RHEUMATOLOGY

RHEUMATOID ARTHRITIS

Boutounniere Deformity
Peri - Articular / Juxta - Articular osteopenia
• Seropositive chronic inflammatory, symmetric
• Narrowing of joint space can occur in any
polyarthritis (> 5joints)
arthritis/ arthropathy ,only exception can be
• Common in females, 30-60 yrs age, females gout & acromegaly related arthropathy.
develop more severe symptoms
• Extra articular manifestation-
Genetic association - HLA DR4
Q
•
1. Lymphadenopathy (MC)
• Environmental association – smoking
2. MC malignancy associated with RA- NHL
• Seropositive - RF +, ACPA +, anti CCP + Ab, anti (DLBCL)
Q

MCV + Ab.
3. MC cardiac manifestation- pericarditis , RCM
• When ↑↑ titres, severity ↑, ↑risk of extra-
articular involvement. 4. MC pulmonary manifestation is pleuritic, with
exudative pleural effusion with low glucose.
• Acute - <6 weeks, chronic - >6 weeks
5. MC skin manifestation- subcutaneous nodules,
• Inflammatory - ↑CRP / ↑ESR
mobile, on extensors, painless
• Any inflammatory arthritis: Early morning
stiffness for >1 hour, pain ↓ with exercise / 6. MC ocular manifestation- keratoconjunctivits
movement, ↑with rest. sicca/dry eyes → MCC of 2° Sjogren’s
syndrome.
• It is an Additive arthritis - more & more joints
will keep on adding 7. Late kidney involvement seen in amyloidosis
• MC joint – MCP joint > PIP joint &wrist joint. (AA type) {early kidney involvement is seen
in SLE} MGN also seen.
• MC large joint involved – knee joint
8. Pulmonary – RA nodules in upper limb,
• Spared joint - DIP > thoracolumbar spine associated with pneumoconiosis like silicosis
(RA+pneumoconiosis- Caplan syndrome)
Q
• Can develop erosions, erosive arthritis.
• Deformities - Boutounniere, swan neck (hyper 9. MC ILD seen in RA- UIP (all other CTD have
flexion at DIP, hyper - extension at PIP), Z – NSIP as MC ILD)
deformity of thumb
Q

10. Hematological – Anemia (AOCD)

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11. Felty syndrome- late erosive RA with • TOC in acute flare - corticosteroids, <2 joints
extremely high titres + massive splenomegaly - intraarticular corticosteroids, >3 joints -
+ neutropenia
systemic corticosteroids. (before starting tx,
– D/D of felty syndrome - T-cell LGL (CD16+, always r/o joint infection)
Q

CD57+)
– In case of large joint, do joint aspiration
12. MCC death - CV risk
before starting steroids.
13. Pregnant female- good prognosis

• Triple Therapy c. Other anti-TNF – used upto 3rd trimester

Conventional synthetics- BIO-DMARDS
d. Azathioprine – not much used as it is less
sulfasalazine + HCQ
effective in RA, but used in pregnancy
1ST choice- anti TNF Target synthetics-
DMARDs because it is safe. Give extra folate as there
DMARDS- methotrexate, alternate- Leflunomide is ↑risk of NTD.
– Before starting anti – TNF, r/o latent TB
e. NSAIDs- SOS. Avoid in >30 weeks.
{Mantoux test, IGRA}
f. Low dose corticosteroids can be continued.
– s/e of anti TNF- drug induced LE. It can
result in HBV reactivation as well. Rituximab
has highest risk of HBV reactivation.

