Petra Emtiaz
Lecture Notes Of
Medicine
Dr. Hassan Abd Al-Majeed Alkhatatbah
Assisted by
Dr. Mohammad Abdel jalil Amrosisoxqyg 0986)
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Sa1{PSMedicine
Pulmonary embolism
Sarcoidosis
Obstructive sleep apnea
Respiratory failure
Pulmonary edema
Occupational lang diseases
Fosinophilic lang diseases
SVC syndrome
Homer syndrome
Chapter
Hematology
Anemia
Hemostasis
Bleeding disorders
pic
Polyeythemia
‘Thrombocytopenia
Functional platelet disorder
Thrombocytosis
Pancytopenia
Multiple myeloma
“Myeloproliferative disorders,
Leukemia
Lymphoma
‘Nephritie syndrome
Nephrotic syndrome
Electrolyte
Chapter 5
Infections diseases
Jomune system
Antibioties
Herpes zoster
Infectious mononcleasus
‘Typhoid fever
Brucellosis
Diarrhea
Meningitis
HIV/AIDS
Syphilis
Cat soratch diseaso
‘Toxic shock syndrome
Pericarditissaree,
Anamyeusssody,
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Chapter 9
Neurology
Stroke
Subarachnoid hemorrhage
Headache
M
sclerosis
ops
Myasthenia gravis
Lambert Eaton syndrome
Parkinson
Aphasia
UMN
Meiosismyerasis
Press
Wemicke encephalopathy
Cranial nerves
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is abnormal heart rythm
Sinus rythm, Is the normal heart rhythm jnormaly heart rate is
60-100 beat/minute ,every p wave is followed by QRS and
every QRS followed by T wave. With regular interval .p wave
representsatrial depolarization(contraction). QRS represents
lar depolarization, T wave represents ventricular
repolarization(relaxation),
Atrial repolarization wave(relaxation) is not seen on
ECG(nasked by QRS).
sinus tachyeardia(HR more than 100 but normal rhythm) .
causes of sinus tachycardia (Pain ,fever,anemia, fear,Exercise,
hyperttryroidism,drugs like atropine and adrenaline)
Sinus bradycardia(HR Jess than 60 but normal rhythm).
(Hypothyroidism, athletes,B-blocker _Drug,increased
intracranial pressure) are causes of bradycardia Bradycardia
if asymptomatic necd no treatment,but if symptomatic
treated by atropineayn pre Jo somereadde yoo) KS
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> Supra-ventriculer tachycardia (SVT)
° No P wave, regular, narrow QRS,HR>180
ECG showing SVT
Treatment
Learotid massage. first done to increase Vagal tone &
decreaseHR,done unilateral because bilateral carotid massage
simultaneously can cause sever bradycardia.
2-valsalva maneuver increase intrathoracic pressure and
stimulate vagus nerve which decrease HR.
3-Oceular massage
4-Adenosin LV 6/12/12mg regimen(the drug of choiceif the
above methods failed). Adenosine can cause bronchospasm
and hypotentionso it is contraindicated in asthma or
hypotention(systolic BP<90). Inasthma patient with SVT give
Diltiazem(calcium channel blocker).
5-DC shock(cardioversion). If hypotensive (systolic BP<90) or
if not responding to medication.
Medic
Remember that:
> Adenosin Contraindicated in pt. With systolic BP less
‘than 90 & in asthma pt. Instead you should give Catt
channel blocker ( verapamil, deltiazem ).
> Dmug of choice in SVT is adenosin
> Adenosin side efect
* Bronchospasm.
© Hypotension
> Ventricular tachycardia :
Regular, wide QRS,no ?’ or T wave
ECG showing ventrienlar tachycardia(Goqoey ys
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‘Hyperglycemia (due to DM or other)
Type A Behavioral pattems (Nervous serious personality)
Lack of exercise
Anemia
‘Consumption of alcohol
Stress
Diet rich in saturated fats
Saturated fat (animal fats) >barmfl
‘Unsaturated fat
1) useful
Obesity
Men over 60; women over 65
Male (M>F)
Aartic stenosis icrease the risk of CAD
Hypermocystinuria (Increase homoeystein increase the risk of
CAD) .Treatment folic acid decrease h
CAD includesAngina(stable or unstable) and myocardial
infaretion(STEMLor NON STEMI).
Coronary artery syndromeincludes unstable angina,
STEMI,non STEMI(but not stable angina).
Medicine
Pathophysiology: cholesterol plaques deposit in the coronary
vessels ,these plaques release chemicals that attract platelet
which result in narrowing of blood vessels.Left anterior
descending(LAD)coronary artery is most common site for
atherosclerosis,
most common cause of acute coronary syndrome is rupture of
plaque.
Angina
Anginadoesn’t cause myocardial muscle necrosis (unlike MI
which cause necrosis) so angina doesn’t cause elevation of
cardiac enzymes,
1-Stable angina
Precipitated by some activity (running, walking, etc.) with non-
existent symptoms at rest.Present with chest pain that start after
yual
ity,Last 5-15 minutes and relieved by rest or su
nitrate.
Occur with stable frequency.
