LAST MINUTE

REVISION BOOK
MEDICINE
by
DR. ASEEM DEWAN
MD MEDICINE (MAMC),
EX SR (AIIMS DELHI)

DR. SHARAD MALHOTRA

MBBS (TMC – GOLD MEDALIST),
DNB MED, DNB GASTRO (GOLD
MEDALIST)

DR. RAHUL CHAUDHARY

MD MEDICINE (AIIMS DELHI),
DM CARDIO (PGI CHD), MAX HOSP
DELHI
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 LMR - CARDIOLOGY

GENERAL PHYSICAL EXAMINATION

JVP - Normal 8 cm from sternal angle; 1 mm HG = 1.36 cm H2O/blood

Raised JVP • Absent pulsation – SVC syndrome

• Present pulsation – Fluid overload /HF
‘a’ wave – Atrial • Prominent ‘a’ – TS, RHF, PAH
contraction (Tricuspid • Canon ‘a’ wave – CHB, VT, AV dissociation
Valve is open) • Absent ‘a’ wave – AF
‘x’ descent – Right atrial • Prominent ‘x’ descent – CCP, Cardiac Tamponade (CT)
relaxation
‘c’ wave – TV closed and • Prominent – Severe TR (as a part of ‘cv’ wave)
bulges into RA; (carotid
pulsation)
‘v’ wave – Venous filling • Prominent – Severe TR – Large ‘v’ (cv) wave , rapid ‘y’
(from SVC/IVC) – RA descent ; (Lancisi’s sign – Giant ‘v’ wave in TR)
tense /TV closed • ASD (a = v)
‘y’ descent – RA emptying • Slow descent – TS
as TV opens • Rapid descent – TR
• Sharp descent, deep ‘y’ trough, rapid ascent to
baseline – CCP (FRIEDREICH’s sign – prominent ‘y’
descent)
• Absent ‘y’ descent - CT
Paradoxical JVP • CCP, CT
(Kussmaul’s sign - ↑ JVP
on Inspiration)
H wave • In between ‘y’ descent and ‘a’ wave – seen in
bradycardia
Abdomino Jugular Reflux • Positive AJR predicts HF and PAWP > 15 mm Hg
(AJR)

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PULSE: (NORMAL 60 – 100 BPM)

< 60/min bradycardia; > 100/min tachycardia; Pulse pressure = (SBP – DBP) normal 30 – 40
mmHg; Proportional Pulse Pressure = (SBP – DBP) /SBP: correlates with Cardiac Index
• Irregularly irregular: AF/AFl with variable block /MAT/ Frequent ectopics
• Regularly irregular: Sinus arrhythmia (Inspiration Increases HR)/ atrial or ventricular bi
or trigeminy /pulsus alternans
• Apex pulse deficit > 10 bpm: AF; < 10 bpm – VPC’s or MAT
• Pulsus parvus et tardus – Severe AS
• Bifid pulse: 2 systolic peaks (Chronic severe AR, AR + AS , HOCM – spike and dome pattern);
systolic and diastolic peak – IABP
• Pulsus alternans: Severe LVSD, LVF, hypovolemia; Pulsus bigeminy – digitalis toxicity – ECG
shows bigeminy; Water hammer pulse (Corrigan’s pulse) – Severe AR (N.B. – CORRIGAN’s
sign is name given to DANCING CAROTID’s which is also seen in Severe AR)
• Pulsus paradoxus: Inspiratory decline in SBP by > 10 mm Hg – Cardiac Tamponade , CCP,
Severe obstructive lung disease , Tension Pneumothorax, massive PTE
• Diminished Pulse
➢ Radio radial delay → Takayasu arteritis, Thoracic outlet/subclavian steal syndrome,
peripheral arterial disease (Atherosclerosis/embolism of upper limb arteries)
➢ Radio femoral delay → Coarctation of aorta, Peripheral arterial disease (lower limb)

BLOOD PRESSURE

• BP = CO (SBP) x PVR (DBP); CO = HR X SV

• (SV) = EDV – ESV (50 -120 ml; Normal 70 ml in 70 kg man)
• SV → preload/afterload/LV contractility
• LVEF = SV /EDV
• SBP – DBP = Pulse pressure (PP)
• MAP = DBP + 1/3 PP = 1/3 SBP + 2/3 DBP = (SBP +2DBP)/3; 70 – 110 mmHg
• Cardiac Index = CO/BSA in m2
• Korotkoff sound: K1 (SBP) K5 (DBP)
• Cuff length & width: 80% & 40% arm circumference respectively
• DBP – zero: Pregnancy, children, large AV fistula, chronic severe AR
• BP difference > 10 mmHg between UL→ subclavian artery stenosis, supravalvular AS,
Coarctation of aorta, aortic dissection
• ABI: 0.9 – 1.3 (normal); < 0.9 PAD; > 1.3 non compressible calcified arteries
• Orthostatic hypotension: fall in BP > 20/10 mm Hg within 3 min of standing

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• White coat HTN: Clinic BP HIGH, normal Avg. Day time BP
• Masked HTN: HIGH avg. day time BP, Normal clinic BP

HEART SOUND

• Due to closure of valves (M1T1-A2P2)

• ASD: wide & fixed split of S2; VSD – Variable split; PDA – Paradoxical split
• S3 -early diastole: rapid ventricular filling – physiological (children, pregnancy) pathological
– Heart failure/ Regurgitant lesion /Shunts
• S4 - late diastole (presystolic atrial contraction) – always pathological – HTN, AS, HCMP
• Systolic sounds: Ejection (Valvular AS/PS) and Non ejection click (MVP); pulmonary EC is
the only right sided event that ↓ Inspiration.
• Diastolic sounds: Opening snap (MS), Pericardial knock (CCP), tumor plop (LA myxoma)
• Systolo – diastolic → Triphasic – Pericardial friction rub (Pericarditis)
• Pan Systolic Murmur: MR, TR, VSD
• Continuous murmur: PDA, RSOV / coronary arterial fistula to RA/RV, Coarctation of aorta,
pulmonary/femoral/renal artery stenosis
• Valsalva maneuver & Standing → ↓ Length & Intensity of all murmur EXCEPT MVP (long
& loud), HOCM (loud)

CARDIOMYOPATHY

• DCMP – Systolic dysfunction

• RCMP/HCMP – Diastolic dysfunction
• MC – Autosomal dominant Inheritance
• DCMP – TTN (Titin mutation)
• HCMP – βMHC, MYBPC3, MYL 2/3
• RCMP – TNNI3 (cardiac troponin), DES (Desmin)
• X linked – Dystrophin (DMD, BMD); α galactosidase A (Fabry’s disease)
• Mitochondrial DNA (maternal) – MELAS, MERRF, Kearns – Sayre syndrome
• RCMP – Right sided congestion predominantly

DILATED CARDIOMYOPATHY

• 2/3rd Idiopathic: Inflammation, toxin (drug, alcohol), metabolic (hemochromatosis), genetic,

familial, Peripartum (PPCM), Tachycardia related
• Viral MC infective etiology (coxsakie, adeno, HIV, HCV)

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• PPCM – last trimester to 6 months after pregnancy – 15% have TTN mutation – HF in early
pregnancy k/a PACM (pregnancy associated CMP)
• Alcohol – 4 ounces (118 ml pure ethanol daily for 5-10 year but frequent binge also
sufficient); Holiday Heart (MC arrhythmia AF – but can have VT/VF; role of Magnesium
deficiency)
• Beri Beri, Selenium def (Keshan’s disease), ↓Ca 2+, Carnitine def, ↓Mg 2+↓Phosphate

RESTRICTIVE CARDIOMYOPATHY

• Infiltrative: between myocyte (Amyloid, transthyretin, atrial peptide); Storage – within

myocyte (Hemochromatosis, Fabry’s ds, Glycogen SD II, III); Endomyocardial (Endomyocardial
fibrosis, HES – Loffler’s endocarditis); Fibrotic (radiation, scleroderma)
• Cardiac amyloid: Transthyretin mutation on Chromosome 13; Light pink (H&E), greenish
blue/turquoise (sulfated Alcian blue), apple green birefringence (congo red stain); low
voltage on ECG, Tc pyrophosphate imaging for TTR amyloidosis; Primary amyloid worst
prognosis (6-12 month survival) – bortezomib (protease inhibitor)/cardiac transplant
• Loffler’s endocarditis (HES): ↑Eosinophil (>1500/µl, > 6 month) – inflammation /fibrosis – AV
valvular regurgitation/ Heart Failure/ AF/ Thromboembolism/Fibrosis of ventricular apex,
inflow, AV valve
• Endomyocardial fibrosis (EMF aka Davies disease): earlier prevalent in Kerala (triad of
↑JVP, massive ascites, hepatomegaly); no pedal edema - managed with steroid and
chemotherapy/diuretics/anticoagulants/

HYPERTROPHIC CARDIOMYOPATHY

• Obstructive (70%), non-obstructive (30%); (apical – k/a Yamaguchi syndrome)

• ASH – asymmetric septal hypertrophy (septum > free wall) – banana shaped LV cavity
• SAM – systolic anterior motion of anterior mitral leaflet (AML)→ MR
• Microscopy – myocyte disarray & interstitial fibrosis
• ECG – Diffuse TWI (T wave inversion) in precordial leads and Q wave in inferolateral
leads
• HCMP – leading cause of SCD (sudden cardiac death) in young
• C/F: ↑’a’ wave in JVP; double /triple apical impulse; LVS3 ,S4; Systolic late peaking murmur
becomes loud with STANDING & VALSALVA
• SPIKE & DOME pattern on aortic pressure trace
• Hyper contractile LV
• Diagnosis – Echocardiography, cMRI, genetic mutation analysis

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• Athlete’s heart (c.f. with HCMP) → Symmetric LVH, dilated LV cavity, normal LV diastolic
function, resolution of LV hypertrophy with deconditioning
• Management – β blocker’s / rate reducing CCB, disopyramide, alcohol septal ablation,
surgical myomectomy → for LVOTO (Left ventricular outflow tract obstruction); AICD
(automated implantable cardioverter defibrillator) for 10&20 prevention of SCD

HEART FAILURE

• Impaired Ventricular filling (leading to Pulmonary and systemic venous congestion) &
Impaired Ejection of blood (leading to ↓ cardiac output and hypoperfusion of organs);
Laplace law – wall stress = (pressure x radius)/2 (wall thickness)
• ↑SNS, ↑RAAS; LV remodeling (microscopy – myocytolysis, necrosis, apoptosis, autophagy,
myofibrosis, degradation of ECM/cytoskeletal protein; Gross – Dilation & ↓ contractility of
LV, ↑ sphericity, thinning of LV wall, Mitral regurgitation)
• Framinghams criteria: (MAJOR – orthopnea PND, Neck venous distension (NVD), JVP > 16
cm H2O, HJR, S3, Rales, Cardiomegaly/Pulmonary edema on Chest Xray; MINOR – dyspnea
on exertion , night cough, tachycardia, ankle edema, hepatomegaly, pleural effusion, ↓ vital
capacity) (MAJOR or MINOR – weight loss > 4.5 kg in 5 days in response to treatment);
diagnosis requires at least 2 major or 1 major + 2 minor criteria
• Any disease of the heart can cause Heart failure (just remember all the chapters in
cardiology in Harrisons)
• Based on LVEF – HFrEF (LVEF < 40%), HFmrEF (40-50%), HFpEF (>50% LVEF); Around 50%
patients of HF have preserved LVEF (HFpEF)
• Stage of HF (A – At high risk for developing HF – HTN, DM, CAD) (B – Asymptomatic HF) (C
– Symptomatic HF) (D – Refractory end stage HF)
• Warm & Dry (C.I. >2.2, PCWP < 18)
• Warm & wet (C.I. > 2.2, PCWP > 18)
• Cold & dry (C.I. < 2.2, PCWP < 18)
• Cold and wet (C.I. < 2.2, PCWP >18)
• Diagnosis: Framingham’s criteria, Pulmonary congestion on Chest Xray; Echo – LVEF;
Biomarkers – BNP, NT – pro BNP, soluble ST-2, galectin – 3; cardiac MRI – LVEF calculation,
amyloidosis/ myocarditis; Chest Xray – pleural effusion, Kerley B line, Batwing appearance,
cardiomegaly, reverse moustache/ Antler’s sign
• BNP < 100pg/ml and NT pro BNP < 300 pg/ml rules out Heart failure (biomarkers ↑in both
HFrEF & HFpEF)

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• MANAGEMENT: Decongestion (diuretics), improve survival and prevent adverse remodeling
of LV (ACE’I, ARNI, ARB, β blockers, Mineralocorticoid Receptor Antagonist, CRT – cardiac
resynchronization therapy), prevent SCD (AICD)
• Diuretics: Metabolic & electrolyte imbalance (↓Na, ↓or↑K ↓Mg ↓or↑Ca ↑ glycemia/ lipidemia/
uricemia); Hypotension, azotemia, ototoxicity
• Newer Drug →ARNI – angiotensin receptor neprilysin inhibitor (Sacubitril Valsartan);
Ivabradine – acts on funny current SA node
• Device therapy → AICD (to prevent SCD in LVEF <35%); CRT – LVEF <35% & Broad QRS
(LBBB with QRS ≥150 ms); LVAD (Left ventricular assist device – Impella/Tandem Heart)
• ACUTE LVF – MC causes ACS, Accelerated HTN, Valvular heart disease, Myocarditis - Prop
up position , high flow oxygen, Non-invasive ventilation , Diuretics, Inj Morphine, Inj
Nitroglycerine, Intubation and mechanical ventilation
• Most common cause of right heart failure is left heart failure
• CARDIOGENIC SHOCK – end organ hypoperfusion (urine output <30 ml/h or cool
extremities); SBP may or may not be decreased; Hemodynamic criteria (C.I. ≤ 2.2 L/min/m2
& PCWP ≥15 mmHg) – manage with inotropes/ Mechanical circulatory support (MCS –
Impella, LVAD, IABP – intra aortic balloon pump)
• HFpEF – No specific management, decongestion with diuretics + control of comorbid
condition, ACEI/ARNI/β blocker/MRA – have not demonstrated benefit in HFpEF
• CARDIORENAL SYNDROME – Type I (Acute Cardiorenal –Acute LVF causing AKI) Type II
(chronic cardiorenal – Chronic CHF causing kidney damage) Type III (Acute renocardiac – AKI
causing acute LVF) Type IV (Chronic Renocardiac – CKD causing cardiac hypertrophy
/remodeling) Type V (Secondary cardiorenal – systemic condition like diabetes affecting
both heart and kidney)

PERICARDIAL DISEASE

• 15 – 50 ml normal pericardial fluid

• Left atrium is extra pericardial
• Normal pericardial contact pressure 2 – 4 mmHg (↑25 in cardiac Tamponade, CT)
• Pericarditis: Acute (<6 week), Sub acute (6 week – 6 month) Chronic (> 6 month) – causes
Infection (viral, bacterial, TB, fungal, protozoal parasite); Non-infectious (idiopathic, renal
failure, tumor, trauma, MI, radiation); Hypersensitivity or autoimmune (Rheumatic fever,
collagen vascular disease, drugs like INH Phenytoin Procainamide Hydralazine)
• Acute pericarditis: chest pain (radiating to trapezius ridge and ↓on sitting up and leaning
forward), pericardial friction rub, diffuse concave ST elevation (concave upwards) with PR
segment depression and PR elevation in aVR on ECG, Pericardial effusion on ECHO

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• Massive pericardial effusion → Ewart’s sign (aka PINS sign) – dullness on
percussion/bronchial breath sound beneath angle of left scapula; Electrical alternans on
ECG (also seen in massive PTE); Water bottle configuration on Chest Xray
• Acute pericarditis treatment with anti-inflammatory (NSAID’s, Aspirin, Steroid, Colchicine);
ANTICOAGULANTS are CONTRAINDICATED (can cause hemopericardium) – Cardiac
Tamponade is RARE
• CARDIAC TAMPONADE – medical emergency – diastolic RA/RV collapse – TRIAD of ↑JVP,
Hypotension, Muffled heart sounds ( Distended JVP, Decrease BP, Decrease heart sounds);
JVP – Prominent ‘x’ descent absent ‘y’ descent and absent Kussmaul’s sign; pulsus
paradoxus (Inspiratory decline in SBP > 10 mmHg) ; Urgent pericardiocentesis
• Chronic Constrictive Pericarditis (CCP): causes → TB (MC); suspect CCP when
Ascites/Hepatomegaly is present with prominent neck vein distension ; JVP – distended ,
prominent ‘x’ and ‘y’ descent (FRIEDERICH’s sign); KUSSMAUL’s sign (↑ or failure of
Inspiratory decline of JVP); 1/3rd can have Pulsus Paradoxus ; BROADBENT’s sign ( reduced
apical impulse with systolic retraction); PERICARDIAL KNOCK (diastolic sound at LV apex
due to abrupt cessation of LV filling); ECG – low voltage complex, 1/3rd AF; Chest Xray –
pericardial calcification (MC in TB Pericarditis); SQUARE ROOT sign on cardiac
catheterization ; treatment – decongestion by diuretics, surgical resection of pericardium
(pericardiectomy)

CARDIAC TUMOUR

• 20 involvement (MC from CA breast and Lung) of heart & pericardium MC

• 10 tumour – benign (MC - MYXOMA) & malignant (MC - SARCOMA)
• MYXOMA: MC 10 cardiac tumor in adult, 3rd to 6th decade, more common in females, 90%
sporadic, 10% familial
➢ CARNEY complex: mutation of PRKAR1A – myxoma with lentigines/pigmented nevi and
endocrine overactivity of adrenal cortex/pituitary/testicles
➢ NAME syndrome – Nevi, atrial myxoma, Myxoid neurofibroma, Ephelides
➢ LAMB syndrome – Lentigines, Atrial myxoma, Blue nevi); TUMOR PLOP; Treatment –
surgical resection
• PAPILLARY FIBROELASTOMA: MC tumor of cardiac valve (aortic > mitral), solitary, SEA
ANEMONE appearance, can present with stroke/TIA/MI/acute limb ischemia
• RHABDOMYOMA: MC cardiac tumor in infant and children, multiple, strong association
with tuberous sclerosis, some association with CMV

