Medicine

TABLE OF CONTENT
Subjects Page No.
Medicine Quick Revision Notes 1-205
Surgery Quick Revision Notes 208-297
Pediatrics Quick Revision Notes 300-371
OBG Quick Revision Notes 374-454

MEDICINE
QUICK REVISION NOTES
CLINICAL CARDIOLOGY AND cardiac injury - Troponin
Q
ARRHYTHMIAS •• Early biomarkers (rise early & fall early) -

myoglobin, H-FABP (heart type fatty acid
Approach To Chest Pain & ACS binding protein), IMA (ischemia modified
albumin)
Q
Features suggesting ACS

•• Others - CKMB (comes back to baseline
Chest Pain - Ischemic within < 48-72 hrs and its not a marker of
1. Location of pain - Retrosternal / Substernal reinfarction anymore), LDH (LDH flip – LDH1
> LDH2)
Q
(Levine’s Sign - retrosternal crushing pain)

2. Nature of pain - Crushing / Constricting / Pressure •• Out of early biomarkers, IMA rises earliest
/ discomfort in 3-6 mins & falls back to baseline in 6-12hrs.
Peak of IMA achieved in 3-6hrs.
3. Radiation of pain - Left Chest / shoulder/arms/
neck / angle of jaw •• IMA > Myoglobin > HFABP (sequence of rise &
fall)
•• The probability of ACS is even higher if patient
c/o rest pain. Stable angina will never have rest •• With advent of high sensitive cardiac troponin,
pain, it will have exertional pain. earlybiomarkers measurement are obsolete
now. Hs-cardiac troponin can detect even
•• New onset acute pain (acc to ACC/AHA
normal levels of troponins, therefore they are
guidelines, 2 months) is ACS unless proved
preferred now.
Q
otherwise
•• Crescendo pain (pain intensity keeps on Myocardial Infarction
increasing)
It is an ischemic + acute myocardial injury.
4. Associated features - cardiogenic shock,
hemodynamic instability •• Acute myocardial infarction - rise & fall of
•• Acute heart failure (eg- pulmonary edema) cardiac biomarkers (troponins)
•• Ventricular arrhythmias (VT /VF if patient •• Ischemia - clinical features of ischemic chest
present with chest pain)
pain
•• Diaphoresis present along with chest pain OR
a. ECG: new ST-T changes + new pathological Q
excessive diaphoresis
wave
Q
Three step protocol for ACS work up b. Imaging:

i. 2D ECHO - new RWMA (Regional wall
motion abnormality), it corresponds to
the area of infarct.
ii. FDG-PET scan - new loss of viable
myocardium seen
Q
iii. Coronary angiogram - specially done in

emergency, for STEMI and high risk
NSTEMI.
Biomarkers
c. Autopsy (if patient dies) - intracoronary
•• Most specific & most sensitive biomarker for
thrombus
2
Cerebellum Quick Revision Notes
Types of MI •• Rise of troponin to detectable level (time lag is

2-4hrs)
1. Type 1: A/c/a spontaneous MI. Here, the cause •• In case of thrombolysis, PCI the peak is
is Coronary artery disease, atherosclerotic plaque achieved earlier (peak and fall is seen earlier)
ruptures and it causes thrombus → MI. MC form •• Area under the curve will tell the total amount
of troponins released and it will be proportional
of MI in world to severity of myocardial injury.
2. Type 2: Here, demand-supply mismatch is there. •• Normal cardiac troponin does not rule out ACS/
MI. That’s why opt for serial troponin. Because
Plaque is stable & not ruptured. Eg. severe anemia, cardiac troponins are not only diagnostic but
severe left ventricular hypertrophy. also prognostic.
•• Chronic myocardial injury will show elevated
3. Type 3: MI causing sudden death. Diagnosed on steady levels of troponins.
autopsy only
Level of troponins:
4. Type 4: Post PCI. It is of 2 types, 4A - Peri PCI
Onset 3-6hrs
MI (<48 Hrs of PCI & Troponin ↑ >5x upper ref.
-ve + Acute myocardial injury
limit) and 4B - Instent thrombosis + + Acute /chronic myocardial injury
5. Type 5: Post CABG. Troponin ↑ >10x upper ref. If initial and after 3-6hrs value
difference is >20 %------->> acute
limit
myocardial injury.
Behaviour of cardiac marker in setting of It can be used to diagnose
MI reinfarction.
Troponin dynamics If difference is <20%

-------chronic myocardial injury
Reinfarction – if there is repeat MI in next 28 days.
Most reinfarction occurs within first 2-3days.
Q
Difference of >20% rise can also be used to diagnose

reinfarction. To make a diagnosis of reinfarction,
troponin levels should be falling, already reached
baseline, or it should be stable. It cannot be diagnosed
in the rising phase of troponin levels.
Difference between STEMI & NSTE-

ACS (NSTEMI & Unstable angina)
STEMI NSTEMI
No flow, 100% occlusion State of some flow,
plaque ruptured.
Involves single vessel Multivessel problem
Acute Subacute
* For Making Notes

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Medicine
STEMI NSTEMI iv. Prasugrel (L.D. 60mg,
↓collateral Extensive collaterals M.D. 10mg/d), Preferred for PCI

↓comorbid conditions More comorbid conditions v. Ticagrelor (L.D.180mg,
Young patient Older patients M.D. 90mg / twice a day)
Transmural ,focal Subendocardial ischemia
C/I of Prasugrel:
ischemia and it causes ST depression+/-
produces ST elevation T wave inversion (non- I. H/o TIA/ Stroke
(localizing) localizing)
II. Age >75, weight <60kgs
Troponins ↑↑ Troponins normal/↑
•• Clopidogrel ,Prasugrel are prodrugs metabolized
Goal of therapy: to Goal of therapy- to reduce
by CYP2C19. Omeprazole ,also metabolized by
reopen the vessel overall thrombus burden.
same CYP2C19, now can be given together.
Main tx- anticoagulation
Immediate reperfusion
•• Aspirin + P2Y12 receptor inhibitor are must in
(thrombolysis /-in next High risk patients- CAG in
STEMI.
2hr next 2-24hrs
•• P2Y12 receptor inhibitors are optional in
INITIAL TX OF ACS- NSTEM-ACS.
5. B - Beta blockers –
Mnemonic - MONABC
•• Reduce overall infarct size because they
1. M – Morphine → used only in anxiety / refractory ↓myocardial oxygen consumption.
Q
chest pain
•• ↓ Risk of ventricular arrhythmias.
2. O- Oxygen → only in low saturations and shortness
of breath. Target saturation >94% •• Drugs used- Metoprolol, Esmolol
C/I of Beta blockers -
Q
3. N - Nitrates → NTG –short acting nitrate, can

be used as IV, sublingual . i. Severe reactive airway disease –Bronchial
•• Used as iv in----- refractory chest pain, ↑↑BP. Asthma / COPD
•• Nitroglycerin is avoided in preload sensitive ii. Hemodynamic stability- low BP/ shock
conditions like RVMI (right ventricular MI), iii. Bradycardia
hypotension.
iv. 2nd /3rd degree heart block /AV nodal block/
•• MOA of nitroglycerin- works by ↓preload PR interval > 0.24sec
(RV is preload sensitive , LV is inotrope v. MI specific C/I- SBP< 120 mmHg /HR >110/min
sensitive.)
vi. Heart failure - KILLIP scoring:
•• In RVMI- Avoid NTG , diuretics
–– KILLIP class I- no heart failure (no jvp/
4. A - Antiplatelet drugs S3/crepitation)
i. Aspirin (L.D. 150-300mg & M.D of 75-81mg) –– KILLIP class II-mild heart failure (JVP/
ii. +/- P2Y12 receptor inhibitors Clopidogrel, S3/Crepitations only at base of lungs)
ticagrelor, Prasugrel. –– KILLIP class III-frank pulmonary edema
iii. Clopidogrel (L.D. 300-600mg, M.D. 75mg/day) - –– KILLIP class IV- cardiogenic shock (↓BP)
preferred for thrombolysis
6. C - Anticoagulation - UFH – used when planned for
PCI <24-48hrs / Renal failure
* For Making Notes

4
LMWH – Enoxaparin- Preferred when no procedure is infusion @0.5mg/kg (max dose- 50mg) and one
planned 1 hr infusion @0.35mg/kg (max dose-35mg).
Total dose = 100mg
Fondaparinux
Bivalirudin – Shortest acting & fastest acting- used C. TPA analogues - Reteplase - 10 units iv bolus
in planned PCI. f/b 10 units iv bolus after 30mins.
Tenecteplase –given as single bolus 0.5mg/kg
In STEMI patients – PCI is planned , therefore UFH
preferred. (max dose-50mg)
In NSTEMI/UA ,high risk- CAG ,Enoxaparin used. How to choose reperfusion strategy ?
In NSTEMI/UA, if renal failure- UFH preferred. STEMI
If patient has h/o heparin induced thrombocytopenia

(HIT)- Fondaparinux, Bivalirudin Pt is at-
DEFINITIVE TX- a. PCI centre → <60mins → PPCI (10 PCI )

b. non PCI centre look for door to
1. STEMI
c. emergency medical balloon time(DTB)
STEMI centre
•• If DTB >120 mins –thrombolyse within next

Chest pain 10mins →shift patient to PCI center to assess
<12hrs if effective lysis done .
Reperfusion for all patients i. If yes----do PCI in next 24hrs.
If patient presents >12 hrs- ii. If not effective lysis- do PCI asap (rescue
PCI)
•• Reperfusion done only in selected patients-
•• If DTB <120 mins- shift to nearby PCI center
•• Ongoing ischemia (persistent ST elevation or → PPCI
persistent chest pain) and cardiogenic shock
patients •• Markers of effective thrombolysis-
i. Chest pain should come down
Reperfusion Strategies: ii. Evidence of ischemia i.e. ST elevation should
(a) Thrombolysis- best useful when done within 3hrs come down by >/=50% (Ecg should be taken
of onset of chest pain,can be done upto24hrs 60-90mins from beginning of thrombolysis).
(b) PCI- Preferred, best because it is evidence •• If c/I to thrombolysis is present, do PPCI
based
Q
irrespective of DTB
THROMBOLYSIS 2. NSTEMI-ACS (NSTEMI / UA) - Anticoagulation
4 drugs used in this are: + CAG in very high risk / high risk patients.
A. Streptokinase - dose-1.5million units ,given as
infusion over30-60 mins
B. rTPA or alteplase – 0.15mg/kg iv bolus (max
dose-15mg) f/b one 30min
* For Making Notes

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Medicine
Very high risk patient- Absolute Relative

a. Cardiogenic shock •• Any prior ICH or h/o •• BP>180/110 at
b. Acute heart failure stroke of unknown origin presentation
c. Mechanical complications of •• Intracranial neoplasm, •• Ischemic

MI-like acute MR aneurysm, AVM stroke>3months prior
d. Ventricular arrhythmias <24hrs •• Ischemic stroke< •• Other intracranial

3months diseases
High risk patients-
•• Closed head •• CPR>10mins
a. Troponin elevation
trauma<3months •• Major surgery <3weeks
b. Any new/dynamic ST changes
•• Intracranial or •• Internal bleed<2-
c. ↑↑risk score – TRS score >/=3
intraspinal surgery 4weeks or active PUD
GRACE score >140 <2months •• Noncompressible
TIMI risk score (TRS) – 7 components •• Active internal bleeding vascular

or known bleeding puncture<24hrs eg- LP,
Mnemonic - AMERICA
diathesis (except liver biopsy
A - Age >/=65 (single most important risk factor) menses) •• Current use of
M - Markers (↑↑troponins) •• Suspected aortic anticoagulants
E - Ecg changes- new or dynamic changes dissection •• TIA<6 months
R - Risk factors (>/=3) – diabetes/htn/dyslipidemia/ •• For STK, prior •• Infective endocarditis
smoking/family h/o of premature CAD Rx<6months •• Advanced liver
I-Ischemia (>/= 2 anginal attack in <24hrs) •• Severe uncontrollable diseases
C- K/c/o CAD >50% stenosis HTN
A- Aspirin use <7days
ECG 1:
Score (0-7) : 0-2 –low risk
>/=3 –intermediate high risk
C/I to thrombolysis : NSTEM-ACS (cause

its clot has no to very less fibrin) Q
EXTENSIVE ANTERIOR WALL STEMI:

•• Convex / Tombstone ST elevation
* For Making Notes
6
•• Pathological Q waves (sign of dead myocardium) •• Tombstone upsloping with convex ST elevation
with reciprocal ST depression in lateral leads
Q
•• Reciprocal ST depressions
Sequence of changes in STEMI: Causes of ST Elevation:
a) Hyperacute stage – Tall T waves (if height of T 1. Myocardial causes : STEMI mimics -
wave >5mm in limb leads &>10mm in chest leads)
A) Prinzmetal’s angina: Mostly are smokers, present
b) Acute stage - ST elevation ,a/k/a Pardee sign is as chronic chest pain in night/early morning.
d/t injury current caused by transmural ischemia,
•• MC vessel to undergo vasospasm in this is RCA.
small Q waves
•• Ecg- transient ST elevation.
c) Subacute stage - ST elevation , deeper Q waves,
T wave inversion •• Confirm dx-CAG: Provocative test (Ach /
ergonorine/hypoventilate)
d) Chronic stage/ old MI- only pathological Q waves
seen •• Excellent response to NTG. Acute tx- NTG
Localization of STEMI: (only STEMI can •• TOC- CCB.

be localized) B) Cardiomyopathy: MC takotsubo cardiomyopathy
Q
a) II/III/aVF – inferior MI – PDA (originate from •• Old >50yr history of stress

RCA >LCx)
•• Presents with chest pain +ST↑
b) V3-V4 - anterior MI - LAD
C) LVH
c) V1-V2 - septal MI - LAD (proximal LAD) - can D) LV aneurysm: POST MI.
have associated aVR elevation
•• Persistent ST elevation
d) I/ aVL +/- V5-V6 - lateral wall MI - LCX •• IOC: 2D ECHO
e) V1 ST↑ - RV MI E) Acute myocarditis: rarely
Gold std for confirming RVMI – V4R - RCA •• IOC : Cardiac MR (non invasive gold standard
for acute myocarditis)
f) V1-V8-V9- posterior wall MI - RCA >LCx •• Lake Louise criteria is used
ECG 2: 2. Pericardial causes:

•• Acute pericarditis: Causes ST elevation
3. Conduction causes: LBBB

4. Electrical changes: Brugada syndrome (CCD in
young)
5. Electrolyte changes: Hyperkalemia / Hypercalcemia
Dx : II/III / aVF-INFERIOR WALL MI
* For Making Notes

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Medicine
ECG 3: STEMI Pattern:

•• Critical LAD occlusion.
•• Clot moved when patient presents to emergency,
so chest pain also gone.
•• Biphasic T waves seen in mid precordial leads
(V2,V3,V4) .
ECG 6:
Dx: NSTEMI
Multifocal ST depression in V2, V3, V4, V5, V6, II,
III, Avf. Downsloping of ST depression.
Left main coronary artery (LMCA/LMS)- LAD (widow
maker’s artery + LCx ). LMCA has highest mortality.
aVR & V1 has ST↑ (V2 will not show ST↑)
ECG 4: TYPE B WELLEN’S PATTERN

•• When patient presents little late to emergency.
•• Deep symmetrical T wave inversions are seen in
precordial leads (V2, V3, V4, V5, V6)
•• D/D for Type B Wellens’s pattern – Apical Type
of HCM.
•• Raised ICP (d/t SAH) - a/k/a cerebral T waves
Complications of MI:
Dx: NSTEMI/UA
1. Arrhythmias - MCC reason for death out of
T wave inversions in lateral leads (I,aVL, V5,V6) hospital
ECG 5: Arrhythmias – Tachyarrythmias (VT/VF) or

bradyarrythmias (Sinus bradycardia, 2nd / 3rd
degree heart block)
Q
As general rule,
•• Tachyarrythmias are common with anterior
MI (LAD)
•• Bradyarrythmias are common with inferior
MI (RCA)
Tx: Standard arrhythmia treatment.
Dx:WELLEN’S PATTERN TYPE A. TOC for MI complications: Reperfusion.
* For Making Notes

8
2. Cardiogenic shock – MCC of in hospital death. V. Mortality – 85-100%

Causes: C. Free wall rupture- presents with cardiac
tamponade
I. Pump failure - Can be due to
Q
I. Clear chest
LV pump failure Rv pump failure
II. Presents as PEA /Asystole (cardiac arrest)
Anterior MI- LAD RVMI- RCA
III. ↑JVP
Crepitations seen d/t Jvp ↑↑
backward congestion PCWP normal/↓ Treatment : reperfusion
Jvp normal/↑
•• Immediate Treatment (if patient in shock): ↓
PCWP ↑↑ afterload – by using IABP (extremely useful
Tx: Tx: here)
Inotropes –non vasodilators Iv fluids- NS bolus •• Shift patient to cath lab for reperfusion +/-
like Noradrenaline Target JVP- 10-14 mm Hg CTS
>dopamine +/- inotropes •• Immediate treatment (if no shock and LV
+/- IABP (if PCI is delayed) failure & mechanical complications ): ↓preload
+ ↓afterload only
Advantages of IABP-
3. LV aneurysm-
•• ↓ Afterload
•• ↑ Mild CO True aneurysm Pseudo aneurysm
It’s a myocardial rupture
•• ↑ Diastolic pressure
sealed by pericardium under
•• ↑ Cardiac blood flow thrombus. Can develop
In ECHO – broad neck
II. Mechanical complications- into cardiac tamponade at
anytime.
A. Acute MR-
In ECHO- narrow neck
I. Due to papillary muscledysfunction (posteromedial
Managed conservatively Urgent intervention
papillary rupture d/t inferior wall MI-PDA blood
supply)
Q
4. Pericarditis: Have fever/↑CRP/ ESR / +/-rub
II. Systolic murmur in the apex. (multiphasic sound heard in small effusions only)
III. Patient have risk for flash pulmonary edema Early pericarditis Late pericarditis
(asymmetrical) Occurs within <1 week >1 week ( 2 week- 2 months)
IV. PCWP - ↑↑, large V waves. Transmural ischemia/stemi

→ inflammation in that area a/k/a dressler syndrome
B. Acute ventricular septal rupture-
→ can spread to adjacent autoimmune
I. Can occur with Ant wall MI (apical rupture) / pericardium
Inferior wall MI (basal VSR). NSAIDS are C/I Large pericardial effusion
Apical rupture Basal VSR Because can cause free wall +/- left pleural effusions
MC More dangerous rupture. +/-left lower lobe
consolidation
II. Pan systolic murmur at left lower sternal border
+/- arthralgia/arthritis
III. Patient have risk for developing flash
NSAIDS- 1st line
pulmonary edema
Treatment : high dose aspirin 650mg QID.
IV. PCWP- ↑↑
* For Making Notes
9
Medicine
Approach To SIHD (Stable Ischemic i. Patient should be able to exercise

Heart Disease)- ii. Should not be having significant baseline ECG
1. Can presents with chronic chest pain or chronic changes-
heart failure. Features suggestive of SIHD- a. LBBB
•• Chest pain < 10mins
if 3/3 + → typical angina b. WPW
•• ↑ with exertion
•• ↓ with rest /NTG
if 2/3+ → atypical angina c. ST ↓ >1mm
(<30 second-5mins) If 1/3+ → non cardiac chest pain
d.Any ST ↓+ LVH / Patient is using drugs like
3P- Pleuritic pain digoxin
Positional pain
iii. Bruce protocol - Exercise protocol. When
Palpable pain
to stop exercise?
2. Work up for SIHD- a. When patient becomes symptomatic-

angina/ shortness of breath/ fatigue/
(a) Stress test – C/I:
dizziness
a. ACS with in 48hrs
b. If you reach high risk criteria- ST↓
b. Severe AS >2mm / Ventricular tachyarrythmias/
ST elevation /SBP ↓>10mmHg.
c. Severe pulmonary HTN
c. Reach the target HR. Target HR is 85%
d. Unstable arrhythmia
of the maximum HR achievable by
e. Aortic dissection/ IE patient
f. Acute pulmonary embolism Duke’s treadmill score = exercise ( mins) – 5 (max
g. Acute myocarditis ST deviation )- 4 (Ai)
(b) Stress ECG AI (Angina Index)-

Stress imaging – localizing ischemia 0 - No angina
1. ECHO- exercise, dobutamine. 1 - Non limiting angina
Look for RWMA.
2 - Limiting angina
2. SPECT- exercise, adenosine,
look for Duke’s treadmill score-
3. PET- adenosine look for perfusion
perfusion defect. defect. >/= +5 -low risk- can be managed conservatively.
4. Cardiac MR- adenosine +4 to -10 – intermediate risk
</= -11-high risk
SPECT: Th201/Tc99m → MIBI
t1/2- 6hrs
Tx:
High risk patients – do CAG
t1/2- 7hrs TETROFOSMIN Low risk patients- medical tx
PET: Rb82 (t1/2- 75-90seconds) /O15 water Intermediate risk- stress imaging (MC- SPECT)
(t1/2- 2mins) /N13 ammonia (t1/2-10mins)
Management of SIHD Q
(c) Indications for exercise ECG-

↓ Mortality
* For Making Notes

10
1. Aspirin 2. CABG-only absolute indication is

Clopidogrel LMCA disease.(regardless of angina)
2. Statins (high statins) – rosuvastatin – 20-40mg Severe/refractory Angina with DM
Atorvastatin- 40-80mg Triple vessel disease
↓mortality
Target LDL <70
Double vessel disease (+proximalLAD)
3. ACEI/ ARBS- DM
HTN 3. Grafts – SVG ( GSV- free graft)
HFrEF
LIMA ( insitu)- best graft ,has max patency ,but
4. Antianginals – can be used once in a lifetime.
•• 1st choice : Short acting NTG + Beta blockers ECG 1: Determining Rate
(doesn’t improve survival)
If bronchial asthma/ COPD patient- non
dihydropyridine –CCB, eg- Verapamil,diltiazem
•• 2nd choice: D-CCB , Dipines
CAG + revascular
Others:
•• Ivabradine (IF channel current blocker) - s/e of
Q
Ivabradine- bradycardia ,Luminous phenomena

•• long acting nitrate- ISDN/ISMN – s/e-
tolerance , to break tolerance adequate nitrate
free interval at least for 12-16hrs.
•• Nicorandil – has nitrate like action + potassium
channel opener,vasodilator ,↑ coronary blood
flow, s/e – oral and anal ulcers 1) To determine HR, calculate distance between 2R
waves.
•• Ranolazine- inhibit late inward sodium current,
↓diastolic tension , pfox inhibitors converts HR= 300 / no. of large box between 2 large
metabolism from FFA→ Glucose
Q
HR>180 in this ECG.
•• Rrimetazidine- pfox inhibitors, s/e-
parkinsons’s, chorea. ECG 2: Axis Determining
Revascularization:
•• 1. elective PCI → DES (drug eluting stent-
preferred cause have ↓risk of restenosis, but
DAPT duration should be > 6months ) / BMS
(bare metallic stent)- rarely
DAPT – Dual antiplatelet therapy – Aspirin+
P2Y12 inhibitor
Q
I -, aVF + : RAD
* For Making Notes

11
Medicine
Axis Determining
I aVF Axis Causes
Normal axis
+ +
(-30° to + 90°)
RVH, COPD, ASD (ostium
Q
secundum)
Pulmonary HTN eg-

pulmonary embolism, TCA
RAD (+90 deg to Toxicity, Dextrocardia,
- +
180 deg) RBBB
Ventricular ectopic
I -, aVF-, aVR+ : Northwest/extreme Axis Hyperkalemia, WPW
Lateral MI.
North west
a x i s / e x t r e m e Hyperkalemia, ventricular
- -
axis (-90deg to ectopic, Lead misplacement
180 deg)
ASD (Ostium secundum)
Normal axis/ LAFB

+ -
LAD LH, Inf wall MI
WPW with Rt sided pathway

Universal Causes - Hyperkalemia, ventricular ectopic
I+, aVF+ : Normal axis Chamber enlargement 1: Left Atrial

Enalargement
I+, aVF- ,II- : LAD
* For Making Notes

12
In lead II- Tall P waves (>2.5mm) / P-Pulmonale

Ebstein anomale .
Chamber enlargement 3 : LVH
Normal appearance of P wave-
Lead II- upright
Lead V1- Biphasic appearance
Left atrial enlargement: MCC is systemic hypertension
Lead II – Wide P wave ( >3mm wide), bifid /M

appearance/ ‘M’ mitrale LVH - Xray – Schmou sign → seen in PA view
appearance. - Hoffman rigler → seen in lateral view

ECG - Sokolov lyon criteria- S V1/V2 + R V5/V6 >35mm
Lead V1 – negative deflection is strong = LVH
Q
X-ray R wave in aVL >11mm
•• Straightening of left heart border Chamber enlargement 4: RVH

•• Right side, double heart border seen
Q
•• Splaying of carina (carinal angle increased)

•• Indentation of anterior surface of esophagus-
left atrial enlargement
•• Indentation of posterior surface of esophagus-
dysphagia lusoria
Chamber enlargement 2: Right Atrial