ECG and cardiac enzymes are normal
Diagnosis treadmill stress test, cardiac catheterization
‘Treatment
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Combination of troponin I and CK-MB are the most sensitive
2ECG
STEMI shows ST elevation Whi
Mi(affect whole thickness of cardiac wall).non STEMI
transmural
shows ST depression and other ECG changes but not ST
clevation.(non STEMI is not transmural).
‘Treatment:
IMER.......GIVE MONA-B and anticoagulate with heparin
and then emergency reperfusion _therapy(cardiac
catheterization (PCIand stenting(best) or fibrinolytic
‘therapy(urokinase or streptokinase)
M: morphine (as MI pain doesn’t respond to nitroglycerine )
: oxygen (02)
N: nitroglycerine (nitrates) angina respond but MI less or no
A: Aspirin (crushed) 325 mg
B: B Blocker
PCI (percutaneous coronary intervention) is the best
reperfusion therapy in ACS ,and best done in the first 90
minutes.
Wibrinolytic therapy: includes streptokinase and urokinase.
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Streptokinase is derived from bacterial protein(streptococcus
protein.its antigenic which produce antibody that decrease its,
efficacy with repeated use.
Urokinase isn’t antigenic ,doesa’t produce antibody and
doesn’t loss efficacy with repeated use(more expensive than
streptokinase).
mechanism of action : activate plasminogen into plasmin
which dissolve the fibrin around the thrombus.
Indications: STEMI(not used in non STEMD),If no PCI
available or the nearest PCI need >90 minutes.if no
contraindications. Bestto use it in 1 4 hrs of STEMI (but
not used after 12 hours of STEMI symptoms:
Contraindications:
Previous hemorrhagic stroke ,suspected aortic
disscction,beeding disorder,active bleeding.brain tumor, HIN
>180/110.pregnancy ,recent major trauma or surgery in the last
2-4 weeks.Aspirinand clopidogrel should be continued for 1
year post PCI and coronary stenting to prevent stent
thrombosis,then topped and patient continue on
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(more with inferior MI due to increase risk of AV block) AV
block with inferior MI usually transient and no need
for pacemaker but AV block in anterior MI aeeds
pacemaker (AV block here from ischemia not vagal
stimulation)
S-Ventricular aneurysm develop 3-7 days post MI
(persistent ST elevation is indication for that)
6-ventricular rupture usually occur 1 week post MI.
7-Papillary muscle rupture and mitral regurgitation(more
ferior MD).
8-VSD in case of anteroseptal MI occur 3-7 days post MI.
9-Acute cardiac tamponade.
10-right ventricular dysfunction (more with inferior M1)
‘Note: avoid nitrate in inferior MI with right ventricular
dysfunction,and give I:V fluid and dobutamine.
11-pericarditis(ressler syndrome) occur 2 weeks post
MI
12-intramural thrombus due to blood stasis with risk of
systemic embolization(stroke bowel ischemia lower
limb ischemia)
|
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Medien
Notes
ECG in pericarditis show diffuse ST clevationMI doesn't cause diffuse
elevation,
‘Ml usually present with epigastric pain not chest pain and occur more in
iabetio,
‘New left bundle branch block(but not right) on ECG can indicates transmural
ML
ECG sequence in STEMI 1" is peaked T wave followed by ST
clovation followed by T wave inversion and finaly Q wave
‘Q wave persst(doesn’tdisappeat) and when you find it on ECG means old M1)
STEMIalso called Q yrve Mii tranemural necrosisynon STEMI(non Q
wave) is superficial necrosis co venticular rupture and aneyrysm occur with
‘STEMI not non STEMI
Indications for coronary artery bypass grafting(CABG)
1-3 vessels diseases 2- occlusion of the proximal left main
coronary artery 3-significant atherosclerosis in left proximal
anterior descending coronary artery with ejection fraction less
than 50% 4-chronic disabeling angina, Vesselsused in CABG.
are great saphenous vein (7O%patency after 10 years) or
intemal thoracic (mammary)artery (the best 90% patency after
10 years)or
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Decrease myocardial ability to pump blood to other organsIs
Ejection fraction < 40% (By echocardiogram). Ejection
fraction(EF)=strokevolume/end diastolic volume. Normaly
EF=50-75%
Classification
I-Systolic Vs Diastolic heart failure
In systolic HF EF <40% due to left ventricular dysfunction
in Diastolic HF ...mormalWF but decrease filling of the
heart during relaxation (diastole)
2-Left Vs Right HF or Biventricular HF(congestive HF)
Causes of Li side HF
Ischemic heard disease (MD)isThe mast cor
‘cause(in.c.c),cardiomyopathy, HTN,valvular heart
disease, myocarditis arrhythmia other causes like sever anemia.
Causes of Rt side HP
L-Lt side HF is the m.c.c(long standing It side HF will cause
eventually Rt side HF)
2-Core pulmonale is Rt side HF not caused by Lt side
(isolated Rt side HF,causcs of core pulmonale include
Medicine a
chronic respiratory diseases like COPD Bronchiectasis,lung
fibrosis primary pulmonary HTN.