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• SARCOMA: MC malignant primary cardiac tumor (angiosarcoma m/c in adults &
rhabdomyosarcoma m/c in children) – fulminant course with death within weeks to
months of presentation ; poor response to therapy ( resection/chemotherapy)
• METASTATIC TUMOUR TO HEART: MC from CA breast and Lung; Pericardium > myocardium
> rarely endocardium; MALIGNANT MELANOMA – high incidence of cardiac metastasis

ATHEROSCLEROSIS & IHD

• Ischemia – demand supply mismatch leading to decreased blood supply (decrease

oxygen/nutrient delivery and reduced waste removal) → different from hypoxemia (↓
oxygen content of blood)
• Commonest cause of ischemic heart disease (IHD) – atherosclerotic narrowing of coronary
arteries (LAD, LCx & RCA which supply the heart)
• LDL cholesterol at birth is usually < 30 mg/dl → as the level increases with ↑ age → lipid
deposition in arterial wall (fatty streak) → gradually progresses to form PLAQUE →
progressive luminal narrowing → leading to varied manifestation (CAD/CVA/Peripheral
artery disease) together known as ASCVD (Atherosclerotic Cardio Vascular Diseases)
• Tunica intima – innermost layer of arterial wall – keeps the blood in liquid state →
Thrombomodulin, Heparan sulphate, PGI2 (ANTICOAGULANT factors); Tissue Factor & vWF
(PROCOAGULANT); if thrombus forms – tPA/ uPA converts plasminogen into plasmin
which then causes fibrinolysis (THIS IS COUNTERED by PAI – plasminogen activator
inhibitor); activated Protein C (along with Protein S) inactivates factor V and VIII
• Tunica media – SMC (smooth muscle cells) – modulates arterial tone – SMC also synthesize
ECM, engulf lipids (Lipid laden FOAM cells)
• WHAT CAUSES ATHEROSCLEROSIS (systemic inflammatory disease)? → Endothelial
dysfunction with progressive Intimal Lipoprotein (Lp) accumulation → Lp oxidation and
glycation – role of CAM/MCP – 1 causing transcytosis of monocyte – inflammation – SMC
migration & proliferation – formation of lipid laden Macrophage and SMC (Foam cells) –
cell apoptosis – PLAQUE PROGRESSION → Progressive luminal stenosis/ plaque rupture,
fissure, erosion causing thrombosis and leading to MI, Stroke, peripheral ischemia, SCD
• Stable plaque (Thick fibrous cap, Large ECM component, Low number of macrophages and
small necrotic area) – responsible for SIHD (Stable Ischemic Heart disease) a k/a CCS
(Chronic Coronary Syndrome)
• Unstable plaque (Thin fibrous cap, small ECM component, High number of macrophages,
Large necrotic core, positive remodeling) – more likely to cause ACS (Acute coronary
syndrome –by plaque rupture/erosion) causing NSTEMI (nonocclusive thrombus)/ STEMI
(occlusive thrombus)/ Arrhythmias/SCD

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• Risk factors for ASCVD: Age, Gender, Race (non modifiable); Cigarette smoking,
Hypertension, Elevated lipids/cholesterol, DM, Obesity, Sedentary lifestyle, psychoSocial
factors (modifiable risk factors – CHEDOSS); Non-conventional risk factors – hs CRP, LP(a),
Apo B/Apo A1 ratio, serum homocysteine levels
• Atherosclerosis complication: Arterial stenosis, Thrombosis (MC due to plaque rupture >
plaque erosion > calcific nodule), Aneurysm/ectasia (e.g. AAA abdominal aortic aneurysm)

10 Hyperlipidemia (familial) Lp
Type Hyperchylomicronemia (LPL ↑Chyl – A/c pancreatitis, eruptive
I deficiency) xanthoma
Type Familial Hypercholesterolemia (FH) ↑LDL (ASCVD)
IIa
Type Familial combined ↑LDL &VLDL (ASCVD)
IIb hypercholesterolemia (FCH) – MC
Type Dysbetalipoproteinemia (Apo E ↑IDL (Palmar & tuberous xanthoma)
III deficiency)
Type Familial hypertriglyceridemia ↑VLDL (eruptive xanthoma)
IV
Type Familial Lipoprotein Lipase ↑VLDL &Chyl (pancreatitis)
V deficiency

SECONDARY (ACQUIRED HYPERLIPIDEMIA)

1. ↑Cholesterol: Hypothyroidism, Nephrotic syndrome, obstructive liver ds, Drugs (OCP, thiazide
diuretics)
2. ↑TG: DM, Chronic renal failure, alcohol

FH: High LDL – C from birth , early onset CAD, Tendon xanthomas (Achilles tendon , tendon on
dorsal surface of hand, elbow), LDL Receptor mutation (most common), gain of function PCSK9
mutation, apoB3500 mutation
Tangier’s disease: ABC1 cholesterol transport gene deficiency - ↓HDL & LDL in blood (as
cholesterol accumulates inside cells) – ORANGE TONSILLS, hepatosplenomegaly,
polyneuropathy, atherosclerosis
METABOLIC SYNDROME: – (ATP III CRITERIA) At least 3 of the following

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 1. Central obesity waist circumference >40 inch,102 cm men and > 35-inch, 88 cm women
2. Fasting Triglyceride ≥ 150 mg/dl
3. HDL – C (< 40 mg/dl in men and <50 mg/dl in women)
4. BP ≥ 130/85 mm hg
5. Fasting glucose ≥100 mg/dl

SIHD/CSA/CCS

• Can manifest as CSA aka CCS (Chronic Coronary Syndrome) (Stable plaque) or ACS (Acute
Coronary syndrome (Unstable plaque) → causing Unstable angina/NSTEMI/STEMI;
Arrythmia /SCD; ICMP (ischemic cardiomyopathy) and Heart Failure.
• Demand (MVO2 – Myocardial oxygen consumption) → Heart rate/Myocardial contractility
/wall stress (Laplace Law – wall stress = pressure x radius/2(wall thickness )
• Supply – depends on CBF (coronary blood flow, O2 carrying capacity (depends on FiO2 –
fraction of oxygen in inspired air and Hb/PaO2/SaO2) of the blood. Cardiac output = HR x
SV (Stroke volume – depends on Preload/afterload/LV contractility)
• 90% coronary blood flow occurs in DIASTOLE
• Demand supply mismatch – causes Ischemia
• Liver >kidney >muscle >brain (Liver receives the maximum cardiac output – 25% of total
cardiac output); Heart receives only 5% of total cardiac output. However, since the weight
of kidney is less than liver – if the question is maximum cardiac output /gram of tissue
→ Answer will be KIDNEY
• Of all these organs MAXIMUM OXYGEN EXTRACTION (i.e. max A – V oxygen difference ) is
by heart, heart has nearly 100% oxygen extraction from the capillaries which means ↑O2
Demand by the heart is met by ↑supply through increased coronary blood flow and not
by increased oxygen extraction as in OTHER tissues
• Typical Angina → 3 features
1. Substernal chest discomfort of characteristic quality and duration
2. Provoked by exertion or emotional stress
3. Relieved by rest or nitrates within MINUTES
• Stable angina – pain duration 2 – 10 min; unstable angina: 10 – 20 min ; MI: > 30 min
• Angina pectoris – diagnosis by HISTORY
• Chest pain in ER → STEMI, Aortic Dissection, Pulmonary thromboembolism (PTE)
(remember MAD PT)
• Unstable angina - ↑ frequency/intensity/duration of angina; angina occurring at lower
work threshold/ new onset angina/ nocturnal angina; crescendo angina/ rest angina/post
MI angina

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• PRINZMETAL’s VARIANT ANGINA – is a vasospastic disease →young patient , no traditional
risk factor (except heavy smoking) → may present with angina and ST elevation on ECG
or MI or VT/VF or even SCD (sudden cardiac death); rare association with Raynaud’s
phenomena and migraine; diagnosis using provocative test during coronary angiography
(using hyperventilation or intracoronary acetylcholine); AVOID ecospirin; managed by
quitting smoke/ CCB (calcium channel blockers)
• > 1mm ST depression in 2 consecutive ECG leads – positive TMT
• CORONARY ANGIOGRAPHY – GOLD STANDARD for diagnosis of CORONARY ARTERY
DISEASE
• Medical management – Single antiplatelet / high intensity statins (meaning target to
reduce LDL by > 50%)/ beta blockers / antianginals (beta blockers, calcium channel blockers,
nitrates, nicorandil – K channel opener, Ranolazine – inhibits late Na current, Ivabardine –
inhibits funny current in SA node, Trimetazidine – inhibits fatty acid oxidation and shifts
myocardial metabolism to more efficient pathway
• Angioplasty and stenting in CSA/SIHD/CCS only if medical therapy fails
• Indication for CABG (coronary artery bypass graft) – Left main disease, Triple vessel
disease , diabetics, Left ventricular systolic dysfunction

ACS – NSTEMI

1. Results from NON-OCCLUSIVE thrombus formation inside the coronary artery from
rupture or erosion of an unstable plaque.
2. Chest pain + ECG changes + raised cardiac Troponin T/I (cTn T/I) → NSTEMI
3. MI definition requires a change in cTn T/I plus at least one of → 1. Symptoms of ischemia,
2. ECG changes ,3. Finding on ECHO, 4. Identification of thrombus on coronary angiography
(CAG) or autopsy
4. Universal definition of MI (5 types)

1 Spontaneous – plaque rupture

2 20 to demand supply mismatch
3 SCD presumed to be due to MI
4 MI related to PCI/ Stenting
5 MI related to CABG
5. Management – Two antiplatelet (c.f. CSA where single antiplatelet is used), high intensity
statin (Atorvastatin 40/80 mg ; Rosuvastatin 20 or 40 mg), betablockers, Heparin ,
antianginals
6. Coronary angiography and revascularization by PCI (Stenting) or Bypass surgery (CABG)

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ACS – STEMI

• Results from OCCLUSIVE THROMBUS inside coronary artery causing abrupt complete
cessation of blood flow to a portion of the heart supplied by that coronary artery – can
lead to NECROSIS if flow is not immediately established.
• STEMI → Chest pain (>30 min), ST elevation of > 1mm in 2 consecutive leads.
• Treatment of choice → PRIMARY PCI (target should be FMC – D ≤ 120 min i.e. First Medical
Contact to Device (balloon inside coronary artery for simple understanding) should be
within 120 min; if this time > 120 min then patient should be Thombolysed (within 30 min
of coming into hospital a/ka – Door to Needle time).
• All patient with STEMI to be given → two antiplatelets/ high intensity statin/ Heparin/ anti
angina.
• Thrombolysis/Fibrinolysis (Streptokinase/Reteplase/Tenecteplase) if facility for PRIMARY
PCI is NOT available.
• Window period (upto 12 hours of onset of chest pain) i.e. PCI/Thrombolysis can be done
upto 12 h.
• STK – 1.5 million units; TNK – 0.53 mg/kg body weight single bolus; Reteplase – 2 boluses
of 10 IU 30 min apart
• ABSOLUTE CONTRAINDICATION of THROMBOLYSIS
• CNS (previous intra cranial hemorrhage, AV malformation ,Malignant intracranial
neoplasm, ischemic CVA within last 3 months except within 4.5 hours, significant head or
facial trauma in last 3 month ,intracranial or intra spinal surgery in last 2 month );
Uncontrolled severe HTN; Aortic Dissection; Active bleeding (excluding menstrual bleed); for
STK – previous use within last 6 month ( 5 days – 2 years).
• RV MI – 1/3rd of patient with IWMI can have RVMI → suspect if patient with IWMI has
Hypotension, ↑JVP and clear lungs → IVF bolus, DO NOT give nitrates
/diuretics/morphine/beta blockers
SIHD NSTE- STEMI
ACS
Antiplatelets Single DUAL
Statin HIGH INTENSITY
ẞ blockers + + +
Anticoagulants - + +
Fibrinolysis - - +
ACE’I or ARB - If LVEF < 40%
Antianginals + + +

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HYPERTENSION

• 2 or more seated BP > 140/90 mm Hg at 2 or more outpatient visit; > 95th percentile for
Age/sex/ height for children
• Why treat high BP → HTN ↑ risk of CAD/CHF/CVA (ischemic and hemorrhagic), Renal
Failure/PAD (peripheral arterial disease), and Retinopathy.
• BP increase with ↑ng age; DBP ↑ till age 55 years then↓ so PULSE PRESSURE (SBP – DBP)
increases after age of 55 years.
• All risk factor for ASCVD are also risk factor for HTN
• > 98% - Polygenic; < 2 % - monogenic (e.g. - 17 ᾳ and 11ẞ hydroxylase deficiency, Liddle’s and
Gordon’s syndrome, PKD, Pheochromocytomas)
• 10 or Essential HTN (80 – 95%) – familial
• 20 HTN – specific cause of HTN can be identified → Renal diseases (Polycystic kidney disease,
renin secreting tumor, Renal parenchymal disease , obstructive uropathy), Renovascular
HTN, Endocrine disorders (↑or↓ Thyroidism, ↑ calcemia, Acromegaly), Coarctation of aorta,
Adrenal Cortex (Primary hyperaldosteronism, Cushing’s syndrome, 11ẞ and 17 ᾳ hydroxylase
deficiency, 11 HSD deficiency), Adrenal Medulla (Pheochromocytomas), Drugs, Obstructive
Sleep Apnea Syndrome (OSAS).
• RAAS, ANS (autonomic NS), intravascular volume and vascular structure and function →
regulates BP.
• MAP = 1/3 SBP + 2/3 DBP (70 – 110 mmHg)
• Augmentation Index (A.I.) = A.P./ P.P x 100 (AP is augmentation pressure – pressure at
inflection point or anacrotic notch; and PP is the pulse pressure) → measure systemic
arterial STIFFNESS.
• JNC 7 criteria for HTN in adults (≥18 years)

SBP (mmHg) DBP(mmHg)

Normal < 120 AND < 80
Pre HTN 120 – 139 or 80 – 89
HTN
• Stage 1 140 – 159 or 90 – 99
• Stage 2 ≥160 or ≥100
Isolated Systolic HTN (ISH) ≥140 AND < 90

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WHITE COAT HTN → ↑Clinic BP, Normal ABPM
MASKED HTN → Normal clinic BP, ↑ABPM
ABPM (Ambulatory BP monitoring)
• 24 h BP recording
• Normally night time BP is 10 -20% lower than day time (k/a – NOCTURNAL DIP)
• Average Awake BP ≥ 135/85 mmHg and Average Sleep BP ≥ 120/75 mmHg → corresponds
to Clinic BP > 140/90 mmHg and hence is used as criteria for HTN based on ABPM

RENO-VASCULAR HYPERTENSION

• Due to occlusion of renal artery stenosis (RAS)

• Cause
➢ Atherosclerosis (Affects ostio-proximal part of renal artery, usually seen in > 50 y
➢ FMD – fibromuscular dysplasia – young female, usually bilateral involvement, affects
distal portion of renal artery, STRING of BEAD appearance
• RAS → Asymptomatic, Renovascular HTN, Ischemic nephropathy, Flash pulmonary Edema
(k/a – PICKERING SYNDROME)
• When to SUSPECT RAS?
➢ HTN with unexplained loss of renal function or worsening of renal function when ACE’I
or ARB is started as a treatment
➢ Recent loss of BP control in a patient who was previously doing OK
➢ Resistant HTN (failure of BP control despite ≥3 drugs including a diuretic)
➢ New onset refractory or severe HTN
➢ 50% of RAS patient can have ABDOMINAL BRUIT in para umbilical region
Treatment of Renovascular HTN – Drugs, Renal revascularization (provided kidney function
is preserved) by angioplasty (PTRA) with or without stent or surgery (aorto-renal , spleno
renal bypass)

PRIMARY ALDOSTERONISM

• 90% cases due to either Adenoma or adrenal hyperplasia

• Suspect in young (3rd – 5th decade), with refractory HTN and unprovoked HYPOKALEMIA (i.e.
in the absence of vomiting, diarrhea, diuretic use).
• ↑Aldosterone – Na+/H2O retention (but PEDAL EDEMA is rare), Hypokalemia (25% patients
can have normal potassium), Hypokalemic alkalosis (muscle weakness, paresthesia,
polyuria, polydipsia)

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 DIAGNOSIS
➢ Plasma aldosterone/ plasma renin activity > 30:1 + Plasma aldosterone >20 ng/dl:
together has > 90% sensitivity and specificity as a screening test
➢ Failure to suppress PA < 10 ng/dl in response to 2L Normal Saline infusion over 4h or
in response to oral NaCl/Fludrocortisone/Captopril → confirm Primary Aldosteronism
➢ Imaging – abdominal CT scan / Adrenal scintigraphy (131I – Iodo Methyl Norcholetsrol)
after dexamethasone suppression
➢ Invasive testing – bilateral adrenal venous sampling to measure aldosterone levels
TREATMENT
➢ Adrenalectomy for Adenoma
➢ Medical therapy with aldosterone antagonist for bilateral adrenal hyperplasia and
non-operable adenoma

Glucocorticoid Remediable HTN

➢ Rare monogenic, Autosomal DI, HTN at early age

➢ ↑Aldosterone, ↓K+, HTN – triad
➢ Defect in Chimeric gene on Chromosome 8
➢ Diagnosis - ↑urinary levels of Hybrid steroids (18 hydroxy and oxo cortisol)
➢ Treatment – Low dose glucocorticoids to suppress ACTH and Aldosterone antagonists