Enlargement
* For Making Notes

13
Medicine
Sokolov-lyon criteria- R in V1 >7mm Before every QRS, pacer spike is present.

Or alternatively, Q/S >1 in V1 •• In leads with +QRS ,-ve ST depression and
slight T wave inversion : normal discordance in
QRS <0.12 sec
LBBB.
RVH in X-ray- clear crescentic air shadow seen in left •• Its difficult to dx ACS in the setting of LBBB.
border ,more clearer on lateral view.
•• STEMI can be diagnosed in setting of LBBB/RV
Since RV is most anterior structure in mediastinum, if pacing. SGARBOSSA criteria is used to predict
there is RVH ,there will be obliteration of the clear or dx STEMI in LBBB/ RV pacing.
retrosternal airshadow.
Conduction block : RBBB
Conduction blocks : LBBB
•• In V1- wide QRS + positive deflection / M

•• Wide QRS, > 0.12 sec in V1 + negative deflection
shaped pattern
in S.
•• RBBB- is a true conduction block. RBBB like
•• Conditions that produce LBBB like pattern- morphology is produced by –
–– Ventricular ectopics –– Ventricular ectopic ( LV)
–– WPW (right sided) –– WPW (left sided pathway)
–– RV pacing. •• WILLIAM PATTERN – V1- W pattern , V-6- M
pattern . Seen in LBBB.
LBBB – due to RV pacing •• MARROW PATTERN- V1- M pattern, V-6- W
pattern . Seen in RBBB.
HEART FAILURE:
1. Symptoms of heart failure-
A) Congestive HF symp- edema/ ascites/JVP or
+ Hepatojugular reflex / Hepatomegaly/b/l
transudative effusions /crepitations
Q
B) ↓ perfusion - cold &clammy extremities/

oliguria/fatigue/sever dizziness/syncope/
comatose/ hypotension &cardiogenic shock
2. Investigation :
A) BNP or NT-pro BNP → if normal values → r/o HF
Q
* For Making Notes

14
→ if ↑ values → cannot confirm dx of HF. d) Beta - blockers- metoprolol succinate /

B) ECHO- either r/o HF / confirms HF bisoprolol/ carvedilol
If EF </= 40% : HFrEF → CV death (85%) > non e) Aldosterone antagonist- spironolactone,
CV death (15%) eplerenone.
If EF 41-49%: HFmrEF → f) SGLT2 inhibitors- ↓HF + antidiabetic :

dapaglifozine/empaglifozin >canagliflozin .
If EF >/=50% : HFpEF →CV death(60%) > non
CV death (40%) It can’t be used in low eGFR state, if <30 for
dapa/cana & <20 in empaglifozin.
3.Death
SGLT2i → If EF improved >40 / 50%, dx will remain
•• CV death - If patient dies within 1 hr of
HFrEF
presentation or within 1 hr of symptom onset-
sudden cardiac death/ progressive HF Not improved then STEP 2
•• Non CV death – d/t infections/ suicide/cancer/ STEP 2: done in patients with EF< 35% +NYHA II-IV
accidents.
a) Hydralazine-ISDN – improves survival in black
4. Classification b) Interventions –
NYHA class–most powerful prognostic marker of •• CRT – a/k/a biventricular pacing. LV is paced
HF. from surface epicardium.RV is paced from
endocardium.
•• Class 1- asymptomatic with ordinary activities
Indications for CRT- EF<35%
•• Class 2- symptomatic with ordinary activities NYHA II-IV LBBB > RBBB
•• Class 3- symptomatic with < ordinary activity QRS >/= 120ms
•• Class 4- symptomatic at rest
•• ICD – indications for ICD- EF<35%, NYHA II,
5. ACC/AHA stages HF into-
NYHA III.
•• Stage A- patient has risk factors only ,no
structural abnormalities
•• Stage B- patient has structural abnormality, •• If patient is persistent NYHA II-IV
but asymptomatic. Drugs that can be used:
•• Stage C- Symptomatic. Most patients presents –– digoxin
in this stage.
–– Ivabradine (HR>70 & sinus rhythm must )
•• Stage D- refractory HF
–– Vericiguat (SGCS)
6. Management of Chronic HF (Chronic HFrEF) - To
↓hospitalization & ↑survival
STEP1:
REFRACTORY HF
a) Diuretics – if congested
b) ARNI- sacubitril ( neprilysin inhibitor) + •• LVAD (LV assist device)
valsartan (ARB) >> ACEI/ARBS •• Heart transplant
c) Omapatrilat- withdrawn from market d/t
angioedema
* For Making Notes

15
Medicine
Drugs that don’t have any survival •• In CMR- Late Gadolinium enhancement is seen
benefit -
Q
which denotes scar tissue.
•• Diuretics Nonischemic CM-

•• Digoxin a. DCM – titin gene mutation
•• CCB
b. HCM
7. Management of Acute HF - to ↓congestion &
c. Restrictive (RCM )
↑perfusion.
•• Congestive symptoms - crepitations/ shortness d. Unclassified- ARVC
of breath /JVP /edema/ ascites/ effusions /
congestive hepatomegaly . PCWP ↑↑ a. DCM –
•• Titin gene mutation
Q
•• Low perfusion – fatigue/ oliguria/ altered
mental status/ comatose/ cold clammy skin( •• FLNC , PLN , LMNA , SCN5A – if these mutation
↑CRT>3sec) /frank shock/ low BP. ↓Cardiac
+, risk of sudden death is very high.
index
•• These patients are prone ventricular arrythmia
•• L - Lasix +/- thiazides
and conduction block.
•• M - morphine (↓preload)
•• Presents like HFrEF → later can develop
•• N - nitrates – NTG (↓preload )/ NTP (↓afterload) ventricular arrhythmia
•• O - Oxygen •• Tx :similar to HFrEF
•• P - position – fowler position +/- PPV (CPAP )
•• 20 causes of DCM :
To ↑Perfusion: A. Alcoholic CM (Dx of exclusion)
a). Inotropes – look at BP- B. PPCM - 1 month before delivery to 5 month
If normal BP- vasodilating inotropes- dobutamine after delivery. Prolactin fragments are the
cause. Therefore BROAD therapy used
Milrinone
BROAD - Risk of recurrence - 30-35%
Levosimendan
If low BP- non vasodilating inotrope- NS/ BR - Bromocriptine,
dopamine O - Oral HF drugs,
b). If patient is having refractory cardiogenic A - Anticoagulants
shock→ MCS
D - Diuretics
2 Types- temporary & permanent
C. Stress CM-
Temporary MCS- IABP ( used in anterior MI),
IMPELLA, ECMO (V-V ECMO &V-A ECMO . V-A a. Postmenopausal women with chest pain/
ECMO preferred for cardiac problem) ST↑/ +/- HF,+/-Tn↑ (ACS like)
Permanent MCS- LVAD , BiVAD ( used in b. ECHO: Apical ballooning (RMWA , non
extreme cases) coronary)
c. CAG: Needed to dx : takotsubo
Cardiomyopathy :
d.Dobutamine should be avoided.
•• 2 Types – ischemic and non ischemic
cardiomyopathy
•• Non invasive gold standard Ix for all CM: CMR
* For Making Notes
16
D.Myocarditis - •• Non sarcomeric mutation – Fabry’s disease

(XLR) : HCM + PN + Cutaneous Angiokeratoma.
Etiology :
α-galactosidase deficieny
○○ Infectious causes – viral (MC is
parvovirus b19> hhv 6> coxsackie TOC- ERT ( Fabrazyme)
virus) , bacterial (streptococcal lyme
•• MC CM in world
disease, diphtheria), parasitic (chaga’s
disease)
Q
•• MCC of sudden death in young people.
○○ Non-infectious causes – •• >90% undiagnosed- out of that <10% diagnosed

– out of 10% ,only >6% asymptomatic &<4% are
Autoimmune – idiopathic/giant cell
symptomatic
myocarditis
•• Dx: unexplained LVH thickness >/= 15mm
Hypersensitivity/ hyperesonophillic
•• C/F- asymptomatic MC /incidental finding
○○ Immune checkpoint
inhibitors(pembrolizumab) If symptomatic : exertion induced VT/VF
leading to syncope &sudden death HFpEF
C/F :
•• Ix:
○○ ACS like
–– ECG: LVH +/- septal hypertrophy
Q
○○ Acute HF
○○ Subacute to chronic HF –– ECHO: LVH +/- LVOTO ( 70% may have
LVOTO → k/a HOCM +/- ASH
Ix:
–– 30% may not have LVOTO→k/a HCM)
○○ ECG /ECHO – nonspecific( global LV
dysfunction ) –– These 70% patient have dynamic obstruction,
depends on preload, afterload, contractility .
○○ CMR- lake louis criteria
○○ Endomyocardial biopsy( EMB)- gold –– Preload/afterload opposite to obstruction.
standard. Sensitivity is poor. DALLAS –– Only contractility ↑ with ↑in obstruction
criteria.
–– Brockenbrough effect is due to dynamic
Tx: obstruction
○○ Autoimmune- steroids
–– In cath lab, premature ventricular contraction
○○ Antibacterials is induced. Normally , Premature contraction
○○ Hypersensitive- withdraw the drug PVC contractility is low but post PVC
contractility beat is powerful &this results
○○ Antiparasitic drug in ↑SV →↑SBP →↑PP.
○○ Viral- supportive tx
–– But in HCM patient, increase in contractility
will result in ↓SV &↑obstruction
Drug induced DCM- Anthracyclines/ trastuzumab
–– Myocardial biopsy- myocyte disarray
b) HCM-
•• Tx: ICD can be used without dx of VT/VF as 10
•• Sarcomeric gene mutation. Non treatable. AD. prevention in high risk patients.
•• MYH7 (beta myosin heavy chain), C-MYBPC Indications –
(cardiac myosin binding protein)- >/= 70%
mutation
Q
•• LVH >/= 30mm
•• Family h/o SCD
* For Making Notes
17
Medicine
•• Unexplained syncope •• AA type – seen in chronic inflammation

•• Apical aneurysm •• ATTR- 2 types- familial amyloidosis (mutated
TTR) & senile systemic amyloidosis (wild type
•• Extensive Late gadolinium enhancement
TTR)
Q
Tx of HF associated HCM- •• C/F- presents like RCM :RHF >> LHF

•• 1ST line- beta blockers
Q
Edema/ascites/ JVP/ Hepatomegaly
•• ND-CCB- alternative •• Ix- ECHO- thick ventricle / severe
diastolic dysfunction ,HFpEF
↓if persistent HF s/o cardiac
initially.
amyloidosis
•• Add Disopyramide ECG- low voltage complexes
↓ •• Tx: Tafamidis- FDA approved for
ATTR amyloidosis.
•• Septal reduction therapy
–– Myomectomy- in young ,fit patients •• 2 Drugs that should not be used in amyloidosis-
Digoxin & nifedipine
–– Alcoholic septal ablation –in old,unfit patients
d) ARVC-
c) RCM-
•• Strong genetic mutation. Desmosomal mutation.
•• Acquired AD.
•• it could be due to endomyocardial process/ •• Syndromic forms- NAXOS, CARVAJAL → will
myocardial process have palmoplantar hyperkeratosis
Q
•• Myocardial – infilteration → amyloidosis/ •• Presents with ventricular arrhythmias first

sarcoidosis/hemochromatosis/storage disorder
then develop HF.
•• Endomyocardial process →
•• RV failure first then LV failure
1. chronic esosinophillic state : Loffler’s
•• Fibro fatty replacement, initially start in RV
endocarditis in temperate climate .
Q
then to LV.
2. Endomyocardial fibrosis( EMF) :
•• ECG – E wave / ↓ T in V1-V4
in poverty stricken areas, in tropical
climate •• ECHO- RV dysfunction
+/- eosinophilia •• IOC- CMR

•• TOC- ICD + beta blockers
Q
Caused by – toxins, radiation, serotonergic
mechanism
Cardiac amyloid – AL (10) /AA (20)/

ATTR
•• AL type- seen mainly in plasma dyscrasia like
MM
* For Making Notes

18
Sudden Death In Young Q
Features HCM ARVC LQTS BRUGADA CPVT

Channelopathy
K+ -MC- LQTA1/2
Channelopathy Channelopathy
Sarcomeric Desmosomal Ca2+, Na+-
Genetic MC- SCN5A RYR –AD
AD AD LQTS3,SCN5A
AD CALSQ- AR
AD( romano ward
syndrome)
AR – JLN
Catecholaminergic
Syndrome-
polymorphic VT
deafness
Early after Delayed after
Arrythmia Structural heart diseases, scar tissue
depolarization Phase 2 reentry depolarization
process act as nidus for reenty
(EAD) (DAD)
LQTS1(swim,
diving) /2 (loud
Arrhythmias
Exertion exertion noise)- exertion Rest Exertion
with
LQTS3/ SCN5A-
rest
Yes Yes Yes
Yes No
ECG LVH , Septal E wave, T ↓in V1- Pseudo RBBB
Long QT >450ms Normal ECG
hypertrophy V4 ST elevation
Imaging
Yes Yes No No No
(ECHO)
LQTS1/2- ICD/
beta blockers ICD
Tx ICD/beta blockers ICD/ Beta blockers ICD/beta blockers
LQTS3- ICD , Quinidine
pacing
LVH: ARVC :
S wave in V1, R wave in V5,V6 >35mm . E wave in V1 at J point
Big R waves in V1- septal hypertrophy T wave inversion in V1, V2, V3, V4
Big Q waves in V5, V6, I, Avl – pseudo infarction
pattern
* For Making Notes

19
Medicine
Brugada syndrome : Bazett’s formula to calculate

corrected QTc :
Pseudo RBBB
in V1,V2 QTc= QT /√RR
Coving of ST segment
Q
QTc > 0.44sec in males & >0.46 sec in females-

long QTc
Risk of ventricular arrythmia due to early after
depolarisation ↑ if QTc >0.50 sec
Short QTc causes- digoxin, hyperkalemia,
hypercalcemia .
Q
Clinical Cardiology & Arrythmias
3 Golden rules: pressures ↓ with inspiration & ↑

with expiration
Rule 1: Pressures –ITP/JVP/BP ↓ with inspiration &
Congenital: ↑ with expiration
Rule 2: HR ↑ with inspiration & ↓ with expiration .
Q
•• AD- LQTS1/2/3
•• AR- JLN (deafness) Rule 3: Flows to right side ↑ with inspiration & Flows
to left side ↑ with expiration. E.g. of - TR murmur
Acquired: MC
(DE- CARVALLO’s law). Only exception to this rule
•• Hypokalemia/hypocalcemia /hypomagnesemia/ is pulmonary valvular click (pulmonary stenosis)- ↑
hypothermia
with expiration.
•• Drugs
E.g. of murmur that ↑ with expiration- MS/MR/
–– Antibiotics - quinolones ,macrolides, AS/AR. Only exception to this HOCM/MVP click &
Antihistamine murmur .
Q
–– Antitubercular –bedaquiline, Antipsychotic

Blood Pressure
–– Azoles ,Antiarrhythmic drugs- class III>Ia
1. BP difference between the arms and legs:
•• ↑ICP, SAH, MI >20mmHg. AR- Hill sign, CoA, PAD, Aortitis
2. BP difference between the arms: >10mmHg.
Aortitis /Aortic dissection/PAD/
Supravalvular AS (Coanda effect - Rt arm
pressure> Lt arm pressure).
3. Pulsus paradoxus: BP ↓ in inspiration
>10mmHg. Seen in cardiac tamponade/Acute
exacerbation of Bronchial asthma, COPD,
tension pneumothorax /Pulmonary embolism/
Rt HF/ 25% of Constrictive pericarditis.
4. Orthostatic hypotension: ↓ in SBP>/= 20mmHg/
↓ DBP>/=10mmHg in <3mins of standing.
* For Making Notes

20
Valsalva BP response: thyrotoxicosis/pregnancy /anemia /paget’s

disease of bone)
It is a straining maneuver
AR- (Pulsus magnus)
b) ↓- shock (hypovolemic/cardiogenic shock/
obstructive shock)
Stenotic – MS/AS (Pulsus Parvus)
2.Character-
a) Collapsing pulse (rapid rise with dramatic fall)-
run off. 2 types.
•• Peripheral run off- when blood doesn’t stay in
central vasculature.
•• Central run off
Phase. •• E.g. – AR, PDA, RSOV (rupture of sinus of
Valsalva), AVF, truncus arteriosus.
Phase 1- ↑ BP .
•• In AR- Watson water hammer Pulse
Q
Phase 2- ↓ BP (d/t ↓Venous return).

b) Pulsus parvus et tardus- seen in AS
Q
Phase 3- ↓BP transiently.

c) Double beating pulse-
Phase 4- ↑BP (d/t ↑Venous return) → overshoot
phase •• Systolic beating pulse
–– Both peaks in systole
Abnormal curves-
–– K/a bisferians.
•• Systolic dysfunction- absence of overshoot.
–– Seen in – severe AR, HOCM(spike &dome
•• Diastolic dysfunction- square wave response. pattern), AS+AR
Q
–– Never seen in AS alone.

PULSE
–– Anacrotic notch- severe AS
•• Diastolic beating pulse –
–– one peak in systole, one in diastole
–– Dicrotic pulse – cardiogenic shock/sepsis/
IABP
d) Alternating small &large volume pulse-
•• Pulsus alternans- regular pulse. E.g. severe LVF
Q
•• Normal pulse - Catacrotic

•• Pulsus bigeminy –irregular pulse. E.g. digoxin
•• Dicrotic notch= closure of aortic valve.
toxicity
Abnormalities in pulse – e) Pulsus paradoxus
1. Volume –
a) ↑-hyperdynamic (fever/beri-beri/
* For Making Notes

21
Medicine
Wave Hemodynamics Abnormalities

Q
a) Absent a wave- A.fib
Q
b) large a wave- TS
c) Pulmonary HTN
Q
a wave Atrial contraction d) Cannon a wave
regular- SVT(AVNRT)-frog sign
irregular-AV dissociation (causes-complete heart block,
VT)
c wave Isoventricular contraction CV fusion –severe TR
Q
Rapid ejection phase+ atrial ↑X descent- constrictive pericarditis/tamponade
x descent
relaxation ↓X descent- TR/ RHF /AF
v wave Venous filling of RA Large V waves- CP/ TR /RHF/ ASD/ TAPVC& PAPVC
↑Y - Friedrich sign-tamponade
y descent Rapid passive filling ↑Y – CP/TR/RHF
Q
↓Y – TS/Tamponade
Mnemonic
PAY –TAX- Pericarditis- ↑ Y: Tamponade-↑ X
JVP :
1.
TS- large a waves

2.
AV Dissociation – irregular cannon a waves
* For Making Notes

22
3. Kussmaul’s sign – No respiratory variation in JVP.

Classically seen in CP. Also seen in some tamponade
patients
Q
Normally, JVP ↓ with inspiration & ↑ with expiration.

Hepatojugular reflex (HJR) – when right
hypochondrial pressure is given, JVP ↑.
A.Fib- Absent a wave
If JVP ↑ >3cm + >15sec → + HJR , it indicates RHF
4.
↑JVP + no Pulsations + absent HJR → SVC obstruction
Heart Sounds:
Severe TR - CV wave (Lancisi sign) and no x.

5.
Cardiac cycle with JVP correlation :

Constrictive Pericarditis –accentuated X & Y sign
Atrium - Atrial systole: 0.1s + ventricular diastole
(Friedrick sign)
0.7s
6.
Ventricle - Ventricular systole 0.3s + ventricular
diastole 0.5s
Heart Sound:
S1 HS- @IVC
S2 HS- @IVR : A2-P2
S3 HS- with Y descent
ASD – large V wave S4 HS- with atrial kick
Almost all HS are high pitched except S3, S4, tumor
plop sound.
* For Making Notes

23
Medicine
Sound Comments
S1- intensity is imp Loud S1- MS/TS (only in pliable valve not calcified valve)/ hyper dynamic state/ PR <120
ms , e.g.- WPW /Tachycardia
Soft S1- MR/TR / calcified MS/calcified TS/ HF /PR >200ms/ Bradycardia
S2-split +intensity both imp INTENSITY :
Q
Loud S2 -
1. Loud A2- HTN/Supravalvular AS/ CoA /Ascending aortic aneurysm
2. Loud P2- Pulmonary HTN/Supravalvular PS
Soft S2-
1. Soft A2- AS/valvular AR
2. Soft P2- valvular PS/PR
SPLITTING :
•• Narrow splitting- pulmonary hypertension
Q
•• Wide splitting –
A. Early A2- VSD
B. Delayed P2- RVOTO /RBBB
Q
•• Fixed splitting- ASD/ RHF
•• Reverse splitting- Late P2, Early A2 - LBBB, severe LVOTO (Severe AS/HCM)
HOW TO KNOW THE TYPE OF SPLIT?
Inspiratory Expiratory
+ - Normal
+ + Wide split
- - Narrow split
- + Reverse split
If there is no change in timing of split in both inspiration &expiration even after
Valsalva maneuver = Fixed split.
S3 Indicates ventricular volume overload.
Q
MR/AR/PDA/VSD/ Hyperdynamic state/ HF(MCC)
In <35 yrs, S3 is physiological.
Q
In pregnancy/exercise- S3 is physiological
S4 d/t stiff ventricles (↓compliance)/ pressure overload- e.g.-AS/HCM/ HTN/acute
Q
MR/acute AR
Systolic sounds Ejection click –in rapid ejection phase – aftr IVC
Ejection click :
Vascular – root dilatation
Valvular – AS ,e.g.- Bicuspid aortic valve/PS
Non ejection click –in slow ejection phase ,e.g. – MVP click
Diastolic sounds Early diastolic sound :
•• Opening snap –in early passive filling phase –after IVR, e.g.- MS,TS
•• Pericardial knock- occurs between OS and S3 HS, eg- CP
•• S3 HS
Late diastolic sound : S4 HS
Q
Multiphasic Pericardial rubs- acute pericarditis
Hamman’s crunch – pneumomediastinum
* For Making Notes

24
No’s in A.Fib- Pan systolic murmur- causes –

a) No P wave in ECG, •• MR - apical murmur with radiation towards
axilla & back.
b) No A wave in JVP
•• TR- left lower sternal border(LLSB), ↑ with
c) No S4 HS. inspiration , ↑ JVP (cv fusion ,large V wave ,
d) Presystolic accentuation is lost. blunted X wave)
•• VSD –LLSB, ↑ with expiration, JVP normal until
Murmurs: patient develops pulmonary hypertension
1. Systolic murmurs -
2. Diastolic murmur
•• Early systolic murmur-

–– Acute MR (acute mi) •• Early diastolic murmur –
–– Small VSD/ 10 TR –– AR- Erb’s point
–– PR- left upper sternal border(pulm area)
10 PR-
20 PR- Pulm. Htn .
a/k/a hypertensive PR murmur and graham
steel murmur
•• Mid systolic murmur (ESM)-
–– LVOTO-AS/HCM
–– RVOTO-PS ISCHEMIC MR
•• Mid diastolic murmur-

–– MS-
•• Late systolic murmur- MVP
↑flow- ASD /VSD/PDA/MR
Q
with MR
Rytand murmur- CHB
•• TS
–– Carey comb murmur (ARF)
Q
–– Austin flint murmur- severe AR
* For Making Notes

25
Medicine
•• 2 physiological causes: mammary soufflé ,

venous hump
Dynamic auscultation Q
Most murmurs MVP & HOCM

Respiration Inspiration→
↑right sided
murmurs
Continuous Murmur
Expiration →
•• PDA (gibson’s murmur)
Q
↑left sided
murmurs
•• AVF ↑Preload ↑ ↓
↓Preload ↓ ↑
•• Lutembacher (ASD + MS)
↑Afterload AS ↓ (MS -/ ↑) ↓
•• ALCAPA (Anomalous coronary artery from
AR /MR ↑
pulmonary artery ) ↓Afterload AS ↑ (MS -/ ↓) ↑
•• RSOV aneurysm MR /AR ↓
Valvular heart disease – MS (RHD)

Features Comments
Pulse/ BP Pulse ↓↓/ BP-normal
JVP Normal (pulmonary htn- ↑↑ & large a wave Atrial fib- absent a waves )
Apical impulse Non displaced (tapping type )
Sounds S1- Loud S1
Q
S2- S2- OS α 1/severity
Murmur MDM (at apex)
Duration of murmur α severity of murmur (not intensity of murmur)
Indication for surgery Indication :
Symptomatic severe MS
Asymptomatic severe MS-
•• If patient has new onset A.fib
•• Pulmonary hypertension →Epasp>50mmHg at rest or >60mmHg at exercise
MC intervention done in MS is PMBV (percutaneous mitral valve balloon
valvuloplasty)
Rarely – MV replacement
C/I To PMBV-
•• LA clot
•• Moderate to severe MR
•• Non pliable valve
* For Making Notes