Signs & Symptoms
= Left-sided failure
© Dyspnea, orthopnea, paroxysmal nocturnal
dyspnea (PND)
= Pulmonary edema, laterally displaced apex beat,
gallop rhythm (Si, $2, $3)
= Right-side failure
Peripheral edema, ascites, hepatomegaly,increase
jugular venous pressure(JVP)
Increased jugular venous
pressare(JVP)> distended neck veins
Diagnosis
«= Echocardiography (EF-><40%)
History and physical exam....signs of HF
= CXR look for pulmonary edema and cardiomegaly
differentiate
wy edema if it caused by left side
‘* Atrial natriuretic peptide(ANP)
Pp
HF(cardiogenic)or non cardiogenic,ANP increase in
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SUPIPOTMedicine ——————____—
Treatment of toxicity
Stop digoxin,02,LV fluid,clectrotyte correction
Antidote is digoxine immune Fab
Lidocaine is the drug of choice for digoxin induced
arrhythmia,
Note that
ACE. Inhibitor,ARB,spironolactone,B. Blockers _(metaprolol,bisoprolol,
decrease the mortalityimprove survival)
But thiazide, furosemide, digoxin don’t decrease mortality (only decrease
symptoms).
24
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“Hypertension
HIN or high blood pressure
Normal blood pressure at rest 100-140 mmkig systolic and 60-
90 mmHg diastolic
Classified as primary (essential) hypertension with no
underlying cause
or secondary hypertension due to secondary cause
About 90-95% of cases are “primary hypertension”
5-10% are secondary hypertension
Signs & Symptoms
= Usually asymptomatic
= Usually Diagnosed accidentally by screening
Classification
PreHTN systolic BP(120-139) and diastolic HTN (80-89)
Stage L HTN Systolic BP (140-159) and diastolic (90-99)
Stage 2 HTN systolic 160-179 diastolic 100-109
Stage 3 HTN(emergency HTN) systolic >~180 or
>=110
Note thatdiastolic HTN is more dangerous Than systolic HIN
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* Liddle syndrome activation mutation in aldosterone
le
receptors, s8s
syndrome but in
low(unlike conn)
syndrome aldosterone level
+ Drugs->cortisone, oral
ine, MAOI,NSAID, adrenergic
contraceptive
Fever and pain can increase BP
White coat syndrome due to anxiety of patient during
doctor clinic visit.
5- coarctation of aorta
Narrowing of aorta distal to the origin of left subclavian
artery(post ductal)
‘M>F 2:1 more in Turner syndrome (45 XO)
S&Sincrease BP in upper extremities but decrease it in
lower extremities,intermittent claudication and pain in lower
limbs, lower limb atrophy,radiofemoral — delay,systolic
murmer,CXR rib notching from collaterals
‘Treatment surgery
|
|
|
|
Medieine
Hypertensive Crises (malignant or —_ accelerated
hypertension)
Severely elevated blood pressure ( or = 180 (systolic) or 110
(@iastolic))
High risk of
Diagnosed when there is direct damage to one or more
organs as a result of severely elevated blood pressure
Complications
«Hypertensive encephalopathy
Altered si
¢ of consciousness (confusion or drowsiness)
Retinal papilledema and/or fundal hemorthages
Chest pain
Left ventricular failure
Pulmonary edema
© Emergency HIN BP >180/110 & one or more organ
damage don’t rapidly reduce BP(cisk of brain
ischemia) so diuretics should not be used in HTN
emergency
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uoysuopiodéyy Jo suomnMedicine ——
Choice of Initial Medication
°
°
°
°
NoteBblocker and cat+ channel blocker are wrong, com
© Thiazide diuretics are effective >best fi
* ‘Thiazide causes Hypercalcemia, Hypokalemia
© Diabetes>ACE inhibitors and angiotensin receptor
the renal and retinal complications of
TheACE inhibitors decrease Nephropathy &
decreased retinopathy in DM(Decrease proteinurea)
Heart Failure ACE inhibitor (decrease mor
Benign prostatic hyperplasia(BPH)>can be improved
with the use of an alpha blocker
Kidney stones improved with thiazide-type diuretics
Increased absorption of Ca2+ so decrease risk of stone
formation
Pregnancy->alpha-methyldopa (Best), labetalol
Post-MI >B-Blocker
‘Also ACE Inhibitor and ARB are wrong combination.