PHAEOCHROMOCYTOMA

• Associated with MEN type 2A and 2B, von Hippel Lindau disease, Neurofibromatosis
Type I
• May present with persistent or paroxysmal HTN or Hypotension (Postural hypotension
occurs because of volume contraction and downregulation of adrenergic receptors)
• Head & neck paraganglioma – mutation in SUCCINATE DEHYDROGENASE gene
• DIAGNOSIS
➢ Plasma Metanephrines (higher sensitivity)
➢ 24 h urinary catecholamine and metanephrines (higher specificity)
➢ Imaging – Abdominal CT/ MRI/ Scintigraphy (123I – MIBG)/PET
➢ Genetic mutation – ret proto oncogene
➢ Other lab finding – hyperglycemia / hypercalcemia /erythrocytosis
• TREATMENT
➢ Adrenalectomy – for adrenal pheochromocytomas
➢ Initiate ẞ blocker ONLY after at least 2 days of ᾳ blockade

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 ➢ DOC – ALPHA BLOCKERS – Phenoxybenzamine, Prazosin, Terazosin, Intravenous
Phentolamine (DOC for Adrenergic crisis during e.g.- pheochromocytomas surgery)

MONOGENIC HTN

• Rare defects in Adrenal steroid biosynthesis – Mineralocorticoid induced Hypertension

and ↓K+
• 17 ᾳ hydroxylase deficiency
➢ CYP17 gene on chromosome 10
➢ ↓sex hormone (pseudo hermaphroditism in male and primary amenorrhea in
female) and ↓cortisol (loss of negative feedback - ↑ACTH - ↑Mineralocorticoid – HTN
and ↓K+
➢ Treatment – Low dose Glucocorticoid
• 11 ẞ hydroxylase deficiency
➢ Salt retaining ADRENOGENITAL syndrome
➢ ↓cortisol → ↑MC (mineralocorticoid) ↑androgen synthesis → virilization and
ambiguous genitalia in female and penile enlargement in male)
➢ HTN is less common
• 11 ẞ Hydroxy Steroid Dehydrogenase (HSD) deficiency
➢ Licorice containing GLYCYRRHIZIN ACID may cause acquired 11 ẞ HSD deficiency
Liddle’s syndrome
➢ Epithelial Na+ Channel (ENaC) mutation
➢ Treatment – Amiloride

HTN MANAGEMENT

• ACE’I /ARB preffered→ Heart failure /Diabetics/ Left Ventricular Hypertrophy (LVH)/LV
Systolic dysfunction/ Proteinuria /CKD
• Safe in pregnancy – MCH (Methyldopa, Calcium channel blockers, Hydralazine)
• Acute Aortic Dissection – beta blockers (Esmolol, Labetalol)
• Acute LVF – Loop diuretics/ Nitroglycerine/Enalaprilat (beta blockers are contraindicated)
• ACS – Esmolol, Nitroglycerine
• Acute Renal Failure – Clevidipine, Nicardipine
• Eclampsia – hydralazine, Labetalol, Nicardipine
• Perioperative HTN – Nitroglycerine, Esmolol,
• Acute Intra Cranial Hemorrhage – Nicardipine, Nitroprusside, Labetalol
HYPERTENSIVE CRISIS can be of 2 types

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• URGENCY - ↑↑ BP without EOD (end organ damage)
• EmERgency - ↑↑ BP with EOD – BP to be aggressively lowered within minutes to hours
(remember ER – for emergency)
• Malignant HTN – when papilledema is present on fundus examination by ophthalmoscopy
End Organ Damanage in HTN Emergency
• Brain – encephalopathy /Stroke
• Eye – Retinal hemorrhage papilledema
• Heart – MI, Acute LVF, Aortic dissection
• Kidney – Acute renal failure, Micro Angiopathic Hemolytic Anemia (MAHA)

AORTIC ANEURYSM

Pathological dilation of a segment of aorta – aneurysm

• True aneurysm – wall of aneurysm by all three layers of aortic wall
(intima/media/adventitia). False aneurysm – wall by adventitia or just perivascular clot
(hence more likely to rupture)
• Fusiform – affects entire circumference of aorta. Saccular – affects a portion (eg only
lateral wall of aorta out pouches as aneurysm)
• Based on location – Thoracic/Abdominal / Thoraco-abdominal

Etiopathogenesis:

➢ Atherosclerosis (MC)/Degenerative / genetic/ inflammation / infection / Trauma →

degradation of ECM (extra cellular matrix) -↓ tensile strength and compliance of aortic
wall → aneurysm
➢ Marfan’s: fibrillin 1 mutation - ↑TGF ẞ signaling. LDS – TGFBR1 & TGFBR 2 mutation.
Ehler-Danlos type IV syndrome – Type III procollagen mutation
➢ Mycotic aneurysm: due to infection of atherosclerotic plaque by bacteria/fungus –
usually saccular
➢ AAA strong association with SMOKING

C/F:

➢ Mostly asymptomatic
➢ Due to effect on surrounding structure: – dyspnea/dysphagia/hoarseness due to TAA
(Thoracic aortic aneurysm). Aortic Regurgitation/ SVC syndrome → Ascending AA
➢ Pain abdomen – in a known case of AAA: sign of impending rupture; medical
emergency as rupture can be FATAL

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 Investigation

➢ X – Ray → mediastinal widening in TAA and calcification in AAA

➢ USG/Echocardiography: Screen all smokers between 65 – 75y & family members of
patient with TAA/AAA by USG
➢ Contrast CT/MRI angiography
➢ Invasive aortography/angiography

Treatment:

• Beta blockers, ARB – in patients with Marfan’s to reduce rate of dilation in TAA. Statins
to reduce atherosclerosis progression in AAA.
• EVAR – Endo Vascular Aortic Repair or Surgical repair with placement of graft
➢ All symptomatic patient
➢ Asymptomatic Asc aorta → BAV (bicuspid aortic valve) + Asc aorta ≥ 5.5 cm ; BAV +
Asc Aorta > 4.5 cm + Severe AS/AR; Marfan’s with Asc Aorta between 4-5 cm
➢ Asymptomatic DTA (descending thoracic aorta) > 5.5 cm or rate of growth > 1 cm/year
➢ AAA if ≥ 5.5 cm

AORTIC DISSECTION

Type-A Type-B

Stanford Type A – Ascending aorta involved (proximal dissection); B - Distal dissection

(involves arch and descending aorta).
Debakey – Type I (Entire aorta), Type II (Ascending aorta ONLY), Type III (descending aorta only)

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C/F:

CHEST PAIN (CP) – quality (sudden onset TEARING type); intensity (Very severe within
seconds); radiation (typically to back interscapular region). Rarely patient may present with
altered sensorium/syncope /focal neurological deficit (N.D.) without CP.
CP + anyone (think of Aortic dissection)
• CVA (focal N.D.)
• Paralysis
• Limb ischemia
• Aortic regurgitation
• Hoarseness
Diagnosis: Chest X – Ray → Calcium sign (due to intimal displacement), Left apical PLEURAL
CAP
CT/MRI Angiography

Management

1. Pain relief – fentanyl

2. Reduce cardiac contractility and heart rate → negative inotropy to reduce Shear stress -
ẞ Blocker’s (Inj Labetalol – DOC)
3. Nitroprusside, Nicardipine → only after giving beta blockers → target HR < 60/min and BP
< 120 mm Hg(systolic) within 20 min
4. Type A – Surgical correction
Type B
• Medical therapy for uncomplicated and stable dissection
• EVAR/ surgery → pain, visceral ischemia, impending rupture, increasing propagation

PERIPHERAL ARTERY DISEASE

• Stenosis of aorta or its branches. MC cause in adults – Atherosclerosis. Risk factors same
as risk factors for ASCVD (mnemonic –CHEDOSS).
• Stenosis of arteries supplying limb – ischemia – VASCULAR CLAUDICATION
(pain/cramps/muscle ache/numbness or sense of fatigue in muscle precipitated by
exertion relieved by rest) distal to site of occlusion
• Differentiate from Neurogenic claudication – produced by nerve compression – associated
with low back pain /sensory motor symptoms/muscle weakness/changes in
reflexes/aggravated by erect posture of extension of spine and relieved by sitting or

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 bending forward/ease of pain on walking uphill or cycling /present pulse /absent arterial
bruit

C/F:

• 50% asymptomatic
• Intermittent claudication (vascular claudication)
• Rest pain (critical limb ischemia) – severe impairment of resting blood flow - more at
night when legs are horizontal (gets better when legs are in dependent position.
• Physical examination - ↓ or absent pulse, arterial bruit, ulcer, gangrene, peripheral edema
Non-Invasive Testing
ABI
• Normally ankle pressure ≥ brachial pressure (because of pulse wave amplification)
• Normal – 1 – 1.4; Abnormal < 0.9 (diagnosis of PAD); value >1.4 – suggest non compressible
calcified arteries – in such a case one may use TBI (Toe Brachial Index) – TBI ≤0.7 is diagnostic
of PAD
TCOM (Trans cutaneous oxygen monitoring) – normal value 50 – 70 mmHg (<30 mmHg –
suggestive of critical limb ischemia)
Duplex USG, Post exercise measurement of ABI, CT or MR angiography
Invasive Testing: Conventional angiography
Treatment:
• Smoking cessation (nicotine patch, bupropion, varenicline)
• Risk factor modification
• High intensity statin, Antiplatelets, Vorapaxar (PAR – 1 antagonist), Cilostazol (PDE 3
inhibitor)
• Pentoxifylline (substituted xanthine derivative has hemorheological effect – i.e. affects
blood viscosity)
• Endovascular (angioplasty +/- stenting) or surgical repair

FIBRO MUSCULAR DYSPLASIA (FMD)

String of beads appearance, MC in female, affects medium and small size arteries (renal,
carotid, subclavian, iliac). Treatment – PTA (percutaneous transluminal angioplasty) or surgery

THROMBO ANGITTIS OBLITERANS (TAO, Buerger’s disease)

• Inflammation of arteries and vein (ANGITTIS) leading to THROMBUS/fibrosis and

OCCLUSIVE vascular disease m/c of distal upper and lower limb vessels

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• Strong association with cigarette smoking and in age < 40 years
• TRIAD of – Raynaud’s phenomena/ Claudication (calf feet or forearm – DISTAL) and
superficial vein thrombophlebitis. Severe disease –gangrene, ulceration
• O/e:- ↓radial/ulnar/tibial (i.e. distal pulses) palpable brachial and popliteal (proximal pulses).
• Diagnosis– CT/MRI/ conventional angiography – confirmation by biopsy of involved vessel.
• Treatment– NO SPECIFIC TREATMENT; Smoking cessation, antibiotics,
debridement/amputation – NO ROLE of steroid and anticoagulant

ACUTE LIMB ISCHEMIA

• Sudden cessation of arterial flow; causes – embolism (MC from heart (AF, Infective
endocarditis, atrial Myxoma, LV thrombus), aorta and large arteries), thrombus in situ,
arterial dissection, trauma , polycythemia and hypercoagulable state
• Paradoxical emboli – from venous system in to arterial system through a PFO (Patent
foramen ovale) or ASD (atrial septal defect).
• C/F: – severe pain, coldness, numbness within an hour and paralysis later. Physical
examination - loss of pulse, pallor, cyanosis, coolness, and gradually sensory motor loss.
• Treatment – Anticoagulation, catheter directed thrombolysis/thrombectomy, surgical
thromboembolectomy and surgical bypass procedures.
• Intra – arterial thrombolysis with Reteplase/Tenecteplase if < 2 weeks. Surgical
revascularization if occlusion > 2 weeks

ATHEROEMBOLISM

• Multiple small cholesterol/fibrin/platelet fragment embolize – acute pain and tenderness

at site of embolization → involvement of digits causing cyanosis and impending necrosis
→ BLUE TOE SYNDROME.
• No specific treatment – analgesic, antiplatelet and statin may be tried.

THORACIC OUTLET COMPRESSION

• compression of neurovascular bundle (vein, artery, nerve) at the thoracic outlet

• Due to cervical rib/scalene muscle/pectoralis minor muscle
• If artery is compressed → claudication, Raynaud’s, ischemic tissue loss, gangrene ;
diminished arterial pulse , presence of bruit → abduction and external rotation of upper
limb /and other maneuver → can precipitate symptoms/cause bruit
• If nerve is compressed → shoulder/arm pain, paresthesia →Nerve conduction study
• If vein is compressed → subclavian/axillary vein thrombosis → Paget – Schoettler
syndrome

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• Treatment – physiotherapy, surgical resection on scalene muscle/removal of first rib

ARTERIOVENOUS FISTULA

• Abnormal communication between artery and vein bypassing the capillary

• Palpable pulsatile mass with continuous thrill and bruit (systole and diastole)
• Chronic veinous insufficiency causing varicose vein pedal edema; High output heart failure
& cardiomegaly
• Nicoladoni – Branham sign → reflex bradycardia on compression of large AV fistula
• Manage with elastic support, surgery, radiotherapy, embolization

VALVULAR HEART DISEASE

AORTIC STENOSIS

• Etiology

➢ Congenital (bicuspid, unicuspid), Degenerative calcific, Rheumatic fever, radiation.

➢ BAV – bicuspid aortic valve – NOTCH 1 gene, NKX2.5 → associated with Coarctation of
Aorta, intracranial aneurysm, aortopathy (aortic especially ascending
aneurysm/dissection). SHONE’s complex - Sub aortic stenosis, CoA, supramitral ring,
Parachute mitral valve

• C/F: TRIAD of exertion (remember as SAD or DAS)

➢ Dyspnea
➢ Angina
➢ Syncope

• Severity: Symptomatic patient – symptoms of Dyspnea/Angina/Syncope

• O/E:

➢ Pulsus parvus et tardus

➢ Apico-carotid delay
➢ Delayed peaking of ESM
➢ Paradoxical S2 split
➢ LVS4; thrill
➢ PH, CHF, Cardiomegaly

• ECHO:

➢ Mean gradient > 40 mm Hg

➢ Aortic forward velocity > 4 m/s

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 ➢ Effective aortic orifice area < 1 cm2 (< 0.6 cm2/m2 BSA)
• Treatment: SAVR or TAVR (surgical or Trans catheter Aortic Valve replacement) –
Symptomatic Severe AS

AORTIC REGURGITATION

Etiology:

VALVULAR

• Congenital (Bicuspid)
• Endocarditis
• Rheumatic Fever *** highlighted – cause of Acute AR (AIR –
• Traumatic Aortic dissection, Infective endocarditis,
• Myxomatous, syphilis RSOV)

• Ankylosing spondylitis

ROOT DISEASE

• Aortic dissection
• Bicuspid aortic valve
• Marfan’s, Cystic medial degenrtn
• Aortitis / HTN

Severity

• Hills sign (>60 mmHg)

• Short murmur duration
• Austin flint murmur
• LVS3
• PH, CHF, Cardiomegaly

Echo

• Dilated LV, ERO ≥ 0.3 cm2, Regurgitant fraction ≥ 50%, Regurgitant volume ≥ 60 ml/beat,
Vena contracta > 0.6 cm , holo-diastolic aortic flow reversal

Peripheral signs of AR (Absent in Acute AR)

• Water hammer or Corrigan’s pulse

• Quincke’s pulse – alternating flushing and paling at root of nail
• Duroziez’s Distal Diastolic ( Diastolic bruit on distal compression and systolic on
proximal)

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• De Musset’s sign – Head bobbing
• Traube’s sign – pistol shot femoral
• Hill’s sign – popliteal SBP > brachial SBP by > 60 mm Hg (SENSITIVE)
• Rosenbach’s sign – Hepatic pulsation
• Gerhardt’s sign (Sailer’s sign) – splenic pulsation
• Becker’s sign – retinal arteriole pulsation
• Landolfi’s sign – systolic contraction and diastolic dilation of pupil
• Shelly’s sign – pulsation in cervix
• Mayne’s sign - ↓DBP by 15 mm Hg on raising hand ( non specific)
• Light house sign – alternate flushing and paling of forehead
• Pulsus bisferien’s – double peaking in systole

Treatment: SAVR – Surgical Aortic Valve Replacement

MITRAL STENOSIS

Etiology:

• Rheumatic fever
• Congenital (Parachute MV, cor triatriatum)
• LA Myxoma / Large IE vegetation
• RA/SLE
• Severe MAC (mitral annular calcification) extending to mitral leaflets

Severity:

• Prolonged Diastolic murmur

• Diastolic Thrill
• Short A2 – OS gap
• PH, CHF, Cardiomegaly
Normal MV area – 4 – 6 cm2
Echo – MVA < 1.5 cm2 (FISH MOUTH like opening of mitral valve)

Complication of MS PARIS

• Pulmonary HTN
• Atrial Fibrillation
• Right heart failure
• Infective endocarditis
• Systemic Embolism

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Treatment

• Mitral Valvotomy (Balloon or Closed) – BMV/CMV

• Mitral Valve Replacement

MITRAL REGURGIATATION

Etiology

Acute (PIR – trauma)

• Papillary muscle rupture
• Infective endocarditis
• Rupture of chordae tendinae
• Trauma
Chronic
• Primary (disease affecting leaflet or chordae) - Rheumatic fever , MVP, healed IE, congenital
cleft mitral leaflet or AV canal defect
• Secondary (Dilation of Mitral annulus) – Ischemic or Dilated Cardiomyopathy, LA
enlargement in chronic AF, HOCM with systolic anterior motion on mitral leaflet causing
MR
• Mitral annular calcification

Severity:

• Cardiomegaly
• LVS3
• Wide split S2
• PH, CHF
ECHO: Dilated LV, ERO ≥ 0.4 cm2, Regurgitant fraction ≥ 50%, Regurgitant volume ≥ 60
ml/beat, Vena contracta > 0.7 cm
Treatment Mitral valve repair or replacement (MVR); Trans catheter MITRA CLIP

MITRAL VALVE PROLAPSE

Aka – systolic click murmur/ Barlow’s/ floppy valve / billowing mitral leaflet syndrome.

