Head and neck

Thyroid gland :

- ID
Arterial supply :-
- superior thyroid art. from ECA supplies the superior part –
- Inferior thyroid art. from thyrocervical trunk from
subclavian art. supplies the inferior part
-Thyroida ima art.(10%) from the aortic arc

Venous drainage :

- superior thyroid vein to IJV

- middle thyroid vein to IJV
- inferior thyroid vein to lt. brachiocephalic vein.

Lymphatic drainage :
to (pre-laryngeal,pre-tracheal,para-tracheal,upper and lower
deep cervical,brachiocephalic ) lymph nodes.

Strab muscles: infrahyoid muscle

Deep: sternothyroid,thyrohyoid
Superficial: sternohyoid , omohyoid
Nerve supply: all parts by ansa cervicalis c1 to c3 except for thyrohyoid which is innervated
by c1
 Action: depress the hyoid bone and larynx during swallowing and speaking

Embryology of thyroid :
The thyroid gland develops from the foramen caecum ( 2/3 along the length of tongue from
the tip) to pass forward and loop around beneath the hyoid bone
Incomplete descent ------> lingual or pyramidal thyroid
Incomplete closure of the pathway of descent --------> thyroglossal cyst

Vertebral level of thyroid cartilage: c4

Why thyroid moves up with deglution:

As the thyroid gland present within the pretracheal fascia which is attached to the thyroid cartilage
and hyoid bone , when the diagastric muscle contract it pulls the hyoid bone upward which pulls the
the thyroid cartilage which pulls the pretracheal fascia with its contents

Commonly injured nerves during thyroidectomy:

ELN (close to the superior thyroid art.)
RLN( close to the inferior thyroid art.)
Cervical sympathetic chain ( lateral ligature of the inf. Thyroid artery trunk causing ischemia induced
neural damage)

Papillary thyroid cancer is the only type to spread lymphatically

Cell origin of medullary carcinoma ....> parafollicular c cells

Late complications of thyroidectomy: hypothyroidism , hypocalcemia

Larynx

. Nerve supply:
Motor ----- > all laryngeal muscles are supplied by RLN except for cricothyroid m. Which is
supplied by ELN (branch of SLN) from the vagus

Sensory----- >above vocal cord------- > ILN (from SLN)

Below vocal cord-------- > RLN (from vagus)

. . Attachements of vocal cords:

Ant.------> thyroid cartilage

Post.-----> arytenoid cartilage

Lat.-------> laryngeal m.

Med.------> free border

. Oppening vocal cords: by the 2 post. Cricoarytenoids by externally rotating the arytenoids

.Closing the larynx during swallowing: : by lateral cricoarytenoid m.

. Tensing vocal cords: by the 2 cricothyroid m.

. Cricothyrodotomy------> crcothyroid membrane ( between thyroid and cricoid cartilage)
Parathyroid
. Location: on the post. aspect of the thyroid gland 2 on each side
. Hormone secretion: parathormone which plays a role in cacium homeostasis
. Embryology: inferior parathyroid ------> 3rd branchial arch with the thymus
Superior parathyroid -----> 4 th branchial arch
. Blood supply: inferoir thyroid artery

RLN
. Supplies all laryngeal muscles except cricothyroid m. And gives sensory innervation of the
mucuous membranes of the larynx below the vocal cords
. Injury on one side during thyroidectomy may lead to hoarsness of voice
. Bilateral injury may lead to :
* partial ( midline ) -----> respiratory compromise
* full (half abducted) -----> the patient will not be able to speak or cough

Skull
. Age cranial sutures ossify: by 18 to 24 months
. If fused at birh; craniosynostosis
. Mastoid bone develops: by the age of 2 years
. diploic veins: veins found in the skull that drain the diploic space to the dural venous sinus
. Pterion: ID

bones forming: frontal,parietal,temporal,sphenoid

Clinical signficane; middle meningeal art. runs behind and injury here may lead to
extradural hematoma
.TMJ: synovial joint (hinge)
Articulating surfaces: head of the mandible+ mandibular fossa of the temporal bone
Movements: opening,closing,protrusion,retrusion, side to side)
. Layers encounterd on pterional burrholing: (scalp+temporalis m.)
*skin *connective tissue * aponeurosis of occiptofrontalis m. * loose areolar tissue. *
temporalis m.
* periosteum
. Foramina:
 * foramen lacerum : - inf. part is occlude by a fibrocatilage and doesn't transmit any vessels or
nerves.
- sup. part transmits .internal carotid art.
. Greater and deep petrosal nerves before they enter
the ptrygoid canal.
* foramen rotundum: (c5v2) maxillary division of the trigiminal nerve
* foramen ovale: ( MALE) .mandibular division of trigiminal n.
. Accessory meningeal art.
.lesser superficial petrosal n.
.emissary veins from ptrygoid plexus to cavernous sinus
* foramen spinosum: middle meningeal art.
* optic canal: . Optic nerve (+ 3 layers of dura)---> infection of meninges is seen as papilledema
. Ohthalmic art.
. Sympathetic nerves
*superior orbital fissure:(3,4,5,6)
. Occulomotor n.
.trochlear n.
. Ophthalmic n. ( nasociliary,frontal,lacrimal)
. Abducent n.v
 * stylomastoid foramen:
Facial nerve

* foramen magnum:
Veseles: Nerves : Tissues :
-tectorial
-vertebral artteries -spinal root of accessory n. membranes
- lower end of medulla -apical ligament
- ant. And post. Spinal arteries oblongata of the
dens
*jugular foramen: (give voice to america)
- glossopharyngeal n. - internal jugular vein
- vagus n. - inferior petrosal sinus
- accessory n
*Middle cranial fossa:

.ID
. Boundaries: ant.-----> lesser wing of sphenoid+ ant. Clinoid process
Post.----->petrous part of temporal bone+ dorsum sellae
Laterally------>squamous part of the temporal bone
. Contents: the temporal lobe

ID :
. Trigiminal impression ID for trigiminal ganglion
. Squamous part of the temporal bone
. Tegmen tympani
. Frontal crest
. Clivus
. Groove for the transverse sinus
. Internal occipital protuberance
. Hypoglossal canal
* ethmoidal sinus ID ( skull x-ray)
* Coronal suture ID ( skull x-ray)
* carotid canal : (SIDE)
. Sympathetic plexus around arteries
. Internal carotid artery.
. Deep petrosal nerve
. Emissary veins

* Cavernous sinus:
. There are 2 cavernous sinuses each lying laterally on either side of the sella turcica.
.draining blood from: * sup. ophthalmic veins + facial vein
*emisary veins from ptrygoid plexux.
*sphenoparietal sinuses

.drains blood to: *superior and inferior petrosal sinuses.

*IJV
* intercavernous sinus
.contents:

Contents :
O -occulomotor n. - ICA
CAT. -trochlear n. - abducent n.
O -ophthalmic n.
M -maxillary n.

. Cavernous sinus thrmbosis :

Due to infections from the dangerous area of the face ( drained by ophthalmic and facial veins)
may soread to the cavernous sinus as the draining veins are valveless
Signs of thrombosis: - painful swelling of the eye - 3rd,4th,5th,6th cranial palsies
- gradual loss of vision
- ID Temporalis muscle
Blood supply: deep temporal arteries( ant. and post.) from maxillary artery
What supplies the scalp over the temporalis muscle? Superficial temporal artery from ECA
A. Sphenoparietal sinus
B. Intercavernous sinus
C. Sigmoid sinus
D. Occiptal sinus
E. Confluence of sniuses
F. Basilar plexus
G. Transverse sinus
H. Superior petrosal sinus
I. Inferior petrosal sinus
J. Cavernous sinus
K. Superior sagittal sinus
 DURAL VENOUS SINUSES

4 unpaired + 6 paired sinuses

Sinus Site Drain from Drain to

Superior border of the -superior cerebral vein

Superior sagittal sinus falax cerebri -diploic veins Confluence of sinuses
-emissary veins

Inferior border of falax Medial part of cerebral

Inferior sagittal sinus cerebri hemispheres Straight sinus

-great cerebral vein

Straight sinus Superior border of - inferior sagittal sinus Confluence of sinuses
tentorium cerebelli

Occipital sinus Inner surface of the Internal vertebral venous Confluence of sinuses
occipital bone plexuses

Sphenoparietal Lesser wing of the Superior cerebral vein Cavernous sinus

sphenoid

Superior aspect of the -cerebellar veins

Superior petrosal petrous part of the -inferior cerebral vein Sigmoid sinus
temporal bone -labrynthine veins
( superior petrosal - cavernous sinus
sulcus)

Inferior petrosal Between the petrous part Cavernous sinus Sigmoid sinus
of the temporal bone and
the basilar part of
occipital bone(inferior
petrosal sulcus)

Transverse sinus Groove of the transverse Confluence of sinuses Sigmoid sinus

sinus on the inner aspect
of the occipital bone
( transverse sulcus)

Floor of the posterior -transverse sinus Jugular pulp to IJV

Sigmoid sinus cranial fossa -inferior petrosal sinus
( sigmoid sulcus)

Cavernous sinus See above

Boundaries of the posterior cranial fossa:
Ant.: The apex of the petrous part of the temporal bone
Post. : occipital bone
Lat.: squamous + mastoid parts of the temporal bone

Bones forming posterior cranial fossa:

Occipital bone + temporal bone

ID Internal auditory meatus (IAM)

Structures passing through:
Facial nerve, vestibulochoclear nerve
What can make irreversible damage to vestibulochoclear nerve: accoustic neuroma
Why patient with acoustic neuroma hear sounds loudly on affected side: affection of facial nerve with
paralysis of stapedius
What is the cranial nerve tracks on the clivus: Abducent nerve
What is the name of the juvenile structure that form the clivus: spheno-occipital synchondrosis
Begnin tumours of the posterior cramial fossa:
, , Medulloblastoma, Ependymoma and ependymoblastoma
. Foramina to be identified on the skull:
Middle cranial fossa: .superior orbital fissure . Optic .foramen
canal rotundum
. Foramen . Foramen
. Foramen ovale spinosum lacerum
+ petrous part of temporal bone + trigeminal impression+
IAM
. Tegmen tympani
. Clivus
External surface of the base of the
skull:
. Carotid canal .jugular foramen .foramen magnum
. Stylomastoid
foramen . Hypoglossal canal

. Muscles attached to the styloid process:

- styloglossus - stylohyoid -stylopgaryngeus.
-
- . Causes of lytic skull lesions:
-lytic skeletal metastasis -multiple myeloma - paget's disease - sarcoidosis -
osteomyelitis -hemangioma

Tongue:
.Nerve supply(general + taste):
Post 1/3: general plus taste-----> glossopharyngeal nerve
Ant. 2/3: general----> lingual nerve Taste----> chordatympani nerve
.Extrinsic muscles: SHPG
stylo,hyo,palato,geni (glossus)

. Muscle retracting the tongue: styloglossus

.Nerve supply: all by hypoglossal nerve except for the palatoglossus by vagus nerve

Facial nerve:
Intra-cranial Course: origin between pons and medulla -----> IAM -----> facial canal(petrous part of
temporal bone)-----> exit through the stylomastoid foramen
 Branches in the face: THE ZEBRA BUGGED MY CAT
( temporal,zygomatic,buccal,marginal mandibular,cervica

Spinal accessory nerve:

. ID
 . Surface anatomy: it crosses the post.triangle of neck between the point of the junction between
upper 1/3 and lower 2/3 of the sternomastoid to the junction between upper 2/3 and the lower 1/3 of
the trapezius
. Supplies: trapezius( shrug the shoulder)
Sternomastoid ( turns the head to the contralteral side)

. Great auricular nerve: ID

Supply: (c2-c3)
- skin over the angle of the mandible
- skin over the parotid gland
- skin of the lower 1/2 of the auricle

Parotid gland:
.ID
.surface anatomy:
*upper end: curved line from the tragus to the center of mastoid bone
* posterior border: straight line from the center of the mastoid process to a point 2 cm below and
behind the angle of the mandible
* Ant. Border: al aline from the tragus of the ear to the center of the posterior border of the
masseter then to the point 2 cm below and behind the angle of the mandible
.parotid duct:
*ID
*surface anatomy: the middle 1/3 of a line drawn between intertragic notch to the middle of the
philtrum
* opens by piercing buccinator m.oppsite the upper 2nd molar tooth
* Blood supply: arterial ----->branches from ECA within the gland
* Venous-----> to the retromandibular vein
* Parasympathetic ganglion supplying parotid: otic ganglion
* Structures passing through: from superficial to deep
1-facial nerve and its branches
2-retromandibular vein formed by the union of maxillary vein and sperficial temporal vein.
3-external carotid artery with its 2 terminal branches( maxillary artery and sperficial temporal art.)
4- auriculotepmoral nerve.
5- deep parotid lymph nodes
*type of parotid salivary secretions: serous
* dd of parotid lump: .infection(parotitis,mumps)
.obstructed duct( calculus or ext. compression)
.neoplasm(pleomophic adenoma,wartin tumour)
. Deep parotid lymph nodes

* frey syndrome: damage of the parasympathetic fibers from the auriculotemporal nerve resulting
in excessive gustatory sweating in response to salivary stimulus

*lymphatic drainage : to deep,and superficial parotid lymph nodes

Triangles of the neck:

Anterior triangle Posterior triangle

Post.: ant.border of the sternomastoid Post.:ant.border of the trapezius

Ant.: midline of the neck Ant.: post.boder of sternomadtoid
Sup.:lower border of the mandible Inf.:middle 1/3 of clavicle
Divided by( diagastric m.+ sup. belly of omohyoid )to:
diagastric ,carotid,muscular,1/2 submental triangles
External carotid artery:
* ID
* course: begining-----> one of the 2 terminal branches of CCA at the upper border of the thyroid
carilage (c4)
termination---->behind the neck of the mandible inside the parotid gland by dividing into
superficial temporal and maxillary branches
* nerve passing ant.to it : hypoglossal nerve
Branches: Some American Ladies Found Our Pyramids Most Satisfactory
*
-superior thyroid a. -
ascending pharyngeal art. -
lingual art.
- facial art.
- occipital artery.
-post. Auricular.art. -
maxillart art.
- superficial temporal art.
* carotid body:
on the post.aspect of the bifurcation of CCA contains
chemoreceptors sensitive to changes in PH
* carotid sinus:
the carotid sinus is a dilated area at the base of the internal carotid artery just superior to the
bifurcation of the internal carotid and external carotid at the level of the superior border of thyroid
cartilage. It contains baroreceptors for maintaining blood pressure
Muscles of mastication: masseter,temporalis,lat. ptrygoid,medial ptrygoid
Muscles of opening the mouth: DLGM diagastric, lateral ptrygoid, genihyoid,mylohyoid

Regions drained by pre-auricular lymph nodes: -

upper half of the face
-temporal region
-auricle and external auditory meatus -
gums

microscopic picture of malignant melanoma lymph node metastasis ( note pigmented cells)
Facial art. ( can be palpated as it crosses the inferior border of the mandible adjacent to the
anterior border of the masseter)

Submandibular duct -----> opens in the floor of the mouth on either side of the lingual frenulum
Submandibualr gland type of secretion----> mucous+serous
Nerves at risk of injury on submandibular gland exicion:
.lingual nerve.(above)
.hypoglossal nerve ( below)-----> deviation of the tongue to the affected side on protrusion
.marginal mandibular branch of facial nerve.

NEUROANATOMY:

ID vessels on cerebral angiogram:

A--------->internal carotid art.
B--------->ant.communicating art.
C--------->ant.cerebral art.
D--------->middle cerebral art.
F--------->post.communicating art.
E--------->basilar art.
*ICA enters the skull through the carotid canal in the petrous part of temporal bone
*what branch gives off before ACA,MCA? Ophthalmic art.
*berry aneurysm rupture: subarachinoid hemorrhage
*signs of MCA infarct: -hemiplegia of the lower 1/2 of the contralateral face -
hemiplegia of the contralateral upper and lower extrmities
- aphasia if in the dominant hemisphere
* vertebral artery: .enters the skull through the foramen magnum
* .crosses transversly across the post.arch of the atlas
*vertebral artery course?
Inside the skull, the 2 vertebral arteries pass upwards , forwards and medially in the
subarachinoid space to reach the anterior aspect of the medulla oblongata, then
they unite together at the lower border of the pons to form the basilar artery
What the vertebral artery and basilar artery supply in the brain?
The vertebrobasilar arterial system perfuses the medulla, cerebellum, pons,
midbrain, thalamus, and occipital cortex

Roof of the middle ear : tegmen tympani

How middle ear infections cross the skull: by direct erosion of

tegmen tympani It may also spread to mastoid air cells causing
mastoiditis
C/ p of meningism: photophobia, neck stiffness, fever

Which vein drain the dangerous area of the face: inferior ophthalmic vein

Difference between UMNL and LMNL facial palsy?

In upper motor neuron lesion upper part of face will be spared, only lower part will be
affected but in lower motor neuron lesion both upper and lower part of face will be
affected.
Relations of the middle ear?
Arnold chiari malformations:
is a condition affecting the brain. It consists of a downward displacement of the cerebellar tonsils
through the foramen magnum causing non-communicating hydrocephalus as a result of
obstruction of cerebrospinal fluid (CSF) outflow.

The only cranial nerves that transmit parasympathetic fibers are the oculomotor, facial,
glossopharyngeal, and vagus nerves

ID parasagittal hyperdense mass in ------> meningioma

Where it arise from: They arise from the arachnoid "cap" cells of the arachnoid
villi in the meninges
- id. Tentorium cerebelli
- Ant. Attahement: superior angle of the petrous part of the temporal bone
- id optic nerve
- Id ICA
- Id optic chiasm
- id oculomotor nerve

Muscles supplied by occulomotor nerve :

* superior rectus m.
* Levator palpebrae superioris
* Sympathetic fibres to Muller's muscle
* Inferior rectus m.
* Inferior oblique
* Medial rectus
* Sphincter pupillae

Paralysis of oculomotor nerve leads to :

* The eye will be displaced outward and displaced downward; outward because the lateral rectus
(innervated by the sixth cranial nerve) maintains muscle tone in comparison to the paralyzed
medial rectus. The eye will be displaced downward, because the superior oblique (innervated by
the fourth cranial or trochlear nerve), is unantagonized by the paralyzed superior rectus, inferior
rectus and inferior oblique.
* The affected individual will also have a ptosis, or drooping of the eyelid, and mydriasis (pupil
dilation).

What is the exact structure on which the occulomotor nerve is pressed against?
Petrous part of the temporal bone

Blood vessel supplying the inner table of temporal bone: middle meningeal artery
If there is a tumour in the precentral gyrus , what is the bone to penetrate?
Parietal bone

What is the aggressive form of glioma: glioblastoma multiforme (GBM)

 Spine and limbs

Other than the fracture , what are the abnormal signs in this radiograph:
1-abnormal alignment( the distance between the dens and the lateral masses of c1 on
both sides is not equal
2-prevertebral soft tissue swelling due to fracture edema

Page 1
Ligaments attached to the odontoid process:
- transverse Atlantal ligament
- Apical odontoid ligament
- Alar ligament

Type of Atlanto axial joint: synovial pivot

Ligaments between C1 and C2:

- ant. Atlanto axial ligament
- Post. Atlanto axial ligament
- Transverse ligament

1st spinous process to be felt: of C7 ( has a long spine = vertebra prominence )

Demonstrate it on the subject

Why we can not feel the upper spinous processes:

As they are short, bifid and attached to the nuchal ligament

Page 2
Atypical cervical vertebrae and the atypical features:

C1( atlas): no body , no spine

C2( axis): body projects upwards to form the ofontoid process, thick spine
C7(vertebra prominence): very long spine, smaller foramen transversium

How many vertebrae make the spinal column: How many spinal nerves:
7 cervical. 8 cervical
12 thoracic. 12 thoracic
5 lumbar 5 lumbar
5 fused sacral. 5 sacral
3 fused coccygeal. 1 coccygeal

Lumbar vertebrae:

Page 3
Intervertebral foramen: structures passing

- the root of each spinal nerve,

- dorsal root ganglion,
- the spinal artery of the segmental artery
- communicating veins between the internal and external plexuses,
- recurrent meningeal (sinu-vertebral) nerves
- transforaminal ligaments.

Level of the lumbar puncture: L4/L5. ( at the supracrestal line)

Layers to pass through:

- skin,sc fat, fascia
- Supraspinous ligament
- Interspinous ligament
- Ligamentum flavum
- Epidural space
- Dura matter
- Arachinoid matter
Page 4
- CSF

IV disc anatomy:
Internal nucleus pulposus surrounded by fibrocartilagenous annulus fibrosus

Type of IV joint: secondary cartilagenous joint

Movement on lumbar vertebrae:

Flexion, extension, lateral flexion, axial rotation
Level of the spinal cord in newborn and adult:
L3 ( at birth) , L1/2(adult)

Contents of the spinal canal below L2:

Cauda equina

Location of the paravertebral venous plexus:

- anterior external vertebral venous plexus, the small system around the vertebral bodies;
- posterior external vertebral venous plexus, the extensive system around the vertebral
processes;
- anterior internal vertebral venous plexus, the system running the length of the vertebral
canal anterior to the dura
- posterior internal vertebral venous plexus, the system running the length of the vertebral
canal posterior to the dura

Contents of epidural space:

Page 5
space contains lymphatics, spinal nerve roots, loose connective tissue, fatty tissue, small
arteries, and a network of internal vertebral venous plexuses

How does spinal mets happen:

- Spread from primary tumors is mainly by the arterial route

- Retrograde spread through the Batson plexus .
- Direct invasion through the intervertebral foramina .

Tumours metastatising to the spine:

Lung - 31%
Breast - 24%
GI tract - 9%
Prostate - 8%
Lymphoma - 6%
Melanoma - 4%
Unknown - 2%
Kidney - 1%
Others including multiple myeloma - 13%

Demonstrate the boundaries of the post . Triangle on a subject:

Demonstrate the hyoid bone(c3) and the cricoid

cartilage(c6) on a subject:

Page 6
Structures found at c6:
- termination of the pharynx and begining of the oesphagus
- Termination of the larynx and begining of the trachea
- Entry of the vertebral artery to the foramen transversium
- Intermediate tendon of omohyoid crosse the carotid sheath
- Middle thyroid vein emerging from the thyroid gland
- Inferior thyroid artery entering the thyroid gland

Demonstrate where brachial plexus run on a subject

Upper limb:
Brachial plexus:

Page 7
Page 8
Where are parts of brachial plexus found:
- roots: exits from iv foramina between scalenus ant. And medius
- Trunks: base of the post. Triangle of the neck behind the 3rd part of subclavian artery
- Divisions: behind middle 1/3 of the clavicle
- Cords : related to the 2nd part of axillay artery

Erb's paralysis:

- damage to the uppert nerve roots (c5,c6)

- Motor affection: ( waiter's tip deformity)
* paralaysis of arm abductors( supraspinatous + deltoid) ------> arm adduction
* paralysis of arm external rotators( infraspinatous +teres minor) ------> arm internal
rotation
*paralysis of forearm flexors and supinators( biceps ,brachialis, brachioradialis) ------->
forearm extension and pronation
- sensory affection: loss of sensation of radial side of arm and forearm

Klumbek's paralysis:
- injury to lower trunk ( C8,T1)
- Motor affection: (claw hand deformity)

* paralysis of all intrinsic muscles of the hand

* Paralysis of wrist flexors( except flexor carpi radialis)
* Hyperextension of MCP joints with flexion of IP joints

- sensory affection: loss of senastion over ulnar border of forearm and hand

Page 9
Page 10
Articulate
humerus, radius
and ulna:

-Capitulum of the
humerus + radial
head
-trochlea of the
humerus +
trochlear notch of
the ulna
-olecranon of the
ulna+ olecranon
fossa of the
humerus
Page 11
Muscles flexing the elbow joint:
- biceps ,brachialis, coracobrachialis
- Brachioradialis,pronator teres,flexor carpi radialis

Strucutres passing in spiral groove:

- radial nerve, profunda brachii vessels

C/p of radial nerve injury at the spiral groove:

- paralysis of wrist extensors ------> wrist drop

- Paralysis of finger extensors ------> finger drop
- Loss of sensation in the 1st web space

Supracondylar fracture humerus:

Associated injuries:- - brachial artery injury( absent distal pulses)

- Anterior interosseus nerve injury( unable to flex the interphalangeal

joint of his thumb and the distal interphalangeal joint of his index finger)
- Ulnar nerve injury ( claw hand)
- Radial nerve injury ( wrist drop,finger drop)

Page 12
ID Median nerve , ulnar nerve

Median nerve sensory distribution in the hand:

a) lateral 2/3 of the palm of the hand
b) lateral (radial) three and a half digits on the palmar side
c) dorsum of the tips of index, middle and thumb

Median nerve motor distribution in hand :

LOAF muscles:

Page 13
Lateral 2 lumbricals, oponence policis, abductor policis brevis, flexor policis brevis

C/p of median nerve injury at elbow:

Ape - like hand:

- Hyperextended thumb( paralysis of FPB)
- Adducted thumb( paralysis of abductor policis brevis)
- Flat thenar eminence
- Loss of sensations from:
- * lateral 2/3 of the palm of the hand
* lateral 31/2 digits ( palmar and distal dorsal aspect)

C/p of ulnar nerve injury at wrist: ( complete claw hand)

- clawing of the 4th and 5th digits ( paralysis of the medial lumbricals and interosseii)
- Loss of sensation of the medial 1/3 of the palmar and dorsal aspects of hand and
fingers

Why ulnar paradox:

In proximal ulnar nerve injuries, there will be paralysis of the medial 1/2 of the FDP which
will decrease flexion of the IP joints

ID Ulnar art., radial art., superficial palmar arch

Page 14
Superficial palmar arch: formed mainly by the arch of the superficial division of the ulnar
artery and is completed by the superficial palmar branch of the radial artery

ID carpal bone

Navicular bone blood supply:

It receives its blood supply primarily from lateral and distal branches of the radial artery, via
palmar and dorsal branches. These provide an "abundant" supply to middle and distal
bone, but neglects the proximal portion, which relies on retrograde flow
Attachement of flexor retinaculum:

Proximal: pisiform+ tubercle of scaphoid

Distal: hook of hamate + trapezium

Structrues passing through carpal tunnel:

- 4 tendons of flexor digitorum superficialis
- 4 tendons of flexor digotorum profundus
- 1 tendon of flecor policis longus
- 1 tendon of flexor carpi radialis
- Median nerve.

Page 15
Page 16
How to test FDP:
By fixing the PIP

How to test FDS:

adjacent digits must be held in extension, in order to eliminate FDP motion in adjacent
fingers, which otherwise might give the impression of FDS motion in the examined finger

Where are tendons of FDS and FDP insert?

FDS: splitted tendon on both sides of the middle phlanax
FDP: passes throgh the splitted tendon of FDS to be inserted into the terminal phalanx

How to test ulnar artery( allen' s test):

- elevate the hand and ask the patient to make a fist for 30 sec..
- Apply pressure on both ulnar and radial aa. To occlude both
- While still elevated, open the hand, it should be blanched
- Release pressure over the ulnar artery, colour should return in 7 seconds

Page 17
Page 18
Structures attached to the coracoid process:
1- ligaments: coracoclavicular- coracohumeral- coravoacromial
2- muscles: pectoralis minor( insertion)'- coracobrachialis( origin)- short head of
biceps( origin)
Page 19
Rotator cuff muscles:
Supraspinatous:
Origin : supraspinous fossa Insertion : greater tubrosity. N. Supply: suprascapular n.

Infrainatous:
Origin: infraspinous fossa. Inserion: greater tubrosity. N.supply: suprascapular n.

Teres minor:
Origin: upper 2/3 of lateral border of scapula. ( dorsal aspect)
Insertion: greater tubrosity
N.suuply: axillary n.

Subscapularis:
Origin: sbscapular fossa. Insertion: lesser tubrosity. N.supply: upper and lower
sbscapular n

Muscles inserted in bicepital groove : ( lady bw 2 majors)

- teres major: ( medial lip)
- Latismus dorsi(floor)
- Pectoralis major( lat. lip)
Page 20
Tendon of long head of biceps lies in the groove

Page 21
Shoulder joint abduction:
- supraspinatous ( 0-15)
- Deltoid ( middle fibres) 15-90
- Trapezius and serratus anterior ( over 90): which will require upward rotation of the
scapula with lateral rotaion of the humerus

Factors decreasing the stability of the shoulder joint:

1- shallow glenoid cavity

2- lax capsule with few ligaments
3- inferior aspect is not supported due to the presence of quadrangular space

The main stabilizer of the shoulder joint is the rotator cuff muscles

Page 22
Quadrangular space:
- sup. : teres minor
- Inf. : teres major
- Lat.: durgical neck of humerus
- Med. : long head of triceps
- Contents: axillary n.--post. Circumflex humeral vessels.
-
Axillary nerve:
Motor : deltoid + teres minor
Sensory: skin to the lower half of deltoid ( badge area)
Injury: inability to abduct the shoulder over 15, loss of sensation over the badge area

Pectoralis major:
Origin :
Clavicular head: from the medial half of the anterior surface of the clavicle
Sternocostal head: ant. Surface of the sternum- upper 6 costal cartilages- EOA

Insertion:
Lateral lip of bicepital groove

Nerve supply: medial ( c8-T1) and lateral pectoral nerve ( c5-c7)

Action:
- adduction and medial rotation of the arm( the whole muscle)
- Clavicular head: flexion of the arm
- Sternocostal head: extends the flexes arm
- Acts as accessory respiratory muscle by elevating the ribs

Axillary artery: divided by pectoralis minor to 3 parts: [ screw the lawyer save a patient]

- 1st part: medial to pectoralis: superior thoracic artery

- 2nd part: behind the pectoralis: thoracoacromial, lateral thorcic
- 3rd part: lateral to pectoralis: ( subscapular, ant.circuflex humeral, post, circumflex
humeral)

Cubital fossa:
Boundaties:
- superolateral: bravhioradialis muscle
- Medially: pronator teres
- Floor: brachialis
Contents: (M--L)

- median nerve
- Brachial artery
- Biceps tendon
Page 23
.upper limb reflexes:

1. Biceps reflex (C5/6) – located in the antecubital fossa -tap your finger overlying the
triceps tendon

2. Triceps reflex (C7) – place forearm rested at 90º flexion

3. Supinator reflex (C6) – located 4 inches proximal to base of the thumb

Biceps muscle:
Origin:
- long head : ( supraglenoid tubercle)
- Short head ( coracoid process)
Insertion:
- biceptal tendon into radial tubrosity
Relation to tendon:
Median nerve , brachial aa.( medially)
Radial nerve ( lateral)
N.supply: musculocutaneous nerve
Page 24
Triceps muscle:
Origin:
Long head: infraglemoid tubercle
Lat . Head: anove the spiral groove
Med. head: below the spiral groove
Insertion:
Olecranon
N.supply: radial nerve

Trapezius muscle:
Origin: ext.occipital protuberance,superior nuchal line ,spinous process of c7, spinous
processes of all thircic verterae
Insertion: lateral 1/3 of clavicle,medial acromion, aponeurosis over the spine of the scapula
N.supply: spinal accessory n.

Serratus anterior:

Origin:
9-10 slips from the 1st to 8 th ribs
Insertion:
Medial border of scapula
N.supply:Long thoracic nerve of bell( c5,c6)

Lower limb:

ID foot bones:

Page 25
Arches of the foot:

What are the components of the Medial Longitudinal arch?

Bones - calcaneum, talus, navicular, all 3 cuneiforms, medial 3 metatarsals

Ligaments - Interosseous and spring ligaments

Muscles - flexor hallucis longus, digitorum longus and brevis; tibialis anterior and posterior

What are the components of the Lateral Longitudinal arch?

Bones - Calcaneum, cuboid and lateral 2 metatarsals

Ligaments - long and short plantar ligaments

Muscles - peroneus longus; flexor digitorum longus and brevis (to 4th and 5th digits)

What are the components of the Transverse arch?

Bones - the bases of all 5 metatarsals (each foot actually forms one half of an arch)

Ligaments - interosseous

Muscles - peroneus longus

Page 26
ID ligaments on the medial and lateral aspects of the ankle:

Attachements of deltoid ligament:

Superior: medial malleolus

Inferior: 1- tubrosity of the navicular. 2- spring ligament. 3- neck of talus. 4- sustanecukum tali

5- body of talus

Page 27
What movements occur at the subtalar joint?

Inversion and eversion of the foot occur at the subtalar joint.

Which muscles perform these actions?

Inversion - Tibialis anterior and posterior (with some help from the extensor and flexor hallucis longus muscles)

Eversion - Peroneus longus and brevis

What is the type of the subtalar joint: synovial( ball and socket)

What are the bones forming ankle joint: ( synovial-hinge)

Trochlear surface of talus, lower end of tibia and fibula

Movements at the ankle joint:

Plantar flexion: gastrocnemius ,soleus. Plantaris. + tibialis post. , flexor didgitorum longus, flexor jalicius
longus

Dorsiflexion: tibialis ant., extensor halicius longus, extensor digitorum longus, proneus tertius

Ankle joint is most stable in dorsiflexion why?

Dorsiflexion is more stable than plantarflexion. The talus is stabilized due to the wider anterior side of the
trochlea being immobilized by the tibial articulation. In plantarflexion, the narrower posterior side is articulating
more and so more movement is possible since it does not completely fill the space allowed the anterior side.

What is the type of inferior talofibular joint? Syndsmosis

Associated injury in syndesmotic fracture: fractures lateral mallelus

Where to palpate dorsalis pedis and post. Tibial aa:

Lateral to the EHL tendon---- halfway between the post.border of the medial mallelus and tendoachilles

Structures passing behind the medial malleolus: (TOM DOES VERY NICE HATS)

- tibialis post . Tendon. - flexor digitorum longus tendon. - post. Tibial vessels.

- Post. Tibial nerve. - FHL tendon

Demonstrate the foot pulses on this actor

The dorsalis pedis pulse is found between the first two metatarsal bones

The posterior tibial pulse is found 2-3cm below and behind the medial malleolus
Page 28
Page 29
Point to the Achilles tendon

What muscles make this up?

Three muscles insert into the Achilles or calcaneal tendon:

Soleus
Gastrocnemius
Plantaris

ID tendons on the dorsum of the foot:

What nerve supplies the muscles in the posterior compartment of the leg?

The tibial nerve supplies the posterior compartment of the leg including plantaris, soleus and gastrocnemius
muscles; the muscles of the superficial posterior compartment and flexor hallucis longus, flexor digitorum
longus and the muscles of the deep posterior compartment: tibialis posterior and popliteus.

Where would you test sensation of:

S1
L4
Deep peroneal nerve
Superficial peroneal nerve
Sural Nerve
Page 30
S1 is tested on the lateral aspect of the foot

L4 is tested over the medial malleolus

The deep peroneal nerve is tested at the first web interspace

The superficial peroneal nerve is tested over the dorsum of the foot, other than the first web interspace

The sural nerve is tested over the lateral malleolus

What movements does extensor hallucis longus perform?

It extends the big toe, dorsiflexes the foot and assists with inversion of the foot.

What vessels would you find deep to extensor hallucis longus?

The anterior tibial artery and vein

And what nerve that lies deep to it?

The deep peroneal nerve

On an actor demonstrate how you would test the knee and ankle reflexes.

Knee reflex: The foot should be unsupported, relaxed and off the ground. The thigh should be fully exposed.

Test by tapping the patellar tendon with a tendon hammer. You are looking for reflex contraction of the
quadriceps muscles.

Ankle reflex: The foot should be pointing laterally, be flexed, and relaxed. the leg should be fully exposed.

Test by tapping the Achilles tendon with a tendon hammer. You are looking for reflex contraction of the calf
muscles.

What nerve roots do these reflexes originate from?

Page 31
Ankle: S1
Knee: L3/4

What movement is ankle dorsiflexion?

Dorsiflexion is the upwards movement of the foot in relation to the leg

At what joint does dorsiflexion occur?

At the ankle joint between the tibia/fibula and the talus

What muscles are involved in dorsiflexion?

Muscles of the anterior compartment of leg are involved:

Tibialis anterior
Extensor hallucis longus
Extensor digitorum longus
Peroneus tertius

What nerve supplies the anterior compartment of the leg?

The deep peroneal nerve

How would you demonstrate ankle plantarflexion?

Plantarflexion is the downwards movement of the foot in relation to the leg.

What muscles are involved?

Both the superficial and deep posterior compartments of the leg are involved

Superficial posterior compartment:

Page 32
Gastrocnemius
Soleus
Plantaris (only weak participation)

Deep posterior compartment:

Flexor hallucis longus

Flexor digitorum longus
Tibialis posterior
Popliteus

What action occurs when tibialis anterior and tibialis posterior contract together?

Ankle inversion

At what joint does this occur?

Inversion and eversion both occur at the subtalar joint

What muscles are responsible for ankle eversion?

Peroneus brevis and peroneus longus

Which nerve innervates them?

The superficial peroneal nerve

What motor and sensory function is lost with damage to the superficial peroneal nerve?

Inability to evert the foot and loss of sensation over the dorsum of the foot, apart from the first web space,
which is innervated by the deep peroneal nerve

How many compartments are there in the leg and what structures are in each compartment?

The leg (below the knee as opposed to the thigh) has four components.

The anterior compartment contains four muscles – Tibialis anterior, Extensor hallucis longus, Extensor
digitorum longus and Peroneus tertius – as well as the deep peroneal nerve and the anterior tibial artery and
vein

Page 33
The lateral compartment has two muscles – peroneus longus and brevis, and the superficial peroneal nerve.

There are two posterior compartments of the leg:

The deep posterior compartment contains tibialis posterior, flexor hallucis longus, flexor digitorum longus and
popliteus, as well as the tibial nerve and the posterior tibial artery and vein
The superficial posterior compartment of the leg has three muscles, gastrocnemius, soleus and plantaris as
well as the medial sural cutaneous nerve

The anterior and posterior compartments are separated by the interosseus membrane whilst the anterior and
posterior facial septum separate the anterior compartment from the posterior compartment respectively.

Surface marknigs of EHL:

Demonstrate on the subject the actions of tibialis ant., post. ,peroneus longus,brevis, gastrocnmius, soleus

Page 34
How would you recognise compartment syndrome in the lower leg?

Compartment syndrome is an emergency that presents with pain out of proportion to the injury sustained, in
someone with a swollen leg, particularly acute on passive stretching of the ankle. There may be paraesthesia,
pulselessness and paralysis, all late signs and suggestive of impending limb necrosis.

Orientate and articulate Tibia and Fibula

Page 35
 Describe the blood
supply to the head of the
femur

The majority of the blood

supply to the head of the
femur is from retinacular
arteries, which arise as
ascending cervical branches from the extracapsular arterial anastomosis. This is formed posteriorly by the
medial femoral circumflex artery and anteriorly from branches of the lateral femoral circumflex artery with minor
contributions from the superior and inferior gluteal arteries.

There is also supply from the artery of the ligamentum teres, also know as the artery of the round ligament of
the femoral head (a branch of the obturator artery).

Where do these arteries originate?

The medial and lateral circumflex femoral arteries originate from the profunda femoris

The artery of the ligamentum teres originates from the obturator artery

What muscles attach to the lesser trochanter of the femur?

Psoas major and illiacus attach to the lesser trochanter

Where does the psoas major originate?

Page 36
The deep part of psoas major originates from the transverse processes of L1-L4. The superficial part originates
from the lateral surfaces of T12-L4 and the intervening vertebral discs.

What is the action of psoas major?

Psoas major flexes and externally rotates the hip

Where does the iliotibial tract attach?

The Iliotibial tract is attached to the anterolateral iliac tubercle of the iliac crest proximally and the lateral
condyle of the tibia distally.

What muscles insert onto it?

Gluteus maximus and tensor fasciae lata muscles insert onto the iliotibial

What is its clinical significance?

The iliotibial tract stabilises the knee in extension and in partial flexion. It is important in walking and running

Where else does the gluteus maximus muscle insert?

Onto the gluteal tuberosity of the femur

What is the nerve supply and nerve roots of gluteus maximus?

Gluteus maximus is supplied by the inferior gluteal nerve (L5,S1,S2)

What are the actions of gluteus maximus?

Page 37
Gluteus maximus performs external rotation and extension of the hip

What nerve supplies tensor fasciae lata?

The superior gluteal nerve supplies tensor fascia lata.

Where does the gluteus medius muscle insert?

Onto the lateral surface of the greater trochanter

Gluteus minimus also inserts onto the greater trochanter deep to gluteus
medius.

What is the action of gluteus medius?

Page 38
During standing, it is a hip abductor. During gait, gluteus medius, together with gluteus minimus, support the
body whilst one leg is in the air, preventing the pelvis from dropping to the opposite side

What clinical sign is evident with weakness of gluteus medius and minimus?

A Trendelenburg gait or a positive Trendelenburg test

Damage to what nerve can produce this distinctive gait?

Damage to the superior gluteal nerve

What are the surface markings of the sciatic nerve?

The sciatic nerve (L4,5,S1,2,3) exits the pelvis via the

greater sciatic foramen from below the piriformis
muscle.

The surface marking of the sciatic nerve is a curved line

drawn from 2 points: halfway between the posterior
superior iliac spine to the ischial tuberosity to halfway
between the ischial tuberosity and the greater
trochanter.

Which vessels exit the greater sciatic foramen from

above the

The superior gluteal vessels and nerve exit above

piriformis.

What variations do you know with regard to the

sciatic nerve exiting the pelvis?

In the majority of cases the sciatic nerve exits beneath

the piriformis. Alternatively either the whole nerve may
pass through piriformis, or it may divide high with one
division passing through or around the piriformis

Page 39
ID LOWER LIMB DERMATOMES

ID origin and insertion of quariceps muscle on the skeleton:

Page 40
Quadratus femoris:
Origin : lateral border of the upper part of the ischial turosity
Insertion: quadrate tubercle of the femur
N. supply: nerve to quadratus femoris
Action: lateral rotation of the thigh

Popliteal fossa:

Boundaries:

- upper medial: semimebrnosus

and semitennosus

- Upper lateral: biceps femoris

- Lower medial: medial head of

gastrocnemius

- Lower lateral : lateral heaad of

gastrocnemius

Contents ( superficia to deep):

- common peroneal nerve

- Tiibial nerve

- Politeal vein

- Popliteal artery

Page 41
- Lymph nodes draining the area along the lateral leg and foot along the course of SSV

DD of lump from popliteal fossa:

- backer's cyst. - pop. Artery aneurysm. - lipoma

- Schwanoama. - Popliteal vein varicosities

A- common femoral a

B- lateral circumfkex femoral

C- SFA

D - profunda femoris aa

Page 42
Hamstrings:

Femoral triangle:

Page 43
What are the boundaries of the femoral triangle?

Superiorly: inguinal ligament

Laterally: medial border of sartorius

Medially: medial border of adductor longus

Floor: medially are the pectineus and adductor longus muscles with illiacus and psoas laterally

Roof: fascia lata

Contents:

- femoral nerve

- Common femoral and profuna

- Femoral vein and GSV

What is Hunter's canal?

Hunter's canal, also known as the subsartorial or adductor canal, runs from the apex of the femoral triangle to
the popliteal fossa.

What are the boundaries of Hunter's canal?

Anterolaterally - Vastus medialis

Anteromedially/Roof - Sartorius

Posteriorly - Adductor longus and magnus

What are the contents of Hunter's canal?

Hunter's canal contains:

Femoral artery and vein

Page 44
Saphenous nerve

Nerve to vastus medialis

What is the surface marking of the adductor hiatus?

The adductor hiatus lies 2/3rds along the line between the ASIS and the adductor tubercle of the femur.

What are the surface markings of the femoral artery?

The femoral artery can be palpated at the mid-inguinal point, which lies halfway between the pubic symphysis
and the ASIS

Vascular lacuna : is an anatomical structure placed behind/below the

inguinal ligament. Lacuna vasorum is medially, while muscular lacuna is
laterally.
Contents of lacuna vasorum (order from medial part)
deep inguinal lymph nodes,
femoral vein,
femoral artery,
femoral branch of the genitofemoral nerve.
Page 45
Contents of lacuna musculorum:
Femoral nerve
Iliopsoas
Lateral femoral cutaneous nerve

Page 46
 Trunk and thorax

Abodominal aorta:
.ID
.ID branches supplying GIT
.ID IVC

Page 1
.branches of abdominal aorta:
[Course T12-L4]
T12 -------- >4 cm above transpyloric plane in midline
L4 ----------> supracristal line in midline

Page 2
Surface marking of the transpyloric plane:
located halfway between the jugular notch and the upper border of the pubic symphysis.

Vertebral level Single branches Paired branches

T12 Coeliac trunk Rt.+ Lt. Inf. phrenic aa.

L1 Superior mesentric a. Rt. + lt. Middle supra-renal aa
L2 ---------- Rt. + lt. Renal aa.
L3 Inferior mesenteric a. Rt. + lt. Gonadal aa.
L4 Median sacral a. Rt. + lt. Common iliac aa.

*Posteior branches--------> 4 pairs of lumbar arteries from the back of aorta opposite each vertebral
Level(L1-L4)

*Ant.relations: celiac trunk and

branches,body of the pancreas,SMA,
3rd part of duodenum,root of
mesentry,splenic vein,lt renal vein

*ID branches on mesenteric

angiogram:

A ---abdominal aorta
B --- Rt. common iliac
C---- Lt. Common iliac
D --- Lt. Renal a.
E --- Rt. renal a.
F --- splenic a.
G --- common hepatic
H --- SMA
I --- gastroduodenal a
J---- Lt. Hepatic a.
K --- Rt. hepatic a.
L --- IMA
Page 3
 *ID AAA on CT angiography ------> saccular. Infrarenal
AAA
*Define aneurysm: abnormal dilatation of an artery.
*pathogenesis: median cystic necrosis ( true
aneurysm), post- traumatic ( false aneurysm)
*Causes( risk factors):
-HTN secondary to astherosclerosis secondary to
smoking
-Marfan syndrome
-Syphilis
-bicuspid aortic valve
* dissecting aneurysm: separation of the layers of the arterial wall with propagation of dissection
proximally and distally
* Complications: harmorrhage due to rupture
Ascending aorta---> acute MI
arch of aorta ---> stroke

IVC
*tributaries: (L5-T8)

T8: paired inferior phrenic veins.