26
Valvular heart disease- MR Feature Comment
•• Acute MR Hypokinetic, pulsus parvus et tardus,

Pulse /BP
anacrotic pulse, SBP ↓↓
–– Causes Normal (large a wave- Bernheim effect),
JVP
parvus
Papillary muscle dysfunction/IE/ARF
Apical impulse Undisplaced, heaving type character
(mitral valvulitis)
•• S1 - normal
2° MR- CCF (HF/DCM), Ischemic MR •• S2 - soft A2, narrow or reverse
Sounds
•• Chronic MR- causes- RHD/CTD/ MVP (severe AS) split
•• S4 - common
Features Comments
•• Ejection systolic murmur - right upper
Pulse /BP •• Hyperkinetic, normal volume
sternal border, radiates to both the
•• Pseudo collapsing pulse, Normal BP
carotids
JVP Normal Murmurs
•• Classic diamond shaped crescendo-
•• If patient has pulmonary HTN + MR - decrescendo murmur → late peaking
JVP ↑↑ + large a wave kite murmur (↑ severity)
•• If A.Fib - absent a wave •• Symptomatic severe AS
Apical impulse Displaced (down & out) → hyperdynamic A - Angina - 5yr
Sounds S1 - Soft, S2 - wide split (early A2), S3 - S - Syncope
common, S4 - acute MR D - dyspnea
Indication for •• Asymptomatic severe AS + EF <50% +

Murmur •• Early MR - early systolic murmur,
Q surgery other coronary surgery
•• Chronic MR - pansystolic murmur
•• AV Replacement is preferred
•• MVP - late systolic murmur
•• Surgical AVR (fit patients) > Trans
•• Ischemic murmur - mid to late systolic
catheter AVR (done for old, high risk
murmur
patients)
Indication for •• Any severe symptomatic MR
surgery •• Asymptomatic severe MS- •• High pitched murmurs (AR, AS) - heard by
diaphragm of stethoscope.
–– If patient has new onset A.fib
•• Low pitched murmurs (MS) - by bell of
–– Pulmonary hypertension → ePASP stethoscope.
>50mmHg at rest or >60mmHg at •• Aortic murmurs are heard best in leaning
exercise, if LV is dilated and ESD forward position
>40mm
•• Mitral murmurs are best heard in left lateral
•• MC surgery: MV repair >> MV
position
replacement
Valvular heart disease – AR
Valvular heart disease- AS •• Acute AR - S4 Present. No Peripheral signs.
Causes: –– Valve problem - IE
•• Old age – degenerative & calcific –– Root problem – aortic dissection

•• Chronic AR -
•• Young – bicuspid aortic valve
–– Valve – RHD/ CTD
–– Root – Aortitis (syphilis, large vessel
vasculitis, AS, Bechet’s)/ aortic aneurysm,
chronic aortic dissection, CoA.
* For Making Notes

27
Medicine
Feature Comments 4-6hrs of anticipated labour → SC LMWH

(enoxaparin) → stop LMWH < 24-36 hrs of
•• Hypervolumic pulse/pulsus magnus,
anticipated labour
Q
hyperkinetic
Pulse/BP •• ↑SBP , ↓DBP (↓SVR) •• Postpartum: Can continue with any. Both
warfarin/ heparin are safe. Started 4-6hrs
•• Bounding pulse , peripheral signs present.
after delivery. Initially, heparin + warfarin dual
•• Hill sign present therapy given because warfarin action takes
JVP Normal time. After reaching target INR, heparin is
Apical impulse Displaced (down & out) , hyperdynamic stopped.
•• S1 - normal
•• S2 V - variable – soft A2: valve problem Drugs avoided in pregnancy & breastfeeding:
Sounds •• Normal/loud A2: root problem DOAC
•• S3 - common in most chronic AR D - Dabigatran – direct thrombin inhibitor
•• S4 - acute AR
O - Apixaban
•• Early diastolic murmur (heard in Erb’s
Murmurs
Q
points) (murmurs of HOCM & regurgitation A - Rivaroxaban Oral factor Xa inhibitor
is located at Erb’place)
C - Edoxaban
•• Symptomatic severe AR
•• Asymptomatic severe AR + EF <50% + other
Indication
coronary surgery + ESD > 50 mmHg / EDD CHD
for surgery
>65 mmHg Disease Comments
•• AV Replacement >> TAVR
Types:
Q
•• Ostium secundum – MC (RAD)
ANTICOAGULATION FOR •• Ostium primum - (LAD)
PROSTHETIC VALVES •• Sinus venosus

•• Coronary sinus type
•• Antibiotic of choice: Warfarin O/E:
•• Bioprosthetic valve: Warfarin X 3 months, •• Pulse – normal
target INR: 2-3 → continue aspirin lifelong •• JVP - large v waves
•• Mechanical valve: Lifelong warfarin, target •• BP - normal
INR – •• S1 - normal
1. If MV - 2.5-3.5 ASD •• S2 - wide fixed split

•• S3 - occurs d/t RV dilatation
2. If AV -
•• Murmurs - ESM in PA (left upper sternal
•• 2-3 (without risk factor) border)
•• 2.5-3.5 with risk factors like - •• No shunt murmur,only flow murmur (only
exception is lutembacher syndrome -
–– A.Fib, hypercoagulable state
continuous flow murmur)
–– h/o TIA, stroke •• Apical impulse – RV apex, hyper dynamic
–– EF <30% precordium.
Q
•• Lowest risk of IE among all CHD
Anticoagulant in pregnancy Indication for closure:
•• 5-12 weeks: warfarin → <5mg /dl → warfarin •• RA/RV enlargement

Warfarin → >5mg/dl → LMWH (Enoxaparin)
•• 12-36 week: warfarin
•• >36 week: Heparin → IV UFH → stop UFH <
* For Making Notes

28
2 types: •• Young + HTN + pulse & BP difference between

•• Muscular - closes spontaneously arms & legs
•• Membranous (MC) Murmurs:
–– Outlet VSD (associated with AR) •• ESM @site of coarct
–– Inlet VSD (associated with AV cushion •• Continuous murmur in the posterior
defects)
infrascapular region because of collaterals of
–– Cleft MV/ Ostium primum type VSD Q
coarctation of aorta (suzman sign)
O/E:
CoA Indication for surgery –
•• Pulse - hyperkinetic with normal volume
•• If complication – HTN /HF
•• BP - normal
•• Gradient > 20mmHg
•• JVP - normal
VSD •• c/o collaterals
•• Apical impulse - displaced d/t LV overload
down & out, hyperdynamic character •• Neonates critical CoA
•• S1 - low •• Turner syndrome
•• S2 - wide split Ioc: – CTA/ MRI
•• S3 - common, because of LV volume overload Toc: Balloon angioplasty
•• Murmur - pansystolic murmur, heard best in 4 components:
LLSB ↑ with expiration
•• Infundibular PS
Indication for closure:
•• Large VSD
•• QP/QS >/= 2:1
•• RVH
•• h/o IE
•• Over riding of aorta
•• LV dilatation
•• Triology of fallot – ASD + infundibular PS +
Common in preterm → Tx- NSAIDS – Ibuprofen , RVH
indomethacine •• Pentology of fallot – TOF + ASD/PDA
Term infants →Tx- intervention (percutaneous / •• Episodic cyanosis - aka cyanotic spells/ tet
surgical) spells
O/E - •• First 2-6 months, no cyanosis, d/t HbF
•• S1 - Loud •• Polycythemic
ToF
•• JVP - normal O/E-
•• Narrow split, continuous murmur in gibson’s •• Single S2 (absent P2)
Q
Q
area
•• ESM in LLSB – disappears in cyanotic spells
PDA
Ductus obligatory conditions: Triggers for cyanotic spell: fever, feeding,
•• Mitral atresia playing
•• Triscuspid atresia Tx: complete primary repair by 6 months –
•• Aortic atresia definitive tx
Q
•• Pulmonary atresia Cyanotic spell tx – oxygen + knee-chest position
•• TGA with intact septum –– IVF bolus + IV morphine
•• Hypoplastic left heart syndrome –– IVF beta blocker+ IV phenylephrine
To keep ductus patent – use PGE1 analogue- –– Palliative shunts- modified blacock tausing
alprostadil shunt + rastelli shunt
•• Any cyanotic CHD can increase risk of thromboemboli manisfestation.

•• ASD, VSD, PDA – L to R shunts → ↑PBF → shortness of breath/failure to thrive → pulmonary HTN → shunt
reverses → cyanosis &polycythemia → ↑risk of thromboemboli: Eisenmenger Syndrome .
Q
* For Making Notes

29
Medicine
Coarctation of Aorta:
AV Cushion Defect – goose neck abnormality

Q
Postero inferior Rib notching (ribs 3-9)
Coarctation of Aorta (Figure of 3)
Q
TGA – egg on side appearance
Q
TOF – boot shaped heart (RVH)
Q
TAPVC – snowman appearance / figure of 8
* For Making Notes

30
•• ECG - global/multifocal ST ↑, not associated

with reciprocal changes, PR↓ (aVR- PR↑) , TP
segment downsloping- spodiac sign
Q
•• ECHO - Mild pericardial effusion
PAPVC
Concave ST Elevation / Saddle Back ST Elevation

•• Tx: NSAIDS + colchicine
•• Alternate - Corticosteroids
•• Post MI Acute pericarditis Tx - high dose
aspirin
•• Uremic pericarditis Tx - urgent dialysis
Q
Q
Ebstein Anomaly - RA enlargement (box shape heart)
PERICARDIAL DISORDERS
•• Acute pericarditis
•• Constrictive pericarditis
•• Tamponade
Acute Pericarditis:
•• Causes: >80% Idiopathic /viral
•• CTD / SLE/RA
•• Uremia → ↑tamponade
•• Any cardiac procedure → ↑ tamponade risk
•• Post MI – Early & late pericarditis
•• C/F - chest pain - positional (↓with leaning
forward position) / pleuritic pain (↑with deep
inspiration), radiate to trapezius
Q
•• Associated signs - rub (multiphasic)
* For Making Notes

31
Medicine
Cardiac Tamponade CP RCM

•• Causes - any cause of acute pericarditis, 7. ECHO - Normal thick,
uremia, after cardiac procedure, post-MI, CTD, ventricle interdependence
7. ECHO- thick ventricles
mediastinal tumors (MC - non small cell lung → ↑respiro phasic variations
cancer), trauma & septal bounce
•• C/F - Beck’s triad - muffled heart sounds+ ↓ 8. LEDP- RVEDP <5 8. >5mmHg
BP+ jugular venous distension
Q
9. Systolic area index >1.1,
done only in patients where 9. Systolic are index <1.1
•• JVP - ↑x descent, ↓y descent
Q
ECHO is not diagnostic

•• ↑RR, ↑HR, Pulsus paradoxus, clear chest. 10. CT/MRI - ↑pericardial 10. ↑ventricular thickness
•• ECG - sinus tachycardia, low voltage complexes, thickness >4mm on CT/MRI
electrical alternans (beat to beat variability in 11. BNP – Normal 11. BNP -↑↑
QRS amplitude and QRS axis. 12. TOC- Pericardiectomy 12. Tx- depends on cause
•• 2D ECHO - pericardial effusion + diastolic RA /
RV collapse Acute Aortic Syndromes:
•• Cardiac catheterization - ↑↑diastolic pressures •• MC risk factor is hypertension
+ equalization (LVEDP- RVEDP <5) 1. Aortic dissection → 80% cases
•• Tx: IVF 2. Aortic intramural hematoma
•• Toc - Urgent pericardiocentesis (<500ml) 3. Penetrating atherosclerotic ulcer
•• Avoid pericardiocentesis: in aortic dissection •• Tx based on Standford classification
Q
–– Ventricular free wall rupture Stanford A Stanford B

•• Definite indication of pericardicentesis: 1. When only ascending 1. Ascending aorta not
jugular venous distension aorta involved. involved
2. Tx: surgery for all
–– ↓BP
Constrictive Pericarditis: ↓BP/↓HR

Causes - MCC in india - TB 1st line - IV beta blockers → IV
Q
NTP (arteriovasodilator)
–– MCC in world- radiation
IV Esmolol > labetalol
•• Anything that causes recurrent acute
pericarditis can result in chronic contrictive •• Target to be achieved in 1 hr of tx: SBP <120mm
Hg, HR <60 bpm
pericarditis.
•• Older classification – Debakey : BAD (mnemonic)
CP RCM
Q B - I: Both ascending +desceding
1. Kussmaul sign 1. Kussmaul rare
2. Pericardial knocks 2. S3/S4 A - II:Ascending only
3. - 3. MR/TR murmurs heard D - III: Descending only
4. - 4. Pulmonary HTN common
→ A – Thoracic alone
5. Poorly felt apical impulse 5. AI Present
Q → B – Both thoracic + abdominal aorta
6. Normal ECG 6. ECG - ↓Voltage
* For Making Notes

32
Tennis ball sign: Aortic Dissection

Q Q
•• C/F - HTN + Chest pain radiating to back to
interscapular region, tearing / ripping quality.
•• MC site of intimal tear - right posterolateral
ascending aorta close to the root of aorta
Q
•• Depending on occlusion of vessels d/t tear-

–– Asymmetric pulse and BP between arms/
stroke/TIA/STEMI (Inf. > Ant. MI) /
Tamponade / Acute AR → AHF
•• Ix - CTA (MC) > MRI (gold std.) > TEE (only for
ascending dissection & unstable)
Q
Bradyarrhythmias - Dr. Dilip's Pathway
DX: 1st Degree AVB
DX: Mobitz 1 (Wenkebach)
* For Making Notes

33
Medicine
Acute Bradycardia: ACLS 2020

yes
Bradyarrythmia observe
No
SBP <90 + Syncope/ AHF/Chest pain
1st line Tx: Atropine, 0.5mg ( repeat X2)
Max dose – should not exceed 3mg in total

NR
DX: Mobitz II / 2nd Degree AVB 2ND line Tx: Pacing (transcutaneous) - best
anterior MI, RBBB / Alternate: chronotropic drugs to ↑HR , eg-
Dopamine / Adrenaline
Transvenous Pacing (RV)
Chronic Bradycardia: Permanent Pacemaker

•• 2 types of pacemakers are:
–– VVI → AF + AVB or SND → complication-
pacemaker syndrome
–– DDD → sinus rhythm + AVB → complication-
pacemaker tachycardia.
•• Pacemaker syndrome - occurs only when patient
DX: Mobitz II with 2:1 Block reverts back to sinus rhythm and presents with
syncope
High Grade AVB
•• Pacemaker tachycardia - occurs because of
excessive sensing
Management of Bradyarrhythmias
•• Indications of permanent pacemaker - Any
symptomatic bradycardia including sinus
bradycardia
AVB SND SYNCOPE CONGENITAL

•• Any 3rd degree block (CHB) •• Sick sinus syndrome, a/k/a •• Corrected sinus •• Any 20/30 AVB +
•• 2nd /3rd degree AVB, but is tachybrady hypersensitivity Neuromuscular disorder
exercise induced •• MC tachycardia is A.Fib •• Depending on •• Congenital CHB
•• 2nd degree AVB with or •• MCC for permanent symptomatic of •• Congenital LQTs (high risk)
without symptom. pacemaker asymptomatic
•• Chronic severe bradycardia
<40/min
* For Making Notes

34
Tachyarrhythmias- Dr Dilip’s Pathway
Q Q
•• Atrial flutter can not be placed in regular or irregular rhythm. Look at lead II. Unstable baseline
sawtooth appearance seen. Negative /inverted p wave seen.
Monomorphic VT
•• > 3 consecutive VPC’s @>/=100-120 /min
•• If occurs @<100/min but >60/min → AIVR (accelerated idioventricular rhythm) - seen post reperfusion
of MI, no treatment required. Its benign.
–– Sustained VT - >30 sec
–– NSVT - <30 sec
* For Making Notes
35
Medicine
Hallmarks of VT
•• Very wide QRS (RBBB >140ms / LBBB >160 ms)
•• Atypical BBB
•• North west axis (verecke’s AVR sign)
•• Brugada positivity /josephson sign
•• AV dissociation (fusion / capture beats)
•• Absence of r/s complexes
DX: Multifocal Atrial Tachycardia
Q
DX:A.Fib - MC sustained arrhythmia in the world .
DX: AVNRT
Q
DX: Atrial Flutter
DX: Regular Wide Complex Tachycardia
DX: Focal Atrial Tachycardia

DX:VT (Concordance)
Narrow Complex Tachycardia
* For Making Notes

36
adenosine- 6+12+12, max - 30mg)

•• Alternate drugs- iv beta blockers and ND-CCB
•• NCT → rhythm → irregular → 1st line beta
blockers /alternate-ND-CCB
Wide Complex Tachycardia

•• Monomorphic VT→ regular /irregular →
antiarrhythmic infusions
Q
–– Procainamide
DX: Irregular Wide Complex VT
–– Sotalol
–– Amiodarone: bolus 300mg → 1mg/min X 6hr
= total 360mg
0.5mg/min x 18 hrs = total 540mg
Total dose = 1200mg
Q
•• Polymorphic VT (PMVT) - DOC - MgSO4 +/-

Pacing
MANAGEMENT OF A.FIB
DX: V.FIB A.All → heparin (UFH/enoxaparin):
•• Give warfarin if
Management of Tachyarrhthmias Q
no –– If moderate-severe MS present
pulse –– Mechanical Prosthetic valve
TACHY cardiac arrest ACLS Cardiac
arrest pathway •• If not severe MS /Mechanical prosthetic valve-
–– Calculate CHA2DS2-VASC score
Q
With pulse (r/o sinus tachycardia)
no / SBP <90 –– If score 0, no need of long-term

Stable SHOCK –Synchronise DCC anticoagulation
C/I of DCC – Sinus tachycardia –– If score 1 in male/2 in female - anticoagulation
Yes considered
- M.A.T
- Digoxin toxicity –– If >2 in males and >3 in females, then
See Width of VT mandatory anticoagulation therapy
If WCT >0.12 sec Therapy given: DOAC / Warfarin
If NCT <0.12 sec
B. Better symptom control:
Narrow Complex Tachycardia •• Rate control – most important

–– 1st – beta blockers /alternate is ND-CCB .
•• NCT → rhythm → regular → vagal maneuver –
corrected sinus massage / Valsalva → AVNB –– Only exception to this rule is patient who is
drugs (adenosine in regular rhythm. Dose of having AHF.
* For Making Notes
37
Medicine
–– In AHF- Digoxin –– Rosuvastatin -20-40mg/dl
–– In CHF or no HF- beta blockers /alt – ND- –– Atorvastatin – 40-80mg/dl

CCB
–– Target LDL <70mg/dl
–– AVN Ablation + VVI pacing
–– If remains more than 70mg/dl
•• Rhythm control- optional
–– Electrical > pharmacological (IC/III) Add :1. EZETIMIBE (NPCILI inhibitor)
2. PCSK-9 inhibitors - Evolocumab
C. Control of risk factors Alirocumab
Q
Special Situations •• 1° Prevention – LDL >190 - high intensity statins

LDL > 100 Ezetimibe / PCSK-9 inhibitor
–– Target LDL for 1° prevention is >100 mg/dl
2 groups-
•• Age - 40-75
•• LDL - 70-180
Age:
1. 40-75 with DM – Statins LDL>/100 add
Ezetimibe
2. 40-75 without DM – see 10 yrs cardiovascular risk

DX: WPW Syndrome (ACC/AHA) →
Q
Short PR Interval, Delta Wave
–– If < 5% Risk - low risk → Statin not required
–– If 5-19% risk - Consider statin
–– If > 20% risk – high risk → Statins Given
•• In intermediate risk, consider ASCVD risk –
–– LDL > 160/ ↑ hsCRP/ CKD/H/O preeclampsia/
premature menopause/family h/o premature
ASCVD/Chronic inflammatory diseases
•• CT coronary calcium - can also be used (Agatson
score)
1. If score is 0 → no need for statins
DX: Osborne Waves / J Waves 2. If score is >0 → consider statins

Q
Hypothermia •• Fibrates are indicated only if TGL >500 mg/dl
to reduce the risk of Pancreatitis. If TG <500 -
CHOLESTEROL GUIDELINES 1st choice is still statins.
•• 2° Prevention → k/c/o ASCVD → Statins
(irrespective of LDL levels):
* For Making Notes

38
PERIPHERAL ARTERIAL DISEASE Neuropathic Ulcers

1. 1st metatarsal
Venous Ulcer
2. Callus
1. Medial malleolus
3. DM
2. Superficial
Q
4. Foot deformity
3. Pulse present
5. Foot arches are lost
4. Warm
6. Painless ulcer
Q
5. Trophic changes
6. Hyperpigmented
Pressure Ulcers
Arterial Ulcer 1. At bony prominences in immobilized patients
1. Deep ulcer on toes, lateral malleolus

Q
2. Disuse atrophy
2. Pulse absent 3. Seen in sacrum/back/heel
3. Cold periphery 4. Macerated ulcer
4. Intermittent claudication
5. Critical limb ischemia - can be gangrenous
•• Tx of pressure ulcer and neuropathic ulcer

is shifting the pressure to another place to
decrease pain.
* For Making Notes

39
Medicine
Rutherford classification
Audible Doppler Sensory /
Category dx
Arterial venous motor loss
Anticoagulant
+ + None Viable I +urgent
revascularization
Chronic PAD Acute PAD Non Anticoagulant
Intermittent Claudication → - + some viable +emergency
inflow and outflow ,III revascularization
Inflow - aortoiliac region → Non
leriche syndrome (buttock/ MCC - Embolus > - - complete viable, Amputation
thigh claudication present ↓/- thrombus III
femoral pulses present, erectile
dysfunction
Outflow - Femoro-popliteal
6 P’s- pain, pallor,
Rest pain → critical limb ischemia
pulselessness,
→ endovascular intervention
poikilothermia,
(angioplasty +/- stenting)
paralysis, paresthesias
Workup:
ABI → 0.9-1.4
•• If <0.9 → PAD → segmental
ABI
•• If >1.4 → non compressible Deep femoral artery stenosed before and after stenting
vessel → TBI (toe brachial
index) INFECTIONS IN CARDIOLOGY –ARF
Tx:
•• ↓ MACE (major adverse
cardiac events)
•• ASA/ STATINS +/- ACEI /
ARBS
•• ↓ Symptoms - Cilostazol
(PDE3)
•• Naftidrofuric (5HT2)
↓
Refractory symptom –
Intervention Aschoff Body
Ix to be done while planning
intervention:
•• Evidence of gas infection /streptococcus
pyogenes – Modified Jones Criteria
Q
•• Duplex US
•• DSA – gold standard –– Throat swab culture /RAT
•• CTA
–– ASO Titres / ADB titres - positive
–– >2 major or >1 major + 2 minor
•• Modified Jones Criteria - Major (CASES) &
minor (PEACH)-
* For Making Notes

40
MAJOR INFECTIONS IN CARDIOLOGY – IE

C - Carditis, if severe myocarditis → can lead to HF, Tx
•• Organisms –
– corticosteroids
Valvulitis - MR (MC), Carey Coomb murmur –– Overall MCC - Staphylococcus aureus
A - Arthritis – MC –– NVE- Staph aureus – acute onset/ IVDU/
hospitalized with CVC
Q
Mono / polyarthralgias, TOC - NSAIDs
S - Subcutaneous nodules on extensor surface of upper –– NVE- Viridans group strep – subacute/SABE/
limb dental procedure/poor oral hygiene
E - Erythema marginatum, centrifugal expansion, non
–– PVE- <2-12months- Staph (CONS/S.aureus)
pruritic
→ >12month- same like NVE
S - Sydenham’s chorea - longest latency period
Emotional lability – Earliest to occur •• Criteria - Dukes criteria
Tx – Haloperidol, if refractory then tx - corticosteroids
MAJOR CRITERIA
+ IV Ig
1. Blood culture positivity - > 3 blood cultures from
Q
MINOR different sites (20ml blood for 1 culture)
For Coxiella burnetti, single ↑ in titre of phase 1 IgG
P - Prolonged PR interval
>1:800 – Diagnostic
E - ESR ↑↑
2. Imaging:
A - Arthralgia - mono / poly
•• MC- ECHO
C - CRP ↑
H - High temperature / fever •• 1st – TTE
•• Best – TEE: friable mitral valve vegetations
•• Prophylaxis – antibiotics
Q
are seen. In new PV, dehiscence is seen.