2
Medicine
Most common bacteria is streptococcus viridans
Inflammation of the inner tissue of the heart (valves)
‘Most common bacteria in [V drug abusers is staphylococcus
aureus
Signs & Symptoms
Fever (97%), Heart murmur or changing murmur, Weight joss,
ing
Finger etal
Vascular phenomena(Septic embolism->cause
thromboembolic problems (stroke in parietal lobe of brain or
gangrene of fingers) Janeway lesions-> painless hemorrhagic
cutaneous lesions on palms or soles, Intracranial hemorrhage
Conjunctival hemorrhage, Splinter hemorrhage,Renal infarcts
Splenic infarcts
Splenomegaly, Stroke,abscess (Brain, lung, kidney)
Osler’s nodes>painful subcutaneous lesions in the distal
fingers
Roth's spots on the retina
Causes
* Bacteremia would be cleared quickly->no adverse
‘consequences
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An inflammatory disease thet occurs following a streptococcus
pyogenes infection(group A b hemolytic streptococcus)
Caused by antibody cross-resetivity that can involve the heart,
Joints, skis
appears in children between the ages of 6-15
and brain, Acute rheumatic fever commonly
Diagnosis
= Major Criteria (John’s Criteria)
© Polparth) Carditis, Erythema marginatum,
Sydenahm’s chorea, Subcutaneous nodules
» Minor Criteria
© Fever, Arthralgia, Raised erythrocyte sedimentation
rate (increased ESR) or C reactive protein,
Leukocytosis (increased WBC),ECG prolonged PR
interval
Diagnosis needs
Evidence (Anti-streptolysin O antibody ASO titer) & 2
major criteria
OR Evidence (ASO titer) & 1 major & 2 minor
OR Evidence (ASO titer) &chorea alone
‘Treatment
* High dose antibiotic (Penicillin) andNSAID (Aspirin)
© Lipid Lowering Agents
© Statins (HIMG COA reductase inhibitors) simvast
© Fibrates (Gemfibrozil)
© Bile acid bindings (Cholestyramine)>GI side effect
© Nicotinic acid
© Fish oil (Omega 3)
d “5 Syncope
Is temporary impairment of consciousness
non cardiac cuases of syncope include, seizure,
hypoglycemia,hepatic encephalopathy,electrolyte changes,
encephalitis.
Cardiac Syncope Causes include
-Arrhythmia
Aortic stenosis,
-Hypertroph
Cardiac Syncope is sudden,without warning symptoms,
usually occur after exercise,Lasts for 1-2 minutes,with
Completes recaveryafter that.6¢
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Treatment warfarin is indicated if MS associated with atrial
fifrilation. Surgery if pulmonary pressure>50 mmbg,
Mitral regurgitation
‘Most cominon cause is rheumatic fever
Other causes include(papillary muscle rupture in ML infective
ventricular dilatation,mitral valve prolapse)
S&SLeft atrial enlargement, pulmonary edema,atrial fibrillation
is common in MR and MS
Signs>pan-systolicor holosystolic murmur ,S3 in sever MR
‘Treatment medical ACE inhibitor and diuretics. If sever
surgery
Mitral Valve Prolapse
© Mc valve proplem....may be normal variant.
° PM
© Associated with Marfan Syndrome & Hyperthyroi
© Signs>mid- Late systolic elick(increase with standing and
decrease in supine position)
40
9M hi $$
Tricuspid Regurgitation
M.c.c is Right ventricular dilatation
Causes pan-systolic or holosystolic murmur that increase
with inspiration increase JVP,ascites lower limb edema(as Rt
side HF symptoms carcinoid tumor),Pulsatile liver.
Tricuspid stenosis,
Causes include rheumatic _fever,endoc: carcinoid
tumor,congenital
S&SDiastolic murmur increase with inspiration enlarged
right atrium, increase JVP,lower limb edema and ascites.
Notes
‘Tricuspid valve disease murmur increase with inspiration while mitral
valve murmurs increase with expiratic twicuspid valve diseases
causes lowe Iimb edema and ascites while mitral valve diseases causes
pulmonary edema,
Carcinoid tumors’ are asso ith tricuspid valve diseases but not
mitral valve diseases.
Aortic Stenosis,
‘Most common cause
* In old age->caleification(degenerative valve disease)
"In children>Bicuspid aortic valve
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3-Restrictive Cardiomyopathy
Most common cause is Amyloid
Rigid ventricles
4-Constrictive Pericarditis
Most coramon cause is idiopathic
Other causes> TB, sarcoidosis
S&S-Right side heart failure (lower limbs edema, ascites,
Hepatomegaly, increased JVP)
Signs>Kussmual sign(Increased JVP with inspiration) ,
Palsus paradoxus(decrease of systolic blood pressure of more
than 10 somhg with inspiration
ADDITIONAL NOTES:
‘+ Normal Stroke volume =70 CC
‘+ End-diastolic volume (EDV) is the largest yolume in the leftt
ventricle just at the end of ventricular relaxation.
jection Fraction (EN) = Stroke volume / EDV
(© Normal level EF > 55-70%
© Heart failure if EF <40%
* Congestive heart failuro-Pright & left side heart failure
44
|
‘Medicine
+ Most common cause of right side heart failure is left side heart
failure
+ Core pulmonale->right side heart failure;Not caused by left side
heart failure
Causes-> COPD, Pulmonary HTN, chronic respiratory diseases
+ ACE inhibitor (captopril, enlepril)
© Rest for heart falure,and DM(decrease proteinuria)
© Side effects
= Dry coughPswitch to ARB if cough occur(ARB don’t cause
cough)
+ Hyperkalemia
= Angio edema
© Contraindication
© Prognaney
+ Renal failure
+ Bilateral renal artery stenosis
‘© Drugs that decrease mortality in Heart failure are
* ACE inhibitor
ARB
+ B-Blocker (Carvedilol, Metaprolol, Bisoprolol)
Spironolactone
© Drugs that don’t decrease mortality in HF->Furosemide,
‘Thiazide, Digoxin
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# ‘Systolic Murmir | “Diastolle Murmur
Aortic Pulmonary —_| Stenosis ‘Regurgitation
Mitral Tricuspid | Regurgitation Stenosis
Pan Sy
regurgitation and Ventricular Septal Defect (VSD)
Murmur seen in mitral regurgitation,tricuspid
Pulsus paradoxus
sever asthma,tamponade,pericardial
effusion o constrictive pericarditis.