T8: hepatic veins (3)
L1: right suprarenal vein.
L1: renal veins.
L2: right gonadal vein.
L1-L5: lumbar veins.
L5: common iliac veins (origin)

Page 4
* ID RT,LT gonadal vein :

* Renal veins( ant. relations) :

Rt side: 2nd part of duodenum
Lt side: body of pancreas,SMA,splenic vein

Page 5
Spleen
* ID
* Blood supply: art.----> splenic art. ( from the celiac trunk)
Venous---> splenic vein to SMV to portal vein
* related ribs: opposite 9th,10th,11th ribs
* Structure to warry during splenectomy: tail of the pancreas
* Describe the course of splenic aa:
Arises from the coliac trunk ----> passes to the left above the upper border of the pancreas ---->
behind the stomach separated from it by the lesser sac-----> lienorena. Ligament-----> ends by
giving up terminal branches inside the hilum of the spleen
It supplies: pancreas, stomach, spleen

Duodenum:
* 4 parts
* Ampulla of vater opens into the posteromedial aspesct of the 2nd part
* Strucutres open in duodenal papilla: CBD+ pancreatic duct
* Blood vessels post. To D1: gastroduodenal vessels
* 2nd , 3rd, 4th parts are retroperitoneal
* Vessels related to the 3rd part of the duodenum:
Ant: SMA.SMV post. : IVC, abdominal aorta

Pancreas:
*parts: head.neck.body and tail
*islet cells produce:
Alpha cells: glucagon
Beta cells: insulin
D cells: somatostatins
*blood supply: ( 3 sources)
1- superior pancreaticoduodenal aa( from gastrduodenal aa)
2- inferior pancreaticoduodenal aa ( from SMA)
3- pancreatic branches ( from splenic aa)
* ducts:
1- main pancreatic duct : drains head,body and tail -----> opens into major duodenal papilla
2- accessory pancreatic duct: drains the uncinate process----> opens into minor duodenal papilla
* vessels encounterd during whipple:
Abdominal aorta,SMA, Lt.renal vein, sup. and inf. pancreatico duodenal aa., splenic vein ,SMV,

Liver and gall bladder:

* the 1st. 2 organs injured in stab epigastrium: Liver ( lt. Lobe), stomach
* What demarcates left and right lobe :
Anatomical: -falciform ligament (ant.), fissure for ligamentum teres and ligamentum
venosum(posteroinferiorly)
Surgical: a line passing from IVC to the fossa of GB
*venous drainage: hepatic veins to IVC
* what art.of the celiac trunk supplies both liver and stomach: hepatic art.( runs in the free border
of lesser omentum to porta hepatis)
*
* ID
-quadrate lobe ( bw the GB and the fissure for ligamentum teres)
- H-shape

Page 6
- porta hepatis: strucure open in:
Ant.: Rt. and Lt.. Hepatic ducts
Intermediate: hepatic art.
Post. : portal vein

- ligament supporting:
1- falciform ligament ( to the diaphragm and AAW)
2- lesser omentum ( to the stomach and 1st part of duodenum)
3- Rt. and Lt. Triangular ligament ( to the diaphragm)
4- upper and lower coronary ligament ( to the diaphragm)

Page 7
 GB :

surface marking: at the angle between the 9th costal cartilage and the lateral margin of the
rectus sheath
Why shoulder pain in cholecystitis:
An inflammed gb may irritate the diaphragm
Roots of phrenic nerve that supply the diaphragm as the same as the suprclavicular nerve
supplying the shoulder tip.

Urinary bladder:
*ID
*Art. Supply: sup. and inf. vesical arteries from the internal iliac art.
Venous drainage: to vesical venous plxus to internal iliac vein
* ID internal iliac art. ( mcmin page 261)
* Nerve supply to detrusor m.:
Sympathetic: inhibit contraction of the muscle ( from L1,L2)
Parasympthetic: stimulate contraction of the muscle ( ftom S2-S4)
* most common bladder cancer:
TCC,SCC, mixed,adenocarcinoma
*c/p of bladder cancer:,painless hematuria
*risk factors of bladder cancer: aniline dyes,smoking,b-naphthalamine, s.hematobium
* how does ureter enters the bladder: at the base of the bladder at the corner of the trigone
* Peritoneal relations of the bladder: covers the superior surface and the upper part of the post.
Surface
* Layers encounterd during suprapubic catheterization:
Skin ,sc tissue,scarpa's ,linea alba,fascia transversalis,preperitoneal fat
* post. Relations of the bladder:
Male: rectovesical pouch+ 2 vas defrens+ terminal part of the 2 ureters
Female: vesicouterine pouch+ terminal part of the 2 ureters

Stomach:
* parts:,fundus,body,pylorus

* Blood supply:
Art. Venous
Lt. Gastric a. From celiac trunk Lt.gastric+ rt. gastric vv.-------> portal vein
Rt. gastric a. From hepatic a. Lt. Gastroepiploic+short gastric vv.>splenic vein
Lt. Gastroepiploic from splenic a. Rt. gastroepiploic v. -----> SMV
Rt. Gastroepiploic from gastroduodenal from hepatic a.
Short gastric a. From splenic a.

Page 8
appendix :
*positions: retrocecal,pelvic,subcecal,pre-ileal,post-ileal
* blood supply: appendicular art. From ileocolic art.
Appendicular vein to SMV

* why appendicitis pain is referred to umblicus:

Pain initially starts in the perimubilical region as visceral pain from the appendix is conveyed in nerve fibres
entering the spinal cord at the T10 level (the T10 dermatome covers the level of the umbilicus).

Irritation of the parietal peritoneum by an inflamed appendix later on causes localisation of pain to the RIF.

ID on a plastic model : uterus,

fallopian tubes, ovaries, douglas
pouch, ceacum, terminal ileum ,
appendix

Diaphragm:

*Openings:
Vena caval Oesphageal
Aortic

T8 T10 T12
central tendon Rt. Crus Behind median arcute ligament
IVC+ rt. phrenic n. Oesphagus+ 2 vagi Aorta,azygous,thoracic duct

Page 9
* attachements:
Origin:

Sternal Costal Vertebral

Xiphoid process(back) Inner surface of the lower 6 costal cartilages .Rt. crus(upper 3L)
.Lt. Crus(upper 2L)
.Median arcuat lig.
(Bw 2 crurae)
. Medial arcuate lig
(Bw the
crus&transverse process of L1)
.lat. arcuate lig.

(Bw the
transverse process of L1& the 12 th rib)
Insertion: in the central tendon

External oblique muscle:

*origin: outer surface of the 5th to 12th rib
* insertion: xiphoid process,linea alba,pubic crest,pubic tubercle,ASIS
* nerve supply: lower 6 thoracic nerves (T7-T12)
* Directions of fibres: downwards ,forwards and medial

Internal oblique muscle:

* origin: lumbar fascia,iliac crest,ing.ligament
* Insertion: conjoint tendon,pubic crest,linea alba
* Nerve supply: lower 6 thoracic nerves,iliohypogastric n.&ilioinguinal n.

Page 10
Inguinal canal:

*boundaries: ant. Wall: skin,sc,EOA,Internal oblique m.( lateral 1/3)

Post. Wall: conjoint tendon
Fascia transversalis
Reflected part of inguinal ligament
Roof: lower arched fibres of int. oblique and transversus abdominis m.
Floor: grooved surface of the ing. Ligament

Page 11
Oesphagus:

*Begins: at the lower border of cricoid cartilage(c6)

*Blood supply:

Arterial Venous

Neck: inferior thyroid a. Neck: inferior thyroid vein

Thorax: branches from aorta Thorax: azygous veins
Abdomen: lt.gastric a.+ inferior phrenic a. Abdomen:azygous vein( systemic)
Lt.gastric vein(portal)
*cells lining: stratified squamous epithelium

*barret's oesphagus: columnar metaplasia with increased risk of developing adenocarcinoma

* achalasia: Esophageal achalasia is an esophageal motility disorder involving the smooth muscle
layer of the esophagus and the lower esophageal sphincter (LES). It is characterized by
incomplete LES relaxation, increased LES tone, and lack of peristalsis of the esophagus

* Microscopic picture of achalasia: hypetrophied musculature with absence of myentric plexus

*lymphatic drainage : cervical: deep cervical L.ns

Thoracic : post. Mediastinal L.ns
Abdomen: lt. Gastric L.ns

* what makes an indent on the oesophagus: lt bronchus- aortic arch- lt. Atrium
* Complications of perforated oesphagus: mediastinitis

Thorax:

Heart:
* ID tricuspid valve,chorda tendinae,papillary m.,pulm.trunk
* ID right atrium,left ventricle,pulm. Trunk,pulm. Valve,ascending aorta,auricle of right
atrium,infundibulum

Page 12
 *Pulm.
Valve: 3
cusps,, lt. 2nd ICS parasternal edge

* ID azygous vein

Page 13
 Tributaries: RIGHT HANDED PM LOVES EAT BURGER
-right sup. intercostal vein
-hemiazygous and accessory hemiazygous
- pericardial veins
- mediastinal veins
- lower right post. Intercostal veins
- eosphageal veins
- bronchial veins.
* branches of ascending aorta:
Rt. and left coronary arteries arising from the aortic sinus opposite the aortic valve

Sympathetic trunk:
* Where preganglionic fibres come from----> the corresponding spinal nerves T1-L2
* What connects it to the spinal nerves: ganglion+ white ramus communicans + grey ramus
communicans

* How sympathetic nerves leave the sympathetic chain:

1-)through the spinal nerves
2- forming plexuses around blood vessels( cardiac and pulmonary plexuses, greater
splanchanic nerve , lesser splanchanic nerve)

Lungs:
* ID main bronchus

Page 14
* ID Structures passing through the hilum of lung:
-pulm. Artery and vein( most. Ant.)
- rt. and lt. Main bronchus(most. Post.)
-bronchial art. And vein
-lymph nodes
- autonomic nerves

*Pulmonary ligament:
Pleural fold that connects
the mediastinal surface of the lung and the pericardium to allow expansion of pulm. Veins with
increased blood flow

*ID surface anatomy of the lung on the skeleton:

Page 15
- Apex: curved line from the stenoclavicukar joint to 3 cm above the junction bw the medial 1/3 and
the intermediate 1/3 of clavicle
-Ant. Border: sternoclavicular joint to the xiphisternal joint behind the lateral border of the
sternum(lt lung deviates laterally from the sternum at the 4 th costal cartilage to form the cardiac
notch
- Inferior border: line drawn bw 6th rib MCL,8th rib MAL,10 th rib vertebral column
- Post. Border: transverse process of C7 to transverse process of T 10
- Hilum: oppsite T5,T6,T7
- Carina: at the level of T4

How many bronchopulmonary segments in each lung? 10

What is the nerve relation anterior and post.? Phrenic nerve , sympathetic chain

Describe the course of a clot from deep veins of the calf to pulmonary artery?

Pop. Vein--- femoral vein----EIV ---- CIV ---- IVC ---- atrium ---- AV valve ----- pulmonary valve ----
pulmonary artery

Branches of the aortic arch:

Page 16
* Subclavian steal syndrome:

Retrograde flow of blood flow down to the vertebral art. Due to stenoocclusive disease in the
subclavian artery proximal to the vertebral artery
This will lead to brainstem ischemia on arm excercise
.

Page 17
Thoracic outlet syndrome:
Compression of the neurovascular bundle (brachial plexus+ subclavian art.) between the scalenus
medius and scalenus ant.------> neurological and vascular symptoms in the arm

* show on the skeleton where to put a chest tube: 5th ICS midaxillary line

* Why bradychardia after chest tube insertion: due to irrirritation of the vagus nerve.

Posterior mediastinum:

Boundaries:
Ant: pericardium+ vertical part of the diaphragm
Post.: lower 8 thoracic vertebrae
On each side: mediastinal pleura
Contents:
-oesphagus
-descending aorta
-sympathetic trunk and vagi
-thoracic duct
-Azygous, hemiazugous veins

Page 18
 ASSCC
Acute pancreatitis:
Stem: 45 y old male diagnosed and managed for acute pancreatitis 2 weeks later, now having
tachycardia,tachypnea, SOB
Differentials:
- acute relapsing pancreatitis
- Acute cholecystitis
- Ascending cholangitis
- Pancreatic peseudocyst

The patient is tachypnic why?

- abdominal pain
- Pressure by pseudo cyst
- ARDS

Scoring systems:
1- Glascow criteria: PANCREAS

- pao2 < 8 kpa ( 10-13)

- age > 55
- neutrophils > 15.000
- calcium < 2 mmol [ after 48h]
- renal ( urea) > 16 ( 2.5-6.7) mmol/L
- enzymes (LDH) > 600 [after48h]
- Albumin < 32 g/L [ after 48h]
- Sugar(glucose) > 10 mmol/L

( at least 3 of the above = severe episode = ITU admission)

Page 1
2- Ranson's criteria:

3-Balthazar CT scoring system:

A: normal pancreas
B: enlargement of pancreas
C: inflammatory changes in pancreas and peripancreatic fat
D: ill-defined single peripancreatic fluid collection
E: two or more poorly defined peripancreatic fluid collections

4- Apache 2

Pathophysiology of hypocalcemia:
* saponification of the omental fat by the pathologically released pancreatic enzymes----> free fatty
acids---> chelate calcium-----> hypocalcemia
* ARF ----> hypocalcemia
Pathophysiology of hyperglycemia:
Pancreatic enzymes destroy B- cells of islets of langerhans ---> increase in serum glucose

Ct findings in acute pancreatitis:

- edema
- Fat strandings
- Collection
Page 2
- Necrosis
- Abscess
- Pseudocyst

Management of nutrition:

- TPN is usually needed in severe cases

- Recently , there is growing trend towards early institution of enteral feeding with a nasojeujenal
tube
- Take into account : * premorbid nutritional status
- * current nutritional needs
- * estimated return to normal feeding
Complications:
- hypovolemic shock
- Haemorrhagic pancreatitis ( grey turner sign, cullen's sign)
- ARDS,SIRS,sepsis, MOF
- pseudocyst formation

Functions of the pancreas:

Endocrine : cells of ilets of langerhans
Alpha ---> glucagon
B -cells----> insulin
Delta cells---> somatostatins
pp cells-----> pancreatic polypeptide
Exocrine : pancreatic enzymes ( digestion of fat ,carbohydrates, proteins)
Enterokinase ( trysinogen---> trypsin )
Lipase,amylase

Cause of normal amylase in pancreatitis: ( too early , too late )

It returns back to normal levels 48 h after the onset of the attack , it doesn't correlate with the
severity of pancreatitis, it is not specific fir pancreatitis

Causes of acute pancreatitis:

- gall bladder stone
- Alcoholism
- Abdominal trauma
- Post ERCP
- Hyperparathyroidism
- Hypercalcemia
- Viral infection( mumps)
- Drugs ( thiazide direutics)
- Idiopathic

Pseudocyst:

Def: collection of amylase rich fluid enclosed in a wall of fibrous or granulation tissue
It requires 4 weeks or more from the onset of the attack

Symptoms: epigastric swelling, dyspepsia,vomiting ,mild fever)

Complications:
Page 3
- rupture ( into bowel or peritoneum)
- Infection
- Bleeding from splenic vessels
- Cholangitis
- CBD obstruction
- Portal vein thromosis

Management of pain:
According to WHO analgesic ladder
( no morphine. No NSAID's)
- epidural analgeisa is a good option
- PCA

Management :
1- CV line for :
* rehydration( because of the fluid sequestration and 3 rd space loss)
* Monitoring
* TPN
2- pain management
3- nasogastric tube , urinary catheter
4- octreotides ( somatostatins) to decrease pancreatic secretions
5- antibiotics
6- i.v ppi to prevent stress ulcers and erosive bleeding

Management of pseudocyst:
> 6 weeks
> 5 cm
> thick cyst wall
---------> internal drainage: cystogastrostomy, cystdudonostomy+ biopsy of the cyst wall to rule out
malignancy

Nutrition options:
Stem: lady with crohn's ------> ileocecal resection------> POD4 anastmotic leakage ------>
defunctioning ileostomy

Page 4
 - what does AXR show ? Small bowel dilatation ( stack of coins appearance)
- What may be the cause in this patient: stricture

Feeding options: parentral vs non-parentral(enteral)

Types of non-parentral feeding: oral,nasogastric, nasojeujenal,percutaneous endoscopic

gastrostomy, jeujonostomy

Nasojeujenal tube :
- smaller in diameter ( more prone to kinking)
- Needs endoscopic guidance for placement
- Bypass the Stomach ( less liability to pneumonia)

Complications of enteral feeding:

Tube related: kinking, misplacement, migration,infection( sinusitis) , aspiration pneumonia
Feed related: diarrhae,nausae, vomiting, refeeding syndrome, fluid & electrolyte imbalance,
deranged liver functions

Complications of parentral feeding :

Line related: infection, thrombosis, pneumothorax, hemothorax
Feed related: fluid and electrolyte imbalance, hypo or hyperglycemia

TPN:
Indications:
General critical illness:
- severe malnutrtion( > 10 % weight loss)
- Multiple trauma
- Sepsis with MOF
- Severe burns
Gut proplems:
- enterocutaneous fistula
- Short bowel
- IBD
- radiation enteritis

Routes of TPN administration:

- central line or PICC

Types of electrolytes in TPN:

sodium chloride, calcium chloride, potassium chloride, magnesium chloride

Complications:
- Hypo-and hyperglycaemia
- Hyperlipidaemia
- Hyperchloraemic metabolic acidosis (if there is an excess of chloride)
- ---Hyperammoniaemia, e.g. if there is liver disease, or a deficiency of L-glutamine and
arginine
- Essential fatty acid deficiency
- Ventilatory problems due to excess production of CO 2 if too much glucose is used in the
mixture. In the ventilated critically ill patient, the amount of glucose given in 24 hours may
have to be restricted to 5 g/kg
- Other complications include infection, from line sepsis, and thromboembolic phenomena,
due to micro-embolic formation at the IV cannula site.
- The most potent risk is that of the re-feeding syndrome, particularly in the chronically
malnourished.

Page 5
 - Gut atrophy: due to the absence of trophic signals released in response to luminal
nutrients, during regular feeding which will lead to bacterial translocation

How it is given:
In a central line because of high osmolarity ( must be < 900 mosm/L)

Components:
Water, carbohydrates (50%), lipids (30%) ,proteins, vitamins, nitrogen ,trace elements

From which sources may the energy requirements be satisfied? How much energy does each of
these provide?
The predominant sources of energy are from carbohydrates and lipid, but protein catabolism also
yields energy
-Fats provide 9.3 kcal/g of energy
-Glucose provides 4.1 kcal/g of energy
-Protein provides 4.1 kcal/g of energy

What are the disadvantages of using glucose as the main energy source?

The problems of glucose are

- Glucose intolerance : as part of the stress response, critically unwell patients are often in a state
of hyperglycaemia and glucose intolerance. Therefore, if glucose is the only source of energy,
patients will not receive their required daily amount due to poor utilisation of their energy source
- Fatty liver : the excess glucose occurring as a consequence of the above is converted to lipid
in the liver, leading to fatty change. This may derange the liver function tests
- Respiratory failure : the extra CO 2 released upon oxidation of the glucose may lead to
respiratory failure and increased ventilatory requirements
- Relying solely on glucose may lead to a deficiency of the essential fatty acids.

Therefore, ∼ 50% of the total energy requirement must be provided by fat.

Epidural:
[ lobectomy using thoracic epidural ]---> hypotensive, bradychardia, desaturation, upper limb
parasthsia

Differentials:
1- High epidural block
2- distributive shock 2ry to epidural
3- paralysis of intercostal muscles
4- paralysis of diaphragm
5- hemothorax or pneumothorax
6 - post operative hypovolemic shock

Why patient having bradycharia:

High epidural block----> blocking of the cardioaccelerator fibres ( sympathetic fibres) from T1-T5----
> unopposed parasympathetic action of the vagus nerve

Page 6
Management plan :
- call the operating consultant and anathesia consultant
- Sit the patient upright
- 100% o2
- Stop any injections in the epidural catheter
- Rule out any concomitant hypovolemic shock
- Epinehrine , phenylepherine, metaraminol ( inotroic agents)

Factors affecting epidural efficency:

- level of injection
- Dosage
- Type of medications
- Vasoconstrictors
- Posture
- Age, height , weight

Why epidural:
- post operative analgesia
- Improves outcomes

How to test the level of the block:

Using temperature sensation ( ice packs)

Why we use temp. Sensation ?

Because of the arrangements of fibers , the motor fibers are the last to be affected

How to differntiate high epidural block from hypovolemic shock :

Eidural: warm and pink periphries ( due to vasodilatation)
Bradychardia
Hypovolemia:cold ,clammy peripheries
Tachycardia

Gastric outlet obstruction:

Causes: 1- begnin: pyloric stenosis secondry to cronic peptic ulceration
2- malignant ( gastric or pancreatic ) carcinoma

ABG: metabolic alkalosis

Biochemical abnormalities:
Hypocholeremic,hypokalemic, metabolic alkalosis
Hypocholeremia: loss of chloride in the vomitus
Hypokalemia: increased aldosterone in response to hypovolemia

Why bicarbonate is increased:

* there will be increased uptake of bicarbonates in renal tubules in response to loss of chloride in
order to maintain electrochemical neutrality
* Reduction of pancreatic juice secretion due to loss of acid load in the duodenum , pancreatic
juice is rich in bicarbonates which will be retained

Why paradoxical acuduria:

Hyponatremia------> stimulation of angiotensin aldosterone system----> more Na+ and h2o
reabsorption in exchange of H+ and K+ -----> hypokalemia and the urine becomes acidic due to
the prescence of H+

Page 7
Why hyponatremia:
In metabolic alkalosis , kidneys excrete more NAHCO3 to reduce blood alkalinity----->
hyponatremia

Management: normal saline 0.9% + K+ supplementation

Causes of hyponatrmia:

Depletional : diarrhea, direutics, burns

Dilutional : heart failure, post- operative over adminstration of 5% glucose
Endocrine: Addison's disease , hypothyroidism
Pseudohyponatrmia: multiple myeloma
SIADH

Atrial fibrillation+ rupture viscus:

[ CXR+ ECG]

Identify the pathology in CXR-----> air under the diaphragm

Identify the pathology in ECG -----> AF ( there is no p- waves), irregular rhythm

Count the heart rate in ECG------> count the No. Of QRS in 30 blocks and multiply it by 10

Why it is different from recorded by the automatic machine:

because automatic machine can not measure irregularity ( because AF causes inadequate heart
contraction resulting in a small volume pulse)

Page 8
What is the cause of AF in this patient :
Hypokalemia, sepsis

Management of AF:
1- cardioversion : chemical ( amiodarone) , DC shock
Give 300 mg of amiodarone in a large vein over 10–20 minutes and repeat the shock, followed by
900 mg over 24 hours
2- anticoagulation : unfractionated heparin 70 units /kg as a bolus then 15 units / kg/ h till adjusting
APTT to 40-60 seconds

Differntials of perforated viscus:

- ruptured diverticulum
- Perforated DU
- Ischemic bowel
- Necrotising enterocolitis

How to consent in such case :

Patient is confused , i will proceed for the operation for the patient best interest with 2 consultant
signature on the consent.

Preoperative aortic stenosis:

[ elective TURBT]

Pathophysiology of aortic stenosis:

Fixed cardiac output -----> limited coronary blood supply-----> can not respond to decreased
afterload which may occur with anathesia or blood loss

Coronary perfusion pressure = systemic diastolic art. Pressure - LVED pressure

Clilnical picture of aortic stenosis:

Symptoms: syncope , anginal pain, dyspnea
Orthopnea, paroxysmal nocturnal dyspnea
Signs:
Pulse: pulsus alternans, narrow pulse pressure
Paradoxical splitting of s2
Ejection Systolic murmur ( right 2nd IC space on right sternal border)

Page 9
ID (ECG)
+ve lead 1 , + ve lead avL
-ve lead 2 , -ve lead avF
Left axis deviation = left ventricular hyperatrophy

How to calculate HR based on this ECG :

300/ No. of large squares between two R-R intervals

What are the complications of aortic stenosis?

- LVH
- HTN
- CHF
- VT, VF
- Angina

Investigations : 2D echocardiography

What to do :
- inform the consultant and the anathesist
- Cancel the operation
- Call the operating theatre to cancel listing
- Explain to the patient
- Discuss in MDT
-
If this patient had a bladder cancer , will you proceed to bladder surgery or valve surgery first?
This will depend on the severity of aortic stenosis:
Normal aortic valve surface area is 2.5-3.5 cm2
< 1cm2 = severe stenosis = transvalvular gradient > 40mm.h

If the operation was cancelled , what are you worried about?

Spread of cancer

if you will proceed to surgery :

preoperative antibiotics for prophylaxis against infective endocarditis ( according to NICE guidlines)

Page 10
Respiratory acidosis:
[ morphine overdose]
How CO2 is transported in the blood:
1- carbaminogroup (20%): between the co2 and proteins or peptides most of which with the globin
portion of Hb.
2- dissolved co2 ( 10%)
3- bicarbonate ( 70% ) :
Carbonic anhydrase [inside RBC's]
H2O+ CO2----------------->H2CO3 ----------> H+ + HCO3-
<--------------- <---------- [alveoli]

HCO3- -------> diffuses out of red cell to the plasma

H+ ------> binds to Hb

Chloride shift: chloride diffuses into the red cell to maintain cellular balance

Why still no metabolic compansation:

Kidney takes time to react

What type of respiratory failure is that?

Type 2 ( hypercapnia)

How morphine act:

By binding to mu receptors on the respiratory center causing respiratory depression

Why pao2 is in normal range:

Because Fio2 is 0.6 = 60%

Management: (ITU)
- ABC
- Ensure adequte oxygenation by humidified o2
- Ensure adequte ventilation either non- invasive or invasive ( entubation and invasive respiratory
support or CPAP)
- Management of the underlying cause
- Morphine antagonist: ( NALOXONE)
Dose : 0.4 -2 mg i.v intially and repeat every 2-3 min. If no response to a maximum dose of 10 mg
Side effects: nausea, vomiting, sweating, tachycardia, abdominal cramps, pulmonary edema,
cardiac arrest

Ruptured AAA:
Perioperative hypothermia: Under anaesthesia hypothermia is defined as a core temperature less
than 36°C.

How to measure core temp.?

Oral, axillary, tympanic membrane, rectal ,oesphageal
Page 11
Risk factors:
- major surgery
- Exposed surgery
- Massive blood transfusion
- Combined general and regional anesthesia
- Preoperative temp. Less than 36

Ways of heat loss:

- radiation (50%)
- Evaporation
- Conduction
- Convection
- Specific:
Vasodilatation
Cold anesthetic gases and i.v fluids
Depressed hypothalamic function and muscle relaxants which will prevent shivering

Complications:
-Cardiovascular –decreased cardiac output (anaesthetised), arrhythmias, vasoconstriction, ECG –
increased PR interval, wide QRS complex
. • Respiratory –increased pulmonary vascular resistance and V/Q mismatch, decreased ventilator
drive. Increased gas solubility
. • Renal –decreased renal blood flow and glomerular filtration rate, cold diuresis.
• Haematological –reduced platelet function and coagulation, increased fibrinolysis, increased
haematocrit, left shift of oxygen dissociation curve.
• Metabolic –reduced basal metabolic rate, metabolic acidosis, insulin resistance, hyperglycaemia.
• Gastrointestinal / hepatic –reduced gut motility.
• Neurological –reduced cerebral blood flow, impaired conscious state leading to coma.

How to prevent thsese complications:

NICE GUIDELINES:
- theatre temp. Is maintained at 21 c
- Warm i.v and irrigation fluids are used
- Patient exposed only as needed
- Postoperative the patient should not leave the recovery room to the ward until core temp. Is
above 36 c
- Bair hugger

DIC:
Def. : it is a pathological consumptive coagulopathy due to activation of the coagulation and
fibrinolytic systems , activation of the latter leasds to formation of microthrombi in many organs with
the consumption of the clotting factors and platlets.

Characterised by:
- widespread hemorrhage
- Thrombocytopenia, decreased fibrinogen, increased FDPs

Cause of DIC in this patient:

Severe hemorrhage, massive blood transfusion, hypothermia

Treatment of DIC:
FFP, platlets, cryoprecipitates

Who to involve in care:

Hematology consultant
Page 12
Indications of platelet transfusion:
Platelet loss, consumption, dysfunction
any cause of thrombocytopaenia, e.g. <50 × 10 9 , disseminated intravascular coagulation (DIC)
and post-cardiopulmonary bypass.

Shelf life : 5 days

Stages of hemostasis:
1- vasoconstriction: smooth muscle contraction by local reflexes , thromoxane A2, serotonin
released from activated platlets
2- platlet activation: adherence, aggregation, plug Thrombin
3- coagulation: intrinsic and extrinsic pathway -----> fibrinogen ---------------> fibrin

Massive blood transfusion:

Replacement of more than 50% of the patient's blood volume in 12-24 hours

Complications: - fluid overload

- electrolyte disturbances: hyperkalemia due to K+ leakage from the stored RBC's
Hypocalcemia due to chelation of ca+2 by citrate
- ARDS( TRALI)
- thromocytopenia : stored blood has decreased No. Of functioning platlets
- hypothermia
Measures to reduce blood loss intra-operative :
- Cell savers
- hypotensive technique.
- Good hemostasis

Burns + ARDS:
-calculate the surface area of the burn

According to Wallace rule of nine's

Management: ABC
1- airway : look for signs of airway burns and inhalational injury as it may cause airway edema
Consider entubation of there airway edema
Page 13
2- breathing and ventilation:
Ensure that adequete ventilation can be achieved as tracheal
or pulmonary burns can impair effective gas exchange , also
full thickness chest burns can impeded chest expansion
3- circulation : 2 large bore cannulae and fluid resuscitation by
crystaloids usisng (PARKLAND FORMULA):
- any patient > 15% TBSA
- any child > 10%
Volume of crystalloids (ml) = 4 X % TBSA X patient
weight-------------> divided into 2 halfs
1/2 in the first 8 hours
1/2 in the subsequent 16 hours

Consider C.V line and urinary catheter

How do you assess the adequacy of fluid therapy?

A number of clinical parameters may be used - --

- Clinical measures of the cardiac index includes peripheral warmth, capillary refill time and urine
output
- Central venous pressure and its response to fluid challenges
- Core temperature, e.g. rectal temperature
- Haematocrit (Hct), which determines the plasma volume and the red cell mass. This is
unreliable if there has been a recent transfusion or haemolysis

ARDS:

Def.: acute respiratory failure and non cardiogenic pulmonary edema which will lead to hypoxemia
and decreased lung compliance refractory to o2 supply
Charcterised by:
1- diffuse pulmonary infiltrates on CXR
2- normal PAWP ( < 18 mm.Hg)
3- pao2/ Fio2 < 26.6

Pathophysiology of ARDS:
Two phases are recognised in ALI / ARDS:
• An acute phase, characterised by widespread destruction of the capillary endothelium,
extravasation of protein-rich fluid and interstitial oedema with extensive release of cytokines and
migration of neutrophils; the alveolar basement membrane is also damaged, and fluid seeps into
the airspaces, stiffening the lungs and causing ventilation/perfusion mismatch.
• • A later reparative phase, characterised by fibroproliferation, and organisation of lung tissue. If
resolution does not occur, disordered collagen deposition occurs leading to extensive lung
scarring.
•
Management:

- Management of the initial predisposing insult

- Adequate nutritional support.
- Low tidal volume –This lung protective strategy protects the lungs from over distension and
prevents the release of inflammatory mediators.
- . Moderate PEEP –Used to prevent lung injury and improve oxygenation. Lower doses are
generally preferred to minimise cardiovascular compromise and risk of pulmonary oedema.
- -Prone positioning –This has been found to significantly improve oxygenation (up to 65%).
- High frequency oscillation –This lung protective mode of ventilation includes low positive
pressure together with high respiratory rates. It prevents ventilator-assisted lung injury.
Page 14
- Extracorporeal membrane oxygenation (ECMO) –Can be used for profound refractory
hypoxaemia. No significant advantage has been identified although its role in combination
therapy is under investigation. Major bleeding is the potential complication.
- Low dose steroids –Certain studies have identified improved oxygenation and survival with
steroid therapy. However it is recognised that therapy should not be commenced 2 weeks after
the onset of ARDS due to the increased risk of infection and mortality.
- Haemodynamic management –Studies have reported the benefit of conservative fluid
management maintaining a low central venous pressure. This reduces the pressure in the
pulmonary microvasculature thereby preventing the development of pulmonary oedema.
- Inhaled nitric oxide/prostacyclin –Both treatments cause pulmonary vasodilation, reducing
pulmonary hypertension and improving gaseous exchange.
- Antibiotics –These should be administered in cases of infective causes after obtaining the
appropriate cultures.
- Nutrition –Enteral nutrition should be commenced after 48–72 hours of mechanical ventilation. A
low carbohydrate, high fat formula containing anti-inflammatory and vasodilating agents such as
eicosapentaenoic and linoleic acids is

Pneumothorax + cv line insertion:

System for reading CXR:

The ABCDE mnemonic is a useful one when trying to ensure that the examination of a chest x ray
is a systematic one.
A-airway

B-bone

C-cardiac

D- diaphragm

E&F- equal (lung) fields

G- gastric bubble

Page 15
H- hilum and mediastinum

I also have to add the T which stands for technicals.

Types of pneumothorax:
Simple vs tension Primary vs secondary

Difference between tension and simple pnemothorax:

Tension Simple
-trachea is shifted to the oopsite side
- tachycardia , hypoxia
- Emergency situation requiring urgent tube thoracostomy - needle thoracostomy in the 2nd
ICS
- midclavicular line
- There is continuous entry of air through a one way valve

Safe triangle of insertion of chest tube:

Ant.: lateral border of pectoralis major
Post. : mid-axillary line
Inf. : a line drawn from the nipple line backwards

Indications of central line insertion:

- monitoring of fluid balance and fluid resuscitation
- TPN
- certain fluids and medications ( K+ rich fluids)
- Failed peripheral venous access
- Hemodialysis
- Transvenous cardiac pacing

Complications of central venous line insertion:

- infection + thrombosis( DVT)
- Air embolism
- Arterial puncture: hemorrhage, pseudoaneurysm, hemothorax)
- Pneumothorax
- Left IJV canulation: damage of the thoracic duct ---> chylothorax
- Perforation of right atrium ----> cardiac tamponade
- Arrythmias

NICE guidlines for insertion:

- insertion under ultrasound guidance
- Post procedure radiograph for:
* position of the radioopaque tip in SVC just superior to its entry in RA
* pneumothorax

Technique for insertion of central venous line : ( IJV)

- locate: - clavicle - 2 heads of sternomastoid

- In the center of the triangle formed by the previous land marks , palpate the carotid artery and
insert the needle lateral to it.
- The needle is directed at 30 angle towards the patient in the coronal plane aiming towards the
ipsilateral nipple
- Aspirate as the needle advances ,once the blood is aspirated, cannulate the vein with seldinger
technique
- Suture the line in place

Removal technique:
Page 16
Head down to prevent air embolism

Sites for inserting a central venous line:

IJV, subclavian vein, femoral vein, PICC( peripherally inserted central catheter)

Organism causing infection: staph. Epidermidis

How to prevent line infection:

- Perform hand hygiene
- Apply appropriate skin antiseptic
- Ensure that the skin prep agent has completely dried before inserting the central line
- Use all five maximal sterile barrier precautions:
Sterile gloves
Sterile gown
Cap
Mask
Large sterile drape
- Once the central line is in place:
Follow recommended central line maintenance practices
Wash my hands with soap and water or an alcohol-based handrub before and after touching the
line
- Remove a central line as soon as it is no longer needed. The sooner a catheter is removed, the
less likely the chance of infection.

Steroids:
Stem:RA patient on steroids / immunomodulators

Layers of adrenal cortex: GFR

- zona glomerulosa: aldosterone
- Zona fasiculata: cortisol
- Zona reticularis: sex hormones

Actions of aldosterone : ( mineralocorticoid)

- Na reabsorption and k excretion in DCT and collecting ducts
- Water balance: salt and water retention
- Acid base balance: metabolic alkalosis ( excretion of k)

Actions of cortisol:
- anti-insulin effect: increase blood glucose
- Stimulate gluconrogenesis: increase blood glucose
- Stimulate protein synthesis in the liver
- Stimulate lipolysis
- Metabolic effect as aldosterone
- Anti inflammatory effect
- Immunosupressive effect
- Control body strss response

Hypothalamic pit. Adrenal axis:

Advice to patients starting steroids:
- they should not stop the drug suddenly , the drug shoud be tappered off slowly
- Make doctors aware that they are on steroids if they are admitted to hospital or prior to
surgery( carry steroid card, wear medicalert bracelet)
- There is increased possibility for infection, delayed wound healing
Page 17
- Steroids may lead to osteoprosis with incraesd risk of fractures
- Steroids may lead to wight gain
- Steroids incraese blood sugar , if diabetic you will encounter poor glycemic control, if not you
can develop diabetes
- Steroids can lead to muscle weakness
- Steroids can lead to mood or behviour changes
- Steroids incrase the risk of peptic ulcers, don not take NSAID's

Addisonian crisis:
Def: it is acute reduction of the circulating steroids due to:
Primary: addisons disease: adrenal supply of cortisol can not meet the body requirements
Secondary: to trauma, surgery, infection: exogenous steroids are suddenly stopped rayher than
being tappered off

Cardinal features:
- abdominal pain
- Nausea,vomiting
- Unexplained shock
- Hyponatremia, hyperkalemia

Management:
- CCRISP protocol
- ABC protocol
- I.v steroids
- Adjust metabolic disturbances

Prevention:
- increase the patient steroid dose prior to surgery
- Convert to i.v steroids.

Calcium homeostasis:
Stem: post thyroidectomy hypocalcemia, calcium 1.8 ----> pod4 0.7

Causes of post-thyroidectomy hypocalcemia:

- removal of parathyroid glands
- Ischemia of parathyroid glands
Page 18
How calcium is transported in the blood:
As dissolved ions or bound to proteins such as serum albumin

Physiologic role of calcium in the body:

- muscle contraction
- Nerotransmitter and nueromodulator
- Activation of some enzymes
- Glycogen metabolism
- Cell division
- Mineralization of bone
- Blood coagulation

Actions of parathormone:
Parathyroid hormone regulates serum calcium through its effects on bone, kidney, and the
intestine:

Bone: stimulates osteoclasts for bone resorption

Kidneys:
- influences the reabsorption that occurs in the distal tubules and the renal collecting ducts
- inhibition of the reabsorption of phosphate (HPO42-) from the tubular fluid
- increase 1- alpha hydroxylase activity
Intestine: enhances the absorption of calcium in the intestine by increasing the production of
activated vitamin D

Hormones involved in ca+2 homeostasis:

1-PTH: (increases calcium)

. Increase bone resorption
. Increae kidney reabsorption
. Increase 1alpha hydroxylase activity

2- calcitonin: ( decrease calcium)

. Decrease bone resorption
. Increase kidney excretion

3- 1,25 dihydroxycholecalciferol:( increase calcium)

. Increase kidney reabsorption

. Increase gut absorption

How it is formed:
UV
Cholesterol -----------> Cholecalciferol
Skin

Liver
Cholecalciferol --------> 25,hydroxycholecalciferol

1 alpha hydroxylase
25,hydroxycholecalciferol ----------------------> 1,25 dihydroxycholecalciferol
Kidney

Signs of hypocalcemia:
- Trousseau sign: carpopedal spasm while inflating the blood pressure cuff above systolic pressure
for 30 sec.
Page 19
- Chovstek sign: contraction of the facial m. On tapping the facial nerve anterior to the ear.
- Convulsions
- Anxiety,depression
- Arrythmias
- Circumoral parathesia
- ECG: prolonged QT interval
- hyperactive tendon reflexes

Which muscle are you worried about in tetany?

Laryngeal muscle for the fear of laryngeospasm
How to treat hypocalcemic tetany?
10 ml ampoule of 10% calcium gluconate should be diluted in 50-100 ml of 5% dextrose and
infused slowly over 10 minutes

Pain management:
Stem: post operative pain , drug chart ----> had only panadol and arcoxia( selective COX2
inhibitor)

How will you manage this patient after this drug chart:

IMMEDIATE MANAGEMENT:

In the critically ill patient in pain, patient assessment is vital. It should follow the same CCrISP
system of assessment as in any other circumstance.:

1- Airway: Start at the beginning by checking that the patient has a patent airway.
2-Breathing: Check the respiratory rate, pattern and depth of breathing. Is your patient’s
respiratory function impaired by inadequate analgesia? Can he or she cough and expectorate
properly to avoid problems later?
3-Circulation: Tachycardia should not automatically be assumed to be caused by pain–there is
commonly an underlying cause. A persistent tachycardia or hypertension caused by inadequate
analgesia may potentiate the development of myocardial ischaemia, particularly in the patient who
is already hypoxaemic.
4- Disability : It is important to assess whether the method of analgesia is contributing to the
patient’s clinical deterioration. Particular attention should be paid to the patient’s level of
consciousness as decreasing conscious level is an early indicator of opioid toxicity.

FULL PATIENT ASSESSMENT:

- Chart review : If pain relief is felt to be contributing to the patient’s deterioration, the drug charts
should be reviewed with the following questions in mind:
•is effective analgesia prescribed?
•is effective analgesia being given?
•is the treatment appropriate for this patient?

- History and systemic examination

- Investigations : Serial ABG analysis and chest X-rays
- Decide and plan: If pain relief is adequate and the patient is improving then continue and
review. If pain relief is inadequate determine why:
- •is it due to failure of the method of analgesia?
- •is it due to incorrect implementation of the method chosen?
- •is it due to the development of a surgical complication?

Page 20
- liase with acute pain multidisplinary team ( acute pain services): multidisciplinary acute pain
team consisting of surgeons, anaesthetists, nursing staff and pharmacists.

Side effects of opioids:

- respiratory depression ( apnea)
- Confusion
- Hypotension
- Nausea and vomiting
- Pin-point pupil
- Itching
- Constipation

What is the pain pathway?

Pain is transmitted via fast A-delta fibers ( sharp pain) and slower C fibers ( dull pain) to lateral
spinothalamic tract then to the thalamus

Page 21
Patient controlled analgesia: (PCA)
- it's a syringe pump connected i.v to allow the patient to self adminster boluses of morphine
- Overdosage is avoided by limiting both the size of the bolus and the frequency of adminstration
- A lock -out time is set within which pressing the button again will not result in a bolus of
analgesia
- One- way valve preventing backflow of opiates into the infusion chamber which may lead to over
dose when redelivered

Poplems :
-patient has to be alert and oriented to be able to use it
-Can break down, run out of battery
-Sleep disturbance
-Not suitable for handicapped patients
-Limits patient mobility

Complications of pain:
- CVS: increased HR, increased Bp, Increased myocardial consumption-----> MI
- GIT: delayed gastric empying, reduced bowel motility,------> paralytic ileus
- RESP. : Limit chest movements leading to atelctasis, retained secretions , pneumonia
- MSK: immobility leading to DVT

Hypothyroidism:
Stem: a lady with a neck swelling, lethargy,malaise

Labs show: low T3 and low T4 with high TSH , anemia

Hypothalamic pit. Thyroid axis:

Difference between T3 and T4:
- T3 is more biologically active, less protein binding capcity
Page 22
- T4 is, in vitro inactive, more protein binding capcity

Synthesis of T3 and T4:

- iodide ions enters the thyroid follicular cell by active pumping
- Iodide is converted to iodine by TOP
- Iodine combines with tyrosine forming : monoiodotyrisine(MIT) and diiodotyrosine( DIT)
- MIT+ DIT= T3 ( triiodotyrosine)
- DIT+DIT=T4 ( tetraiodotyrosine)

Type of anemia in this case: Macrocytic anemia = pernicious anemia

( lack of absorption of vit. B12 due to antiparietal cell antibodies leading to lack of intrinsic factor)

Causes of hypothyroidism:
- primary :
- autoimmune ( hashimoto's)
- iatrogenic ( thyroidectomy, carbimazole)
- transient thyroiditis ( Dequervian's thyroiditis)
- iodine deficiency
- infiltrative ( amyldosis, sarcoidosis)
-Secondary: to TSH defciency

Signs of hypothyroidism:
- weight gain
- Memory loss
- Cold intolerance
- Constipation
- Myxedema
- Bradychardia
- Muscle weakness
- Pretibial edema

- patient with hypothyroidism not compliant to medications comes for an emergency surgery, what
are the risks:
* myxedema coma
Page 23
* Delayed recovery from anasthesia
* Cardiac arrythmia

- Involve endocrionolgist in care , anasthesia consultant

- How to increase patient compliance with the treatment:

- to make the dose of replacement in the early morning

- make the dose single not divided
- involve carer or a family member
- regular follow up visits
- emphasize that relapse is inevitable if therapy is interrupted

Extradural hematoma:
Stem: RTA-----> GCS 15------> 2 episodes of
Vomiting-----> amnesic events-----> GCS 8

- Biconvex shape, hyperdense

- Midline shift
- Compression on the ventricles

When to consider CT brain for trauma:

High Risk Criteria

-GCS < 15 at 2 hours post-injury

-Suspected open or depressed skull fracture
-Any sign of basilar skull fracture
*Hemotympanum
*Racoon Eyes
*Battle's Sign
*CSF oto-/rhinorrhea
-≥ 2 episodes of vomiting
-Age ≥ 65

Medium Risk Criteria

-Retrograde Amnesia to the Event ≥ 30 minutes

-"Dangerous" Mechanism
*Pedestrian struck by motor vehicle
*Occupant ejected from motor vehicle
*Fall from > 3 feet or > 5 stairs

Normal value of ICP: ( 7-15 ) mm.Hg ( supine)

( -10 ) mm.Hg ( standing)
Ways to measure ICP:
- invasive :
* external ventricular drain(EVD)
Page 24
* ICP tranducer
* Subdural catheter
- non- invasive:
* transcranial doppler can measure MCA velocity and derive a pulsatility index correlating with ICP

What is the danger of lumbar puncture in increased ICP?

Herniation and conning

Pathophysiology of increased ICP:

(Monoro - Kellie hypothesis)

-the skull is fixed box containing 3 components

Brain (80%), blood (10%), CSF ( 10% )
- ICP/ volume relationship is governed by these 3 components
- Increase in volume in one component may result in compansatory decrease in the volume of
another component in order to prevent rise in ICP ( compensation)
-However, once the ICP has reached around 25 mmHg, small increases in brain volume can lead
to marked elevations in ICP; this is due to failure of intracranial compliance.( decompensation)
leading to brain herniation

Lucid interval :
Page 25
A temporary improvement in a patient condition after traumatic brain injury after which the condition
deteriorates with rapid decline of consciousness
During this period , blood accumulates in the extradural space leading to increaes in ICP leading to
cerebral edema

CPP= MAP - ICP

MAP auto-regulation range is between 50 - 150 mm.Hg to maintain a constant cerebral blood flow
In cases of traumatic brain injury , this will be disruption of MAP autoregulation----> cerebral
ischemia

C/p of increased ICP:

- headache
- Nausea, vomiting
- Papiledema
- Fall in GCS : . Pressure symptoms( hematoma)
. Ischemia( loss of autoregulation of MAP)
- dilated pupil ( occulomotor nerve palsy)
- Defect in lateral gaze ( abducent nerve palsy)
- Cushing's triad involves an increased systolic blood pressure, a widened pulse pressure,
bradycardia , irregular respiratory pattern

Managemnent:

- ABC
- Positioning : tilting the end of the bed 20–30° (head up) and loosening of tracheal tapes and
neck collars to aid cerebral venous drainage
- Fluid restriction : to prevent cerebral oedema, e.g. a life-threatening complication of managing
diabetic ketoacidosis (DKA)
- Diuretics : e.g. mannitol, which is an osmotic diuretic given at a dose of 0.25–1.00 g/kg over 20–
30 minutes. It rapidly decreases ICP and is useful before hospital transfers
- Controlled ventilation : keeping the P aCO 2 between 4.0 and 4.5 kPa enables CO 2 to control
the degree of intracranial vasodilatation
- Drainage : this can be done by direct tapping of CSF from a ventricular catheter
- Barbiturates : e.g. thiopentone
- Surgery : a decompressive craniectomy can be performed for malignant increases in ICP
refractory to optimal medical therapy. It is controversial and has gained widespread scrutiny

Diverticular abscess + septic shock

Stem: old lady ,critically ill, with LIF pain and tendeness

DD:
- diverticulitis -
- sigmoid volvulus -
- gastroentrits -
- acute constipation -
- pelvic tumour -
- uretruc colic -
Page 26
Interpret ABG, FBC:
Metabolic acidosis with partial compansation
Increased total lecocytic count

Define shock:

Shock is circulatory failure resulting in inadequate organ perfusion, e.g. cannot meet the metabolic
.demands

What kind of shock this patient having?