• Treatment in Pregnancy–

a. HCQ / Sulfasalazine – safe

b. Anti-TNF – Certolizumab is safest

Q

* For Making Notes

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Medicine

Seronegative Spondyloarthropathies
• Common features - RF-, ACPA-, ANA -. Peripheral arthritis. Variable association with HLA-B27.
• Inflammatory back pain, early morning stiffness >1hr that improves with exercise. NSAIDS very useful. Most commonly involved
is thoracolumbar spine (only exception is psoriatic arthopathy). Sacroilitis present. Peripheral arthritis - oligoarticular &
asymmetric, LL > UL. Achilles enthesities. Dactylitis. Sausage shaped digits. MC extra - articular manifestation - Ant. uveitis.
Distinguishing features
Disorder AS PsA ReA EA
Axial 1° peripheral arthritis +/- axial
Disease type Oligoarticular /asymmetric
Sometimes, PsA can mimic RA by involving small joints of upper limb
Males / <40yrs Males =females Males /<40yrs Males =females
Gender/ Mean age (yrs)
>40yrs /<40yrs
Axial involvement, Correlates 100% 20-40% 40-60% 5-20%
with HLAB27
Sacroilitis – 1st Ix to be done Symmetric Asymmetric symmetric
when Sacroilitis is suspected is
XRAY - ankyloses/fusion.
MRI – gold standard. BM
edema.
Peripheral distribution UL>LL UL>LL LL>UL UL>LL
Enthesitis ++ ++ ++ Rare
Dactylitis Rare ++ ++ Rare
Q Q
Ocular Ant uveitis Episcleritis +/-ant uveitis conjunctivitis Rare
Rare Psoriatic skin & nail changes Circinate balanitis, Erythema
(80%) keratoderma nodosum,
Skin
blenorrhagicum Pyoderma
gangrenosum
Q
Shiny corner sign / Pencil in cup DIP deformity Asymmetric No specific
bamboo spine/ dagger syndesmophytes
Imaging
sign/symmetric
syndersmophytes
Q
UL fibrosis Types: • Arthritis (sterile) h/o IBD
MC valvular disease- 1. asymmetric oligoarticular + conjunctivitis 2 Types
AR 2. symmetric polyarticular (sterile) + urethritis Type 1 –
3. isolated DIP (sterile/non sterile) oligoarticular /
4.psoriatic spondylitis asymmetric
• Reactive arthritis correlates with
Other features 5.athritis mutilans
occurs as a reaction IBD activity.
to infections -
GIT - shigella /
GU - chlamydia (l2b
serovar)
Treatment: DMARDS -
1. Pain- NSAIDs • Conventional- no efficacy on axial disease
2. Control- DMARDS • Target synthetic- can be used for both axial &peripheral if disease is refractory to conventional
3. Apremilast – PDE4i – PsA DMARDs & anti TNF.
Q
4. Antibiotics – doxycycline in • Biological DMARD - best .
PsA
- Anti-TNFα- infliximab /adalimumab
- Anti IL-17 inhibitor- Secukinumab / Ixekizumab – approved for AS/ PsA
- Anti IL-12/23 inhibitor- Ustekinumab
* For Making Notes
- Anti IL-23 inhibitor- GuselkUmab
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Cerebellum Quick Revision Notes

B/L Symmetric Ankylosis - AS

Pencil in Cup Deformity, Classic of PsA.

CRYSTAL ARTHROPATHIES &

AOSD
Dactylitis- Reiter Syndrome & PsA Gout (d/t deposition Pseudogout (d/t
Features of monosodium urate deposition of calcium
crystals) pyrophosphate crystals)

Sudden onset, severe

nocturnal pain, MC • Monoarticular
joint involved is 1st / asymmetric
metatarsal jt (k/a
oligoarticular
Psoriatic Nail Changes Acute PODAGRA), initial
• MC joint involved is
attack is monoarticular
→ later polyarticular Knee / MCP , Wrist
attacks. Can have joint
associated cellulitis.

• Tophi deposition
seen in Joints (toe
• Pseudo RA- Early
jt/ finger jt/wrist
morning stiffness
Chronic jt/knee jt.)
• Pseudo OA- non
Enthesitis - seen in all arthropathies except enteropathic • Soft Tissue (pinna
inflammatory
arthritis / olecranon bursa/
Achilles)
3H-
Associated Metabolic syndrome / hyperparathyroidism
conditions CKD/HF Hypomanesemia
hemochromatosis

* For Making Notes

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Medicine

Gout (d/t deposition Pseudogout (d/t HIGH YIELD POINTS

Features of monosodium urate deposition of calcium
crystals) pyrophosphate crystals) • Rasburicase – approved and used only for tumor
• MSU
lysis syndrome not chronic gout
• IOC- joint
• IOC- joint
aspiration .
• Pegloticase – can be used for chronic gout, not
aspiration approved for tumor lysis syndrome.
Crystals • Rhomboid shape,
• Negatively
birefringent, needle
weakly positive • C/I of Pegloticase & Rasburicase – G6PD
Q birefringence deficiency
shaped
• Acute – non specific
• Chondrocalcinosis
Q • Uricosurics- Probenecid –organic anion
• Chronic – Martel transport inhibitor
Imaging • MC seen in knee
G sign, MSK USG - Benzbromarone - selective uric
joint, wrist joint
double contour seen transporter Selective urate
inhibitor
Lesinurad