–– No carditis / valvulitis: total duration of 5
•• Severe valvular regurgitation → severe HF.
yrs /upto 21 yrs of age (whichever is later)
•• Complications seen on TEE - abscess seen
–– Carditis present / valvulitis- total duration
of 10 yrs / upto 21 yrs of age
MINOR CRITERIA
–– Valvulitis present & severe manifestation – 1. Predisposing conditions
eg: HF / MVR Lifelong prophylaxis 2. Fever>38
–– If only valvulitis- total duration of 10yrs / 3. Blood culture not meeting major criteria
till 40 yrs of age (whichever is late) 4. Immunological – roth spots (nonspecific) / osler’s nodes
•• Antibiotics: (painful, in fingers & toes) / MPGN / RF present
5. Vascular - emboli / mycotic aneurysm → ICH /
1. 1st line – penicillin
conjunctival hemorrhage/janeway lesions (painless ,in
a. Oral penicillin IV/IM benzathine penicillin palms & soles)
b. Dose of benzthine penicillin - <27kg - •• DX: 2 major / 1 major + 3 minor / 5 minor
0.6mu / >27kg – 1.2mu
•• Empirical TOC : Ceftriaxone + Vancomycin +
2. 2nd line - sulfadiazine Rifampicin(+/-) +Gentamycin
3. 3rd line - macrolides
•• For HACEK – TOC is Ceftriaxone
* For Making Notes

41
Medicine
Prophylaxis Indications For Surgery In Ie

Indications When to give ? What ? 1. Severe valvular regurgitation → Severe HF
1. H/o IE 1. Dental 1. Amoxicillin /
2. Uncontrolled infection – invasive (periannular abscess/
2. Prosthetic valve procedures ampicillin – 30-
Conduction block) / persistent (cultures + >1 week of
3. Any untreated 2. Invasive 60 mins prior
antibiotics)
cyanotic CHD respiratory tract to procedure
procedures single dose 3. Organism – indicating poor prognosis- MDR /fungal
4. Any congenital
HD – after 2. If penicillin –– If fungal endocarditis not treated with
repair defective allergy – surgery – Azoles Prophylaxis For Lifetime
→leak &during clindamycin 4. Prosthetic valve – dehiscence / dysfunction
repair prosthetic – p/o or iv
material was used 5. Risk of embolism – if vegetation size>1 cm
→1st 6 month
prophylaxis given
* For Making Notes

ENDOCRINOLOGY
HYPOPITUITARISM
Etiology
Q
Sheehan syndrome Apoplexy RT Infiltration
•• Post partum pituitary •• Haemorrhage in the •• More sensitive: •• 3 main examples:
Q
necrosis pituitary Hypothalamus > –– Sarcoidosis,
•• Cause: Severe post partum •• Cause: 90% due to pituitary –– Hemochromatosis,
haemorrhage pituitary macro adenoma •• If radiation is >12-18 –– Langerhans cell
•• History of multiple blood •• Other causes: DIC, gy: GH affected first, histiocytosis
transfusion during delivery / Malignant hypotension, mainly somatotropes •• Mainly damage anterior
labour trauma, coagulopathy •• If radiation is >30 pituitary
•• Mother presents with •• Clinical features: gy: lead to multiple •• Patients presents with
lactation failure nausea, vomiting, intense pituitary hormone central DI, polyuria,
•• Deficiency of GH, headache because of deficiency polydypsia
prolactin, TSH (central raised ICP, diplopia •• History of childhood •• Sarcoidosis can lead to
hypothyroidism) due to 6th CN damage, brain tumor central & Nephrogenic
•• Investigation: MRI → empty visual field defect, DI
Q
sella is seen Adrenal insufficiency •• Lymphocytic

(hypotension, Tachycardia, hypophysitis:
•• Normally ACTH /
hyponatremia) Idiopathic condition,
gonadotropin spared in
Sheehan syndrome, but •• Investigation: mainly associated
incase if rarely ACTH –– CT / MRI: huge with pregnancy (3rd
deficiency is seen, we replace mass in sella with trimester), IgG4 disease
cortisol with hydrocortisone intralesional density & iplimumab also cause
(haemorrhage) Q
pituitary insufficiency .
•• Gold standard -
insulin tolerance test •• Treatment: IV fluids & It is associated with
(contraindications: coronary hydrocorticosteroids ACTH > TSH deficiency.
artery disease, seizure) (Dexamethasone / Treatment - Steroids
Methylprednisolone) •• To differentiate between
•• Other tests - glucagon
stimulation test, GHRH lymphocytic hypophysitis
arginine test, macimorelin & pituitary adenoma,
stimulation test we should check stalk
–– Serum prolactin thickness, bulky pituitary
Estimation test to (symmetric enlargement
detect prolactin in Lymphocytic
deficiency & simple hypophysitis)
thyroid function testing
to check central
hypothyroidism (T3, 4
low, normal or decrease
TSH)
45
Medicine
PITUITARY ADENOMA •• >200 → confirms the prolactinoma

•• Associated with Hyper prolactinemia
Other causes
•• Drugs
–– D2 receptor blockers: Anti emetic →
metaclopramide, domperidone
–– Anti psychotic: haloperidol, risperidone
–– Amine depletors: tetrabenazine, verapamil
Classification based on size & functional
status •• CKD
1. Size •• Focal seizures

•• <1 cm: Microadenoma •• Stress
•• >1 cm: Macroadenoma
•• Pregnancy/ Post partum periods
•• Macroadenoma lead to VFD (mainly bitemporal
Heminopia), headache, diplopia, cranial nerve •• Anything that stimulates the reflex arch
palsy
•• Primary hypothyroidism
2. Functional status
•• Idiopathic
•• Functioning tumor: prolactinoma
•• Non functioning tumor: gonadotropin adenoma Clinical features
–– Most common pituitary adenoma overall:
•• Most common: Gonadal dysfunction
prolactinoma
–– 2nd Most common: Gonadotropin adenoma –– Prolactinemia → decrease gonadotrophs →
decrease FSH, LH → Hypogonadotrophic
–– 3rd Most common: Somatotroph adenoema
hypogonadism
–– 4th Most common: ACTH secreting pituitary
adenoma / corticotroph adenoma •• Common in females → present with infertility
–– Least common: Thyrotroph adenoma → cause •• 2nd Most common feature: galactorrhea
central hyperthyroidism
Investigation Indications for treatment

•• Dynamic contrast enhanced MRI •• Any Symptomatic adenoma (micro / macro)
•• Macroadenoma: Seen as figure of 8 or snowman •• Macroadenoma (with or without symptoms)
appearance
Treatment
PROLACTINOMA –– Dopamine receptor agonist (bromocriptine
•• Normal Prolactin <20 → in case of females desiring pregnancy
or already pregnant, cabergoline → in
•• >20 = suspect prolactinoma
case of non pregnant female, pergolide
* For Making Notes

46
→ have impact on heart valves so annual

echocardiogram is mandatory
Q
•• 2nd line treatment: trans sphenoidal surgery
•• 3rd line treatment: pituitary radiotherapy
•• If patient have infertility then start

bromocriptine
check prolactin levels after 3-6 months → if normal,
then female can conceive → if it is not normal, then
do trans sphenoidal surgery or radiotherapy
If patient conceives, then stop bromocriptine &

assess headache, visual field defect etc.
Clinical features
↓ •• Bony changes (hypertrophy) → skull - frontal
If patient have stable tumor → just observe bossing, enlargement of mandible & maxilla,
enlarge frontal sinus seen in X-ray
↓
•• Soft tissue changes → results in obstructive
If unstable tumor & have symptoms like headache, sleep apnoea, increased ring size and shoes size,
VFD widening of joints, spade-shaped distal phalanx
↓
Do MRI → if enlarged mass present → start

bromocriptine
•• Increased heel pad thickness > 23-25 mm

Q
If treatment effective, If treatment fails,
continue bromocriptine do surgery (TSS), •• Metabolic changes → Impaired glucose
tolerance, DM
ACROMEGALY •• Hyperhydrosis → hypertrophy of sweat glands
- Earliest sign
•• Due excess of Growth hormone in adults
•• Patient may also have LVH, cardiomegaly,
•• Most common cause of GH excess in acromegaly thyromegaly & renomegaly, colonic polyp -
is somatotroph adenoma (among them 40% have increase risk of colonic cancer
GS alpha mutation)
•• Very rarely, patient have Hypothalamus

hamartoma, ectopic tumors like small cell
Lung tumor, medullary cancer, pancreatic
neuroendocrine tumors that leads to excess GH
* For Making Notes

47
Medicine
Investigation •• Ends up with permanent Central DI
•• Serum IGF -1 → screening test Hook effect

Q
•• Patient have functioning macro adenoma

Q
if normal, then if value is increased, •• Assay → normal or mild increase in prolactin

level → dilute the sample (1:100) → if value is
rule out GH excess do 75 gm of OGTT
normal or mildly increased, the dilution will be
undetectable
If decreased, then rule if GH increases, then it •• If the value is detectable / increased, then it is
known as hook effect
Out GH excess confirms GH excess
•• To localize, do dynamic contrast enhanced MRI Macroprolactin

•• Mass in pituitary confirms somatotroph adenoma •• They bound to immunoglobulin segments,
mainly IgG
•• If no mass seen in MRI, then cause would be
ectopic •• Assays: Higher prolactin values
•• Investigation of choice: PEG precipitation
Treatment (polyethylene glycol)
Q
•• 1st line treatment: trans sphenoidal surgery

•• 2nd line: medical treatment
SIADH (SYNDROME OF
INAPPROPRIATE ANTIDIURETIC
–– Somatostatin receptor agonist (2 & 5):
Octreotide, Lanreotide, Pasireotide HORMONE)
–– GH receptor antagonist: Pegvisomant
Q
•• Have ADH excess / increase ADH effect
–– Pituitary radiotherapy •• Most common cause is hyponatremia in

hospitalized patients
Stalk effect
Clinical features
•• If we transect the stalk, there will be deficiency
of all pituitary hormones except prolactin - it •• Euvolemia (normal JVP & BP, no Ascites &
increases because it is controlled by Dopamine edema, no Pleural effusion)
•• Non functioning macro adenoma can compress •• Hyperosmolar hyponatremia (decrease serum
osmolality)
the pituitary stalk which can produce
hyperprolactinemia •• Increased urine osmolality
•• Trans sphenoidal surgery also does the stalk Treatment
transection
•• Check if severe symptoms (coma, seizures)
•• Leads to classic triphasic response present, give 3% NaCl → if no severe symptoms,
do standard SIADH management
Q
•• Most commonly after TSS, patient have

Transient central DI (treatment of choice = •• To reduce total body fluid, restrict water (1-
desmopresssin) lasts for 1-2 weeks, then there 1.5 L/day water is sufficient) → to increase
will be degeneration of neurons of posterior effect, patient can use strongest drug Vaptans
- tolvaptan (hepatotoxic), conivaptan (aquaretic
pituitary → release the stored SIADH →
agent) → increase urine excretion
results in Transient SIADH
* For Making Notes
48
Etiology –– History of subarachnoid haemorrhage,

polyuria
•• Tumor: small cell lung cancer
•• Treatment: IV fluids (0.9% NS)
•• Pulmonary causes: pneumonia (mainly legionella
infection), TB, PPV
Approach to polyuria
•• Neurological: GBS
•• >3 L/day or >2 L / m2 / Day or 40 ml / kg / day
•• Drugs: anti cancer drugs (cisplatin, vincristine,
Cyclophosphamide), antidepressants, •• If UOSM decreased→ water diuresis → seen in
DI, 1° polydypsia
Q
antipsychotics, anti epileptics (carbamazepine,
oxcarbamazepine), clorpropamide, thiazide
•• Endocrine patients
Differential diagnosis
•• Cerebral salt wasting syndrome
–– Defect of CNS → increased release of BNP,
increased urinary sodium & osmolality
–– Total body salt decreases → patient will be
Hypovolemic
Conditions S. Na+ Baseline Post H2O Post dDAVP Pituitary MRI Baseline AVP
UOSM deprivation
PP N/↓ ↓ ↑ Same N N/↑
CDI N/↑ ↓ Same ↑ Stalk thickening ↓↓
NDI N/↑ ↓ Same Same N N/↑
Treatment of choice for CDI - Post neuro surgery

Desmopresssin Any CNS infections
•• Causes of CDI
–– Congenital
Treatment of choice for NDI -
thiazide
Didmoad syndrome / wolfram syndrome
Q
•• Causes of NDI
is mitochondrial transmitted disease
DI - Diabetes insipidus –– Congenital
DM - Diabetes mellitus Due to vasopressin 2 receptor mutation
OA - Optic atrophy Male > female

Aquaporin 2 mutation, AR pattern
Q
D - Deafness
–– Acquired –– Acquired
Infiltrative cause Drugs-related Causes: Lithium,
Metastasis demeclocycline, Amphotericin B
CNS causes
* For Making Notes
49
Medicine
Electrolytes problems: ↑ Ca2+, ↓ K+
Other: Sarcoidosis, amyloidosis, multiple myeloma, sickle cell disease
MEN SYNDROMES
MEN 1
Features MEN 2A (Sipple) MEN 2B MEN 4
(Wermer)
Inheritance AD, Chromosome 11 AD, chromosome 10 AD, Chromosome 10 AD
RET gene (proto onco Q
MEN 1 (menin Q RET gene
gene)
Mutations protein – tumor •• Codon: 918 (worst CDK N1B
Q •• Codon Mutations: 634,
suppressor protein) mutation)
88
Present, cause
PHPT + - +
hypercalcemia
present, MC is
Pituitary adenoma - - +
prolactinoma
present, non
functioning >
Pancreatic NENs gastrinoma - - +
•• Most common
cause of death
present, most
common cause
MTC - +
of death, most
aggressive
Present, Bilateral &
Pheochromocytoma - Present, Bilateral & benign
benign
Familial medullary thyroid
Angiofibroma, Reproductive organ
cancer, Hirschsprung Mucosal neuroma,
Others lipoma, foregut tumors: Testicular
disease, cutaneous lichen marfanoid habitus
Carcinoid tumor
amyloidosis
≥ 2 major features
present or 1 major
2 major manifestations
feature with FDR
Diagnosis or FDR with proven RET Same as MEN 2A
with MEN 1 or
mutation
positive MEN 1
gene mutation
In 634, 883 mutation:
do Total thyroidectomy In 918 Mutation: do
Treatment before 5 years of age in Total thyroidectomy
case of intermediate to within 1 year of age
high risk of Mutations
* For Making Notes

50
IPEX (immune poly endocrinopathy X

linked):
•• FOX P3 Mutation
(IBD, Ulcerative colitis)
DIABETES MELLITUS -
DIAGNOSIS
APS (AUTOIMMUNE
Normal Pre-diabetes DM
POLYGLANDULAR SYNDROME)
FPG (mg/dl) < 100 100 – 125 ≥ 126
APS Type 1 2h PG (mg/dl) < 140 140 – 199 ≥ 200
•• Rare HbA1C (%) < 5.7 % 5.7 – 6.4 % ≥ 6.5 %

Classic symptoms of diabetes + random blood sugar
•• Mutation: AIRE gene
Q
≥ 200 → DM
•• APS 1 also known as Autoimmune poly
endocrinopathy with candidiasis & ectodermal Types of DM
dystrophy
1. Type I DM
•• Characteristic triad
•• Due to Ab like IAA (insulin auto Ab), ICA (islet
cell Ab), Zn8T8 (zinc transporter Ab), GADA
(anti CAD 65) → cause beta cell destruction
Q
•• Features:
–– Osmotic symptoms: polyuria, polydipsia
•• Ectodermal dystrophy
–– Catabolic symptoms: weight loss
APS Type 2 –– Age of onset: juvenile
•• Female > male •• Treatment
•• Polygenic inheritance –– Insulin
•• Triad
* For Making Notes

51
Medicine
2. Type II DM Diabetes Mellitus - Management

•• Most common in adults, now common in children Effect Drugs
also Insulin, insulin secretagogues,

Hypoglycemia risk
sulphonylurea, meglitinides
•• Features: •• Weight loss: SGLT 2 inhibitor,
GLP 1 receptor gonist
–– Metabolic symptoms
•• Normal: metformin, alpha
–– Obesity Weight glucosidase inhibitor, DPP4
inhibitor
–– PCOS
•• Weight gain: sulphonylurea,
–– Acanthosis nigricans meglitinides
•• Treatment •• Reduced by SGLT 2 inhibitors,
MACE GLP 1 agonist
–– Oral drugs mainly +/- insulin
•• Induced by rosiglitasone
3. MODY (Maturity onset diabetes in young Reduce heart failure: SGLT 2

inhibitors
= age <25) HF Induce heart failure event: DPP4
inhibitors (saxagliptin / alogliptin),
•• Monogenic, AD pattern
Pioglitazone
•• Strong family history DKD SGLT 2 inhibitors, GLP 1 agonist
Safe in ESRO Linagliptin & pioglitazone
•• Beta cell dysfunction → decrease release of
Metformin, incretin drugs, DPP4
insulin
GI side effects inhibitors, GLP 1 agonist, alpha
•• Most common is MODY type 3 → HNF 1 alpha glucosidase inhibitor
gene mutation Incretin group of drugs (DPP4

Pancreatitis
inhibitors & GLP 1 agonist)
•• Treatment: sulphonylurea •• Pioglitazone
•• MODY type 2 is least severe •• Increase risk of Bladder cancer

Cancers
(GLP 1 agonist increases risk of
•• Weight of latent is normal medullary & pancreatic cancer
Osteoporosis (by pioglitazone),
4. LADA (latent Autoimmune diabetes in Bone issues
Canagliflozin
adults) •• NAFLD & NASH: metformin,
Q
•• Most common in age of > 30 pioglitazone

Non DM uses
•• Late dumping syndrome reduced
•• Type 2 diabetes with Ab by acarbose - liraglutide
•• Most common anti body is anti GAD Ab
Q
•• NIDDM is maintained atleast till >6 months,

then it is converted into IDDM
* For Making Notes

52
Effect Drugs Types of insulin

•• Bromocriptine, Bile acid •• Rapid acting insulin:
sequesters
–– Analogs: lispro, aspart, glulisine
–– Colesevelam, renolazine
–– Saroglitazar: dual PPA alpha –– Short acting: regular insulin → cheapest and
Q
& gamma agonist easy to use, IV
Misc drugs used
–– Teduglutide: GLP 2 agonist,
in DM Analogs & short acting are Prandial insulin
→ decreases intestinal
motility Given before meal
–– Dapiglutide: GLP 1 & 2 agonist
•• Intermediate acting: NPH
–– Tirzepetide: Max. weight loss
•• Long acting: Glargine, detemir, degludec
Q
→ GLP 1 & GIP analogue
–– Intermediate & long acting are used as Basal
Complications of diabetes insulin
•• Vascular diseases –– Given irrespective of meal time
–– Micro
•• Insulin Given subcutaneously in
Retinopathy
–– Abdomen
Neuropathy
–– Lateral thigh
Nephropathy
–– Posterior arm
DKD
•• Never Given on buttocks
–– Macro
Coronary artery disease •• Site should be rotated every time otherwise it
can lead to lipodystrophy
Peripheral artery disease
•• Complications
Cerebral artery disease
–– Hypoglycemia
•• Infections
•• Cataract: Due to excessive sorbitol production
Q –– Weight gain
•• Glaucoma –– IV insulin → hypokalemia

–– Subcutaneous insulin → lipodystrophy, lipo
Effects of insulin
atrophy
Features Dawn effect Somogyi Insulin def.
effect DKA vs HHS
7 am glucose ↑ ↑ ↑
DKA HHS
3 am glucose N ↓ ↑
Blood Glucose 250 – 400 mg% >600- 800 mg%
Treatment ↑ ↓ ↑
Comorbidities Less More
•• Dawn effect: Natural increase in counter Coma / surgery Less More
regulatory hormone
-/ may little
Plasma ketone ++++
•• Somogyi effect: Mid night Hypoglycemia & present
early morning hyperglycemia S. HCO3 <18 mmol/L >18 mmol/ L
•• Insulin def.: Night dose of insulin is not Arterial pH <7.3 >7.3
sufficient → effect seen as hyperglycemia in Normal ( < 12 –
morning AG ↑ ( >12-14)
14)
* For Making Notes

53
Medicine
DKA HHS (Bevacizumab, Ranibizumab)

S. Osm ↑↑ ↑↑↑(>320 osm/L) –– Indication for PRP
Sodium 125 -135 135-145 Severe non proliferative diabetic Retinopathy
Potassium N/ ↑ N
Proliferative diabetic Retinopathy
Creatinine N/ ↑ ↑↑
Mortality <1% 15%
Vitrectomy: for vitreous haemorrhage
•• In DKA, plasma ketone is detected best by VEGF: for diabetic retinal edema
Beta hydroxy butyrate level → >30 mmol /L
Diabetic neuropathy
•• In HHS, beta hydroxy butyrate is <1.5 mmol / L
•• Distal symmetric polyneuropathy
•• Treatment
–– Length dependent atonal neuropathy
–– DKA
–– Earliest site involved: feet
FLIP : Fluid (in 1st 3 hours → 2-3 L or
10-20 ml / kg/ hr of NS 0.09% → After –– Painful but 70% painless, burning, numbness
3 hours shift the fluid to 0.45% NaCl), –– Treatment for painful form: SNRI, tricyclic
Insulin, potassium
Q
antidepressants, calcium channel blockers
If capillary blood glucose value is <200- •• Diabetic autonomic neuropathy
250 mg/dl → add Dextrose 5% solution
to prevent Hypoglycemia –– GI (bladder & bowel problems: constipation,
diabetic diarrhea, gastroparesis), GU
–– Use FDII regime (erectile dysfunction), CVS (Tachycardia)
If S. Potassium: problems
1. 3.3–5.2 - give insulin + IV fluid + KCl •• Diabetic amyotrophy
2. <3.3 - give KCl → when K+ gets normal → –– Asymmetric involvement

give insulin –– Focal pain in hip, thigh, buttock
3. >5.2 → insulin + close watch potassium –– Proximal weakness because of radial & nerve
–– S. PO4 2-
<1 mg/dl → risk of rhabdomyolysis root involvement in diabetes
If pH is <7 → add IV NaHCO3 •• Mononeuropathy

–– Can affect the peripheral nerves
Microvascular Complications of
Most common: Median nerve (carpal tunnel
diabetes syndrome)
•• Non proliferative diabetic Retinopathy
Common fibular nerve: foot drop
–– Micro retinal Aneurysm
–– Can affect the central nerves
–– Hot spot
Most common: CN 3 > 6 > 4
–– Cotton wool spot
CN 3 palsy + Pupil sparing = Diabetes
•• Proliferative diabetic Retinopathy
–– Neovascularization near the disc
Q Diabetic nephropathy
•• Check Microalbuminuria → proteinuria → GFR
–– Treatment: Pan retinal photo coagulation
drop → end stage kidney disease
Q
+/- vitrectomy + intra vitreal anti VEGF

* For Making Notes
54
•• Biopsy: Kimmelstiel Wilson lesion also known as –– Beta hydroxy butyrate <2.7 → not insulin
nodular glomerulosclerosis mediated
•• Treatment: <2.7
–– ACE inhibitors or ARB blockers
–– Finerenone: non steroidal MRA if insulin value <3 → cause is IGF 2
>3
When to start screening for diabetes
•• Type 2 diabetes: at the time of diagnosis C peptide <0.2 → exogenous insulin abuse
•• Type 1 diabetes: after 5 years of diagnosis, >0.2
then start screening
•• Retinopathy: do fundus examination Rule out sulphonylurea abuse → if positive,
•• Nephropathy: do EGFR + urine albumin: it is an induced cause
creatinine If -ve
•• Neuropathy: do 10 gm mono filament testing
+ deep tendon reflexes + pain & temperature Do Imaging
assessment
•• Check for Type 2 diabetes:
•• If screening is normal → do annual screening
–– MRI of pancreas → mass lesion present →
METABOLIC SYNDROME due to insulin
•• Criteria
Q
–– If MRI is normal, do Ab testing because
insulin auto Ab can cause Hypoglycemia
I. Central obesity - check by waist → do SACST (selective arterial calcium
circumference stimulation test to diagnose Nesidioblastosis
Males ≥ 102 cm, females ≥ 88 cm (benign beta cell hyperplasia) - can be
Idiopathic (known as NIPHS – non insulinoma
In Asian males ≥ 90, females ≥ 80
pancreatogenous Hypoglycemia syndrome)
II. Impaired fasting glucose, Impaired glucose or occur after gastric bypass)
tolerance, frank Type 2 diabetes
•• Whipple’s traid
Q
III. Hypertension
Symptoms of Hypoglycemia
IV. Triglyceride ≥150 mg/dl
– Low HDL: males <40, females <50
•• If any 3 of these 5 Criterias are present, it is
diagnosed as Metabolic syndrome
APPROACH TO HYPOGLYCEMIA
•• Check for diabetes
–– Present: Most common cause is drugs - Documentation of Complete resolution
insulin, sulphonylurea, pioglitazone
Q
Hypoglycemia of symptoms with
glucose
–– Absent: Do 72 hour fast (CBG <45 – take
blood sample – end the fast)
* For Making Notes

55
Medicine
•• Level 1: ≤ 70 mg/dl Any 1 is positive

•• Level 2: ≤ 54 mg/dl
•• Level 3: incapacitated Endogenous cortisol excess → endogenous
Cushing syndrome
CUSHING SYNDROME
•• Excess cortisol Level True Cushing Pseudo Cushing
•• Most common cause: exogenous corticosteroid •• Conditions associated with pseudo Cushing
use syndrome:
•• Clinical features: –– Severe depression
–– Weight gain (centripetal obesity)
–– Severe obesity
–– Round or moon face
–– Critical illness
–– Dorso cervical fat pads / Buffalo hump
–– Clinical alcoholic patient
–– Purple striae (due to spontaneous bruising)
•• After resolution of these symptoms, test CRH
–– Proximal myopathy stimulation after dexamethasone suppression
Q
–– Metabolic disturbances: –– If the test is negative → pseudo Cushing