Septic shock

Define septic shock:

This is the presence of sepsis associated with hypotension (systolic BP <90 mmHg) or
hypoperfusion resulting in organ dysfunction despite adequate fluid resuscitation (or the
.requirement for inotropes), e.g. persisting lactic acidosis, decreased urine output and altered GCS

basic principles of management of septic shock?

,Circulatory support : to maintain the cardiac index and oxygen delivery to the tissues -
- use IV fluids, e.g. colloids and crystalloids such as 0.9% saline -
- Inotropes may be required to increase the systemic vascular resistance . -
-
Respiratory support : non-invasive or invasive ventilation -
may be required for the management of ARDS and respiratory failure -

.Renal support : to ensure that the urine output is >0.5 ml/kg/h

.- Dopamine or a furosemide infusion may be required to support the failing kidney
- Cardiac support helps maintain the renal perfusion pressure -
- Renal replacement therapies may also be required -

Nutritional support : may be enteral or parenteral. Enteral nutrition helps maintain mucosal integrity
and reduce bacterial translocation

Antimicrobials:
During the early phases there is empirical use of broad spectrum antibiotics and surveillance of
infection, but in the latter stages, agents are targeted to grown microbiological sensitivities from
general, e.g. blood, and local sources

CT confirmed the presence of diverticular abscess, what are the management options?
1-Open drainage:
Advantages:
-proper drainage with peritoneal toilet - has the ability to make a stoma if needed -
Disadvantages: -
- liability of wound infection -genral increase in morbididty -

2- image guided aspiration:

Advantages:
no wound infection - less hospital stay - possbilty to leave peg-tail catheter for repeated -
darinage abd administration of antibiotics
Disadvantages: -
- less adequate drainage - does'' t have the ability to make a stoma -
-
Page 27
 -
Pregnant lady undergoing open chole : -
Stem: 34 weeks undergoing open chole for necrotising cholecystitis, BP is decreasing, HR is -
decreasing, reversed telendenberg position, combined GA, epidural, the operation is taking
longer duration than expected)

Benefits and risks of this patient undergoing this operation:

* Benefits: control of infection which may lead to sepsis and induction of pre- term labor
* Risks: IUFD , DVT ( long duration) , pre term labor

Who to involve in care:

Neonatologist ( in case of pre-term labor) , ITU registrar, obstetrician , anasthesist

Where to mange this case post- operative?

Obstetric HDU

Why blood pressure is decreasing?

- Compression of IVC by the uterus which will decrease the venous return which will decrease
preload thus decreasing the cardiac output
- Reversed telendenberg position

Pre-load:
is the end diastolic volume that stretches the right or left ventricle of the heart to its greatest
dimensions
Or
The amount of myocardium that has been stretched at the end of diastole

Shock:
Shock is circulatory failure resulting in inadequate organ perfusion, e.g. cannot meet the metabolic
demands.

What will be the body response to decreased blood pressure?

The autonomic response is due to decreased venous return (preload) which causes a drop in
cardiac output and arterial pressure by the Frank–Starling mechanism

- Reflexes: Baroreceptor : stimulates sympathetic activity producing a compensatory tachycardia,

increased stroke volume and peripheral vessel constriction ( ↑ SVR). This increases the cardiac
output and maintains blood pressure.
- Hormones :
- Catecholamines : the adrenal medulla is stimulated by pain and injury and releases hormones
to cause peripheral vessel constriction, e.g. noradrenaline ( ↑ SVR)
- Mineralocorticoids : the adrenal cortex releases hormones to stimulate salt and water
retention, e.g. cortisol to increase the blood pressure The reduction in the circulating volume,
and increased sympathetic activity, stimulates renin release from the macula densa of the
juxtaglomerular apparatus of the kidney, e.g. renin–angiotensin–aldosterone (RAA) cascade.
A resultant increase in salt and water retention helps to restore circulating volume over
several hours .

Baroreceptors?

Page 28
mechanoreceptors located in the carotid sinus and in the aortic arch. Their function is to sense
pressure changes by responding to change in the tension of the arterial wall.
Supplied by sinus nerve of Hering, which is a branch of cranial nerve IX (glossopharyngeal nerve).

Factors affecting venous return?

- Muscle contraction. Rhythmical contraction of limb muscles as occurs during normal locomotory
activity (walking, running, swimming) promotes venous return by the muscle pump mechanism.
- Decreased venous compliance. Sympathetic activation of veins decreases venous compliance,
increases central venous pressure and promotes venous return indirectly by augmenting cardiac
output through the Frank-Starling mechanism, which increases the total blood flow through the
circulatory system.
- Respiratory activity. During respiratory inspiration, the venous return increases because of a
decrease in right atrial pressure.
-Vena cava compression. An increase in the resistance of the vena cava, as occurs when the
thoracic vena cava becomes compressed during a Valsalva maneuver or during late
pregnancy, decreases return.
- Gravity.: decreses venous return

Can you name some devices used in mechanical DVT prophylaxis may be used to improve
circulatory parameters in this patient?
Intermittent pneumatic compression devices, TEDS ( thromboembolic deterrent stockings)

What can be done to improve the preload of this patient:

Fluids , inotropic and vasopressor agents

Actions of inotropes:

- Adrenergic agonists : adrenaline, noradrenaline, isoprenaline increase the systemic vascular

resistance (SVR) through vasoconstriction, heart rate, stroke volume and resultant cardiac
output to increase the systolic blood pressure
- Dopaminergic agents : (with some adrenergic activity) : dopamine, dobutamine, dopexamine
increase the heart rate, stroke volume and resultant cardiac output and contractility to increase
the blood pressure, but depending on dose, decrease the SVR to produce vasodilatation

Polytrauma:
Stem: RTA

Management of airway and breathing according to ATLS protocol: ( primary survey)

1- airway and cervical spine control:

Assesment:
- speaking to the patient if can speak ----> secure airway
Can not speak :
(Look): in the mouth for FB or in the face for maxillofacial injuries
( listen) : to abnormal breath sounds stridor or hoarsness
( feel) : the breath on your cheek

Management:
Page 29
- chin lift or jaw thrust
- Remove any FB in the mouth
- Oro-naso pharyngeal airway
- Cricothyrodtomy
- Trachestomy
- Endotracheal entubation
- Immobilise the cervical spine by hard collar or sandbag or tape

2- breathing:

Assesment:
Inspection: - any obvious chest injuries
-Open wounds, flail segment
-Count R.R
-symmetrical chest wall movement
Palpation: -central trachea
- surgical emphysema

Percussion and auscultation :

For obvious hemo or pneumothorax
Management:
- high flow o2 via non rebreath mask
- needle thoractomy or chest tube
- Occlusive dressing for open pneumothorax

Comment on this CXR:

Pneumothorax + rib fracture + surgical emphysema

Page 30
How will you manage this ?
Urgent needle thoracostomy in the 2nd ICS mid-clavicular line then chest tube insertion

Now, patient is shocked , how will you manage the circulation?

Assesment:
- pulse rate and character
- Blood pressure
- Class of hemrrhagic shock:

Class 1 Class 2 Class 3 Calss 4

Blood loss ( ml) 750 750-1500 1500-2000 > 2000

Blood loss % 15 15-30 30-40 >40

Pulse <100 100-120 120-140 >140

R.R 12-20 20-30 30-40 >40

UOP (ml/h) >30 20-30 5-15 Anuric

Mental status Slightly anxious Anxious Confused Lethargic

Management:

- stop any obvious source of bleeding

- Gain venous access by 2 large bore cannulae
- Take blood for FBC, GLUCOSE, U&E
- Cross match for 4 units of blood
- Commence i.v fluid resuscitation with 2litres of crysytalloid
- Consider blood transfusion if no response to fluids

How will you monitor the response?

- Heart rate
- Blood pressure
- Capillary refill time
- Urine output
- Mental status

Comment on this CT:

Page 31
There is a liver tear

Management of liver tear:

- conservative : blood transfusion , monitoring of the hemodynamic status of the patient

- Surgical:
- damage control : perihepatic packing
- repair
- resection

Is CT was a good investigation of this patient?

No , patient is hemodynamically unstable , FAST was the investigation of choice

Obstructive jaundice:
[epigastric pain, nausea,vomiting ,diarrhea, increases ALT, AST, ALP, GGT,
urobilinogen undetectable in urine ]

Normal bilirubin level: 3-30 umol/L

apparent jaundice ---> 35 umol/L

Why clotting derranged:

- liver synthesize most of the clotting factors
- vit. K required to activate factors 2,7,9,10
- in severe liver damage and biliary obstruction there will be decreased absorption of vit. k
Page 32
- this will lead to increased prothrombin time

Alkaline phosphatase :
- increases in cholestasis to a far greater extent than ALT,AST
- located in the epithelium of bile canaliculi
- Present also in bone and placental tissue
- ALT,AST present in hepatocytes and their increase is suggestive for liver damage rather than
obstructive jaundice.
- ALT> AST in liver pathology

Function of bile:
Emulsification of fat into fatty acids which can be absorped from the small intestine

What is bilirubin conjugated to ?

- in the liver
- Conjugates with glucouronic acid by the enzyme glucuronyltransferase,

Bilirubin metabolism :
- congugated bilirubin goes into the bile and thus out into the small intestine. Though most bile
acid is resorbed in the terminal ileum to participate in enterohepatic circulation, conjugated bilirubin
is not absorbed and instead passes into the colon

- There, colonic bacteria deconjugate and metabolize the bilirubin into colorless urobilinogen,
which can be oxidized to form stercobilin: these give stool its characteristic brown color.

- 10% of the urobilinogen is reabsorbed into the enterohepatic circulation to be re-excreted in the
bile: some of this is instead processed by the kidneys, coloring the urine yellow.

Page 33
What is urobilinogen ? How it is formed?
It is a byproduct of bilirubin metabolism formed in the intestine by gut flora

Enterohepatic circulation :
Reabsorption of bile salts from the terminal ileum and return them back to the liver ( 95%)

What is the function of bile salts? And what they need to achieve this function?
- aid digestive enzymes
- Reduce surface tension and break fat globules into droplets
- Enhance absorption of fatty acuds and cholesterol
- Help absorption of fat soluble vitamins
To do these functions, they have to be negatively charged through conjugation with glycine and taurine

How to correct clotting abnormality:

- i.v vit. K
- fresh frozen plasma
- Prothrombin complex concentrates
- Consult hematologist

Other investigation you want to do ?

Abdominal ultrasound

If you find a CBD stone? ERCP

If the patient had fever, pain, chills?

Ascending cholangitis

Causes of jaundice:
Pre-hepatic Hepatic Post-hepatic( obstructive)
Hemolytic anemias: Viral hepatitis Gall stones
-hereditary spherocytosis Drug induced Sclerosing cholangitis
- G6PD Chronic autoimmune hepatitis Cholangiocarcinoma
- Sickle cell disease Wilson's disease Cancer head pancreas
Congenital defects:
- gilbert
- Crigler-Najjar

Pulmonary edema ( fluid overload):

Stem: [post-operative pt.,fluid chart+vitals chart= taken
crystalloids plus colloids about 7 litres, 4 litres of them are
normal saline, now he is tachycadiac, hypertensive,
desaturated, oliguric]

What are your expected physical findings?

- congested neck veins
- Puffiness of face
- Lung crepitations
- Cinfusion
Page 34
Management:
- ABC
- stop all i.v fluids
- Commence high flow o2
- I.v frusemide
- GTN infusion if systolic B.P > 100
- Liaise with ITU registrar
- Request CXR
- Request ABG, elctrolytes
- Request ECG

Chest x ray findings in pulmonary edema:

A: alveolar edema ( bat wing or butterfly)

B: kerley B lines
C: cardiomegaly
D: dilated prominent upper lobe vessels

Why this patient is on high risk of MI?

Tachycardia decreases diastole time which decrease coronary filling , also it increaes cardiac load

What is the minimal UOP?

In adults, the minimum acceptable urine output is 0.5 ml/kg/h

Can you explain why the patient is oliguric?

- The most common cause is due to the physiological stress response to surgery in the first 24–36
hours post-operatively. This is due to circulating glucocorticoids and mineralocorticoids inducing
salt and water retention.
- Surgical trauma and various anaesthetic gases also stimulate the release of vasopressin from
the posterior pituitary, stimulating post-operative solute-free water retention.
- congestive heart failure with low renal perfusion

Explain what are the fluids given to this patient:

Crystalloids and collids
Amount of Na in 0.9 % saline: 150 mmol/L
Amount of Na in Hartman's solution: 131 mmol/L

Page 35
Daily requirement of Na and K:
Na: 1-2 mEq/kg
K: 0.5 - 1 mEq/kg

Prevention:
- Insert a CV line , monitoring the central venous line
- Monitoring UOP
- report to the hospital incident reporting system
- Better training of junior staff.

Inotropes and vasopressors:

Inotrope: drug increases cardiac contractility
Vasopressor: drug increases vasoconstriction, MAP
both are acting through autonomic nervous system

Receptors acting on :
- adrenergic alpha 1 receptors: ( vessel wall, heart) -------> vasoconstriction, inotropic
- Adrenergic beta 1 receptors: ( heart) ----------> inotropic , chronotropic, minimal vasoconstriction
- Adrenergic beta 2 receptors: ( vessel wall) ---------> vasodilatation
- D1, D2 receptors: ( kidneys) -----------> direusis

Indications:
- hypotension refractory to fluid resuscitation
- Low cardiac output states
- Low SVR

SHOCK:
def. : inadequete tissue perfusion to meet metabolic requirement

SIRS:
Criteria: ( 2 or more)
- temp. > 38 c or < 36
- RR > 20
- Paco2 < 4.3
- Pulse > 90/min.
- Wbc's > 11 or < 4

Sepsis:
SIRS+ documented infection

Septic shock:
Sepsis with organ hypo perfusion leading to organ dysfunction despite fluid replacement

Which inotrope to be used in septic shock:

Noradrenaline ( alpha 1 effect)
Dopamine ( D1, D2 , alpha effect)

How would you monitor :

1- maintain MAP = 65 mm.Hg to maintain end organ perfusion :
- maintain UOP
- optimize intra abdominal perfusion pressure
Page 36
2- monitor blood pressure and heart rate
3- central venous pressure monitoring

MAP: average blood pressure during a single cardiac cycle

( CO x SVR) + CVP

Preload:
The amount of the myocardium that has been stretched at the end of diastole

Starling law of the heart:

The force of the myocardial contraction is directly proportional to the myocardial fiber length , so
the stroke volume of the heart (SV) = the volume of blood ejected from the heart during systole is
directly proportional to the end diastolic volume (EDV) = the voume of the blood entering the heart
during diastole

Control of blood pressure: through baroreceptors located in the aortic arch and carotid sinus
BP= CO X SVR

When blood pressure increases: stretching of baroreceptors -------> reflex reduction in the
vasoconstriction and reduction in heart rate ----------> decrease in SVR, CO --------> decrease in BP

When blood pressure decreases: baroreceptors are less stretched --------> increase in
vasoconstriction and increase in heart rate -------> increase in SVR, CO -------> increase in BP

ITU admission criteria:

- patient requiring or likely to require advanced respiratory support ( endotracheal entubation and
mechanical ventilation)
- Patients requiring support for 2 or more failing organ systems:
Respiratory : ventilation ,CPAP
Renal: hemodialysis
Cardiac: inotropic support
Neurological: icp monitoring
- patient requiring 1:1 nursing care

Enterocutaneous fistula:
Def.: abnormal communication lined by granulation tissue between the skin and gastrointestinal tract

Predisposing factors:
- intestinal anastomosis
- Crohn's disease
Page 37
- Infection
- Cancer
- Irradiation
- Ischemia

Complications of ECF:
- sepsis
- Malnutrition
- Fluid and electrolyte imbalance

Management: SNAP

- sepsis control
- Nutritional support
- Anatomical assessment
- Adequate fluid and electrolyte replacement
- Protect skin to prevent excoriation
- Plan ( conservative, surgical)

- Management of fistulas requires an MDT approach following initial resuscitation and stabilisation with an
ABCDE approach, which is particularly pertinent in patients with high-output fistulas

- For nutritional support, one would liaise with a dietician asking him to recommend a TPN regimen that
adequately meets the patient's calorific needs.

- To ensure adequate fluid and electrolyte replacement, one would arrange bloods tests with the U&Es
guiding electrolyte replacement, and WCC and CRP acting as a measure of inflammation or infection.

- Imaging such as an MRI, CT or US scan of the abdomen can exclude an underlying collection or abscess.

- With conservative management, 60% of fistulae will close spontaneously when sepsis is controlled and
distal obstruction is relieved.

- Surgical management is normally delayed until after a trial of conservative measures has been undertaken;
however, peritonitis with ongoing sepsis will require more urgent surgical intervention. In general terms the aim
of surgery is to excise the fistula tract with resection of the bowel involved and anastomosis or exteriorisation of
the remaining bowel, followed by delayed anastomosis.

Factors preventing spontaneous healing:

- distal obstruction
- Malignancy
- Infection
- Radiation
- Crohn's
- Malnutrition
- High output

Imaging:
- CT abdomen and pelvis with contrast
- Fistulogram: - to delineate the track length
Locating the fistula
Locating any distal obstruction

Page 38
Fluid management:

High output fistula: TPN

Nutritional assessment are normally performed by a dietician. It is based on a patient’s body weight and how
unwell they are. The energy requirement is 25-30 kcal/kg/day for a normal person and 45-55 kcal/kg/day for a
patient following extensive trauma. In addition the protein, fats, glucose, electrolytes and fluids are calculated
and adjusted based on regular blood tests

TURP syndrome:
[ post TURP confused , hypoxic, hypotensive]

Possible causes:
- TURP syndrome
- Effects of analgesia and sedation
- Hyponatremia
- Blood loss
- Cerebrovascular disease

Def:
Dilutional hypotonic hypervolemia due to the use of glycine rich hypotonic irrigation solution which
will be absorbed leading to severe dilutional hyponatremia
( glycine is used instead of saline because isotonic solutions limit diathrmy use)

C/p:
- restlessness
- Confusion
- Blurred vision
- Intial HTN followed by hypotension
- HF
- Pulmonary edema

Causes of confusion:
- hyponatrmia: cerebral edema
- High ammonia: glycine is broken down to ammonia in the liver

Cause of hypoxia?
Pulmonary edema

Management:
- ABC according to CrISP protocol
- Stop the opeartion if ongoing and prevent futher irriagation by hypotonic fuid
- Cosider entbation according to the consiousness level
- Order ABG and electrolytes
- Correct hypothermia using bair hugger, infusion of warm fluids
- Fursemide to correct fluid overload
- Refer to HDU
- Replacement of sodium but not more than 10 mmol/ day

Page 39
Will you give hypertonic Saline?

If Na is < 110 mmol/L , i will give 250-500 ml of 3% saline through a central line but not more than
10 mmol/L

Other system can be affected by TURP?

Cardiac system

Action of furesmide:
Site of action : thick ascending limb of loop of henle
Mechanism : inhibit Na/K pumb thus preventing Nacl absorption , so the distal convluted tubules
tries to prserve Na and lose K

Other direutics :
- Osmotic diruetics: mannitol ( osmosis)
- Thiazide direutics: DCT ( inhibit Na reabsorption)
- K+ sparing direutics: spironolactone ( aldosterone antagonist) acts on DCT on Na/K pumps
- Amiloride ( binds to Na+ channel at DCT)

Crush injury:

[ compartement syndrome + rhabdomyolysis]

Stem: leg crushed for few hours in 28 y old male, left unobserved on ortho ward
Bloods: AKI, Urine dipstick : blood

Labs of rhabdomyolysis:
- increased creatine kinase( CK ) > 5 times the normal
- Incraesed lactate , LDH, creatinine
- ABG: hyperkalemia with metabolic acidosis

C/p of compartement syndrome:

- worsening pain out of proportion to injury on Passive stretching on the affected compartement
- Not responding to analgesia

Normal compartement pressures (0-15 mm.Hg) , >20 = indication of fasciotomy

Treatment:
4 compartement fasciotomies through 2 incisions as an emergency procedure

Acute renal failure: (why)?

Acute tubular necrosis due to the nephrotoxic effect of myoglobin pprecpitating in the renal tubules
Myoglobin : o2 binding protein found in muscles

Rhabdomyolysis:
Def. : the release of potentially toxic muscle cell components into the systemic circulation
Causes:
- trauma : fracture or lengthy compression of muscle
- Massive burns
- Hypo or hyperthermia
Page 40
- Acute ischemia with reperfusion injury

Management :
- Vigrous fluid reuscitation
- forced direusis ( mannitol)
- Alkalinization of urine
- Correction of hyperkalemia

Fluid management post operative :

Stem: 48 year old lady presented by persistent hypotension and tachycardia post
operative THR, transferred to the ward 3pm, hypotensive and tachycardiac 70/30 at 2am

Fluid chart: 2X250 ml bolus with small improvement initially

Explain the fluid chart:

Persistent hypotension and tachycardia with 2 fluid challenges and nothing in between

Is that adequate:
No

How would you manage this case:

In view of response to previous fluid challenges, i will do more fluid challenges and monitor
the response

Formula of fluid challenge:

500 ml crystalloids over 10-30 min. And monitor the fluid responsiveness

The patient is on 2 hours monitoring , is that adequate?

No, he should be monitored hourly

Who to notify ,when?

I will notify my consultant when no response to multiple fluid challenges

How blood pressure is calculated?

Blood pressure (BP) is the product of the cardiac output (CO) and the systemic vascular
resistance (SVR). The CO is the product of the heart rate (HR) and stroke volume (SV)

How to incraese blood pressure?

Inotropic support and fluids to increase CO, vasopressor agents to increase SVR

PERFORATED GASTRIC ULCER:

Stem: middle aged man ,OA, NSAID's, peritonism

Comment on CXR: air under diaphragm

The most likely diagnosis: perforated gastric ulcer or duodenal ulcer

Page 41
Risk factors of perforation:
- NSAID's
- H-pylori
- Steroids
- Previous peptic ulcers
- Malignancy

How can NSAID's causes peptic ulceration?

- topical irritant effect of these drugs on the epithelium,
- impairment of the barrier properties of the mucosa,
- suppression of gastric prostaglandin synthesis, ( inhibition of Cyclooxygenase)
- reduction of gastric mucosal blood flow
- interference with the repair of superficial injury.

Management options:
Omental patch repair , good peritoneal toilet, intraabdominal drain
In perforated gastric ulcers , we will take a biopsy to rule out malignancy

Post- operative medications:

Long term PPI

Mechanism of action of PPI:

The PPI binds irreversibly to a hydrogen/potassium ATPase enzyme (proton pump) on
gastric parietal cells and blocks the secretion of hydrogen ions, which combine with
chloride ions in the stomach lumen to form HCL

Actions of HCL:
1- activated pepsinogen to pepsin which help in proteolysis
2- antimicrobial

Phases of gastric secretions:

Page 42
Esophageal varieces and hematemesis:
Stem : chronic alcoholic, 3 times of hematemesis, decreased blood pressure, increased HR

Differentials:
- bleeding esophageal varieces due to pertal HTN caused by cirrhotic liver
- Mallory-weiss tear
- Boerhave's syndrome
- Bleedding peptic ulcer

Pathogenesis of portal HTN in chronic alcoholism:

- cirrhosis resulting from chronic liver disease and is characterized by liver cell damage, fibrosis
and nodular regeneration. The fibrosis obstructs portal venous return and portal hypertension
develops.
- Arteriovenous shunts within the liver also contribute to the hypertension.

Sites of portosystemic anastmosis

Page 43
Which varieces are usually bleeding?
Varices in the submucosa of the lower oesophagus are the common source of major bleeding

How will you manage this patient ?

- Active resuscitation:
• Group and cross-match blood
• Establish i.v. infusion line( s)
• Monitor (Pulse Blood pressure Hourly urine output Central venous pressure)
• Fresh blood transfusion , FFP, Platlets
• Assessment of coagulation status: • Prothrombin time • Platelet count
• Control of bleeding :
• • Endoscopic banding or injection sclerotherapy
• • Tamponade (Minnesota tube) if bleeding uncontrolled
• • Pharmacological measures (e.g. vasopressin/ octreotide)
• Urgent endoscopy

Cause of thrombocytopenia in this case?

- hypersplenism
- DIC

Patient with macrocytic anemia, what could be the cause?

Nutrition deficiency with chronic alcoholism

Surgical treatment options:

Page 44
- Portosystemic shunts ( splenorenal shunts- TIPSS: a metal stent is inserted via the transjugular
route using a guidewire passed through the hepatic vein to the intrahepatic branches of the
portal vein.)
- (stapled oesophageal transection): The gastric vein and short gastric veins are ligated, and the
distal oesophagus is transected and reanastomosed just above the cardia using a stapling gun
- Orthotopic liver transplantation (OLT) - Treatment of choice in patients with advanced liver
disease

If the patient is to go for liver transplant , what will you tell his family?
- Counseling regarding patient condition , proposed treatment options, outcome of treatment,
lifestyle modifications
- Abstinence from alcohol 6 months later
- ABO matching
- Immunosupression

Sangstaken Blackemore tube:

Double ballon tamponade

Ports:
- port for gastric ballon
- Port for oesphageal ballon
- Port for gastric suction

Modifiaction:
Oesphageal suction port to help suction of oesphageal contents ( Minnesota tube)

If there is no modification: insert NG tube

Technique:
Page 45
- position the patient and elevate the head of the bed to 45
- Anathesize the posterior pharynx and nostrils with topical anathetic
- Coat the ballons with lubricating jelly
- Pass the tube from the nostrils to at least 50 cm mark
- Suction from the gastric and oesphageal ports
- When the gastric ballon is correctly positioned in the stomach , infalte the ballon with 500 ml of
air and clamp,the port, pull the tube back until resistence is felt against diaphragm
- Inflate the oesphageal ballon by the sphygnomanometer to 30-45 mm.Hg and clamp the port
- When bleeding is controlled , reduce the oesphageal ballon by 5 mm.Hg every 3 hours until 25
mm.Hg is reached without bleeding then keep the tube form 12-24 hours
- Deflate the oesphageal ballon for 5 min. /6 hours to prevent oesphageal necrosis

RENAL FAILURE WITH HYPERKALEMIA:

Stem: 78 y , dementia, renal impairment, history of recurrent UTI , baseline creat. 250, now
developped UTI, nausea, vomiting

Bloods:
- K+= 8 mmol Na+ = 121 Creat. = 700

Interpret : AKI, obstructive uropathy , pre-renal due to decreased oral fluid intake due to dementia

This patient had urinary catheter inserted , drained 1500 ml , then 4 L/day , why?
This is the direutic phase of AKI , which occurs after correction of the cause

Why are uraemic patients anaemic?

Uraemic patients may develop a normocytic, normochromic anaemia for a number of reasons:
- Deficiency of erythropoietin (most important cause)
- Presence of circulating bone marrow toxins
- Bone marrow fibrosis during osteitis fibrosa cystica
- Increased red cell fragility caused by uraemic toxins

Functions of potassium:

Potassium is essential for maintaining proper fluid balance, nerve impulse function, muscle
function, cardiac (heart muscle) function.

Homeostasis of k+ :

There are a number of influential factors on serum potassium :

- Gastrointestinal Diet : the Western diet may contain 20–100 mmol of potassium daily
- Endocrine:
- * ( Aldosterone) : this mineralocorticoid, produced by the zona glomerulosa of the adrenal gland,
stimulates sodium reabsorption in the distal convoluted tubule and cortical collecting duct,
through an active exchange with potassium. It promotes its excretion
- * (Insulin) : stimulates potassium uptake into cells, reducing the serum level

Page 46
- Renal:
- * ( Acid–base balance) : potassium and H + are exchanged at the cell membrane, producing
reciprocal changes in concentration, e.g. acidosis leads to hyperkalaemia. Similarly, alkalosis
can lead to hypokalaemia. Also, renal reabsorption of one causes excretion of the other
*(Tubular fluid flow rate) : increased flow promotes potassium secretion, one method by which
diuretics may cause hypokalaemia

What use does knowledge of the cardiac effects of potassium have for surgical practice?

Potassium-rich cardioplegic solutions are used to arrest the heart in diastole to permit
cardiac surgery once cardiopulmonary bypass has been established.

What is the emergency management of hyperkalaemia?

- immediate ABCDE assessment,

- implement Continuous cardiac monitoring
- Stop all potassium-containing intravenous fluids, including Hartmann's
- Calcium gluconate (10 ml of 10%) is given IV over 10 min, which provides a short-term
cardioprotective effect but does not decease the serum potassium
- Give 5–10 U of insulin in 50 ml of 50% dextrose IV over 30 minutes, which increases cellular
uptake of potassium
- Calcium resonium (15 g PO or 30 g PR) can be given to provide longer term potassium
depletion
- haemodialysis might be needed if the potassium is persistently high or if there is severe acidosis
(pH <7.20).

Ethical issues of dialysis of 77 y old man with dementia:

- the patient will be unable to give a consent , so i will proceed for dialysis for the patient best
interest with two consultant signatures,
- Also i have to involve the staff of his residentiary house , special nurse

Bloody diarrhea:
Stem:
55 y old abdominal pain, bloody diarrhea, hypotensive, tachycardiac, feverish, adimitted , fluid
resuscitation done, 10 episodes of bloody diarrhea, stopped after 6 hours

Labs:
FBC : Hb: 8.7 g , platlets: 666000 , wbc's: 12000
Hyponatremia, hypokalemia, increased CRP
Creat. : 109 , urea: 9'

What type of anemia ?

Microcytic hypochromic anemia

Why platlets are elevated?

- Secondary to acute inflammation( acute phase reactants)
- Dehydration
Abdominal x-ray :
Dilatation of the ascending and transverse colon , with narrowing of the descending colon With
thumbprinting sign ( Thumbprinting is a radiographic sign of large bowel wall thickening, usually
caused by oedema, related to an infective or inflammatory process (colitis). The normal haustra
become thickened at regular intervals appearing like thumbprints projecting into the aerated
lumen.)

DD of bloody diarrhea:

Page 47
- Ulcerative colitis and Crohn’s disease ( IBD)
- Ischaemic colitis
- Amoebic colitis
- Bacillary dysentery
- Carcinoma colon
- Infectious colitis by Clostridium difficile, Campylobacter jejuni

Why not to transfuse blood?

State of sepsis
Not indicated as Hb is not below 7g

Why there is hyponatremia and hypokalemia?

Due to losses from diarrhea

How else would you investigate the patient?

- ESR , CRP
- Stool analysis and culture
- CEA
- Antiobodies for UC, Crhon's
- Colonoscopy ( later stage)
How will monitor the patient response?

- clinically : fever settles, diarrhea stops

- Lab. : decrease CRP, decrease TLC
Indications of urgent surgical management ?
Page 48
- Toxic megacolon refractory to medical management
- Fulminant attack refractory to medical management
- Uncontrolled colonic bleeding
- Perforation (free or walled off)
- Obstruction and stricture with suspicion for cancer
Surgical management :
Pan-proctocolectomy with ileostomy

Page 49
 Pathology
Infective endocarditis:
Def.: inflammation of the endocardial surfaces of the heart including heart valves which is caused
by certain micro organisms

why rheumatic heart and valve replacement patients are more susceptible to IE:
Blood usually flows smoothly over valves, when these valves are damaged as in RH or valve
replacement, there will be an increased chance for bacterial colonization on damaged tissues

Diagnosis: using Dukes criteria :

2 major criteria
Or 1 major + 3 minor criteria
Or 5 minor criteria

Major criteria:
*major blood culture criteria:
- 2 blood cultures positive for micro organisms typically found in patients with IE
- blood cultures persistently positive for one of these micro organisms drawn 12 hours apart
- 3 or more separate blood cultures drawn at least 1 hour apart .

*major echocardiographic criteria:

- Valve vegetations.
- Myocardial abscess
- New partial dehiscence of a prothetic valve.

*minor criteria:
-predisposing factor.: known cardiac lesion or iv drug abuser
-fever: > 38
-vascular problems: arterial emboli, janeway lesions,conjuctival hge
-immunological proplems: glomerulonephrits, roth's spots, osler nodes
- positive blood cultures that doesn't meet the criteria above
- Echocardiographic findings consistent with IE that does not meet the criteria above

Common organisms:
- viridans strept or staph.
- Coagulase nagative staph.
- Enterococi
- Hacek group of micro organisms (oropharyngeal commensals)
(Haemophilus species, Aggregatibacter species, Cardiobacterium hominis, Eikenella corrodens,
and Kingella species.)

Signs in hand:
- osler nodes: painful, raised ,red lesions due to immune complex deposition
- Janeway lesions : non painful,nodular or macular red lesions due to septic emboli which deposit
bacteria forming microabscesses
- Splinter hemorrhages: tiny blood clots under nails

Treatment: i.v antibiotics depending on culture and sensitivity for 6 weeks

( i.v ceftriaxone and vancomycin)
Restrictions : * valves do not have specific blood supply so antibiotics can not reach
Page 1
 * organisms lie inside the vegetations
* bacteria forms a biofilm( glycocalyx covering) that shields them from antibiotics
If IE occurs in tricuspid valve in younger persons: -----> right sided heart failure
If no response to medical treatment: -----> valve replacement or heart transplantation
Matching before heart transplantaion: HLA antigen
If not matched: type 1 -----> graft rejection
How to prevent graft rejections: immunosuppresant therapy --> tacrolimus,mycophenolate,steroids
Side effects of long term steroid:
- opportunistic bacterial and viral infections such as EBV,CMV ---> leukemia,lymphoma
- Cushinoid features: obesity,m.waekness,hirsutism,striae
- Cardiovascular: fluid retention, hypertension
- Endocrine: DM
- musculoskeletal: osteoprosis.AVN, proximal myopathy

After valve replacement why on warfarin: to prevent thromboembolism

Mechanism of action of warfarin: vit. K antagonist thus inhibiting clotting factors 2,7,9,10

How to monitor: INR

reversal: vit. K, FFP,PCC

Right sided vegetations:= tricuspid valve IE = I.V drug abuser

Inflammatory bowel disease:

[ STEM: lady known to have ulcerative colitis and on surveilliance colonoscopy found to have a
lesion less than 1cm in sigmoid colon.]

What is ulcerative colitis: inflammtory bowel disease affecting the colon in the form of colitis with
charcteristic ulcers

Pathogenesis: idiopathic

Colonoscopy done with biopsy showing tubular dysplasia in one part , adenocarcinoma in other
part - showing a picture of a tumour eroding through the muscularis layer + 1/4 positive node

What will you offer this lady: total colectomy

Why? The whole colon is suscepitible

Page 2
If there is liver Mets , how will this affect TNM staging : M1

Microscopic features of crhon's :

- cobble stone appearance : odematous islands of mucosa separated by fissures.
- Skip lesions
- Full thickness( transmural ) involvement
- Sinus or fistula formation
- Non-caseating granulomas

Complications :
- intestinal obstruction
- Fistula formation
- Abscess
- Toxic megacolon
- Malabsorption
- Malignancy
- Gall stones ( due to inhibition of enterohepatic circulation so bile salts will not be absorped
leading to increased amount of cholesterol)

Why patinet having diahrrea:

- malabsorption
- Infection
- Increased motility

Why you need endoscopic survilliance : risk of colon cancer

Renal stone formation in crohn's :

Increased intestinal fat ( due to malabsorption) ----> binds to calcium---> leaving oxalates
(hyperoxaluria)

Describe adenoma carcinoma sequence:

Stepwise accumulation of mutations of oncogenes and tumour suppressor genes:

1- loss of APC ( tumour suppressor gene) ----> hyperplasia
2- k-ras (oncogene) mutation-/----> dysplasia
3- loss of p 53 ( tumour suppressor gene) --> adenocarcinoma

How proto-oncogenes and tumour supressor genes act?

Proto-oncogenes: normal cellular genes whose products promote cell proliferation

Oncogenes: mutated or overexpressed versions of proto-oncogenes that function autonomously,
having lost dependence on normal growth promoting signals
Tumour supressor genes (p53, APC) : normal genes whose absence can lead to development of
cancer, they act as :
- gatekeepers: inhibit proliferation or promote the death of cells with damaged DNA
Page 3
Had resection of terminal ileum but diarrhea continued-----> relapse of crhon's or malabsorption

Stoma-----> ischemia----> inform consultant , patient relatives, consider refashioning

Type of vit. Defeciency: A.D,E,K defeciency

Other investigations: - stool analysis

- barium follow throuh
- prothrombin concentration: to detect vit. K def.
- calcium oxalate levels
- full blood count: macrocytic anemia

Familia adenomatous polyposis FAP:

STEM: a young lady with endometriosis concerned that her father fied of a
cancer at an early stage . , she had a colonoscopy just now

ID a picture of FAP : multiple polyps the largest one is about 7mm and ulcerated

Def.: autosomal dominant condition chacterised by loss of APC tumour supressor gene on the
long arm of chromosome 5 leading to development of hundreds of tubular adenomas with 100%
risk of cancer by the age of 40

Function of APC tumour supressor gene:

encodes a factor that negatively regulates the WNT pathway in colonic epithelium by promoting the
formation of a complex that degrades β-catenin

Classification of polyps:
- non -neoplastic : hamartomatous, metaplastic
- Inflammatory: pseudopolyps ad in ulcerative colitis
- Neoplastic: villous(40%), tubulovillous(20%), tubular( 5%)

Page 4
Malignant potential of adenomas depend on:
1- type of adenoma
2- diameter of adenoma: < 1 cm ---> 5%
> 2 cm----->20 %
3- degree of dysplasia

Extracolonic manifestations: in the related gardener syndrome ( mandibular osteomas,desmoid

tumours, sebaceous cyst)

Management: prophylactic near total colectomy by the age of 25

If the patient is having a child 2 y , what is your advice:

Colonoscopic screening by the age of 12

Define endometriosis:
Endometriosis is defined by the presence of “ectopic” endometrial tissue at a site outside
of the uterus

Definitions:
Dysplasia: disordered cellular development charcterised by inreased mitosis,pleomorphism without
the ability to invade the basement membrane
Severe dyplasia= carcinoma in situ

Abscess: collection of pus surrounded by granulation or fibrous tissue

Pus: collection of neutrophils plus dead or dying micro organisms

Ulcer: a lesion in the mucous membrane or the skin resulting from the gradual distingration of
surface epithelial cells

Secondary intention: secondary healing by repithelization and contraction

Life style modifications to reduce risk of cancer colon :

- eat much fibres
- Limit alcohol
- Reduce fat intake
- Stop smoking

T.B
[ A young lady came back from a foreign travel with cervical lymphadenopathy, LOW, Night
sweating]

* diff.:non-Hodgkin'slymphoma or t.b

* Which labs you will send her sputum to : microbiology + cytology labs

* what are the tests of TB?

- sputum examination ( culture, ziel-neelson stain)
- Mantoux test
- PCR to differntiate mycobacteria t.b from other species
- quantiferon ( interferon gamma assays)
- FNAC of lymph node

* How to label the sputum specimens: Category -B UN3373

Page 5
* Where to put: in a biohazard bag

* Organism of T.B: mycobactetium T.B

* other mycobacteria: mycobactetia avium/ intracellulare(MAC)---> disseminated infection in

immunocompromised patients

* what are the culture media for mycobactetia:

- solid media: lowenstein jensen media, middle brooke media
- Liquid media: BACTEC/MIGT ( mycobacteria growth indicator tube)

* how long to culture: 1-8 weeks

* What type of protein deposition: amyloid

* Given the FNAC result: necrotic tissue, histocytes, giant cells -----> TB

* what is giant cells: multinucleated cells comprising of macrophages often forming granuloma
Ex. : langerhan's giant cells, Reed sternberg cells

* Public health concern/ community concerns

* 1- notify the consultant in communicable disease control (CCDC)
* 2- Avoid work in food factory
* 3- Use mask during sneezing or coughing
* 4- takes DOTS anti -TB therapy

* Contact tracing: the identification and diagnosis of persons who may have come into contact with
an infected person

* What is your advice to contacts: councelling,screening and treatment of other family members

* Granuloma: organised collection of macrophages fusing to form langerhan's giant cells.

* Other Causes of granuloma: leprosy, schistomiasis, sarcoidosis,crhon's , rhematoid arthritis

GB cancer + pseudomembranous colitis:

[ cholecystectomy+ surgical site infection]

Causes: chronic cholecystisis, cholelithiasis

Spread: liver( segment 5), cbd, stomach, dudenum, porta hepatis lymph nodes

Pathology: adenocarcinoma

Surgical site infection ------> necrtotising fascitits

Organisms causing necrotising fascititis:

- group A streptcocci( strept. Pyogenes)
- Staph. Aureus
- Clostridium perferngines
- Bacteroides fragilis
- MRSA

DIAGNOSIS: cellulitis,crepitus

Page 6
 Laporatory: LRINEC( laporatory risk indicator for necrotising fascititis)
Score >= 6 ----> necrotising fascititis is highly considered
1-crp >= 150 4points 4- Na < 135 2 points
2- wbc < 15 0 points 5- creat. > 141 2 points
15-25 1 point 6- glucose > 10 1 point
> 25 2 points
3- hb > 13.5 0 points
11-13.5 1 point
< 11 2 points

Pathology: extensive necrosis with thrombosis of blood vessels

Management:

1- hemodynamic support according to CrISP protocol

2- surgical debridement
3- antibiotics according to culture and sesntivity

Who to involve in care: ITU specialist, palstic surgeon

Post. Operative bloody diahrrhaea:

- Pseudomembranous colitis
- Bowel ischemia
- Stress ulcer
- Infective gastroenteritis

Pathogenesis of PMC:
Uses of broad spectrum antibiotics-----> destruction of normal flora----> overgrowth of clostidium
difficile----> produce enterotoxin a,b----> exudative fibrin deposition-----> pesudomembrane
formation

Page 7
MALIGNANT MELANOMA METS:
Stem: a patient with a hard swelling in her right inguinal region ,her GP sent her for biopsy

DD:
Inguinal lymph nodes receive lymphatic drainage from the lower extremities and skin of the lower
abdomen, genitals, and perineum.[6]

*Infections associated with inguinal lymph nodes are as follows:

-Cellulitis of the lower extremities

-Venereal infections - Syphilis, chancroid, herpes simplex virus infection, lymphogranuloma
venereum

*Malignancies associated with inguinal lymph nodes are as follows:

-Lymphomas
-Metastatic melanomas from lower extremity primary site
-Squamous cell carcinomas from genital primary site

Results of histopath. Revealed malignant melanoma, :

What are types of malignant melanoma:

Melanomas are divided into 5 main types, depending on their location, shape and whether
they grow outward or downward into the dermis:
• • Lentigo maligna: usually occur on the faces of elderly people •
• Superficial spreading or flat melanoma: grows outwards at first to form an irregular
pattern on the skin with an uneven color
• • Desmoplastic melanoma: is a rare malignant melanoma marked by non-pigmented
lesions on sun-exposed areas of the body
• Acral melanoma: occurs on the palms of the hand, soles of the feet, or nail beds
• • Nodular melanomas: are lumpy and often blue-black in color and may grow faster and
spread downwards

Where would you examine this lady?

- primary sites: Whole lower limb including nail beds and soles
- Metastatic sites: chest , abdomen and brain

How to treat this lady?

Excision of the primary lesion with safety margin plus block inguinal lymph node dissection plus
radiotherapy

How can you know the phenotype of the tumor?

By immunohistochemistry

Post operative the wound is red and swollen , culture was done revealed diplococci?

Examples of gram-negative diplococci are Neisseria sp., Haemophilus, Moraxella catarrhalis,

Acinetobacter, and Brucella. Examples of gram-positive diplococci would be Streptococcus
pneumoniae and enterococcus.

Next the patient got toxemia with rapidly spreading infection? What do you think?
Necrotising fasciitis

Page 8
What is SIRS

Manifestations of SIRS include, two or more of the following:

- Body temperature less than 36 °C (96.8 °F) or greater than 38 °C (100.4 °F)
- Heart rate greater than 90 beats per minute
- Tachypnea (high respiratory rate), with greater than 20 breaths per minute; or, an arterial partial
pressure of carbon dioxide less than 4.3 kPa (32 mmHg)
- White blood cell count less than 4000 cells/mm³ (4 x 109 cells/L) or greater than 12,000 cells/mm³
(12 x 109 cells/L); or the presence of greater than 10% immature neutrophils (band forms). Band
forms greater than 3% is called bandemia or a "left-shift."
- Hyperglycemia (blood glucose >6.66 mmol/L [120 mg/dL]) in absence of diabetes mellitus
- Altered mental state

What happens to lung in SIRS?

ARDS
Define ARDS?

diffuse alveolar damage and lung capillary endothelial injury

Malignant melanoma:
[ pathology report]

Definition: malignant neoplasm of melanocytes

Skin conditions associated with melanoma:

- Xeroderma pigmentosa
- Albinism
- giant congenital pigmented naevus
- Fitz patric skin type 1
- Dysplastic neavus , multiple nevi

Other risk factors of malignant melanoma:

- hutchinson's melanotic freckles
- Immunocomprimised patients
- Past history of melanoma
- Red hair, sun exposure

Comment on the pathology report:

- Size
- Breslow thickness: measured in mm. From the top of stratum granulosum to the deepest point of
tumour involvement
- Depth of invasion ( clark's levels)
- Ulceration, mitoses, lymphovascular invasion
- Immunohistochemistry staining

How to diff. MM from SCC?