Pulsus alternans seen in sover left side HE.
‘© Pulsus tardus seen in aortic stenosis(slow rising pulse)
‘© Pulsus bisferiens seen in Aortic Regurgitation,and Hypertrophic
bstructive cardiomyopathy.
+ Wide fixed splitting of $2 een in atrial septal defect(ASD)
* Continuous machinery murmur scon in patent ductus
arteriosus(PDA)
+ Normal Beart sounds is St(closure of mitral and tricuspid
valves) and $2(closure of aortic and pulmonary valves)
+ $3. seen in children(uormabpregnancysLeft side heart
failure sever aortic regurgitation sever mitral regurgitation)
Collapsing or bounding — pulse seen_— in
(ARPDA, fever,pregnancy,aneminhepatic failure,CO2
retention,hyperthyroidism),which means large pulse volume.
= Aortic Regurgitation causes wide pulse pressure while Aortic
Stenosis causes narrow pulse pressure
48
Medic
L-Typical vs Atypical
2-Community acquired vs hospital acquired vs ICU
acquired pneumonia
“Typical pneumonia are caused by bacteria and
charachterised by high feverproductive cough(sputum with
cough)and patient look —_unwell(toxic), CXR shows
consolidation(lobar pneumonia)
-M.cc is streptococcus pneumonia(pneumococcus)(also
caused by Hb, staphylococcus, pseudomonas,E-coli,klet
-Atypical pneumonia milder symptoms than typical
pneumonia with no or low grade fever,dry cough(no
sputum),patient looking well,usually caused by viral.fungalor
atypical _bacteria(legionelia,mycoplasma,chlamydia),CXR
shows diffuse patchy infiltration unilateral or bilateral
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oupewMedicine
‘Hospital acquired pneumonia(AP)
“Pneumonia that develop 2 days after hospitalization for
another cause.
Staphylococcus aureus( m.c) and pseudomonas are the most
‘common bacteria in HAP
If patient was on ventilator and developed pneumonia tis
called ventilator acquired pneumonia(VAP)
‘Treatment vancomycin and 2 antipseudomonas antibiotics
like imepinem and gentamycine.
Aspiration pneumonia
-Due to aspiration of GI contents in semicomatosed
ppatient(intubation, vomiting of semicomatosed patient)
-Most common bacteria is anaerobic(bacteroid,fusobacterium)
-CXR finding usually ocor after 6 hrs of aspiration,and moast
‘common infilstration site is Right lower lobe.
‘Treatmentshould include antil that cover anaero
(clindamycin)
Complications of pneumonia
-Sepsis,DIC,arrhythmia(atrial
lure,tespiratory failure,lung _abscess,empyema(exudate
pleural effusion),and death.
Medicine
slung abeess i
ly treated by antibiotics(not drainage).if
not respond to antibiotics then needs drainage(percutaneous or
surgerical)
Additional notes:
CMV pneumonis diagnosed by BAL (inclusion bodies) andtreated by
gancyclovir,
-pneumocysts carini peumonta(PCP) is fungel,m.c.e of pueumonia in
AIDS pati
bilateral infiltrate and treated by
(cotrimaxazole)
sur when CD4 const <200,in CXR shows diffuse
imethoprime/ sulfamethaxazole
mycobacterium avium complex occur in AIDS patient when CD4
count <100,and treated by el
count>100
ithromycin(macrolide)and increase CD4
“sputum culture is indicated when pneumonia doesn’t respond to
antibiaties(not always positive)
-stain for AFB(TB) should be done in upper lobe pneumonia and
‘pneumonia not responding to antibiotics.
Methicillin resistant staphylococcus aureus (MRSA) antibiotic of choice
vancomycin or linezolid.
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—Medicine.
Diagnosis
1-CXR loss of costophrenic angle
2-Aspiration of the fluid and test for protein, LDH, bacteria
to determine if exudte or transudate
CXR SHOWS Right PLEURALEFFUSION
‘Treatment according to the cause
-HF —diuretics,empyema needs drainage(chest tube and
anti
iotics)
-Pleurodysis in case of reccurent pleural effusion which means
introducing tetracycline or bleomycine in pleural space to
obliterate it
Surgery for multilocular empyema either by thoracoscop or
thoracotomy
56
ce
Medicine
Notes =
‘chylothorax has white color (rich in'TG),2nd With exudate features, with
TE>110,
pulmonary embolism can cause both exudate and sransudate pleural
effusion
Airborn transmition(from respiratory droplet) primarly affect
Jung(puimonary TB)
Caused by mycobacterium TB(Aerobi
spore forming,has high lipid contents stain weekly (+)in gram
stain
Mycobacterium TB also called acid fact bacilli(AFB).
‘TB usually affect upper lobe causing upper lobe cavitation.