Treatment
Acute Gout & Acute Pseudogout:
• 1st line - NSAIDs +/- Colchicine (for 3-6 Martel G Sign /Ratbite Erosions
months) → ↓recurrence
• Alternate – corticosteroid / ACTH /anti-IL-1 –
Anakinra < Canakimumab (preferred)
• s/e of colchicine-
– GI disturbances, diarrhea mostly
– Agranulocytosis (dangerous s/e)

Chronic Gout
Double Contour Sign
• Indications for uric acid lowering therapy: >
2attacks / year / Tophi / EGFR <60 / urolithiasis
• Allopurinol – purine based XO inhibitor →
allopurinol hypersensitivity syndrome mainly in
HLA B 5801.
• Febuxostat – non purine XO inhibitor
• Both Allopurinol , Febuxostat → avoided with
Azathioprine / 6-MP (↑BM suppression)
Q
Chondrocalcinosis (Pseudogout)

* For Making Notes

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Cerebellum Quick Revision Notes

• Plasma cell / dendritic cell type – linked to

ADULT ONSET STILL DISEASE pathogenesis of SLE
• Auto inflammatory (innate immunity is • Signature cytokine- IFN-α
affected) disease affecting those in 16-35 yrs
• Constitutional symptom- fatigue (MC) / fever/
of age. {In autoimmune conditions, acquired
malaise/weight loss
immunity is affected}
• MC system involved in body- MSK (>90-95%) –
• Presents like PUO, arthritis, salmon rash, ↑↑ arthralgia / arthritis (non erosive )
TLC, hepatosplenomegaly, ↑ inflammatory
markers like ↑CRP / ↑ESR / ↑↑↑Ferritin, • 25% deformity →Jaccoud’s arthropathy
Q

serology negative – RF- / ACPA - / ANA-

• Mucocutaneous –
• r/o other disorders
a. Oral /nasal (painless) ulcers
• It is diagnosis of exclusion.
b. Alopecia ( non scarring)
• Yamaguchi criteria
c. Skin-
• Tx: DMARDs , anti IL-1 therapy .
ƒ ACLE- malar rash , mainly face
JIA
ƒ SCLE- anti Ro antibody, spare face
• <16 yrs of age
ƒ CCLE- DLE , MC face>scalp , scarring type,
• 3 Types- over time ↑risk of squamous cell cancer
– Oligoarticular / asymmetric
– All SLE related skin lesions are
– Polyarticular / symmetric photosensitive.
– Systemic JIA – still’s disease • Serositis can result in pleuritic (associated with
• +/- Growth affected small pleural effusions ) / pericarditis
• +/- anterior uveitis • Major organ development- MCC of death in SLE
is CV risk
• Serology negative – RF-/ACPA-/ANA-
Hematological Kidney Neuropsychiatric Lungs
TOC- DMARDs
Q
•
1. Anemia (anti 1. Lupus 1. MC- ↓cognition 1. <5% - ILD
SLE erythrocyte Ab)– nephritis (associated (MC- NSIP)
AOCD / warm (anti ds with anti NMDA 2.
type AIHA(IgG) DNA Ab/ receptor Ab/anti endocarditis
– DCT+ anti smith glutamate Ab) – libman
2. Leukopenia / Ab) – MC 2. Headache sach’s
lymphopenia (anti & most 3. Seizures endocarditis
lymphocyte Ab) / severe –sterile
4.Psychosis (anti
thrombocytopenia form is vegetations
ribosomal P ab /
(20 ITP)
Q class IV. 3. RCM – HF
APLA ab)
Wire loop d/t diastolic
5. Vascular
lesions are failure.
complications-
seen in
• Middle age female in reproductive age group stroke (APLA Ab)
this.
• Genetic association- early classic complement
pathway deficiency (C1q/ C4/C2). SLE - Antibodies
• C1q- severe disease, TREX gene associated • C3/C4 can be used as marker of disease activity.
• Environmental → EBV / hormonal → estrogen /
If low C3/C4- active disease
Q

drugs → procainamide, hydralazine •

* For Making Notes

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Medicine

• CRP can be normal in active disease, if ↑↑- Anti histone Ab- drug induced SLE. Drugs causing this –
suspect infection in SLE. MD - SHIP