Melanoma: arise from the lower layer of the epidermis from any part of the body
SCC : arise from upper and mid layer of epidermis with keratin pearl formation usually on sun
exposed areas

Page 9
Poor prognostic factors:
- increased tumour thickness( Breslow thickness)
- Increased depth of invasion
- Type of melanoma: Nodular , amelanotic melanoma
- Prescence of ulceration
- Prescence of lymphatic or perineural invasion
- Prescence of regional or distant metastsis

Genes responsible for familial MM:

CDKN2A and CDK4

Lesion excised , Breslow thickness 1.5 mm, margins 0.5 mm , what to do? Re- exision

Management: excision + safety margin

Size of the safety margin is based on the Breslow thickness

<0.76mm thickness=
Melanoma 1 cm
in situ margin margin 5 mm
— excision

0.76-1mmMelanoma < 1.02mm
thickness= cm— excision margin 1 cm
margin

> 1mm= Melanoma 1.0–2.0 mm — excision margin 1–2 cm
3 cm margin
 Melanoma 2.0–4.0 mm — excision margin 1–2 cm
 Melanoma > 4.0 mm — excision margin 2 cm
What to do to ensure adequate margins:
Frozen section,Moh's microsurgery

Post excision the patient developped regional lymphadenopathy:

Management: FNAC
whole body CT
Post excision the patient developped painful swelling of the arm + dyspnea:-----> axillary vein
thrombosis-------> pulmonary embolism

Risk factors for thrombosis:

Virchow's triad : hypercoagulable state, venous stasis, endothelial injury

Management: - CTPA
- SC LMWH if the patient is hemodynamically stable
- thrombolysis or embolectomy ( massive embolism)

Breast cancer:
[mamogram+ pathology report]

*What can you recognize in mammogram:

Speculated mass+ microcalcifications
* what other tests to do:
Tissue biopsy ( tru-cut ,FNAC)
* most common type of breast cancer:
Invasive duct carinoma
* exision----> pathology report----> what to look for:

-type of cancer
-No.of positive lymph nodes
-Margins status
-HER2 receptors status
-ER/PR receptor status
Page 10
- Ki 67 proliferation index

Her2: transmembrane epidermal growth factor and it is overexpressed in 15% of breast cancer
cases and associated with bad prognosis

Herceptin: ( trastazumab) causes antibody mediated destruction of cells overproducing HER2

3 times weekly for 12 months .
What else in management: radiotherapy, chemotherapy, hormonal therapy

Hormonal therapy:
Premenopausal: tamoxifen ( 20mg /d ) for 5 years
Postmenopausal: aromatase inhibitors ( anastrazole) to prevent peripheral conversion to
oestrogen

Peptic ulcer disease+ hyperparathyroidism:

[gastric ulcer----> hematemsis ---> OGD----> peptic ulcer, biopsied] + hypercalcemia

Def. ulcer: a local defect of the mucous membrane or the skin due to gradual distingration of the
surface epithelial cells

Risk factors of PUD: H-pylori infection

NSAID's
Smoking
H- pylori: gram negative microaerophilic spiral bacteria found in the stomach

CLO test: ( campylobacter like organism) :

It depends on urease production by H-pylori
A gastric mucosal biopsy is taken during gastrosopy and is placed in a medium containing urea
and an indicator such as phenol red,urease production by H-pylori converts urea to ammonia
which increase pH changing the colour ( yellow to red)= positive test

Eradication of H-pylori:
7 days twice daily of :
Full dose of ppi+ metronidazole 400 mg+ clarithromycin 250mg or:

Full dose of ppi+ amoxycillin 1g + clarithromycin 500mg

Other causes of hematemesis in this patient:

Hypercalcemia-----> incresaed gastrin release-----> incraesed hcl production

Common causes of hypercalcemia:

- Malignancy
- hyperparathyroidism(PTH adenoma)
- Renal failure

Cause of UTI in this patient: renal stones

How to localise parathyroid glands: sestamibi scan, frozen section

What is frozen section : is a pathological laboratory procedure to perform rapid microscopic

analysis of a specimen.

Page 11
How the specimen is fixed:

The surgical specimen is placed on a metal tissue disc which is then secured in a chuck and frozen
rapidly to about –20 to –30 °C. The specimen is embedded in a gel like medium called OCT and
consisting of poly ethylene glycol and polyvinyl alcohol.Subsequently it is cut frozen with the
microtome portion of the cryostat, the section is picked up on a glass slide and stained (usually
with hematoxylin and eosin, the H&E stain).

Histopathology report: ( frozen section)

1 gland 0.2 g chief cells
3 glands ranging from 0.08 to 0.09 g oxiphilic cells and fat cells

Interpret: parathyroid adenoma in one gland with involution to the other glands

Histology of parathyroid adenoma:

parathyroid adenomas are mostly composed of uniform, polygonal chief cells with small,
centrally placed nuclei . At least a few nests of larger oxyphil cells are present as well;
uncommonly, adenomas are composed entirely of this cell type (oxyphil adenomas).A rim of
compressed, non- neoplastic parathyroid tissue, generally separated by a fibrous capsule, is
often visible at the edge of the adenoma

Where to find parathyroid gland if you do not see them in the normal position:
the superior mediastinum
As the thymus originates from the third branchial arch ,it occasionally drags the inferior glands
down to the mediastinum

Treatment of parathyroid adenoma: exicsion

Types of hyperparathyroidism:
1ry-----> parathyroid adenoma( hypercalcemia)
2ry-----> chronic renal failure( hypocalcemia)
3ry-----> chronic stimulation of parathyroid gland due to hypocalcemia in 2ry hyperparathyroidism
leading to overactivation ( hypercalcemia)

Treatment of hypercalcemia:
- hydration
- forced direusis
- Bisphosphanates: i.v pamidronate
- Calcitonin

Testicular teratoma:
[35 y man with left groin mass+single palpable testis]

On ultrasound , lt groin mass turned to be undescended testis with solid and cystic components----
> tissue diagnosis -----> pathology report -------> comment:
-Teratoma
-Positive margins
-Lymphovascular invasion
-T4, Nx,Mx

Page 12
Define cryptorchidism:
Cryptorchidism is a complete or partial failure of the intra-abdominal testes to descend into the
scrotal sac and is associated with testicular dysfunction and an increased risk of testicular cancer.

How does undescended testis contribute to increased risk of testicular cancer?

The cryptorchid testis carries a 3- to 5-fold higher risk for testicular cancer, which arises from foci of
intratubular germ cell neoplasia within the atrophic tubules

What will be your management: Ct abdomen and pelvis

Satging
Discuss in MDT
orchiectomy+ chemotherapy
RPLND ( if nodal disease)
Discuss pathology report with family in 3 simple lines:
-This is cancer in the testis
-With incomplete resection
-With lymphatic spread

Where teratoma spread to first : to the para-aortic lymph nodes

Where does it spread to next : locoregional

Serological markers:
biologic markers include HCG, AFP, and lactate dehydrogenase
value of serum markers is fourfold:
• In the evaluation of testicular masses
• • In the staging of testicular germ cell tumors. For example, after orchiectomy, persistent
elevation of HCG or AFP concentrations indicates stage II disease even if the lymph
nodes appear of normal size by imaging studies.
• • In assessing tumor burden
• • In monitoring the response to therapy. After eradication of tumors there is a rapid fall
in serum AFP and HCG. With serial measurements it is often possible to predict
recurrence before the patients become symptomatic or develop any other clinical signs of
relapse.

Post - operative developped hematoma, mention stages of hematoma resolution:

Page 13
. Lysis of the clot by macrophages (about 1 week)
• Growth of fibroblasts from into the hematoma (2 weeks)
.

After few months developped small pneumothorax-----> lung metastasis

Define metastasis: survival and growth of cells at a site distant from their primary origin

1year later the patient came with para-aortic lymph node compressing renal artery and vein + SOB
+ PE Why PE in this patient?
- hypercoagulable state
- Venous stasis

Which part of Virchow's triad doesn' t contribute ?

Endothelial injury

What is choriocarcinoma and what is its tumour marker?

Choriocarcinoma is a highly malignant form of testicular tumor.
Histologically the tumors contain two cell types, syncytiotrophoblasts and cytotrophoblasts
Tumour marker is B-HCG

What is the common tumour in this age group?

Seminoma

Non–Hodgkin lymphoma is the most common testicular tumor in men older than 60 years.

What is the cell origin of seminoma?

Most testicular germ cell tumors originate from a precursor lesion called intratubular germ
cell neoplasia (ITGCN)

Histopath showed papillary thyroid tissue and GIT adenocarcinoma, why?

Teratoma has the 3 germ cell lines

Temporal arteritis:

60 y old female with headache and skull tenderness on mastication, transient

loss of vision
Biopsy from the temporal artery -----> giant cell arteritis( granulomatous pan - arteritis with mono-
nuclear cell infiltrates)

Describe the pathological changes in microscopic picture:

MORPHOLOGY
Page 14
- Involved arterial segments develop intimal thickening (with occasional thromboses) that reduces
the luminal diameter.
- Classic lesions exhibit medial granulomatous inflammation centered on the internal elastic
lamina that produce elastic lamina fragmentation;
- there is an infiltrare of T cells (CD4+ > CD8+) and macrophages.
- Although multinucleated giant cells are seen in approximately 75% of adequately
biopsied speci- mens, granulomas and giant cells can be rare or absent
- Inflammatory lesions are only focally distributed along the vessel and long segments of
relatively normal artery may be interposed

One simple blood test to prove: ESR ( elevated)

Why blindness: ophthalmic artery involvment

Treatment-----> corticosteroids

One year later developped fracture NOF why?

1- AVN
2- osteoprosis

Why osteoprosis in this patient: steroid therapy , post-menopausal

Pathological changes in osteoprosis:

- histologically normal bone that is decreased in quantity.
- postmenopausal osteoporosis the increase in osteoclast activity affects mainly bones or
portions of bones that have increased surface area, such as the cancellous compartment
of vertebral bodies. The trabecular plates become perforated, thinned, and lose their
interconnections , leading to progressive microfractures and eventual vertebral collapse

Mechanism by which corticosteroids cause osteoprosis:

- direct inhibition of osteoblast formation
- direct stimulation of bone resorption
- inhibition of GIT calcium absorption
- Stimulation of renal calcium losses
- Inhibition of sex steroids

Other causes of pathological fracture:

- skeletal mets
- paget's disease
- Multiple myeloma

Multiple myeloma :
Is a plasma cell neoplasm commonly associated with lytic bone lesions, hypercalcemia,
renal failure, and acquired immune abnormalities.it produces large amounts of igG 55% or
igA 25%.It is the most common primary bone tumour in elderly

Diagnosis:
- punched-out lytic skull lesions on x-ray
- M spike on protein electrophoresis
- Ig light chains in urine ( Bence Jones proteins)
- CRAB :

.HyperCalcemia (corrected calcium >2.75 mmol/l, >11 mg/dL)

Page 15
.Renal insufficiency attributable to myeloma
.Anemia (hemoglobin <10 g/dl)
.Bone lesions (lytic lesions or osteoporosis with compression fractures)

Bence Jones protein:

Are monoclonal globulin proteins or immunoglobulin light chain found in the urine,The
proteins are produced by neoplastic plasma cells. Bence Jones proteins are present in 2/3
of multiple myeloma cases.

Concerns if going to surgery: Addisonian crisis

How to prevent:
- increase the patient steroid dose prior to surgery
- Convert to i.v hydrocortisone

The patient went for THR , died in POD1 suddenly-------> fat embolism

Gangrene+ mesothelioma:
[ worker,smoker, toe gangrene, ]

Define gangrene:
Gangrene (or gangrenous necrosis) is a type of necrosis caused by a critically insufficient blood
supply

Define necrosis:
accidental” and unregulated form of cell death resulting from damage to cell membranes and
loss of ion homeostasis

Types of cell death:

Necrosis, apoptosis

Page 16
Pathogenesis of necrosis:
Severe/prolonged ischemia: severe swelling of mitochondria, calcium influx into mitochondria and
into the cell with rupture of lysosomes and plasma membrane. Death by necrosis and apoptosis
due the release of cytochrome c from mitochondria

Define atherosclerosis:
Pathological process of the vasculature in which an artery wall thickens as a result of accumulation
of fatty materials such as cholesterol

Risk factors: smoking,HTN,D.M, family history, Increased LDL

Patient developed cough------> one bedside test to do : sputum analysis

xray -----> pleural plaque
Pleural plaques, the most common manifestation of asbestos exposure, are well-circumscribed
plaques of dense collagen that are often calcified
Significance: increased malignancy risk of mesothelioma and lung adenocarcinoma

Give one classification of lung cancer:

adenocarcinomas (most common), squamous cell carcinoma, large cell car- cinoma, and small cell
carcinoma.

Now the patient is presented with Mets, poorly differntiated, how to tell its epithelial origin?
Immunohistochemistry

If the tumour was epidermal growth factor positive, what will be the chemotherapeutic agent?
Tyrosine kinase inhibitor

Diverticulitis + endometriosis:
Stem: ( LIF pain+ peritonism -------> ruptured diverticulitis -------> Hartman's procedure ------->
histopath --------> diverticulitis+endometriosis)

Pathophysiology of diverticulitis:

Colonic diverticula result from the unique structure of the colonic muscularis propria and
elevated intraluminal pressure in the sigmoid colon. Where nerves, arterial vasa recta, and
their connective tissue sheaths penetrate the inner circular muscle coat, focal discontinuities
in the muscle wall are created. In other parts of the intestine these gaps are reinforced
by the external longitudinal layer of the muscularis propria, but, in the colon, this muscle
layer is gathered into the three bands termed taeniae coli. Increased intraluminal pressure
is probably due to exaggerated peristaltic contractions, with spasmodic sequestration of
bowel segments, and may be enhanced by diets low in fiber, which reduce stool bulk,
particularly in the sigmoid colon.

Page 17
How neutrophils migrate to the site of infection?

How did endometriosis got the colon?

theories are as follows:

• The regurgitation theory: proposes that endometrial tissue implants at ectopic sites via
retrograde flow of menstrual endometrium. Retrograde menstruation through the fallopian
tubes occurs regularly even in normal women and can explain the distribution of
endometriosis within the peritoneal cavity.
• The benign metastases theory : holds that endometrial tissue from the uterus can “spread”
to distant sites (e.g., bone, lung, and brain) via blood vessels and lymphatic channels.
• The metaplastic theory: suggests that endometrium arises directly from coelomic
epithelium (mesothelium of pelvis or abdomen), from which the müllerian ducts and
ultimately the endometrium itself originate during embryonic development. In addition,
mesonephric remnants may undergo endometrial differentiation and give rise to ectopic
endometrial tissue.
• • The extrauterine stem/progenitor cell theory: is a recent idea that proposes that stem/
progenitor cells from the bone marrow differentiate into endometrial tissue.

Page 18
Is endometriosis can increase the risk of cancer?
Yes, especially ovarian cancer ( 3.5 fold risk increase)

Few days later developped LIF collection why?

retained collection( pelvic abcess)

What antibiotics to give?

-Amoxycillin clavulinic (1.2 g BD for 7 days) to cover G+ve organisms

- gentamycin ( 80 mg BD for 3 days) to cover G-ve organisms
- Clindamycin ( 600 mg BD for 5 days) to cover anaerobes

Aortic stenosis:
Causes:
- Post- inflammatory scarring (rheumatic heart disease)
- Senile calcific aortic stenosis
- Calcification of congenitally deformed valve
-
How stenosis occur ?

- lipid accumulation, inflammation, calcification ----------> valve thickening and stenosis

Cause of sudden death in AS?

aortic dissection, MI

Aortic valve endocarditis, after a while weakness in Arm ?

Thromboembolism which lead to cerebrovascular stroke

Which coagulation system will not be affected by warfarin ?

Extrinsic patway

Define thrombus:

thrombus is defined as solid material formed from the constituents of blood in flowing blood

If metallic valve replacement was done and the patient developped IE, why the valve should be
removed?
-The valve will be a septic focus
- the valve will be dehiscent

If we found micrscopic branching hyphae on a removed metallic valve:

This is fungal infection:

- candida
- Aspergillus
- microsporum
- Trichophyton
- Epidermophyton

Page 19
Gastric carcinoma:
(Gastrectomy with splenectomy, pathology report)
Stem: surgery done -------> histopath ------> signet ring carcinoma

2 major risk factors for gastric cancer:

• H. pylori infection, chronic atrophic gastritis

. Intestinal metaplasia
. Pernicious anemia
. Adenomatous polyps more than 2 cm
. Previous gastric surgery
. HNPCC
. FAP

Discuss pathology report with the family in 4 simple lines:

- this is cancer of the stomach
- With incomplete resection
- With high possibility of recurrence
- The patient will require further resection and chemotherapy

7-10 days later the patient had axillary vein thrombosis ,what prediposes to that?

- hypercoagulable state in malignancy

6 months later came with ascites,derranged liver functions, hepatic mets/ mention 2 pathological
tests to do?

1-Ascites tap and cytology

2- liver biopsy from mets
3- FNAC from the left supravlavicular lymph node
4- tumour marker : CA72-4

Treatment of this patient:

- feeding jeujnostomy
- Palliative chemotherapy
- Palliation of ascites by repeated tapping
- Pain relief using opioids

Page 20
Polycystic kidney disease:
Stem: ADPK going for bilateral nephrectomy due to intractable abdominal pain

Describe gross pathology:

Enlargement of the kidney with multiple cyst formations

Mode of inheritence:
Autosomal dominant condition due to mutations in 2 genes: PKD1, PKD2

Pathogenesis of cyst formation:

The cells of the renal tubules divides repeatedly until causing an out-pocketing of the tubular wall
with the formation of a saccular cyst that fills with fluid derived from glomerular filtrate that enters
from the afferent tubule segment. Progressive expansion eventually causes most of the emerging
cysts to separate from the parent tubule, leaving an isolated sac that fills with fluid by
Page 21
transepithelial secretion. This isolated cyst expands relentlessly as a result of continued
proliferation of the mural epithelium together with the transepithelial secretion of sodium chloride
and water into the lumen

Other organs in the abdomen causing cyst formation:

Liver, ovaries,pancreas ,spleen

Copmlications:
- renal failure
- Infection
- Hypertension
,

Associated lesion in the brain:

Cerebral aneurysm

Type of matching before transplant:

-ABO blood matching

HLA matching: Human Leucocyte Antigens. HLA-

A, HLA-B and HLA-DR are the most important.
They are proteins located on the surface of WBC.

Types of graft rejections:

-Hyper-acute:
Due to presence of recipient antibodies against the donor tissue
Occurs within minutes
There is complement activation, clumping of red blood cells and platelets leading to interstitial
hemorrhage
Kidney swells and becomes discolored
Nephrectomy must be performed on transplanted organ
-Acute rejection:
Classified as accelerated if it occurs in the first week.
Acute if it occurs within first 100 days
T cell mediated with diffuse lymphocytic infiltration, arteritis and tubulitis
Can be reversed with high dose steroids
-Chronic rejection:
Occurs months to years after transplant
Humoral system is responsible for this type of rejection
There is graft fibrosis and atrophy

What types of malignancy occuring with immunosupression:

Malignancy: this is 5 times greater than the normal population. Most commonly squamous cell
carcinoma of skin, cervix, basal cell carcinoma’s, lymphoma and Kaposi’s sarcoma.

Sickle cell disease + brain tumour:

Page 22
(Stem: a lady known to have sickle cell didease, had head injury, CT done
and a temporal mass of 3.8 cm accidentally discovered)

What is sickle cell disease:

Sickle cell disease is a common hereditary hemoglobinopathy caused by a point mutation
in β-globin that promotes the polymerization of deoxygenated hemoglobin,that leads to the
replacement of a glutamate residue with a valine residue. The abnormal physiochemical
properties of the resulting sickle hemoglobin (HbS) are responsible for the disease. leading
to red cell distortion, hemolytic anemia, microvascular obstruction, and ischemic tissue
damage.
Complications:
- vaso-occlusive crisis: triggered by infection,dehydration, acidosis,affecting the bones( painful
bone crisis as in hand-foot syndrome),lungs( acute chest syndrome), brain( stroke and
retinopathy), spleen ( autosplenectomy)
- Sequestrtion crisis: in children , massive entrapment of sickle cell in the spleen will lead to rapid
splenic enlergement and hypovolemic shock
- Aplastic crisis: due to infection of red cell progenitors by parvo-virus
- Chronic tissue hypoxia: organ damage ( spllen, heart,kidney,lungs)
- Increased susptibility of infection with encapsulated organsims

Mechanism of autosplenectomy;
In early childhood, the spleen is enlarged up to 500 gm by red pulp congestion, which is
caused by the trapping of sickled red cells in the cords and sinuses . With time, however,
the chronic erythrostasis leads to splenic infarction, fibrosis, and progressive shrinkage, so
that by adolescence or early adulthood only a small nubbin of Fibrous splenic tissue is
left; this process is called autosplenectomy

What are the surgical relevance of sickel cell diseae?

- gall stones
- Autosplenectomy
- Avascular bone necrosis
- Osteomyeitis
- Pulmonary hypertension
- Heart failure

Why the patient is immunocompromised:

Because of autosplenectomy with increased susptibility of infection with encapsulated organsims

Most common brain tumour in elderly:

High-grade:
Gliomas and glioblastoma multiforme.
Medulloblastomas.

Low-grade:
Meningiomas.
Acoustic neuromas.
Neurofibromas.
Pituitary tumours.
Pineal tumours.
Craniopharyngiomas.

Secondaries:
Page 23
Manifestations of brain tumours:

The presentation will depend on location and rate of growth but includes features of a space-
occupying lesion and raised intracranial pressure (ICP) :

Headache, which is typically worse in the mornings.

Nausea and vomiting.
Seizures.
Progressive focal neurological deficits - eg, diplopia associated with a cranial nerve defect, visual
field defect, neurological deficits affecting the upper and/or lower limb.
Cognitive or behavioural symptoms.
Symptoms relating to location of mass - eg, frontal lobe lesions associated with personality
changes, disinhibition and parietal lobe lesions might be associated with dysarthria.
Papilloedema (absence of papilloedema does not exclude a brain tumour).

What if the tumour left untreated, -----> death

Biopsy showed squamous cells:

Metastatic SCC

Possible primary sources:

Scc of skin, lung, oesphagus, nasopharynx, cervix

Post biopsy had wound infection:

Common organisms:
Staph aureus

Wound discharge showed glucose :

CSF communication

Polytrauma+ transfusion:
Stem: hepatitis c patient ---- > trauma-----> blood loss/----> splenectomy+transfusion
------> DIC

Define DIC: it is a pathological consumptive coagulopathy due to activation of the

coagulation and fibrinolytic systems , activation of the latter leasds to formation of
microthrombi in many organs with the consumption of the clotting factors and platlets.

Characterised by:
- widespread hemorrhage
- Thrombocytopenia, decreased fibrinogen, increased FDPs

Functions of the platlets:

Platelets contribute to the hemostatic process in two different ways. First, through their
adhesive and cohesive functions that lead to the formation of a hemostatic plug. Second,
they can activate coagulation mechanisms

How platlets are formed from bone marrow?

From megakaryocytes

Page 24
Why this patient has bleeding tendency:
Because of the liver affection

Very late manifestations of HCV: cirrhosis, HCC

What activates intrinsic and extrinsic pathways:

Intrinsic pathway is activated by vessel injury which will lead to activation of factor 12
Extrinsic pathway is activated by tissue thromboplastin released by the damaged cells

APTT tests for intrinsic pathway

PT tests for extrinsic pathway and the common pathway

Hypersenstivity reactions:

Type1:This is due to mast cell degranulation mediated by IgE.

The reaction is almost immediate.
Examples include anaphylaxis, atopy and asthma

Type 2: due to antibodies directed towards antigens present on the surface of cells
Examples include transfusion reactions and autoimmune haemolytic anaemia

Type 3: due to the formation of antibody-antigen complexes (immune complex mediated)

An example is SLE

Type 4: delayed hypersensitivity reaction mediated by T-lymphocytes. Takes 48-72 hours

to see the effects.
An example is contact dermatitis

Type 5: due to formation of stimulatory autoantibodies in autoimmune conditions such as

Graves’ disease and myasthenia gravis.

Which blood product will you give?

Packed RBC's

Percentage of white blood cells in packed RBC's?

<5x10^6 cells/L ( leucoreduced Packed RBC's)-LPRC

Life span of RBC's:

120 days

What tests to do before blood transfusion:

ABO- RH

What is GXM:
Group cross matching: to test donor red cells against recepient serum to detect any
potential incompatibility through which antibodies in recipient cause hemolysis to donor
cells

Antigen in cross matching: ABO

Stages of bone healing:

Page 25
1. Hematoma formation (mass of clotted blood) at fracture site.
Tissue in fracture site swells, very painful, obvious inflamation, and bone cells are dying.

2. Fibrocartilaginous callus developes over a 3 to 4 week period.

This process involves

-capillary growth in the hematoma

-phagocytic cells invading and cleaning-up debri in injury site
-fibroblasts and osteoblasts migrating into site and beginning
reconstruction of bone

Note that the fibrocartilaginous callus serves to splint the fracture.

3. Bony callus begins forming after 3 to 4 weeks after injury and is prominent 2 to 3
months following the injury. Continued migration and multiplying of osteoblasts and
osteocytes results in the fibrocartilaginous callus turning into a bony callus.

4. Remoldeling. Any excess material of the bony callus is removed and compact bone is
laid down in order to reconstruct the shaft. Remoldeling is the final stage.

Effects of prolonged immotility on bone:

Loss of bone density and increased risk of osteoprosis

Infected implant, why you should remove?

Septic focus

What the 1st test to do?

Wound swab for culture and sentivity

What is PVL staph aureus?

Panton–Valentine leukocidin (PVL) is a cytotoxin—one of the β-pore-forming toxins. The

presence of PVL is associated with increased virulence of certain strains (isolates) of
Staphylococcus aureus. It is present in the majority of community-associated Methicillin-
resistant Staphylococcus aureus

What is the effect of this cytotoxin?

PVL creates pores in the membranes of infected cells and is the cause of necrotic lesions
involving the skin or mucosa, including necrotic hemorrhagic pneumonia.

MEN 1 syndrome:
Man with parathyroidectomy, pancreatic mass

Define hyperplasia:
Increase in the No. of cells in tissue or organ in response to a stimulus

How many parathyroid glands mostly affected?

Page 26
The 4 glands

Microscopic picture of hyperplasia?

- Microscopically, the most common pattern seen is that of chief cell hyperplasia,
which may involve the glands in a diffuse or multinodular pattern.
- Less commonly, the constituent cells contain abundant water-clear cells
(“water-clear cell hyperplasia”).
- In many instances there are islands of oxyphils, and poorly developed,
delicate fibrous strands may envelop the nodules.

The patient developped stupor , confusion and hypoglycemia( 1.2 mmol/l)

Why do you think ?
Insulinoma

What cell derived from ?

β-cell of islets of langerhan's

What other causes of unresponsive hypoglycemia do you know?

- abnormal insulin sensitivity,
- diffuse liver disease,
- inherited glycogenoses,
- ectopic production of insulin by certain retroperitoneal fibromas and
fibrosarcomas

C/p of insulinoma:
- -The clinical manifestations include confusion, stupor, and loss of
consciousness.( blood gucose 2.5 mmol/L) or less
- - These episodes are precipitated by fasting or exercise
- promptly relieved by feeding or parenteral administration of glucose.

Biochemical diagnosis:

- high circulating levels of insulin ( <10 µU/mL)

- high insulin-to-glucose ratio

What do you suspect as another pathology in this patient?

Pit. Adenoma( MEN 1)

What are the 3 gene mutations in insulinoma?

1- MEN1, which causes familial MEN syndrome, type 1, also is mutated in a

number of sporadic neuroendocrine tumors•
2- Loss-of-function mutations in tumor suppressor genes such PTEN and TSC2 (,
which result in activation of the oncogenic mammalian TOR (mTOR) signaling
pathway.•
Page 27
3- Inactivating mutations in two genes, alpha-thalassemia/mental retardation
syndrome, X-linked (ATRX) and death-domain associated protein (DAXX), which
have multiple cellular functions, including telomere maintenance..

What is double hit hypothesis?

Like all genes, tumor suppressor genes may undergo a variety of mutations;
however, most loss-of-function mutations that occur in tumor suppressor genes are
recessive in nature. Thus, in order for a particular cell to become cancerous, both of
the cell's tumor suppressor genes must be mutated. This idea is known as the "two-
hit" hypothesis

What is telomere?

A telomere is a region of repetitive nucleotide sequences at each end of a

chromosome, which protects the end of the chromosome from deterioration or from
fusion with neighboring chromosomes

What is apoptosis?
Programmed cell death

PROSTATE CANCER:
Stem : A man with BPH , Poor urine stream , low back pain

How to take a prostate biopsy?

Trus guided from: midlobe parasagittal plane at the apex, the midgland, and the
base bilaterally.

Why multiple biopsies?

- There is often only a scant amount of tissue available for histologic

examination in needle biopsies,
- malignant glands may be admixed with numerous benign glands
- Moreover, the histologic findings pointing to malignancy may be subtle
(leading to underdiagnosis),
- there are also benign mimickers of cancer that can lead to a
misdiagnosis of cancer

How to differntiate between rectum and prostate cells in a needle biopsy?

-Using immunohistochemical marker ( α-methylacyl-coenzyme A-racemase)

(AMACR)
- CEA ( in rectal cells)
Page 28
What are the gene mutations involved in pathogenesis of prostate cancer?

The most common acquired genetic lesions in prostatic carcinomas areTPRSS2-

ETS fusion genes and mutations or deletions that activate the PI3K/AKT signaling
pathway.

Patient went to radical prostatectomy , PSA is 7 3 months later

How can you judge the scuccess of radical prostatectomy ?

Fall in the level of PSA below detectable levels within 4-6 weeks

High PSA after prostatectomy-----> i should consider recurrence

Why PSA is not reliable?

- PSA is organ specific, but not cancer specific.

- Although serum levels of PSA are elevated to a lesser extent in BPH than
in prostatic carcinomas, there is considerable overlap.
- Other factors such as prostatitis, infarction of nodular hyperplasias,
instrumentation of the prostate, and ejaculation also increase serum PSA
levels

What is the grading system ?

Gleason score

It grades prostate tumors from 2 – 10, 10 being the most abnormal and therefore
the most likely to spread.
The pathologist allocates a number from 1 - 5 for the most common histological
pattern in the specimen, then does the same for the second most common
pattern.
The sum of these two numbers gives the Gleason score
One test to exclude bony Mets?
Alkaline phosphatase
What kind of metastases? Sclerotic
Why? Due to increased bone deposition due to increased osteoblastic activity

Post operative, patient developed fever, dusky red urine?

Page 29
Why? UTI
Which of the blood components will rise?
WBC's - neutrophils
Most common organisms?
E-coli
What is the rational in treating prostste cancer by bilateral orchidectomy?
Androgen depriviation
the growth and survival of prostate cancer cells depends on androgens,
which bind to the androgen receptor (AR) and induce the expression of
pro-growth and pro-survival genes.

What are the cells producing testosterone?

Leydig cells
BASAL CELL CARCINOMA:

Describe the lesion:

Pearly papule with a central ulcer with rolled in ( inverted) edges
Why the surrounding skin is red?
Due to the presence of dilated subepidermal blood vessels ( telengectassias)
Most propable diagnosis?
BCC
Natural hx of BCC?
Page 30
indolent with slow progression

locally destructive but limited potential to metastasise(never metastasize)-

what is your concern in pathology report?

Deep margin involvement

How would you manage a pt with deep margin involvement.

Re-excision

Treatment options for basal cell carcinoma.

:Surgical

Curettage and Electrodissecation: - (scraping away the tumour and stopping-

bleeding with cautery

Excision with primary closure, flaps, grafts, and secondary intention healing --
excision margin of 4 mm around the tumour is recommended where possible

Cryotherapy (with liquid nitrogen), but can't obtain tissue biopsy-

Mohs micrographic surgery – Serial tangential horizontal sections are taken and-
examined histologically until all margins are clear

:Radiotherapy

Topical photodynamic therapy - δ-aminolaevulinic acid made up in a 20% emulsion-

and applied topically, Tumour tissue absorbing this porphyrin metabolite becomes
photosensitive with its conversion to protoporphyrin IX and subject to
photodestruction when exposed to light, usually in the wavelength range 620-670
nm

-Topical fluorouracil 5%

Topical imiquimod 5%-

How to prevent recurrence of deep margin involvement during re-operation.

If recurrent, go for moh’s micrographic surgery(frozen section)

Skin graft placed for pt and subsequently had graft failure.

Cause for graft failure

Page 31
Wound infection

Common organism? S. aureus.

Wound c/s grew MRSA,What is MRSA.

Methicilin-resistant Staphylococcus aureus.

How would you manage this pt with MRSA wound infection.

if abscess---I&D-

Outpatient Inpatient

ANTIBIOTICS: ORAL-

oral as clindamycin,amoxicillin plus tetracyclin or tmp/smx,linezolid*

Hospitalized patient

Vancomycin Dose to target trough level 7-14days

Linezolid 600 mg twice daily, PO or IV 7-14

Daptomycin 4 mg/kg once daily 7-14

Telavancin 10 mg/kg once daily 7-14

Clindamycin 600 mg IV or 300 mg PO 3times daily

Decolonization with mupirocin nasal or chlorhexidine for body decolonization-

After exicision , the patient devlopped regional lymphadenopathy? FNAC Done

revealed (lymphocytes, PMNL, Histocytes, cells with an biloped nuclei)

Interpret:

Reed-Sternberg cells: (owl eye appearance)-------> lymphoma

Parotid tumours:

- What is the most common parotid begnin swelling ?

Pleomorphic adenoma
- What is the meaning of pleomorphic ?

Page 32
 remarkable histologic diversity
- describe pleomorphic adenoma appearance?
benign tumors that consist of a mixture of ductal (epithelial) and
myoepithelial cells, and therefore they show both epithelial and
mesenchymal differentiation
- clinical signs of malignancy?
* Facial nerve affection
* Rapid increase in size
* Fixity to the underlying structures
* Invasion of the overlying skin

- types of parotid tumours?

- features of malignant cells?

* Invasion: Malignant cells do not respect tissue boundaries, and can be seen infiltrating or
invading into surrounding structures
* Increased mitotic rate:.Malignant cells will often have increased numbers of mitoses.
* Differentiation and Anaplasia: Normal cells are usually structured in a particular way that
corresponds with their function. This is known as differentiation. Malignant cells may
become less differentiated as part of their path to malignancy. This is known as
anaplasia.
Well differentiated maligant cells show features similar to the parent tissue. For example,
well differentiated adenocarcinoma cells will tend to form gland-like structures; well

Page 33
differentiated squamous cell carcinomas may show intercellular bridging or keratin
formation.
Poorly differentiated cells have lost most of their resemblance to the parent tissue, which
may be difficult to identify without special staining techniques.
Anaplastic cells have no resemblence to their parent tissue, and usually indicate a very
aggresive malignancy.

* Anaplastic Features:

- Loss of normal tissue architecture: Normal cells are usually arranged in an orderly
fashion. Epithelial cells often have polarity, with their nuclei at a specific location.
Malignant cells lose this architecture and are arranged haphazardly
- Pleomorphism: Malignant cells may show a range of shapes and sizes, in contrast to
regularly sized normal cells. The nuclei of malignant cells are often very large (often
larger than the entirety of a normal cell) and may contain prominent nucleioli.
- Hyperchromatic nuclei: The nuclei of malignant cells typically stain a much darker colour
than their normal counterparts.
- High nuclear-cytoplasmic ratio: The nuclei of malignant cells often take up a large part of
the cell compared with normal cell nuclei
Giant cells: Some malignant cells may coalesce into so-called giant cells, which might
contain the genetic material of several smaller cells.

Single best test to differentiate between begnin and malignant cells? FNAC

Difference between cytology and histology?

Cytology is the study of cellular structure and function

Histology is the study of tissue under the microscope

How to rule out malignany intraoperative ?

Frozen section

If you find : lymphocytes, langerhan's giant cells -----> granuloma

If you find: brown pigmented cells ----> malignant melanoma
If you find : -------- > lymphoma

High senstivity test:

the ability of a test to correctly identify those with the disease (true positive rate)

High specificity test:

The ability of the test to correctly identify those without the disease (true negative rate).

Page 34
Scenario: Ca Oes Hist
Code Cairo

Scenario data sheet History taking

Scenario: Carcinoma of the Oesophagus
Code
Source: Prospero
Last updated: MCAP Aug 2011
Actor gender and age Male ideally 50-60
range
Couch or chair for actor Chair
Instr. outside prep. bay N/A
cand instr inside prep bay N/A
The time is: 14:00 weekday
The scenario takes place Outpatient clinic
Inst. outside the exam. Take a history from this patient who has been sent to the outpatient clinic, by
bay his GP because of increasing dysphagia
Instr. inside the exam. bay N/A

INFORMATION FOR THE ACTOR

The patient

Name Jack White

Date of birth 1/1/55
Sex Male
Job Landlord of The Black Lion
Patient's address: The Black Lion, Oak Road Anytown, Anyshire
The character the actor is to play:

Age range for actor from 40-65

Character: Patient
costume Casual
personal props: Newspaper, packet of cigarettes and a lighter
Scenario location and Outpatients 2.00PM weekday
time
Actor's instructions You have been the landlord of a local pub for 24 years. You are everybody's
best friend always; the life and soul of the party; nothing gets you down. You
will chat to anyone about anything.
Lunch is usually some of your wife's sandwiches eaten while you work behind
the bar. Some months ago you realized that it was taking longer and longer to
get them down. You found that you sometimes needed a second pint to help
wash them down. You joked that it was due to modern bread full of "genetic
flour", but you became quite worried about this although you tried not to show
it. You have been getting more indigestion for which you take some tablets
from the GP (which helped at first but not now) and several packets of
"Rennies" every day.

From time to time during the consultation, you take out your packet of
cigarettes, then realise where you are and hurriedly put them away.
You were generally well until 6 months ago, apart from Indigestion on and off
for a couple of years. You now have increasing difficulty in swallowing, meals
take longer and longer. Bread and meat are the most difficult. Drinking fizzy
drinks (bottle of beer) with meals helps. For the last few weeks you can eat
1
Scenario: Ca Oes Hist
Code Cairo

only sloppy food like porridge. When you vomited and brought up blood you
panicked and went to your GP who sent you urgently to out-patients.
You have lost at least 1 stone in 3-4 weeks

Medication:
Voltarol - pain killers for hip 2-3 every couple of days, used to be much more
before hip operation
Omeperazole (Zantac) for indigestion many prescriptions over the last 2 years

Things to say:
• It's just an ulcer isn't it
• I don't drink much ( a lie)
• I don't smoke much (another lie)
• I haven't got cancer, have I?
• Will I be alright?

You are terrified about cancer, a big operation and death.

Patient’s expectations You would like to be reassured that all is well, but you fear that you have
cancer of the gullet
Actor's background This patient probably has cancer of the oesophagus (gullet), which typically
information: presents with increasing difficulty in swallowing.
The previous history of testicular tumour is probably irrelevant, as is the history
of a hip replacement
Smoking and excessive drinking are well known risk factors for oesophageal
cancer.
This patient will need an oesophagoscopy (telescope test) and biopsy and
then if cancer is confirmed possibly a combination of radiotherapy
chemotherapy and surgery, but the outlook is not good.
There is an outside chance that this is benign oesophagitis.

Presenting Increasing difficulty with swallowing for a couple of months

Complaint Weight loss of about 1 stone in last month
History of Generally well until 6 months ago Indigestion on and off for a couple of months. Then
presenting increasing difficulty in swallowing, meals took longer and longer. Bread and meat were
complaint the most difficult. Drinking fizzy drinks (bottle of beer) with meals helped
For the last few weeks you can eat only sloppy food like porridge
When you vomited and brought up blood you panicked went to you GP who sent you
urgently to out-patients
You have lost at least 1 stone in 3-4 weeks
Normal For this patient
Cardio-vascular
system
Chest pain none
Palpitations none
Faints / none
Blackouts
Ankle swelling none
Claudication none
2
Scenario: Ca Oes Hist
Code Cairo

Respiratory
System
Short of breath no A bit on the stairs
Wheezing no
Cough no
Sputum no
Exercise capacity normal Probably getting less
Alimentary
System

Appetite normal Decreased now only eating sloppy foods and fluids
Change in weight no One stone weight loss in 3-4 weeks
Indigestion none Yes and getting worse
Dysphagia none Yes initially for bread and meat now for almost everything
Nausea no
Vomiting no Very occasionally but it was blood stained last week
Abdominal pain none Perhaps just a bit of upper abdominal pain
Bowels once/day A bit constipated lately
Urogenital
system

Urinary 2-3/day
frequency
Haematuria none
Nocturia no
Stream good
Periods( normal
Females)
Nervous system

Sleep OK
Headache no
Vision OK
Speech Ok
Fits never
Parasthesia none
Weakness none
Hearing Ok
Loss of- no
consciousness
Past Medical
History
Operations none Operation aged two for undescended testicle
This testicle (right) developed a tumour and was removed through a cut in
the groin when you were 20. You then had chemotherapy and have had no
trouble since.
Left hip replacement for osteoarthritis in this hospital 3 years ago
Tb no
Diabetes no
Jaundice never
DVT/PE no
Other none
3
Scenario: Ca Oes Hist
Code Cairo

Family History
A&W=alive and well
Mother A&W Dead- old age
Father A&W Dead - old age
Brothers A&W 4 all well, a mechanic, a newsagent, a baker and a professional magician
Sisters A&W none
Spouse A&W Works in the pub with you –a bit overweight
Children none Because of the chemotherapy
Familial disorder none
Medication
History
Medication none Voltarol 2-3 every couple of days for pain in your hip used to be a lot more
before operation
Omeprazole (Zantac) for indigestion on and off over the last two years
Allergies no
Social History

Job clerical Publican

Smoking no 20-30 per day
Alcohol none 2-3 pints per day at least and a bottle of rum per week
Accomodation house Over the pub
Sexuality Hetero.
Other factors none

INFORMATION FOR THE EXAMINER

Examiner instructions

Point of concern 1 Consider a diagnosis of carcinoma of the oesopghagus

Point of concern 2: Realise this patient will need early admission for investigation and treatment
patient will need urgent upper GI endoscopy
Point of concern 3 Note history of heavy drinking
Point of concern 4 Note history of heavy smoking
Point of concern 5 Enquire about barium meal
Point of concern 6: Concern about this patients nutritional status

Point of concern 7: Previous history of testicular tumour is probably irrelevant

Point of concern 8:

Point of concern 9:

Point of concern10:

CLINICAL EXAMINER 1 MARK SHEET

Knowledge: Knows symptoms of carcinoma of oesophagus

4
Scenario: Ca Oes Hist
Code Cairo

Knows risk factors for carcinoma of oesophagus

Professionalism 1: Is truthful with the patient about the probable diagnosis but does not remove
all hope
CLINICAL EXAMINER 2 MARK SHEET

Comms 2: Gets the facts about the dysphagia

Comms 3: Presents a clear history does not focus on irrelevant details

NOTES

For Editor none

Issues of Surgical Fact None of which I am aware.

5
 History taking
Pre- operative confusion :
- hello, i'm .... One of the surgical doctors , how are you today?
- Would you mind if I asked you some questions to test your memory?
Abbreviated mental test scoring:
*How old are you?
*What time is it to the nearest hour?
*Can you remember this address? 24 West St. I will ask you this at the end
*What year is it?
*What is the name of this place?
*What is my job? And what is the job of this person (e.g. a nurse)?
*What is your date of birth?
*When did WW2 end?
*Who is the current prime minister?
*Can you count backwards from 20-1?
*What was that address I asked you to remember?

Discussion:
The patient has AMS SCORE 2/10
She has a short term memory loss

Fitness for the operation?

Not fit for giving a consent , as she can not retain informations and she can not make an informed
decision

Should the operation go ahead?

No. The operation is non urgent, therefore it can be postponed until the cause of the confusion has
resolved. I would talk to my consultant and the anaesthetist in charge of the case to inform them of
the confusion and ask their advice before cancelling it.

What is your differential diagnosis?

- differential for this lady’s acute confusion is a urinary tract infection.

- Other causes include: . other sources of infection, metabolic abnormalities such as renal or
hepatic failure, hypoglycaemia and hyperthyroidism, hypoxia, hyperthermia, vitamin deficiency
such as thiamine deficiency, medication such as steroids, opiates or other sedating medication,
and being in an unfamiliar environment on the background of dementia.

Management: ?

I would take a history from the patient, the notes, family members and her GP and perform a
thorough systemic examination.

My initial investigations would include a urine dip and MSU, blood tests including inflammatory
markers, haematinics and thyroid function tests.

Imaging should be arranged, firstly a chest X-ray and then a CT head if there are any neurological
signs, or after other investigations return as negative.

Page 1
I would consider asking the medical registrar to see the patient to either take over care or give
appropriate advice.

Bleeding per rectum:

Scheme of history taking:
- identify your self
- Confirm the patient name and date of birth.
- Start by an open question: how can i help you today? Or what seems to be the proplem ?
- History of the presenting complaint( onset , duration, course, severity, ppt factors, releving
factors, associated features)
- Past medical and surgical history
- Drug history : doses, allergies
- Social history: occupation, home situation, mobility, smoking, alcohol
- Family history
- ICE: ideas, concerns, expectations
- Systems review

Discussion:
[History of the presenting complaint: ]
- onset: did this started suddenly or gradually?
- duration: when did you first noted this?
- course: does this bleeding comes and goes.? Does it get previously worse?
- Severity:what is the colour of the blood? , how much blood you notice every time?Streaks?
Teaspoon? More? Is that bleeding is painful when you pass stool?
- Releving factors: is there anything makes this bleeding stops
- Ppt factors: is there any thing makes that bleeding increases?
- Associated features: - do you have noticed any slime or discharge? Or pain in your tummy.?
- Do you have any disturbances regarding bowel habits?
- Abroad –Have you been abroad recently? If so , where?
- Tiredness –Have you been feeling more tired than normal recently? -
- - Swallowing/upper-GIT symptoms –Have you been nauseous or sick? ( If
so, ask about haematemesis. ) Any difficulties swallowing? Heartburn?
- Pain/pruritis ani
- Have you had any pain in your tummy? If so, SOCRATES. Have you
noticed any itching around the anus?
- Anorexia –How has your appetite been?
- Weight loss –Have you noticed any unintentional weight loss?
- Systemic features –Have you had any mouth ulcers? Fever? Painful red
eye? Joint or back pain?

[Past medical and surgical history: ]

Do you have any other medical conditions, see your GP for any thing, ever had surgeries?

[Drug history: ]
Do you take any medications? Dose? Do you have any allergy against any drug?

[Social history: ]
- What is your occupation?
- who is at home with you?
- do you have any difficulty with the stairs
- do you smoke ? How many packs/ day
- do you drink alcohol? How many units/ week

[Family history: ]
Page 2
Is there any one else in the family has had a similar problem?

[Elicit ICE: ]
Before i go any further, could i ask:
- what do you think the cause is?
- What are you the most concerned about?
- What are you hoping us to do for you?

[Systems review: ]

- resp., cvs: is there any chest pain,SOB, cough

- Malignancy: have you had any unintentional weight loss ,difficulty in swallowing, change in
bowel habits, night sweats
- Urinary: any proplems in passing urine?
- Rheumatic : any muscle or joint pain?
- Any thing i have missed?

Discussion:
What is your differential diagnosis?

The weight loss, change in bowel habit and PR bleeding are concerning. My main differential is
colorectal cancer, which would need thorough investigation. Other differentials for PR bleeding

Page 3
include haemorrhoids, inflammatory bowel disease, angiodysplasia, diverticular disease, benign
polyp, and an anal fissure. It may also be secondary to medication or a hematological condition.

What is the most important investigation to carry out?