Hyperglycemia
–– If test is positive → true Cushing
Hypokalemia
•• True Cushing
Hypertension low = source is Adrenal → CT /
S. ACTH MRI
hirsutism
Fungal infections (ex: candidiasis) Normal / High = source is
pituitary/ ectopic (Pituitary
Cataract adenoma = cushing’s disease)
Nephrolithiasis
Polyuria –– Difference between Pituitary vs ectopic
source
Psychosis, depression, dementia
Use high dose dexamethasone test or
–– Blood changes: neutrophilia, eosinopenia, CRH stimulation test
lymphopenia
If there is response = problem is pituitary
–– Facial plethora adenoma
•• Work up:
–– 3 am cortisol level check → if low → exogenous
Cushing disease Do MRI → mass present → Cushing disease
If normal / increased If not response = ectopic ACTH production
Do screening → low dose dexamethasone

suppression test, 24 hour urinary free Do CECT abdomen → mass present → ectopic
cortisol, late night salivary cortisol source
If Imaging is normal → do Bilateral IPSS
(inferior petrosal sinus sampling)
* For Making Notes
56
ADRENAL INSUFFICIENCY •• Work up
A.1° insufficiency
•• Problem with adrenal gland
•• Low cortisol production → increased ACTH
•• Most common cause in India - infectious,
leprosy, in western world – Autoimmune
adrenalitis
Q
•• Low level of adrenal Androgen → so low level of

DHEAS
•• Low aldosterone level results in salt wasting →
Hypovolemic hyponatremia PHEOCHROMOCYTOMA
•• Treatment: hydrocortisone, fludrocortisone •• Tumor of chromatin cells
B. 2° insufficiency •• Type of paraganglioma
•• Problem with Pituitary gland •• Most common site is Adrenal gland (in medulla)
•• Low level of ACTH → low S. Cortisol •• Most common extra Adrenal site is Para Aortic
region near the organ of zuckerkandl
Q
•• Lead to Risk of Adrenal crisis
•• Low Adrenal Androgen •• Genetic syndromes associated:
•• Aldosterone level normal –– MEN 2A, 2B
•• No salt wasting → euvolemic hyponatremia –– VHL
•• No hyperkalemia, no Metabolic acidosis
–– NF-1
•• Investigation of choice: ACTH stimulation test
–– TMEN 127
•• Non sun exposed area are quite specific for this
disease features (gingiva, nails, nipples) –– SDH
•• Clinical features: –– MAX

–– Weakness & fatigue •• Biopsy: histopathology
–– GI symptoms, abdominal discomfort
–– Neutropenia, eosinophilia, lymphocytosis
–– Zellballen pattern: nest of tumor cells

surrounded by supporting cells known as
sustentacular cells
Q
* For Making Notes

57
Medicine
–– By giving alpha blockers → phenoxybenzamine

Q
•• Clinical features: 6 P’s

–– Pressure (BP) - paroxysmal hypertension or –– After 24 hours, give beta blockers →
sustained hypertension propranolol
–– Palpitation –– Liberal use of salt & fluid
–– Pain – headache, chest pain (most common •• Surgery

cause of death) –– Increased BP → treat with NTP
–– Pallor due to vaso constriction –– Tumor removed → hypotension → manage by
–– Perspiration IV fluids
–– Postural hypotension –– If metastasis present, treatment will

continue for that even after removing tumor
–– Weight loss
Most common site for Metastasis → liver
–– Hyperglycinemia
Best treatment → I131 MIBG
–– Constipation
Congenital Adrenal hyperplasia
–– Hypercalcemia
•• AR inheritance
•• Low cortisol, high ACTH - reason for
hyperpigmentation
Q
•• 21-hydroxylase deficiency, 11-OH deficiency,

17-OH deficiency, 3-beta-hydroxy steroid
deficiency
•• Work up
•• 21 & 11 OH-deficiency affects Adrenal gland
–– Urinary Metanephrines test - elevation is
specific for chromaffin cells
Q
•• 17 OH & 3 beta hydroxy Steroid deficiency
affects Adrenal & gonads
–– Plasma metanephrines test - preferred only
in high risk patients
Q
•• In 21 & 11-OH deficiency, female child will
have ambiguous genitalia → excess Androgen
–– If test value is mildly increased → it is false
from Adrenal glands
positive due to some drugs reaction like
alpha, beta blockers, diuretics etc. •• In 17-OH deficiency, male child will have
ambiguous genitalia
–– If significant elevation in value → do imaging
of abdomen > chest •• In 3-beta hydroxy steroid deficiency, both
Normal imaging, no mass - can be false male & female children will have ambiguous
positive genitalia
Abnormal imaging, mass present → •• In 17-OH & 3-BHS deficiency, there will be
Pheochromocytoma decreased Testicular Androgen
For metastatic & multifocal disease •• 21-OH deficiency is also known as non classic
congenital Adrenal hyperplasia
•• Nuclear imaging: I123 MIBG, PET scan, Ga68
(DOTATOC / DOTATATE scan) –– Post puberty → PCOS-like presentation
→ hyperandrogenism features, oligo /
•• Preparation: reduce BP → target <160 /90
amenorrhea
* For Making Notes
58
–– Treatment: hydrocortisone or Prednisolone Treatment: Conservative

–– Prenatal Treatment: dexamethasone
Q
–– With high T4 → central hyperthyroidism
Continue Treatment if karyotype is 46xx •• High TSH
+ recessive defect till delivery
–– With low T4 → 1° hypothyroidism
Stop Treatment if karyotype is 46xy + no
recessive defect Treatment: T4 replacement
Integrated approach to TFTs & Thyroid –– With normal T4 → subclinical hypothyroidism
disorders
Treatment - T4 replacement
•• Low TSH & T4 → Central hypothyroidism
•• Etiology: 2° pituitary > 3° Hypothalamus cause Indication: TSH >10, symptoms present
•• High T3, Normal T4 - Isolated T3 toxicosis –– With high T4 - central hyperthyroidism

•• Normal T3 & T4 - Sub-Clinical hyperthyroidism –– Dose of T4 replacement therapy:
•• TSH low, T4 high - 1° hyperthyroidism
1.5 – 1.7 mg / kg / day
•• Radioactive iodine ablation: I123 → t1/2 = 13
hours Better to give levothyroxine at empty
stomach
•• Alternatively, we can use Tc99m pertechnetate
→ t1/2 = 6 hours Starting dose - 100 kg/day
•• Diffuse increased uptake of thyroid: Grave’s
Check TSH every 6-8 weeks
disease → TRAG Ab test should be done to
confirm •• Most common cause of hypothyroidism in world
is Autoimmune thyroiditis (Hashimoto’s)
Q
•• Patchy increased uptake:
–– Focal: Solitary toxic adenoma •• Risk of Malignancy with cold nodules is highest
–– Multiple: Toxic multinodular goiter (plummer’s
disease)
Q
•• Thyroglobulin
–– Low level - Source is exogenous - Factitious
hyperthyroidism
Q
–– High level - source is endogenous- thyroiditis,

also from ovarian tumor (do abdominal USG)
•• Normal TSH
–– With low T4 - central hypothyroidism
–– With normal T4 → look for T3
Low T3 → low T3 syndrome or sick
euthyroid syndrome
In early stage of this syndrome: Low T3,

reverse T3 is high, T4 & TSH is normal
In late stage: Low T3, high revers T3, low

T4 & TSH
* For Making Notes
59
Medicine
Graves disease –– Moderate to severe: corticosteroid ,

Teprotumumab
•• Type 2 hypersensitivity reaction mediated by
TRAB antibody
Q
–– Surgical decompensation of orbit
•• Example of autoimmune thyroiditis •• Most specific investigation is Ab detection test
•• Clinical features •• Doppler shows excessive vascularity
–– Thyrotoxicosis (high T3 & T4 + low TSH)
Treatment of hyperthyroidism
–– Euthyroid profile (normal TFT) also present
in some patient •• For child & pregnant female: anterior thyroid
drugs
–– Tachycardia
–– 1st line: PTU - less teratogenic
–– Palpitations
–– 2nd & 3rd line: methimazole - teratogenic,
–– Systolic hypertension
aplacia cutis
–– High pulse pressure
–– Non pregnant females: Beta blockers & anti
–– Diarrhea thyroid drugs (methimazole > carbimazole),
–– Menstrual irregularity CCB
–– Thyroid eye signs –– Continue till euthyroid levels
–– Extra thyroidal Clinical features –– Definitive Treatment: Radio iodine ablation -
Graves orbitopathy (mostly asymmetrical) I131 = t 1/2 = 8 days
Q
→ orbital fibroblast → exophthalmos

Contraindicated in pregnancy, breast
→ exposure keratitis → Corneal ulcer &
blindness, leads to edema, Restrictive feeding mother, suspecting cancer,
extra ocular myopathy (most common is moderate to severe orbitopathy
inferior Rectus muscle)
Q
Thyroid Storm
Dermopathy (pre tibial myxedema)
•• Most common cause is inadequate preparation
Acropachy (bone disease - rare)
of gland for surgery
•• Clinical features
–– Undetectable TSH, detectable T3, T4
–– Increased HR
–– Increased systolic BP
•• Treatment
–– Beta blockers (esmolol, metaprolol, propranolol),
•• Investigation
CCB (verapamil, diltiazem), anti thyroid
–– IOC: MRI of orbit drugs (PTU), lugol’s iodine/potassium iodine,
dexamethsone, plasma exchange
•• Treatment
Myxoedema coma Q
–– Mild to moderate disease: conservative

•• Hypothermia
* For Making Notes

60
•• Reduced mentation •• Very high TSH, very low T4

•• Bradycardia, bradypnea •• Treatment:
•• Hypotension –– IV / oral T4
•• Hypoglycemia –– Hydrocortisone
THYROIDITIS
Chronic Subacute Subacute
Features Acute suppurative Riedal’s
lymphocytic lymphocytic granulomatous
Autoimmune,
Etiology HLA DR 3, Autoimmune Viral Infection -
DR5, B8
Pain - - ++ ++ -
Fever /
- - ++ ++ -
malaise
1° Hypothyroid to
TFT Thyrotoxicosis N TFT N TFT
hyperthyroid euthyroid
Persistence Yes Variable No No Yes
Lymphocytic Lymphocytic Giant cells & Fibrosis +
Pathology Abscess
infiltration infiltration granulomas seen inflammation
Beta blockers,
Antibiotics, incision Immuno suppressent
Treatment Levothyroxine NSAIDS,
& drainage (tamoxifen), surgery
corticosteroids
•• Presence of germinal centres indicate chronicity. •• Hashimoto patients are at increased risk of PTC
& Thyroid lymphoma
•• Presence of Hurthle cells is common in
Hashimoto’s (but not specific).
Calcium & bone disorders

Hypercalcemic Disorder
Disorder Ca PO4 PTH ALP Comments
PHPT ↑ ↓ ↑↑ ↑ •• Asymptomatic, picked incidentally, renal stones, abdominal pain
•• Most common cause: parathyroid adenoma (right inferior
parathyroid gland involves most commonly)
•• Less common cause: hyperplasia, carcinoma
Q
•• Diagnosis: Tc99m sestamibi scan
•• Treatment: Surgery in case of >65 years age, severe
hypercalcemia, low bone mineral density
•• If no surgery then give cinacalcet
FHH ↑ ↓ ↑ ↑ Calcium sensing defect, asymptomatic, benign
PTHrP ↑ ↓ ↓ ↑ Most common mechanism of hypercalcemia in Malignancy, renal cell
cancer
Lyrics mets ↑ ↑ ↓ N Multiple myeloma, activate osteoclast
* For Making Notes
Vit D toxicity ↑ ↑ ↓ Variable Marker: 25 HCC value
Sarcoidosis ↑ ↑ ↓ Variable Lymphadenopathy, lymphomas, 25 HCC & 1, 25 HCC level increases
•• Treatment: Corticosteroid
61
Medicine
Other causes of hypercalcemia –– Severe dehydration, shock, low BP, Tachycardia
•• Thiazide –– Altered mental status
•• Endocrine conditions such as hyperthyroidism, –– Weakness

Adrenal insufficiency –– Lethargy
•• Vitamin A toxicity •• ECG changes: ST elevation, short QT, J waves
•• Milk alkali syndrome - chronic form is known as •• Treatment:
Burnett syndrome
–– Correct shock by normal saline
•• 3° Hyperparathyroidism
–– Reduce S. Calcium → by calcitonin ,
Hypercalcemia Bisphosphonates (IV pamidronate ,
zolendronate)
Q
•• Other:
–– Loop diuretics only in case of hyper volemic
state
Milk alkalosis AKI
–– Dexamethasone in case of vit D excess
Hypercalcemic crisis –– Denosumab → subcutaneously, safe in renal
failure
•• Clinical features
–– Dialysis
–– Severe polyuria
Hypocalcemic disorders
Disorders Ca PO4 PTH ALP Comments
Q
Cause: Autoimmune , APS 1, post thyroid surgery – have
1° Hypoparathyroidism ↓ ↑ ↓↓ N Transient hyperparathyroidism, post parathyroidectomy
(rare), Wilson disease, Hemochromatosis
•• Rickets, osteomalacia, cod fish vertebrae, looser’s zone
In diet↓ / pseudo fractures
Vit D deficiency ↓ ↑ N /↑
In CKD↑ •• Elevated ALP in CKD → renal osteo dystrophy → rueger
jersey
•• IA, Ib , Ic, II → IA & Ic have skeletal defect called as
Albright hereditary osteo dystrophy
PHP (GNAS gene #) ↓ ↑ ↑↑ N
•• Features: Short stature, round face, brachydactyly
Q
(knuckle Dimple sign)
PPHP (GNAS gene #) N N N N Albright hereditary osteo dystrophy
•• High bone turnover
•• X-ray: cystic & blastic lesion
•• Abnormal bone remodelling
•• If symptoms present: bone pain (tibia)
PDB N N N ↑↑
•• MC neurological symptoms: headache
•• CN affected commonly: 8th CN
•• Increased risk of osteosarcoma (giant cell tumor of bone)
•• Treatment in Symptomatic patient: Bisphosphonates
Osteoporosis N N N * ForNMaking
BoneNotes
metric problem, trabecular bone affected
62
–– -1 to -2.5 = osteopenia → do therapy >

Other causes of hypocalcemia
decide by FRAX tool (tells about 10-years
•• Critical illness risk of any major fracture & hip fracture)
•• Excessive bone turnover (post parathyroidectomy) –– < - 2.5 = osteoporosis - do treatment
•• If patient is heavily immobilized- paget’s disease
Approach
•• Sequestration (high PO4, excess citrate, •• History of fragility fracture ( colle’s fracture )
pancreatitis, alkalosis, Bisphosphonates)
•• Check if Kyphosis is present or not
Clinical features •• History of wedge compression fracture
•• Neuromuscular Irritability (perinoral parasthesia, •• If patient does not have history of fragility
Chvostek sign, Trousseau sign, tetany, seizures) fracture → do BMT screen - DXA scan
•• Target for screening: Elder patient (>65 years
•• Cardiac irritation
age) or <65 years of age + risk factors present
•• ECG: ST depression, long QT
Q
•• Risk factors:
Treatment –– Advancing age
–– Glucocorticoids use
•• If patient have severe symptoms: IV calcium
gluconate –– Personal history of fracture after 40 years
of age
Diagnosis & management of post –– Family history of hip fracture
menopausal osteoporosis –– Active Smoking
–– Excess alcohol consumption
Diagnosis
–– Malabsorptive state
•• Bone mineral density
–– Chronic liver disease
•• DEXA scan - check T score –– Rheumatoid arthritis
–– > -1 = normal - no treatment require , take –– IBD
vitamin supplements (800 units of vitamin
D / day) –– Early menopause
* For Making Notes

63
Medicine
Treatment •• MRKH: Patient have low testosterone level,

female patient, pubic & axillary hair present, no
•• 1st line = Bisphosphonates
Q
palpable gonads
–– Oral: arendronate, risedronate •• Complete AIS: Testosterone high, male patient,
Side effect: pill-induced esoohagitis pubic & axillary hair absent, palpable gonads
Contraindication: GERD •• If Uterus is present
–– IV: zolendronate •• Breast development present
Side effect: hypocalcemia, osteonecrosis •• For outflow tract obstruction, do MRI → if

of jaw, atypical femoral fracture, present → vagainal atresia, Transverse vaginal
nephrotoxic
Q
septum, imperforate hymen
•• 2nd line = anabolic agents - teriparatide, •• If no outflow obstruction → constitutional delay

abaloparatide, anti sclerostin (romosuzumab) puberty, Hyper androgenic states (early PCOS,
non classic Adrenal hyperplasia), prolactinoma
•• Denosumab: subcutaneous
•• If Secondary sexual characteristics are absent:
•• SERM: raloxifene (hot flushes risk present) -
only give if high breast cancer risk present –– Look at the height of patient
•• Bazedoxifene - with Conjugated estrogen Short: look FSH → if low - central causes
•• Hormone replacement therapy: estrogen ○○ High FSH - Turner syndrome
–– Oral ○○ MCC of 1° amenorrhea - Turner

syndrome
–– Transdermal patch
Normal:
Approach to primary amenorrhea ○○ Low FSH: Isolated gonadotropin
•• No menstruation till Age ≥ 15 years or > 5 years deficiency-kalmman syndrome
of breast development ○○ High FSH: Gonadal dysgenesis
•• Look for the uterus first → if absent, do
karyotype
–– 46xx (+) → MRKS
–– 46xy → CAIS
* For Making Notes

NEUROLOGY
APPROACH TO WEAKNESS
Feature UMN LMN NMJ Myopathy
Distribution •• UL - extensors Distal /segmental •• Ocular - Symmetrical
ptosis / proximal weakness
•• LL - flexors +
bulbar
hip abductors
•• Limb -
proximal
weakness
Atrophy •• Not seen +++ Not seen Not seen
•• Disuse atrophy
seen very late
and rarely in
UMN lesions
Fasciculation (Ant. Horn Not seen +++ Not seen Not seen
cells damage indicate
fasciculation)
Tone ↑↑↑ (spasticity) ↓↓↓(flaccidity) Normal Normal
DTR ↑↑↑ +/- clonus ↓↓↓ /-ve Normal Normal
Plantar reflex Extensor – Babinski Flexor – Babinski
+ve –ve
•• In pure myopathy + myasthenia gravis → 3. Biceps reflex - Biceps brachii muscle →

no sensory involvement → bladder/bowel Musculocutaneous nerve
Q
involvement is rare
4. Brachioradialis – Radial nerve
IMPORTANT REFLEXES 5. Triceps reflex - Radial nerve
6. Finger flexion reflex - Median nerve & Ulnar nerve
7. Cremastric reflex – L1 → Genital branch of

genitofemoral nerve
Q
8. Bulbocavernous reflex – S2-S4 → Pudendal nerve
9. Plantar reflex – S1
Q
Normal – Flexor hallucis Abnormal – Extensor

+ Toe flexors → Tibial hallucis +Toe extensor
1. Ankle reflex - Gastrocnemius /Soleus muscle → nerve → deep peroneal nerve
Tibial nerve
2. Knee reflex - Quadriceps femoris muscle →
Femoral nerve
67
Medicine
Myotomes & Dermatomes SPINAL CORD SYNDROMES

Level Dermatome Myotome
C5 Lateral antecubital Shoulder abduction /
fossa External rotation
C6 Thumb Elbow flexion / Wrist
extension
C7 Middle finger Elbow extension /Wrist
flexion
C8 Little finger Thumb extension /ulnar
deviation of wrist
T1/T2 Medial antecubital •• Finger abduction/
fossa adduction
•• T1- supplies all the
intrinsic muscles of
hand Causes of spinal cord syndromes
•• All intrinsic muscles •• Trauma / tumors / demyelinating diseases /
supplied by ulnar vascular conditions / syrinx → central cord
nerve except – syndrome / infections
L-Lateral 2 lumbricals
O-Opponens pollicis
Columns
A-Abductor pollicis •• Posterior column – fine touch /pressure /
vibration /conscious position (proprioception)
brevis
→ I/L loss of posterior column
F-Flexor pollicis brevis
L1/ Over anterior thigh Hip flexion –– Romberg’s test – test of posterior column &
L2
vestibular apparatus.
L3 Over medial femoral Knee extension –– Lhermitte sign – nonspecific, can be seen in
condyle MS, NMO ,Cervical spondylitis
L4 Medial malleolus Ankle dorsiflexion –– Sensory ataxia – high stepping stamping gait
L5 Dorsum of 3rd Great toe extension –– Pseudoathetosis
metatarsophalangeal
joints
•• Anterolateral tracts -
S1 Lateral heel Knee flexion /ankle –– Spinothalamic tract – if lesioned →→ C/L

plantar flexion loss of Pain & Temperature
Erb’s palsy Klumpke’s palsy

–– Corticospinal tract –
•• C5/C6 affected •• C8/T1 affected If lesioned → I/L weakness (UMN)

•• Lateral sensory •• Medial sensory loss If anterior horn cells damaged → I/L
loss •• Wasting of intrinsic muscles
weakness (LMN)
•• Policeman’s tip +/-complete claw hand If intermediolateral nucleus of T1-L2

•• Horner syndrome is also damaged → Horner’s syndrome
common in this setting
* For Making Notes

68
Syndrome Features
•• B/L loss of sensations
Complete •• B/L UMN weakness below level of lesion + Bladder-bowel incontinence
•• B/L LMN palsy @ level of lesion
•• I/L loss of posterior column sensations
•• I/L UMN weakness
Q •• C/L loss of pain & temperature – below level of lesion
Brown – Sequard
•• +/- I/L loss of Pain & temperature only for 1-2 segments @ level of lesions → Tract of
Lissauer
•• +/- I/L LMN weakness @ level of lesion
Anterior cord – •• B/L loss of pain & temperature /B/L UMN weakness
dissociated sensory loss •• Spared: Posterior column sensation +/- incontinence
•• MCC - syringomyelia
•• Posterior column orientation – (lateral) C T L S (medial)
•• Spinothalamic tract orientation – (lateral) S T L C (medial) → sacral sparing →
characteristic of central cord
•• Anterior horn cell - (lateral) L T A (medial) → medial arm is affected first.
•• Involves intermediolateral nucleus → Horner syndrome
Q •• When corticospinal tract is involved → UMN weakness
Central cord
•• B/L pain & temperature loss (spinothalamic tract) → cape-like /suspended sensory loss
→ extensive sensory loss – descending kind of sensory loss & sacral sparing → motor loss
– UL > LL
•• Upper Limb: LMN type of weakness (wasting of intrinsic muscles / atrophy / fasciculation)
•• Lower Limb: UMN weakness
•• B/L burns of hands
•• Incontinence – rare/at last
•• L1-L2 vertebral level → Sacral spinal cord (S1-S5)
•• Back pain
•• Sensory loss not prominent / saddle anesthesia
•• Motor deficit not common – if seen, distal motor deficit → only ankle reflex is affected
Q
Conus medullaris (UMN weakness), symmetric motor weakness
•• Bladder/bowel involvement – early
•• Early sexual dysfunction
•• Bulbocavernosus reflex +ve
•• Dissociated sensory loss seen
•• Below L2 level → lumbosacral nerve roots
•• Radicular pain prominent / saddle anesthesia
•• Motor deficit – early, common, both knee & ankle reflexes involved, asymmetric motor
Cauda equina weakness
•• No bladder/bowel involvement or sexual dysfunction at time of presentation.
•• Bulbocavernosus reflex –ve
•• No dissociated loss seen → it is a nerve root lesion
* For Making Notes

69
Medicine
VISUAL FIELD DEFECTS craniopharyngioma- inferior fibres >> superior

fibres / ACOM artery aneurysm
Q
C. C/L Homonymous hemianopia → optic tract

D. Parietal (Baum’s) optic radiation fibres - C/L
inferior quadrantanopia PITS
E. Temporal (Meyer’s) optic radiation fibres → C/L
superior quadrantanopia
F. C/L Homonymous hemianopia with macular
sparing → occipital cortex lesion
•• PITS:
A. I/L mononuclear vision –– Parietal = inferior