• ESR – normal M - Minocycline , Methyldopa

Ab Significance D - D- penicillamine
Most sensitive, >98-99%, poor S - sulfonamides
ANA
specificity , >1:80 titres H - hydralazine
Specificity >95%, poor
I - isoniazid, interferons, infliximab
Anti ds DNA sensitivity - 50-70%, correlate
P - Procainamide
to lupus nephritis /vasculitis
Anti histone SLE → mild arthritis / serositis Lupus Nephritis
• Specific for sjogren
syndrome. Class I – Minimal mesangial Asymptomatic →
• Seen in SLE-Sjogren Class II- mesangial proliferative
Q
Tx: observe &ACEi
overlap

Anti Ro/La (SSA/ • SCLE, Photsensitivity, Class III- focal

myocarditis, myositis, Nephritic →hematuria ,
SSB) Class IV- diffuse
shrinking lung syndrome, rbc cast +/- proteinuria
proliferative
neuromyelitis optica +/-AKI/HTN
immunosuppression
spectrum disorder,
neonatal lupus → CHB (need
Class V- membranous → Nephrotic → proteinuria/
permanent pacemaker)
edema
Anti U1 RNP MCTD
Class VI- advanced sclerosing → ESRD → standard
Anti Ribosomal P Specific for SLE (Pschiatric?) ESRD Tx.

Anti cardiolipin Ab /lupus SLE – management

anticoagulant Ab/ anti β2
glycoprotein Ab
C - Clotting, venous >arterial
APLAs
L - livedo reticularis
O - obstetrics complication
(recurrent pregnancy loss)
T - thrombocytopenia
Anti smith – 30% sensitive< 99-
Others
100% specific

• SLEDAI – SLE disease activity index

– When SLEDAI = 0 + Patient is not on
glucocorticoids → REMISSION
• HCQ reduces flare.

* For Making Notes

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SYSTEMIC SCLEROSIS • 1° vascular disease, skin thickening is a reaction

to underlying vascular damage and resultant
hypoxia.

• Every patient has 2° raynaud’s phenomenon

abnormal nail fold capillaroscopy.

• Female, middle age group

Limited Scleroderma Diffuse Scleroderma

Constitutional symptoms more common
General
. fever/fatigue/arthalgia
Skin (LEROY CLASSIFICATION)
Face &neck involvement common in Distal to knees/elbows Distal & proximal
both. + +
Raynaud’s phenomenon
Type 1 PAH >ILD ILD(MC is NSIP) > PAH
Pulmonary
PAH is the MCc of death ILD is the MCc of death
Esophageal dismotility → severe GERD ↓ intestinal motility
GI
1° biliary cirrhosis Constipation
SRC common (early )
Renal Scleroderma renal crisis rare (late) High dose corticosteroids ↑risk of
SRC, therefore avoided.
Cardiac rare RCM, conduction block common
Others Crest syndrome Raynaud’s
Anti Th/To Ab
ANA+ (>90-95%), RF+( 30%)
Anti topo I(anti SCL-70 Ab)→↑risk of
Ab Anti centromere Ab (40-50%)→↑risk
Q ILD & ↑SRC (anti RNA poly III)
of PAH Q
Anti U3 RNP
Prognosis Decent. >70% in 10years Poor prognosis, 40-50% in 10 yrs

– H/o diffuse cutaneous systemic sclerosis

Treatment +MAHA (hemolysis / schistocytes) +
• Skin thickening - Mtx /MMF ↓Platelet + severe AKI + ↑BP
• ILD – MMF /Tocilizumab /Nintedanib • PAH (Type 1) - Ambrisentan + Tadalafil +/-
Prostanoids
Q

• Scleroderma renal crisis – ACEi only

* For Making Notes

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Medicine

SJOGREN SYNDROME GLANDULAR EXTRAGLANDULAR

• MC , develop early • constitutional symptoms
• Dry eyes →↓quality of • MSK – Arthralgias /arthritis
life (abnormal sensation) • ILD- MC NSIP
→ corneal ulceration • RCM , Conduction block
• Dry mouth → bad • Distal RTA
odour/dental caries/
• Hemat- MC is anemia (AOCD)
dysphagia/taste
• Monoclonal gammopathy
• Dyspareunia
-20%→↑risk of lymphomas
• Dry skin- xerosis
• MC cancer- NHL (Maltoma)
• b/l parotid enlargement
• Peripheral neuropathy (small
(symmetric & painless)
fibre) → Ix with skin biopsy

Ix: Triad
1.Serology –
1° Sjogren syndrome-
• Idiopathic • Anti Ro (SSA) - specific
Q