As I am suspecting colorectal cancer, the most important investigation is a colonoscopy +/- biopsy
to examine the whole colon.
If immediately available in clinic, a rigid sigmoidoscopy may be carried out in the first instance

• Haematology: FBC (anaemia, leucocytosis of infective colitis, inflammatory bowel disease,

ischaemic colitis), low platelets (bleeding disorder), clotting screen, group and save / cross match
for transfusion.
• Biochemistry: U&Es, LFTs (hepatic failure with variceal bleed, malignancy)
• Arterial blood gases: Raised lactate (ischaemia), metabolic acidosis.
• ECG: Mesenteric ischaemia, atrial fibrillation (emboli).
• Endoscopy: OGD (to exclude upper gastrointestinal cause), sigmoidoscopy / proctoscopy
(haemorrhoids, anorectal lesion, distal colitis, rectal ulcer) and colonoscopy (malignancy,
diverticular disease, colitis, angiodysplasia).
• Mesenteric angiography (CT or invasive) / Technetium scan / Labelled red cell scan, if source not
identified by endoscopy (looking for angiodysplasia / Meckel’s diverticulum).
• Radiology: AXR (obstruction, toxic megacolon of inflammatory bowel disease) and US scan / CT
(if suspected malignancy, for liver metastases and staging).
• Microbiology: Stool cultures (infective colitis).

Dysphagia:
- Solids or liquids? –Do you have difficulty swallowing solids, fluids or both? Timing –Is it there all
the time or does it come and go?
- Onset –When did this start? Progression –Has it worsened over time?

Associated features:

- Stuck –Does the food get stuck in your throat when swallowing?
- Halitosis –Have you noticed having bad-smelling breath recently?
- Lump –Do you ever feel a lump in your throat?
- Gurgle –Do you ever notice gurgling or a wet voice after swallowing?
- Pain –Is there any pain when swallowing? Any chest pain?
- GORD/dyspepsia –Do you ever taste acid at the back of your mouth? Heartburn? Pain in your
tummy?
- Hematemesis –Have you vomited at all? If so, was there any blood?
- Bowels –Have you noticed any change in your bowels? How many times a day do you go to the
toilet? Has that changed at all? Have you noticed any blood in your stools? Is it darker or more
smelly than usual?
- Neuro –Have you noticed any weakness anywhere? Any problems walking?
- Autoimmune –Do you suffer with painfully cold hands? Dry eyes or mouth?
- Constitutional –Have you had any unintentional weight loss? If so , how much have you lost and
over how long?

Page 4
Severity:
Do you experience this difficulty of swallowing to solid or to liquid foods or both?

History taking as previous

Discussion:

Considering : difficulty in swallowing, weight loss, heavy smoking, alcohol drinking, hematemsis
my main diagnosis will be esophageal carcinoma causing mechanical obstruction of the
oesophagus
I also have to consider:
- lung cancer , pharyngeal pouch, retrosternal goiter ( compression from outside)
- Oesphageal web, plumer vinson sundrome
- Achalsia ( motility disorder)
- Myathenia gravis

Investigations:
- Full clinical examination checking for lymphadenopathy
- Bloods –FBC, U&Es, LFTs and clotting and bone profile
- Chest X-ray
- Oesophageal manometry: achalasia, GORD
- Barium swallow
- Endoscopy and biopsy
Page 5
- Oesophageal endoluminal US, also for staging of carcinoma.
- Videofluoroscopy –assessing for aspiration
- Staging CT scan, depending on what the previous investigations reveal

Treatment :
Operable cases: oesphagectomy + chemoradiotherapy
Non-operable cases: palliation: self expanding metallic stent, palliative chemotherapy and
radiotherapy , feeding jeujnosomy

Change in bowel habits (IBD)

- Open question –Can you tell me what has been going on?
- Specify –When you say constipation/diarrhoea, what do you mean exactly? Do you
mean you are going more/less often or the consistency has changed?
- Onset –When did you first notice this? Has this changed recently?
- Character/colour –What are the stools like? Are they watery, semi-solid or solid? Is
there any blood or mucus in the stools or on the tissue paper?
- What colour are your stools?
- Radiation (from upper GIT) –Do you get any dark, foul-smelling stools?
- Associated features :(BOWELS)
* Bloating –Do you tend to suffer from bloating and flatulence?
* Ouch! –Are you suffering from any abdominal pain? If so, SOCRATES
* Weight loss –Have you lost any weight recently? How is your appetite?
* Exhaustion –How have your energy levels been?
* Lasting urge –Do you feel like you always need to go to the toilet, even after you’ve just
been? Is this despite not passing very much stool? ( Tenesmus )
* Swallowing/upper-GIT symptoms –Any vomiting? ( If so, ask about haematemesis. )
Any difficulties swallowing? Heartburn?
* Extra-intestinal features IBD –Have you had any mouth ulcers? Fever? Painful red
eye? Joint or back pain?
* Foreign travel –Have you been abroad anywhere recently?
- Timing –How many times a day do you go to the toilet to pass faeces now? How often
do you normally go? What are your stools normally like? Have you ever suffered from
the opposite? (i.e. constipation/diarrhoea)
- Exacerbating/relieving factors –Does anything relieve the constipation/diarrhoea?
Does anything make it worse?
- Severity –How badly is this affecting your day-to-day life

Discussion:
Considering weight loss, diahrrhea, PR bleeding, mucous discharge, extra-intetinal
manifestations,my main diagnosis will be crhon's disease or ulcerative colitis
I will also consider:
- infective gastroenteritis
- Colrectal cancer
- Diverticular disease

Management:
Investigations:
-Abdominal examination including DRE
Page 6
-Routine bloods – FBC, U&E, CRP, LFTs, calcium, magnesium, phophate, Coagulation screen, -
Group and Save. (Looking for raised inflammatory markers, dehydration, electrolyte disturbance
secondary to diarrhoea, albumin as a guide of nutritional status, coagulation defects.)
-Stool sample
-Faecal occult blood test
-Abdominal Radiograph - assess for toxic megacolon
-+/-CT or MRI abdomen and pelvis if concerning features on examination and for pre-operative
planning if surgery is indicated
- colonscopy
Treatment:
Medical : mesalazine, prednisolone, immunomodualtors( infliximab)
Conservative: dietary control ( low residue diet)
Surgical : in toxic megacolon, IO, maignant transformation, fistulation, refractory cases

Thyroid status: (female with hyperthyroidism)

History taking as usual

Assiciated features:
Compressive symptoms:
1- changes in voice
2- difficulty in swallowing
3- do you breath well?

Toxic symptoms:
1- changes in vision or difference in eyes
2- diarrhea
3- menstruation ( do you menstruate regularly)
4- sleep disturbances
5- hot or cold intolerance
6- weight loss
7- mood or behavioral changes
8- appetite

Discussion:
Mr ... Is .... Y old , previously fit and well, presents with a lumb in her neck, the lumb has grown
over the past .... Years, in addition she has symptoms indicating hyperthyrodism such as .......
She has also compressive symptoms such as ..........
My main differentials will be:

- Toxic MNG
- simple MNG
- thyroid neoplasm
- Thyroiditis

Management:
Tripple assement:
. Full clinical examination
. Ultrasound imaging
. FNAC

Other investigations: radioisotope scan

Possible causes of sudden enlargement:

- hemorrhage inside a cyst.
Page 7
- Malignant: papillary, follicular , medullary carcinoma

Treatment: thyroidectomy ( hemi, near total or total) with such compressive symptoms

What possible complications of surgery do you advise this patient about?

- risk of RLN injury: hoarsness of voice, aphonia, stridor and possibility of tracheostomy
- Risk of hypocalcemia
- life long thyroxine replacement

Abdominal pain : ( IBS) female referred from her GP as chronic calcular cholecystitis

O’SOCRATES
- Open question –I believe that you are suffering from pains in your tummy. Can you tell me a bit
more about your problem?
- Site –Where exactly do you get this pain? Can you point to it precisely? Where did the pain first
manifest? Has it moved?
- Onset –When did this pain start? Minutes, hours, days, weeks, months?
- Character –What does the pain feel like? You may need to provide examples, such as cramping,
aching, sharp, knife-like, dull, twisting, excruciating, like an electric shock, etc.
- Radiation –Does the pain move anywhere else? Can you show me? Does it go into your back/
around the side/groin/testicles? Do you get shoulder-tip pain?
- Associated features :
* Have you noticed any weight loss? How has your appetite been?
* Have you had any difficulty swallowing? Any heartburn? Any vomiting? If so , have you noticed
any blood in the vomitus?
* Any change in your bowel motions? Any blood or mucus in your stools?
- Timing –Is the pain there all the time or does it come and go? What is the periodicity if any
( length of time the pain is present and how long between bouts )? Is there any particular time
where you have noticed you get the pain ( day, night, mealtimes, menses )? Have you ever had
this pain before? If so, what happened?
- Exacerbating/relieving factors –What, if anything, brings the pain on? Does anything make it
worse? Does anything make it better? Have you taken anything to relieve the pain? Is it getting
better/worse with time? Does body position make a difference?
- Severity –If you had to rate the pain from 1 to 10, with 10 being the worst pain you can imagine,
how would you rate it?

Social history: social stress( her husband left his job with some financial problems)

Discussion:
Mrs ..... Is ..... Y old , presented by abdominal pain, the pain is colicky in nature, it is not related to
meals, she experience it in the middle of her abdomen, has no special timing, no aggrevating or
relieving factors, associated with disturbed bowel habits, she also has some social stress
My main diagnosis will br IBS, I will also consider IBD, colon cancer, chronic calcular cholecystitis.

Management:
Investigations: abdominal ultrasound, AXR, colonscope, stool analysis, FBC
Treatment: fiber diet, antispasmodics, antidepressants

Abdominal pain ( chronic pancreatitis) :

History summary:

Page 8
40 y . Old divorced male with chronic epigastric pain radiating to the back for the past 1 year,with
steatorrhea, takes 5 glasses of beer/ day, previously admitted for acute pancreatitis. Takes 30 mg
of morphine / day to numb the pain, depressed

SOCRATES approach as usual

Differentials:
- chronic pancreatitis ( in view of epigastric pain, steatorrhea, previous attack of acute
pancreatitis, being an alcohol drinker)
- Pancreatic pseudocyst
- PUD

What do you think about the history of taking 30 mg of morphine, what should be the normal dose?
15-30 mg /4hours as needed

Investigations :
- secretin stimulation test
- Serum amylase and lipase ( elevated)
- Serum trypsinogen
- CT scan ( pancreatic calcifications)
- MRCP : identify the presence of biliary obstruction and the state of the pancreatic duct
- Endoscopic ultrasound

Treatment:

Medical treatment of chronic pancreatitis:

1- Treat the addiction :̔ Help the patient to stop alcohol consumption and tobacco smoking
̔ Involve a dependency counsellor or a psychologist
2-Alleviate abdominal pain:
̔ Eliminate obstructive factors (duodenum, bile duct, pancreatic duct) ̔ Escalate
analgesia in a stepwise fashion
̔ Refer to a pain management specialist
̔ For intractable pain, consider CT/EUS-guided coeliac axis block
3- Nutritional and digestive measures:
̔ Diet: low in fat and high in protein and carbohydrates
̔ Pancreatic enzyme supplementation with meals
̔ Correct malabsorption of the fat-soluble vitamins (A, D, E, K) and vitamin B12
̔ Medium-chain triglycerides in patients with severe fat malabsorption (they are directly absorbed
by the small intestine without the need for digestion)
̔ Reducing gastric secretions may help Treat diabetes mellitus
4- treat DM
The role of surgery is to overcome obstruction and remove mass lesions

Lower limb claudication:

Analysis of pain:

- Open question –Can you tell me about the pain?

- Site –Where do you get the pain? (buttock, thigh, calf)
- Onset –Did it come on suddenly or gradually?
- Character –What does it feel like? (cramping, tightening of muscles)
- Radiation –Does the pain go anywhere else?

Page 9
- Associated factors –Do you get any pain at night? Have you noticed any ulcers in your legs or
feet? If so , are they painful? , do you have any numb in your legs or feet? Do you have any
back pain
- Timing –Do you get the pain when walking or at rest?
- Exacerbating & relieving factors –Is it relieved by rest? Is it made worse if you walk faster or up
a hill? Does cold weather affect it?
- Severity –How badly does it affect you? How far can you walk before stopping?

Discussion :
My main diagnosis will br chronic lower limb ischemia causing vascular caludication
I will also consider : spinal canal stenosis, DVT, disc lesion causing spinal
claudications,osteoarthritis ,muskloskeletal injury

How to diff. Between spinal and vascular caludications:

Peripheral vascular disease :
- Claudication pain is a cramping pain in the calf, thigh or buttocks
- Brought on by exercise and relieved by rest (patients often pretend to ‘window-shop’ until the
pain disappears)
- Exacerbated by walking faster or up hills and also by cold weather
- Risk factors/associated factors for atherosclerosis: Diabetes Hypercholesterolaemia Stroke
- Rest pain may indicate critical limb ischaemia
Spinal claudication :
- Often relieved when walking up a hill
- Often has associated limb numbness
Sciatica :
- Shooting pain down the back of a leg to the feet
- History of lower-back pain

Management:.
Investigations:
- Full peripheral vascular, cardiovascular and neurological examination
- Assess gait and balance
- arterial duplex
- ct angiography ( if surgical intervention was needed)
- MR Angiography
Treatment:
- optimise blood sugar , cholesterol, blood pressure
- Antiplatlet agents: aspirin, clopidogrel
- Antilipemic agents: simvastatin
- Surgical treatment: endovascular stenting, surgical bypass, amputation

Anxious patient : ( SOB ) in pre-admission clinic

Lady planning for chlecystectomy, SOB for few minutes, increasing in frequency 6 weeks after
being scheduled for operation

- Onset –How long has this been going on for?

- Frequency –Are you always breathless or only sometimes? What sets it off?
- Relieving factors –Does anything help you get your breath back? If you rest for a while, does it
improve? Do inhalers help?
- Exacerbating factors –Does anything make it worse? Is it worse lying flat? Sleeping upright –
How many pillows do you sleep with? Do you have to prop yourself up? Do you ever wake up
gasping for air?

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- Severity –How far can you walk before the breathlessness stops you? Can you climb a flight of
stairs in one go? If not , how many can you manage?
- Associated features:
- Cough –Have you noticed a cough? If so , for how long? Do you bring anything up?
Have you noticed any blood?
- Wheeze –Do you get wheezy? Is it worse at any time of the day?
- Fever –Have you recently had a cough or cold? Do you have a fever?
- Constitutional –Have you had any weight loss? How is your appetite?
- Chest pain –Do you suffer from chest pain? If so, SOCRATES
- Palpitations –Do you get palpitations with the breathlessness
- Anxiety –If relevant , do you only get breathless when you are anxious?

Discussion:

The SOB described does not fit with cardiac or pleuritic chest proplem , and the patient tells me
that she has been investigated and ruled out. My top differential would therefore be anxiety
related to her impending operation.
I will also consider: anginal pain, pneumonia, pleurisy.

Management:

- I should contact the GP to get hold of all the notes regarding investigation of the patient’s chest
pain.
- I would examine the patient and ensure that we repeat the patient’s bloods, ECG, CXR and get a
baseline ABG on room air.
- I would want to ensure she had a recent echo and angiogram and discuss these with a
cardiologist.
- I would reassure the patient that she is going to be well looked after, and ask her is there was
anything we could do to allay her fears.
- I would also suggest that we involve her close relatives or friends so that she has an adequate
support network in place before and after the operation

Can the operation go ahead:?

As long as we have no documented evidence that there is no cardiac or resp. Illness, the
operation should go ahead

- FEV1: Volume that has been exhaled at the end of the first second of forced expiration
- FVC: is the amount of air which can be forcibly exhaled from the lungs after taking the deepest
breath possible
- FEV1/FVC ratio: It represents the proportion of a person's vital capacity that they are able to
expire in the first second of forced expiration

In obstructive lung disease, the FEV1 is reduced due to an obstruction of air escaping from the
lungs. Thus, the FEV1/FVC ratio will be reduced

In restrictive lung disease, the FEV1 and FVC are equally reduced due to fibrosis or other lung
pathology (not obstructive pathology). Thus, the FEV1/FVC ratio should be approximately normal

Page 11
Knee pain: (OA)
Footballer, had right knee injury 30 years ago, had knee operation that he has no idea about,
developed worsening right knee pain 4 months ago

Analysis of pain (SOCRATES)

-Site –Where is the pain?
-Onset –When did you first notice the pain? Was there any history of trauma?
-Character –What does the pain feel like?
-Radiation –Do you have pain anywhere else? (other joints)
- Associated features :
*Did you notice any changes in the shape of your knee?( deformity)
- Did you experience locking of your knee?( menisci)
- Did you experience giving away when walking? ( ACL)
- Did you notice any numbness?( neurology)
- Stiffness –Have you noticed any stiffness in your joint(s) when you wake up in the
morning? How long does that last for?
- Swelling –Have you noticed any swelling, redness or heat in your knee
- Extra-articular features:
* Rashes –Have you noticed any rashes anywhere on your body?
* Enteropathy –Have you had any diarrhoea?
* Uveitis/iritis –Have you had painful or red eyes?
- Spondyloarthropathy –Have you had any back pain?

- Timing –When do you get the pain? Is it there all the time or does it come and go? Are the
symptoms worse at any particular time of the day?
- Exacerbating/relieving factors –Does anything make it better? Does anything make it worse? Is
it made better or worse by the cold? Is it made better or worse by exercise? Does resting the
joint help the symptoms at all? What painkillers have you tried so far? Do they help?
- Severity –If you had to rate the pain from 1 to 10, with 10 being the worst pain you can imagine,
how would you score your pain? How do your symptoms affect your day-to-day life? Is there
anything you find you cannot do now as a result of your symptoms?

Discussion:

Mr ......... a ....year old gentleman who has been referred with increasing pain from his right knee.
This started approximately .......years ago and has been increasing in severity over the past 4
months. He is experiencing a dull constant ache that is increased on exertion and at the end of the
day. However, the joint does not swell, lock or become unsteady on walking. The pain is limiting
his daily routine., the patient has a past history of knee trauma and surgery

My main differential will be:

- OA ( traumatic)
Page 12
- RA
- Referred pain from hip or spine pathology

Managenent:

Invesigations:
- knee x- ray ( standing and weight bearing) : a-p , lateral views
Treatment:

Conservative

• Maintain or achieve a healthy weight i.e. aim to decrease weight, and therefore force, going
through a joint
• Regular exercise, with particular attention to strengthening the muscles around the joint.
For example in OA of the knee, cycling is beneficial
• Analgesia: care to be taken with NSAID's with relation to gastric irritation
• Heat application to the joint may offer relief
• Physiotherapy
• Intra-articular steroids

Surgical:
. Arthroscopy and arthrocentesis
• Realignment osteotomy
• Total or partial knee replacement

Will the patient be likely to play soccer in 9 months? No

Headache: ( subarachinoid hemorhhage)

- Open question –Would you please tell me about your headaches?
- Site –ask about frontal, occipital, temporal, unilateral, all over
- Onset –Did it come on suddenly? Do you have any warnings prior to the headache?
- Character –Was it one episode or multiple? Describe the pain
- Radiation –Does the pain move anywhere else?
- Associated symptoms :
* Fever –Have you been feeling ill or had a fever?
* Trauma –Have you banged your head, had a fall recently?
* Sensorimotor changes –Have you had any arm or leg weakness? Any visual disturbances? Any
other sensory disturbance? Have you ever lost consciousness?
* Meningism –Are you sensitive to light? Do you have any neck stiffness? Have you noticed a rash
anywhere?
* Seizures/blackouts –Have you ever had seizures or blacked out?
* Vision –Any eye pain? Visual disturbances? Nausea or vomiting
- Timing –When can you remember this starting? Was it continuous or intermittent? How long do
they last? When was the last time you had a headache?
- Exacerbating or relieving factors –Does it get worse on coughing? Is it worse at night or in the
early morning? Any particular activities or movements? Does anything relieve the pain?
- Severity –How bad is the pain on a scale of 1–10, with 10 being the worst pain you can
imagine? Has it changed over time? How is it now? Is it painful to touch or press over?

Past medical history:

polycystic kidney ( relevant history)

Page 13
Family history:
My aunt died suddenly of an aneurysm in the brain

Discussion :
My main differential is a subarachnoid haemorrhage, but I would also consider other causes of an
acute severe headache including :
meningitis, encephalitis, and a migraine, increased ICP due to brain tumour

Management:
I would manage him in an ABC manner, ensuring that he is stable and arrange appropriate bloods
and a plain CT head.

Investigations:
- CT BRAIN
- CSF Tapping

Treatment:
- I would refer this patient to a neurosurgical unit.
- bed rest, 3L of IV fluids /24h.
- oral nimodipine 60mg every 4 hours, and laxatives
- attempt to coil the aneurysm is made
- Burr holes
- Craniotomy
- Discuss in neurovascular MDT

Seizures: ( brain tumour)

- *Before:
- Open question –Can you talk me through what happened exactly? Where and when? What
were you doing at the time?
- Aura –How did you feel immediately before the episode? Any aura? Chest pain, anxious or
fearful? Did you have any warning that something was about to happen?
- Environmental –Did you trip over anything or slip?
- LOC –Did you lose consciousness? How long for?
- Witness –Did anyone witness the episode? How did they describe the episode?
- During Fall :
- How did you fall exactly? Did you hit your head?
- Seizure –Did you have a fit? Can you describe it? Did your whole body shake or only part of it?
-- Continence –Did you pass any urine or soil yourself?
- Tongue –Did you bite your tongue?

-After:
- Post-ictal state –How did you feel immediately after the fall/when you regained consciousness?
Were you confused? Drowsy? Aching muscles?
- Previous episodes –Has something like this ever happened before? If yes , can you describe
exactly what happened those times?

Page 14
Discussion:

Management:

Investigations : CT BRAIN , MRI BRAIN, EEG

Treatment:
- start anticonvulsant therapy after discussing that with my consultant :
Phenytoin ( 1g loading dose) then 300 mg once daily
Ensure that the patient is on steroids( 4mg dexmethasone QDS)
- discuss in neuro-oncology MDT
- stealth guided biopsy
- Resection and debulking

Hematuria ( bladder cancer) :

CLOTS

- CLarify –When do you notice the blood? Is it only when you pass urine? Is there any chance it
could be coming from elsewhere? What colour is it? Have you recently eaten any beetroot?
- Onset –When did you first notice the blood?
- Timing –Is there always blood in your urine or does it come and go? Have you had this before?
Is the blood present at the start of urination, the end or throughout?
- Severity –Do you pass any clots?
- Associated symptoms:
- Pain –Do you have any pain when you pass urine? Any pain in your tummy or back? If so,
SOCRATES
- Frequency –Any change in frequency? Any trouble with incontinence? Do you get sudden
irrepressible urges to pass water?
- Nocturia –How often do you get up at night to pass urine? Urinary stream –Do you have
difficulty getting the stream started? Is there prolonged dribbling at the end? Is your stream
powerful or weak?
- Constitutional –Have you been unwell recently, or had any fever or chills? How is your appetite?
Have you lost any weight?
- Trauma –Have you had any trauma to your stomach or groin recently?

Social history: occupation? Aniline dyes and beta-naphthylamine

Discussion:
Mr........ Is .......y old , presented by painless hematuria one month ago, with associated weight
loss over the last ........ , there is no any abdominal or loin pain, there is no proplems in urine
stream, he is concerned about the possibility of having cancer

DD:
- my main dd will be bladder cancer, renal cell carcinoma considering (his hemorrhage, weight
loss, occupation)
- Stone kidney, bladder, ureter
- Infection
- Trauma
- Bleeding tendency

Page 15
Management:
- urine dipstick to confirm hematuria, assess infection, send a sample for cytology
- Bloods: FBC, U&E, clotting screen , PSA
- Cystoscopy And biopsy
- u/s, CT

Treatment:
Depends on the stage and the grade of the tumour
- surgical: TURBT, Radical cystectomy
- Non- surgical: chemotherapy and radiotherapy and immunotherapy

Urine retention: (BPH)

History taking as usual

Associated features:

- do you have any pain during urination?

- Any redness or blood in your urine?
- Any bone pains?
- do you have proplems in urination that awakes up from sleep
- Do you have any hesitancy in starting micturition?
- Do you have any senasation about incomplete evacuation
- Do you have any proplems with erections

Drug history:
Patient takes nasal sprays containing phenylephrine ( which may cause additive effect to
tamsulosin espcially in decreasing blood pressure and postural hypotensions)

Discussion:
Mr ..... Is ..... Y old, presenting with difficulty in intiating urination, slow stream, hesitancy ,urgency
and incraesed frequency. He does not have dysuria, hematuria, bone pains, or weight loss

DD:
- begnin prostatic hyperplasia
- Overactive bladder
- Prostatic cancer
- Obstructive bladder pathology( malignancy or calculi)

Management:
Investigations:
- full clinicaL examination including DRE
- Bloods : PSA , Urine analysis, U&E
- imaging : abdominal u/s , transrectal u/s
-
- Treatment:
Medical:
- Tamsulin ( 1alpha adrenergic blocker)
- Finasteride ( 5 alpha reductase inhibitor)

Surgical:
TURP

Page 16
Unilateral tonsillar enlargement: ( SCC tonsils)
Systems review:

Asks specifically about the following:

Weight loss
Fevers
Night sweats
Difficulty swallowing
Cough / sputum

Discussion:

Mr....... Is ...... year old previously fit and well gentleman, has presented with a 2 month history of
an enlarging left tonsil. He has lost approximately half a stone in weight and has increasing
discomfort on swallowing, with no other symptoms.

Dd:

-Squamous cell carcinoma (SCC) tonsil

-Lymphoma
-Asymmetrical tonsils (unlikely)
-Tuberculosis
- glandular fever.

Management:
Investigations :

-FBC: looking for raised WCC associated with infection

-U+E’s: looking for renal impairment if patient has had decreased oral intake
-LFT’s: derangement may indicate glandular fever or metastasis
-Monospot test (detecting glandular fever)
-Biopsy and EUA (examination under anaesthesia)
-panendoscopy

Treatment:
- Staging: MRI neck, CT neck, u/s liver
- Discuss in MDT
- Block neck dissection ( radical, modified radical, selective)
- Radiotherapy

Depression : ( reactive depression post operative on discharging )

Opening the consultation:

-Introduce yourself – name/role

Developing a rapport:

-“How have you been feeling recently?”

Page 17
Screening for core symptoms:
Screen for core symptoms of depression – feelings of depression, anhedonia and fatigue.

“In the past days during your hospital stay have you…”

Felt down, depressed or hopeless?

Found that you no longer enjoy, or find little pleasure in life?
Been feeling overly tired?

Assessing biological symptoms of depression:

Screen for the presence, and assess extent of any biological symptoms

Biological symptoms
Sleep cycle:

“How has your sleep pattern been recently?”

“Have you had any difficulties in getting to sleep?”

“Do you find you wake up early, and find it difficult to get back to sleep?”

Mood:

“Are there any particular times of day that you notice your mood is worse?”
“Does your mood vary throughout the day?”
“Do you find that your mood gradually worsens throughout a day?”

Appetite:

“Have you noticed a change in your appetite?”

“What is your diet like at the moment?”
“What are you eating in a typical day?”

Libido:

“Have you noticed a change in your libido?”

“Since you have been feeling this way, have you noticed a difference in your sex drive?”

Past psychiatric History:

Previous episodes of depression or dysthymia:

“Have you ever felt like this before?”

“Have you ever had any other periods of feeling particularly low?”
“In the past, have you had any problems with your mental health?”
“Have you had any counselling for any issues before?”
“Have you ever been admitted to hospital because of your mental health?” If so, obtain details –
time, method of admission, result.

Management :
Mild :
- Regular exercise
Page 18
- Advice on sleep hygiene (regular sleep times, appropriate environment)
- Psychosocial therapy –CBT
Moderate to severe:
- Regular exercise, advice on sleep hygiene,
- CBT
- Medication –SSRIs
- High-intensity psychosocial intervention (CBT or interpersonal therapy)
- Immediate and considerable high risk to themselves or others: Admit to psychiatric ward (use
Mental Health Act if necessary)

Impotence: ( psychological)
Ask about:
- Are you ever able to obtain an erection suitable for penetration, even momentarily?
- Is your ED getting worse or stable?
- How long have you had trouble attaining or maintaining an erection?
- How hard is the erection, on a scale of 0-100?
- Are you able to achieve orgasm and ejaculation?
- Approximately how long are able to have intercourse before ejaculating?
- Do you experience nocturnal or morning erections?
- Is penile curvature ( Peyronie disease) a problem?
- Drug history:
* Anti hypertensives
* Antiulcer drugs (eg, proton pump inhibitors [PPIs] and cimetidine)
* Lipid-lowering (eg, statins and fibrates)
* 5-Alpha reductase inhibitors (eg, finasteride and dutasteride)
* Antidepressants
* Antipsychotic drugs
* Testosterone and anabolic steroids

- Did the onset of ED coincide with a specific event

- Do you have diminished sexual desire? If so, how long have you had this? Is your diminished
sexual desire a primary symptom, or is it a reaction to poor sexual performance?
- Do you have any feelings of performance anxiety?

DD:
- psychological impotence ( considering the presence of morning erection and the stresful
conditions of his life)
- I will also consider:
- Venogenic erectile dysfunction
- uncontrolled D.M
- atherosclerosis
- renal failure
- M.S
- hyperprolactinemia
- BPH
- leriche syndrome
- anti hypertensive drugs.

Investigations:

- Haematology: FBC, erythrocyte sedimentation rate, haematinics, clotting screen, group & save. -
- Glycated haemoglobin (cardiovascular risk assessment).
Page 19
- • Biochemistry: U&Es, LFTs, CRP, lipid profile.
- • Prostate specific antigen (if relevant history).
- • Serum free testosterone.
- • Serum prolactin.
- • Serum FSH / LH.
- • ACTH (synacthen) stimulation test.
- • Urinalysis: Microscopy to exclude a genitourinary cause.
- • Radiology: –Duplex ultrasonography to assess vascular function of the penis. –
Ultrasonography of the testes to exclude any abnormality. –Transrectal ultrasonography to
exclude any pelvic or prostatic abnormality.

- Angiography: It can be useful for planning vascular procedures / reconstruction, particularly

following trauma.

Back pain: ( functional back pain ) / cauda equina

5 year history of back pain ,worse in the last 3 years, MRI 4 years ago showed mild degenerative
change , no neurological symptoms , no trauma, disabled husband, work commitment.

- Site –Where exactly do you feel the pain? Can you point to the area?
- Onset –When did you first notice the pain? Did it come on suddenly or gradually? Was there
any history of trauma? Have you had it before? If so , is it the same pain or different?
- Character –What is the pain like?
- Radiation –Does the pain go anywhere else? Does it travel down your legs? If so, how far? - --
- Associated features :
* Cord compression / cauda equina: –Have you had any problems with your waterworks?
Bowels? Have your legs been feeling weaker than usual? Have you had any strange sensations
down your legs or buttocks? Have you had any difficulty in gaining an erection?
* Inflammatory –Is your back stiff in the morning? If so , how long does that last for? * * *
* Constitutional –Have you noticed any significant weight loss over the past few months? How is
your appetite? Have you been feeling feverish or ill recently? How has your mood been?
- Timing –Is the pain always there or does it come and go? Is it worse at any particular time of
the day?
- Exacerbating/relieving factors –Does anything make the pain better? Anything make it worse?
Is it made better or worse by movement? Is it made better or worse by rest? Is it worse when lying
down or standing? Is it tender when you press on it? Have you tried taking any painkillers for it? -
-- Severity –If you had to score the pain between 1 and 10, with 10 being the worst pain you can
imagine, how would you score your pain?

Social history:
Who is at home with you?
Her husband is bed ridden and she has to take care of him

Discussion:

My main differential diagnosis will be :

- functional back pain (Mechanical lower-back pain) :
.localised pain that worsens with movement and changes in posture
.history of heavy lifting
. history of previous similar episodes over a number of years
. No features of systemic illness, nor neurological symptoms
- I have also to rule out organic pathology: Prolapsed intervertebral disc, spinal mets,
Seronegative spondyloarthropathy( ankylosing spondylitis),Spinal canal stenosis,Non-spinal
causes of back pain( AAA, fibromyalgia, pancreatitis, renal calculi)
Page 20
Cauda equina:
- Urinary and faecal incontinence
- Sensory numbness of buttocks and backs of thighs and weakness of legs

Investigations:

- A full examination is required, particularly looking for perianal sensory loss and anal tone.
- I would carefully check for a reduction in power and decreased reflexes.
- Back examination and lower-limb neurological examination
- Bloods –FBC, LFTs, U&Es, CRP and ESR Chest X-ray and QuantiFERON-TB Gold if TB
suspected
- MRI (not needed if the history suggests uncomplicated mechanical back pain)
- Urgent MRI/CT scan if cord compression or cauda equina is suspected
- X-ray and a subsequent DEXA scan if a crush fracture is suspected

Management :
Simple back pain (including prolapsed intervertebral disc):
- Advise to stay active and avoid prolonged bed rest Physiotherapy, regular analgesia and
consider short-course muscle relaxants
- Serious pathology or red-flag symptoms: Cord compression –dexamethasone and urgent
surgery; radiotherapy in malignancy
- Cauda equina syndrome –urgent surgery
- refer to social worker

Chest pain : ( PE)

- Site –Where exactly is the pain? Can you point to where it is?
- Onset –When did it start? Did it come on suddenly or gradually? What were you doing at the
time?
- Character –How would you describe the pain?
- Radiation –Does the pain go anywhere?
- Associated factors :

* Breathlessness –Do you get breathless?

* Orthopnoea –Do you ever get breathless when lying flat? How many pillows do you sleep with at
night?
* Paroxysmal nocturnal dyspnoea –Do you ever wake up gasping for breath?
* Cough –Have you noticed a cough? Do you bring anything up? Any blood?
* Constitutional –Have you noticed any weight loss? How is your appetite?
* Musculoskeletal –Is the pain worse on movement? Does it hurt to press on the area?
Page 21
* Do you have any lower limb pain or swelling?

- Timing –Is the pain always there or does it come and go? What brings the pain on? Have you
ever had this pain before?
- Exacerbating/relieving factors –Does anything make the pain better or worse? Is it worse when
you walk? Does it go away with rest? Is there any relation to eating food? Is it better when you
are in any particular position, e.g. sitting up? Is it worse when taking deep breaths? Severity –
How bad is the pain on a scale of 1–10, with 10 being the worst pain you can imagine? How
would you score it at its worst?

Discussion:
Considering :pleuritic chest pain, acute onset of SOB,hemoptysis, my main diagnosis will be
pulmonary embolism , i will also consider:

- pneumonia
- Basal atelectasis
- MI

Manegement:
Investigations:
- CTPA
- V/Q scan
- CXR
- ECG
- ABG
Treatment:
- ABC PROTOCOL
- Non massive : heparin untill APTT 50-60 sec.
- Massive : thromolysis/ embolectomy

Inguinal hernia :
History taking as usual:

-How long have you noticed this symptom?

- What were you doing when you first noticed the bulge?
- Is the bulge always present or does it appear and disappear.
- When does it appear and when does it disappear or what do you do to make it disappear?
- Is there pain on the swelling?( uncomplicated hernia is classically painless)
- Is there change in the overlying skin?
- Is there wound or sore over the bulge?
- Is there discharge ( pain, change in overlying skin and discharge may suggest strangulation or
inflammation )

Ask for other GIT symptoms:

Abdominal pain, abdominal rumbling, abdominal distension, vomiting or constipation (can the
patient link these symptoms with the appearance of the bulge?)

- Is there straining at defecation

- Is there abdominal mass or distension

Review of other systems:

Page 22
All other systems must be reviewed starting from the nervous system. But the clinician should pay
attention to symptoms of chronic obstructive airway disease and obstructive uropathy such as
chronic cough and straining at micturition respectively

Special notes:
ICE:
How does a henia happen?
With straining like you do, there will be muscle tearing , and some gut will protrude through the
defect

Could it be better?
It usually needs a surgical operation for repair, the operation may be in open fashion or key hole
surgery

Where to get back to work?

Few weeks

History:
Stamina tonic : what are the components of it? Is it contains any steroids
Visit of the GUM clinic, foreign travel: did you make test for HIV, When you came back , did you
repeat it?

Page 23
Page 24
[Code] [Title] Summary

MRCS OSCE
Scenario summary sheet

Code
Title
Syllabus area Imflammatory bowel disease
Content area Clinical, communication and procedural skills
Station type History taking
Double manned – surgeon and lay examiner
Domains assessed Clinical knowledge and its application 4 marks
Clinical skill 2 x 4 marks
Communication 4 marks
Professionalism 4 marks

Source roger Vaughan 15/6/2014

Last updated
Used

Props and equipment

Actor
24year old male/female Actor to receive full scenario in advance of diet.
College
Desk/table.
Pencil and paper for candidate’s notes.
Chairs for candidate and two examiners.
Specify chair or couch for actor, depending on condition
 [Code] Candidate instructions

Candidate instructions
A 24year old patient has been referred by their GP with
diarrhoea and abdominal pain.
You are to take an appropriate history in 6 minutes. If you
complete your history within the 6 minutes you should
indicate to the examiners that you are ready.

In the remaining 3 minutes the examiners will ask you to

present a summary of the history [amend as appropriate for
assessment of capacity/mental state etc.]. They may also
ask you to discuss any particular physical signs you would
look for on examination, the likely differential diagnosis,
appropriate investigations and a management plan.
You may make notes while taking the history and refer to
them during you presentation. Paper is provided for this.
You will be able to refer to the front sheet of the patients
notes which are with the patient.
 [Code] [Title] Actor instructions

Information for the actor

Patient details
Name: George/georgina paston Age: calculate from DOB DOB: 20/4/1990
Sex: Job: Hospital number:
Patient’s address: GP address:
16 victoria avenue Dr PR Smith
Anytown High Street Surgery
High Street
Anytown, AB12 3XY

Character: Patient Age range for actor from 24 to 40

Costume: not special
Personal props:
Time and place: This scenario takes place outpatients
The scenario
You are a 24 year old who has presented with 9 month history of diarrhoea and
vomiting. This started following a camping trip to France in the summer. You took this trip
with a now former male/female partner ( opposite sex) You started passing mucous and
blood ( you describe this as slime in your stools and find it abhorrent ) intermittently This has
become frequent in last 2 months You now pass stools 4 to 5 times per day . You think it is
getting worse.

You have a weight loss of 12 kilos of weight. You are finding it difficult to cope by yourself
and carrying out work as a living in house nanny .You are struggling to look after flat and
have been feeling weak

When asked about your stools .They are not smelly and flush away normally. The blood in
the stools is mixed. On opening your bowels you have considerable pain.

3 weeks ago you saw your gp because your left knee has become swollen and painful as
have your toes.
Your gp asked whether you were on aspirin because he had noticed bruise like areas on
your shins. ( you thought it was due to bumping into furniture )
You do not volunteer the candidate about joint pain or bruising unless asked)

In past you have had no major illnesses in past

You have no allergies and was fit and well.
Drugs you take Imodium recently to help diarrhoea
You are a vegetarian

Medications Imodium self-medication if asked

Ibuprofen 40mg tds for back pain

Non smoker Alcohol 2 glasses wine per night and 4 to 8 at weekends

Background
You are very anxious teacher who has had a steady relationship for 2 years before
the holiday in France . You think this was caused by an infection you caught when there
and ask whether this was a infection caused by unprotected sex

Specific worries is this due to camping holiday in France as you were living rough and
 [Code] [Title] Actor instructions

drinking fresh milk

Have you got cancer as young man died recently who got the MBE
Why are you losing weight
Is it a food allergy or the drugs
[Code] [Title] Examiner instructions

Examiner instructions
In this scenario, the candidate has 6 minutes to take an appropriate, focused and relevant clinical
history from a simulated patient. They will then have 3 minutes to produce a sensible summary of
relevant positive and negative points from the history and a differential diagnosis. They should be
able to suggest appropriate investigations.
Both examiners should listen to and observe the candidate (who may make notes) taking the
history without interruption. If the candidate does not appear to be performing the required task
properly, invite them to re-read the candidate instructions.
After 6 minutes (or sooner if the candidate is ready), Examiner 1 (surgeon) uses the remaining time
to ask the candidate the following.
1. To summarise the history.
2. To give the differential diagnosis and explain how they would justify their answer and which
tests are essential .
3. To explain how the diagnosis would be confirmed and treatments (see below).
.
Examiner 1 (surgeon) marks the domains clinical skill and clinical knowledge.
Examiner 2 (lay) marks the domains communication and professionalism.
The examiners should not swap roles between candidates during the circuit.
Both examiners will assess the overall performance of the candidate.
Examiner 1 looks at whether the candidate has gathered accurate information relevant to the
specific scenario along with important systemic effects of the condition under consideration through
the use of proper closed questions and systematic enquiry.
Examiner 2 assesses the candidate’s general approach to the taking of the history as instructed on
the mark sheet. They examine the candidate–patient interaction and check for shared
understanding between candidate and patient. During the discussion with Examiner 1 after the
history-taking, they should consider whether the information is being fed back with synthesis and
prioritisation.
If the candidate finishes early they must remain in the bay and wait for the indication to move on.
Scenario-specific guidance

Critical points
1. History of Chrohns ? ulcerative colitis
2.Must mention leg bruising and eye problems and joint pains

Investigations essential FBC ESR Abdominal CT Endoscopy/colonoscopy Stool culture essential

Check haematinics i.e. Folate B12 Iron

Treatment options Mezalazine , Prednisolone If Chrohns Bilologics Surgery if toxic dilation .

Dietary control (low residue diet)
[Code] [Title] Examiner instructions

Generic domain descriptors

Clinical knowledge
Possesses the clinical knowledge specified in the syllabus.
Able to understand, synthesise and apply knowledge in a clinical context.
Clinical skill
Capable of applying sound clinical knowledge, skill and awareness to a full investigation of problems to
reach a provisional diagnosis.
Communication
Able to assimilate information, identify what is important and convey it to others clearly using a variety of
methods.
Capable of adjusting behaviour and language as appropriate to needs of differing situations.
Actively and clearly engages patient/carer/colleague(s) in open dialogue.
Professionalism
Able to accommodate new or changing information and use it to manage a clinical problem.
Anticipates and plans in advance.
Prioritises conflicting demands and builds contingencies.
Demonstrates effective management of time and resources.
[Code] [Title] Examiner 1 mark sheet for examiner 2 info

EXAMINER 1 MARK SHEET Candidate number:

for examiner 2 info only Examiner number:
Date:
Signature:
Scenario code and title
Domains assessed Clinical skill 2 x 4 marks
Clinical knowledge and its application 4 marks

Domain Mark
Clinical skill 1 0–4
Elicits necessary detail/information from patient/colleague.
Accurately identifies key clinical symptoms.
Accurately interprets key clinical symptoms.
Has a systematic, complete and organised approach.
General assessment of patient is satisfactory.
insert scenario-specific criteria
Clinical skill 2 0–4
Presents a well organised history.
Accurately describes key clinical symptoms.
Understands key clinical signs.
Overall assessment of patient is satisfactory.
insert scenario-specific criteria
Clinical knowledge 0–4
Demonstrates knowledge in the essential areas tested.
Demonstrates knowledge in the majority of areas examined.
insert scenario-specific criteria

Examiner 1 overall assessment (circle one):

Fail Borderline Pass

Agreed joint overall assessment (circle one):

Fail Borderline Pass

This is required whether the examiners’ individual overall assessments differ or not.
[Code] [Title] Examiner 2 mark sheet for examiner 1 info

EXAMINER 2 MARK SHEET Candidate number:

for examiner 1 info only Examiner number:
Date:
Signature:
Scenario code and title
Domains assessed Communication 4 marks
Professionalism 4 marks
Domain Mark
Communication 0–4
Uses appropriate opening/introductions and establishes purpose of the interview.
Uses technical/non-technical language appropriately, accurately and with fluency.
Confirms that there is common understanding.
Establishes relationship of respect with others.
Adapts language/behaviour as needed and adjusts style of questioning (open/closed) as
appropriate.
Establishes rapport with others.
Uses appropriate body language and eye contact.
Demonstrates clarity and focus in communication.
Demonstrates active listening towards others.
Demonstrates empathy and responds appropriately to patient’s concerns and questions.
Adequate closure of interview.
insert scenario-specific criteria
Professionalism 0–4
Plans ahead, identifies requirements and prioritises accordingly.
Demonstrates strategic and tactical planning ability.
Able to recognise and manage complex and competing needs.
Manages time and resources effectively.
insert scenario-specific criteria

Examiner 2 overall assessment (circle one):

Fail Borderline Pass

[Code] [Title] Examiner 1 (surgeon) mark sheet

EXAMINER 1 (SURGEON) Candidate number:

MARK SHEET Examiner number:
Date:
Signature:
Scenario code and title
Domains assessed Clinical skill 2 x 4 marks
Clinical knowledge and its application 4 marks

Domain Mark
Clinical skill 1 0–4
Elicits necessary detail/information from patient.
Accurately identifies key clinical symptoms.
Accurately interprets key clinical symptoms.
Has a systematic, complete and organised approach.
General assessment of patient is satisfactory.
insert scenario-specific criteria
Clinical skill 2 0–4
Presents a well organised history.
Accurately describes key clinical symptoms.
Understands key clinical symptoms.
Overall assessment of patient is satisfactory.
insert scenario-specific criteria
Clinical knowledge 0–4
Demonstrates knowledge in the essential areas tested.
Demonstrates knowledge in the majority of areas examined.
insert scenario-specific criteria

Examiner 1 overall assessment (circle one):

Fail Borderline Pass

Agreed joint overall assessment (circle one):

Fail Borderline Pass

This is required whether the examiners’ individual overall assessments differ or not.
[Code] [Title] Examiner 2 (lay) mark sheet

EXAMINER 2 (LAY) Candidate number:

MARK SHEET Examiner number:
Date:
Signature:
Scenario code and title
Domains assessed Communication 4 marks
Professionalism 4 marks
Domain Mark
Communication 0–4
Uses appropriate opening/introductions and establishes purpose of the interview.
Uses technical/non-technical language appropriately, accurately and with fluency.
Confirms that there is common understanding.
Establishes relationship of respect with others.
Adapts language/behaviour as needed and adjusts style of questioning (open/closed) as
appropriate.
Establishes rapport with others.
Uses appropriate body language and eye contact.
Demonstrates clarity and focus in communication.
Demonstrates active listening towards others.
Demonstrates empathy and responds appropriately to patient’s concerns and questions.
Adequate closure of interview.
insert scenario-specific criteria
Professionalism 0–4
Plans ahead, identifies requirements and prioritises accordingly.
Demonstrates strategic and tactical planning ability.
Able to recognise and manage complex and competing needs.
Manages time and resources effectively.
insert scenario-specific criteria.