Etiology

• Marfan’s , Ehlers – Danlos syndrome

• Osteogenesis imperfecta
• Straight back syndrome

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• Rarely rheumatic fever
Click murmur occurs earlier with standing and Valsalva.
Treatment – Mitral Valve repair

TRICUSPID VALVE DISEASE

Etiology

TS – Rheumatic /congenital
TR – Primary (organic) →rheumatic/IE/Ebstein’s anomaly/ Carcinoid; Secondary (functional) –
RV and tricuspid annular dilation due to Pulmonary HTN, Cardiomyopathy

TS/TR → features of RHF → ↑JVP, ascites, hepatomegaly, pedal edema

CV wave in JVP in TR
Carvallo’s sign → Increased systolic murmur with inspiration in TR and diastolic murmur in
TS
Treatment → Tricuspid valve repair

PULMONARY VALVE DISEASE

Graham Steell murmur – Diastolic murmur in pulmonary area associated with Loud P2 & RV
parasternal lift (or heave) suggestive of Pulmonary HTN.

Pulmonary Stenosis – associated with Noonan’s syndrome (PTPN1 mutation).

JONE’S MAJOR CRITERIA

Low risk population Moderate & high-risk population

CARDITIS: clinical and /or subclinical Carditis: clinical and /or subclinical

ARTHRITIS: polyarthritis only Arthritis: Monoarthritis or polyarthritis,

Polyarthralgia

Chorea Chorea

Erythema marginatum Erythema marginatum

Subcutaneous nodules Subcutaneous nodules

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 JONE’s MINOR CRITERIA

Low risk population ** Moderate & high risk population $$$

Polyarthralgia Monoarthralgia

Fever ≥ 38.5⁰ C Fever ≥ 38.5⁰ C

ESR ≥ 60mm/hr or CRP ≥ 3mg/dl ESR ≥ 60mm/hr or CRP ≥ 3mg/dl

Prolonged PR interval Prolonged PR interval

$$$
: Those with higher incidence and Prevalence rates
**: ARF incidence 2/1000 or all age RHD prevalence ≤ 1/1000 population at any age during 1 y.

DUKE’S CRITERIA – IE

Major Criteria

Blood culture positive for IE

1. Typical microorganisms consistent with IE from two separate blood cultures

a. Viridans streptococci; Streptococcus bovis, HACEK group, Staphylococcus aureus, or
b. Community-acquired enterococci, in the absence of a primary focus
2. Microorganisms consistent with IE from persistently positive blood cultures, defined as
follows:
a. At least two positive blood cultures of blood samples drawn > 12 h apart; or
b. All of three or a majority of 3 or 4 separate cultures of blood (with first and last
sample drawn at least 1 h apart)
3. Single positive blood culture for Coxiella burnetii or antiphase I lgG antibody titre > 1: 800

Evidence of endocardial involvement

1. Echocardiogram positive for IE defined as follows:

• Oscillating intracardiac mass on valve or supporting structures, in the path of
regurgitant jets, or on implanted material in the absence of an alternative anatomic
explanation; or
• Abscess; or
• New partial dehiscence of prosthetic valve
2. New valvular regurgitation (worsening or changing of pre-existing murmur not sufficient)

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MINOR CRITERIA

• Predisposition, predisposing heart condition or injection drug use

• Fever, temperature > 38°C
• Vascular phenomena, major arterial emboli, septic pulmonary infarcts, mycotic aneurysm,
intracranial haemorrhage, conjunctival haemorrhages and Janeway lesions
• Immunologic phenomena: Glomerulonephritis, Osler nodes, Roth’s spots, and rheumatoid
factor
• Microbiological evidence: Positive blood culture but does not meet a major criterion as
noted previously. (excluding single positive cultures for coagulase-negative staphylococci
and organism that do not cause endocarditis) or serologic evidence of active infection with
organisms consistent with IE
• Echocardiographic minor criteria eliminated

IE Prophylaxis

• Previous IE
• Prosthetic Heart valve
• Cardiac transplant recipients with diseased valves
• Unrepaired Cyanotic CHD
• Repaired CHD with residual defect
• Repaired CHD with prosthetic material or device for first 6 month

CONGENITAL HEART DISEASE (CHD)

ACYANOTIC
• Shunt: ASD / VSD/ PDA
• Obstructive: CoA, AS, PS
CYANOTIC
• TOF (↓ PBF – Pulm Bld Flow)
• Tricuspid Atresia
• TGA
• TAPVS
• Truncus Arteriosus

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ASD/ TAPVC – Pre-Tricuspid lesion: causes enlargement of RA/RV (right side of heart).
VSD/ PDA – Post Tricuspid lesion: causes enlargement of LA/LV left side of the heart)

Ebstein’s anomaly: HIMALAYAN ‘P’ wave (tall ‘P’ wave > 5 mm lead II); associated with WPW
syndrome
Most common congenital anomaly recognized at birth – VSD
Most common cyanotic CHD – TOF (Nonrestrictive VSD, Over riding of Aorta, Infundibular PS,
RVH); TOF + ASD or PDA → Pentalogy of Fallot
Most common Cyanotic CHD at birth → TGA (Arterial switch operation)
BT shunt, Pots shunt Waterston shunt → palliative for TOF
X – Ray appearance
• Boot shaped heart – TOF
• Snowman’s sign (figure of 8) – Supracardiac TAPVC
• Egg on string or side appearance – d TGA
• Waterfall appearance – L TGA, Truncus
• Figure 3 sign – Coarctation of aorta (CoA)
• Notching of inferior border of ribs - CoA

❑ ❑ ❑

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 LMR GASTROENTEROLOGY

LIVER

1. Largest organ of the body, approx wt: 1 – 1.5 kg

2. Dual blood supply – 80 % from portal vein and 20 % from hepatic artery
3. Functional unit is acinus- blood enters from the portal area (zone 1), flows through
sinusoids to terminal hepatic veins (zone 3), hepatocytes are zone 2. The secreted bile flows
in opposite direction zone 3 to zone 1
4. Kupffer cells – largest collection of macrophages in body; stellate cells seen – in space of
disse
5. Serum bilirubin – measure of hepatic conjugation and excretion, serum albumin and
prothrombin time - measure of protein synthesis
6. Jaundice without dark urine – indirect / unconjugated hyperbilirubinemia, typical hemolysis
and genetic disorder of bilirubin conjugation
7. Signs of advanced liver disease - muscle wasting, ascites, edema, dilated abdominal veins,
fetor hepaticus, asterixis, mental confusion, stupor/coma & GI bleeding
8. Pain in liver disease is due to stretching of Glisson capsule which surrounds liver and is
rich in nerve endings.
9. Ascites is caused due to cirrhosis, low albumin levels, medications, heart failure and venous
insufficiency
10. Bruit in liver disease is heard in hepatocellular carcinoma, AV malformations and Alcoholic
hepatitis
11. HPS - Hepato pulmonary syndrome: characterised by platypnea and orthodeoxia (shortness
of breath that occurs paradoxically on assumption of upright posture)
12. Fibroscan is good for initial detection and follow up for liver stiffness. MR elastography is
better for detecting liver fat / fibrosis but is expensive. Liver biopsy provides assessment
of mild fibrosis also hence is the gold standard
13. MELD-Na (Model For Endstage Liver Disease – Na ) score is used for pre-transplant
assessment of a individual with liver disease. It consists of three variables- PT/INR, Bilirubin
and creatinine . Recently serum sodium levels have been added to improve its sensitivity
14. In jaundice, if direct fraction is less than 15% of total, then total bilirubin can be considered
all indirect
15. Unconjugated bilirubin is albumin bound hence cannot be filtered by kidney. Any bilirubin
in urine is always conjugated

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16. AST/ALT ratio is usually < 1 in chronic viral hepatitis and reverses to > 1 once cirrhosis
develops
17. In alcoholic liver disease,
• AST levels are typically elevated above 300
• ALT levels are usually normal due to alcohol induced deficiency of pyridoxal phophate.
• GGT levels are typically high in alcohol consumption
• AST/ALT ratio is typically > 2: 1 in alcoholic liver disease
18. ALP > 4 times normal occurs in cholestasis, infiltrative liver disorders and bone conditions
of high turnover like Paget’s
19. Gamma globulins are produced by B lymphocytes in cirrhosis, It is usually due to increased
antibody synthesis against intestinal bacteria
20. Prothrombin time – measures factors II, VII , IX and X
21. Shortest half life is of factor VII – 3-6 hours and longest half life is 5 days for fibrinogen
22. Ammonia is generated in colon with bacteria and in course of normal protein metabolism.
Liver helps in detoxification by converting it into urea which is removed by kidneys
23. Multi drug resistance associated protein 2 mutation causes Dubin Johnson syndrome.
MRP 3 mutation is associated with Rotor syndrome
24. Gall stones which develop in hemolysis are always bilirubin stones. Bilirubin levels are
usually not more than 4-5 mg%. Pattern of bilirubin will be predominantly unconjugated
only
25. Gilbert Syndrome is characterised by AR inheritance, males more common than females,
prevalence of 5-8 % population, normal colored bile, normalisation of bilirubin on giving
phenobarbital.
26. Progressive Familial Intrahepatic Cholestasis causes growth retardation, malnutrition and
end stage liver disease. Type I is known as Byler disease. GGT is abnormal in type III PFIC
only. Treatment is liver transplantation only
27. BRIC is having AR inheritance, Presents with hepatitis like illness initially and then pruritus
and jaundice . Usually seen in childhood and adolescence. Due to FIC 1 gene mutation

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VIRAL HEPATITIS

1. Hepataitis B
3 forms – most numerous 22 nm particles
42 nm particle – intact hep b virion
• 8 subtypes and 10 genotypes
• GENOTYPE D – More likely to develop - hepatocellular CA
• GENOTYPE A – More likely to clear hep b and develop seroconversion
• HbsAg positive mother with positive HBeag – 90% rsik of child transmission , if
HBeag negative -risk 10 %
• Anti HbS antibody – protective antibody
• Molecular variants
A. PRECORE MUTANTS – high risk of chronic and severe liver disease
B. ESCAPE MUTANTS – loss of protective antibody to anti -h bs

2. HEPATITIS D
• Only co-ifection / superinfection with hepatitis b
• Isolated infection not possible
• Usually suppresses HBV replication

3. HEPATITIS C
• 9600 nucleotide RNA virus
• 3 structure protein and 7 non structural protein
• 6 major genotypes ( 1 minor 7th type )
• Genotype 3 more common in india
• Quasispecies phenomenon- deifference in sequence homology by few percent –
prevents development of vaccine and development of hormonal antibody
IL-28 association for treatemnt response

4. HEPATITIS E-
• 3 open reading frames
• Genotypes 1 to 4
• Genotypes 1 and 2 more common in Asia (more virulent)

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VACCINE AVAILABILITY

• Hepatitis A and B have excellent vaccines

• Hepatitis E has an experimental vaccine
• Hepatitis C has no vaccine

Acute hepatitis – diagnosis

1. HAV- IgM Anti HAV

2. HEPATITIS B – HbsAG AND IgM ANTI Hbc
HbeAG- Marker of relative infectivity
3. Anti Hbs- Marker of immunisation
4. HEPATITIS C – Anti HCV + HCV RNA – Quantitative
HEPATITIS E- IgM ANTI HEV

• Suggested Acute Hepatitis panel should have 4 markers: HbsAG, IgM Anti HAV, IgM Anti
Hbc and Anti HCV

Other special associations:

1. Hepatitis A is associated with Relapsing and Cholestatic hepatitis

2. Hepatitis E virus is associated with increased mortality in pregnancy
3. Firosing cholestatic hepatitis is associated with Hepatitis C in a post transplant setting

TREATMENT OF HEPATITIS :

• Hepatitis A and E: supportive care

• hepatitis B –
1. Acute setting: supportive care except for acute liver failure
2. Chronic setting: oral drugs: entecavir, tenofovir, telbivudine, adefovir, lamivudine, and
injectable – interferon
• Hepatitis C
1. Acute: usually not detected
2. Chronic: 3-6 months course of direct acting antivirals with/ without intrefron and
ribavirin

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PROPHYLAXIS

1. HEPATITIS A VACCINE: 2 doses 6-12 MONTHS apart

Post Exposure Prophylaxis: Immunoglobulin single dose 0,02 ml/ kg Body weight
2. HEPATITIS B: Recombinant Vaccine 3 doses ( 0,1, 6 MONTHS )
Dose: 10 mcg, always give in deltoid only
Post Exposure Prophylaxis:
A, New born: 0.5 ml HBIg after birth in thigh with 3 doses of vaccine schedule
b. Adult: IM dose of HBIg 0.06ml/kg - single dose
3. Pregancy and Hepatitis B – only approved drug for use is tenofovir

ESOPHAGUS

Achalasia

• Loss of ganglion cells with in the myenteric plexus

• Incidence 1-3 /100000 population
• Age usually 25-60
• Both excittaory and inhibitory ganglionic neurons are involved
• Most common symptom – regurgitation
• Pseudoachalasia: carcinoma of distal esophagus or gastric fundus
• Diagnosis:
1. Barium swallow
2. Esophageal manometry
3. Endoscopy only to r/o pseudoachalasia
• Criteria on manometry: impaired LES relaxation and absent esophageal peristalsis
• Therapy:
1. 1, Oral drugs - Nitrates / Calcium Channel blockers/ Sildenafil
2. Botulinum toxin injection
3. 3. Endoscopic and surgical options
a. pneumatic balloon dilatation
b. poem – per oral endoscopic myotomy
• Surgical – Heller's Myotomy

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GASTRIC ULCERS

• Definition: Breaks in mucosal surface < 5 mm with depth to submucosa

• Most common cause – H. pylori infection and NSAID abuse
• H. pylori association: > 90 % duodenal ulcers and 60-70 % gastric ulcers
• Treatment for H pylori – 14 days triple therapy (PPI + amoxycillin or clarithromycin or
tinidazole)
• Quadruple therapy includes Bismuth

ZOLLINGER ELLISON SYNDROME – ZES

• 80 % tumors in gastrinoma triangle

• Duodenal tumors: most common - non pancreatic lesions
• Symptoms: > 90 % peptic ulcers and diarrhea

MENETRIER DISEASE

• Characterised by large tortuous mucosal folds

• Most common in body and fundus
• Histology: foveolar hyperplasia
• Due to over expression of groath factor TGF – beta

IRRITABLE BOWEL SYNDROME

• Diagnositic criteria: Rome IV criteria

• Recurrent abd pain on average once / week in last 3 months associated with > 2 of the
following:
a. a, Related to defecation
b. b. Associated with change in frequency of stool
c. c. Associated with change in form (appearance) of stool
• Newer therapies for IBS
1. Serotonin receptor agonists and antagonists:
▪ Alosteron (5 HT 3 antagonist) for IBS -diarrhea (concern: ischemic colitis)
▪ Tegaserod (5 HT 4 agonist) for IBS – constipation
2. Choliride channel activators
▪ Lubiprostone for IBS – constipation
3. Guanylaste cyclase - C agonist
▪ Linaclotide – IBS -constipation

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DIAGNOSTIC STUIDES IN STEATORRHEA OF VARIOUS ETIOLOGIES

Duodenal
D – Xylose test Schilling test
mucosal biopsy

Chronic Normal 50 % abnormal, Normal

pancreatitis improves on
treatment

Bacterial Normal or modestly Often abnormal, Usually normal

Overgrowth abnormal improves with
Syndromes course of antibiotics

Ileal Disease Normal Abnormal Normal

Celiac Disease Decraesed Normal Abnormal,
probably flat
biopsy

Intestinal Normal Normal Abnormal, dilated

Lymphangiectasia lymphatics

PANCREAS

1. More than 90% of pancreas needs to be damaged before maldigestion of protein and fat
occurs
2. Single best enzyme for diagnosis of pancreatitis is lipase
3. Serum amylase and lipase are elevated in acute pancreatitis within 24 hrs and remain so
for 3-7 days
4. Best initial investigation for diagnosis of pancreatic disorders: contrast enhanced CT
abdomen
5. Endoscopic ultrasound - EUS is inv of choice if we have to diagnose chronic pancreatitis,
take FNAC from pancreatic masses and endoscopic drainage of pseudocyst
6. Cambridge criteria should be used for diagnosis of chronic pancreatitis (at least 5/9 need
to be positive)
7. Test of exocrine function of pancreas - direct stimulation of pancreas - IV infusion of

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 secretin - measurement of duodenal contents (dose of secretin 0.2 mcg/ kg) bolus inj
8. Maximal bicarb conc appears to be the most reproducible once diagnosis of chronic
pancreatitis is being considered, < 80 mmol/l is considered abnormal
9. Decreased elastase activity in stool is an excellent test to detect severe pancreatic
insufficiency
10. Fecal elastase levels values less than 50 mcg /g are definitive for pancreatic insufficiency
11. pancreatic secretion: 1500-3000 ml of iso-osmotic alkaline secretion and contains 20
different enzymes and bicarbonate
12. Release of cholecystokinin (cck) from duodenal and proximal jejunal mucosa (ito cells) is
triggered by gastric acid, essential amino acids and long chain fatty acids
13. Parasympathetic nervous system –affects the enzyme secretion, water and bicarbonate
are dependent on the hormonal effect of secretin and cck
14. Neurologic control of pancreatic secretion-stimulatory neurotransmitters are acetylcholine
and gastric releasing peptides
15. Acute pancreatitis – caused by alcohol and gall stones in 80-90 % cases
16. Hypertriglyciredemia may cause pancreatitis, levels usually > 1000 mg/ dl
17. Autodigestion is currently accepted theory for pancreatitis
18. Diagnosis of acute pancreatitis: •2 out of 3 criteria

a. Pain epigastrium radiating to the back

b. > 3 fold elevation in serum lipase/ amylase

c. Confirmatory findings on cross sectional imaging of pancreas

19. Autoimmune pancreatitis – IgG4 levels help in diagnosis, criteria used for diagnosis is
hisort criteria
20. Annular pancreas-when ventral anlage fails to migrate correctly to make contact with
dorsal anlage, result is a ring of pancreatic tissue encircling the duodenum, treatment is
surgery - retrocolic duodenojejunostomy (procedure of choice)
21. Macroamylasemia- circulating amulase in polymer form and can't be cleared by the kidney,
seen in cirrhosis and NHL

❑ ❑ ❑

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 Respiratory System, ABG & Mechanical Ventilation

Treatment of COPD

• 3 interventions that improve survival:

1. Smoking Cessation
2. LTOT (Long term Oxygen therapy)
3. LVRS (Lung Volume Reduction Surgery)
• Varenicline: Partial agonist at nicotinic receptor – helps in smoking cessation
• Bronchodilators – Muscarinic antagonists are superior to beta-agonists in COPD (due to
airway destruction)
✓ Beta-agonists
o SABA: Albuterol; Terbutaline
o LABA: Olodaterol, Vilanterol, Indacaterol, Arformoterol, Formoterol, Salmeterol
(“Ola VilaINs Are Former Slaves”)
✓ Muscarinic antagonists
o SAMA: Ipratropium
o LAMA: Umeclidinium, Tiotropium, Aclidinium, Glycopyrrolate
(“U-me Tied ACross the GLacier”)
• Roflumilast: PDE4 inhibitor (given in COPD when FEV1 < 50%)
• Long-term macrolide prophylaxis can be beneficial in COPD

Treatment of AECB

• Broncho dilator
• Antibiotics
✓ Pneumococcus, H. influenzae, Moraxella catarrhalis
• Systemic Glucocorticoid
• OXYGEN (sat ≥ 90)

Ventilatory Support

• NIV: pCO2 > 45 (if acute – pH)

• C/I:
✓ Hypotension (septic shock);
✓ Altered sensorium (Hypoxia & Hypercapnia);

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 ✓ Copious secretions;
✓ Facial abn (retrognathia); Extreme obesity
✓ Cardiorespiratory arrest
• IPPV
• The contraindications for NIV (non-invasive ventilation) are indications for invasive
intermittent positive pressure ventilation.