15-20% have extrapulmonary TB which is more in
immunocompromised patient and childrens,and genitourinary
‘TB(kidneyand ureter) is the m.c.c of extrapulmonary TB.
primary sites for TB inchide(ung,genitourinary,bone(m.c in
vertebra and is called potts disease)Gi(m.c. in ileocecal
region),brain and meninges,pleura,tonsils)‘srompo at, sdnos ystx Moy ur mag [<—
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Note:
nergies are better than B2 agonists in COPD
'B2 agonist is better than Anticholinergics in asthma
Signs of Hypercapnia (increased CO2) which can be seen in
exacerbations:
Headache, decreased conscious increase intracranial
pressure,papilledema, coma, vasodilation, warm extremities
‘Tremor (asterixis), large volume pulse (collapsing pulse).
68
i
|
Medtetme
Asthma
Is the common chronic inflammatory disease of the
airways characterized by
variable and recurring symptoms(unlike COPD which
irreversible and not variable)
reversible airflow obstru airway obstruction in
asthma is usually reversible
airway byper-responsiveness and bronchospasm
increased mucus produc
mn (increase mucus and gob)
cells)
airways edema and smooth muscle hypertrophy
increase inflammatory cells in airways (esepi
2 types
Atopic" children. Increased IgE
Non-atopic>> or = to 40 years/ normal IgE
‘Causes and Risk factors
It is thought to be caused by 2 combination of genetic and
environmental factors
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irMedicine
Asthma exacebations
Acute attack of ashma could be precipitated by
Infection(m.c.c),smoking,dust,old furniture, pets,pollens,strong
odorlike perfiumes,cold _air,cxercise. Drugs(NSAID,aspirin,B
blocker)
Signs of sever life threatening asthma
‘amental status change -hypotention<90mmhg peak flow <33%
cyanosis -arythmia -silent chest (no wheezes) -normal or high
C02 -PO2 <60 or saturation <92% -RR>25 - inability to complete
sentence in one breath —use of breath accessory muscles of neck
-Note thet asthma usually has low CO2 level (hyperventilation
‘wash out CO2),but in sever life threatening, asthma because of
sever bronchospasm CO2 not eliminated wich result in normal
and then increase CO2
-also no wheezes(silent chest) in sever ashma due to sever
bronchospasm
Medicine
Asthma medications
Quick relief medications | Controller medications
Used in acute asthma attack to | Not used in acute attack but used to
abort it decrease frequency of ashma
attacks
L-short acting ——B2 | L-long acting B2
agonist(salbutamol.albuterol) | medication(salmetrol,formetrol)
2-short acting | 2-long acting
anticholenergicsGpratropium | anticholenergics(tiotropium)
bromide) 3-methylxanthine
3esystemic cortisone ecg bees
Scrafiricukast,montelukast,zeliuton
6-sodium cromoglycate
Status asthmaticus is sever life threatening asthma not
responding to routin short acting B2 agonist
‘Treatment
OXYGEN, Corticosteroids (IV), Adrenaline (IV),Intubation
Prognosis of ashma
-The prognosis for asthma is generally good especially for
children with mild disease
-54% of children with asthma no longer have the disease after
10 years,(euajaeq 2m aq st senomopnasd)uonsazut
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Tru'sezzaqasis60 means CF
‘Treatment
Antibiotic prophylaxis, mucolytics.physiotherapy.vitamin
KEDA supplements,pancreatic enzymes
supplement....... symptomatic treatment
APE is a blockage of the main artery of the lung or one of
°
its branches
© PE most commonly results from deep vein
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© Mesite for DVT.
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°-For PE pulmonary angiogram is the gold standard but not
routine(invasive)
~CT pulmonary angiography (Best initial)( contraindicated in
renal failure).
-ventilation/ perfusion sean in case of renal failure and
allergy to contrast.
-for DVT do Doppler us (best initial test) if not seen do
venography (best,definitive test for DVT)
-Norma! D-dimer is enough to exclude or rule out the
of thrombotic PE(sensitive),but positive d-dimer
don’t rule in the disease as d-Dimer increased in many
conditions also(aot specific)
-BCG:sinus tachyeat the mec.finding on ECG.
~The classic signs for PE on ECG are a large $ wave in lead I, @
Jarge Q wave in lead Ill, and an inverted T wave in lead II
(S1Q3T3)
80 ——
el
‘Mesieine =
‘Treatment
-Anticoagulation(heparin and warfarin) >d
thrombus but prevents its progression.—Target INR is2-3,
dissolve
~ length of treatment is 3-6 month in provoked (occur with risk
factor) DVT Or PE,6-12 mont
mut risk — factors)),
if Unprovoked(occur in
patient wit fe long in case of
thrombophilia
‘Thrombolysis: (Streptokinase, urokinase, Tissue Plasminogen
activators-Dissolves thrombs
= used onl
inBlemodynamic instability->low blood pressure
<90 pressure.
-IVC filter used to prevent PE in patient with DVT and has
contraindication for anticoagulation(internal bleeding)
-IVC filter not used for treatment of PE(only prophylactic to
prevent PE)
-IVC actually increase risk of DVT
-thrombectomy in case of PE with contraindication for
anticoagulation,eae
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granuloma
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cparcps>4
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on BAL but CD4/CD8<1)
Chest X-Ray changes are divided into four stages
© Stage 1: bihilar lymphadenopathy
‘= Stage 2: bihilar lymphadenopathy and reticulonodular
infiltrates
‘© Stage 3: bilateral pulmonary infiltrates
© Stage 4: fibrocystic sarcoidosis typically with
fibrosis > ground-glass appearance
-inerease serum ACE level which used to monitor response
to treatment.