Examiner 2 overall assessment (circle one):

Fail Borderline Pass

Scenario: Inguinal hernia history
Code Cairo

Scenario data sheetHistory

Scenario: Inguinal hernia
Code
Source: MCAP
Last updated: 18/8/2011
Actor gender and age 20-40 male
range
Couch or chair for actor chair
Instr. outside prep. bay
candinstr inside prep bay
The time is: 10:30 weekday morning
The scenario takes place Surgical out-patient clinic
Inst. outside the exam. This man presented to his GP with a lump in his right groin. He has now been
bay referred to the surgical out-patient clinic.
Instr. inside the exam. bay

INFORMATION FOR THE ACTOR

The patient

Name Jason White

Date of birth 1/1/1980
Sex M
Job Personal trainer
Patient's address: 17, Holly Heights, Anytown, Anyshire
The character the actor is to play:

Age range for actor from 20-40

Character: patient
costume Track suit
personal props: newspaper
Scenario location and Out-patient clinic 10:00 weekday morning
time
Actor's instructions You are a personal trainer and therefore consider yourself quite
knowledgeable about anatomy and muscles in particular, although in reality
you don’t know much more than the average person. You are a bit precious –
obsessed with your body and health and a bit of a hypochondriac and take lots
of vitamins and supplements including a “stamina tonic” that you buy from a
man at the gym. You will want to know a lot of detail about what has happened
to you, what the treatment is, what could go wrong and what the long term
effects will be especially to your l

A few months ago you felt something “give” in your right groin while weight
training, it was uncomfortable but not particularly painful. Later that day in the
shower you noticed a lump in your right groin. It is firm, not hard and not
painful. It disappears when you lie down and relax, but comes back after you
have been walking around for 30 or 40 minutes. It gets bigger if you cough or
when you are straining at some athletic manoeuvre.

You are a non smoker and drink alcohol very occasionally and take no
prescription medication, you have never been to hospital before, although you
did attend the ”special clinic” 18 months ago because you had a genital
1
Scenario: Inguinal hernia history
Code Cairo

discharge after a friend’s stag weekend in Estonia when you made full use of
the local attractions.
You have lived with a gym teacher (opposite sex ) for the last year and
comment, full of embarrassment, that you have not had sex for months
because it makes your hernia ache, and you partner has for that reason
accused you of being “ a complete wimp” which was the main reason for you
seeking help.

After the candidate has asked you a few questions say knowingly “It’s an
iguana hernia isn’t it”(note malapropism, should be inguinal) when the
candidate agrees ask “just what is an iguana hernia?”

You can go on to ask: ”how does a hernia happen?”.”What if it is not a hernia,

what else could it be?” “Will it get better?”” what will happen if I just leave it?”
“How is the operation done” “what are the side effects?” “Are there any
complications?” “When can I get back to work” and so on .the torrent of
questions is due to your fear and anxiety which lurk just below you superficial
bluster. The candidate should be aware of your apprehension and answer
your questions, but he must also retain control of the interview in order to
obtain a good history on which to base a diagnosis.

Patient’s expectations To have an explanation of what is wrong and to be reassured that it can be put
right as it affects his livelihood
Actor's background A groin hernia that suddenly appears with straining, like yours, is due to the
muscles tearing and some gut protruding through the defect
The “stamina tonic should raise some alarm bells in candidates he should be
concerned that it might contain anabolic steroids or some herbs that might
interact with anaesthetic agents. (in fact it is totally harmless)
This is a fairly straight forward history and the candidate should be au fait with
inguinal hernias the challenge her is to address your concerns but at the same
time get a comprehensive history. There is a risk that you have not considered
that you could have picked up HIV in Estonia a test immediately after returning
would not have been reliable the clinic doctor asked you to return in a few
months, but you did not.

HISTORY DETAILS

Presenting Lump in Right groin

Complaint
History of Lump appeared few months ago during weight lifting.
presenting
complaint
Normal For this patient
Cardio-vascular
system
Chest pain none
Palpitations none
Faints / none
Blackouts
Ankle swelling none
Claudication none
Respiratory
2
Scenario: Inguinal hernia history
Code Cairo

System
Short of breath no
Wheezing no
Cough no
Sputum no
Exercise capacity normal
Alimentary
System

Appetite normal
Change in weight no
Indigestion none
Dysphagia none Occasional heart burn
Nausea no
Vomiting no
Abdominal pain none
Bowels once/day
Urogenital
system

Urinary 2-3/day
frequency
Haematuria none
Nocturia no
Stream good
Periods- Females normal
Nervous system

Sleep OK
Headache no
Vision OK
Speech Ok
Fits never
Parasthesia none
Weakness none
Hearing Ok
Loss no
ofconsciousness
Past Medical
History
Operations none
Tb no
Diabetes no
Jaundice never
DVT/PE no
Other none
Family History
A&W=alive and well
Mother A&W
Father A&W
Brothers A&W One - he is a florist
Sisters A&W
Spouse A&W

3
Scenario: Inguinal hernia history
Code Cairo

Children none None known

Familial disorder none
Medication
History
Medication none
Allergies no
Social History

Job clerical Personal trainer

Smoking no no
Alcohol none occasional
Accommodation house Flat with partner
Sexuality Hetero.
Foreign travel none Estonia 18 months ago
Other factors none

INFORMATION FOR THE EXAMINER

Examiner instructions This is a straight forward history of an inguinal hernia (probably direct) the
challenge is to get a good history from this talkative and somewhat obsessive
patient
Point of concern 1 Candidate should explore the issue of the “stamina tonic”
Point of concern 2: The visit to the GUM clinic raises the possibility that this patient is HIV positive
Point of concern 3
Point of concern 4 Particularly, he should be able to give a good account of what the hernia is
and how it will be fixed
Point of concern 5 The candidate should be allowed to describe what he is used to, either
minimally invasive or open operation
Point of concern 6: It will be a few months before he is back to full fitness and can use weights

Point of concern 7:

Point of concern 8:

Point of concern 9:

Point of concern10:

CLINICAL EXAMINER 1 MARK SHEET

Knowledge: The causation nature and repair of inguinal hernias

Professionalism 1: Deals with the issue of ”the tonic” and the visit to GUM clinic

CLINICAL EXAMINER 2 MARK SHEET

Comms 2: Deals well with this patients bantering questions due to his fear and anxiety
Comms 3: Separates out all the unnecessary trivia and presents a clear focussed history

4
Scenario: Inguinal hernia history
Code Cairo

NOTES

For editor
Issues of Surgical Fact Recovery times are a bit vague on NHS Direct website. need to check with a
real hernia surgeon

5
Scenario data sheetSurgical and Lay examiner
Scenario: Lay Appendicitis in a child
Code Cairo
Source: Prospero
Last updated: MCAP April 20111
Actor gender and age Male 30-40
range
Couch or chair for actor Chair
Instr. outside prep. bay Standard text
candinstr inside prep
bay You are the SHO on call for emergency general surgical
admissions. A 10-year-old girl has just been admitted as an
emergency with peritonitis. She has been unwell for 2 days and
very unwell for one day. The child is extremely ill. A perforated
appendix is suspected and she is being resuscitated by your
registrar before being taken to the operating theatre. Your
consultant, Mr. Mann is on his way in from home, and will
perform the operation. You have been instructed to see the
child’s father, and explain the situation. You did not have an
opportunity to see the child yourself before she was taken to
theatre.

The time is:

The scenario takes Office in A&E
place
Inst. outside the exam. Standard text
bay
Instr. inside the exam. Please talk to the patient’s relative about the issues he raises
bay

INFORMATION FOR THE ACTOR

The patient

Name Jayne White

Date of birth 12/4/2001
Sex female
Job School girl
Patient's address: 190 Sycamore Street
AnytownAnyshire AY56 3JH
The character the actor is to play:

Age range for actor 30-40

from
Character: Patient’s father
costume casual
personal props: none
Scenario location and Office in A&E
time Weekday 23:00
Actor's instructions You are a single parent who has been working extra weekend
shifts in the local biscuit factory to make some money to take
your daughter on holiday. This would be her first holiday for two
years since her mother died in this hospital following a major
operation for cancer of the gullet.Your daughter has been left with
your neighbour for the last few days while you have been
working.
The problem started 40 hours ago with central abdominal pains.
Your neighbour delayed calling the GP. You are now feeling very
guilty about what has happened. You have come to the hospital
straight from your shift.Your daughter, previously a normal
healthy 10-year-old child, has been admitted to hospital
extremely ill with peritonitis, which is probably due to a ruptured
appendix The registrar, not the doctor you will see, has seen your
daughter; she is to have an emergency operation
The consultant is on his way into the hospital. He will see you
inthe theatre reception and take formal written consent.
You are becoming aware that this is a serious situation and you
are becoming increasingly anxious exhausted, guilty and scared.
You are worried that your neighbour delayed too long. You
cannot understand why something like appendicitis which you
thought was quite simple, can be so dangerous.
Assuming that she comes through all this, you are worried about
the long-term effects. Scarring may have been mentioned.

Looking to the future helps you to cope with the present threat.
You have read that severe infection can block the reproductive
tubes in young girls. Bring this up if there is time.

Actor's background: Appendicitis is a common condition. If the appendix perforates,

the released pus can lead to peritonitis. This can lead to a
systemic inflammatory response, which may be fatal. There is
less fat in the abdomen of young children so perforation can be
particularly dangerous
You are upset at the high risk with a simple condition An outline
of sequence of events, including resuscitation with intravenous
fluids and antibiotics, and a description of the surgery is
appropriate. The size and direction of the incision used will be
according to the judgment of the surgeon.

INFORMATION FOR THE EXAMINER

Examiner instructions The candidate must try to calm the father with a clear and honest
description of the situation putting the risks into perspective
Point of concern 1 A small horizontal incision will leave little in the way of scarring,
but if she does need a long midline incision or lengthy transverse
incision this will undoubtedly be disfiguring.
Point of concern 2: The child may need to go a high care area
Point of concern 3 Future sub-fertility is a possibility
Point of concern 4 The candidate must understand the additional risks in young
children because of the underdeveloped omentum
Point of concern 5 There are risks but ultimately she should make a full recovery
Point of concern 6: The candidate should not enter into a discussion about blame

Point of concern 7:

Point of concern 8:

Point of concern 9:

Point of concern10:

CLINICAL EXAMINER MARK SHEET

Scenario: Child appendicitis

Code: Lay examiner
Clinical Knowledge: Risks of appendicitis in a child
Professionalism 1: Gives a factual account without apportioning blame

LAY EXAMINER MARK SHEET

Comms 2: The candidate can deal with this distraught mother and try to
allay some of her anxieties
Comms 3: An account of the surgical situation is given in clear lay language
 CASENOTE FRONT SHEET

Case record number P238756

Surname White

Title Miss

First names Jayne

Sex Female
Date of Birth 12 April 2001

Address 190 Sycamore Street

Anytown
Anyshire

Postcode AY56 3JH

Telephone

Occupation School child

General Practitioner Dr PR Smith

The Surgery
High Street
Anytown
Consultant…Mr ARD Mann Number P238756 Name: Jayne WHITE
Date of Birth 12/04/2001Sex Female
Ward..ward paeds3 190 Sycamore Street
Anytown
Anyshire

12/04/2011

22:00

10 yr old girl sent in by deputising service

(Vague history from neighbour, father on her way Patient crying

and too distressed to give any useful history)

Generalised abdo pain for 1-2 days

For last 6 hours v. Painful in RIF

Vomited once yesterday not eaten since and had only a few sips of
water. Does not know about bowel actions

Previously fit and well

No Medication

No other sibs lives with father mother died from post op. leak after
oesophagectomy by Mr Mann 2 yrs ago in this hospital)

O/E

Temp 41degrees cent. Pulse 120

Rapid shallow breathing chest clear

Mouth v dry

Abdo very tender in RIF generalised guarding no bowel sounds.

Needs IVI fluids

Bloods

Miss Sparrow to see

John Smith FY1 Bleep 1234

Consultant…Mr ARD Mann Number P238756 Name: Jayne WHITE
Date of Birth 12/04/2001Sex Female
Ward..ward paeds3 190 Sycamore Street
Anytown
Anyshire

12/04/2010
22:15
I agree probable appendicitis with generalised
peritonitis
Needs urgent resuscitation with fluids and antibiotics.
I will ask Mr Mann to come in
And get the on-call anaesthetist to see her - will probably
need on-call consultant anaesthetist to be around
Also get paeds reg to come down and help with resus and
then post op. care
Alison Sparrow SpR Bleep 6789

12/04/2011
22:30
Message from on call anaesthetist can we send patient up to recovery he will
see her there with the paediatrician while they wait for consultant anaesthetist
and surgeon to arrive

Sister Amanda Goodbody MSc RGN

 ST VINCENT’S HOSPITAL

Laboratory report

Name Jayne WHITE Hospital Number P238756

Date of birth 12/04/2011 Sex Female

Address 190Sycamore Street

Anytown
Anyshire

LIVER PROFILE

Test Result Units Normal

Serum albumin 40 g/L 35-50

Serum alkphos 50 IU/L 30 - 115

Serum AST 37 IU/L 5-45

Serum bilirubin 9 µmol/L 1-22

Serum total Protein 70 g/L 60-80

Calcium 2.3 mmol/L 2.20-2.70

Phosphate 1.6 mmol/L 1.00 – 1.80

3
Report Date 12/04/2011 Time 22:30
 ST VINCENT’S HOSPITAL

Laboratory report

Name Jayne WHITE Hospital Number P238756

Date of birth 12/04/2011 Sex Female

Address 190Sycamore Street

Anytown
Anyshire

Biochemistry

Test Result Units Normal

Serum sodium 140 mmol/L 135- 145

Serum potassium 4.2 mmol/L 3.4-5.0

Serum urea 10.0 mmol/L 2.5-7.0

Serum creatinine 110 µmol/L 50 -100

Plasma glucose 5.0 mmol/L <6

Serum amylase 40 IU/L <80

C-reactive protein 50.0 mg/L <6

4
Report Date 12/04/2011 Time 22:30
 ST VINCENT’S HOSPITAL

Laboratory report

Name Jayne WHITE Hospital Number P238756

Date of birth 12/04/2011 Sex Female

Address 190Sycamore Street

Anytown
Anyshire

Haematology

Test Result Units Normal

Haemoglobin 10.1 g/dl 13.0 - 16.5

RBC 4.80 1012/L 3.80-5.60

Hct 0.48 0.34-0.50

MCV 85.0 fl 80.0-98.0

MCH 30.0 pg 27.0-34.0

Platelets 320 109/L 150-400

WBC 20.42 109/L 4.0 1 - 10.5

Neutrophils 17.2 109/L 2.00-8.00

Lymphocytes 2.3 109/L 1.00-4.00

Monocytes 0.6 109/L 0.10-0.80

Eosinophils 0.2 109/L 0.10-0.50

Basophils 0.1 109/L 0.10-0.10

5
Report Date 12/04/2011 Time 22:30
 ST VINCENT’S HOSPITAL

Laboratory report

Name Jayne WHITE Hospital Number P238756

Date of birth 12/04/2011 Sex Female

Address 190Sycamore Street

Anytown
Anyshire

Arterial blood gases

Test Result Units Normal

pH 7.35 – 7.45

PaCO 2 Kpa 4.0 – 6.0

Pa0 2 Kpa 10 - 13

HCO 3 Mmol/L 22 - 26

O 2 saturation% 95 – 98%

Base Excess

6
Report Date 12/04/2011 Time 22:30
Scenario: Mastectomy complications phone
Code Cairo

Scenario data sheetSurgical examiner with telephone

Scenario: Mastectomy complications telephone
Code Cairo
Source: Prospero
Last updated: 4/10/2010
Actor gender and age N/A
range
Couch or chair for actor N/A
Instr. outside prep. bay Standard text
cand instr inside prep bay The daughter of the patient whose notes you have, has arrived at the hospital.
The patient was due to go home tomorrow but some complications have
arisen.Notwithstanding this the daughter wants to take her mother home this
afternoon to her house which is 60 miles away. She has persuaded her
mother that this would be the best course of action. You have spent the last 20
minutes trying, unsuccessfully, to persuade the daughter that discharge today
is not in the patient’s best interest especially to a house 60miles away.

The patient was keen to go home to her own bungalow, however in view of her
complications she should stay in hospital until she is better

The daughter is very determined and wants to have her own way and does not
suffer fools gladly. She is convinced that her mother will be fine going home
with her today You have perceived that it would certainly be a lot more
convenient for the daughter because it will save her from coming to visit her
mother in hospital or at her bungalowShe has convinced her mother that it will
be best for her to go home with her today, although the patient would almost
certainly prefergo to her own house when she is well enough to go home. The
daughter is a school teacher and is out at work all day, as is her husband.
Theyhave two teenage daughters and a labrador so the house is busy and
noisy.
The patient has another daughter who lives near to the hospital, but she is a
paranoid schizophrenic.
The time is: Sunday 15:00
The scenario takes place Ward Office
Inst. outside the exam. Standard text
bay
Instr. inside the exam. bay Ring the on-call consultant surgeon, who is not the patient’s consultant, and
explain that this patient’s daughter wants to take her mother home.

INFORMATION FOR THE ACTOR

The patient

Name Janice Green

Date of birth 1938
Sex Female
Job Widowed house-wife
Patient's address: 13 Ash Avenue
Anytown,
AnyShire
AY23 7FG
The character the actor is to play:
1
Scenario: Mastectomy complications phone
Code Cairo

Age range for actor from N/A

Character: N/A
costume N/A
personal props: N/A
Scenario location and N/A
time
Actor's instructions N/A

Actor's background: N/A

Examiner instructions Ask the candidate how he/she tried to persuade the daughter to allow her
mother to stay in hospital,

Point of concern 1 Has the PATIENT made their own decision or has she been bullied into
making a decision to go home to day
Point of concern 2: Is it safe for the patient to go 60 miles away -
Point of concern 3 What plans are there for care in the event of complications
Point of concern 4 Does the candidate understand the risks to the patient
Point of concern 5 Is the patient sufficiently alert to make their own decision
Point of concern 6: What is the blood in the drain due to

Point of concern 7: The candidate must understand the ‘discharge against medical advice
procedure’- it is ultimately the patient’s own decision without duress
Point of concern 8: Ask the candidate how he/she appraised the daughter of the risks of
premature or inappropriate discharge
Point of concern 9:

Point of concern10:

CLINICAL EXAMINER MARK SHEET

Scenario: Complications of mastectomy telephone

Code: Cairo
Clinical Knowledge Does the candidate understand the complications of mastectomy
Communication 1 Can the candidate explain clearly and succinctly what has happened to the
patient.
Communication 2 Can the candidate give a satisfactory account of what has transpired between
him/her and the daughter
Professionalism 1 Does the candidate understand about discharge against medical advice.
Professionalism 2 Has the candidate a clear plan for what to do next.

2
 CASENOTE FRONT SHEET

Case record number B456791

Surname Green

Title Mrs

First names Janice

Sex Female
Date of Birth 13/3//1938

Address 13 Ash Avenue

Anytown
Anyshire

Postcode AY23 7FG

Telephone

Occupation Retired

General Practitioner Dr PR Smith

The Surgery
High Street
Anytown

1
 B456791 GREEN Janice
Consultant…Mr ARD Mann Date of Birth 13/3/1938 Sex Female
23 Ash Avenue
Ward.. . W4 Anytown
Anyshire

11/10/2010
10:30
Outpatient note
Elderly female with 3-month history of a lump in upper outer
quadrant left breast reported as cancer on mammogram done last
week.
Menopause age 50 No HRT
Family:No sisters, mother died of colon cancer
2 daughters alive with no history of breast disease
O/E
Right breast normal Left breast hard lump UOQ mobile not fixed
to skin no axillary nodes right or left side clinically this is cancer

For biopsy today and then probably TCI for Left simple
mastectomy or lumpectomy and sentinel node.

ARD Mann

Consultant surgeon
 B456791 GREEN Janice
Consultant…Mr ARD Mann Date of Birth 13/3/1938 Sex Female
23 Ash Avenue
Ward.. . W4 Anytown
Anyshire

21/10/2010

15:20

Pre-admission Clinic

Discussed at MDT last week Bx confirms malignancy

History as before

Lives alone in her own house manages shopping etc

Smokes 20/day since her teens

Alcohol occasionally

Drug history

Statin

Diuretic

Aspirin

O/E

Examination of breasts unchanged since OP visit

Chest

Has chronic cough

No wheezing widespread coarse ronchi

And creps

Will need anaesthetic opinion

Get CXR

John Smith FY1 1234

 B456791 GREEN Janice
Consultant…Mr ARD Mann Date of Birth 13/3/1938 Sex Female
23 Ash Avenue
Ward.. . W4 Anytown
Anyshire

27/10/2010

10:00

ANAESTHETIC NOTE

Elderly lady for lumpectomy and sentinel node biopsy on Mr Mann’s list
tomorrow

Smokes 30/day

COPD and mild LVF not well controlled mild pulmonary oedema
recommend cardiology opinion as out-patient

Will need close monitoring ?HDU

CXR Mild upper lobe diversion and prominent hilar vessels

with some blunting of both costo-phrenic angles

ABG Boyles Anaes SpR 7891

28/10/2010

17:00

Operation cancelled today as no time in theatre.

For operation on tomorrow’s list

I have explained this to Mrs Green

John Smith FY1 1234

 B456791 GREEN Janice
Consultant…Mr ARD Mann Date of Birth 13/3/1938 Sex Female
23 Ash Avenue
Ward.. . W4 Anytown
Anyshire

29/10/2010

10:30

Operation note

Lumpectomy and sentinel node biopsy

Frozen section +ve at the margins and tumour in the node therefore proceed to
mastectomy and complete axillary clearance

Haemostasis satisfactory

Vacuum drain inserted

Skin closure with clips

See typed report for full details

Allison Sparrow SpR 9876

30/10/2010 10:30

First PO day

Pain well controlled

P80 BP 120/70 T=36.5centigrade

A little drowsy

Wound satisfactory

Drain 30mls clear fluid since opn

John Smith FY1 1234

 B456791 GREEN Janice
Consultant…Mr ARD Mann Date of Birth 13/3/1938 Sex Female
23 Ash Avenue
Ward.. . W4 Anytown
Anyshire

31/10/2010

09:00

2nd PO day

Complains of increased discomfort in left axilla

P 95 regular BP 130/80 T=37.8

Slightly SOB today

90 mls of bloody fluid in drain in last 24 hours

Axilla looks a bit puffy

Needs registrar review

John Smith FY1 1234

 St VINCENT’S HOSPITAL

Laboratory report

Name Janice Green Hospital Number B456791

Date of birth 13/03/1938 Sex Female

Address 23 Ash avenue

Anytown
Anyshire

Test Result Units Normal

LIVER PROFILE

Serum albumin 40 g/L 35-50

Serum alk phos 50 IU/L 30 - 115

Serum AST 37 IU/L 5-45

Serum bilirubin 9 µmol/L 1-22

Serum total Protein 70 g/L 60-80

Calcium 2.3 mmol/L 2.20-2.70

Phosphate 1.6 mmol/L 1.00 – 1.80

Report Date 27/10/2010 Time 16:00

 St VINCENT’S HOSPITAL

Laboratory report

Name Janice Green Hospital Number B456791

Date of birth 13/03/1938 Sex Female

Address 23 Ash avenue

Anytown
Anyshire

Biochemistry

Test Result Units Normal

Serum sodium 140 mmol/L 135- 145

Serum potassium 4.2 mmol/L 3.4-5.0

Serum urea 9.0 mmol/L 2.5-7.0

Serum creatinine 115 µmol/L 50 -100

Plasma glucose 5.0 mmol/L <6

Serum amylase 40 IU/L <80

C-reactive protein 5.0 mg/L <6

Report Date 27/10/2010 Time 16:00

 St VINCENT’S HOSPITAL

Laboratory report

Name Janice Green Hospital Number B456791

Date of birth 13/03/1938 Sex Female

Address 23 Ash avenue

Anytown
Anyshire

Haematology

Test Result Units Normal

Haemoglobin 13.9 g/dl 13.0 - 16.5

RBC 4.80 1012/L 3.80-5.60

Hct 0.48 0.34-0.50

MCV 85.0 fl 80.0-98.0

MCH 30.0 pg 27.0-34.0

Platelets 320 109/L 150-400

WBC 6.42 109/L 4.0 1 - 10.5

Neutrophils 3.2 109/L 2.00-8.00

Lymphocytes 2.3 109/L 1.00-4.00

Monocytes 0.6 109/L 0.10-0.80

Eosinophils 0.2 109/L 0.10-0.50

Basophils 0.1 109/L 0.10-0.10

Report Date 27/10/2010 Time 16:00

 St VINCENT’S HOSPITAL

Laboratory report

Name Janice Green Hospital Number B456791

Date of birth 13/03/1938 Sex Female

Address 23 Ash avenue

Anytown
Anyshire

Arterial blood gases

Test Result Units Normal

pH 7.4 7.35 – 7.45

PaCO 2 6.2 Kpa 4.0 – 6.0

Pa0 2 9.8 Kpa 10 - 13

HCO 3 23 Mmol/L 22 - 26

O 2 saturation% 93 95 – 98%

Base Excess -1

Report Date 27/10/2010 Time 16:00

 Communication skills : phone call
Oliguria pod1:
( after right hemicolectomy for cecal tumour)

Hello, i'm ......... (SHO, ST1, CT2) working for mr. ..... . I am calling to speak to mr. .......to
ask him an advice about a patient who underwent right hemicolectomy for cecal tumour ,
he has been oliguric now. Could i check that i am speaking to ........

Who is the consultant of the case?

Mr. ........

Summarize your case?

Mr .... Is ....y old , he has been operated 24 h ago by right hemicolectomy for cecal tumour,
,his urine output in the last 8 hours is about (10-20 ml) ,i checked the urinary catheter
which was not blocked. He is tachycardiac , has low grade fever, with mild hypotension,
his abdomen is lax.
His bloods show his Hb dropped from 12-10 , urea is moderately raised, creatinine is
borderline high

What do you think the cause is ?

I think the patient is dehydrated, he received only 1100 ml of normal saline for pod1. Also
on checking the operative notes, there was a blood loss but he received 2 units of blood

Plans of action?

I will start fluid resucitation by giving 1 liter of normal saline over 1 hour and will continually
monitor the patient in the ward . I will repeat bloods tomorrow morning , if no response to
fluid challenge overnight , i will transfer the patient to HDU to insert a central line and
monitor. If bloods shows Hb more dropping, i will start blood transfusion

Do you think that the patient is bleeding?

May be, but i will monitor the vital signs continuously, i will do serial abdominal
examinations.if i found any signs of bleeding i will let you know

Do you think it is anastmotic leak?

For now , the patient is not toxic, his abdomen is lax , but i will do serial abdominal
examinations and prepare for abdominal ultrasound and will let you know if the patient
becomes peritonitic

If you need me to come back?

I will start fluid challenge , will update you subsequently

1
Bile leakage pod4 after lap. Interval cholecystectomy:
Hello, i am .........( SHO, ST1, CT2) working for MR. ...... In ...... Hospital . I am calling to
speak to MR. ......., the hepatobiliary consultant to ask him an advice about a patient , can i
check that i am speaking to Mr....

Summarize your case:

Mr. ..... Is .... Y old previously fit and well who underwent lap. Cholecystectomy 4 days ago.
He has been complaining of abdominal pain since . Today we noticed bile in his abdominal
drain.
Clinically, he is tachycardiac, pyrexic, slightly jaundiced, has generalised abdominal pain,
but his abdomen is lax. His bloods (taken 2 days ago )show elevated bilirubin, elevated
TLC and increased CRP. We have arranged for an abdominal ultrasound which showed
free intra-abdominal collection. We think that this patient has had a bile leakage and we
were hoping to transfer him to your specialist care for definitive treatment.

What are the possible sources of bile leakage?

May be due to:

- cystic duct stump leakage due to slipped clippage or retained CBD stone
- CBD injury
- Accessory cystic duct
- Leakage from the liver bed

What will be your management?

- I started fluid resuscitation and antibiotics

- I will order new set of bloods when i am off the phone
- We need to make an ERCP to delineate the source of leakage and probably to put a
stent ,but this is not available in our hospital now.

Is this urgent?

Yes, for the fear of developing biliary peritonitis

Do you need to arrange with anyone?

Yes, with the bed manager of both hospitals to discuss creating bed whether by facilitating
discharge or repartitioning of patients

Refer polytraumatized patient to a cardiothoracic consultant:

Hello, i am ......... (SHO, ST1, CT2) working for mr. ........ In ......... Hospital. I am calling to
speak to Mr. ....... The cardiothoracic consultant to ask him to accept a referral of a

2
polytraumatized patient with a widened mediastinum on the chest x ray. Could i check that
i am speaking to mr.....

Summarize your case?

A man aged ...... Came to us on motorcycle RTA , on examination, his GCS= 14 ,his pulse
rate was 120/ min, his BP= 100/80, he has a swollen left thigh.
We did a chest x ray which revealed a widened mediastinum with bilateral hemothorax, we
put a chest drain which drained 200 cc of fresh blood,we could not make CT as the
machine is being serviced for the next 3 hours.
His AXR showed absent psoas shadow , his x-ray on the femur showed fracture of the
shaft .
His bloods: Hb 8.9 , PH 7.32, with low HCO3 ,the patient is known to be diabetic.
We started fluid resuscitation by 4 litres of crystaloids and we cross matched 6 units of
blood but not yet transfused.

What will you do for the cervical spine?

I will support it using a hrad collar

What will you do for the leg?

I will use a Thomas splint

What will you do for the blood pressure?

We started fluid resuscitation and cross matched for blood , but we should not let the blood
pressure rises for the fear of increased hemorrhage

Why having metabolic acidosis?

Patient has a closed fracture of the femur, so compatement syndrome is a possible cause
The patient has a hemorrhagic shock
The patient may have diabetic ketoacidosis

What about the abdomen?

Absent psoas shadow denotes the presence of intra-abdominal collection , so he may

require exploratory laprotomy.

Who will accompany the case?

I will come with one of our anathesia colleagues or ITU colleagues

3
Call consultant to update him about a pod2 mastectomy patient
who her daughter wants to discharge her against medical advice

78 y old lady , with a background of COPD , milld LVF , underwent mastectomy + axillary clearance
for breast cancer, pod2 she developed axillary discomfort with axillary swelling with SOB
Her daughter wants to take her home .

The daughter of the patient whose notes you have, has arrived at the hospital.
The patient was due to go home tomorrow but some complications have
arisen. Notwithstanding this the daughter wants to take her mother home this
afternoon to her house which is 60 miles away. She has persuaded her mother
that this would be the best course of action. You have spent the last 20 minutes
trying, unsuccessfully, to persuade the daughter that discharge today is not in
the patient’s best interest especially to a house 60miles away.

The patient was keen to go home to her own bungalow, however in view of her
complications she should stay in hospital until she is better

The daughter is very determined and wants to have her own way and does not
suffer fools gladly. She is convinced that her mother will be fine going home
with her today You have perceived that it would certainly be a lot more
convenient for the daughter because it will save her from coming to visit her
mother in hospital or at her bungalow She has convinced her mother that it will
be best for her to go home with her today, although the patient would almost
certainly prefer go to her own house when she is well enough to go home. The
daughter is a school teacher and is out at work all day, as is her husband.
They have two teenage daughters and a labrador so the house is busy and
noisy.
The patient has another daughter who lives near to the hospital, but she is a
paranoid schizophrenic.

Ring the on-call consultant surgeon, who is not the patient’s consultant, and
explain that this patient’s daughter wants to take her mother home.

Hello, i am ......... (SHO, ST1, CT2) working for mr. ........ In ......... Hospital. I am calling to
inform you about a pod2 patient who underwent mastectomy with axillary clearance

Summarize your case

Mrs Janice green 78 y old who had mastectomy with axillary clearance 2days ago for
breast cancer, now she has an axillary swelling and her wound suction drain has 90 ml of
fresh blood , also she experiences SOB. The patient has also a background of COPD and
mild LVF. Now her daughter wants to take her home which is 60 miles away. I spent 20
min. Trying unsuccessfully to persuade her daughter that discharge today will not in the
patient best interest

4
Has the PATIENT made their own decision or has she been bullied into making a decision to go
home today?

I think the daudhter has convinced her mother that it will be best for her to go home with her today,
although the patient would almost certainly prefer go to her own house when she is well enough to
go home.

Is the patient is suffeciently alert to make her own decision?

Yes, she has the competence to make an informed decision

What do you think has happened to this patient?

In view of the fresh blood in the vacuum drain and the swelling in the axilla , there is a
possiblity of a reactionary hemorrhage in the wound site
Also i have to consider the presence of DVT and pulmonary embolism in the view of SOB

What will be your plans of action in the event of these complications?

As for hemorrahge , i will order FBC to check Hb if there was continued bleeding
A wound hematoma may require evacuation later on. If i suspect DVT and PE , i would
arrange for a CTPA and i will manage accordingly

So, what will you do if they were insisting to go home?

I will inform the patient and her daughter about the possible complications which may
occur due to this premature discharge especially for a 60 miles away home. Also i will
inform that the patient will have to sign on a legal document stating that she has the full
responsibility of the discharge against medical advice.
Also i will inform the patient about the warning signs and symptoms that she has to be
alert for such as increasing wound discharge or being more unwell and increasing
shortness of breathing and that she has to seek advice immediately in a nearby hospital or
to come back here

Update the trauma head about a trauma case:

( RTA +open tibio fibular #+ pulsless foot+ abd. Collection)

Hello, i am ...... ( SHO, ST1, ..) , i am calling to speak to MR .....to update him
anout a trauma case ,could i check that i am speaking to MR .....

Summarize your case?

21 y old male came to A&E departement after RTA , his GCS is 15 at time of
examination, he is hemodynamically stable . He has an open tibiofibular fracture on
his left lower limb. Abdominal ultrasound shows free intra abdominal collection , on
examination of the left distal pulses, there was no felt pulses on the left foot

What is the most urgent?

5
The patient has an open fracture with an arterial damage on his left lower limb, so it
is urgent to interfer with him to avoid ischemia and compartement syndrome

Is the patient is wearing a c-collar?

( info. Is not given in the notes) , i will check for this
Is the patient id dehydrated?
info. Is not given in the notes) , i will check for this
Plans of action?
- I will inform the orthopedics consultant and the vascular consultant
- I will reduce and immobilize the fracture
- I will order Ct - abdomen and pelvis
- I will order CT- head and brain

Speak to ITU registrar to book a post- operative bed and

ask about pre-op. Advice:
( COPD + perforated viscus+ ARF+ metabolic acidosis)
- 73 y old lady brought by her daughter due to sudden abdominal pain and confusion after
she ate her breakfast
- Assesment revealed suspected perforated viscus
- Urgent laparotomy was required
- Call the ITU registrar
(Remember to write down his advice , he will ask you to repeat at the end)

Hello, my name is Mr ....... I am the surgical SHO working for Mr .......at ........ Hospital. I
am calling to speak to the ITU registrar to ask advice on an unwell patient who has been
today admitted and is going to require a laparotomy. I would also like to arrange an HDU
bed postoperatively. Could I check who I am speaking to, please?

Summarize your case?

Mr...... is a 73 year old with a background of COPD, presented with a perforated viscus
and has gone into acute renal failure, with hypokalemia. His bloods tests show an
potassium of... an creatinine of ...up from a baseline of ........
Her ABG shows a metabolic acidosis, with a high lactate and high negative base excess.
Please could I have some advice on optimisation before theatre and would it be possible
to arrange an HDU bed post_ operative?

Why do you think it is a perforated viscus?

On examination, there is signs of peritonisim, Hb dropped by 2 g,CXR showed air under
the diaphragm , abdominal ultrasound showed free intraabdominal collection .

What fluid resuscitation will you do?

I will start by crystalloids, rapid flush , then to colloids if poor response , i will cross match
for blood in view of rapid Hb drop

What are the pre-operative arrangements do you suggest?

6
- ECG: to look for arrythmias , AF, signs of hyopkakemia
- repeat CXR
- IDC insertion
- Antibiotics
- check if the patient is on steroids , to give I.v hydrocortisone
- I will keep the o2 saturation lower in the view of chronic COPD
- I will contact the anasthesist to review the patient pre-operative

What are the criteria of admission to ITU ?

- 2 organ systems impaired with acute reversible causes

- Impaired respiratory system requiring mechanical ventilation
- 1:1 nursing care
- 1 organ system chronically impaired with a possible 2nd system is being affected

What if i only have 1 ITU bed left and there is asthmatic young lady coming first ?

I will continually monitor the patient in the recovery room untill a bed is available

Call a vascular consultant to refer a case of acute limb

ischemia:

- lady admitted for mild diverticulitis,symptoms improving with I.V Abs and I.V fluids,
- now complaining of sudden acute right lower limb pain
- ECG AF+ preventricular complex, sudden right acute limb ischemia,
- ABG metabolic acidosis, hypokalemia
- arterial duplex showing acute ischemia

Question asked:
- summarize your case?
- Is it urgent, can we send it tomorrow morning instead?
Yes , it is urgent, patient has a critical limb ischemia , so early intervention is
extremely needed for the fear of losing the limb

- Do you need cardiologist to review for PVC before transfer?

No, this can be assesed later on

- What do you think of her presumed diagnosis of diverticulitis?

Now , in view of acute limb ischemia and AF , i have to consider the presence of
mesentric ischmia as a cause of this patient abdominal pain

- Do you want to scan the abdomen first?

We will need to scan her abdomen , but i think after the transfer
- Could it be mesentric ischemia?
Yes, it could be , but for now the abdomen is soft and not tender, i will do serial
abdominal examination and if we need we may do CT Scan of the abdomen with
contrast if the renal functions were normal
7
- Management plan
* correction of hypokalmia
* Correction of AF
* Anticoagulation
* Correction of metabolic acidosis
- What will you tell her family?
I will tell them that the patient has devolpped acute reduction of ciruclation in her
lower limb which may need an urgent intervention and that is why we are going to
transfer her to a vascular consultant

- Ok you can send the patient over

8
 CLINICAL EXAMINATION
peripheral lower limb arterial examination: lower limb chronic
ischemia ( intermittent claudiaction)
WIPER:

Wash your hands

Introduce yourself
Permission( explain the procedure)
Exposure
Reposition

A- INSPECTION: (with the patient lying on the couch)

General:
1. Inspect the hands looking for nicotine staining, tendon xanthomata, nail fold infarcts and
splinter haemorrhages and nail changes
2. Look at the skin and hair for changes suggestive of arterial disease, i.e., thin/shiny skin
and hair loss.
Specific: :
1- Look at the legs for Colour of the legs do they appear pale, cyanosed or red?
2- Scars suggestive of previous surgery (e.g., femoro-distal bypass) or amputated digits
3- Signs of venous insufficiency such as lipodermatosclerosis, venous eczema and atrophy
blanche
3- Venous guttering seen when veins collapse in limbs with peripheral vascular disease and
appear as shallow grooves
4- Ulceration comment on the location, shape depth and size of the ulcer
NB: Arterial ulcers typically have a “punched out” appearance and are generally found around
pressure areas, i.e., lateral and medial malleoli, tips of the toes, head of the 1st and 5th
metatarsals, the heel and the interdigital clefts –so remember to look between toes and under the
heel. (May often be confused with neuropathic ulceration; venous ulceration commonly occurs
around the gaiter region (medial side) of the leg)
5-Gangrene

B-PALPATION:
1- Compare the temperature on both legs using the dorsum of your hand.
- 2- Check the capillary refill time in toes of both feet. ( NB: normal = <2 sec)
- 3- Say you would like to perform BUERGERS TEST:

With the patient lying supine, ask if they have any pain or restriction in hip movements. Then lift
both legs slowly (ideally in about 10 degree increments and waiting for 10 seconds at each stage)
and evaluate the angle at which the leg becomes pale or white . This is known as Buerger’s angle
–in normal subjects it should be greater than 90 degrees (even if the limb is flexed further at the
hip, there should be no colour change in the limb). In patients with peripheral vascular disease, the
limb may go pale as it is lifted and reaches a certain angle. If the angle is less than 25-30 degrees,
it suggests severe ischemia.

Once you have established Buerger’s angle, sit the patient up and swing the legs over the side of
the couch. Watch for the foot to reperfuse –in normal subjects there should be no colour change
but in patients with peripheral vascular disease, you will observe the legs becoming a dusky
crimson/purple colour, which is caused by reactive hyperaemia. This represents a positive
Buerger’s test.

4- Palpate the pulses on both legs:

- Femoral –felt in the mid-inguinal point , halfway between the pubic symphysis and ASIS.
Page 1
- Popliteal –felt deep in the midline of the popliteal fossa with the knee flexed to ~30 degrees
- Posterior tibial –felt posterior to medial malleolus, 2/3rd of the way between the medial malleolus
and the insertion of the Achilles tendon
- Dorsalis pedis felt in the 1st webspace, just lateral to the extensor hallucis longus tendon on the
dorsal surface of the foot (dorsiflexion of the hallux may aid palpation)
- Remember also to check the radial pulse and assess for radio-femoral delay.

C- Auscultation : for iliacs and femoral bruits

D- ABPI: =Ankle Systolic Pressure/Brachial Systolic Pressure

The ABPI gives an indication of the severity of peripheral vascular disease where present
. A normal ABPI is >1.0
. If the ABPI is:
- 0.7 –1 = mild disease (i.e., patient may present with intermittent claudication)
- 0.5 –0.7 = moderate disease (i.e., likely to have rest pain)
- < 0.5 –0.3 (or absolute pressure <50mmHg) = severe disease (i.e., critical ischemia)

Complete the exam: Say you would like to:

-Perform a complete neurological examination of the lower limbs
-Perform a full cardiovascular examination
-Perform a vascular examination of the upper limbs
-Feel the abdomen for any evidence of an aortic aneurysm and auscultate for renal and aortic
bruits.

Discussion:

A male/female patient who presents with leg pain on walking. He seemed generally stable, but I
noticed a toe amputation on the right. On closer examination he had difficult to palpate dorsalis
pedis and posterior tibial pulses on the right,ABPI was 0.9 on the left and 0.5 on the right,
consistent with claudication in the right leg. My main differential would be atherosclerotic or
diabetic peripheral vascular disease.

Management:
- Diagnosis:
Imaging: arterial duplex
CT angiography
MR angiography
Lab.: Blood glucose level
Lipid profile ( LDL)
- treatment:
1- the patient should have an assessment of their risk factors and be actively discouraged from
smoking, have their cholesterol, blood pressure and blood sugar control optimised and be
considered for an antiplatelet agent.
2- The patient will probably need surgical or endovascular intervention. Options include
endovascular stenting of a stenosed portion of an artery, surgical bypass or amputation of the
affected part of the limb.
3- Conservative treatment alone is only an option if the patient were unfit or unwilling to have
surgery.

Critical limb ischemia:

Critical ischaemia can be defined by the presence of ischaemic pain at rest, or tissue loss in the
form of gangrene or ulcers. It is consistent with an ABPI of < 0.4.

Page 2
Thyroid : ( goiter)
Inspection:
- lumb
- 6s: site ,size, shape, symmetry, overlying skin, scars
- Neck veins.
- Swallow water .
- Protrude tongue.

Palpation:
Explain to the patient that you will examine him from behind

- feel the lumb: surface,edge,consistency,fixity,pulsatility

- Feel below the lumb:
- Trachea :
- Swallow water
- Protrude tongue
- Lymph nodes: submental, submandibular, preauricular, postauricular, occipital, post. Cervical,
ant. Cervical, pretracheal, supravlavicular.

Percussion:
Sternum

Auscultation :
Bruits

Thyroid status:
- 1- Hands:
- radial pulse
- tremors:
- Ask the patient to place their arms straight out in front of them
- Place a piece of paper across the backs of their hands
- Observe for a tremor (the paper will quiver)
- 2- Eyes:
- exophthalmos: examine from above
- lid lag:
*Hold your finger high & ask the patient to follow it with their eyes (head still)
*Move your finger downwards
* Observe the upper eyelid as the patient follows your finger downwards
- eye movement:
* Ask the patient to keep their head still & follow your finger with their eyes
* Move your finger through the various axis of eye movement (“H“ shape)
* Observe for restriction of eye movements & ask the patient to report any double vision or pain
- 3- Leg:
- pretibial myxoedema
- ankle reflex
- proximal myopathy:
*Ask patient to stand from a sitting position with arms crossed
*An inability to do this suggests proximal muscle wasting

Discussion:

Differntial diagnosis:
Page 3
-simple MNG
- thyroid neoplasm
- Graves diseaes
- Thyroditis

How would you manage this patient?

I would perform a triple assessment, taking a history as well as my examination, arrange an

ultrasound and a fine needle aspiration or a biopsy.

If the patient come back with pain on swallowing, difficulty in breathing few months later, does it
change your management?
Yes, these are obstrucive symptoms requiring thyroidectomy

Her FNA comes back showing a follicular cell tumour. The report says “unable to differentiate
carcinoma from adenoma”. Why is this?

Follicular carcinomas are differentiated from follicular adenomas as they invade the tumour
capsule or surrounding vessels. Therefore histology rather that simply cytology is needed.

What is the next step in the patient's management following this histological result?

This lady needs to be discussed in the MDT and worked up for a total or hemithyroidectomy

5year survival rate of follicular carcinoma: 99%

Parotid:
Inspection:
- 6s
- The contralateral side
- Facial nerve: raise your eyebrow, shut your eyes aganist resistence, blow out your cheek, show
your teeth, tense your neck muscles.
- Oral cavity: inspect the stensen's duct ( at the level of the upper 2nd molar tooth)

Palpation:
Explain to the patient that you will examine him from behind
- palpate the lumb: ( ask the patient to clench his teeth) surface, consistency, fixity, edges,
pulsatility
- Lymph nodes( as above)
- Palpate the stensen's duct
- Bimanual examination
- Palpate the contralateral side

Discussion :

Diffrential diagnosis of parotid lump:

- infective: parotitis
- Inflammatory: sjögren syndrome, mikulicz's syndrome
- Bengin neoplasm: pleomorphic adenoma, warthin's tumour
- Malignant neoplasm: mucoepidermoid carcinoma, adenoid cystic carinoma, adenocarcinoma,
lymphoma

Page 4
Investigations:
- CT , MRI to assess the extent of local, bony, or perineural invasion
- Us
- FNAC

Submandibular gland :
Inspection :
- 6s
- The contralateral side
- The oral cavity : wharton duct on either side of the lingual frenulum
- Marginal mandibular nerve: show your teeth
- Hypoglossal nerve: take out your tongue ( deviation to the affected side)

Palpation:

Explain to the patient that you will examine him from behind
- palpate the lump: surface, edges, consustency, fixity, pulsatility
- Wharton duct
- Bimanual
- Lymph nodes
- Lingual nerve: touch sensations to ant. 2/3 of the tongue
- Palpate the contralateral side
Discussion:
Examination revealed a diffusely enlarged left / right submandibular gland, approximately 4cm in
diameter. There was no associated cervical lymphadenopathy and there was normal flow of clear
saliva into the oral cavity. The neck examination was otherwise normal.

What is your differential diagnosis?

Submandibular sialolithiasis
Dental infection
Submandibular neoplasm

How would you investigate this patient?

Sialogram if a salivary stone is suspected
X- ray
Ct scan
FNA if a neoplasm is suspected

What are the treatment options?