• Female, 40-50 yrs of age

• MC ANA + (>95%) non specific
• Extraglandular manifestation - CD4 T cell
infilteration 2.Dry mouth- sialometry
• Dry eyes - schirmer test
2° Sjogren syndrome-
3. Labial biopsy – focus score >1/4mm2
• Some associated disease.
• Treatment – Conservative &supportive
• MCc- RA
• Dry eyes- CMC ,cyclosporine eye drops
• Dry mouth - pilocarpine

INFLAMMATORY MYOSITIS
Features DM PM sIBM NAM
Females>males, 30-40yrs age , Female>males, 30-40 Female>males, Any age
Epidemiology Males, >50 yrs
Can affect children also yrs age
Skin +/- proximal weakness Both proximal(MC
• if only skin is involved – affected – quadriceps)
k/a Amyopathic DM (anti Proximal muscle +distal (long finger
Clinical Proximal muscle weakness
CADM 140/MDA5 Ab) weaknesss flexors) muscle
• abnormal nail fold weakness + associated
capillaroscopy neuropathy

CPK ↑↑(>50X) ↑↑ (>50X) Normal/mild↑(<10X) Mildly ↑(<10X)

• Anti SRP Ab (NAM
+cardiac involvement)
Anti NXP2 Ab • Anti mup44 Ab, • Anti HMG CoA
Q
Ab Anti TIF18(P155/140)Ab Anti Jo-1 Ab • Anti 5’cytonucleotide reductase Ab
Q
Anti mi2 Ab Ab • Anti 200/100 AG Ab
• Both are associated
with statin exposure

* For Making Notes Inflammation less, No inflammation.

Peri-fascicular/peri fascial Endomysial inflammation
Biopsy inclusion body seen → β Necrosis , macrophage
inflammation(CD4) (CD8)
amyloid infiltration
Response to CS yes yes No yes
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Cerebellum Quick Revision Notes

• Anti amino acyl tRNAsynthetase Ab

– Histidyl = anti Jo-1 (MC synthetase antibody)
Q

SYNTHETASE SYNDROME
1. Fever
2. Raynaud’s
3. Myositis (polymyositis)
Holster Sign
4. ILD
5. Mechanic’s hands
• Malignancy + myositis → can be associated with
polymyositis or dermatomyositis. Anti TIF-1ϒ
(p155/140)

V Sign

Heliotrope Rash

Mechanic’s Hands

RAYNAUD’S PHENOMENON

Shawl Sign

Triphasic Response. Pallor-Cyanosis-Reperfusion

Gottron Rash

* For Making Notes

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Medicine

1° Raynaud - MC (>70—80%) 2° Raynaud (<10-20%)

Vessel wall Functionally abnormal Structurally abnormal
• CTD (SLE/RA)
• PAD(Buerger’s)
Etiologies idiopathic
• Hematological
• Drugs- ergot compound/cocaine
Epidemiology Females, 20-40 yrs of age Females, >30yrs age
Clinical Mildly symmetric, no tissue injured Severely asymmetric, thumb
Auto Ab No present (CTD related)
Nailfold Normal Abnormal (dilation & tortuosity seen)
Mild- moderate- CCB like nitrates
Moderate- severe- PDE5-
Treatment
Digit threatening- prostanoids
Recurrent /refractory – digital sympathectomy

VASCULITIS
Large Vessels Medium Vessels Small Vessels
Feature
TAKAYASU GCA PAN AAV IC
Female ,<40yrs Females , >50yrs, Variable, middle aged HSP, males, <20 yrs, Cryoglobulinemia-
Epidemiology Caucasians Variable variable
Asians 5-10% are HBV+
• Microaneurysms
• Infarcts to
Renal artery kidney.
stenosis / • ++GN → Hematuria, RBC casts/ HTN/AKI
Renal renovasular rare • HTN,↑S.
• RPGN
hypertension Creatinine
• Hematuria,
• No RBC casts
Pulmonary rare - rare common Cryo >HSP (rare)
PN Rare/uncommon + + +
+
GI rare + + ( HSP> CRYO)
microneursym
+→palpable
purpura
Skin Rare none + + Raynauds
phenomenon,
PLT count
normal
Granulomas Yes no Yes, except MPA No
TRIAD-
MC artery involved
Wegener’s granulomas- Skin - palpable
is superficial
ENT involvement, pulmonary purpura –
temporal artery,
renal syndrome (MCc of death). common in LL/
temporal Q
MC artery C-ANCA + butts
Headache (MC), jaw
involved is Churg strauss syndrome +
claudication (2nd Q
subclavian HBS Ag+ , Testicular (EGPA) - bronchial asthma. MCC GI – abdominal
Others MC)
artery, arm pain, involvement of death is cardiac involvement. pain, +/-
ESR↑↑
pulseless radial P-ANCA + bleeding
Q Ophthalmic artery-
artery MPA - present with pulmonary +
artery AION , * For Making Notes immune syndrome, no ENT / Arthralgia
Blindness
no eosinophilia/ no bronchial +/- renal- IgA
IOC- Temporal Q
asthma. P-ANCA+ mesangial
artery bx
deposits
TOC-
Treatment HSP- NSAID’S
corticosteroids
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Cerebellum Quick Revision Notes