‘Treatmentif asymptomatic no need for treatment.
Corticosteroids, prednisolone, have been the standard treatment
84
‘Medicine
Prognosis
‘The disease can remit spontaneously or become chronic
Increased risk for cancer (lung cancer) and malignant
lymphomas
Good prognosis Bad prognosis
young old Fee
Stage 1 ee Stage 4 or organ involvement
| white Black
Erythema nodosum or Lofgren | Lupus perinio
syndrome
_ | Obstructive Stedp ‘Apnea (OSA)
~Most important cause is obesity
-Can cause episodes of apnea during sleep
-Symptoms
* Snoring
* Day-time sleeping (Because of poor sleep)
* Sleep apnea due to airway obstruction
°
Complication
Pulmonary HTN
Right side heart failure (Core pulmonele)
85-dund worreg
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upayMedicine
-Lung diseases that occur due to long exposure to certain
substances in certain occupations, which can cause lung
fibrosis.
latency period 20-30yr.
-Include:silicosis(m.c),asbestosis,beryllium,and berylliosis.coal
worker pneumoconiosis(black lung)
-all of the above mentioned diseases affect upper lobe except
asbestosis which affect lower lobe.
silicosis asbestosis Coal worker
pneumoconiosis
Lobe Upperlabe | Lower lobe (mainly | Upper lobe
pleura causing bilateral
ickening)
CXR gg shell | Bilateral pleural | Less fibrotic
‘calcification | thickening and pleural | than silicosis
in upper lobe _| effusion(m.c)
‘Associated | Increase TB | Strongest risk factor
risk risk 30 times. | for pleural
ceancer(mesothelioma)
More than smoking
occur after 40 years of
‘exposure
Medicine
Rare diseases that charachterised by increase eosinophil count
in airway and hung parenchyma
Causes,
1-ascaris infection(loeffler syndrome) and other helminthic
infection.
2-allergic bronchopulmonary aspergillosis
3-churg-strauss syndrome
4-eosinophilic pneumonia
S-drugs and toxins: like inhaled cocaine, phenytoin,
tryptophan,some antibiotics)
Diagnsis
“Rare diseases so should be suspected in any patient with
respiratoty problems with increase eosinophil in CRCor
BAL or lung biobsy
-Remember that sarcoidosis and hypersensitivity pneumonia
increase lymphocyte but not cosinophil on BAL so are not
Eosinophilic lung diseases.mye e9y 10A98 J)
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oupaIWMedicine:
°
°
specific signs
Koilonychias(spoon nails),angular stomatitis, glossitis,
(een in iron deficiency anemia
Jaundice (seen in hemolytic anemia)
Bone deformities (sees Jassemnia major
Leg ulcers (seen in sickle cell disease)
Anemia workup:
CBC (look at Hb level,mean cell volume(MCV),other
cells( WBC. platelet to see if the are pencytopenia or not)
4 parameters (RBC count, hemoglobin concentration,
MCV(mean cell volume) and BDW)
Reticulocyte count{immature RBC) is the measure of the
bone marrow’s activity (increase reticulocyte if bone
marrow is active)
iron,ferritin,total iron binding capacity(TIBS)vitamin B12
or folic acid
Blood film
Medicine:
According to MCV (normal 76-96)anemia is classified as
Mierocytie(MCV=7
6
Normocytie(aormat
me)
“Macrocytic(mev>96
Lilron deficiency
anemia IDAGm.c
anemia)
-scute blood loss
of chronic
3-pemitious anemia
2-thalasemia
‘A-liver diseases(cithosis)
3-sideroblastic iseasescithosis)
snemia S-alcoho!
Alead toxicity 6-hypothyroidism
5- anemia of chronic | S-hypothyroidism | 7
iseases(in 25%) drugs(methotrexate;phem
alproic acid cotrimexezele)
IDA is the mec.anemia
-megaloblastic anemia is macrocytie anemia that result from
vitamin B12 or folic acid defici
-methotrexate,phenytoin,valproic acid,cotrimaxazole, all
can decrease folic acid resulting in megaloplastic anemia,
-Pernitious anemia(autoimmune atrophic gastritis):
~ is autoimmune discase ,antibody against gastric parictal cell
(normaly produce HCL and intrinsic factor(IF) H
be no IF( which normaly complex with VitaminB12 to aid in its,
so there
absorbtion in terminal ileum)...cesult in vitamin B12
defeceincy and megaloblastic anemia.