Permissive hypercapnia

• Trying too hard to correct pCO2 too soon can cause volume trauma / barotrauma
• Therefore - Intentional Hypoventilation allowed
• TV 5ml/kg (10ml/kg)
• To limit airway plateau pressure < 35cmH2O
• Tolerated to a pH – 7.15

Drugs causing ILD / Pulm fibrosis

• Methotrexate
• Azathioprine
• Rituximab
• TNF-α blockers
• Nitrofurantoin
• Amiodarone
• Bleomycin
Ritu MetX he was TALL & had Bleached hair - they had Pizza-topping at the Fountain where
Adrone saw them

Pneumothorax with 1 / more of – Hypotension / Tachycardia / Electromechanical Dissociation /

Hypoxia / Cyanosis = TENSION PNEUMOTHORAX … immediate wide-bore needle insertion in 2nd
ICS in mid-clavicular line (with a water seal) – followed by – ICD (intercostal drain)

Light’s criteria:

• Pleural fluid rich in protein / LDH – exudate (Ratios / absolute values)

• If clinically transudate, but identified as exudate by Light’s criteria – SPFPG (serum-
pleural fluid protein gradient) – if > 3.1 = transudate

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TB Effusions

• Usually PRIMARY TB (less common in secondary TB)

• Usually DTH reaction
• Exudate
• Lymphocyte-rich
• High ADA / IFN-gamma
• Usually ZN stain / AR stain –
✓ Unless TB empyema: teeming with TB bacilli

• High ADA pleural fluids: TB, Synpneumonic effusion, Malignant effusion

Pleural Effusion Essentials

• Low glucose: Synpneumonic, TB, RA

• High Cholesterol: RA
• Eosinophils: Drugs (Nitrofurantoin, Bromocriptine, Amiodarone)
• High Amylase: Esophageal rupture; Acute pancreatitis; malignancy
• Left-sided: Esophageal rupture; Acute pancreatitis; post-CABG
• Low mesothelial cells: TB, Synpneumonic effusion, Malignancy

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Mnemonic for the DVT Score:

1 point for all parameters; -

2 for alternatives possible

Mnemonic for the PE score:

3 points each for DVT signs

/ symptoms & alternative
diagnoses less possible;

1.5 points each for HR>100,

prior DVT-PE, Immobility

1 point each for

haemoptysis & cancer

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ACID-BASE DISORDERS

ABG analysis:
1. Assess pH first – Whether it’s obviously acidotic / alkalotic.
2. Check if HCO3 matches with the pH (e.g. an acidotic pH matches with a low HCO3; but an
alkalotic pH does not)
3. Similarly check if the pCO2 matches with the pH (e.g. an acidotic pH matches with a high
pCO2 - not with a low pCO2)
• If the pH matches with the HCO3 – it’s a primary metabolic disorder
✓ e.g. pH 7.55 & HCO3 35 (alkalotic pH & raised HCO3)
✓ pH 7.25 & HCO3 15 (acidotic pH & low HCO3)
• If the pH matches with the pCO2 – it’s a primary respiratory disorder
✓ e.g. pH 7.55 & pCO2 24 (alkalotic pH & low pCO2)
✓ pH 7.25 & pCO2 65 (acidotic pH & high pCO2)

Compensation for the metabolic disorders:

• Metabolic acidosis: pCO2 = (1.5 x HCO3) + 8 ± 2

• Metabolic alkalosis: pCO2 = HCO3 + 15 (but never > 55) – if pCO2 > 55: implies respiratory
acidosis
• EXAMPLE 1: pH 7.15 HCO3 10 pCO2 21
• This is metabolic acidosis (a low pH & a low bicarb tells you that – if this were a primary
respiratory disorder, pH should have been alkalotic)
• The appropriate pCO2 as compensation for this severity of metabolic acidosis
(Kussmaul’s breathing) – should be 21 to 25 (as calculated from the above formula) –
which is what it actually is: therefore, this is partially compensated metabolic acidosis.
• In this very example, if pCO2 were < 21 – it would have meant an added respiratory
alkalosis & if pCO2 were > 25 – it would have meant an added respiratory acidosis

Compensation for respiratory disorders:

• “14-24”
• Change in HCO3 for 10mmHg change in pCO2
• Respiratory acidosis – 1 & 4 meq/l rise in HCO3 for every 10mmHg rise in pCO2 (acute &
chronic resp acidosis, respectively)
• Respiratory alkalosis – 2 & 4 meq/l fall in HCO3 for every 10mmHg fall in pCO2 (acute &
chronic resp alkalosis, respectively)

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EXAMPLE 1: pH 7.22 pCO2 70 HCO3 29

• The CO2 is elevated by 30mmHg (above 40 – which is normal pCO2)

• pH is grossly acidotic – so, it’s an acute disorder (kidneys have not yet fully compensated)
• The appropriate elevation of HCO3 will be 3 mEq/l (1meq for every 10) – so bicarb should
be between 25 to 29: which is what is seen here
• So, this is an acute respiratory acidosis with partial metabolic compensation

EXAMPLE 2: pH 7.34 pCO2 70 HCO3 45

• The CO2 is elevated by 30mmHg (above 40 – which is normal pCO2)

• pH is near normal (N is 7.35 – 7.45): so, it’s a chronic disorder (kidneys have fully
compensated)
• The appropriate elevation of HCO3 will be 12 mEq/l (4meq for every 10) – so bicarb should
be between 34 to 38: but much more bicarb is seen here
• Therefore, this is a chronic respiratory acidosis with a metabolic alkalosis
• High Anion Gap Metabolic Acidosis

Causes of HAGMA

• “Keto Diet Lacks SPICE – KIDs take Marijuana”

• Ketoacidosis – Diabetic, Alc, Starvation
• Lactic Acidosis
• Salicylates
• Pyroglutamic acid (5-oxoproline)
• ICE: antifreeze – ethylene glycol
• Kidney failure
• Methanol (not marijuana!)

HAGMA: Important Points

• SALICYLATES
✓ Resp alkalosis + HAGMA
✓ T/t: Lavage, activated charcoal & IV NaHCO3
• ETHYLENE GLYCOL & METHANOL
✓ OSMOLAR GAP
✓ Can damage CNS & optic nerve
✓ DOC: Fomepizole

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Respiratory Failure

• Type 1 RF: pO2 < 60

• Type 2 RF: Hypercapnic Resp failure (pCO2 > 50)
• Type 3 RF: Peri-operative RF
✓ Reduced FRC after GA
• Type 4 RF: Shock (Resp muscle hypoperfusion)

Indications of MV

• pO2 < 60 (despite fiO2 > 0.5)

• RR > 40
• pCO2 > 50 with pH < 7.25
• Respiratory Muscle Fatigue
✓ Paradox, Tachypnea-Bradypnea, Accessory muscle, Speech (Mono)
• Type 4 RF

Weaning modes:

• SIMV (synchronized intermittent mandatory ventilation)

• PS (pressure support)
• PEEP (positive end expiratory pressure)
• (*CMV, ACMV & PCV are not weaning modes)
✓ CMV – continuous mandatory ventilation
✓ ACMV – assist control mandatory ventilation
✓ PCV – pressure control ventilation

ARDS – ventilation: Low TV, High PEEP (& fluid-restrictive)

❑ ❑ ❑

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 HEMATOLOGY

Vitamin B12

Metabolizes only 2 reactions in the body:

1. Methylmalonyl CoA isomerization (therefore deficiency of B12 → methylmalonicaciduria)

2. Methylation of HC (homocysteine) to Methionine

Dietary sources & transport of B12:

• The MC naturally occurring form of B12 is the ado form: 2-deoxyadenosyl (found in
mitochondria); methylcobalamin is the 2nd MC form – found in plasma & cytoplasm
• The only source of B12 for humans is meat, fish & dairy – so, vegetarians who don’t take
milk – def
• There are two B12 carriers: TC-I & TC-II (each carries 1 molecule of B12)
• While TC-I does not help in B12 entry into tissues, TC-II (synth by liver, macrophages, ileum
& vasc endoth) provides B12 to BM & placenta

Methylfolate trap / THF starvation (when folate administered alone in a combined FA-B12
deficiency):

• Large doses of FA circumvent the methylfolate trap (DHFRase)

• So, dTMP gets formed – the anemia improves
• But the methionine synthesis reaction does not occur – methyl group needed for MYELIN
BASIC PROTEIN not available
✓ Neuropathy progresses & can become irreversible
• In a previously normal person - Complete absence of B12 from the diet – deficiency in 4
years
• Complete absence of folic acid – deficiency in 4 months
• Red cell folate: better marker of folate levels than serum folate

Chronic Gastritis

• Type A (AI: auto-immune)

• Type B (H. pylori)
• AI Gastritis
✓ Parietal cell antibodies (No acid: Bacterial overgrowth)

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 ✓ IF-antibodies (No IF: B12 malabsorption) *anti-IF antibodies are more specific for AI
gastritis
✓ Intestinal Metaplasia (precancerous)

Lead poisoning: Coarse basophilic stippling of RBCs; mild hypochromia (same picture seen in
P5N – pyrimidine 5’ nucleotidase deficiency); increased ZnPP (zinc protoporphyrin) levels are
seen in lead poisoning & IDA

Hemolytic anemia: red cell morphology is variable: e.g. bite / blister cells in G6PD deficiency;
Cabot rings (nuclear remnant); HJ bodies (nuclear remnant); Schistocyte / helmet cell of
MAPHA – pictures needed; size is usually normocytic

Causes of macrocytosis:

• Pregnancy
• MDS – myelodysplastic syndrome
• Alcohol abuse / ALD
• ARV (antiretroviral – Zidovudine)
• Newborn
• AA – aplastic anemia
• RETICULOCYTOSIS

“If PREGNANT MaiD DRINKS, Z NEWBORN has APLASTIC RETICS”

Causes of Hypersegmented Neutrophils:

• Steroid (for ITP)
• Kidney Failure
• 5FU / hydroxyurea therapy

“Many lobed Stars make Kids Feel Happy”

Differential Diagnosis – Patient Snapshots –

In a patient with - Hb: 9 MCV: 104 TLC: 2500 Platelets: 80k

• Hypersegmented polymorphs & hypercellular marrow – B12 deficiency
• Hyposegmented polymorphs & hypercellular marrow; dysplastic appearing precursors -
MDS
• Fatty marrow (HYPOCELLULAR) with normal appearing precursors – AA (aplastic anemia)

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 Thal
Tests IDA AI Sidero A
trait

MCHC NC MCHC V
Smear
Target

S. Iron LOW N - High

TIBC H L N

% Sat LOW N - High

Ferritin L N N - High

TfR H N

• For IDA & AI – the 3 distinguishing features are: TIBC; Ferritin; TfRP (transferrin receptor
protein)
• In thal trait – everything is N except for smear; The only way to definitively diagnose
Thalassemia trait is Hb electrophoresis
• Sideroblastic anemia – it is one of the categories of MDS & can also occur without MDS –
mitochondrial dysfunction causes iron to accumulate in a ring fashion around nucleus of
the erythroblast: RING SIDEROBLAST: combination of HYPOCHROMIC RED CELLS in PB &
EXCESS BM IRON
• If TfR: log (Ferritin) > 1.5: IDA <1.5: AI (Anemia of inflammation)

What does each test measure?

• TIBC: transferrin
• S. iron: circulating Fe bound to Tf
• T. sat: s. iron * 100 / TIBC
• Ferritin: TBI (Total body iron) - *Iron bound to protein in tissue – ferritin / hemosiderin
✓ Better indicator than marrow Fe stain
• RCPP (red cell protoporphyrin)
✓ Protoporphyrin: I-M in heme synthetic pw;
✓ If heme synth impaired – PP accumulates in RBC

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 ✓ Causes: IDA & lead poisoning
• TfRP: Total erythroid marrow mass (RBC: have highest numbers of TfR of any cell in the
body – and TfRP is freely released by RBCs)

AML

APL – acute promyelocytic anemia

• PML – chromosome 15
• RARA – chromosome 17
✓ PML: cell growth, apoptosis
✓ RARA: Nuclear hormone receptor transcription factor
• Fusion product: Suppresses transcription; block at promyelocyte stage
• Treatment: ATRA / ATO: break the fusion protein

NOVEL THERAPIES IN AML

• FLT3 inhibitors: Midostaurin, Sorafenib, Crenolanib

• Hedgehog inhibitor - Glasdegib
• BCL2 inhibitor – Venetoclax

Differential Diagnosis – Patient Snapshots

• Anemia, thrombocytopenia with high TLC: Acute Leukemia (additionally – blasts on PS,
clinically ‘sick’ patient with peri-rectal abscess / bleeding)
• High TLC with all precursor types in PS: CML (additionally, large spleen **massive
splenomegaly is seen in Primary Myelofibrosis)
• All 3 cell lines increased: PRV (also, aquagenic pruritus, JAK2 mutation – V617F)
• Generalized LNs + lymphocytosis: CLL (> 5000 lymphocytes / mm3)

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• Circumscribed LN masses + normal CBC & B-symptoms: NHL/HD
✓ single LN mass – say, axillary – HD
✓ Multiple sites (mediastinal, abdominal) – NHL (& in our country, it could also be TB –
but if they want to you to answer TB, there will be convincing evidence for that
diagnosis – like infiltrate on Xray / positive Mantoux)
• Anemia, infection, hyperglobulinemia, hypercalcemia, azotemia: MM (multiple myeloma)
• Primary myelofibrosis:
✓ Features of EMH – nRBC, teardrop RBCs, myelocytes, promyelocytes
✓ Dry tap (BMA)

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CML

Philadelphia chromosome – t (9;22) – the BCR-ABL adduct forms on chromosome 22

The BCR-ABL has constitutive (unregulated) tyrosine kinase activity
Blasts on PS < 5%
Treatment: TKI (tyrosine kinase inhibitors) – C/I in pregnancy (pregnancy with CML –
leukapheresis & hydroxyurea)
• Imatinib
• Nilotinib, Dasatinib
• Ponatinib T315-I mutation (gatekeeper mutation)

CLL

Treatment of choice: FCR (Fludarabine + Cyclophosphamide + Rituximab)

BTK (Bruton Tyrosine Kinase) inhibitor: Ibrutinib, Acalbrutinib

HD

Regimen of choice: ABVD (Adriamycin, bleomycin, vinblastine, dacarbazine)

❑ ❑ ❑

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 RHEUMATOLOGY

Antibodies

• ANA: Most sensitive marker for SLE (positive in many auto-immune disorders)
• Anti-dsDNA: Most specific marker for SLE; associated with lupus nephritis
• Anti-Ro (mother): Risk for congenital lupus / neonatal heart block
• Anti-cardiolipin; lupus anticoagulant; Beta-2 glycoprotein I, prolonged aPTT: Antiphospholipid
syndrome
• Anti-centromere: limited SSC
• Anti-Scl 70 (anti-topoisomerase I): diffuse SSc
• Anti-CCP (cyclic citrullinated peptide); RA factor: RA
• Anti-histone antibody: Drug-induced lupus
• Drug-Induced Lupus: “Doping, hiding, isolating, promising but procrastinating;
Intermittently Taking My Cycle, pencils & pants”
▪ Methyldopa, Hydralazine, Isoniazid, Chlorpromazine, Procainamide, Interferon, TNF-
alpha blocker, Minocycline, Penicillamine, Phenytoin
• Anti-MDA5: Amyopathic dermatomyositis (no muscle weakness)
• Anti-TIF1: DM with cancer
• Anti-HMGCR: IMNM (Immune mediated necrotizing myopathy)
• Anti-U1 RNP: MCTD (Mixed conn tissue ds) – Poly RAScaL (polymyositis, RA, SSc, Lupus)
• Anti-U3 RNP: SRC (scleroderma renal crisis)
• Treatment of lupus nephritis: Prednisolone + Cyclophosphamide (+ Leuprolide – to preserve
fertility); maintenance with azathioprine / mycophenolate
• Glucocorticoids in SLE: Hemolytic anemia; Severe thrombocytopenia; CNS manifestations;
cardiac lupus; vasculitis;
▪ (no glucocorticoids for dermatitis / arthritis / fatigue in SLE – use HCQS / paracetamol
/ Belimumab)
• Glucocorticoids in pregnancy: Prednisolone is safe for the fetus (HCQS & azathioprine can
also be used in pregnancy with active SLE)
• Genetic signature of SLE: Upregulation of genes induced by IFN