BEHCET’S DISEASE KAWASAKI DISEASE

HLA B51 Medium vessel vasculitis
Q
• •
Recurrent oral apthous ulcers Coronary artery aneurysm
Q
• •
• Recurrent genital apthous ulcers- male : scrotum • Children <5yrs, males, Asians
> shaft of penis
• Gold standard Ix - Coronary angiography
• Females: labia
• Monitor disease - ECHO
• Skin – erythema nodosum
Tx: IV Ig + aspirin
Q
•
• Eyes- posterior uveitis >anterior uveitis,
F - fever, > 5days
hypopyon formation
E - enathems
• Pathergy positivity
B - bulbar conjunctivitis (sterile)
• Superficial thrombophlebitis +DVT
R - rash- groin /perianal
• Arthritis /fever
I - internal organ involvement : coronary artery
• CNS – brainstem involvement
involvement → aneurysm → AF/MI → death
L - Lymphadenopathy
E - extremity changes

* For Making Notes

Telegram - @nextprepladdernotes
Telegram - @nextprepladdernotes
 Chapter - 3 Autacoids
- Have autocrine effects [Local effects] H1 Blockers
- Based on chemical Structure 1st Generation 2nd Generation
Peptide Autacoids Amine Autacoids Lipid Autacoids Cross BBB, cause sedation Do not cross BBB, no
→ Angiotensin → Histamine → Prostaglandins sedation
→ Bradykinin → 5-HT → Leukotrienes Have Anti-cholinergic action No Anti-cholinergic action
→ Thromboxane → Anticholinergic S/E occur
Useful for allergy and Useful only for allergy
HISTAMINE Possess : Prophylaxis of
Receptors motion sickness
Anti : Akathisia
Location Action Blockers
Cholinergic : Common Cold

H1 CNS Allergy First and Property : Parkinsonism

Bronchus second (Drug induced)

Stimulates RAS
Generation Promethazine FexofenadineQ
Promote
Drugs • Terfenadine metabolite
wakefulness
Loratidine
H2 Stomach Secrete Acid Ranitidine
Cetirizine
Cimetidine
H3 PreSynaptic BRAKE H3 Inverse
Agonist
Tiprolisant
[Pitolisant]
Used for
Narcolepsy
H4 WBC Chemotaxis

5-HT (SEROTONIN)
Serotonin Receptors

Location Action Drugs Example Uses

5HT1A Presynaptic Brake Agonist Buspirone Q
Anxiety
5HT1B/ID BV of Brain Vasoconstriction Agonist Sumatriptan Naratriptan DOC for
Eletriptan Rizatriptan Acute Severe Migraine
5HT2A/2C Brain Blockers Clozapine , Olanzapine Atypical Antipsychotics
5HT3 CTZ Emesis Blockers Ondansetron Granisetron DOC for vomiting due to
Tropisetron Dolasetron Chemotherapy
PalonosetronQ Radiotherapy
Post-operativeQ
5HT4 GIT Prokinetic Agonist Cisapride , Mosapride, As prokinetics for GERD
Prucalopride
24
Cerebellum Quick Revision Notes

MIGRAINE:Q
→ Drug of choice for mild to moderate headache – NSAIDs (Paracetamol, Diclofenac)
→ Drug of choice for Acute severe attack – Triptans
→ Other drug for Acute severe migraine – Ergotamine
→ DOC for prophylaxis of migraine – Propranolol

New Drugs for Migraine: 1. General Effects

Q
1. Lasmiditan (DITANS) • Fever
• Stimulates 5HT1F receptor and decreases CGRP • Pain
release. • Inflammation
• This prevents the vasodilation and neuronal
inflammation. 2. Platelets