1. Conservative management: Analgesia, oral antibiotics, good hydration and gland massage

2. Sialogram can occasionally be therapeutic, as the injection of contrast can 'wash out' the gland

3. If the stone is within the duct then the duct can be laid open and the stone retrieved. The duct is
then left open as suturing would result in a stricture

4. Sialendoscopy: stone retrieval via endoscopic techniques

5. Submandibular gland excision

Page 5
Cardiovascular examination:
[ mitral reguarge , aortic stenosis, valve replacement, pacemaker]
Patient going for elective hernia repair

Inspestion+palpation:
- General: walking aids, o2, medications, observation charts, ECG, midline sternotomy scar
- Hands: . Signs of IE( splinter Hges, janeway lesions)
- Tar staining
- Capillary refill
- Palpate the radial pulse ( rate , rhythm, radioradial delay, collapsing pulse)
- Clubbing
- Blood pressure measurement
- Neck: JVP assesment, palpate the carotid pulse
- Eye: mucous membranes, corneal arcus, xanthelasma
- Mouth: oral hygiene, central cyanosis
- Face: malar flush
- Chest : scars( sternotomy, thoracotomy, infraclavicular)
Visible apex pulsations
Palpate for: apex beat( 5 ICS midclavicular line)
Heaves( ventricular hypertrophy)
Thrills ( palpable murmurs)
Auscultation:
(Put your left hand on the carotid pulse to time systole and diastole)
- Mitral area: 5th ICS midclavicular line
Pan systolic murmur radiating to the axilla
- Tricuspid area: 4th ICS left parasternal edge
- Pulmonary area: 2nd ICS left parasternal edge
- Aortic area: 2nd ICS right parasternal edge
Ejection systolic murmurs radiating to the carotids
- Accentuation maneuvers:
These maneuvers cause particular murmurs to become louder DURING expiration:
*Roll onto left side & listen to mitral area with bell during expiration – mitral murmurs (stenosis &
regurgitation)
*Lean forward & listen over aortic area during expiration – aortic murmurs are louder (stenosis &
regurgitation)
- Metallic heart sounds:
One metalic click corresponding to S1= mitral valve replacement
Two metalic clicks corresponding to s2 = aortic valve replacement
- Carotid bruits
- Lung bases

Check lower limb for :

Edema
Vein graft harvest scars

Discussion:

Male patient who I assessed in preadmission clinic. On examination of his cardiovascular system
from the end of the bed I noted a midline sternotomy scar. There were no peripheral stigmata of
cardiovascular disease, he was haemodynamically stable with a narrow pulse pressure of 120/100
millimetres of mercury, and slow rising pulse. On closer inspection of his chest, there was an old
midline sternotomy scar; the apex beat was not displaced. On auscultation I heard a metallic
second heart sound, but no murmur. There were no signs of heart failure; however I noted

Page 6
abdominal bruising, perhaps consistent with the use of subcutaneous heparin injections, and a vein
harvest scar over the right great saphenous area. His signs are consistent with a CABG and
metallic aortic valve replacement for which he is on anticoagulation. I am slightly concerned that he
has signs of aortic stenosis - a slow rising pulse and narrow pulse pressure although I did not hear
a murmur - despite the valve replacement, therefore I would investigate this thoroughly.

What investigations would you order preoperatively?

This patient appears well, but would require a baseline ECG and echo preoperatively. In addition
he would require bloods including an INR as he is on warfarin.

How would you manage this patient’s anticoagulation?

The patient presents with fever 5 days postoperatively:

Might have infective endocarditis

Page 7
Note the pacemaker spikes, no p- waves

Indications of pacemaker:

Who would you inform about the pacemaker?

An anaesthetist, ideally the consultant who will be doing the case. I would ensure it is clearly
documented in the notes.

What precautions would you take?

I would arrange a pacemaker check pre- and postoperatively and contact their pacemaker follow-
up clinic to inform them of the operation and ask for advice.

During the operation I would avoid monopolar completely, or limit its use to short bursts only.

The return electrode should be placed so that the pathway between the diathermy electrode and
return electrode is as far away from the pacemaker and leads as possible

I’d ensure that appropriate resuscitation equipment was available

Respiratory examination:
Inspection+ palpation:

-general: o2 , medications, SOB, ask to take a deep breath and cough

-Hand: tar satining, clubbing, radial pulse, repsp. Rate
-Mouth: central cyanosis
-Lymph nodes: cervical
-Trachea: central or not
-Chest:
*Scars for thoracotomy: can you put your hand on your hips and bend your elbows forward for
me please

Page 8
 *Chest expansion:
-Place your hands on the patient’s chest, inferior to the nipples
-Wrap your fingers around either side of the chest
-Bring your thumbs together in the midline, so that they touch
- Ask patient to take a deep breath
- Observe movement of your thumbs, they should move apart equally
- If one of your thumbs moves less, this suggests reduced expansion on that side
Reduced expansion can be caused by lung collapse / pneumonia
Percussion :1st : supraclavicular
2nd: medial 1/3 of the clavicle
Auscultation:

- from the same levels of percussion:

Ask patient to take deep breaths in and out through their mouth.

* Assess quality – Vesicular (normal) / Bronchial (harsh sounding) – consolidation

* Assess volume – quiet breath sounds suggest reduced air entry – consolidation / collapse /
fluid
* Added sounds:

- Wheeze – asthma / COPD

- Coarse crackles – pneumonia / fluid
- Fine crackles – pulmonary fibrosis

‫*ء‬Vocal resonance:

Ask patient to say “99” repeatedly & auscultate the chest again
Increased volume over an area suggests increased tissue density – consolidation/fluid/tumour

Back of the chest:

- repeat *chest expansion

*Percussion and auscultation
*Vocal resonance

Discussion:

What is your differential diagnosis?

Main diagnosis is COPD in a smoker of this age; however asthma is also a possibility

Who would you inform about this?

I would inform an anaesthetist, ideally the consultant who will be doing the case, otherwise the
coordinating anaesthetic consultant and the operating surgeon.

What further investigations would you arrange?

A chest X-ray to rule out a preop pneumonia or underlying malignancy

Spirometry and respiratory function tests

A baseline ABG to identify preoperative paO2 and PaCO2

How could you try to reduce the risks in a patient with COPD about to undergo an operation?

Page 9
I would ask the GP to optimise medication before the operation and refer to a respiratory medic if
necessary.

Any infection should be treated before the operation.

The patient should be encouraged to stop smoking

I would arrange chest physio before and after surgery to encourage excretion of excess mucus

In addition I would inform HDU in case more intensive care is required post operatively

Use open surgery , not laparoscopic because of co2 pneumoperitoneum

Use regional anathesisa instead of grneral anathesia

Cranial nerve examination: ( bitemporal hemianopia, conductive hearing loss -

anterior cranial fossa tumour)

-olfactory nerve:
With eyes closed, ask patient to identify various scents – e.g. coffee,vinegar

- optic nerve: (5)

. Visual acuity:

1. Stand the patient at 6 metres from the Snellen chart.

2. If patient normally uses distance glasses, ensure they wear them for the assessment.
3. Ask the patient to cover one eye & read to the lowest line they can manage.
4. Visual acuity is recorded as chart distance (numerator) over number of lowest line read
(denominator).
5. Record the lowest line the patient was able to read (e.g. 6/6 which is equivalent to 20/20)
Page 10
 . Colour vision :( not done)

. Pupils:
- Direct reflex– shine torch into eye – look for pupillary constriction in that eye
- Consensual reflex – shine torch into eye – look for pupillary constriction in opposite eye
- Swinging light test– move light in from side of each eye rapidly – relative afferent pupillary defect
(RAPD)
- Accommodation reflex:

1. Ask patient to focus on a distant point (clock on a wall / light switch).

2. Place your finger/object approximately 15cm in front of the eyes.
3. Ask the patient to switch from looking at the distant object to the nearby finger / object.
4. Observe the pupils, you should see constriction & convergence bilaterally.

. Visual fields( visual inattention, confrontation):

Visual inattention (visual neglect):

1. Ask patient to focus on your face & not move their head or eyes during the assessment.
2. Hold both arms out, with one hand in the upper right and the other in the upper left quadrant of
your visual field.
3. Remind the patient to keep their head still & their eyes fixed on your face.
4. Move one of your fingers (on only one hand) and ask the patient to point at the hand on which
the finger is moving.
5. Move the finger on the left and right hand individually in whichever order you prefer.
6. Then move the finger of both hands simultaneously.
7. If patient only reports a finger on one of the hands moving (whilst both are moving
simultaneously), it suggests the presence of visual neglect.

8. Repeat the process with your hands in the lower quadrants of vision.

..
Confrontation:
1. Ask the patient to cover their left eye with their left hand.
2. You should cover your left eye and be staring directly at the patient (mirror the patient).
3. Ask patient to focus on your face & not move their head or eyes during the assessment.
4. Ask the patient to tell you when they can see your fingertip wiggling.
5. Outstretch your arms, ensuring they are situated at equal distance between yourself & the
patient.
6. Position your fingertip at the outer border of one of the quadrants of your visual field.
7. Slowly bring your fingertip inwards, towards the centre of your visual field until the patient sees
it.
8. Repeat this process for each quadrant – at 10 o’clock /2 o’clock / 4 o’clock / 8 o’clock.
9. If you are able to see your fingertip but the patient cannot, this would suggest a reduced visual
field.
10. Map out any visual field defects you detect.
11. Repeat the same assessment process on the other eye.

. Fundoscopy:
Assess for red reflex

1. Position yourself at a distance of around 30cm from the patient’s eyes.

2. Looking through the ophthalmoscope observe for a reddish / orange reflection in the pupil.

Page 11
An absent red reflex may indicate the presence of cataract, or in rare circumstances
neuroblastoma.

Move in closer & examine the eye with the fundoscope

- Begin medially & assess the optic disc – colour / contour / cupping
- Assess the retinal vessels – cotton wool spots / AV nipping / neovascularization
- Finally assess the macula – ask to look directly into the light – drusen noted in macular
degeneration

- occulomotor + trochlear+ abducent:( eye movement)

-
- Eye movements:
- 1. Ask the patient to keep their head still & follow your finger with their eyes.
- 2. Move your finger through the various axis of eye movement (“H” shape).
- 3. Ask the patient to report any double vision.
- 4. Observe for restriction of eye movement

- trigeminal nerve:
Sensory: close your eyes, use a cotton wool
Ophthalmic : forehead , corneal reflex ( not done)
Maxillary: cheek bones
Mandibular: jaw angles
Motor: muscles of mastication
Close and open your jaw against resistance
Clench your teeth and feel temporalis and masseter
Reflexes: corneal reglex , jaw jerk ( not done)

- facial nerve:
*Temporal ( raise your eye brows)
*Zygomatic ( close your eyes against resistance)
* Buccal ( blow your cheeks)
* Marginal mandibular( show your teeth)
* Cervical ( tense and flare your neck muscles)
* Chorda tympani( is there any taste sensations)

Page 12
- vestibulochoclear nerve:
*Whisper no. And repeat
* Rinne test :

1. Tap a 512HZ tuning fork & place at the external auditory meatus & ask the patient if they are
able to hear it (air conduction)
2. Now move the tuning fork (whilst still vibrating), placing its base onto the mastoid process (bone
conduction)
3. Ask the patient if the sound is louder in front of the ear (EAM) or behind it (mastoid process)

Normal = Air conduction > Bone conduction (Rinne’s positive)

Neural deafness = Air conduction > Bone conduction (both air & bone conduction reduced equally)
Conductive deafness = Bone conduction > Air conduction (Rinne’s negative)

* Weber test:
1. Tap a 512HZ tuning fork & place in the midline of the forehead.
2. Ask the patient where they can hear the sound:

Normal = sound is heard equally in both ears

Neural deafness = sound is heard louder on the side of the intact ear
Conductive deafness = sound is heard louder on the side of the affected ear

- glossopharyngeal+ vagus:
*Open your mouth and say AAH ( look for any deviation of uvula and soft palate)
* Ask the patient to cough( asses adduction of both vocal cords by vagus nerve)
* Gag reflex( not done)

- spinal accessory:
Trapezius( shrug shoulder against resistance)
Sternomastoid ( turn head against resistance)

- hypoglssal nerve:
Protrude your tongue ( deviation towards the affected side)

Discussion:
[Bitemporal hemianopia]

Where might the lesion be to cause this symptoms?

A bitemporal hemianopia is suggestive of a lesion affecting the optic chiasm, where the more
medial fibres cross over to the contralateral eye. This may be either a lesion of the optic chiasm
itself or a mass pressing on it (e.g. a pituitary tumour).

If a mass arises from above the chiasm (e.g. pituitary craniopharyngioma), the initial symptoms
may be of a bitemporal inferior quadrantanopia, progressing to a bitemporal hemianopia.
Conversely, masses arising below the chiasm may present at first with bitemporal superior
quadrantanopia.

What else might you expect if a pituitary tumour were the cause of this lady's bitemporal
hemianopia?
Page 13
The other signs and symptoms of a pituitary tumour can be general or specfic to hormone
production:

General - raised intracranial pressure may cause papilloedema (as seen on fundoscopy) or
headaches.

Specific - hyperpituitarism: this depends on the type of hormone secreted. The most common are
growth hormone and prolactin from pituitary adenomas. The former causes acromegaly and the
latter hyperprolactinaemia.

Signs of acromegaly - prognathism, prominent brow, macroglossia, thickening of the skin,

enlargement of hands and feet, hyperhidrosis, carpal tunnel syndrome.

Signs of hyperprolactinaemia - increased lactation, loss of libido, erectile dysfunction in males,

amenorrhoea and infertility (anovulatory) in females.

Management:
Invesigations: hormone assays
MRI
CT (disadvantages: poor soft tissue visualization, need for contrast)
Treatment: antiprolactin ( bromocryptine)
Surgery( trans-sphenoidal, trans-frontal)

[Hemotympanium: ]

Cause of conductive hearing loss in this patient:

Hemotypnum secondary to skull base fracture

What cranial nerves to examine together:

Vestibulochoclear+ facial ( they exit together from IAM)

How to fit otoscope:

1. Pull the pinna upwards & backwards – to straighten the external auditory meatus
2. Position otoscope at the external auditory meatus:
Otoscope should be held in your right hand for the patient’s right ear and vice versa
Hold the otoscope like a pencil and rest your hand against the patient’s cheek for stability
3. Advance the otoscope under direct vision

Page 14
4. Look for any wax, swelling, erythema, discharge or foreign bodies
5. Examine the tympanic membrane:

-Colour – pearly grey & translucent (normal) / erythematous (inflammation)

-Erythema or bulging of the membrane? – inspect for a fluid level e.g. otitis media
-Perforation of the membrane? – note the size of the perforation
-Light reflex present? – absence / distortion may indicate ↑ inner ear pressure e.g. otitis media
-Scarring of the membrane? – tympanosclerosis – can result in significant hearing loss

6. Withdraw the otoscope carefully

Management:
Ct brain ,audiogram , ENT review

[ anterior cranial fossa tumour]:

Do AMTS:

Abbreviated mental test scoring:

*How old are you?
*What time is it to the nearest hour?
*Can you remember this address? 24 West St. I will ask you this at the end
*What year is it?
*What is the name of this place?
*What is my job? And what is the job of this person (e.g. a nurse)?
*What is your date of birth?
*When did WW2 end?
*Who is the current prime minister?
*Can you count backwards from 20-1?
*What was that address I asked you to remember?

Score less then 6/10 suggests dementia / delerium

What do you want to look for in fundoscopy:

Ophthalmoscopy serves to identify:

- Papilloedema suggestive of sustained raised intracranial pressure (e.g. caused by a tumour or
hydrocephalus). This may be absent in the context of acutely raised intracranial pressure, or there
may be atrophic changes in longstanding chronic disease.
- Haemorrhage into the vitreous humour (Terson's syndrome) or other intraocular haemorrhage
secondary to a subarachnoid haemorrhage.

Differential diagnosis of anterior cranial fossa tumour:

Meningioma, olfactory neuroblastoma, sinonasal malignancies

Management:
- CT scan
- MRI with gadolinium
- Streotactic biopsy
- Involve neuro-oncology MDT
- treatment is by surgical resection and proton beam radiotherapy

Page 15
Knee examination:[ LCL + meniscus injury] or [OA]
Look:
Look for:
- Swelling: pre-patellar / infra-patellar Scars Muscle wasting Erythema
- Deformities (valgus and varus)
- Asymmetry
- Baker’s Cyst in Popliteal Fossa
- Accessories , e.g., walking stick / crutches
- Observe gait :Ask the patient whether he/she uses any walking aids, then ask him/her to walk
across the room

Feel:
Ask the patient if there are any areas of localized pain
- assess temp.
- Palapte joint lines:
Palpate the following with the knee flexed at 90°:

Patella – palpate the borders for tenderness / effusion

Tibial tuberosity
Head of the fibula – irregularities / tenderness
Tibial & Femoral joint lines – irregularities / tenderness
Collateral ligaments – both the medial and lateral
Popliteal fossa – feel for any obvious collection of fluid (e.g. a Baker’s cyst)

- Measure quadriceps circumference and compare( 10 cm above patella)

- Effusion: patella tab test( large effusuions) :
1. Empty the suprapatellar pouch by sliding your left hand down the thigh to the patella.

2. Keep your left hand in position and use your right hand to press downwards on the patella with
your fingertips.

3. If fluid is present you will feel a distinct tap as the patella bumps against the femur.
Bulge test ( small effusions);
1. Empty the suprapatellar pouch with one hand whilst also emptying the medial side of the joint
using an upwards wiping motion.

2. Now release your hands and do a similar wiping motion downwards on the lateral side of the
joint.

3. Watch for a bulge or ripple on the medial side of the joint.

4. The appearance of a bulge or ripple on the medial side of the joint suggests the presence of an
effusion.
Move:
- ROM: test active and passive flexion and extension + feel crepitus
- Hyperextension: lift the leg from the heel and look

Special tests:
- post. Sag sign: (post. Cruciate)
- Ant. Drawer and post. Drawer test:
1. Flex the patient’s knee to 90º.

2. Inspect for evidence of posterior sag as this can give a false positive anterior drawer sign.

Page 16
3. Wrap your hands around the proximal tibia with your fingers around the back of the knee.

4. Rest your forearm down the patient’s lower leg to fix its position.

5. Position your thumbs over the tibial tuberosity.

6. Ask the patient to keep their legs as relaxed as possible (tense hamstrings can mask pathology).

7. Pull the tibia anteriorly – significant movement suggests anterior cruciate laxity /rupture

8. Push the tibia posteriorly – significant movement suggests posterior cruciate laxity /rupture
- Lachman's test( ant. Cruciate);
The knee is flexed at 20–30 degrees with the patient supine.
The examiner should place one hand behind the tibia and the other grasping the patient's thigh.
It is important that the examiner's thumb be on the tibial tuberosity.
The tibia is pulled forward to assess the amount of anterior motion of the tibia in comparison to the
femur
- Valgus stress test: (MCL)

1. Extend the patient’s knee fully.

2. Hold the patient’s ankle between your elbow and side.
3. Place your right hand along the lateral aspect of the knee.
4. Place your left hand on the lower limb (e.g. calf or ankle).
5. Push steadily inward with your right hand whilst supplying an opposite force with the left.
6. If the MCL is damaged your hand should detect the medial aspect of the joint opening up.
- Varus stress test: (LCL)

1. Extend the patient’s knee fully.

2. Hold the patient’s ankle between your elbow and side.
3. Place your right hand along the medial aspect of the knee.
4. Place your left hand on the lower limb (e.g. calf or ankle).
5. Push steadily outward with your right hand whilst supplying an opposite force with the left.
6. If the LCL is damaged your hand should detect the lateral aspect of the joint opening up.

If after this assessment the knee appears stable you can further assess the collateral ligaments by
repeating this test with the knee flexed at 30°. At this position the cruciate ligament are not taught
so minor collateral ligament laxity can be more easily detected.

- Mcmurray's test ( medial and latetal menisci)

To test the medial meniscus, the examiner palpates the postero-medial aspect of the knee while
extending the knee and externally rotating the tibia.
To test the lateral meniscus, the examiner palpates the postero-lateral joint line while extending
the knee and internally rotating the tibia.
If pain is felt by the subject or if a ‘click’ is felt by the subject or examiner, the test is considered
positive

Discussion:

Male pateient had a non-contact sporting injury where he twisted his knee. On examination he has
an antalgic gait, . His range of passive movement was not affected, but active movement was
limited by pain. He did not have localised joint tenderness. Varus stress test and mcmurray's test
were positive, fitting with lateral collateral ligament and meniscal tear.

What is your differential diagnosis?

Page 17
Medial collateral ligament tear
Cruciate injuries
Combination injuries
Bony injuries

What investigations would you perform?

Initially I would arrange a weight bearing X-ray of the knee; however the most important
investigation would be a knee MRI.

What to look for in MRI?

-increased internal signal intensity in the meniscus.

-abnormal meniscus shape

Management:

Nonoperative treatments:

Rest (with weight bearing as tolerated or with crutches)

Ice
Compression bandaging
Elevation of the affected limb to minimise acute swelling and inflammation.

Operative :
Repair or partial menisectomy

X ray of OA:
There are four main radiographic signs in osteoarthritis:

• Narrowing of the joint space

• Subchondral sclerosis
• Cyst formation
• Osetophyte formation

How is osteoarthritis of the knee managed?

Conservative

• Maintain or achieve a healthy weight i.e. aim to decrease weight, and therefore force, going
through a joint
• Regular exercise, with particular attention to strengthening the muscles around the joint.
For example in OA of the knee, cycling is beneficial
• Analgesia: care to be taken with NSAID's with relation to gastric irritation
• Heat application to the joint may offer relief
• Physiotherapy
• Intra-articular steroids

Surgical:

• Arthroscopy and arthrocentesis

• Realignment osteotomy
• Total or partial knee replacement

Page 18
Hip examination: [hip ostearthritis]
Look:
- front ,sides,post.
- gait( antalgic gait, telendenberg's gait)
- Walking aids
- Scars, pelvic tilt, quadriceps wasting, gluteal wasting, lumbar lordosis

Do telendenberg's test:

1. Place hands on the iliac crests on either side of the pelvis.

2. Ask the patient to stand on one leg for 30 seconds.
3. Observe your hands to see which moves up or down.
4. Normally the iliac crest on the side with the foot off the ground should rise up.
5. Repeat the test on the opposite side.

The test is deemed positive (abnormal) if the pelvis falls on the side with the foot off the ground.

This abnormal result suggests weak hip abductors on the contralateral side of the pelvis
Feel:
- palpate the joint( tenedrness or warmth)
- Palpate the greater trochanter
- Measure ( apparent leg length:umbilicus to the tip of medial malleolus)
( true leg length: ASIS to the tip of medial malleolus)

Do Thomas test:

1. Place hand under patient’s spine.

2. Passively flex both legs (hips/knees) as far as you are able to.
3. Your hand should detect that the lumbar lordosis is now flattened.
4. Ask patient to fully extend the hip you are assessing:
Incomplete extension suggests a fixed flexion deformity at the hip joint.
5. Repeat the test to assess the contralateral hip joint

Move:
- ROM ( active+ passive ) , crepitus:
- Flexion( bring your knee towards your chest)
- Adduction
- Abduction
- Internal rotation(passive only)
- External rotation( passive only)
- Extension( prone or lateral, passive)- ( don't perform if Thomas +ve)

To complete my examination I would assess the neurovascular status of the lower limbs and
examine the joint above and below - knee and spine.

Discussion:
Male patient who presents with right sided hip pain. I note that he has an antalgic gait and a scar
overlying the left hip suggesting a previous operation. Positive findings include reduced range of
movement in hip flexion, extension and internal and external rotation on the right. Trendelenburg
and Thomas’ test were negative and there was no discrepancy with respect to true or apparent leg
length.

What is your differential diagnosis?

Page 19
My top differential for this patient with hip pain and reduced range of movement is osteoarthritis.
Other arthritides should be considered. These include rheumatoid arthritis, pseudogout, gout,
inflammatory or infective arthritis and a reactive arthritis.

How would you investigate and manage this patient?

I would take routine bloods, paying particular attention to raised inflammatory markers, which
would alert me to possible infection, and order hip and knee X-rays. If required an MRI of the
affected joint could also be ordered but may be unnecessary.

If this patient had osteoarthritis then management is aimed at alleviating pain and improving the
patient’s functional status. Non-operative measures include weight loss, exercise, physical and
occupational therapy. Simple analgesia such as regular paracetamol and prn NSAID can be
prescribed. More invasive measures such as a corticosteroid injection can be considered, but
ultimately the patient may need surgery in the form of an arthroplasty.

Spine + peripheral neurological examination: [ disc prolapse+

sciatica]

Look:
- general: walking aids- gait
- Behind: scars, muscle wasting, scoliosis, abnormal hair growth
- Side: cervical lordosis, thoracic kyphosis, lumbar lordosis
- Front: posture of the head and neck, symmetry of shoulders

Feel:
Palpate: spinous processes and sacroiliac joints
Paraspinal muscles

Move:
Assess active movements

Cervical spine: flexion, extension, lateral flexion, rotation

Lumbar spine: flexion , extension, lateral felexion
Thoracic spine: rotation

Special tests:
- straight leg raise: +ve in sciatic nerve root impingement due to prolapsed disc
1. Position the patient supine on the bed.
2. Holding the ankle, raise the leg (passively flexing the hip) – keeping the knee straight
3. Normal ROM is approximately 80-90º of passive hip flexion.

4. Once the hip is flexed as far as the patient is able, dorsiflex the foot.
5. The test is positive if the patient experiences pain in the posterior thigh / buttock.
If this causes pain in lower back /thigh/ buttocks, it suggests sciatic nerve root impingement.

- Femoral nerve stretch: +ve in femoral nerve root compression

1. Position patient prone
2. Flex knee
3. Extend hip
4. Plantar-flex foot
Positive test = pain felt in thigh/ inguinal region.

Page 20
- Schobber's test: ankylosing spondyolitis
1. Identify position of the posterior superior iliac spine (PSIS) – “dimples of Venus”p
2. Mark the skin in the midline 5cm below PSIS
3. Mark the skin in the midline 10cm above PSIS
4. Ask the patient to touch their toes – full lumbar flexion
5. Measure the distance between the two lines (started at 15cm)
Normally the distance between the two marks should increase to >20cm.
Reduced range of motion can indicate conditions such as ankylosing spondylitis.

Peripheral neurological examination:

TOPCARS

Tone:
1.leg roll:roll the patient’s leg & watch the foot – it should flop independently of the leg
2. Leg lift – briskly lift leg off the bed at the knee joint – the heel should remain in contact with the
bed
3. Ankle clonus:
Position the patient’s leg so that the knee & ankle are 90º flexed
Rapidly dorsiflex & partially evert the foot
Keep the foot in this position
Clonus is felt as rhythmical beats of dorsiflexion/plantarflexion (>5 is abnormal)

Power:

Hip:
- flexion ( L2,L3):raise your leg off the bed & stop me from pushing it down
- Extension ( L4,L5):stop me from lifting your leg off the bed”
Knee:
- extension ( L3,L4) :
- Flexion ( L5, S1):bend your knee & stop me from straightening it”
Ankle:
- dorsiflexion ( L4,L5):point your foot towards your head & don’t let me push it down”
- Plantar flexion (S1,S2):press against my hand with the sole of your foot
Big toe:
- halux extension( L 5):don’t let me push your big toe down”

Co-ordination:
Heel to shin test:
run your heel down the other leg from the knee & repeat in a smooth motion”

Reflexex:
- knee jerk : ( L3, L4)
- Ankle jerk: ( L5,S1)

Sensations:
- light touch ( dorsal column)
- Pin - prick ( spinothalamic tract)

Discussion:

I examined the peripheral neurology of the lower limbs of this patient with back pain. His gait was
normal, he had a positive Lasegue’s sign on the right, with normal tone, power, co-ordination and
Page 21
reflexes throughout both lower limbs. He had impaired sensation over the L5 dermatome on the
right leg, to both light touch and pin prick.

Diffrentials:
-Disc herniation between L4-5 impinging on the L5 spinal nerve.
- spinal canal stenosis
-Diabetes Mellitus (peripheral neuropathy)
-Vitamin B12 deficiency(subacute combined degeneration of the cord)
-Drug therapy (e.g. anti-retrovirals, thalidomide, phenytoin)
-Heavy metal/chemical exposure (lead, arsenic, mercury)
-Carcinoma (most likely spinal metastases)
-Tabes dorsalis (syphilitics myelopathy).

Management:
Imaging : x ray on lumbosacral spine
MRI of lumbosacral spine

Treatment: conservative
Surgical : discecctomy , laminectomy

Ankle examination:
Simulated patient, played soccer, sprained ankle
Look:
(Gait)

Is the patient demonstrating a normal heel strike / toe off gait?

Is each step of normal height? – increased stepping height is noted in foot drop
Is the gait smooth & symmetrical?

Swelling / erythema of the foot or ankle – may suggest injury / inflammatory arthritis / infection
Scars – suggestive of previous injury / surgery

Feel:

Ask the patient to lay on a bed.

Assess temperature & compare between legs – ↑ temperature may indicate inflammatory
pathology
Assess pulses in both feet – posterior tibial & dorsalis pedis
Palpate the achilles tendon – assess for thickening or swelling

Palpate the joints / bones

Work distal to proximal – assess for tenderness / swelling / irregularity

Squeeze MTP joints – observe patient’s face for discomfort

Tarsal joint
Ankle joint
Medial / lateral malleoli
Proximal fibula

Move:
Page 22
Assess each of the following movements actively & passively (feeling for crepitus).

Foot plantarflexion – “push your feet downwards, like pushing a car pedal” – 30-40 º
Foot dorsiflexion – “point your feet towards your head” – 12-18 º
Foot inversion – grasp ankle with one hand & heel with the other – turn sole towards midline –
passive assessment only
Foot eversion – grasp ankle with one hand & heel with the other – turn sole away from midline –
passive assessment only

Special tests:
Simmonds’ test

Simmonds’ test is used to assess for rupture of the achilles tendon

1. Ask patient to kneel on a chair with their feet hanging off the edge.
2. Squeeze each calve in turn.
3. Normally the foot should plantarflex.
4. If the achilles tendon is ruptured there will be no movement of the foot.

Differentials:
- Ankle llgament sprain
- Fracture lateral maleolus, cuboid, cuneforms
Management: x-ray on ankle joint

Xray showed undisplaced fracture of fibula with swelling of the ankle? Management
- Backslab and analgesia
- Rest , ice , elevation to reduce edema

Inguinoscrotal examination: (inguinal hernia, hydrocele)

Expose the patient from umblicus to feet

- inspect the lumb , ask the patient to cough

- Palpate the other side
- Palpate the lumb: ask the patient to cough
- Id ASIS, Pubic tubercle: show the position of the lumb in relation to the inguinal ligament
- Ask the patient to reduce the hernia
- Perform DIR test
- Auscultate the lumb
- Examine the scrotum : scrotal neck, transillumination, testis seprable or not

Discussion:

Diffrentials:

What are the differentials for a scrotal swelling?

Page 23
Common differentials include a hernia e.g. a inguinal or femoral hernia, lymph nodes, varicocoele
or a swelling related to the testes, such as a hydrocoele, epididymal cyst, lipoma of the cord or
testicular tumour. Other differentials include infection such as orchitis or epididymitis, testicular
torsion, and a spermatocoele

Management:
Inguinal hernia: mesh repair
Hydrocele : evacuation and eversion of the tunica vaginalis

Abdominal examination:
Acute cases: ( all will be presented with observational charts,
lab. Data + ECG)
- pod6 (post left hemicolectomy anastmotic leakage)- CCRISP
APPROACH
- Acute diverticulitis
- Acute cholecystitis
- Acute appendicitis
Chronic cases:
- paraumblical hernia
- Incisional hernia

POD6 ANASTMOTIC LEAKAGE ( after left hemicolectomy)

Stem : patient is presented with shotness of breathing, left shoulder tip pain,abdominal lower
midline covered scar with dressing)

- WIPER
- Note that the patient will simulate SOB , Note the nearby O2 mask
- Ask the patient if he is having any pain at the moment, the patient will point to his abdomen
- Tell the patient that you will examine his tummy and that you will be gentle, and take verbal
permission
- Start by light palpation of the RIF , Note : the patient will jump in pain simulating acute abdomen
- Tell the examiner that the patient is experiencing severe abdominal pain , so further abdominal
examination can not be continued, and that you are going to start assessing the patient using
the CCRISP
- AIRWAY : the patient was talking so his airway is patent
- BRAETHING :
* look for any central cyanosis
* Look for chest wall movements , equal or not
* Palpate for chest expansion
* Percuss the anterior and lateral chest wall only
* Auscultate anterior and lateral chest walls
- CIRCULATION:
* look for the neck veins
* Look for signs of dehydration (dry tongue, sunken eyes)
* Auscultate the heart
- DISABILITY : ( consciousness level)
Page 24
* the patient is alert
- EXPOSURE:
* Offer to remove the dressing to expose the laparotomy wound
* Look and squeeze for the calfs to rule out DVT and PE
- CHARTS: EWS charts( rising temp., risinig pr, incresing o2 requirements) FBC ( leucocytosis) ,
ECG ( AF)

Discussion :
I examined this patient presented by SOB , Left shoulder tip pain. On general inspection, the
patient looks obviously having SOB and generalized abdominal pain. I started by doing light
palpation on his RIF , which showed that the patient was having severe abdominal tenderness,so
this patient looked critically ill and therefore i started assessing the patient according to the
CCRISP .
- his airway is patent
- breathing: no central cyanosis, equal chest wall movements, percussion note was normal, equal
air entry with no added sounds
Page 25
- Circulation: no congested neck veins, no signs of dehydration,normal heart sounds
- The patient was alert
- There was no any swelling or pain in his calves
- His charts showed: rising temp., rising pr, increasing o2 requirements
- FBC ( leucocytosis) ,
- ECG ( AF)

So, my main diagnosis for that case is generalized peritonitis secondary to anastomotic leakage
which caused the patient to have sepsis.shoulder tip pain in such case may be due to the presence
of intrabdominal collection causing irritation of the diaphragm

Managment:

- NBM
- Urinary carheter to monitor output
- NG tube for suction and bowel rest
- May refer the patient to HDU to insert a central line and monitor
- Fluid resuscitation by crystalloids
- I.V antibiotics
- Bloods: ABG, U&E
- Chest x-ray to rule out any respiratory problem
- CTPA to rule out PE
- Abdominal ultrasound to detect any abdominal collections
- CT with gastrograffin enema to identify the leaking anastomosis

This patient will need urgent laparotomy : Harman's procedure plus good peritoneal toilet plus
drainage

ACUTE DIVERTICULITIS:
Perform classic abdominal examination----> tenderness on LIF, otherwise normal findings
Note: do not do deep palpation on LIF
Read the patient charts after completing examination-----> fever, mild tachycardia
Stem: severe left side abdominal pain in patient with a long standing history of constipation

General examination: from the end of the bed

- Does the patient look comfortable?
- How is the general appearance and nutritional status?
- Is there any obvious pallor or jaundice?
- THE HANDS : Nails, Anaemia, Clubbing (Crohn’s disease, Ulcerative colitis, Cirrhosis)
Leuconychia (Caused by hypoproteinaemia associated with liver disease), Koilonychia (Spoon
shaped nails seen in iron deficiency anaemia) ! Asterixis( liver flap), seen in decompensated
liver disease.
- THE FACE Eyes Anaemia (pale conjunctiva) , Jaundice, Mouth Dentition- Ulcers (Inflammatory
bowel disease, herpes simplex) , Tongue Dehydration- red, beefy (B12 deficiency) - Angular
stomatitis Caused by iron, folate and vitamin B/ C deficiency Also seen in herpes simplex and
oral candidiasis- Hepatic Foetor
- THE ARMS & TRUNK: Spider Naevi are found along the distribution of the Superior Vena Cava
(i.e., above the nipple line) and are associated with oestrogen excess , Purpura, petechiae Can
be caused by low platelets or raised prothrombin time, Gynaecomastia , Signs of pruritus –
scratch marks
- SUPRACLAVICULAR LYMPH NODES: Virchow’s Node in the left supraclavicular fossa can be
enlarged in gastric cancer.
Page 26
Local examination:
Inspection:
- Scratch marks
- Swelling,
- distension
- Caput medusae
- Skin changes (bruising, signs of weight loss)
- Scars Striae
- Any visible pulsations
- Ask the patient to cough or lift his/ her head off the bed to reveal any herniae or signs of
peritonism (the patient will exprience pain in LIF)

Palpation:
Tips:
- Kneel down at the patient’s right side
- Ask the patient if there is any generalized pain or localized pain
- Palpate all nine distinct areas of the abdomen starting furthest from you, unless the patient
indicates an area of pain, in which case palpate this area last
- Look at patient’s face for signs of pain while palpating
- Palpate the abdomen with flattened fingers
- start by superficial palpation of the 9 quadrants then by deep palpation and feel the presence of
any masses

- Liver: Start in the right iliac fossa, asking the patient to take deep breaths in and out. Move your
hand upwards towards the costal margin during inspiration until you feel a liver edge on
expiration.
If the liver is palpable check the:
* Size (record enlargement in cm below costal margin)
* Texture (soft / firm / hard / nodular)
* Edge (smooth / irregular) An irregular liver edge suggests metastases
- Murphy’s test: With your hand in the position of the gallbladder, fingers pointing up, ask the
patient to take a deep breath in and out. Pain on expiration as the gallbladder comes to rest
against your fingertips is a positive Murphy’s test.
- Spleen: Start palpating in the right iliac fossa, using the same breathing technique as for liver
palpation. However, this time move gradually towards the left upper quadrant . Note the size,
texture and edge of the spleen.
- Kidneys: ‘Ballot’ the kidneys using both hands
- Abdominal aorta: Palpate in the region of the lower epigastrium/ upper umbilical area, slightly
towards the left of the mid-line, deeply for a pulsatile mass. Note the approximate diameter by
using both hands to feel the lateral edges of the mass.

Percussion:
- Upper liver border
- Spleen
- Bladder
- Ascites: Start by percussing in the midline towards either flank and note any change in pitch
from resonant to dull, indicating fluid . If there is dullness, keep your finger on this area and ask
the patient to roll onto his/ her side so that the dull area is now superior.Percuss again and note
any change in pitch back to resonance . If present, this is shifting dullness.

Auscultation:
- Over the left iliac fossa for bowel sounds
- Over the liver for a bruit
- Over the aorta, iliac vessels and the renal arteries for bruits
Page 27
Say you would like to :
- Feel the hernial orifices
- Examine external genitalia (e.g., for testicular atrophy in chronic liver disease)
- Perform a rectal examination
- Examine the lower limbs for peripheral oedema

Questions:
If CT shows only sigmoid wall thickening with one locule of gas seen, what will be your
management?
- antibiotics: co-amoxiclav, garamycin, clindamycin
- Bowel rest
- DVT prophylaxis

If no response to antibiotics , what will you do?

- percutaneous drainage
- Hartman's procedure

ACUTE CHOLECYSTITIS
Stem: right hypochondrial pain since 4 days
Perform classic abdominal examination ----> positive murphy sign, otherwise normal examination
Note: do not do percussions on the liver
Read the patient charts ------> fever, undetectable urobilinogen in urine, increased liver enzymes

Differentials:
- Acute cholecystitis
- Ascending cholangitis
- PUD
- Lower lobe pneumonia
- Acute pancreatitis
- Renal pathology

Investigations:
- liver function tests
- Urea and electrolytes
- Full blood count
- Crp
- Abdominal ultrasound may show dilated CBD and IHBR or my show CBD stone
- MRCP

Treatment:
- conservative treatment: (nil by mouth, intravenous fluids, antibiotics /3rd generation
cephalsporins + metronidazole, nasogastric suction if appropriate)
- Surgical treatment:cholecystectomy in 5 days if conservative treatment fails

ACUTE APPENDICITIS:
Stem : RIF pain in simulated young lady
Perform classic abdominal examination ------> RIF pain , positive rebound, Rovsing , obturator,
psoas signs
Examine the patient charts : fever, mild tachycardia, leucocytosis

Special signs:

- Rovsing's sign: Pressure in the LIF causes pain in the RIF with appendicitis
Page 28
- Obturator sign: Ipsilateral hip and knee are flexed; internal rotation of the hip (heel moves
outwards) stretches obturator internus, which causes pain if in contact with an inflamed
appendix
- Psoas sign : Inflammatory processes in the retroperitoneum irritate the psoas muscle, causing
ipsilateral hip flexion, Straightening the leg causes further pain.

Differentials:

• acute appendicitis
• leaking duodenal ulcer
• pelvic inflammatory disease
• salpingitis
• ureteric colic
• inflamed Meckel's diverticulum
• ectopic pregnancy
• Crohn's disease
• Complicated ovarian cyst

Investigations:

- urine analysis
- Urea and electrolytes
- Full blood count
- Abdominal ultrasound
- Ct abdomen and pelvis

Treatment :
Appendectomy ( open - laparoscopic )

What will you do if you encountered blood in the peritoneal cavity while doing appendectomy?
- i will call for an obstetric surgeon ( may be ruptured ectopic pregnancy)
- I will order group and save
- I will have to perform appendectomy eventually

PARAUMBLICAL HERNIA AND INCISIONAL HERNIA:

Perform classic abdominal examination

Notes:
Inspection:
- Describe any scars and look for other scars, stomas etc
- Ask the patient to lift their head off the bed and look for bulging of the hernia or the scar
Palpation:
- Enquire about tenderness and palpate the hernia, commenting on any defect you can feel
- Ask the patient to cough and demonstrate weakness in the scar or abdominal wall, feeling for
bulging of abdominal contents against your hand
- Try to determine the size of the defect
- If there is a midline longitudinal abdominal bulging with no scar, consider divarication of the
recti.
Page 29
Auscultation:
Listen for bowel sounds

Questions;
Treatment:
open or laparoscopic mesh repair is possible. At open surgery, the mesh can be inserted as an
onlay, inlay, sublay or intraperitoneal position

Chest pain ( pulmonary embolism) : ( POD8)

This is a potentially unwell patient, therefore you should approach him in an ABC manner

A – you know his airway is patent as he is talking to you

B – inspect chest for respiratory movement, is it equal? Look for central cyanosis, use of accessory
muscles,
Feel for chest expansion,
tracheal position
Percuss the chest for dullness / hyper-resonance,
test vocal fremitus
Page 30
Listen for bilateral air entry, crackles of consolidation or pulmonary oedema
Measure the respiratory rate
Look for ABG and chest X-ray

C- Inspect for cyanosis,

and look at the JVP
Feel the pulse, making note of any rhythm abnormalities and tachycardia, and peripheries (cold
and poorly perfused v hot and septic)
Auscultate the heart – muffled heart sounds could indicate tamponade, a murmur could suggest a
significant valve lesion
Measure the blood pressure
Look for ECG

D – GCS / AVPU

E – make a point of checking the calves for a DVT

Check the drug chart for SC heparin and TEDS – have they been signed for
Check the fluid chart to ensure they are not overloaded

Discussion:

This patient presented with acute pleuritic chest pain and shortness of breath 8 days after a hip
operation. I note from their drug chart that they have missed two dose of their subcutaneous
heparin.

He is haemodynamically stable, but had saturations of 88% on 2L. This improved with high flow
oxygen. They also had a swollen left calf. Otherwise examination showed a clear chest with good
bilateral air entry and a normal percussion note making a pneumonia and pneumothorax unlikely.
An MI is possible but less likely due to the nature of the pain, however I am awaiting an ECG and
troponin. My top differential is a pulmonary embolus.

What investigation would you arrange now?

- Assuming renal function was within acceptable limits I would arrange a CTPA to exclude a PE
- Chest x-ray
- D- dimer
- ABG : respiratory alkalosis
- ECG:
* Right ventricular strain pattern – T wave inversions in the right precordial leads (V1-4) ± the
inferior leads (II, III, aVF).
* Right axis deviation
* SI QIII TIII pattern – deep S wave in lead I, Q wave in III, inverted T wave in III

What is the management of a pulmonary embolism?

Management follows the usual ALS sequence of securing the airway before moving on to breathing
where high flow oxygen is essential and then circulation. Assuming this was all done, the
management can be spilt into massive PE and non-massive PE. Massive PE is characterised by
haemodynamic compromise and may require thrombolysis. I would put out a crash call if the
patient presented in this way to get urgent help.

If the patient is stable, treatment initially with a therapeutic dose of subcutaneous heparin, followed
by warfarin is warranted. I would involve the appropriate medical team to follow this patient up.

Page 31
If you were scrubbed in a the theatre and have been updated with the patient condition, what will
you do?
I will put a crash call immediately

Varicose veins:
- Inspect:
* Inspect with the patient standing up
* Ensure that the patient is adequately exposed whilst dignity maintained.
* Inspect from all sides -easiest done by kneeling in front of the patient then asking the patient to
turn around.
* Look for:
. Varicosities
. Skin changes and ulceration from chronic varicosities and their complications especially the
medial “gaiter” area
, Lipodermatosclerosis
. Venous eczema
. Haemosiderin staining
. “Atrophie blanche” –white patches found in areas of healed ulceration
. Oedema
. Scars from previous surgery, including avulsion scars
. sapheno varix in the groin
- Palpate for saphina varix

- palpate :
- Feel at the sapheno-femoral junction (~4cm below and lateral to the pubic tubercle) for a
sapheno varix. If a swelling is present check for a palpable thrill and a cough impulse which
indicates an incompetent valve between the superficial and deep systems
- Feel down the leg over the course of the long saphenous and then short saphenous veins for
tenderness along the veins which may indicate perforator incompetence.

- Special tests:
. Telendenberg's test:
* With the patient lying supine, lift his/her leg to about 45 degrees and gently empty the veins (this
may be aided by “milking” the veins)
* Occlude the sapheno-femoral junction and ask the patient to stand up ensuring that the finger or
thumb is firmly over the junction
* If the superficial veins do not fill and the varicosities are controlled at the level of the sapheno-
femoral junction by occluding it, it strongly suggests sapheno-femoral incompetence. This can be
confirmed by releasing the pressure from the sapheno-femoral junction that will cause the blood
to return from the femoral vein into the saphenous vein (through the incompetent sapheno-
femoral junction), resulting in the varicosities becoming prominent.
* As the patient stands, if the veins fill from below with the sapheno-femoral junction occluded,
incompetent perforators are the most likely cause for the varicosities.

. Touniquet test:

Page 32
* The tourniquet test follows the same principle but is easier to perform than Trendelenberg’s test
as it uses a tourniquet to control the sapheno-femoral junction rather than the examiner’s fingers.
It also has the added advantage that if varicosities are due to perforator incompetence, it can be
performed further down the leg to identify the level of the incompetence
* Once the superficial venous system has been controlled with the tourniquet you can perform
Perthe’s test to assess the patency of the deep venous system, particularly important if
considering varicose vein surgery

. Perthe's test:
With the patient standing and with the tourniquet still around the thigh ask the patient to go up and
down on his/her tiptoes or ask him/her to walk, thus exercising the calf muscles. If the deep venous
system is intact, the calf pumps encourage venous return. However, if the deep venous system is
occluded or valves incompetent, when the patient performs this action venous return is restricted
and blood is forced into the superficial system from the deep system, causing engorgement of the
superficial veins associated with a bursting pain.