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9%C> St pooyg Wt arKoo]nionE4 Jo [aad PeUIOU-
-YNRL tp Sutaourar Aq Oe
mye opuy (snojonu you nq YN Sey HOM Dey ame)
ayfooqnone Jo WoIsIOAUOD st uOHSNposd Jey ur days yeuy
sraoyds
q paronnsop cjeunou rep sae pue Aep oz st weds eT DER
“YNQT OU pur snojont ou sex Ser (AaupHy ur paonposd
unarodosm sve Aq pareymums)woueur 2u0q ur paonposd st DER
mmonanpoad Dnt
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Suo] apy pur (jes0 jou)uopsafuy 71g unUTETA JuOMNTTAZL
aaoutea auxyseS Jo st osvaxoU erutoue sonnruod-
0p96)-Decreased RBC count and
hemoglobin levels
-Reticulocyte count is decreased
-Macrocytes (larger than normal RBCs) are present
-Hyper-segmented neutrophils on blood film (Neutrophil 6-
10 lobe, normal level 3-5).paamnbow SA 9H8uaH ~T
wouLoyisse|y
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supp
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Jo} eqesuaduroo 0} eatioe si MouEUr auOg ERMINE sNAoUIOT CI
veuadoyXoued asneo 1.U0p VC
‘08 pue voyonpoad Sey 10F juedun st uo ynq‘eruadoréoued
asnea tea Aouraaayap aA3s os (siojere|d Se ‘OeW)sTIO2 Poor
8 Jo sisampuAs soy ueuoduat ore prow ojos pue 21-1 UUM! A-
-Kouotayop ploe 91}OF Jou INg AauaKaFOp
ZIG URMENA WM asearoM CyPApIe omMOjor Apa
‘aYONS pure (LY JOF YSH St YI [Pao MISKoowOK,
aseauoay AousIoaJap TI WUMYA puvsousteayap plow ovoy-
wandompawEN opraTON pe
aioidpea‘usoxsuaydoxexonornong
non qzosqeruruonsasor snap (ps4qous2q
stmomoquyuueWard)paewep asvoxsuy
'sqp[eUE]OYOOPE'uOREAUPEYA,
‘oe Aan ;oajep
Zr wNUREHA go sosmeg | (YSWE>ASUDIDIQ}Op prow oMOp Jo sosRED
torreGenetic or hereditary acquired
I- Membrane abnormalities | -autoimmune hemolytic anemia
Tike HS. HE -microangiopathic hemolytic
2 Enzyme defect like | anemia(DIC,TTP,LUS)
GOPD.pyruvate kinase } pyr
defecei |
ee -infection Tike malaria
3+ Hemoglopinopathies Hike :
SCA, thalassernia -prosthetic heart valve also can
, cause hemolysis.
“SLE
2- Intravascular (RBC destroyed inside blood vessel)VS
extravascular (RBC destroyed in spleen)hemolysis
Intravascular hemolysis Extravascular hemolysis
-prosthetic valve autoimmune hemolytic,
-GorD -heridatary
“PND spherocytosis(HS),0r
eli ssis(HE)
Microangiopathie(DIC,TTP,us) | UP
Acute hemolytic reaction in
incompatible blood transfusion
100
Presi =eeeeeee eereeECeeeeeeeeeereereeeeeeseeeerees eet
‘Aereditary spherocytosis (HS)Heréditary elliptocytosis(A)
-autosomal dominant
-defect in RBC membrane called spectrin so RBC shape
become spherical -RBC in HS do its function in carrying O2
normaly but when recognized by: spleen are destroyed
(extravascular hemolysis)
-Complications Kemicterus in neonate,GB stones,folic acid
deficiency.
-DiagnosisTest osmotic fragility(hemolysis in hypoosmolar
solution)
-Treatment if mild observation if sever splenectomy at 5-7
years.
-pneumococcus,meningiococcus, Hib vaccine should be given at
least 2 weeks before splenectomy
-any chronic hemolysis patient should be given folic
acid(vitamin BO),sc
ur Sunmse: wo ue oy MOY pool raiser ue sonEmdes
JORNSq s[[99 OPIS -(woydarks su)s|sHO aAIsNIIIQ-0seA-
swords
asi ay St SHIP pue seBug uy Soyoms pur ured)sqyAEp
TUM (UG Ie JouIAIG Ye s~pLOU! g-p Te pus suo\dWAE-
surojduidg pur sudig
lo steak (95-cp) €Aourroadxa ayt| aBeso0y-
(11 suosomony)
mgofoury go ueYD MgO aH WY uONEIME yuOg-
(edeys appors
“pedy) Seu podeys sqeunouqe
pneumococcus, meningococcus, Haemophilus influenza(due to
autosplenectomy)
Aplastic crises Triggered by parvovirus B19 which
suppress bone marrow(ususlly active in hemolytic anemia to
compensate),result in sever drop in Hb,and reticulocyte count
Complications
i-Overwhel
post-auto-splenectomy infection (OPSI)
© For encapsulated bacteria
"Streptococcus pneumonia
* Hemophilus influenza (Hib)
* Meningococcus
oie
ieledbhaassee tae
2-Stroke
3-Cholel
sis (pigmented gallstones) and cholecystitis
4-Pulmonary hypertension
5-Priapism (erection for > or = 6 hours) and infarction of the
penis
6-Leg ulcers
lary necrosis in the kidneys and Chronic renal
8-Avascular necrosis of head of femur
9-Osteomyclitis (bacterial bone infection)>cause sal
Diagnosis
Hb electrophoresis (best)
1Lif show increase Jevel of HbS>70% HbF<30%(in sickle ceil
anemia)
2-sickle cell trait if HbS 40-50% and HbA 50-60%
3-HbSC if 50%EbS 50%EbC
411bS60% increase HbA2 HF <30% this HbS -B
thalassemia
Notes -Hb electrophoresis shouldn't be done if patient took
blood transfusion (wait 1 month after blood transfusion)
105£0.
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