• Effective orally. • TXA2 → Aggregation

• It is recently approved for acute attacks of • PGl2 → Inhibition of aggregation

migraine. 3. Heart
• Advantage over triptans is that it does not induce • Ductus Arteriosus is kept open by PGE1
peripheral vasoconstriction.
• PDA [Patent ductus Arteriosus] is treated by
2. Monoclonal Antibodies Against CGRP NSAIDs like
• Approved for prophylaxis of migraine. – Aspirin
• Given by injectable route. – Indomethacin
– Erenumab – Ibuprofen (DOC)
– Fremanezumab
– Galcanezumab
4. Uterus

– Eptinezumab • PGs Contract upper segment of uterus

Q • Used for abortion (Misoprostol is used)
3. CGRP Antagonist: (GEPANTS)
5. Stomach
• Used for acute attack
• PGE2 protect the stomach from peptic ulcer disease
• Effective orally
• For NSAID Induced Peptic Ulcer Disease
• Drugs are
– Most specific drug is MisoprostolQ
– Olcegepant
– DOC is proton pump inhibitors
– Rimegepant
– Ubrogepant
6. Eye
PROSTAGLANDINS PGF2α
→ ↑ Uveo scleral outflow
→ Latanoprost
→ DOC for Primary Open Angle GlaucomaQ
 25
Pharmacology

NON-STEROIDAL ANTI- - Valdecoxib

INFLAMMATORY DRUGS (NSAIDs) - Parecoxib
COX 1 COX-2 - Lumiracoxib
Constitutive Enzyme Inducible enzyme
• These have lesser risk of causing PUD
Present normally at most Present normally in
• These increase the risk of MI and stroke
places • Kidney
• Endothelium - Etoricoxib Longest acting

• CNS - Rofecoxib and Valdecoxib Withdrawn because of MI

and stroke
NSAIDS act by inhibiting COX. These may be:
- Parecoxib is given by Parenteral route
Non-Selective COX Inhibitors Selective COX-2 Inhibitors
- Lumiracoxib is withdrawn Due to Liver toxicity
↑ Risk of PUD Less risk of PUD
GOUT
Non-Selective COX Inhibitors
It is characterized by increase in serum uric acid.
Drugs
Acute Gout
- Aspirin : Irreversible COX inhibitor
1. DOC : NSAIDs (except aspirin and paracetamol)
(Antiplatelet), ↑Uric acid
2. Steriods : If NSAIDs do not work
- Paracetamol : COX - 3 inhibitor, safe in CKD
3. Colchicine (Most effective drug):Q
- Ibuprofen : DOC for PDA
- Can cause myopathy and diarrhea
- Diclofenac : Partial COX-2 selective
- Inhibit granulocyte migration
- Indomethacin : Sedation is adverse effect
- Piroxicam : Longest acting NSAID
Chronic Gout
- Nimesulide : Not used in children (hepatotoxic)
Three types of drugs can be used in chronic gout.
- Ketorolac : Given IV
– Drugs decreasing production of uric acid
– Drugs increasing excretion of uric acid
(Uricosuric agents)
– Drugs increasing metabolism of uric acid

Proteins / Purines

Xanthine
Xanthine oxidase
1
Uric acid Excretion 2

In birds Uricase 3

Allantoin
Selective COX 2 Inhibitors
Drugs
- Celecoxib
- Rofecoxib
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Cerebellum Quick Revision Notes

1. ↓ Formation 2. ↑ Excretion 2. Biological DMARDs:

AllopurinolQ Probenecid i. Drugs Inhibiting TNF-a:Q
• Inhibit xanthine oxidase Sulfinpyrazone
- All are injectable
• DOC for chronic gout Lesinurad
Febuxostat A Adalimumab
→ Plenty of fluids should
C Certolizumab
• Inhibit xanthine oxidase be taken E Etanercept
3.↑ Metabolism Inhibitor lnfliximab
Rasburicase → Recombinant uricase Goli Golimumab
→ ↑ Risk of infections.
Pegloticase → Long acting uricase
These are fastest urate lowering agents for tumor → Contra-indicated in T.B. and Hepatitis B
lysis syndromeQ → Apart from R.A., these drugs can be used for Crohn’s
disease as well as Psoriasis
RHEUMATOID ARTHRITIS
NSAIDs and Steroids DMARDs or SAARDs ii. IL - 1 Receptor Antagonist:Q
• Slow down the disease ANAKINRA
• ↓ Pain and lnflammation
progression
• No effect on disease – A - 1st letter
Progression
– KIN - Interleukin
• Fast acting • Slow acting
– R - Receptor
– A - Antagonist
1. Conventional DMARD:
DMARD of choice in iii. IL - 6 Receptor Antagonists:Q
Cute and Chloroquine
pregnancy Tocilizumab
Used for Cu poisoning/
p Penicillamine → 1st IL- 6 targeted monoclonal Antibody.
Wilson’s disease
→ Approved for treatment of cytokine release
A Azathioprine syndrome also.
G Gold salts Sarilumab
L Leflunomide Fastest acting DMARDQ → Used for rheumatoid arthritis
S - Six
Inhibitors of Tofacitinib
I AR - R.A.
JAK Baricitinib MAB - Monoclonal antibody
DOC, Needs LFT
Malika Methotrexate
Monitoring iv. Co-stimulation InhibitorsQ
DOC for ulcerative • Abatacept
Sherawat Sulfasalazine
colitis
• Inhibit the interaction of T-cell and Antigen
Presenting Cells (APC).
 27
Pharmacology