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Hand deformities in RA

Treatment of RA

SPONDYLOARTHROPAHTIES

• Seronegative (i.e., RA factor negative)

• Strong association with HLA-B27

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• SpA features:
▪ Inflammatory back pain (age < 40; early morning & nocturnal; alternating buttock;
improves with activity but not with rest)
▪ Arthritis
▪ Enthesitis (heel) (entheses: site of tendinous attachment to bone – e.g. tendo-calcaneal)
▪ Anterior Uveitis
▪ Dactylitis (sausage digit)
▪ Psoriasis
▪ CD/UC (Crohn’s disease / Ulcerative Colitis)
▪ NSAID – good response
▪ F/H/o SpA
▪ Elevated CRP

Treatment of AS (ankylosing spondylitis):

• Pregnancy is not a c/I to use of biologicals – but the infant should not be given any live
vaccines for 6 months
• Cause of death in AS: Amyloid nephropathy / Respiratory Failure
• Bath index: Index for activity of disease & disability

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Hypouricemic therapy – must be combined with colchicine to prevent paradoxical precipitation
of acute attack

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• Crystals: Rectangular / box-shaped crystals of pseudogout (pink background)
• Negative birefringent crystals of gout (black background)

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Comparison between limited cutaneous systemic sclerosis (lcSSc) & diffuse cutaneous
systemic sclerosis (dcSSc):

Short stubby fingers with nail pitting, healing ulcers – due to distal phalangeal ischemia in SSc

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• AAV: ANCA-associated Vasculitis
• WG – Wegener’s granulomatosis (Granulomatosis with polyangiitis): cANCA
• Microscopic Polyangiitis: pANCA
• CSS – Churg Strauss Syndrome (Eosinophilic Granulomatosis with polyangiitis): pANCA

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IBM – Inclusion Body Myositis

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 INFECTIOUS DISEASES

SIRS – systemic inflammatory response syndrome (TPRL – temperature, pulse, respiration,

leukocytes)

• SIRS: T >38 or <36; RR > 20/min; HR > 90/min; TLC >12k or <4k or >10% bands
• In the 2003 definition of sepsis (SEPSIS-2), SIRS criteria were used in the criteria for
sepsis. (they were subsequently excluded, since SIRS can occur without an infection)
• In the 2016 definition of sepsis (SEPSIS-3): SIRS was replaced by SOFA (sequential organ
failure assessment, or sepsis-related organ failure assessment) score: the SOFA score
looks at all major organ systems – heart, lung, liver, kidney, nervous system, BP (& even
the dose of vasopressor medication) {suspected (or documented) infection & an acute
increase in >2 sepsis-related organ failure assessment (SOFA) points}
• qSOFA (quick SOFA): “if she’s breathing fast, feeling nervous & feeling low – lay her down
quickly on the SOFA”
✓ RR, Altered mentation, Low systolic BP
• NEWS (National Early Warning Score): “watch NEWS sitting on TOP of SOFA”
• TOP (temperature, oxygen sat, pulse rate) + qSOFA

MICROBE HOST RECEPTOR

Influenza virus Sialic acid

HIV CD4 (CCR5, CXCR4)

EBV CD21

Neisseria CD46

Pseudomonas CFTR

Bordetella, Legionella, CR3

M. tuberculosis

P. vivax Duffy antigen

Also, For P. falciparum: Glycophorin A & for SARS-CoV2: ACE-2

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Antibiotic prophylaxis against Meningococcemia: Ceftriaxone / Ciprofloxacin / Ofloxacin
(Rifampicin not the preferred drug anymore – 20% failures & needs 4 doses – poor
compliance)

Needed for:

1. Close contacts (kissing & household contacts)

2. Health-care workers (those who will come in contact with respiratory secretions)

Additional VACCINE (besides the antibiotic)

a. To provide protection beyond the duration of antibiotic therapy

b. Mass vaccine programs: useful to contain outbreaks in educational & other closed
communities (**Mass antibiotic prophylaxis not useful)

Meningococcal Vaccines

• POLYSACCHARIDE: first vaccine; now used only in underdeveloped world – protective for
max 10 years; booster not useful
• CONJUGATE: Conjugated to diphtheria / tetanus toxoid – used in most of the world now
• SUBCAPSULAR ANTIGENS – to provide a vaccine that covers B serogroup also (B
polysaccharide not recognized as foreign – since it’s also found on neural cells)

FOOD POISONING & INCUBATION PERIODS:

• 1-6 hours: Staph aureus & Bacillus cereus (fried rice); Capsaicin (nonbacterial cause)
• 8-16 hours: Clostridium perfringens & Bacillus cereus
✓ *Bacillus cereus can cause 2 forms of illness – emetic & diarrheal
• >16 hours: Vibrio, ETEC, EHEC

ORAL LESIONS IN HIV

Oral candidiasis – white, cheesy,

adherent, painless

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 ORAL HAIRY LEUKOPLAKIA: Lateral
border of tongue, frond-like (like ferns -
plants); NOT premalignant; associated
with EBV

KAPOSI’s sarcoma: Multicentric

vascular nodules (oral mucosa / skin)

Oral lichen planus – mild white

reticulate eruption of buccal mucosa

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Diphtheria:

Bull-Neck Pseudomembrane

HIV-TB coinfection:

• Disease varies as a function of the CD4 count:

CD4 > 200 CD4 < 200

Typical – pulmonary, upper lobe, cavitary Atypical: extrapulmonary, lower lobe,

no cavities

Sputum + Sputum -

Effusion, LN (hilar) - Effusion, LN (hilar) +

Fever, weight loss + Fever, weight loss -

Mantoux: more NPV Mantoux: poor NPV

ATT in the HIV-positive patient:

Treatment in HIV is also the same as for HIV-negative persons

• IRIS
✓ CD4 > 50: ATT → 2 weeks → cART
✓ CD4 < 50: ATT + cART together

HIV exposure to HCW’s (health care workers)

• Fluids to which universal precautions apply: Blood, any body fluid grossly contaminated
with blood, Semen, Vaginal Secretions, Pleural fluid, Peritoneal fluid, Pericardial fluid,
Synovial fluid, CSF, Amniotic fluid
• Increased risk of transmission with:
✓ Needle placed in vein / artery

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 ✓ High viral load of patient
✓ Patient not on cART
✓ Deep injury
✓ Terminal ill patient
• Risk of transmission: 0.3% (without PEP – postexposure prophylaxis)
• Preferred regimen: Tenofovir + Emtri + Dolutegravir * 4 weeks

JAPANESE ENCEPHALITIS

• Most important cause of encephalitis in Asia

• Only 1% of infections are symptomatic – of the symptomatic cases, 25% mortality rate
• Transmitted by Culex tritaeniorhynchus & Culex vishnui
• Usually exists as an infection of wading (water) birds
• Pigs / horses – amplifier hosts – vaccination of these animals prevents outbreaks
• Man: Incidental / dead-end host (virus levels in blood of infected human never high enough
to infect a feeding mosquito)

POST-MEASLES NEUROLOGICAL COMPLICATIONS:

1. Post-measles encephalomyelitis – 2 weeks after rash – auto-immune disease (virus

undetectable)
2. MIBE (Measles inclusion body encephalitis) – after few months – due to persistent viral
infection; fatal
3. SSPE (subacute sclerosing panencephalitis) – after a latent period of few years –
personality change, decline in school performance seizures, ataxia – quadriparesis – due
to a nonpermissive (non-replicative) infection by measles virus; Bursts of high voltage
sharp, slow waves q3-8 secs; Elevated gamma globulin level in CSF (acellular, mild
elevation of protein); CSF anti-measles antibody is invariably elevated

TREATMENT OF ASPERGILLOSIS:

INDICATION PRIMARY TREATMENT

Invasive Voriconazole
Isavuconazole

Prophylaxis Posaconazole

Aspergilloma Surgery

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 INDICATION PRIMARY TREATMENT

Chronic Pulmonary disease Itraconazole

ABPA Itraconazole

BIOTERRORISM

Category A agents

• Variola major (smallpox)

• Bacillus anthracis (anthrax)
• Yersinia pestis (plague)
• Clostridium botulinum toxin (botulism)
• Francisela tularensis (tularemia)
• Filoviruses (Ebola, Marburg)
• Arenaviruses (Lassa, Junin and related viruses)

“Small ants play in bottle till the arena fils with mud”

Category agents are highest priority – easy to grow in large numbers, easy to spread; person-
to-person transmission; sturdy (difficult to destroy) organism

COVID19 (due to SARS-CoV2; ssRNA virus)

• Host receptor protein: ACE2 (viral spike protein binds here)

• Biosafety level 2 (also Staph. Aureus)
✓ BSL3: M. tuberculosis
✓ BSL4: Marburg virus, Ebola virus, Nipah virus
✓ (BSL1 is lowest risk microbes;, BSL4 is highest risk microbes)
• Tests for COVID19
✓ Direct detection tests
o RT-PCR – gold-standard (target is nucleocapsid gene & human RNAseP)
o Antigen (nucleocapsid & spike protein)
✓ Antibody tests (against the above mentioned antigens)
o 1-3 weeks: appear (therefore not for current infection)
o For surveillance of communities; not useful for the individual
o For identifying potential donors of convalescent plasma

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 RT-PCR Tests Antigen Tests
Intended Use Detect current infection Detect current infection

Analyte Detected Viral RNA Viral Antigens

Specimen Type(s) Nasal Swab, Sputum, Saliva Nasal Swab

Sensitivity High Moderate

Specificity High High
Test Complexity Varies Relatively easy to use

Authorized for Use at Most devices are not, some Yes

the Point-of-Care devices are

Turnaround Time Range from 15 minutes to >2 Approximately 15 minutes

days
Cost/Test Moderate Low

Severity of COVID19:

• Mild: URT manifestations / mild systemic manifestations (anosmia / diarrhea / fever)

• Moderate: Pneumonia without resp distress
• Severe: Pneumonia with RR > 30 or sPO2 < 90
• Critical: ARDS / Organ dysfunction / Shock

Managing Severe COVID:

• Same principles as for ARDS treatment:

• Low TV
• Fluid restrictive strategy
• No hypotonic fluids, no starches
• Prone ventilation if pO2 / fiO2 ratio < 150 (**Normal pO2/fiO2 = 500)
• Permissive hypercapnia
• ECMO if pO2 / fiO2 < 80 * 6 hours
• Keep MAP > 65 & lactate < 2

OXYGEN THERAPY

1. Nasal cannula: Delivers 24% oxygen @ 1L/min (with every increment of 1L/min – add 4%;
cannot deliver more than 40% oxygen)

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2. High-flow nasal cannula (can deliver 100% oxygen @ 60 L/min – when tapering down, when
spO2 maintained with 50% oxygen @ 20L/min – switch to usual nasal cannula)
3. Venturi mask – can deliver 60% oxygen (depending on the attached venturi valve)
4. NRBM – Non-rebreathing mask (gas flow needs to be higher than patient’s minute volume
– otherwise will work as a rebreathing mask) – can deliver 80% oxygen

Approved drugs in COVID19:

• Remdesivir & Glucocorticoids – for hospitalized patients

❑ ❑ ❑

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 ENDOCRINOLOGY

PITUITARY

ANTERIOR PITUITARY

Pituitary Apoplexy
• Acute pituitary hemorrhage
• Endocrine EMERGENCY
✓ Severe hypoglycemia
✓ Shock
• Predisposition: Pregnancy / Adenoma / Diabetes
• Severe headache with meningeal irritation
✓ Visual: ophthalmoplegia / field def
• Treatment:
✓ High dose GC
✓ URGENT Surgery: Visual loss / LOC / CN palsy

All pituitary hormones are secreted in a PULSATILE manner

• Therefore they have peak levels & low levels

• Therefore, SINGLE measurements can be misleading (except Prl & TSH – long t1/2) Q
• Peak levels
✓ Prolactin: REM Sleep; 4-6AM
✓ GH: Sleep-onset (within 1 hour) - SWS
✓ ACTH: 6AM
✓ LH: Mid-cycle (12 h pre-ovulation)
FSH: Mid-follicular phase

PROLACTIN: ESSENTIALS

• Regulation: TONIC INHIBITION BY DA

• Lactotropes & somatotropes: common precursor
✓ Therefore tumors often co-secrete: Prl & GH

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Causes of hyperprolactinemia:

• TIPSY Met Nancy – started to STALK her – Nancy LaCKeD Sleep – was Stressed & ‘tired’ :
• Antipsychotic, metoclop; pregnancy; pit stalk; Lactation; Kidney disease (CKD); Sleep;
Stress; Hypothyroid

In a patient with panhypopituitarism, mineralocorticoid replacement is not required since

Aldosterone production (from zona glomerulosa) is under the control of Angiotensin (not
ACTH)

POSTERIOR PITUITARY

SIADH

✓ Physiological ADH secretion:

✓ Hyperosmolality / very low blood volume
✓ ‘Inappropriate’ ADH (or SIADH)
✓ Uosm > 300 Posm: Low
✓ Urine Na > 20 Serum sodium: Low
✓ Neurologic: Tumor / Stroke / Trauma
✓ Pulmonary: Pneumonia / IPPV
✓ Malignancies: SCLC / Squamous cell cancer of HNF
✓ Drugs: Tricyclics / Desmopressin

• Tolvaptan is a V2 receptor antagonist

• Renal cAMP production is inhibited by Tolvaptan (it’s action in ADPKD)
• A very dilute urine will be produced – therefore urine osmolality will be low

DI (DIABETES INSIPIDUS)

• The posterior pituitary has MC (magnocellular) neurons which produce oxytocin &
Parvocellular neurons which produce AVP
• AVP’s primary action is increased water reabsorption by PRINCIPAL CELLS of collecting
duct (**Thirst is regulated by Posm – AVP indirectly stimulates thirst)
• Plasma osmolality is 280-295: The threshold / set point for AVP is 280mOsm/L (or a Na
of 135). The thirst osmostat is set at 3% higher than the AVP setpoint (this ensures that
polydipsia & dilution of plasma doesn’t occur until Posm exceeds the defensive capacity
of AVP)

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• In absence of AVP – the distal tubule & medullary CD are impermeable to water – so a
very dilute urine will be produced
Drugs causing NDI (Nephrogenic Diabetes Insipidus)
• “LeMe C If i AM-IN”
• Lithium, demeclocycline, Cisplatin, Rifampin, Amphotericin B & aminoglycosides

THYROID

Jod Basedow Disease (Iodine-induced hyperthyroidism)

✓ If patients with Nodular goitres / autonomous thyroid nodules / asymptomatic

Grave’s disease
✓ Take excessive iodine
✓ Sources: iodinated radio-contrast, food (kelp), amiodarone

Wolff-Chaikoff Effect

✓ ↑ Inorganic iodide in the thyroid cell

o Inhibitory effect of IODINE ORGANIFICATION
o Thyroid hormone production is reduced

Thyrotoxicosis factitia

✓ Excessive intake of thyroxine (psychiatric / inadvertent)

✓ Low Tg: CLINCHING EVIDENCE
✓ RAIU – also low
✓ Severe thyrotoxicosis (but INFILTRATIVE ophthalmopathy never)

deQuervain’s thyroiditis

✓ After a Viral URI

✓ Aka Granulomatous / Post-viral thyroiditis
✓ Enlarged & very painful thyroid
✓ Thyrotoxicosis in 50% * 6 weeks
✓ ESR > 100
✓ Tg elevated
✓ RAIU decreased in thyrotoxic phase
✓ Hypothyroidism (with a high RAIU) for a year thereafter
✓ Treatment:

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 o NSAID / Aspirin
o Prednisolone for severe local symptoms

Hashimoto’s thyroiditis

✓ Aka Silent / Lymphocytic / AI thyroiditis

✓ Painless thyroid enlargement
✓ Normal ESR
✓ Anti-TPO antibodies
✓ RAIU decreased in thyrotoxic phase
✓ Hypothyroidism (with a high RAIU) for a year thereafter
✓ Recovery is the rule
✓ No steroids needed
• Hypothyroidism with a low TSH:
• If the TSH level increased in response to TRH administration, that implies a normal
secretion from the pituitary.
• The deficiency / disease is in the hypothalamus
• When the disease is in the thyroid – it’s called PRIMARY hypothyroidism
• When the ds is either in pituitary / hypothalamus it’s called CENTRAL hypothyroidism
• CENTRAL is SECONDARY (when pituitary is diseased) or TERTIARY (when hypothal is
diseased)

Myxedema Coma

✓ Usually elderly
✓ Miss their meds / newly diagnosed
✓ Precipitated by: Drugs / conditions that cause hypoxia-hypercapnia
✓ E.g. Sedatives / Pneumonia / Sepsis
✓ Altered sensorium
✓ Seizure
✓ Hypothermia
✓ Thyroxine, Hydrocortisone, Antibiotic;
✓ Re-warming – if Temp < 300C

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Transient Thyrotoxicosis of pregnancy

• Seen with conditions of hCG excess - multiple pregnancy / hyperemesis gravidarum /

molar pregnancy
• Self-limiting
• Differentiate from Grave’s by TRAB (TSH-receptor antibodies)

Thyroid physiology in pregnancy

• hCG: stimulates the TSH-R (T1)

✓ Therefore fall in TSH (till 20 weeks)
• Estrogen: Rise in TBG (T1 – T3)
• If an autoimmune thyroid disease is present, it can worsen or improve
• New autoimmune thyroid disease can begin
• Increased thyroid hormone metabolism by placenta
• Increased urinary iodide excretion (can cause hypothyroidism)

LABS & POSOLOGY: Pregnancy & Thyroid disease

• TSH levels fall during first 20 weeks – then rise

• Total T4 & T3 levels are 1.5 x higher (throughout pregnancy)
• Free T4 decreases as gestation progresses – T3 levels are lower than LLN
• Subclinical hypothyroidism in 2%
• Overt hypothyroidism in 0.2%
• Thyroxine dose requirement increases by 50%