B. Heteronymous bitemporal hemianopia → central –– Temporal = superior
chiasma – causes can be pituitary adenoma /
STROKE LOCALISATION
Artery Features
ICA •• I/L monocular vision loss (Amaurosis fugax)
ACA •• Stroke causing leg problems – C/L Hemiparesis
•• Leg involvement >> Arm/face involvement
•• Stroke with isolated leg problem
•• Gait apraxia
•• Abulia / Antisocial behaviour / Incontinence
•• Release reflexes – certain reflexes suppressed in childhood/infancy by frontal lobe →
redevelopment of these reflexes on the opposite
•• Cortical stroke mimicking a spinal cord problem → ACA stroke
MCA •• >70% strokes
•• M1 MCA →
–– C/L Hemiparesis / Arm/face involvement >> Leg (feet spared)
–– C/L Hemisensory loss + global aphasia → comprehension, repetition, fluency is lost (only left
sided lesions results in aphasia) + visual field defects involving optic radiation, parietal or
temporal lobes
–– Superior division involvement - C/L hemiparesis +/- C/L hemisensory loss +/- nonfluent aphasia
–– Inferior division involvement - No hemiparesis /no hemisensory +/- visual
–– Field defect +/- fluent aphasia (wernicke’s aphasia – comprehension, repetition lost but fluency
is increased)
–– If non-dominant parietal lobe is involved - constructional apraxia, C/L neglect + Anasagnosia
(awareness of one’s own defect)
–– If dominant angular gyrus in parietal lobe involved → Gerstmann syndrome - Acalculia /
Agraphia/ Rt. or Lt. confusion /finger agnosia
PCA •• U/L - C/L Homonymous hemianopia with macular sparing
•• B/L – Cortical blindness (Anton syndrome) → visual anasagnosia
Q
VA (Or PICA) •• Wallenberg syndrome / LMS (Lateral medullary syndrome)
–– No hemiparesis / sensory involvement (pain & temperature) / crossed signs – I/L LMN type of
loss of pain & temperature in face + C/L loss of pain & temperature in limbs & body
–– I/L Horner syndrome
–– I/L cerebellar syndrome
* For Making Notes
–– Lateral medullary nerves - LMN 9/10 palsy
–– Bulbar symptoms - dysphagia /palatal dysarthria / dysphonia + refractory hiccups are
characteristic
–– Loss of reflexes seen, especially I/L gag reflex
70
Artery Features
Basilar •• Complete basilar lesions/ mid basilar lesions/ top of basilar lesions
•• Complete basilar occlusion – B/L motor sensory symptoms (UMN) + B/L CN palsies (LMN )
•• Mid-basilar occlusion -
–– Locked-in state – quadriparesis (UMN type) – medial part of pons affected on both sides,
therefore, motor tracts are affected
–– B/L LMN type facial palsy – no expression
–– Complete loss of horizontal gaze (as pons affected)
–– Midbrain spared
–– Spared-
Consciousness
Pain & temperature
Limited vertical gaze / blinking
Pupillary reflex +ve
•• Top-of basilar occlusion –
–– No motor/sensory loss
–– Altered mental status/ coma
–– Vertical gaze palsy
–– Peduncular Hallucinosis – dream-like state +/- memory issues
Cerebellar •• I/L cerebellar signs & symptoms
•• Limb /truncal ataxia
•• Dysmetria & incoordination
•• Nystagmus /diplopia
•• Pendular knee jerk / dysarthria
•• Vertigo /nausea/vomiting
Lacunar •• Small vessel stroke – arteriole affected
•• MC vessel affected - lenticulostriate branch from MCA
•• Reason - Microatheroma (HTN >> DM)
•• No cortical signs/symptoms, no aphasia
•• No brainstem signs /symptoms
•• C/L dense hemiparesis (arm = face = leg) +/- C/L hemisensory loss
•• 5 lacunar syndromes-
–– Pure motor stroke – MC
–– Pure sensory stroke
–– Sensorimotor stroke
–– Ataxic hemiparesis
–– Dysarthria – clumsy hand syndrome
STROKE MANAGEMENT
•• Notes
* For Making DWI shows core infarct. Hyper intense areas seen
in DWI are diffusion restricted areas that indicate
Dense MCA sign – clot in M1 MCA
core infarct area.
•• PWI – Hyperintense areas shows salvageable
ischemic areas.
•• Mismatch – if infarct-ischemia mismatch is >1.7 →
consider EVT
71
Medicine
* For Making Notes

72
COMPLICATIONS AFTER
ISCHEMIC STROKE
1. BP management:
•• Target: in lytic candidate = <135 /110 mmHg , in
Q
non-lytic candidate = <220/120mmHg

•• Drugs: Nicardipine – DOC
2. Fever: ↑ cerebral metabolic rate - ↑ infarct
territory
3. Glucose: target blood glucose = <180mg% → both
hypoglycemia and hyperglycemia are dangerous
•• ICU - IV insulin infusions
4. Venous thromboembolism: Intermittent pneumatic
compressions + LMWH (prophylaxis)
•• Enoxaparin 40mg/day s.c
5. Cerebral edema: cytotoxic cerebral edema,
•• 2° prevention → started by D2, peak by D3/D4, starts resolving by
D5-D14.
1. Antiplatelets –
•• Conservative Mx: Head-end elevation to
–– Aspirin / Clopidogrel : if patient is lysed,
Q
30-degree + hyperosmolar agents (Mannitol /
start Aspirin/Clopidogrel only after 24 hrs 3% NaCl)
to reduce risk of bleeding.
If not tx, Refractory
–– Indications for DAPT (Aspirin + Clopidogrel):
high risk TIA / Non-disabling stroke
Decompressive hemicraniectomy (DC)
–– Duration: DAPT X 21 days → switch to
monotherapy
Prophylactic DC
2. Statins: high intensity /max tolerable dose.
S - GCS score < 8
Target LDL <70 (for primary prevention =
<100) T - time <48hrs
3. DM/HTN control: A - age <60yrs

T - territory → malignant MCA >50% MCA territory
DM: SGLT2 inhibitors / GLP1 agonist
/volume >145ml
receptors / Pioglitazone
E - life expectancy ↑↑
HTN: ACEi/ARBs + diuretics
4. Extracranial disease: CDOS (gold std.) / Hemorrhagic Stroke
CTA /MRA → TOC - CEA •• ICH → 30 -50% mortality
Indications for CEA in a symptomatic •• Causes –
patient: if stenosis > 70% OR > 50% + male
–– MCC - HTN
MC hypertensive bleed - putamen > globus
pallidus
* For Making Notes

73
Medicine
HTN bleed - HTN affects small vessels, –– If SBP = 150-220 mmHg, target BP <140mmHg
lenticulostriate branches of MCA (A/k/a 2. Surgery – hematoma evacuation
Charcot’s artery of ICH /Charcot’s
aneurysm) –– Infratentorial cerebellar bleeds of size >3cm
is the only indication for surgery
–– CAA - Cerebral amyloid angiopathy → very
old patient, lobar bleed (large, cortico- 3. Coagulopathy – immediately reverse warfarin
subcortical bleed) affects if patient is taking warfarin + INR
>2 and patient comes with ICH → Tx - IV
Large vessels → present with memory loss/ Vitamin K + 4 Factor PCC (Alternative – FFP)
involves warning TIA in past.
•• ICH score –
C/f - h/o memory loss
– Age >75 years
h/o warning TIA
– IVH
Ix - MRI, gold std. - Brain biopsy
– Location of bleed - supratentorial (better) /
–– Coagulopathy infratentorial (bad prognosis)
–– AVM – Volume of bleed >30ml – poor prognosis
–– Trauma – GCS - lower the GCS, poorer the prognosis
•• ICH Tx -
C/I to Thrombolysis Q
1. BP - Target BP = 140-180mmHg
* For Making Notes

74
SAH •• Tx - ↓ complications
1. Vasospasm – occur by D4-14
–– CCB – Nimodipine
2. Re-bleed (rerupture) – Max. D1. Interventions
done - CLIP (craniotomy/open) vs COIL
(endovascular coiling is better as it ↓ morbidity
& mortality)
3. Hydrocephalus → external vascular drain =
Star of death appearance V-P Shunt
•• MCC - trauma 4. Seizure – antiepileptics
•• Aneurysmal SAH – Berry aneurysm (tunica 5. Hyponatriemia – always consider Cerebral
media defect): CoA / ADPKD salt wasting syndrome (CSWS)
- Size α risk –– Give IVF
↑ risk of rupture
- Size > 7mm •• Grading – 1. Hunt & hess – old
↓ mortality
2. WFNS
•• Site – 3. Modified Fishcer grading
–– MC - ACOM •• Singlemost important prognostic factor – GCS
score
Sometimes, expanding ACOM aneurysm
can result in 2° optic chiasma compression •• MC cranial nerve palsy in SAH is 6th CN (because
→ bitemporal hemianopia 6th cranial nerve has longest subarachnoid
course) → this is regarded as false localizing
–– PCOM
sign
Q
PCOM aneurysm - vague headache + 3rd

Cranial nerve palsy (I/L dilated pupil – TBI- TRAUMATIC BRAIN INJURY
anisochoria)
I.SDH
–– MCA bifurcation
–– Basilar top
–– VA/ PICA
•• C/F - headache / thunderclap headache (max
intensity @onset) +/- neck stiffness +/-
seizures / altered mental status /+/- focal
neurological deficit
•• Low impact trauma in susceptible individuals →

elderly, chronic alcoholics
Q
•• Bleeding – bridging veins

Q
•• Acute SDH - typical traumatic injury

•• Chronic SDH can present like dementia, seen
especially in elderly who are on anticoagulants,
* For Making Notes

75
Medicine
→ C/F - behavioural changes +/- mild focal •• Surgery – burr hole +/- craniectomy
neurological deficit
III.DAI
•• CT - concavo-convex, crescent-shaped bleeding
•• Can cross suture, can not cross midline (falx
cerebri)
•• Indications for surgery–
1. If thickness >10mm
2. ICP
•• Midline shift >5mm
•• Hydrocephalus •• Petechial hemorrhages d/t Shearing of axons @
grey-white junction (acceleration /deceleration
•• Brainstem compression
injury)
3. Progressive / worsening of deficit
•• ↓↓↓ GCS + imaging – CT / MRI Normal
•• ↓ GCS >2
•• Ix - SWI / GRE (gradient ECHO)
Q
•• Anisochoria
•• Conservative Mx
•• Focal neurological deficit
•• Poor prognosis
II. EDH •• GCS – pain
–– Sites of pain in GCS-
Fingertips – near nailbed
Trapezius
Supraorbital ridge
EYES VERBAL MOTOR
1 No eye No verbal No response
opening response
EDH 2 Painful Sounds Extension
•• Any age group, d/t high impact trauma stimulus
•• Vessel ruptured - middle meningeal artery 3 Verbal Words Abnormal flexion
(anterior branch) commands
4 Spontaneous Confused Withdrawl from
•• Lucid interval phenomenon pathognomic of
opening pain
EDH, but can seen in SDH also
5 Oriented Localize pain
•• CT scan – biconvex/ lenticular in appearance
Q
6 Obeys commands
•• Can not cross sutures, practically EDH can not NT Local Local factors Paralysed
cross midline, theoretically it is possible factors – ETT /
tracheostostomy
•• Indications for surgery –
–– Score 13-15 – Mild brain injury
–– Volume >30ml
–– ↑ ICP –– Score 9-12 – Moderate brain injury
–– Progressive/worsening of deficit –– Score <8 – severe, coma – intubate
* For Making Notes

76
CONCEPT OF BRAIN DEATH

Self- Respiratory Cerebral
Condition Sleep wake cycle Motor function Sufferings EEG
awareness function metabolism
Variable ↓, Non Slow
PVS No Yes No Normal Variable ↓
purposeful waves
Variable ↓, Non Slow
Coma No No No Variable ↓ Variable ↓
purposeful waves
Brain death No No Negative No Negative Silent Absent
Quadriparesis,
Purposeful
Locked-in Yes Yes Yes Normal Normal Normal
Eg- blinking /
vertical gaze
Brain Death Q
–– Spinal reflexes present, babinski positive /
thumbs up sign/ lazarus sign
Deep Coma - GCS 3/15
•• Brainstem reflexes that are to be checked-
Afferent Efferent
Pupil II III
Corneal V VII
Apnea Vestibulo ocular reflex

Absent brainstem reflex
- By caloric stimulation
- Don’t use COWS mnemonic here as
Prerequisite
patient is in coma.
•• Temp >35° C - COWS- used only for nystagmus in
conscious patients
•• Normal SBP/DBP - If patient is in Coma, not VIII III/IV/VI
•• No major electrolyte disturbances/metabolic / Brainstem Death →
endocrine disturbances –– Cold - eye movements on
same side
•• No sedation /no paralysis, TOF response >0.9
–– Warm - eye movement on
•• Atleast 2 examination by 2 separate practitioner opposite side
(transplant surgeon should not be an examiner) Gag reflex - only pharyngeal (not
IX X
palatal)
•• Time of death – completion of 2nd examination
Cough reflex (introduce suction
•• Points that r/o brain death- catheter and stimulate carina via ET X X
Tube)
–– Any level of posturing → Decorticate
Doll’s eyes response also lost
(abnormal flexion of arm with leg extension) in brainstem death (can not be
/ Decerebrate (universal extension) performed in conscious patients)
•• To prove apnea
Q
–– Presence of seizures
•• Points that are compatible with dx of –– Disconnect from ventilator
brainstem death– –– Prerequisite to disconnect from ventilator -
normal BP/ saturation normal/ ph -7.3
–– Normal BP /HR without any inotropic/
vasopressor –– PaCO2 >60, but still no breaths
* For Making Notes
77
Medicine
Neurocognitive Disorders
Reversible causes of dementias-
•• D → Drugs – Antiepileptic drugs/Anticholinergics / Opioids
•• E → Emotional – depression, pseudodementia
•• M → Metabolic – electrolytes, mainly chronic hyponatriemia or hypercalcemia/ organ damage
•• E → Endocrine - ↓T4 / ↑PTH / ↑ cortisol
•• N → Nutritional causes - B12 def. / Niacin def. / NPH
•• T → Trauma /tumors
•• I → Infections – HIV /Neurosyphilis
•• A → Alcoholics- Wernicke’s encephalopathy / Karsakoff amnestic syndrome
→ Apnea
Disorder Important feature

AD •• MC dementia in world
•• Affects elderly, 1st symptom - amnesia
•• Short term memory loss is characteristic → earliest site involved is medial temporal cortex, mainly
Entorhinal / Hippocampus
•• Any disease that spares medial temporal lobe is unlikely to be alzheimer’s disease
•• Gold std. - brain biopsy
Q
•• C/F - 4 A’s → Amnesia / Aphasia /Apraxia /Agnosia
•• Normal neurological examination (especially motor examination) + r/o reversible causes – B12/TSH/KFT/LFT
/ VDRL / MRI Brain
•• Tx - 1st line – Central cholinergics (AChEi) – Donepezil /Rivastigmine/Galantamine or NMDA receptor
antagonists - Mematine
•• Pathogenesis–
Q
- Aβ Amyloid plaques (extracellular) – Aβ42 > Aβ40
- Amyloid PET scans (Pittsburg compound B)
Q
- Neurofibrillary tangles (made of tau proteins) – intracellular/intracytoplasmic
- NFT is specific, but Tau is non specific because it can be seen in taupathies – AD/ FTD/ PSP / CBD/ chronic
traumatic encephalopathy
•• Cortical dementia
FTD •• 2 types – Behavioural Variant – MC, → Presents with personality changes
•• PPA - 1° Progressive aphasia → patient presents with aphasia
•• Inclusion bodies seen – Tau bodies (K/A pick bodies in FTD) / FUS /TDP43 (associated with FTD + MND)
•• Calculation spared as parietal lobe is spared.
•• Cortical dementia
* For Making Notes

78
Disorder Important feature

CJD •• 2 types – SCJD (MC) & VCJD (rare)
•• SCJD
–– Age >50yrs, rapidly progressing dementia (Onset to full blown dementia duration is <2 yrs)
with myoclonus
–– +/- extrapyramidal symptoms (eg – bradykinesia or any abnormal movement)
–– +/- Psychiatric changes
–– +/- Exaggerated startled response
–– EEG - Slow background with periodic sharp waves
Q
–– CSF- 14.3.3 protein is seen , non specific
–– IOC - RT QuIC (>95% sensitivity & specificity)
Q
–– MRI – Cortical ribboning
Q
•• VCJD → thalamic hyperintensities manifest as Pulvinal sign or hockey stick sign
–– No Tx
–– Patient can die in 8 months.
–– Cortical dementia
–– Sometimes can have UMN signs @ time of presentation
DLB <2years
•• PD features Dementia
Both DLB &
PD are due to •• Fluctuating consciousness, can be misdiagnosed as delirious
Q
lewy bodies •• Visual hallucination
(aggregate of •• Parkinsonism features - Rigidity and bradykinesia
α-synuclein body •• Extreme sensitivity to neuroleptic drugs
in cytoplasm) •• Memory spared
•• Mixed dementia
PD >1years
PD features Dementia
•• Memory spared
•• Relative dementia
Q
NPH •• HAKIM’s triad →
–– subcortical dementia
–– urinary incontinence - late finding → if present- poor prognosis
–– gait apraxia (magnetic gait) - elderly → earliest symptom
•• MRI – disproportionate ventricular dilatation, dilatation out of proportion of degree of cortical atrophy
•• LP - CSF opening pressure normal
•• TOC - V-P shunt (Miller – Fischer test)
VCD •• Main cause - Typical multiple infarcts
•• Stepwise progression – cognition decreases with each episode of infarct
•• UMN Signs – spasticity, DTRs exaggerated
* For Making Notes

79
Medicine
NORMAL PRESSURE
HYDROCEPHALUS (NPH)
•• out of proportion ventricular dilatation
•• Hyperintensities at sides of ventricles d/t
leakage of CSF into surroundings
Aβ Amyloid plaques
ALZHEIMER’S DISEASE
•• Atrophy in medial temporal cortex NFT – intracellular
•• Ventricular dilatation – correlating with
background severe cortical atrophy → SEIZURE TYPES & TREATMENT
Hydrocephalus Ex-Vacuo
Indication for Starting Therapy
•• Abnormal EEG
•• Nocturnal seizures
•• Structural brain disease
–– Abnormal MRI: Medial temporal lobe epilepsy
– d/t medial temporal lobe sclerosis – MCC of
focal seizure with dyscognitive features
–– H/o trauma /stroke
Indication to Stop Therapy

•• Lower the dose for over 3-6months and then
stop AED
•• Seizure free 1-5yrs (→ 2yrs)
•• Normal EEG
•• Normal neurological examination with normal
intelligence
•• No family h/o seizure/epilepsy
•• Single seizure type (generalised > focal)
* For Making Notes

80
SEIZURE TYPE FEATURE TREATMENT

3 Phases-
•• Aura – few secs to mins 1st line –
•• Ictal phase – few secs to mins Valproate
GTCS
- Tonic phase - clonic phase Lamotrigine
•• Post-ictal phase - confused /lethargic/fatigue/frank 2nd line – Phenytoin/Topiramate /Levetiracetam

muscle weakness
•• Typical absence seizure-
TYPICAL-
–– 4-10yrs children
•• Valproate
–– Present with transient loss of consciousness
•• Lamotrigine
→ blank stare / daydreaming → lasts for few Q
Absence •• Ethosuximide – DOC
seconds
ATYPICAL–
–– No loss of postural tone
•• Valproate → but can not be used in <3yrs
–– No postictal confusion Q
age
–– EEG - 3Hz spike & wave pattern
•• Common in early teens/adolescents
Q
•• Present with B/L Myoclonic jerk – common in morning / •• 1st line - Valproate
Q
sleep deprivation •• Alternative -
JME
•• No loss of consciousness –– Lamotrigine
•• +/- associated with GTCS / Absence –– Topiramate
•• EEG - 4-6Hz spike & wave pattern
•• Involve one hemisphere
•• Automatism /sterotyped movements like lip smacking
•• EEG - Focal epileptiform discharges – PLEDs Q
•• 1st line - Oxcarbamezpine/CBZ
•• Classified into –
•• Alternative –
–– With impaired awareness / with dyscognitive
Focal seizure –– Topiramate
feature → old name complex focal seizure
–– Levitracetam
Medial temporal lobe epilepsy
–– Lamotrigine
–– Without impaired awareness/ without
dyscognitive features → old name simple
focal
CSE With convulsions Tx-

Status epilepticus NCSE •• ICU – No convulsions Follow Status
•• Seizure >5 mins •• CSE can get converted to Epilepticus Protocol
•• >2 consecutive NCSE
seizure •• Need EEG monitoring
without gain of •• Suspected when
consciousness
–– Frequent impaired
•• 2 types – CSE & awareness
NSE
–– Sudden autonomic
changes- ↑ BP/ ↑ HR
–– Pupil diameter changes
* For Making Notes

81
Medicine
Lennox - Gastaut Syndrome Drugs Important ADRs

•• Triad
Q
•• Hirsutism / Gum
–– Multiple seizure type hyperplasia / Osteomalacia
/ B12 def.
–– Cognitive dysfunction
Q •• Rash –SJS / BM
–– EEG changes – slow spike & wave pattern Phenytoin
suppression
(1Hz changes)
•• IV Use- severe
•• TOC - Valproate / Rufinamide → new drug
approved for LGS thrombophlebitis → purple
glove syndrome
Infantile Spasms/ West Syndrome Rash /BM Suppression
•• Sudden jerking in infants Phenobarbitone / Sedation in adults &
•• Associated with tuberus sclerosis hyperactivity in children
•• EEG shows chaotic, disorganized, high amplitude Q Weight loss, Nephrolithiasis,
Topiramate
discharges Cognitive slowing
•• TOC - ACTH (Corticosteroids)
Q
Behavioural changes – rage /
Levetiracetam
anger
Genetics in Epilepsy
Lacosamide Prolonged PR interval
•• SLC2A1 codes for GLUT 1 → TOC - Ketogenic
diet Gabapentin Weight gain / ankle edema
Rare. Rash / behavioural
•• SCN1A defect does not responds to Phenytoin Ethosuximide
/ Lamotrigine changes
•• SCN2A /8A defect will respond to high dose

Phenytoin Management of Status Epilepticus
•• ALDH7A1 defect responds to Pyridoxine
•• HLAB1502 - SJS risk / hypersensitivity with
following drugs
–– Carbamezpine
–– Phenytoin
–– Lamotrigine
ADRs of AEDs
Drugs Important ADRs
Q
Hyponatriemia (SIADH)
CBZ/OxCBZ / BM Suppression / SJS
(HLAB1502 +)
Weight gain / PCOS /Insulin
Valproate (only enzyme resistance /steatosis –
inhibitor) hepatotoxicity (C/I <3yrs) ,
alopecia
* For Making Notes

82
Points to keep in mind while choosing → degeneration of nigrostrial neurons that

drugs in normal patients / pregnant- secrete dopamine
•• If already ongoing treatment / if better •• Ix - DAT scan (dopamine transporter scan)
controlled seizure - continue Valproate even in → shows asymmetric ↓ in uptake of tracer in
pregnancy basal ganglia → seen in idiopathic PD / atypical
•• Alternatives – Lamotrigine (in generalised) / parkinsonism
CBZ (in focal) •• DAT scan is normal in essential tremors →
•• Try lowest possible dose and monotherapy as –– Family history
much as possible.
–– B/L Symmetrical
Teratogenic Risk –– Tremors – coarse, 4-12 Hz, postural tremor
/ titubation
•• In healthy women – 3%
–– No bradykinesia
•• In epilepsy – 6% (Valproate has highest risk –
7-20%)
Q
–– Alcohol /sleep suppress tremor
–– TOC - β blockers
PARKINSON DISEASE •• Tx – medical therapy
1. Dopaminergic therapy
Q
Idiopathic PD – strictly asymmetrical
–– Levodopa – best
•• C/F – T R A P
–– Used with carbidopa
–– T - Tremors → resting , 4-6Hz, Pill rolling
type, Earliest –– Used only in elderly >60yrs
–– R - Rigidity (lead pipe /cog wheel type) –– S/e of levodopa
–– A - Akinesia / Bradykinesia → most
Central s/e Peripheral s/e
specific symptom → can be caught early
by ↓ arm swing •• Levodopa-induced •• Edema
dyskinesia → MC •• GI S/e → N/V
–– P - Postural instability , late manifestation. S/e •• Orthostatic hypotension
If seen early → atypical parkinsonism like •• Psychosis
psp
2. For young patients – dopamine receptor
•• Non-Motor Manifestation agonist
–– Anosmia
Ergot compounds Non ergot compounds -1st choice
–– REM - Sleep behavioural disorder → can be •• Bromocriptine •• Ropinirole
seen years before start of motor symptoms
•• Cabergoline •• Pramipexole
–– Micrographia •• Rotigotine patch
–– Depression •• S/e-
> 1yr
–– Dementia → Motor dementia –– Dyskinesia
–– Psychosis
–– Constipation
–– Peripheral s/e- GI /edema
–– Sexual dysfunction
–– Impulse control disoders-
•• Clinical diagnosis – Gold std → brain biopsy compulsive gambling /
•• On Autopsy, pallor of substantia nigra seen hypersexuality /hypomania
* For Making Notes