- hand held doppler assesment:

hold the Doppler probe at a 45 degree angle to the skin at the level of the sapheno-femoral
junction and the squeeze the patient’s calf. In a patient with a competent sapheno-femoral junction
you will hear a short “swoosh” as you squeeze, but this ceases as soon as you let go of the calf. If
however, the sapheno-femoral junction is incompetent, there is a more prolonged “swooooosh” of
blood as it regurgitates back down though the incompetent valve.

- to complete my examination i would examine the arterial system and the abdomen

Discussion:

- On closer inspection of the legs, she has obvious varicosities bilaterally. There were no ulcers,
but I noted venous eczema, lipodermatosclerosis and haemosiderin deposition reflecting chronic
venous insufficiency. Doppler assessment demonstrated incompetence at the saphenofemoral
junction.

What further investigations would you arrange?

Venous duplex: Duplex ultrasound scan to determine the site of valvular incompetence, ensure
patency of the deep venous system

What are her management options?

Depends on symptoms and effect on quality of life.

• Conservative: Graduated compression stockings, leg elevation, exercise and avoidance of
prolonged sitting or standing.
• Invasive, non-operative: Foam sclerotherapy, radiofrequency or photocoagulation (Laser)
ablation (under local anaesthesia).
• Invasive, operative (under general anaesthesia): Varicose vein surgery is reserved for
symptomatic patients with skin complications. It can involve ligation of the vein (long or short
saphenous) near the site of incompetence and excision (for the long saphenous) by stripping
through small skin incisions to reduce the risk of recurrence.Varicose veins can be avulsed through
small stab incisions (phlebectomies), followed by compression bandaging.

Page 33
Stoma examination:
Inspection

Inspect from the end of the bed and the patient’s right hand side
-Site: quadrant
-Scars
-Contents – liquid stool (ileostomy), formed stool (colostomy), urine (ileal conduit/urostomy/
nephrostomy)
-Output – high, normal, low (high output is associated with ileostomies)
-Lumen – single (end stoma) or double (loop stoma)
-Type - Spout (ileostomy) or flush (colostomy)
-Stoma health – pink, necrotic ulcerations, stenotic
-Surrounding skin – erythematous, excoriation (usually as a result of ileostomy output)
-Retracted or prolapsed
-Parastomal herniation - ask the patient to lift their head off the bed

Palpation

-Digital stoma examination: remove bag and insert your finger into the stoma to assess for patency
and any stenosis.
-Transilluminate to assess mucosa for ulcerations
-Reattach the bag, thank the patient and wash your hands

Further considerations

-Abdominal examination
-Inspect perineum for scars and patency of anus
-Assess stoma position when standing and sitting

How are stomas classified?

Loop v End

Temporary v Permanent

Anatomical site

What is important to consider when siting an abdominal stoma?

It needs to be:
Away from bony prominences, dominant skin folds and scars.
Within the rectus abdominus muscle
Away from the belt line
Visible to the patient
Supplied with good vasculature

What are the possible complications of a stoma?

Early :
Ischaemia/necrosis
High output +/- electrolyte imbalance
Retraction
Obstruction

Page 34
Late :
Obstruction
Stoma retraction or prolapse
Stenosis of the stoma
Parastomal hernia
Parastomal granulomas
Mucocutaneous separation
Fistula formation

Superficial lumb:
Inspection

-Site
-Size
-Shape - hemispherical
-Surface – smooth, irregular
-Skin – any overlying skin changes
-Scars

Palpation
-Tenderness
-Temperature
-Surface
-Margins
-Consistency
-Surrounding area
-Pulsatility
-Compressibility
-Reducability
-Fluctuation

Assess regional lymph nodes

Discussion:

What is your differential diagnosis?

Lipoma
Sebaceous cyst
Abscess
Soft tissue tumour
Bone tumour
Vascular malformation

Management:

Investigations:
Ultarsound
Tru- cut biopsy
Treatment:
Exicision

Page 35
Cerebellar examination:
Gait:
1. Stance – a broad based gait is noted in cerebellar disease
2. Stability – can be staggering and often slow & unsteady – can appear similar to a drunk person
walking
3. Tandem (‘Heel to toe’) walking – Ask patient to walk in a straight line with their heels to their
toes
This is a very sensitive test and will exaggerate any unsteadiness.
4. Romberg’s test – ask patient to put their feet together, keep their hands by their side and close
their eyes (be ready to support them in case they are unsteady!)
This is a test of proprioception – a positive Romberg’s test indicates that the unsteadiness is due to
a sensory ataxia (damage to dorsal columns of spinal cord) rather than a cerebellar ataxia.

Head:
- speech ( stacatto): say british constitution
- Nystagmus : follow my fingers by your eyes

Arms:
*Pronator drift:

1. Ask patient to close eyes & place arms outstretched forwards with palms facing up

2. Observe the hands / arm for signs of pronation / movement

A slow upward drift in one arm is suggestive of a lesion in the ipsilateral cerebellum.

*Rebound phenomenon:

Whilst the patient’s arms are still outstretched and their eyes are closed:

1. Ask the patient to keep their arms in that position as you press down on their arm.
2. Release your hand.

Positive test = Their arm shoots up above the position it originally was (this is suggestive of
cerebellar disease).

*Tone:

1. Support the patient’s arm by holding their hand & elbow.

2. Ask the patient to relax and allow you to fully control their arm.
3. Move the arm’s muscle groups through their full range of movements .
4. Is the motion smooth or is there some resistance?

* reflexes:

Assess the patient’s upper limb reflexes, comparing left to right.

1. Biceps(c5, c6)
2. Triceps (c7)
3. Supinator (c6)

In cerebellar disease, there is often mild hyporeflexia.

* Co-ordination

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Finger to nose test

1. Ask patient to touch their nose with the tip of their index finger, then touch your finger tip.
2. Position your finger so that the patient has to fully outstretch their arm to reach it.
3. Ask them to continue to do this finger to nose motion as fast as they can manage.
4. Move your finger, just before the patient is about to leave their nose, to create a moving target
(↑sensitivity).

An inability to perform this test accurately (past pointing/dysmetria) may suggest cerebellar
pathology.

* Intentional tremors

* Dysdiadokinesia

1. Demonstrate patting the palm of your hand with the back/palm of your other hand to the patient.
2. Ask the patient to mimic this rapid alternating movement.
3. Then have the patient repeat this movement on their other hand.

An inability to perform this rapidly alternating movement (very slow/irregular) suggests cerebellar
ataxia.

Legs:
- tone: leg roll, leg lift
- Reflexes: ( knee, ankle)
- Co-ordination ( heel to shin)

To complete my examination , i would do:

full neurological examination including:

Cranial nerves
Upper and lower limbs

Discussion:

Patient has (DANISH) : dysdiadokinesia, ataxic gait, nystagmus, intention tremors, stacatto
speech, hypotonia
My main diagnosis will be cerebellar ataxia due to posterior fossa tumour, other diffrentials include:
- cerebellar metastases due to lung or breast cancer
- Head trauma
- cerebrovascular stroke
- TIA
- MS
Posterior fossa tumors:
- cerebellar astrocytoma
- Primary neuroectodermal tumors
- Medulloblastoma
- Ependymoma and ependymoblastoma
- Choroid plexus papilloma and carcinoma
- Dermoid tumors
- Hemangioblastoma
- Metastatic tumors
- Brainstem gliomas

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Management:
- investigations:
* Plain x-ray skull: It may show calcification.
* MRI brain ( enhanced) with gadolinum
* CT brain : CT scan of the posterior fossa is inferior to MRI in diagnostic value because of the
artifact produced from the surrounding thick bone. However, CT scan is helpful for postoperative
follow-up.
* CT ( whole body) to detect primary tumours
* guided biopsy
Treatment :
Excision

Hand examination:( carpal tunnel syndrome)

Wash hands
Introduce yourself
Confirm patient details – name / DOB
Explain examination
Gain consent
Expose patient’s hands, wrists and elbows
Position patient with hands on a pillow
Ask if the patient currently has any pain

Look:

Dorsum :
- Inspect hand posture – asymmetry / abnormalities
- Scars or swellings
- Skin colour:
Erythema – e.g. cellulitis (erythema) / palmar erythema
Pallor – e.g. peripheral vascular disease / anaemia
- Deformities:
Bouchard’s nodes (PIP) / Heberden’s nodes (DIP) – OA
Swan neck deformity – distal interphalangeal (DIP) joint hyperflexion with proximal
interphalangeal (PIP) joint hyperextension – RA
Z-thumb – hyperextension of the interphalangeal joint, in addition to fixed flexion and
subluxation of the metacarpophalangeal (MCP) joint – RA
Boutonnières deformity – PIP flexion with DIP hyperextension – RA
- Skin changes:
Skin thinning or bruising – long term steroid use
Rashes – e.g. psoriatic plaques
- Muscle wasting – may indicate chronic joint pathology or motor neurone lesions
- Nail changes:
Nailfold vasculitis – small areas of infarction
Pitting and onycholysis – associated with psoriasis

Palms:
Page 38
- Inspect hand posture – asymmetry / abnormalities (e.g. clawed hand)
- Scars – e.g. carpal tunnel release surgery
- Swellings
- Skin colour:
Erythema – e.g. cellulitis (erythema) / palmar erythema
Pallor – e.g. peripheral vascular disease / anaemia

- Deformity – Dupuytren’s contracture

- Thenar/ hypothenar wasting – isolated wasting of the thenar eminence is suggestive of carpal
tunnel syndrome
- Elbows – psoriatic plaques or rheumatoid nodules

Feel:

Dorsum
- Assess radial nerve sensation by touching:
First dorsal webspace- radial nerve

- Assess and compare temperature using the back of your hand:

Forearm
Wrist
MCP joints

- Gently squeeze across the metacarpophalangeal (MCP) joints – observe for non-verbal signs of
discomfort – tenderness may indicate inflammatory arthropathy

- Bimanually palpate the joints of the hand (MCP / PIP / DIP / CMC) – assess and compare for
tenderness / irregularities / warmth
Metatarsophalangeal (MCP) joint
Proximal interphalangeal (PIP) joint
Distal interphalangeal (DIP) joint
Carpometacarpal (CMC) joint of the thumb (squaring of the joint is associated with OA)

- Palpate the anatomical snuffbox – tenderness may suggest scaphoid fracture

- Bimanually palpate the patient’s wrists

Elbows
Palpate the patient’s arm along the ulnar border to the elbow:
Note any rheumatoid nodules or psoriatic plaques (extensor surface)

Move:

- Assess each of the following movements actively first (patient does the movements
independently). Then assess movements passively, feeling for crepitus and noting any pain.
. Finger extension – “open your fist and splay your fingers”
. Finger flexion – “make a fist”
. Wrist extension – “put palms of your hands together and extend wrists fully”
. Wrist flexion – “put backs of your hands together and flex wrists fully”

- Test separately for both sets of flexor tendons:

Page 39
. Flexor digitorum profundus: stabilise the PIPJ and ask the patient to flex at the DIPJ
. Flexor digitorum superficialis ,: isolate the finger being examined by holding the other fingers in
extension, then ask the patient to flex at the PIPJ

- Assess all movements of the thumb –flexion, extension, abduction, adduction and opposition
NB: To simply check for extension of the thumb, ask the patient to place his/her hand palm down
on the table and see if he/she are able to raise his/her thumb off the table. Feel for integrity of
the Extensor Pollicis Longus tendon.

Function:
- Power grip – “squeeze my fingers with your hands”
-Pincer grip – “place your thumb and index finger together and don’t let me separate them”
-Pick up small object or undo a shirt button – “can you pick up this small coin out of my hand?”

Neurlogical examination:

Motor:

- Median Nerve:
Test the function of abductor pollicis brevis; with patient’s palm facing up, stabilise the rest of
patient’s hand on the table and ask them to point with the thumb to the ceiling.
- Ulnar Nerve:
Palmar interossei –adduct the fingers
Dorsal interossei –abduct the fingers
Froment’s sign: ask the patient to grasp a piece of paper between the index finger and the thumb.
You then try to pull the paper away. If there is an ulnar nerve lesion, the distal phalanx of the thumb
flexes (due to action of the unaffected flexor pollicis longus) to compensate for the weak muscle
(adductor pollicis) that is supplied by the ulnar nerve. This is a positive Froment’s sign
- radial nerve:
ask the patient to extend the fingers and wrist against resistance.

Sensory:
• Volar aspect of index finger (median n. and C6)
• Volar tip of middle finger (C7).
• Volar tip of little finger (ulnar n. and C8).
• First dorsal web space (radial n).

Special tests:

Tinel’s test
Tinel’s test is used to identify nerve irritation and is therefore can be useful in the diagnosis of
carpal tunnel syndrome.
The test involves the following:
Tap over the carpal tunnel
If the patient develops tingling in the thumb and radial two and a half fingers this is
suggestive of median nerve irritation and compression.

Phalen’s test
If the h examination findings are suggestive of carpal tunnel syndrome this test may be used to
further support the diagnosis:
Ask the patient to hold their wrist in complete and forced flexion (pushing the dorsal
surfaces of both hands together) for 60 seconds
If the patient’s symptoms of carpal tunnel syndrome are reproduced then the test is positive
(e.g burning, tingling or numb sensation over the thumb
Page 40
To complete my examination , :

Perform a full neurovascular examination of the upper limbs

Examine the elbow joint.

Discussion:
-Sensory deficit present on the palmar aspect of the first three digits and radial one half of the
fourth digit.
- Motor examination: Wasting and weakness of the median-innervated hand muscles (LOAF
muscles) can be detectable.
- Positive phalen's and tinel's tests

Investigations:
- Electrophysiologic studies including electromyography (EMG) and nerve conductions studies
(NCS) are the first-line investigations in suggested CTS.
- MRI scan can exclude underlying causes in the carpal tunnel.
- lanoratory: blood glucose, thyroid functions

Treatment:

- Treatment of underlying disease, if any.

- Conservative management of mild to moderate disease (EMG and NCS) includes: –Splinting the
wrist at night time for a minimum of three weeks –Steroid injection into the carpal tunnel –Non-
steroidal anti-inflammatory drugs (NSAIDs) and / or diuretics
- Surgical treatment is indicated for severe disease, or when conservative management fails and
includes carpal tunnel release.

Page 41
 Procedural skills

1- ordering a theatre list:

Page 1
- strangulated inguinal hernia ( COPD+Pacemaker)
- Diverticular abscess ( allergic to penicillin and iodine)
- BKA( IDDM+ MRSA+AF)

General principles:
- Patients with diabetes go early in the list. : This prevents complications of
hypoglycaemia and allows early return to normal glycaemic control. Peri and
post-operative normoglycaemia is essential in order to reduce rates of surgical
site infections.
- Patients with latex allergies should be considered to be first in the list.: Natural
rubber allergies require a clean theatre and time must be given for previous latex
“dust” to settle before starting the case. All latex products must be removed form
theatre or clearly labelled.
- Children should be operated on early. This minimises distress to the child and the
parents.
- Procedure under local anaesthesia (minor point) : Some surgeons would put
local anaesthetic cases first or last as a professional courtesy to their anaesthetic
colleagues. However, it is also practical to place small local anaesthetic cases
between major cases to allow the anaesthetist to recover the last patient and
anaesthetise the next to optimise theatre time.
- Major procedures should be considered to be early in the list.: Major procedures
and patients for cancer resection should not be cancelled due to time constraints.
It is often best to put these cases first or early on the list.
- Patients with infection go last in the list. MRSA and C. difficile must go last on a
list to prevent cross contamination between patients. If possible, order a list

Page 2
 according to USA NRCS guidelines (Clean, Clean-contaminated, Contaminated,
Dirty).
- Clinical Priority: . It is important to appreciate the difference in operative priority
between emergency and elective procedures. Life-or limb-threatening conditions
must go first on an emergency list.
- National Confidential Enquiry into Patient Outcome and Death (NCEPOD)
Criteria for emergency surgery
- . 1a. Immediate.:
- * Life or limb threatening.
- * Simultaneous haemodynamic resuscitation and intervention.
- * Ruptured AAA, Ruptured spleen and
- * Haemodynamically unstable pelvic trauma.
-
- 1b. < 6 hours. :
- * Life threatening but not immediate.
- * Intervention following resuscitation.
- * Ischaemic bowel, large bowel obstruction.
-
- 2. <24 hours.:
- * Deterioration of condition that may threaten life.
- * Appendicitis (not perforated).
-
- 3. < 7 days.:
- * Deterioration of elective condition.
- * Acute cholecystectomy.
-
- 4. Scheduled. Elective procedure with no threat to life or limb.

Questions:

- What are the current guidelines for perioperative glycaemic control in the
diabetic patient?

* Patients with diabetes must be prioritised in the operating list.

* Routine overnight admission is not necessary.
* Starvation time should be no more than one missed meal.
* Analgesia and anti-emetics should be used to enable early return to diet and usual
insulin regime.
* Insulin infusions should only be used if a patient is expected to miss
more than one meal.
* 0.45% sodium chloride with 5% glucose and 0.15% or 0.3% KCl is the
recommended IV fluid.
* Capillary blood glucose should be measure hourly during and after the any
surgical procedure.
Page 3
* The target blood glucose should be 6-10 mmol/L (acceptable range 4-12 mmol/L).

- What precautions should be taken in a patient with a pacemaker?

* Preoperatively:
* - the patient should undergo a pacemaker check where a “passport”
containing information on the device model, date of implant, and reason for
implant should be available.
* - They should have had a recent review by their pacemaker follow up clinic
with information regarding degree of pacing dependency, extent of any heart
failure and any particular safety advice communicated to the anaesthetic and
surgical team.

* Intraoperatively :
* - the use of monoplolar should be strictly limited, and not used near the
pacemaker device. Where its use is unavoidable, it should be limited to short
bursts. The return electrode should be placed so that the current pathway is as
far away from the pacemaker as possible.

- The theatre should have cardio-pulmonary resuscitation and temporary pacing

equipment available.
- The patient’s ECG should be monitored throughout from before induction

-What is the difference between bipolar and monopolar diathermy :

In monopolar diathermy current passes from the active electrode through the
tissues being operated on to an electrode plate on the patient. The current is
disseminated thought a larger surface area of at least 70 cm2 than it originated
in, therefore preventing a heating effect at the plate electrode.
In bipolar diathermy, current passes between the two tips of the active
electrodes, therefore only passing though tissue that lies between the tips. There
is no plate electrode

What complications are patients with COPD at particular risk from?

Patients with COPD have a several fold increase (2.7-4.7x) in postoperative complications including
atelectasis, pneumonia, and respiratory failure.

Page 4
How can you reduce these?

The risk of pulmonary complications can be reduced though smoking cessation at least 4-8 weeks before
surgery and early mobilization following surgery.

Pre- and postoperative respiratory physiotherapy to provide deep breathing exercises, intermittent positive
pressure breathing, and incentive spirometry can help reduce complications.

Postoperatively, adequate pain relief and an upright position in bed should aim to ensure the patient is able to
cough and that the diaphragm is not splinted.

How would you manage warfarin?

It depends on her current risk. If the patient has recently been started on warfarin for AF and the AF is the
source of an emboli that has led to vascular problems in the leg to be operated on, then I would place him in
the high risk thromboembolic category. I would take advice from a consultant haematologist. They might advise
that he stop warfarin 4 days before surgery, and commence subcutaneous low molecular weight heparin. This
would be withheld the evening before surgery, and then restarted from 6h after surgery once haemostasis had
been achieved. I would ensure the INR had fallen to below 1.4 before operating.

What to use in case of iodine allergy?

Chlorhexidine based antiseptic instead

What prophylactic antibiotic in patient with penicillin allergy?

Cefazolin, vancomycin

Page 5
2- cannulation of ATLS patient:
Preparations:

-Tell the examiner that you would wash your hands prior to setting up your
equipment.
-Choose an appropriate sized cannula as indicated by the clinical situation :

- Prepare 10mL of 0.9% normal saline flush in a 10mL syringe.

- Introduce yourself and include your full name and grade.
- Ask to check the patient’s identity, “Can I just check you are….. and what is
your date of birth?”
- Explain what you are about to do, why and what the complications are.
- The patient must give verbal or implied consent for the procedure.
- Position yourself and the patient, and select an appropriate vein. It can often
be helpful to allow the patient’s arm to hang over the side of the bed in order to
distend the veins or offer to warm the patient’s hands.
- In general, the veins on the dorsum of the hand should be used and the
antecubital fossa should be reserved for trauma or emergency situations.
Procedure:
- Apply the tourniquet and offer to don two pairs of gloves for high risk patients.
- Sterilise the skin with an alcohol wipe and allow it to dry.
- Do not re-palpate.
- Check the cannula, apply skin traction and insert cannula until flashback is
seen.
- Flatten off the angle of your approach and advance while removing the needle.
- Place the needle in the sharps bin.
Page 6
- If a blood sample is required, it can be taken from the cannula at this point
using a syringe or vacutainer.
- Release the tourniquet and occlude the vein above the level of cannulation.
- Position the hub on the end of the cannula. Flush with 10ml normal saline
ensuring that no resistance is felt.
- Apply the appropriate cannula dressing with the time and date of insertion
written on it.
- Dispose off all equipment into a yellow bag.
- Wash your hands.
- Offer to document date, time and site of insertion in the patient notes.

Q. What the fluid regimen will you administer?

1 liter of crystalloids over 15 min.

3- knot tying:

Tie a braided non- absorbable simple reef-knot:

- The reef knot consists of two throws: the coming down and going up throw.
- To start with, the coming down throw: Pick up the end furthest away from you
(the shortest end or the white end in this example) with your left thumb and
ring finger. Then lay the suture over your index and middle fingers ). Using
your right hand pick up the other (red) end and lay it up over the left middle
and index fingers . Bend (flex) the left middle finger under the white end and
straighten again so that the white end is behind the middle finger under
tension .Keep the red end under tension with your right hand. Now release the
white end and draw it through the loop with fingers of your left hand . Lay the
knot using some tension

Tie an absorbable braided knot at depth:

- Though the throws are the same for a reef knot, your hands have to move in
the vertical plane to tie at depth.
- This can be tricky when operating and the difficulty is replicated by using a
narrow cup on the hand tying jig in the exam.
- Pass a suture around the hook and tie the first throw of a reef knot .
Page 7
- Lay the knot by pushing down with the index finger of your left hand and lifting
the suture vertically with your right hand .
- Tie your second throw of a reef knot
- Lay the knot using your index finger again to put the knot under tension

Perform a hemostatic suture for bleeding tissue using an non- absorbable

monofilament suture:
- You will need to use instruments for this part of station and demonstrate safe
handling of the sharp needle.
- Angle the needle perpendicular to the tissue, to one side of the bleeding area.
- Pass the suture through the tissue and re-mount the needle.
- Aim to put the next suture on the other side of the bleeding tissue, through the
tissue in the same direction as the first pass.
- Tie the two ends of the suture under some tension.

Questions:

-What other knots do you know?

Surgeon's knot - Granny knot
-What is vicryl is made up from ?
Polygalactin
-When vicryl is absorped:
Page 8
within 56–70 days.
- how long it holds a tensile strength?
For two to three weeks

Advantages of braided sutures?

- greater tensile strength
- Better flexibility
How to protect tissues while tying at depth?
- obtain more light in the field
- Retraction of tissues outside
- Making the knot loose then securing it by pushing it down by finger

4- debridement of a contaminated wound :

- Firstly,
dirt and debris must be gently removed to expose any underlying tissue
damage. It is important to use a swab on an artery forcep to keep your fingers
away from the tissue, as there may be sharp materials concealed in the wound.

- Use a systematic approach, starting at the centre of the wound and working out
to the periphery. Gently sweeping the debris away shows that there is a lot of
dirt in this wound. After an initial washout, forceps may be used to inspect the
wound.

- Any foreign bodies should be removed using the forceps; this should prevent
any ongoing infection.
- Deep within this wound, there is a damaged tendon which will need to be
repaired at a later stage. Working systematically around the wound, in an
anticlockwise fashion, any devitalised tissue should be identified and removed.

- The next step is to irrigate the wound with saline. It is the pulsed pressure of
the fluid that is important for clearing the tissues.
- A swab is then used to gently mop out and clear the wound. Any deeper areas
of damage should also be irrigated to ensure that the wound is clear.

Page 9
When is tetanus toxoid / tetanus immunoglobulin indicated?
There are specific guidelines on tetanus prophylaxis for each hospital but in general wound are
considered high risk if they:
- are contaminated with farmyard material such as soil or manure.
- involve the axilla or Feet.
- penetrate into the deep tissues. are animal or human bites.
- have large amounts of devitalised tissue.

- Areas of devitalised tissue must be removed. In general, it is better to remove

too much tissue that too little.

- Once the wound is clear, it is important to insert a pack In this case, a saline
wick is gently inserted to hold the wound open and the tail is trimmed to allow
easy removal.

5- FNAC:

For this technique we will use a 10ml syringe with a green needle and a vial of
heparinized saline.
- The first step is to draw up a little heparinized saline into the syringe. This is
then drawn up and down the syringe as shown.
- The saline is then expelled, leaving the needle and syringe flushed with
heparinized saline.
Page 10
- In this specimen, there is a palpable lesion simulating cystic swelling . It is not
common practice to use local anaesthetic for this procedure, but this may be
required if the patient is particularly anxious. It is necessary to obtain some
cells for cytology.

- After cleaning the overlying skin, the needle is passed directly into the lesion.
- Once the tip of the needle is inside the lesion, the plunger is pulled back with
the thumb whilst keeping the syringe and needle in place with the other
fingers.
- Multiple passes are needed through the lesion to collect an adequate sample.

- The needle is then removed and you should havejj a small sample of aspirate
in the green portion of the needle.
- Using a pair of slides, pre-marked with the patients details, pass a small
amount of aspirate onto one slide as shown. The other slide is then passed
across the first to form two smears.
- One slide will then be air dried and the other sprayed with a fixing agent.
- The rest of the aspirate can be placed in a pot with some saline, to be spun
down for further analysis.( cytospin container)

6- Suturing of a wound:
- You should also ask about the patient's tetanus status, whether they have any
allergy and state that you would like to arrange an X-Ray of the limb to check for
foreign bodies.
- Equipment: Due to time constraints, the correct equipment is usually provided
for you and the patient is already prepared and draped. However, be prepared to
clean and drape the wound if asked.
- Equipment that you may require includes: Sterile gloves and gown. Skin
preparation solution (Iodine or Chlorhexidine in alcohol). Sterile drapes. 10ml
syringe. Needles (1 x 21 & 1 x 25 gauge needle). Local anaesthetic (1%
Lignocaine). Toothed forceps. Skin suture. Suture scissors. Adherent dressing.
Gauze swabs.
- Preparation: If the equipment is not already laid out for you and the patient is
not prepared and draped, firstly open up a wound care pack, pour some
antiseptic solution into the receptacle and open the relevant remaining
equipment onto the sterile field. At this point state the need to wash your
hands before donning a pair of sterile gloves.
Page 11
- Local anaesthetic : Firstly state that you would like to check the local
anaesthetic and its expiry date. Then attach the 21G needle to the syringe and
draw up the desired amount of anaesthetic. Discard this needle into a sharps
bin and mount the 25G needle onto the filled syringe. At this point, if not
already done for you, clean the wound using the antiseptic solution and use
the drapes to create a surgical field. Administer the local anaesthetic
appropriately around the wound, remembering to warn the patient before
introducing the needle. Introduce the needle in a smooth motion, pull back on
the plunger to ensure you that are not injecting into a vessel, and then slowly
administer the local anaesthetic whilst withdrawing the needle. Repeat this
step until the surgical field is anaesthetised adequately. Discard the needle
into a sharps bin and state that you would now leave the anaesthetic to work
for at least 5 minutes. Before starting to suture the wound, always check that
the local anaesthetic has taken effect, either using a needle or pinching with
toothed forceps.
- Closure : It is most likely that the wound will be a clean, straight incision. If it is
not, then state that you would like to debride the unhealthy wound edges to
turn a ‘traumatic wound’ into a ‘clean, surgical wound’ before closing. In this
scenario, when suturing a traumatic wound, it is advisable to use interrupted
sutures to close rather than a continuous suture. This is because if the wound
became infected, then not only could the wound discharge between the
interrupted sutures, but individual sutures could be removed to allow drainage,
without opening up the whole wound. A suitable suture in this scenario would
be a non-absorbable, monofilament suture material such as 4.0 Nylon. Start at
one end, and place a simple interrupted suture. Ensure your needle enters the
skin at 90 o and use the curve of the needle by fully pronating and supinating
your wrist to ensure the wound edges are everted. Bring the needle out into
the wound, grasp the needle again and repeat the same action for the other
side of the wound. Take equal bites (roughly 0.5cm) either side of the wound,
and ensure that they are of the same depth to avoid steps in the wound edges.
Place sutures roughly 1cm apart along the remainder of the wound, until it is
closed adequately. Finish by applying a simple adherent dressing to the
wound.
- Post-operative instructions & follow up Once you have finished the procedure,
the first thing you should do is discard your sharps into a sharps bin, which will
be provided in the station. At this point the patient may ask you a few
questions regarding post-op instructions, but you will appear far more
professional if you offer this information without being prompted. Explain that
the patient will go home with some simple analgesia, and that they must seek
medical attention if they are concerned about any of the following signs/
symptoms:
- Increased pain.
- Redness.

Page 12
- Discharge/blood through the dressing.
- Malodour.
- Systemic symptoms (fever/nausea/malaise).
- Give the patient the appropriate follow-up information with regards to when
and where the sutures must be removed.

Questions:
Xylocaine dose: ( lidocaine 1%)
3mg/kg
Lidocaine+ adrenaline:
7 mg/kg
Mechanism of action:
Blocks Na channels thus preventing depolarization

In this scenario, the patient would need at least a single dose of antibiotic. If
there was a delay in presentation, two further doses would be required post
closure. For the type of antibiotic prescribed, you should follow hospital/
department guidelines where available. In this clinical scenario a broad-spectrum
antibiotic such as Co-amoxiclav is appropriate.

7- Excision of a nevus:
- The best way to excise the lesion is using an elliptical incision. The incision site
should be measured to allow enough clearance on either side of the lesion.

Page 13
- The two points indicate ideal 2mm clearance margins. This distance is then
multiplied by three to indicate the length of the long axis of the elliptical
incision

- To create this incision, it is most effective to hold the blade in a pencil grip.
Whilst holding the skin taught with your other hand, start the incision using the
belly of the blade. Move the blade along perpendicular to the skin, smoothly
along the line of the ellipse.

- At the edge, it is important to make sure that it forms a smooth V shape to allow
excision of the lesion. Make sure that you have cut through all of the skin and
then proceed to remove the lesion, dissecting through the subcuticular plane.
Take care to dissect along the line of the ellipse and not cut into the skin edge.
- Complete the excision with a smooth V shape, keeping the blade
perpendicular at all times. The lesion is then removed.
- It is now necessary to close this ellipse.
- Sometimes you may find that there is a lot of tension in the mid portion of the
ellipse. In these circumstances, it is helpful to undermine the subcutaneous
tissue away from the skin edges
- To close this ellipse, the best method is to place the first sutures at the distal
edges, then gradually work towards the centre. If you try to start the closure at
the widest part of the wound, you may find it difficult to bring the edges
together.
- Post-operative instructions & follow up Once you have finished the procedure,
the first thing you should do is discard your sharps into a sharps bin, which will
be provided in the station. At this point, the patient may ask you a few
questions regarding post-op instructions, but you will appear far more
professional if you offer this information without being prompted. Explain that
the patient will go home with some simple analgesia, and that they must seek
medical attention if there are any worrying signs/ symptoms (increased pain,
redness, discharge/ blood through dressing etc). Give the patient the
appropriate follow-up information with regards to when and where the sutures

Page 14
 must be removed, and that a further clinic appointment will be posted to them
once the results are available from histology.( within 2 weeks)
Langer's lines:
They correspond to the natural orientation of collagen fibers in the dermis, and
are generally parallel to the orientation of the underlying muscle fibers.

8- Male catheterization:

- Consent: It is not necessary to obtain written consent for catheterisation. Talk

through the procedure in layman’s terms. Indication for procedure. Risks, if not
performed. Alternatives. What the procedure entiles. Complications. Failure
(need for alternatives). False passage. Haematuria. Pain (bladder spasm).
Occasional need for monitoring urine output post catheterisation (diuresis).
- Equipment: A second examiner may act as an assistant and offer to get a
trolley ready for you.
- * Basic catheter pack.
- * Kidney dish, gallipot, gauze and sterile drape.
- * Skin preparation solution (sterile water is acceptable).
- * Sterile gloves.
- * Appropriate urinary catheter (14 Ch is probably the most appropriate; ensure
that it is not a female catheter as these are shorter).
- * 10ml syringe + 10ml water (not saline) if not supplied with catheter.
*Instillagel (anaesthetic, antiseptic lubricant) –minimum 10ml.
- * Appropriate catheter bag (large ‘night’ bag or a urometer).
- Positioning : Patient should be as flat as possible to perform the procedure.
- Procedure: .
- Confirm patient’s identity and ask if they have previously had a catheter and, if
so, whether any problem or complications were encountered.
- Ask for allergies (iodine/ n /lignocaine/latex) before positioning the patient
supine and covering them.
- Wash your hands and prepare your equipment.
- Ask the assistant to obtain adequate exposure.
- Cleanse hands with an alcohol-based agent and don non-sterile gloves.
- Use one hand to retract the foreskin with gauze and clean the foreskin, glans
and meatus (separate swabs for each). Change to sterile gloves and apply a
sterile drape.
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- Place the kidney dish or collecting dish between the patient’s legs.
- Instil at least 10ml of gel into the urethra, hold the urethra at the base of the
glans and wait for 3-5 minutes.
- Advance the catheter with the penis held pointing to the ceiling with gentle
traction.
- Pass the catheter all the way to the hilt and wait for urine to drain.
- After urine has started to drain, inflate the balloon with the appropriate amount
of sterile water (usually 10mL, but some such as 3-way catheters require
30mL) and withdraw the catheter gently.
- Replace the foreskin if present.
- Dry and cover the patient before asking them to redress.
- Dispose off the equipment in the appropriate bin.
- Measure the amount of urine draining after an adequate period of time (5-10
minutes) and obtain a CSU for microscopy, culture and sensitivity.
- Document the procedure in the notes
Questions:
-What would you do if no urine drains after catheterisation?
1. Reevaluate presence of urine in bladder by percussing the suprapubic region
if you haven't done this already.
2. Apply suprapubic pressure.
3. Aspirate with a syringe.
4. Flush with a 50ml catheter syringe and sterile water.
-You insert the catheter; it drains no urine and you therefore remove it. You then
examine this patient’s abdomen and there is a supra-pubic mass. What is your
differential diagnosis?
* A bladder that was not catheterised appropriately.
* Colonic carcinoma.
* Large iliac aneurysm.

9- chest drain insertion:

Equipment:
- Sterile gloves and gown.
- Skin preparation solution (iodine or chlorhexidine in alcohol).
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- Sterile drapes.
- 10ml Syringe. Needles (21–25 gauge).
- Gauze swabs. Local anaesthetic (1% or 2% lignocaine).
- Scalpel and No. 11 blade.
- Suture material (1 silk).
- Large haemostat or Spencer-Wells Clamp for blunt dissection.
- Large bore chest tube (24 to 30 French).
- Connecting tubing.
- Closed drainage system(underwater seal).
- Occlusive dressing (sleek tape).
Positioning :
- Patients should be supine with 30 o of head up if possible and the bed slightly
rotated towards the side of insertion.
- The patient’s arm should be placed behind their head to expose the axillary
area. It is essential that the patient undergoes regular haemodynamic
observations and pulse oximetry during the procedure.
-
- Insertion Site : Although variations have been suggested, the 'safe triangle' for
insertion of a chest drain has the following borders:
- * Posterior Margin Mid-Axillary line (some literature states the anterior border
of latissimus dorsi to be the posterior margin but if this is taken as a landmark,
then the insertion point will be in the mid-axillary line where the long thoracic
nerve lies). *
- * Anterior Margin Lateral border of Pectoralis Major.
- Inferior margin 5 th intercostal space (above 6 th rib).
- Apex –Below the axilla.

Ideal placement should be just anterior to the midaxillary line within this triangle
to avoid damage to the long thoracic nerve of Bell. Blunt dissection should be
over the superior aspect of the inferior rib in order to avoid damage to the
intercostal neurovascular bundle.

- Anaesthesia : Lignocaine or similar is infiltrated to the skin and periosteum of

the superior margin of the inferior rib. There is no evidence that local
anaesthetic with adrenaline reduces the risk of iatrogenic haemothorax. The

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 skin is tested before any incision is made. Despite local anaesthetic the
procedure is poorly tolerated by patients and concomitant anxiolytics or
opiates are recommended by the BTS.
- Insertion : Make a skin incision parallel and just above the rib below, slightly
longer than the tube diameter (1French is 1/3mm). Use a large haemostat or
clamp to blunt dissect through the parietal pleura before doing a finger sweep.
A small clamp can be attached to the end of the tube through one of the holes
to guide placement. Aim the tube apically for pneumathoraces and basally for
haemathoraces. Watch for tube fogging to confirm appropriate placement.
Suture the drain in place with a stay suture and pass a horizontal mattress
closing suture but leave this untied. The end of the closing suture can be
covered in sleek or a transparent adhesive dressing with the drain to stop it
coming loose.
- Drainage : A unidirectional closed drainage system such as the underwater
seal drain is most commonly used. Connection tubing is used between the
chest tube and underwater drain. Before the procedure is completed it is
essential to ensure that the fluid within the tube is moving with respiration
(“swinging” or bubbling). Post Procedure It is essential to obtain a chest X-ray
to ensure appropriate tube placement.

Questions:

Indications for contacting thoracic surgeons ?

- A persistent pneumothorax despite drainage may suggest a bronchial tear.
Haemothorax .
- More than 1,500 mL of blood immediately evacuated by tube thoracostomy.
Persistent bleeding 150 mL/h to 200 mL/h for 2 hours to 4 hours.
- Persistent blood transfusion is required to maintain hemodynamic stability.

10-Taking blood culture from HIV + ve patient

Procedure:

.Although you are talking to an arm, you should treat it as a patient.

.Wash your hands, introduce yourself and gain permission to take blood.
.Prepare your equipment You will need
-Gloves
-2% chlorhexidine 70% isopropyl alcohol wipe Tourniquet
-Winged Vacuette blood collecting set or a needle and syringe
-Sterile gauze
-An aerobic and an anaerobic culture bottle
-A microbiology request form
.Wash your hands again
.Wear an apron, eye protection and gloves
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.Once you have chosen vein, make sure you clean thoroughly with the chlohexidine wipe, and then
do not touch the area again before venepuncture. Allow the skin to dry.
.Flip the tops off the two culture bottles and clean with a fresh chlorhexidine wipe. Allow to dry.
. Insert the bottles into the collection port, or the needle and syringe into the bottle depending on
what equipment is available,
.inoculate the aerobic bottle first, then the anaerobic bottle, and rotate 180o to ensure the blood
mixes evenly.
.Label the bottles with the demographics, time and date,
. complete the request form. Send for microscopy, sensitivity and culture.
.Thank the patient and wash your hands.

Discussion:

What is the rate of HIV transmission from a needle stick injury?

It is around 0.3% following a needle stick injury from an HIV positive patient

How does this compare to hepatitis B and C transmission?

Before vaccination the risk of transmission following a needlestick injury from a patient with
hepatitis B was around 30%, but has been reduced significantly by the hepatitis vaccination,
obligatory for at risk health care workers, which is 90- 95% effective.
The risk of hepatitis C transmission is around 1.8%

What should you do if you get a needle stick injury?

Clean the wound with soap and water. Report the incident to your occupational health department
or A&E out of hours. Another doctor should approach the patient and ask permission to take some
blood to test it for HIV, and viral load, hepatitis B and C. They should also take a sample of blood
from you for testing. Retest again at 6 weeks and 3 months for HIV, HBC and HCV antibodies, and
for elevated liver enzymes, which could indicate hepatitis.

11- Scrubbing:
Pre scrub:
1. Mention you would be in scrubs with appropriate footwear and a scrub cap.
2. Remove any watches or rings (make sure you are not wearing nail varnish!)
3. Expose hands and forearms to elbows 4. Put out a gown and appropriate sized gloves
5. Put on a face mask
6. Put a nailbrush on the sink

Scrub:
1. Scrub time - 5 mins for first scrub of the day and 3 mins for each subsequent scrub (look at a
clock!)
2. Hold hands at a higher level than elbows at all times
3. Initial pre-scrub – apply surgical detergent, work up a lather then wash hands and forearms to
elbow and rinse from finger-tip to elbow
4. Then apply more scrub solution to hands
5. Clean each nail under running water with nail stick
6. Scrub each nail against palm of opposite hand
7. Scrub each finger on all 4 sides - 5 strokes/side
8. Scrub back of hand and palm from base of fingers to wrist
9. Small overlapping circles are used to scrub from wrist to 2 inches above elbow 10. Rinse hands
and forearms from finger- tip to elbow

Drying:
1-Lift one of the drying towels up and away from the sterile field
2. Dry fingers and hand then dry remainder of the forearm
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3. Drop towel into bin
4. Lift the other towel and dry the other hand and forearm

Gowning and gloving:

1. With one hand, pick up the gown and hold by the neck and allow to unfold with arm holes facing.
2. Slide arms into sleeves and your assistant will secure at the back
3. “Gloving” is performed by the closed or open method (practice this before the exam so you look
slick)
4. Hand your assistant the belt tie and turn around to then secure waist belt.

12-Abscess Drainage

- The first step is to make a generous incision at this point. This will result in an immediate release
of pus, which should be cleared away using swabs.

We are left with a cavity which still contains pus and an overlying linear skin incision.

- It is vital to ensure that the skin incision cannot close over. This can be achieved firstly by making
a generous skin incision. Usually, an elliptical incision should be made

- At this point, a swab is taken, placed in a container and sent for culture and sensitivity tests at the
bacteriology lab.

- The next stage is to express the remaining pus using two handed pressure and plentiful swabs to
clear away the exudate. We are now left with a cavity and an overlying cruciate incision. It is
sometimes necessary to excise the edges of necrotic skin tissue further.

- A finger is then inserted into the cavity to break down any loculi, leaving one continuous space. If
necessary, the cavity can be irrigated with saline using either a bladder tipped or standard syringe.
On occasion, 3% hydrogen peroxide can be used to help clean out the cavity.

- A pack must the be inserted into the cavity to keep the osteum open and to absorb any further
exudate. Either a saline wick or an alginate dressing can be used. The pack is loosely inserted
and the wick trimmed, leaving a small tail to aid subsequent removal.

- The wick will remain in place for about 24 hours and will then be replaced by an alginate
dressing.
- When removing the pack, make sure that it is moist, as pulling out a dry dressing will disturb the
granulation tissue forming at the base of the cavity.

- If an alginate dressing is used from the outset, it is important to trim this to match the size of the
cavity, as a larger dressing may cause maceration of the surrounding normal tissue.

13- Airway management in ATLS patient:

- How is the airway assessed clinically?

Assessment is based on the principle of: Look, Listen and Feel.
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Look : for the presence of accessory muscles of respiration (neck, shoulders,
chest and abdomen) being used, presence of obvious foreign bodies in the
airway, facial/airway injury ( le forte fractures) and the ‘see-saw’ pattern of
complete airway obstruction (NB. central cyanosis is a late sign)
Listen : for the presence of inspiratory stridor, as this indicates upper airways
obstruction (laryngeal level and above). Also take note of grunting, gurgling
(liquid or semi-solid foreign matter in the upper airways) and snoring sounds
(indicating the pharynx is partially occluded by the tongue or palate). Expiratory
wheeze suggests lower airways obstruction. Crowing indicates laryngeal spasm
Feel : for chest wall movements and airflow at the nose and mouth (for 10
seconds)

What techniques of airway management will you do?

Simple measures:
- Basic airway manoeuvres : these include a[ head tilt, chin lift and jaw thrust]
- Basic airway adjuncts : these include nasopharyngeal and oropharyngeal
airways.

Head tilt : the hand is placed on the patient's forehead and another under the
occipital protuberance to tilt the head back gently
Chin lift : the fingers of one hand are placed under the mandible in the mid-line
and then lifted upwards to bring the chin forward

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Jaw thrust : the angles of the mandible are identified on both sides, the index and
middle fingers are placed behind it and a steady upwards and forwards pulling
pressure is applied to lift the mandible (this is painful, and if a patient tolerates it,
consider an anaesthetic review). Finally, the thumbs are used to slightly open the
mouth by downward displacement of the chin

Nasopharyngeal airway : check for right nostril patency, attach safety pin to end
of tube (if needed) and lubricate the tip, insert it bevel end first and perpendicular
to orifice (towards the ear). Once in place, reassess the airway according to
Look, Listen and Feel

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Oropharyngeal airway : open the mouth employing basic airway manoeuvres.
Suction out debris and insert it upside down (curved side pointing to the palate).
Rotate it 180° between the hard and soft palate and seat the flattened section
between the gums and teeth.OPA should be measured so that it stretches from
the corner of the mouth to the angle of the mandible

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 Ventilations are delivered at 8 to10 per minute(1ventilation every 6-8seconds)

Complex measures:
Endotracheal intubation : this requires anaesthetic expertise and can be
achieved through the mouth (orotracheal) or the nose (nasotracheal) intubation
Surgical airway : this requires a cut down through tissues in the neck and can be
achieved in three ways
There are three types of surgical airway :
- Needle cricothyroidotomy (and jet insufflations of oxygen)
- Cricothyroidotomy
- Tracheostomy, which may be performed in the emergency or elective setting
What are the indications for a surgical airway?
- Failed intubation, e.g. due to oedema
- Traumatic fracture of the larynx
In which anatomic location are the surgical airways sited?
Both types of cricothyroidotomy are performed through the median cricothyroid
ligament. This is the thickened anterior portion of the cricothyroid membrane that
runs between the cricoid and thyroid cartilages.
A tracheostomy may be placed from the 2nd to 5th tracheal rings

Cervical spine control:

- Sizing the collar:
1) Achieve a lateral view of the patient's neck by looking from the side of the body.
2) Bring your fingers and thumb together as if you were going to salute.
3) Rest your outstretched hand on the base of the patient's shoulder, pinky finger
side down.
4) With your eye, draw an imaginary line sticking straight forward from the bottom of
the patient's chin.
5) Note which finger matches the level of that imaginary line.
6) Count the number of your fingers, from the pinky to the imaginary line. For
example: if your index finger matches the line, you have 4 fingers worth of space to
fill with the collar.
Following the manufacturer's guidelines, find the appropriate measurement tool on
the collar itself. It may be line-etched in the plastic or a post. Place your fingers in
the specified space to determine how to select the right collar, or adjust the size of
the collar so it fills the space appropriately.

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- Applying the collar:
- slideback portion of collar under neck until it is just visible. Then slide the collar
up the chest wall until the chin is firmly seated on the chin piece. Correct
placement is evident because the chin will be flush with the end of the chin
piece. IF THE CHIN IS NOT FLUSH WITH THE END OF THE CHIN PIECE,
THE COLLAR IS NOT ON CORRECTLY

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