Hyperthyroidism in pregnancy

• PTU in T1; Methimazole to be re-started in T2

TAO: Thyroid associated ophthalmopathy

• 90% are hyperthyroid

• 10% are euthyroid / hypothyroid (TAO)
• 10% are unilateral (typically bilateral & symmetrical)
• LID RETRACTION – (staring appearance) → due to sympathetic overactivity
• Grave’s: Enlarged EOM – on US / CT
• Early: Grittiness / Tearing
• Sclera can be seen between lower eyelid & lower border of iris

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GO (Grave’s Orbitopathy)

• Proptosis can cause CORNEAL DAMAGE (exposure – failure of closure)

• Lagophthalmos
✓ Incomplete eyelid closure
• Von Graefe sign
✓ Eyelid lags behind eyeball movement on downgaze
• Periorbital edema, scleral injection & chemosis: common
• Eye movement restriction: esp with upward gaze
• Antithyroid DOC in thyrotoxic crisis: PTU (followed by SSKI – Wolff Chaikoff effect)

ENDOCRINE TUMORS

• MC site for gastrinoma: D1 (first part of duodenum)

• Diagnostic for Gastrinoma / ZES (Zollinger Ellison Syndrome): ‘2 – 1000 – 15’
✓ Fasting gastric pH < 2
✓ Fasting serum gastrin > 1000 pg/ml
✓ BAO (basal acid output) > 15 meq/hour
• Imaging modality:
• PET with Ga-DOTATATE (or a DOTATOC scan) is the new gold standard for all patients
with a suspected NET

MEN1 (Wermer Syndrome)

Type (Chromosome) Tumors (Penetrance)

MEN1 (11q) Parathyroid (90%)

GI / Pancreas
(30-70%)
MC: Gastrinoma

Pituitary (Anterior)
(15-50%)
MC: Prolactinoma

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MEN2A

• Aka SIPPLE syndrome

• MTC
• Hyperparathyroidism
• Pheochromocytomas
• GLP1-RA absolutely C/I

MEN2B (MEN3)

• AD (familial)
• ret protooncogene
• Mucosal neuromas
• Marfanoid habitus
• Delayed puberty
• MTC (Aggressive & Early)

NETs (GIT / Pancreas / Lung / Thyroid)

• GEP-NETs: CARCINOIDS
• Divided into Foregut / Midgut / Hindgut
• In the foregut, MC location is: Respiratory system
• In the midgut, MC location is: Ileum
• MC GI-NET with METS: Pancreas

Carcinoid syndrome

✓ Most likely with:

✓ Midgut / Ovarian / Testicular
✓ Least likely with: Appendiceal
• Single most important prognostic factor for Carcinoid: Liver mets

NET diagnosis

24-h Urinary 5-HIAA (100% specific)

*Platelet serotonin: more sensitive (but not available)
Chromogranin A: tumor bulk
Carcinoid syndrome: Flushing, Diarrhea & Pellagra (tryptophan diverted to Serotonin synth
instead of Niacin); more common with liver mets

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PHEOCHROMOCYTOMA

• Classic triad: Headache, Sweating & Palpitations

• HT: Episodic / Sustained
• Most sensitive biochemical test: Fractionated / free metanephrines (urine & plasma)
• Most specific biochemical test: Total urinary metanephrines
• Most sensitive imaging: CT / MRI
• Most specific imaging: MIBG & Fluoro-DOPA PET/CT
• MEN-2A, MEN-2B, VHL syndrome, NF-1
• Resection

Prior to resection: First start Phenoxybenzamine (establish alpha blockade) – after a week,
add beta blocker

HYPERCALCEMIA TREATMENT

• Initial TOC: Hydration (Saline bolus)

• Hypercalcemia of malignancy: Bisphosphonate (Calcitonin as adjunct)
• Emergency (NDI-AKI):
✓ Calcium > 14.8
✓ CaSR activation in CD
✓ Dialysis against a low calcium dialysate
• DENOSUMAB – RANKL monoclonal ab
✓ Bisphosphonate-refractory cases
• Hypercalcemia due to Vitamin D toxicity can be corrected by hydrocortisone -
glucocorticoid inhibits 1-alpha-hydroxylase: the enzyme that activates 25 hydroxy-
cholecalciferol to 1,25 (dihydroxy) cholecalciferol
• (Once vitamin D is not activated to calcitriol – it doesn’t increase calcium absorption
from the GIT – calcium levels decrease)

ADRENAL INSUFFICIENCY

• PRIMARY: Adrenal disease (ADDISON’s disease)

• SECONDARY: Hypothalamic or Pituitary disease

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 PRIMARY SECONDARY

Both GC & MC lost Only GC lost

Hyponatremia & Hyperkalemia Hyponatremia

Pigmentation Pale skin

HPA-axis suppression (IATROGENIC) Combination of

Cushingoid features &
Medication abruptly stopped
Adrenal insufficiency

• ACUTE – ADRENAL CRISIS

✓ HYPOVOLEMIC SHOCK
✓ Severe Intercurrent Illness – T-storm; adrenal hemorrhage with a metastasis
✓ DIAGNOSIS of Adrenal Insufficiency
✓ Short Synacthen test
✓ Cortiso should increase in response to synacthen injection
✓ Treatment: Hydrocortisone
• At dose of hydrocortisone > 50mg / day, it provides sufficient stimulation of
mineralocorticoid receptor activation (additional fludrocortisone not needed)

MINERALOCORTICOID EXCESS

• MC cause: B/L micronodular hyperplasia

• Conn Syndrome: Adrenal adenoma
• HYPOKALEMIA
• ECFV expansion (due to Na retention)
• HYPOKALEMIC HYPERTENSION
• Aldosterone excess + MACE (mild autonomous cortisol excess)= CONNSHING SYNDROME
• DIAGNOSIS: Measure plasma renin & aldosterone
✓ ARR – High aldosterone-renin ratio
Imaging modality of choice: Unenhanced CT of Adrenals

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METABOLIC SYNDROME IN SOUTH ASIANS

• Fasting TG > 150mg/dL

• HDL < 40 (men) or < 50 (women)
Or
• BP > 130/85 {or medication}
Medication
• FPG > 100 {or medication}
• WC 90 (men); >80 (women)

CUSHING’s SYNDROME

CUSHING’s SYNDROME

• Chronic exposure to glucocorticoid (any etiology)

✓ ACTH-dependent
o Pituitary adenoma, Ectopic ACTH (tumors)
✓ ACTH-independent
o Adrenal hyperplasia / adenoma / carcinoma
✓ Iatrogenic
• Cushing’s disease: pituitary adenoma
• Ectopic ACTH: Lung carcinoid (commonest cause)

CUSHING’s SYNDROME: CLINCAL FEATURES

• GLUCONEOGENESIS
• LIPOLYSIS
• PROTEIN CATABOLISM
• Overcomes 11 ß HSD2
✓ Diastolic HT
✓ Hypokalemia
✓ Edema
• Obesity, T2DM / IGT, Hirsutism, Depression, Osteoporosis
• Gonadotropin suppression: Hypogonadism & Amenorrhea
• Skin fragility
• Striae
• Fat redistribution
• Proximal myopathy
• Hypercoagulability (DVT/PE)

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• CVD
• Leukocytosis, Lymphopenia, Eosinopenia
• Ectopic ACTH
✓ More pigmentation
✓ Rapidly progressive
✓ Severe myopathy
✓ HT, hypokalemic alkalosis, IGT
✓ Edema

APS-1

• Aka APECED
• Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy
• Infancy
• 2/3 needed for diagnosis:
✓ Mucocutaneous candidiasis
✓ Addison’s disease
✓ Hypoparathyroidism
✓ Hypogonadism
✓ Grave’s or AI thyroiditis
✓ Type 1DM

APS-2 / SCHMIDT SYNDROME:

• Addison’s disease
• Graves’ disease or AI thyroiditis (either of the 2 AI thyroid illnesses can occur)
• Type 1 DM
• Primary hypogonadism
2 or more of these are reqd to make a diagnosis of APS-2

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DIABETIC KETOACIDOSIS

DKA HHS

T1DM & T2DM T2DM

Glucose 250 – 600 600 - 1200

P(osm) 300 - 320 330 – 380

pH 6.8 - 7.3 > 7.3

Na 125-135 135 - 145

FLUIDS IN DKA

• 0.9% saline @ 20ml/kg/hour * 3 hours

• 0.45% saline @ 250ml/hour

• When glucose < 250,

✓ 5% glucose & 0.45% saline @ 250ml/hour

INSULIN IN DKA

• Bolus: 0.1 U/kg - IV

• Infusion: 0.1U/kg/hour
• Dose varied as per response
• Sugar checked q1hour
• Glucose target achieved (150-200)
• ACIDOSIS resolved
• Patient starts eating

INSULIN EFFECT:

• 3 factories closed,
• 2 products utilized & 1 basic regenerated:
• The liver’s factory of sugar & ketones is shut down.
• Fat breakdown stops.

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• Sugar & KB use increased.
• Bicarb regeneration is increased.

POTASSIUM IN DKA

• K < 3.5: 40-80mEq/hour

• K 3.5 – 5.2: 10mEq/hour
• K > 5.2: no replacement needed
• K < 3.3: no insulin till K > 3.5

DIABETIC RETINOPATHY

• NPDR: @ 10years
✓ Retinal ischemia
• Proliferative DR
✓ Neovascularization in response to hypoxemia
✓ Near optic nerve / macula
✓ Rupture easily
• Intensive glycemic control is the cornerstone of prevention
• BP control
• Fenofibrate
• Laser photocoagulation
• Anti-VEGF (ocular injection) for PDR
• A/w retinopathy
• Albuminuria @ 10 years
✓ CKD, CVD: both increased with albuminuria
• DKD: GFR < 60 ml/min/1.73m2
• Type 4 RTA – hyporeninemic hypoaldosteronism
• Radiocontrast nephropathy: increased risk – stop Metformin for 48 hours; hydrate well
• Glycemic control
• BP control
• ACEI / ARB
• DSPN – distal symmetric polyneuropathy
• Annual screening for DSPN
✓ 5 years after diagnosis of T1DM
✓ At the time of diagnosis if T2DM

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• Autonomic neuropathy – Hypoglycemia unawareness
• MC CN: 3rd (ptosis & ophthalmoplegia, with preserved pupillary reaction to light)
• Prevention: Glycemic control

MACROVASCULAR COMPLICATIONS OF DM

• CVD – Cardiovascular disease

✓ IHD
✓ Cerebrovascular disease
✓ Peripheral arterial ds
✓ CV mortality
• Benefit of intensive glycemic control – questionable; could be detrimental
• Liraglutide, Semaglutide Drugs with proven CV benefit
• Empagliflozin, Canagliflozin – reduce CV events

❑ ❑ ❑

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 LMR NEPHROLOGY

• Prerenal AKI (more likely than intrinsic renal AKI / ATN):

1. Good UOP (urine output) in response to a fluid bolus – Gold standard for distinction
2. Disproportionate elevation of urea (compared to creatinine)
3. Uosm (urine osmolality) > 500
4. FeNa < 1%
• FeNa: fraction of filtered Na which is not reabsorbed by tubules (& therefore, excreted in
urine)
• PRERENAL: avid tubular reabsorption of Na → FeNa < 1% (Tubular function is N in prerenal)
• In Ischemic AKI / ATN: FeNa often >2% (because of the tubular injury, Na cannot be
reabsorbed)

**Sepsis, Rhabdomyolysis, Contrast: ATN with FeNa <1%**

• Calculation of FeNa: UNa x SCl-/SNa x UCl-

• Predictors of poor prognosis in AKI:
1. UOP < 200 ml over 2 hours after a bolus of furosemide
2. Large number of epithelial cells on urinalysis
3. Large number of granular casts on urinalysis
4. Oliguria (preserved UOP is a marker of good prognosis)
• NEW BIOMARKERS OF KIDNEY FUNCTION:

1. KIM-1: Transmembrane protein on PCT cells; enables phagocytosis of tubular debris;

appears in urine shortly after ischemic / toxic injury

2. NGAL: (Siderocalin / Lipocalin 2) – Binds to iron siderophore complexes & protects PCT;
increases after ischemic injury; can differentiate prerenal from intrinsic AKI

3. IGFBP7 & TIMP-2: cell-cycle arrest biomarkers: they predict severe AKI in critically ill
patients (insulin-like growth factor binding protein 7 & tissue inhibitor of
metalloproteinase-2)

4. Cystatin C is a serine protease that has a short half-life in serum & is freely filtered
at the glomerulus – then reabsorbed by tubules & degraded – it’s absent in normal
urine – therefore, it might be a good marker for tubular injury. And because of its

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 short half-life its levels change faster than those of creatinine – and will therefore
signify an AKI earlier than creatinine.

• **BUN & S. creatinine are functional biomarkers & NOT TISSUE INJURY MARKERS – so
they will not reflect renal parenchymal damage for a long time: they will LAG BEHIND GFR
(when serum creatinine is used to calculate GFR – that calculation does not reflect the
true GFR at that instant)

Urine casts:

• Muddy brown epithelial casts are indicative of an acute process – the epithelial cells can
still be identified – this implies that it is an acute process.
• Broad waxy casts – imply tubule dilatation & degenerated casts – these are seen in CKD
• RBC casts: acute GN
• WBC casts: acute interstitial nephritis & acute pyelonephritis
• Hyaline casts: normal urine

RHABDOMYOLYSIS

• Triad: muscle pain (esp proximal muscles & calves), muscle weakness & dark brown urine.
• Myoglobin is a monomer & is not protein bound – is easily filtered across the glomerulus
– and forms a PPT with THprotein – and these casts cause tubular obstruction & AKI
• Myoglobin is a heme-containing protein – therefore the dipstick will reveal heme-positivity.
(*If dipstick positive for heme & few or no RBC’s – either rhabdomyolysis / hemolysis)
• CK levels can be elevated upto a 100,000 also; Uric acid elevated
• Hyperphosphatemia, Hyperkalemia, Hyperuricemia & secondary hypocalcemia (same as
tumor lysis syndrome – distinction by CK enzyme levels)
• Treatment –
▪ Aggressive hydration (upto 10 L of fluids per day)
▪ Desired urine flow of 200-300ml/hour (diuretic may be added to achieve this)
▪ Alkalinization helps: administration of NaHCO3 in 0.45% saline – this prevents cast
formation & tubular injury – but it can worsen hypocalcemia

Diet in AKI:

✓ Energy: 20-30kcal/kg/day

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✓ Protein:
✓ Protein intake:
✓ No hyper catabolism & no haemodialysis: 0.8-1 g/kg/day
✓ Hemodialysis: 1 – 1.5 g/kg/day
✓ Hypercatab & HD: 1.7 g/kg/day
• Part of kidney most susceptible to ischemia: Outer medulla
• Part of kidney with the lowest pO2: Inner medulla (papillary tip)
• Maximum oxygen consumed by the kidney: by Na-K ATPase
• Diseases that preferentially affect distal nephron: Sickle cell anemia, Obstructive Uropathy;
Diabetes
• Pulmonary Renal Syndromes: AAV (ANCA-associated vasculitis; Goodpasture syndrome;
Henoch Schonlein Purpura; Essential Mixed Cryoglobulinemia) (also, Weil’s syndrome of
Leptospirosis & Hantavirus – HFRS)
• Renal disorders preceded by a URI: PSGN, IgA nephropathy, HSP,

CKD

• CKD (as opposed to AKI) – favoured by the presence of:

1. Anemia
2. Shrunken kidneys
3. Bone disease (secondary hyperparathyroidism)

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 **CKD with large (or non-shrunken) kidneys: Diabetes, Amyloidosis, Multiple Myeloma,
Polycystic Kidney disease, HIVAN (HIV associated nephropathy)

• Stopping CKD progression:

1. Administer alkali when bicarb < 20 (alkali stops the protein catabolism due to acidosis)
2. Control BP (& therefore reduce intraglomerular hypertension)
3. Control proteinuria – ACEI / ARB
• Bone disease in CKD
1. Osteitis fibrosa cystica (OFC): due to high PTH
2. Adynamic bone disease: due to low PTH
3. Brown tumors (haemorrhagic cysts of OFC)
4. Osteomalacia – due to deficient 1-alpha hydroxylation of Vitamin D

• The best treatment of secondary hyperparathyroidism & osteitis fibrosa is PREVENTION

(this is because once the PTH gland becomes very large – it’s very tough to control the
disease)

Calcitriol –

• inhibits PTH synthesis directly (in the PTH gland)

• Corrects hypocalcemia – this also inhibits PTH production

CINACALCET:

• Acts thru CaSR – to enhance sensitivity of PTH gland to the suppressive effect of calcium
– therefore reduces PTH & calcium concentrations

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0.8 g/kg/day protein if not on dialysis; 1.2 if on dialysis

• Hyperphosphatemia is associated with increased CV mortality

➢ Low P diet – No Dairy products (milk & ice cream), colas / E-drinks / processed foods
(processed cheese / fast-food) – so, basically, boring home cooked fresh food is good.
• Phosphate binders: Given with food (to bind the P present in food)
➢ Calcium-based: Calcium acetate / Ca carbonate – s/e: hypercalcemia
➢ Non-calcium containing: sevelamer / lanthanum
• MC cause of death in CKD: CVD (Cardiovascular disease)
• CV death in CKD is more commonly dt HF & sudden cardiac death (rather than AMI –
although that occurs as well)
• RISK FACTORS FOR CVD can be divided into traditional & CKD-related risk factors:
o Traditional risk factors exist like they do for all individuals – (“high pressure, sugar,
fats & homocysteine”) - HT, Dyslipidaemia, sympathetic overactivity,
hyperhomocystinemia, DM;
o And then there are risk factors that are because of the CKD: These are – Anemia,
hyperphosphatemia, hyperparathyroidism, increased FGF-23, sleep apnea, generalized
inflammation; the high CO state dt AV fistula (for HD)