83
Medicine
3. Adjunctive drugs -
–– Central anticholinergic – Benztropine / THP
–– Added only if patient is having troublesome
tremors.
–– MAOB inhibitors - Selegiline / Rasagiline /
Safinamide
–– COMT inhibitors – Tolcapone (crosses BBB)/
Lewy body (aggregate of α-synuclein)
Entacapone
•• Α-synuclein →
–– Amantadine – NMDA antagonist
–– Idiopathic PD
–– Istradefylline – adenosine 2A receptor
–– MSA – Papp Lantos bodies
antagonist
–– DLB
–– S.C Apomprphine (infusion) – work by
Dopamine receptor agonism Atypical Parkinsonism – (Age >50-60/ poor
response to levodopa / poor prognosis)
1. DLB
2. MSA – α-synucleinopathy
Q
4. If still refractory – Bilateral deep brain

stimulation a) Symmetric bradykinesia + rigidity → axial &
truncal rigidity (tremors not prominent)
–– Subthalamic deep brain stimulation – best
for idiopathic PD
Q
b) Cerebellar signs and symptoms (old name-
MSA-C ) / late autonomic issues (old name
–– Thalamic DBS – treat only tremors, best for – Shy drager syndrome), bladder / bowel /
refractory essential tremors orthostatic hypotension / arrhythmia
c) On MRI, – MSA-C can show hot cross bun
3. PSP – taupathy
a) Symmetrical bradykinesia + rigidity (tremors
not prominent)
b) Supranuclear gaze palsy (vertical gaze palsy)
→ downgaze > upgaze
c) Early postural instability → falls
d) Square wave jerks in eyes /surprised look
On left - classic PD with pallor of substantia nigra
4. Corticobasal degeneration – taupathy
On right – normal substantia nigra
a) Cortical signs/symptoms - apraxia & alien
hand phenomenon
b) Asymmetric – bradykinesia + rigidity /
dystonia
c) On MRI - asymmetric atrophy of brain
* For Making Notes

84
•• Occurs mostly in evening

•• B/L, band-like headache from frontal to
occipital region
•• Acute TOC - Simple Analegesic
•• Prophylactic Tx - TCA (Amitriptyline)
Q
2. MIGRAINE – (Cortical spreading depression)

•• Underdiagnosed
–– P - pulsatile headache
Hot cross bun sign – MSA-C
–– O - one day duration (4-72hr) –if >72hr →
status migranosus
–– U - unilateral (can be B/L)
–– N - nausea +/- photophobia /phonophobia
–– D - disabling
•• Classified –
–– With aura → classic
–– Without aura → common – MC
–– If aura only, no headache – Acephalegic
Q
Humming bird sign – PSP (sagittal sign)
migraine
•• Aura –
–– Visual aura – MC characteristic – scintillating
scotomas
–– Auditory
–– Sensory
–– Gustatory
–– Motor aura – hemiparesis → family history →
CANa1A / ATP1A / SCN1A
Mickey mouse ears sign – PSP (axial section) –– Basilar migraine – posterior circulation,
stroke like symptoms
PRIMARY HEADACHES –– Ophthalmoplegia
•• Clinical diagnosis •• Tx - (Acute →)
a) Mild – Moderate – acetaminophen / NSAIDs
1. Tension Type Headache (Ketorolac)
•• Mostly in middle age group → d/t stress & b) Moderate-severe – triptans – 5HT1B/1DF →
tension very powerful vasoconstrictor
Q
•• Featureless / characterless headache because Sumatriptan – MC, oral /SC/ nasal spray
it does not have any features or powder
* For Making Notes

85
Medicine
Rizatriptan – oral, ↓ dose if patient is on A. Cluster Headache

propranolol
•• Middle aged males, (headache occurs in cluster
Zolmitriptan – oral / nasal spray
over 2-12weeks f/b period of long remissions)
Frovatriptan – slow acting, less s/e, used
•• Triggers – sleep and alcohol intake ↑ headache
in menstrual migraine
risk
Naratriptan
•• a/k/as middle of night / suicidal headache
–– C/I of triptans–
•• Attack frequency – 1-8/day
○○ Pregnant females/ CAD/ prior stroke
/ PAD/ motor aura/ h/o seizure •• Duration – 30-180mins
–– Alternative to triptans – •• During the attack- Restless patient with
Ditans → Lasmiditans – 5HT1F + - autonomic features
relatively safe in CAD
•• Tx - acute – 1ST line → 100% O2 @ 5-6 litres /
D2 receptor blockers →Metoclopramide min for 5-10 mins, can abort > 95% headache
Q
/ Prochlorperazine
–– Sumatriptan - preferred is SC route >
CGRP inhibitors → oral → Rimegepant / intranasal
Ubrogepant / Zavegepant
•• Prophylaxis – Verapamil
c) Refractory status migrainosus – Sodium
valproate
•• Prophylaxis –
–– Indications -
Decreased quality of life – recurrent
attacks > 4 attack / month
Prolonged > 12hrs attack
–– Drugs used -
Q
Beta – blockers- Propranolol /Metoprolol

TCA /SNRI B. Paroxysmal Hemicrania
Valproate •• Female
Anti-CGRP – •• ↑ frequent attacks – upto 30 attacks / day
○○ Oral → Rimegepant / Atogepant
•• ↓ duration of attacks
○○ S.c Monoclonal Ab → Erenumab /
•• TOC - Indomethacin → 100% response
Fremanezumab / Galcanezumab /
Eptinezumab
C. Hemicrania Continua
3. Trigeminal Autonomic Cephalgia •• Female
•• Involve trigeminal nerve in ophthalmic •• No painfree interval
distribution
•• TOC - Indomethacin
•• Autonomic symptoms - conjunctival redness/
lacrimation / rhinorrhea / frank horner
syndrome, strictly U/L symptoms
* For Making Notes
86
•• When is headache considered dangerous?

–– S - Systemic symptoms/signs (fever / ↑CRP
& ESR)
–– N - Neurological deficit –(Eg- FND- can
suggest underlying space occupying lesion)
–– O - old age ( >50yrs)
–– O - onset (sudden – thunderclap)
–– P - Papilledema (↑ ICP) / Positional headache
(↑/↓ICP) / headache precipitated by
Hemicrania continua Valsalva / sudden pattern change /
headache during pregnancy & postpartum
D. SUNCT (SUNA)
•• Headache in orbital distribution /orbitofrontal 1. Idiopathic intracranial hypertension
distribution (IIH) / Pseudotumor cerebri Q
•• Ultrashort duration – few sec to mins •• Risk factors -

•• ↑↑ frequency (300-400) –– Obesity
•• Electrical / stabbing pain –– OCP use
•• Autonomic symptoms present –– Vit A intoxication
•• Stimulus sensitive - headache increases on –– Hormonal imbalance – acromegaly /
touching that area recombinant GH use
•• D/D - Trigeminal neuralgia –

Q –– Hypothyroidism / sudden corticosteroid
withdrawl
–– electrical stabing pain that lasts for few
•• Present as chronic headache, features
seconds suggestive of ↑ ICP, MC CN palsy is of CN VI.
–– no autonomic symptoms
•• On fundus examination – Papilledema
–– pain in V2/V3 distribution → facial pain & not
•• MRI - normal / empty sella
ophthalmic pain
–– TOC - CBZ / OxCBZ •• LP – CSF opening pressure >25mmHg
–– If refractory – SRS / Glycerol injection in •• Tx -

V CN –– 1st line – Acetazolamide
–– On MRI, - superior cerebellar artery –– Alternative – Topiramate
compressing trigeminal nerve
–– Refractory – Lumbo-peritoneal shunt
•• TOC – Lamotrigine
–– Complication – visual field defects → Optic
nerve fenestration surgery
SELECTED SECONDARY
HEADACHES
•• IIH / CVT / PRES (RPLS)
* For Making Notes

87
Medicine
•• IOC- MRI → posterior white matter Vasogenic

edema
•• Tx - supportive / reversible in >99%, → good
prognosis
MULTIPLE SCLEROSIS
•• MC Demyelienating disease of CNS
•• Affects oligodendrocytes
Papilledema •• Females, young to middle aged
2. Cortical venous thrombosis (CVT)
•• Disease of temperate climates, therefore
•• Risk factor – Virchow’s triad associated with vit D deficiency
–– Stasis – severe dehydration •• MCDonald’s criteria – revised in 2020 →
dissemination in time & space
Q
–– Endothelial injury – neurosurgery / CNS
infections
•• C/F - heavily myelinated areas like posterior
–– Hypercoagulation – thrombophilias / Factor column are targeted mainly
V leiden mutation/ Pregnancy & postpartum
/ OCP use •• MC presenting feature-
•• Presents as acute headache +/- seizure /altered –– sensory symptoms - loss of light touch,
mental status +/- FND vibration, proprioception
•• CN VI involved here as false localizing sign –– sensory ataxia
•• IOC - MRV (contrast filling defects seen )
–– optic neuritis (20%patient’s presenting
•• Ix - On CTV, empty delta sign seen
Q
feature) - blurring of vision/ ↓visual acuity
•• On plain CT- delta sign seen, thrombus will be + color desaturation → RAPD+
hyperdense –– Gold Std Ix- VEP, Pulfrich effect.
•• TOC - Anticoagulation – start with heparin + –– Optic neuritis is U/L in MS →, if B/L, then
warfarin
it is NMO
After reaching target INR Pulfrich effect - lateral moving objects

have 3D like effect, because of differential
elimination of both eyes → signals carried by
Continue with warfarin alone the defective optic nerve in optic neuritis will
be less → Cortex receives less signals from
3. PRES / RPLS defective optic nerve, it will have sense of
•• Risk factors differential elimination of both eyes that will
–– Sudden ↑ HTN at time of presentation create 3D-like effect for laterally moving
–– Use of drugs → CNI /Bevacizumab objects.
–– Pregnancy / early postpartum (those –– +/- Lhermitte’s sign- non specific sign (D/D
eclampsia/ pre-eclampsia) of lhermitte’s sign – cervical spondylosis /
radiation myelopathy /b12 def causing sacd/
•• Present as ↑ BP with headache +/- AMS /seizure
/visual symptoms tabes dorsalis)
* For Making Notes

88
–– UMN Type weakness - spasticity / –– Maintenance therapy (↓ relapse &↑functional

exaggerated DTRs / Babinski + Cerebellar states)- DMD
signs / symptoms → truncal / limb ataxia,
DMD – disease modifying drugs –
incoordination dysmetria, nystagmus, diplopia
Convenience Safety Efficacy approach – for
–– Internuclear ophthalmoplegia – d/t MLF approach- for oral approach – for s.c/ i.v drugs
involvement drugs subcutaneous
drugs
–– Heat intolerance – Uhthoff phenomenon
1. Fumarate – 1. IFN-β- 1. Monoclonal antibodies
•• Ix - MRI •• MC used 2. G l a t r i a m e r •• anti CD20 –
in India acetate ocrelizumab /
•• Clinical types of MS- →dimethyl ofatumumab /
fumarate ublituximab
1. MC – RRMS (Relapsing remitting MS) → 90%
→ SPMS •• Others- •• anti CD 52-
Monomethyl alemtuzumab
–– Disease modifying drugs - ↓ relapses & ↑ fumarate
•• α4β7 integrin
functional states •• Diroximel inhibitors –
fumarate natalizumab →↑
–– Corticosteroids – ↓ duration of acute attack
Q
PML risk (JC
2. Teriflunomide-
virus)
2. PPMS – Tx - Ocrelizumab (anti CD20 Mab) → low efficacy
only drug proven to be effective in this. 2. Others-
3. Cladribine – high
efficacy •• Mitoxantrone
3. Others –
4. S-1-PO4 •• Cyclophosphamide
–– Acute Fulminant MS - a/k/as Marburg receptor
variant modulator –
• Fingolimod –
–– Balo concentric sclerosis – in children s/e 1st dose
bradycardia
•• IOC - MRI with Gadolinium contrast
Q
, Macular
edema
Dissemination in space Dissemination in time
• Siponimod
(DIS) (DIT)
• Ponesimod
MS specific areas – •• Simultaneous presence
cortical / juxtacortical / of gadolinium enhancing
peri-ventricular (dawson (new) /non enhancing
NMOSD
Q
fingers)/ brainstem / lesions (old) Core clinical features
spinal cord •• OCB – Oligo clonal bands MC features •• Optic neuritis – B/L
in CSF , if +ve → added •• Acute myelitis – LETM
to recent MCDonald (longitudinal extensive transverse
criteria to improve myelitis) → / 3 segments >3
sensitivity of diagnosis •• Area postrema – refractory &
unexplained hiccups +/- nausea &
•• CSF findings in MS are nonspecific → OCB + vomiting
(sensitivity >95%) / ↑IgG /↑ Cells (<50 cells) Less common •• Acute brainstem syndrome
features •• Symptomatic narcolepsy (Acute
•• Tx – diencephalic syndrome)
•• Symptomatic cerebral lesions
–– Acute - 1st line Corticosteroids →plasma
exchange (↓duration of acute attack)
* For Making Notes

89
Medicine
•• Signature antibody in NMOSD → anti NMO

IgG (anti AQP4 Ab)
Q
•• If antibody is present → > 1 core clinical

•• If antibody is absent → > 2 core clinical (one
must from MC features)
•• Tx: Acute attack → Corticosteroids → if
refractory Plasma exchange
•• Maintenance therapy - MS – left sided, U/L optic neuritis
–– Eculizumab (anti C5 Ab) / Inebilizumab (anti

CD19 Ab )/ Satralizumab (anti –IL 6 receptor
Ab)
–– Alternative – Mycophenolate mofetil /
Azathioprine /Methotrexate
MS lesions
•• Dawson fingers – multiple white matter

plaques arranged near periventricular region
•• Indicates late stage of MS.
ADEM – ACUTE DISSEMINATED

ENCEPHALOMYELITIS
•• Asymmetric, new enhancing lesions (open ring
enhancing) •• Common in children
•• Juxta-cortical region (typical MS site) •• Monophasic illness

•• Have h/o post viral infection /post-vaccination
•• Patient presents with ataxia /FND
•• Encephalopathy- key feature
•• MRI – B/L symmetric confluent lesions (MS-
U/L lesions)
•• Minimal enhancement
•• TOC - Corticosteroids +/- plasma exchange
Q
•• Old, non enhancing lesions (a/c as T1 black

holes)
•• Peri-ventricular site (typical MS site)
* For Making Notes

90
MOTOR NEURON DISEASE

UMN LESIONS LMN LESIONS UMN + LMN LESIONS
•• Spasticity •• Atrophy 1. Amyotrophic lateral sclerosis -
•• ↑ DTRs •• ↓/ -ve DTRs Lou Gehrig’s disease
•• Babinski positive •• Fasciculation 2. ALS-FTD
Eg- Eg-
3. ALS-PARKINSON (Guam
1. Primary lateral sclerosis (PLS) 1. Progressive muscular atrophy complex)
2. Hereditary spastic 2. Kennedy’s disease - d/t CAG repeat 4. SCA-type 3 – a/k/a Machado
paraparesis joseph disease
3. Spinal muscular atrophy – Exon 7 deletion on SMN1
3. Adrenomyeloneuropathy - defect • MC form of spino
cerebellar ataxia
• X-linked •• SMA1- Werdnig Hoffman disease →infantile
• Weakness + pyramidal
• ABCD1 gene defect → ↑ presentation tract sign + ataxia +
VLCFA •• SMA2- Dubowitz disease → present within 18 incoordination
• MC form of months of life
adrenoleukodystrophy
•• SMA3- Kugelberg-welander disease →juvenile onset
• Presents with spastic
•• SMA4- adult onset disease
paraparesis
•• Tx - DMD –
• Adrenal insufficiency
–– Nusinersin (antisense oligonucleotide)
• ↓cognition / blindness /
deafness –– Onasemnogene abeparvovec (immunologic
4. HTLV-1 related tropical response)
paraparesis •• Infectious causes of LMN -
5. Neurolathyrism – BOAA 1. Poliomyelitis – pure LMN
2. West nile virus - pure LMN
Amyotrophic lateral sclerosis- Variants of ALS -
•• Onset middle age. Median survival - 3-5yrs 1. Mill’s variant – U/L hemiparesis like
presentation
•• Genetics – familial ALS
2. Flail arm variant – B/L arm weakness +/-
–– C9O RF 72 > 40% → associated with ALS- bulbar symptoms
FTD complex •• Atypical for ALS- sensory involvement /
–– SOD-1 gene
Q extraocular muscle involvement/bladder-bowel
involvement /extrapyramidal symptoms
–– FOS gene •• Ix - no definitive Ix
–– TDP43 gene •• Tx – Riluzole (NMDA receptor modulator) -
•• Pathological hallmark – Bunina bodies (inclusion ↑survival
bodies in neurons), >97% Bunina bodies are made –– Edaravone - ↑ functional outcome
up of TDP43 gene •• Supportive Tx - Nocturnal BiPAP
•• Clinical features –
–– Fasciculation / cramping/exertional weakness PERIPHERAL NEUROPATHY & GBS
–– Weakness (focal initially →spread) – UMN + •• 1/3rd – Idiopathic
LMN type weakness in same limb – specific •• 2/3rd – Known cause → out of this
for ALS –– 1/3rd –DM
* For Making Notes

91
Medicine
–– 1/3rd – Alcohol GBS

–– 1/3rd – other causes •• MC demyelinating PN in world
Q
•• Can be divided into axonal PN and demyelinating

PN
Axonal PN Demyelinating PN
Causes- Causes-
•• DM •• AIDP (GBS)
•• Alcohol •• CIDP
•• Vit B12 def. (Vit B12 Def. •• Amiodarone
in Spinal Cord Causes •• Paraproteinemias -
Demyelienation, But In MM/ WM
Pns Causes Axonal Pn) •• HMSN-1
•• HMSN-2
•• Vasulitis
•• Sensory symptoms > •• Diffuse, motor >
B/L LMN VII CN PALSY- bell’s phenomenon
motor symptoms and sensory, Early reflex
•• B/L LMN VII CN Palsy – rare (D/D – GBS / Lyme
length dependent lost
disease / sarcoidosis)
•• NCS - ↓ CMAP amplitude •• NCS- conduction
•• Normal velocity /normal blocked ↓ velocity / ↑
latency latency
AIDP Cytomegalovirus /influenza

•• Precipitants ( >60%) Vaccination
–– Infection - Drugs – immune check point inhibitors
URI - mycoplasma •• Patient presents with early sensory symptoms
– hip/thigh/backpain f/b motor weakness →
Diarrhea – campylobacter acute symmetric and progressive ascending
Other - Zika /covid-19 areflexic flaccid quadriparesis +/- bulbar
symptoms +/- CN involvement (MC involved-
* For Making Notes
92
CN VII) +/- autonomic symptoms (↑ HR, ↓ BP, –– Anti LRP4 Ab → 2%

Arrhythmia)
These Ab do not co-exist
•• MCC of death in GBS- arrhythmia or respiratory
–– Affects all ages → if young – females > males
failure due to diaphgramatic involvement.
•• If old - 60’s / 70’s → males > females and no
•• Acute→ <8 weeks, if >8 weeks → CIDP
Thymoma
•• Progression → > 1-4 weeks
•• Risk factor - Thymoma / AchR Ab
Q
•• Brighton criteria is used to diagnose

•• Clinical features -
•• Ix –
–– No sensory /no autonomic involvement
–– NCS – Demyelination (↓ velocity & ↑ latency,
conduction block)
Q –– H/O eating canned foods
–– No bladder/bowel involvement
–– LP- CSF – Albuminocytological dissociation
→ ↑↑ albumin + normal cells (<10) –– Normal tone/ normal DTR’s /no atrophy
Q
•• Tx –– MC clinical feature in MG patient is ptosis,

seen in >60%
–– ABC
•• Clinically MG can be divided into –
–– ↓ BP – IVF (NS bolus)
Generalised MG Ocular MG
–– Respiratory failure - intubate → 20-30-40 •• 85% •• 15%
rule •• Proximal weakness •• Persist with ocular
If VC < 20ml/kg (fluctuating /diurnal weakness, no limb
•• Variation weakness weakness
MIP > 30cm H2O
→ weakness more in •• Ptosis + diplopia
MEP< 40cm H2O evening than morning) + (ophthalmoplegia)
ocular weakness
–– Look for arrhythmias
•• One clinical test to confirm MG - ice pack
–– TOC - IVIg OR plasma exchange test
Q
–– No role of corticosteroids or –– Keep ice pack and reassess ptosis.

Q
immunosuppression Improvement is seen after ice pack use .
In CIDP - 1St Line Iv Ig, If •• Ix- most sensitive – single fiber EMG >95%
Refractory Then +/- Corticosteroids/ –– Most specific- Ab testing
Immunosuppresion
Q
Mainly → EMG/NCS + Ab is done in practice.
Myasthenia Gravis •• MUSK + features → female > male / ↑↑ face /

↑↑ bulbar /↑↑ limb weakness +/- atrophy
•• NMJ disorder, It is post synaptic disorder
•• CT chest - mandatory for all patients Thymoma.
•• Affects only skeletal muscles –– MC thymic abnormality seen on CT Chest →
•• Type 2 hypersensitivity disorder – antibodies Thymic Hyperplasia (>60-70%)
seen in it are- –– Thymoma – 15%
–– AChRAb > 70-80%
Q
•• Indications for thymectomy
–– Anti MUSK Ab → 4% –– Thymoma
* For Making Notes

93
Medicine
–– Age <50 + AchR Ab present •• Neonatal FcR inhibitor - Efgartigimod α

•• Tx - myasthenic crisis /respiratory failure –
TOC is IVIg or plasma exchange
Corticosteroids may transiently worsen crisis &
should be avoided as 1st line.
–– 1st line – Pyridostigmine –
–– Immunosuppression – Corticosteroids
–– Corticosteroids can cause transient
Ptosis – Myasthenia Gravis
worsening & have to watch for. Onset of
action takes around 2-3 weeks ,therefore
corticosteroids sparing therapy IMPORTANT MUSCULAR
–– CS Sparing Therapy → MUSK + → Rituximab DYSTROPHIES
/Alternative - MMF/ Azathioprine
AChR Ab + seronegative
•• MMF/ Azathioprine
•• Alternative – anti C5 Mab → Eculizumab /
Ravulizumab
Gower Sign positive → seen in all childhood muscular
dystrophies
DMD BMD
•• Both are d/t dystrophin gene defect. XLR.
•• Proximal weakness-
Q
•• Gower sign
•• Waddling gait
•• Skeletal deformities
Q
•• Pseudohypertophy of calf
•• Initially, DTRs preserved → as weakness increases,
DTRs diminished
•• Cardiomyopathy common. In Beckers – Cardiomyopathy
precedes skeletal deformities
•• ↑↑ CPK / ↑↑ Aldolase-B
•• Gold std - muscle biopsy + genetic testing
•• Tx -
–– 1st line – corticosteroids
–– Genetic therapy –
Casimersen → if axon 45 skipped
Eteplimersen → if exon 51 skipped
Golodirsen / Viltolarsen → if axon 53 skipped
Ataluren → nonsense mutation
* For Making Notes

94
DMD BMD
•• Dystrophin gene function completely lost •• Dystrophin gene some part functional
•• Onset – 3-5yrs •• Onset - 10-12yrs
•• Progression – rapid •• Progression - slow
•• Become wheel chair bound by 10 yrs •• Wheel chair bound by 30’s
•• IQ - ↓↓ •• IQ - normal
•• Life expectancy → 20 ‘s •• Life expectancy → 40’s
•• 1st skeletal deformities → cardiomyopathy •• 1st CM → skeletal deformity
Myotonic Dystrophy
•• 2 Types-
Type 1 MD Type 2 MD
•• MC •• d/t mutation in – ZNF9 on chromosome 3
Q
•• d/t mutation in DMPK gene on chrosome 19 •• CCTG repeats
•• CTG Repeat •• Proximal weakness
•• Clinical features – •• Calf pseudohypertrophy
–– Percussion myotonia •• Associated tremors
–– Weakness – distal
Q
–– Facial involvement - HATCHET facies
–– 30% patients have dysphagia –late
–– Cardiomyopathy
–– Arrhthymia
–– Diabetes (insulin resistance), hypoandrogenism
(testicular atrophy)
–– Frontal baldness
–– B/L cataracts
–– Hypersomnolence
–– EMG- myotonic discharge k/a diver bomb sound
•• TOC - Mexiletine
Emery-Driefuss
•• Early contractures
•• Cardiomyopathy /Arrythmias severe
•• Humeroperoneal weakness
LGMT – Limb Girdle Muscle Dystrophy-

•• Multiple types
•• MC- LGMD2 A (CALPAIN 3 gene mutation )
•• Present in late childhood early adulthood
FSHD- Facial scapular humeral dystrophy
* For Making Notes

95
Medicine
IMPORTANT CNS INFECTIONS
* For Making Notes

96
* For Making Notes

97
Medicine
ENCEPHALITIS –– If hydrocephalus – external ventricular drain

or V-P shunt
Diagnosis ?
– – If cerebral edema (encephalitis)-
•• CSF - non diagnostic Dexamethasone / Prednisolone
•• Imaging – normal/ non specific

3. Toxoplasmosis
Options •• h/o HIV-AIDS
•• Triad - Fever + Headache + FND/AMS/Seizure
Q
•• Broad range PCR done → 16S r RNA (bacterial)
/ 18S r RNA (fungal)
•• MRI - ring enhancing lesion
•• Viral PCR panel
•• D/D - Primary CNS lymphoma (DLBCL) → MC is
•• Autoimmune & paraneoplastic panel CNS tumor in HIV
•• Brain biopsy
INFECTIOUS MASS LESIONS
•• Tx - sulfadiazine – pyrimethamine /TMP-SMX
1. Brain abscess - (ring enhacing lesions seen)
Q
•• ENT sources → TOC - ceftriaxone +