Previous Years Questions

Q1. Most specific antiemetic for Chemotherapy induced Q8. A 60 year old female with renal disease was
vomiting is: admitted for pyelolithotomy. Post operative analgesic
of choice in this patient is?
A. Doxylamine B. Tegaserod
A. Diclofenac B. Indomethacin
C. Granisetron D. Domperidone
C. Naproxen D. Acetaminophen
Q2. Buspirone is a drug used in chronic anxiety. It
produce its action by acting on which of the following Q9. Which of the following is the fastest urate
receptors? lowering therapy in tumor lysis syndrome to prevent
renal damage?
A. 5HT1A B. 5HT1B
A. Allopurinol B. Febuxostat
C. 5HT2 D. 5HT3
C. Rasburicase D. Furosemide
Q3. A boy is planning to travel by bus. Which of the
following drug can be used to prevent motion sickness Q10. A female patient presented with pain and redness
in this person? in great toe. Serum uric acid level is 9.6 mg/dL. Apart
from prescribing analgesics for relieving pain, the
A. Promethazine B. Cetrizine physician prescribed a drug which can decrease the
C. Loratidine D. Fexofenadine formation of uric acid. Which of the following enzyme
is likely to be inhibited by this drug?
Q4. Drug of choice for prophylaxis of migraine is A. Xanthine oxidase
A. Propranolol B. Imipramine B. Thymidylate synthase
C. Flutamide D. Flunarizine C. Phosphpribosyl transferase
D. DHFR
Q5. A young female presented with left sided severe
throbbing headache associated with nausea, vomiting,
photophobia and phonophobia. Which of the following Q11. Drug inhibiting granulocyte migration is:
drug can provide immediate relief to this patient? A. Montelukast B. Cromoglycate
A. Propranolol B. Sumatriptan C. Colchicine D. Felbamate
C. Topiramate D. Flunarizine
Q12. Pegloticase is used for treatment of :-
Q6. Drug of choice in paracetamol overdose is A. Ankylosing spondylosis
A. N-acetylcysteine B. Dopamine B. CPPD
C. Hydralazine D. Furosemide C. Chronic tophaceous gout

Q7. A 34 week pregnant female with polyhydramnios D. Refractory Rheumatoid arthritis

presents with labour pain. She was treated with
indomethacin earlier. Which of the following can be
likely outcome in the baby if delivery occurs at this
time?
A. Patent ductus arteriosus
B. Premature closure of ductus arteriosus
C. Patent ductus venosus
D. Premature closure of ductus venosus

Answers
1. - C 3. - A 5. - B 7. - B 9. - C 11. - C
2. - A 4. - A 6. - A 8. - D 10. - A 12. - C
28
Cerebellum Quick Revision Notes
Q13. A patient diagnosed with Rheumatoid arthritis was A. IL-6 B. IL-12
on medications. After 2 years, he developed blurring
C. IL-2 D. IL-3
of vision and was found to have corneal opacity. Which
drug is most likely to cause this?
Q15. A 40 year old male patient presents to hospital
A. Sulfasalazine B. Chloroquine with pain in great toe. It was diagnosed to be a case
of gout. Which of the following drug increases the
C. Methotrexate D. Leflunomide excretion of uric acid in urine?
Q14. Tocilizumab is an immunosuppressive drug used A. Colchicine B. Probenecid
for Rheumatoid arthritis. It is a monoclonal antibody
C. Allopurinol D. Febuxostat
against

Answers

13. - B 15. - B
14. - A