Fetuin

• Is a protein which binds Ca & P – and inhibits their crystallization in blood

• Therefore, a decreased fetuin concentration allows precipitation of calcium-phosphate
• Uremia is a/w low fetuin levels
• In patients on HD: repeated episodes of hypotension/hypovolemia cause coronary ischemia
& repeatedly stun the myocardium

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• Indications for HD: Volume, potassium, acid, uremia
o Vol overload (unresponsive to diuretics OR pulmonary edema); intractable
hyperkalemia (not responding to glucose insulin, K-binders, beta-agonist nebulization);
acidosis; uremic symptoms (pericardial rub, encephalopathy, uremic bleeding); diuretic
resistance with intractable edema & hypertension

Post-renal transplant infections:

➢ Peri-transplant: Wound infection; UTI; Candidiasis; Herpesvirus

➢ Early post-transplant: Pneumocystis; Hepatitis B & C; CMV; Legionella; Listeria
➢ Late post-transplant: Aspergillosis; Hepatitis B & C; BK virus (polyoma virus); Herpes
Zoster; Nocardia

RENAL TUBULAR ACIDOSIS

Type 2: Proximal RTA All 3 are NAGMA (non-anion gap acidosis);

Types 1 & 2 are hypokalemic;

Type 1: classic distal RTA
Type 4 is hyperkalemic
Type 4: generalized distal RTA

Type 2 (Proximal RTA)

• PATHOPHYSIOLOGY: Filtered HCO3-: 80% reabs by PCT; PCT disorder → HCO3- loss →
ACIDOSIS
• Causes:
o Familial disorders: Tyrosinemia, Cystinosis, Hereditary fructose intolerance
o Drugs: Aminoglycosides, Valproic acid, Ifosfamide, cisplatin
o Multiple Myeloma, Vitamin D deficiency
• Commoner in kids (because of the familial disorders)
• Manifestations:
• Renal Fanconi’s Syndrome: Glycosuria; Generalized AA’uria, Phosphaturia, Hypercitraturia
• **Because of hypercitraturia, these patients are protected from nephrolithiasis (and
because of hypocitraturia with hypercalciuria, dRTA patients have stones)
• Kaliuresis – especially with bicarbonate supplementation therapy
▪ Hypokalemia

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• TREATMENT
▪ NaHCO3 therapy
▪ With K-supplement

Type 1 RTA (classic distal RTA)

Causes: Sjogren’s, Primary hyperparathyroidism, Vitamin D toxicity, Amphotericin B, Toluene

• Inability to acidify urine
• Hypercalciuria & Hypocitraturia
• Nephrocalcinosis & Nephrolithiasis
• Osteopenia

Type 4 RTA (generalized distal RTA)

• Mineralocorticoid deficiency^^
• Associated renal failure is common
• Treatment: Treat the hyperkalemia & the underlying cause
✓ ^^Min-cort deficiency can be primary (like Addison’s or 21 hydroxylase deficiency or
ACEI/ARB therapy)
✓ ^^Min-cort deficiency can also be SECONDARY – i.e., HYPORENINEMIC
HYPOALDOSTERONISM (Diabetic nephropathy, NSAID’s, obstructive uropathy)
✓ Urine ammonium excretion is reduced
✓ If UAG is positive – it is a RTA
✓ If UAG is negative – the cause of acidosis is extra-renal

ARAS – atherosclerotic artery stenosis

Screening investigation of choice: Captopril renography with 99m
Tc MAG3
Gold standard investigation for ARAS: Intra-arterial Angiography

THROMBOTIC MICROANGIOPATHIES

HUS & TTP

• Pentad of: Neurologic findings, Renal insufficiency, Fever, Thrombocytopenia & MAHA
(microangiopathic hemolytic anemia)

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• HUS – in kids – STEC (Shiga toxin producing E. coli) associated {aka D+ HUS – diarrhea-
associated} – only supportive treatment (no specific therapy available)
• Renal receptor of Shiga toxin: Gb3 (Globotriaosylceramide) – richly expressed on renal
micro vessels
• HUS – in adults – atypical HUS (aHUS) – complement-mediated HUS: The commonest
cause is factor H deficiency; The combination of low C3 & normal C4 reflect alternate
pathway activation
• Responds well to Eculizumab (anti-C5)

TTP (Thrombotic Thrombocytopenic Purpura)

• Absent ADAMTS 13
• Accumulation of large vWF multimers bcoz of absent ADAMTS 13 (adamts 13 is a
plasma protease)
• The large vWF multimers → clots → MAHA
• Triggers: Infection / Surgery / Pancreatitis / Pregnancy
• Treatment: Plasmapheresis & Prednisolone
• UPSHAW SHULMAN syndrome: congenital deficiency of ADAMTS-13; (USS presents with
severe neonatal Jaundice followed by recurrent TTP episodes which respond to FFP
infusion)

ADPKD

• Complete penetrance & variable expressivity

• Diagnosed incidentally on USG
• No symptoms before middle-age: backpain / flank pain, abdominal mass, HT
• MC cause of death: CV disease (as for all patients with CKD)
• Increased incidence of renal cyst infection, UA stones, liver cysts, intracranial aneurysms
• RCC: no increase in incidence BUT when RCC occurs in ADPKD -
• Cyst infection: Cotrimoxazole / Quinolones / Chloramphenicol

ARPKD

• The more serious form

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• Diagnosed in-utero / in neonatal period
▪ Massively enlarged echogenic kidneys
• Most kids are born with renal failure
• 60% mortality in the neonatal period
• Liver:
▪ Biliary dysgenesis
▪ CHF – congenital hepatic fibrosis
▪ Caroli’s disease – IHBR dilatation
▪ Portal HT

ALLERGIC INTERSTITIAL NEPHRITIS

• Usually due to drugs
• Beta-lactams, Rifampin, Acyclovir, PPI’s, NSAID’s
• TRIAD: fever, rash, eosinophilia: only in 5%
• Oliguric AKI with an enlarged kidney
• **EOSINOPHILURIA** - should NOT be used as a criterion (too insensitive & nonspecific)
• Treatment:
▪ Best: Withdraw the offending drug
▪ STEROID: Reserved use for -
o Need for HD
o Continuing worsening of renal function despite withdrawing the offending drug

SRC (Scleroderma Renal Crisis)

• Increased risk with anti-U3 RNP
• Accelerated HT
• Rapid deterioration of kidney function
• Nephrotic range proteinuria
• Hematuria
• Fluid overload
• ARCUATE artery narrowing
• Treatment: ACEI
• 2/3rd will need dialysis
❑ ❑ ❑

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 NEUROLOGY

SEIZURE DISORDERS

TYPICAL ABSENCE SEIZURES versus ATYPICAL ABSENCE SEIZURES

No loss of postural control (in absence seizures) – postural control is lost in ATONIC seizures

POST-ICTAL CONFUSION

“Complex people are generally confused:

Complex partial seizures, generalized seizures (GTCS) – have post-ictal confusion
“Confusion is typically absent with a simple attitude”
Typical absence, Simple partial seizures, Atonic seizures: No post-ictal confusion

COMPLEX PARTIAL SEIZURES: (Focal seizures with impaired awareness)

(A) AURA: Focal seizure without cognitive disturbance; they are subjective “internal” events
which are not directly observable by someone else; examples – fear / deja-vu / micropsia /
macropsia
(B) Lip-smacking / chewing / picking movements / emotion – are all AUTOMATISMS
(INVOLUNTARY AUTOMATIC BEHAVIOR)
(C) Motionless stare: this is how the ictal phase begins

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EPILEPSY SYNDROMES:

(A) LG syndrome: triad of – multiple seizure types, spike-and-wave discharge (on EEG) &
impaired cognition
(B) MTLE – generalized seizures are rare: 3-FIRE: focal, febrile sz (history), family h/o sz,
intractable, remit-reappear, early-onset; Small hippo; small TL & enlarged Temporal horn;
clinical – FS with impaired awareness
(C) Lafora’s ds: Progressive myoclonic epilepsy – common in India – death in 10 y of onset
(D) JME (Juvenile Myoclonic Epilepsy) - 12 to 18-year olds (juveniles); generalized, B/L myoclonic
jerks; often in the mornings; precipitated by sleep deprivation & alcohol binge;
CONSCIOUSNESS PRESERVED

Treatment of GCSE (Generalized Clonic Status Epilepticus)

GCSE (> 5min)

Midazolam (0.2mg/kg iv)

AED
(Volproic acid /
Phenytoin /
Leveyiracetam)
(20mg/kg iv)

GCSE Focal-complex,
Persisting / Myoclonic or
“subtle SE” Absence SE

Midazolam IV / PO AED
(0.2mg/kg/hour) / (Valproate /
propofol infusion Levetriracetam /
(2mg/kg/hour) Lacosamide)

Thiopentone (1mg/kg iv)

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Refractory SE

• Early refractory SE: (30min to 48h): Midaz / Propofol infusion

• Late refractory SE: (> 48h): Isoflurane / Ketamine / Vagal nerve stimulation / rTMS
(recurrent transcranial magnetic stimulation)

Indications for initiating AED after a seizure:

‘FENTS’: Family history; EEG abnormal; Neurologic exam abnormality; Todd’s paralysis; Status
epilepticus

Criteria for withdrawing AED:

‘FENTT’: Family history -, EEG – normal; Neuro exam- normal (including normal intelligence);
Type – single seizure type – more likely to be able to d/c; patients with generalized sz more
likely to remain seizure-free than focal-onset – after withdrawing AEDs; Time > 2 years
(definitely not before 1 year) of seizure-free interval

1 per second Periodic complexes of CJD (EEG)

3RD NERVE SYNDROMES

(Ipsilateral 3rd nerve palsy in all 4): Name of syndrome;

Structures involved;
BoRN CAT: Benedikt syndrome; Red Nucleus; Chorea, Athetosis,
Contralateral features
Tremor

Not SCePtiCAl: Nothnagel Syndrome; Superior Cerebellar Peduncle; Cerebellar Ataxia

Cat is Not Born: Claude’s syndrome = Nothnagel + Benedikt

With Cerebral Palsy: Weber’s syndrome; Cerebral peduncle; Paresis

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BRAINSTEM SYNDROMES:

MEMORIZE:

PARALYSIS:

(Face Arm Leg) – is always C/L (never I/L); Always with Medial brainstem (never with
lateral)
CN: always I/L (why? Because the brainstem contains CN nuclei & issuing nerve fibres – the
corticobulbar fibres have already crossed above); Only 1 medial brainstem syndrome causes
CN palsy – medial medullary (tongue is in the middle)
Ataxia – Never occurs in medial midbrain & medial medulla; Always I/L (except: lateral
midbrain – only cause of C/L ataxia)
Pain in the lateral syndromes; Touch in the medial syndromes (& lat sup pons)
Lateral Medullary Syndrome aka Wallenberg syndrome

ARTERY SYNDROMES

MCA – Superior division:

• Contralateral face-arm-leg paralysis with sensory loss;

• Dominant Hemisphere – Broca’s (Motor) aphasia

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• Nondominant Hemisphere – Anosognosia / Neglect

MCA – Inferior division:

• No motor weakness
• Dominant Hemisphere – Fluent (Wernicke’s) aphasia
• Nondominant Hemisphere – Anosognosia / Neglect

ACA (Anterior Cerebral artery)

• Paralysis of opposite LL
• Lesser paresis of opposite UL
• U. INCONTINENCE (paracentral lobule)
• Primitive reflexes (Grasp / Sucking)
• Gegenhalten (paratonic rigidity)
• ABULIA (akinetic mutism): medial frontal lobe

Posterior Cerebral Artery

• P1 syndromes: (proximal PCA)

▪ Claude’s / Weber’s
▪ TDR (Thalamic Dejerine Roussy syndrome): C/L hemisensory loss; BURNING pain
▪ A of Percheron: Drowsiness, Abulia, Up-gaze paresis

BASILAR ARTERY OCCLUSION

Bilateral signs
• Long tracts
• Cranial Nerves
• Cerebellum

***Cerebellar Infarction:
• Nausea, Unsteadiness, Dizziness
• Is it LABYRINTHITIS?
• Headache, Neck Stiffness & U/L Dysmetria: FAVOR STROKE
PICA (posterior inferior cerebellar artery / Vertebral artery: Lateral Medullary Syndrome /
Wallenberg syndrome

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APHASIAS

*Broca’s area – IFG (inferior frontal gyrus) – superior division of MCA

*Wernicke’s area – STG (superior temporal gyrus – posterior part) – inferior division of MCA
• In 95% of R-handers & 60% of L-handers, aphasia is due to Left hemisphere lesions
**Crossed aphasia: aphasia due to R-hemisphere lesion in a R-handed person

Global aphasia is a combination of B & W – occurs with complete MCA occlusions

Anomic aphasia – Middle / Inferior Temporal Gyri
• MC language disturbance in AD (Alzheimer’s), after TBI (traumatic brain injury) & in
metabolic encephalopathy
Echolalia (parrot-like repetition): Isolation aphasia

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TREATMENT OF ISCHEMIC STROKE

The first investigation in suspected stroke is an NCCT – Why?

The initial CT rules out 2 things: (A) Hemorrhage (B) A large MCA infarct
With those ruled out, in the ‘window’ & no contraindications to TL – give thrombolytic
therapy

Indications for thrombolysis:

Stroke; window period 3 (to 4.5) hours (important issue about the window: If a patient
wakes up with a stroke – ONSET time is when he went to bed)
Age > 18years
BP lowering in ischemic stroke:
If it’s:
(A) > 220/120
(B) a/w malignant HT (retinopathy / proteinuria – azotemia / encephalopathy /
microangiopathic hemolytic anemia) – best drugs – IV nitroprusside, labetalol or
nicardipine
(C) a/w myocardial ischemia – NTG, nicardipine, labetalol or esmolol
(D) > 185/110 & TL is to be given

What can you identify on the CT?

1. A large infarct
2. Asymmetric ventricles
3. Effacement of sulci in the left hemisphere
4. Midline shift

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Impending Risk: Brainstem herniation & death
HEMICRANIECTOMY – decompression surgery: REMOVE a part of the skull & therefore
remove THE RESTRICTION on brain volume
Also, larger infarcts & cerebellar infarcts are very likely to need decompression surgery
HUNT-HESS scale: severity of subarachnoid hemorrhage
“Worst headache of my life” – most likely diagnosis: Migraine (But a CT is a must: r/o SAH)
MC location of saccular aneurysm (leading to SAH): Terminal ICA

HEADACHES

Headache with autonomic features –

• Lasts few seconds: SUNCT / SUNA
• Lasts few minutes: Paroxysmal Hemicrania
• Lasts few hours: Cluster headache (TOC: 100% oxygen * 15 min)
‘Featureless’ headache: Tension type headache
Headache with photophobia, phonophobia, throbbing, nausea, visual phenomena: Migraine
Drugs for migraine:
• Ditans: 5HT (1f) agonists
• Triptans: 5HT (1B/1D) agonists
• Gepants: CGRP antagonists
• Dihydoergotamine: nonspecific serotonin (5HT) receptor agonists
• DA antagonists: metoclopramide; prochlorperazine

Giant cell arteritis – tetrad of headaches, anemia, high ESR, fever; aortic aneurysms; PMR;
AION; Steroid (without waiting for biopsy); Tocilizumab

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• Cardiac cause of syncope must be ruled out – ECG / Holter / Physical exam / Echo
• Causes of ascending paralysis: RPP – rabies, porphyria, potassium (Rabies, Acute
intermittent porphyria, hypokalemic periodic paralysis); GBS
• DESCENDING PARALYSIS: BDS (Botulism, Diphtheria, Snake bite)
• GBS: Albuminocyto dissociation (high protein with N cells)
• Prolonged F-wave latencies – earliest NCV
• IVIg / PE
• Foville: Dorsal pontine injury – lateral gaze palsy + ipsilateral 7th CN palsy + CL hemiparesis
(lateral gaze palsy: due to abducens NUCLEAR lesion – causes ipsilateral LR & contralateral
MR palsy)
• Millard-Gubler: Ventral pontine injury – Lateral rectus weakness (no gaze palsy) – because
6th nerve fascicle is injured instead of nucleus + ipsilateral 7th CN + CL hemiparesis
• Gradenigo: Mastoiditis – leading to deafness, pain, ipsilateral 6th nerve palsy
• Duchenne Muscular Dystrophy: onset at 1 year; BMD – onset at 5 years; Gower manoeuvre;
CK levels elevated
• Myotonic dystrophy: Temporalis & masseter atrophy; Hatchet facies
• Edrophonium test – MG; anti-AchR, anti-MuSK, anti-LRP4 antibodies; Thymoma
• NPH (normal pressure hydrocephalus) = DIG (dementia, incontinence, gait)
• Daytime somnolence; RBD (REM-sleep behavior disorder); visual hallucinations: DLB
(Dementia with Lewy bodies)

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• Memory loss; loses his way around the neighborhood; nominal aphasia: Alzheimer’s disease
• Eats a lot; disinhibited; compulsive behavior: FTD (Frontotemporal dementia)
• PSP (Progressive Supranuclear Palsy): Falls, Inability to look down, (Supranuclear
ophthalmoparesis), Dysarthria, Hyperextended neck
• CJD: Rapidly progressive dementia & Myoclonus
• Alien limb phenomenon: CBS (Corticobasal syndrome)
• Hashimoto’s encephalopathy: progressive subacute encephalopathy with myoclonus;
triphasic EEG complexes; anti-TPO & anti-TG; response to steroids
• Myxoedema Coma: Thyroxine; Hydrocortisone; Rewarm if T < 30 degree C
• Restless Legs Syndrome: Pramipexole / Ropinirole / Rotigotine (Levodopa not to be used)

MENINGITIS –

CSF profile:

TREMOR

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• Bilateral simultaneous optic neuritis: NMO (neuromyelitis optica), LHON (Leber’s), Toxic
optic neuropathy
• Bilateral INO (internuclear ophthalmoplegia): MS
• Anti-AQP4: NMO
• Anti-GQ1b: Miller Fisher Syndrome
• In MS:
▪ Slowing of conduction: due to demyelination
▪ Permanent sequelae: due to gliosis / sclerosis

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