Metronidazole
–– Otogenic (abscess location → temporal lobe)
–– Sinus (abscess location → frontal lobe)
–– Dental
•• Hematogeneous Seeding → septic emboli, →
lodge in superior division of MCA
•• Post-neurosurgery / penetrative trauma → Cobweb coagulum - TBM
Q
TOC - Vancomycin + antipseudomonal cover -

like Meropenem or Ceftazidime or Cefepime
2. Neurocysticercosis
•• MC c/f → seizures
•• Appear as ring enhancing lesions on MRI (D/D
→ tuberculoma)
•• MRS -
–– Lipid peak – TB
Soap bubble appearance in India Ink – Cryptococcus meningitis
–– Multiple AA without lipid peak -
neurocysticercosis
•• Tx-
–– If viable cysts - antiparasitic drugs like
high dose Albendazole +/- Praziquantel +
Dexamethasone/ Prednisolone
–– If dead cysts (calcified cyst) - No
antiparasitic therapy, AED’s
* For Making Notes
98
MISCELLANEOUS – PHAKOMATOSIS
NF-1 NF-2 TS VHL
Inheritance AD AD AD AD
Chromosome Chr 17 Chr 22 Chr 9/ chr 16 Chr 3
Gene NF-1 NF-2 TSC-1 (Hamartin) VHL
Protein Neurofibromin Merlin TSC-2 (Tuberin) PVHL
1. Cutaneous 1. Rule of 2 - 1. Cutaneous - 1. Hemangioblastomas –
neurofibromas •• Ash leaf macules cerebellar & retinal
•• B/L vestibular
•• Axillary freckling schwannoma •• Shagreen patches •• Pheochromocytoma /
•• Periungual fibromas (a/k paragangliomas
•• Café-au lait •• B/L Cataract
Koenen’s tumor) 2. Renal cysts (progress
macules – 5mm to clear renal cell
•• B/L Meningiomas •• Café- au lait
for prepubertal cancer) / pancreatic
•• B/L Ependymomas •• Adenoma sebaceum
•• 15mm for (angiofibromas) cysts
postpubertal 2. CNS- cortical tubers
2. Iris nodules - lisch (hamartomas)
nodules •• Subependymal nodules
(calcified)- candlewax
3. Tumors - optic nerve
dripping appearance
gliomas
•• Epilepsy
Features
•• Pheochromocytoma 3. Tumors – SEGA
•• Meningiomas (Subependymal giant cell
•• Astrocytomas astrocytomas)
4. Bone problems - •• Glioblastoma
•• Scoliosis 4. Eye manifestations - retinal

hamartomas
•• Sphenoid dysplasia
5. Pulmonary –
lymphangioleiomyomatosis
(LAM)
6. CVS - Rhabdomyoma
7. Renal – renal artery stenosis/
angiomyolipoma
8. Triad - EpiLoiA – epilepsy
+low IQ+ adenoma sebaceum
STURGE WEBER SYNDROME phenomenon / reduces blood supply – cortical

atrophy → low IQ & seizures on C/L sides
•• Sporadic
•• On CT/ X-ray → tram track appearance
•• Port wine stains → CN V1/V2 → d/t cutaneous
angiomas •• Glaucoma /Bupthalmos
•• I/L leptomeningeal angiomas → steal
* For Making Notes

99
Medicine
MISCELLANEOUS- ALCOHOL RELATED

Q
Wernicke’s encephalopathy Korsakoff amnestic syndrome
•• Reversible •• Irreversible
C - global confusion R-retrograde amnesia
O - ophthalmoplegia (MC ocular manifestation in)- MC A-anterograde amnesia
nerve involved = B/L CN VI palsy C-confabulations (false memory)
A - Ataxia K-korsakoff
T - thiamine deficiency •• Ix- MRI- Changes seen in mammillary bodies and
•• Tx- thiamine replacement dorsomedial thalamus → correlate with memory deficit
–– Thiamine f/b glucose
•• Ix - MRI → hyperintensities in mammillary body and
atrophy and problems in Dorsomedial thalamus
•• Causes - Hyperemesis gravidarum /cancer
Others –– CNS manifestations like hallucination,

•• PN (axonal)
disorientation, agitated
•• Myopathy –– Autonomic fluctuations - extreme tachycardia
•• Marchiafava bignami syndrome - rare / ↑BP / ↑ Temp / Diaphoresis
•• Demyelination of corpus callosum /white matter •• TOC – for any alcohol withdrawl condition will
•• UMN like weakness – dementia/ spasticity be Benzodiazepines
•• 1st line – Diazepam (↓risk of rebound withdrawl
Alcohol withdrawl symptoms as it is Long acting)
Q
1. Simple – Headache/ anxiety/ mild tremors (6-

•• Alternative - Chlordiazepoxide / Lorazepam /
48hrs ) → Tx - Benzodiazepines
Oxazepam (best for liver dysfunction)
2. Complicated withdrawl –
a) Seizure –
–– Within 48hrs
–– GTCS
–– Brief, short post-ictal state
–– If not treated- 1/3rd can progress to
delirium tremens @ D3-D4
Q
b) Hallucinations –
–– 12-48hrs
–– Visual hallucinations
c) Delirium tremens-
–– 48-96hrs @D3/D4
–– Violent shaking
* For Making Notes

PULMONARY & EMERGENCY MEDICINE
Approach to pulmonary function testing
SHAPES OF FLOW VOLUME CURVES

•• Small airway obstruction = characteristic coving curve on expiratory limb of curve
•• Restrictive lung disease = when shape is normal but size is small
103
Medicine
–– V/Q mismatch
If ratio is >1 → shock, pulmonary HTN
If ratio is <1 → airway diseases (asthma,
COPD), parenchymal diseases (pneumonia,
ILD )
–– Shunt formation (mixed blood amount should
be atleast >40% for shunting)
V/Q ratio = 0
Anatomical Shunt vs physiological shunt

•• Anatomical
–– EX: cyanotic congenital heart disease
–– Physiological is a pathological process that
causes shunting at microscopic level
–– Ex:- B/L Diffuse process
Alveolar filling process
○○ Fluid: pulmonary edema → could be
cardiogenic (ARDS) or non Cardiogenic
○○ Pus: B/L extensive pneumonia
•• Large airway obstruction = Flattening of ○○ Blood: Diffuse alveolar haemorrhage
inspiratory limb of curve (Suggests variable
U/L total collapse
/ dynamic extra thoracic large airway
obstruction) ○○ Tension Pneumothorax
○○ Massive effusion on 1 side
•• Variable / dynamic intra thoracic large airway
obstruction = Entire expiratory limb Flattening ○○ Right endobronchial intubation
•• Fixed obstruction = Flattening of both Hepato pulmonary syndrome (Cirrhosis,

end stage liver disease, severe Portal
expiratory & inspiratory limb of curve
HTN)
APPROACH TO RESPIRATORY Types 2 respiratory failure

FAILURE
•• Also known as hypercapnic respiratory failure
Q
•• Types 1 respiratory failure

Q
•• Primary problem - ↑ PaCO2 + ↓ PaO2 + Normal

–– Also known as hypoxemic respiratory failure
Q
A-a gradient
–– Primary problem - ↓ PaO2 + ↓ PaCO2 + ↑ A-a
•• Causes
gradient
–– Causes: –– Alveolar hypoventilation
–– Diffusion limitation –– Minute ventilation = tidal volume × RR
ILD –– Low minute ventilation = ex:- neuromuscular

disorders such as:- GBS , myasthenia crisis,
Emphysema etc → because of this, patient is unable to
breath properly
* For Making Notes
104
Low RR causes are: CNS problems – Type 4 respiratory failure

such as drug toxicity, severe alcohol
•• Primary problem – shock / heart arrest
Q
intoxication, Traumatic brain injury, brain

stem compression, raised intra cranial
Mixed Type 1 & Type 2 respiratory
pressure, etc.
failure
Type 3 respiratory failure •• Problem - ↑ PaCo2 + ↓ PaO2 + ↑ A-a gradient
•• Primary problem – post operative atelectasis
Q
* For Making Notes

105
Medicine
ENVIRONMENTAL EMERGENCIES •• Heat stroke : Severe form

–– Temperature >40.5 °C
–– Alter mental status
–– Low BP
–– No Sweating
–– Treatment: IV fluids, active cooling (ice
packs), active internal cooling (cold saline)
Q
–– Stop active cooling if patient starts Shivering

•• Common features of Heat exhaustion & stroke
1. Altitude related problems
–– Tachycardia
•• Acute mountain sickness
–– Increase respiratory rate
–– Complains: fatigue, exercise intolerance, +/-
mild headache (treatment: Acetazolamide) •• Exertional Heat stroke
•• High altitude pulmonary edema: cough, –– Seen in athletes, soldiers

Haemoptysis, dyspnoea (treatment: rapid –– Sweating
descent)
Q
–– Severe electrolyte imbalance (ex:

•• High altitude cerebral edema severe headache, hyperkalaemia)
alter mental status, coma (treatment: rapid –– Rhabdomyolysis
descent)
–– If patient unable to descent rapidly: give 4. Cold related problems
hyperbaric bags + Dexamethasone + O2, +/-
Nifidipine (in case of Pulmonary edema) •• Hypothermia related issues
–– Mild <35°c
2. Diving related problems Features: Shivering, tachypnea, Tachycardia,
•• Barotrauma hypertension, increase urine output
due to increased renal blood flow, clear
–– Tympanic membrane rupture → Deafness consciousness
–– Pneumothorax –– Moderate : <32°c
•• Decompression sickness – also known as caisson Features :- no Shivering, bradypnea,
disease (due to formation of N2 bubble in blood)
Q
bradycardia ,hypotension , variable urine

–– Clinical features: arthralgia, altered mental output , alter mental status , EEG & ECG
status, dyspnea, hypotension changes ( form J wave)
–– Treatment: hyperbaric O2 therapy –– Severe: <28°c
3. Heat related problems Features: coma, respiratory arrest,

apnea, ventricular arrhythmia, no urine
•• Heat cramps output
•• Heat exhaustion: Mild form –– Treatment: rewarming → passive or active
Q
–– Temperature <40.5 °C Passive rewarming: blankets

–– Clear consciousness Active rewarming: external = special
–– BP Normal warming blankets, internal = thoracic >
abdominal lavage with warm fluids (40-
–– Sweating 42°C)
–– Treatment: conservative, hydrate the patient Rate of rewarming: 0.5-2 °C / hour
* For Making Notes

106
–– Best site to measure core body temperature:- Beta blockers/ CCBs

Pulmonary artery < distal esophagus < rectal Bradycardia , hypotension Q
Glucagon
temperature , pulmonary edema , acute
heart failure
•• Freezing injuries: frostbite
TCAs
–– Usual sites of Frostbite: sacral areas / distal
Q
Cardiac effects – wide QRS , IV NaHCO 3
extremities ventricular tachyarrhythmia
–– Clinical features: numbness, chunk of wood LAs 20% IV intra Lipid- given in
Ex: Lignocaine , bupivacaine case of cardiac irritations
sensation → immediately do rewarming (37-
40°C) , if pain present during rewarming,
Q
Opioids
reduce the temperature, & if pain is severe Pin point pupil, Bradypnea, IV naloxone
Q
alter mental status, coma,

– give analgesics → because patient will Hypothermia
develops vesicle, blisters & become cyanotic
Benzodiazepines Flumazenil ( increase risk of
–– Grade of cyanosis: Bradypnea , alter mental
seizures)
Q
status, coma, Hypothermia

I = No cyanosis during rewarming
Methemoglobinemia
II = cyanosis up to the distal phalangeal •• Chocolate cyanosis
•• Treatment:- IV methylene
joint (chocolate colour blood)
blue ( contraindicated in
III = cyanosis extend up to •• High anion gap Metabolic G6PD deficiency – use IV
metacarpophalangeal joint acidosis because of Ascorbic acid)
hypoperfusion of
IV = cyanosis extend up to proximal •• Precipitants :- well water ,
tissues , low SpO2 (real
metacarpophalangeal joint drug intake (dapsone etc..)
SpO2 measured by co-
–– Perform MRA – if patient presents within 24 oximeter), Normal PaO 2
hours Iron (oral Fe)
•• Produce free radical via
If it shows significant Vascular occlusion
Fenton reaction
= rTPA (recombinant tissue plasminogen Treatment:- IV deferoxamine
activator) •• Cardiopulmonary failure ,
hepato cellular necrosis,
–– Perform Bone scan if patient presents after gastric outlet obstruction
24 hours
CO
Perform amputation •• Cherry red discoloration
•• When person is exposed
TOXICOLOGY to fire, automobile

exhaust
Treatment:- hyperbaric oxygen
therapy
Toxin Antidote •• High anion gap Metabolic
Q
N acetyl cysteine ( oral or IV) acidosis, falsely elevated
APAP → NAPQI → hepatic
failure because of severe •• Most common side effect of SpO2
zone 3 central lobular oral is nausea & vomiting Ethylene glycol / methanol
necrosis + renal failure +
•• Safe in pregnancy, safe for Alter mental status, coma,
Lactic acidosis Fomepizole (alternative :- IV
renal failure, high anion
Treatment:- IV fluids > liver liver failure only , not safe gap Metabolic acidosis
Q
ethanol)
transplantation for renal failure with increase osmolal gap,
blindness
Digoxin Q
Digibind OPC
Main problem :-
xanthochromia Treatment:- for bradycardia Cholinergic crisis :-
atropine → for ventricular DUMBELS = Diarrhea,
Main side effect:- Brady & arrhythmia = lignocaine
tachy arrhythmia urination, myosis, IV atropine , pralidoxime
bronchorrhea, bradycardia,
Bronchospasm, emesis,
lacrimation, salivation
* For Making Notes

107
Medicine
Cyanide Catatonic rigidity / Lead pipe rigidity

•• Smell- bitter almonds Treatment: bromocriptine +/- IV dantrolene
•• Cause :- fires
100% O2 , IV hydroxocobalamin –– Malignant hyperthermia is a genetic defect,
•• C/f: high anion gap / IV sodium thiosulfate
Metabolic acidosis,
fuel to RYR gene mutation, Autosomal
altered mental status, dominant
normal SpO2 & PaO2 Due to use of anaesthetic agents &
paralytic agents
Extrapyramidal toxidrome
Most common cause in world =
•• Because of D2 receptor blockers succinylcholine
•• Patient develops acute dystonic reactions , Extreme hyperthermia
oculogyric crisis Rigidity (mortis like rigidity)
•• Treatment :- central anticholinergic = Benzhexol Massive elevation of end tidal CO2 in OT
/ trihexyphenidyl , Benztropine, antihistamines
Treatment: Dantrolene
Q
drug = promethazine, diphenhydramine

–– Common features of all toxidrome:-
•• Treatment for Drug induced parkinsonism =
Fever
central anticholinergic
Tachycardia
•• Akathisia (constant feeling of restlessness) =
beta blockers + clonazepam Tachypnea
Alter mental status
Hyperthermic toxidrome Hypertension
•• Ex:
GIT contamination process
–– Sympathomimetic toxidrome = use of •• Can be done with activated charcoal = 1g/kg -
MDMA, cocaine , amphetamine 50g/kg, whole bowel irrigation by polyethylene
glycol
Patient will have mydriasis, extreme
hypertension •• Contraindication of activated charcoal:
Treatment: alpha blocker → beta blockers –– Altered mental status/ low GCS score
–– Late presentation (after 1-2 hours of
–– Serotonin syndrome caused by SSRIs, SNRI
ingestion of toxin)
Patient will have rigidity , extremities
–– Any evidence of presence of bowel obstruction
clonus, ocular clonus
–– Toxins → alcohol , petroleum products , boric
Treatment: cyproheptadine
acid, inorganic ions , heavy metals
–– Anticholinergic toxidrome due to datura or
•• Indication of whole bowel irrigation
belladonna toxicity
L = Lithium
Dry patient, urinary retention, constipation
severe delirium I = iron
Treatment:- physostigmine M = metals
–– Neuroleptic Malignant syndrome due to P = body packers

consumption of Dopamine receptor blockers S = sustain release preparation
present after 24 hours
* For Making Notes

108
Enhanced elimination REVERSAL OF

•• Urinary alkalization: give IV NaHCO3 & ANTICOAGULATION
maintain urinary pH of ≥ 6.5 – 7 → increase
Anticoagulant Reversal
elimination of salicylate like substances (it is
Warfarin INR >2 + bleeding → treatment – IV
present with high anion gap Metabolic acidosis
vitamin K + 4 FPCC
& mixed respiratory alkalosis), methotrexate,
phenobarbitone , chlorpropamide UFH Protamine sulphate
LMWH Protamine sulphate (but no Efficacy,
•• IV intra Lipid → used for local anaesthetic
give Andexanet alpha)
toxicity
Fondaparinux Andexanet alpha
•• Renal replacement therapy - to eliminate toxin
Dabigatran Idarucizumab
via dialysis
FXai Andexanet alpha
–– Low Vd & less protein binding
–– Drugs which are eliminated by renal SHOCK
replacement therapy
Q
•• Hypoperfusion to tissues / MAP <65 mmHg

B = Barbiturates (not benzodiazepines)
L = lithium
I = Isoniazid
S = salicylate
T = theophylline, aminophylline
M = methanol, metformin, methotrexate
E = ethylene glycol
D = Depakote, Dabigatran
C = carbamazepine
–– Drugs that can not be eliminated by this
therapy:-
Benzodiazepines
Sulphonylurea
Beta blockers (except atenolol) , CCB
Phenytoin
Warfarin, heparin
Amiodarone, digoxin
TCAs , SSRI
* For Making Notes

109
Medicine
Features Hypovolemic Cardiogenic Distributive Obstructive

Pulmonary/RV Mechanical
Hemodynamics
Preload (PCWP) ↓ ↑ ↓ ↓ ↑
Pump function N ↓ ↑ /Variable ↓ ↓
Afterload (SVR) ↑ ↑ ↓ ↑ ↑
Q
Tissue perfusion ↓ ↓ ↑ ↓ ↓
(MvO2)
Clinical Features
JVP ↓ ↑ ↓ ↑
Extremities Cold Cold Warm Cold
Fluid responsive Yes No Yes Variable/ no
LV function N ↓↓ N N
Q
Initial treatment Fluids +/- blood Inotropes +/- •• Septic = •• Tamponade = urgent pericardiocentesis
products MCs, Ab, Iv fluid, •• Tension Pneumothorax = needle
NA, Dopamine vasopressin thoracostomy, chest drain
Atropine Sync. •• Anaphylaxis •• RVMI = IV fluids +/- inotropes
Q
DCC
= adrenaline •• Pulmonary embolism = thrombolysis
(1mg = :1000) (alteplase) + anticoagulation
•• Hypovolemic shock
•• MvO2 or SvO2 measured best at pulmonary
–– Hemorrhagic = road traffic accident , surgery artery by Swan ganz catheter/ white heart
catheter/ pulmonary artery catheter
–– Non Hemorrhagic = vomiting , Diarrhea,
acute pancreatitis Massive transfusion
•• Most common cause : cardiac surgery > trauma
•• Cardiogenic shock
•• Old Definition:- >10 U PRBC / 24 hours
–– Cardiomyopathic shock = poor pump function
•• Now : >4 U PRBC / 1 hour
Q
–– Arrythmogenic shock •• Complications :-

•• Distributive shock –– due to citrate overload → hypocalcaemia,
Metabolic alkalosis
Q
–– Septic shock
–– Hypokalaemia > hyperkalaemia (in case of
–– Non Septic shock = neurogenic shock due to renal failure , neonates + old PRBC )
spinal cord trauma , anaphylactic shock –– Hypothermia
•• Pulmonary RV = due to pulmonary embolism, –– Dilutional Thrombocytopenia (PRBC : FFP :

platelets = 1:1:1)
acute RVF
–– Persistent hemodynamic instability
•• Mechanical obstructive = due to tension
–– Blunt abdominal trauma + eFAST positive +
Pneumothorax, tamponade
unstable patient
* For Making Notes

110
–– High risk scores → ABC ≥ 2 , RABT ≥ 2 , CARDIAC ARREST

shock index >1
•• Treatment of Septic shock patient
–– qSOFA score ≥ 2 = indicates high risk

Q
RR ≥ 22/min
SBP ≤ 100 mmHg
Alter mental status ( GCS <15)
–– SOFA
GCS
PaO2 / FaO2 ratio
MAP & dose of vasopressors
Total bilirubin
S. creatinine , urine output
Platelets
Sepsis + hypotension
Collect alteast 2 sets of blood
culture from different sites
(CBC , BMP , lactate)

IV fluids + antibiotics (within <1 hour)
Not responding
Septic shock
CPR
1. Circulation
Vasopressors ( NA +/- vasopressin +/- Dopamine)
•• Good Chest compression :- rate = 110-120/ min,
–– If Adjunctive therapy: CIRCI (critical depth = 2-2.5 inches (5-6 c ) → uninterrupted
illness related corticosteroid insufficiency) Chest compression
Q
→ add hydrocortisone (also in refractory

shock = 50mg / QID)
* For Making Notes

111
Medicine
2. Airway •• Clinical examination:
•• Basic: Oropharyngeal , Nasopharyngeal airway –– >24 hours :- status myoclonus
•• Advanced: LMA, Endotracheal intubation –– >72 hours :- absent pupil reflex & Corneal
reflex
3. Breathing: •• Serological markers
•• Rescue breath (30:2 → chest compression: –– NSE → increased → poor prognosis
breath)
•• In Advanced airway, compression is: 10/min PNEUMONIA
Drugs used in cardiac arrest
•• Adrenaline
–– used in both Shockable & non shockable
rhythm
–– Dose :- 1:1000 IV 1 mg
–– Repeat Every 3-5 minutes
•• Anti arrhythmia drugs like amiodarone,
lignocaine
–– Used in shockable rhythm (after 3rd shock)
–– Dose: 300 mg amiodarone, 1:1.5 mg/kg for
lignocaine
–– Half Dose of this can be repeated once
•• Not used drugs: atropine, vasopressin
Outcomes of CPR
•• Successful → indicated by ETCO2 >40 mmHg
–– Check brain response of the patient:- if
patient follows the command, outcome is
good
–– If patient dose not follow the commands, Community acquired pneumonia
improve brain condition by using Targeted
•• 65% Idiopathic, 25% viral cause, 15%
temperature management for 24 hours
bacterial cause (most common typical bacteria
(also known as therapeutic Hypothermia
previously). - pneumococcus, atypical – Mycoplasma →
infiltrates, chlamydia, legionella).
•• Not successful → dead people
•• Features:- fever , productive cough, shortness
•• To assess neurological outcome:- of breath, haemoptysis
–– CT (in 1st 24 hours) / MRI (after 24 hours)
•• Examination:- crepitation ,bronchial breath
–– Electrophysiology:- EEG (after 24 hours, if sound , bronchophony / egophony
there is persistent myoclonic seizures, & >72
hours = burst suppression pattern, N20 SSEP •• Investigation :- increased CRP / ESR , x- ray
(>24 hours :- B/L absent = death) :- consolidation, infiltration
* For Making Notes

112
•• Treatment:- CURB 65 score •• Treatment:- beta lactam → cefepime ,

piperacillin & tazobactam , meropenem
–– C = confusion
•• Duration of therapy :- 5-12 days + patient
–– U = BUN >7mmol/L (in India:- ≥40 mg% ) should be stable + afebrile for ≥ 48 hours
–– R = RR ≥30/min •• Most common complication:- Para pneumonic
–– B = BP :- SBP < 90 or DBP ≤60 effusion → if it gets more complicated, do
drainage (loculated effusion is one of the
–– 65 = age >65 Indications of chest drain
Q
–– Score :- –– Signs of complicated Para pneumonia

0-1 = treat as out patient → look for risk effusion :-
factors :- if no risk - give Azithromycin
pH of Pleural fluid <7.2 ( normal is 7.4-
/ Doxycycline, if risk factors present
7.6)
(example:- any comorbidities such
as CKD , heart failure, lung diseases , Glucose <40 mg %
took antibiotics in last 90 days) give
Gram stain +
beta lactam (Amoxicillin- clavulanic
acid, 3rd generation cephalosporin – Pleural fluid Culture +
cefexime) + Azithromycin / Doxycycline
Frank pus – Emphyema
or respiratory (3rd & 4th generation)
Fluoroquinolones = levofloxacin, –– Clue for complicated Para pneumonia effusion:-
moxifloxacin non resolution of Clinical illness
2 = as short impatient → give beta
lactam + Azithromycin/ Doxycycline or Hospital acquired pneumonia &
respiratory Fluoroquinolones Ventilation acquired pneumonia
≥ 3 = admit patient +/- ICU → beta •• HAP = Pneumonia occur after 48 hours of
lactam + Azithromycin/ respiratory hospitalization
Fluoroquinolones, if patient have •• VAP = Pneumonia occur after 48 hours of
penicillin allergy = give Aztreonam Endotracheal intubation
Community acquired MRSA •• Look for MDR risk
•• Can Produce Panton valentine leukocidin –– Infection occurs after 5 days of hospitalization
•• History of post influenza pneumonia, –– Patient in Septic shock at the time of

pneumatoceles presentation
•• IE / iv drug users who are is on renal replacement –– ARDS
therapy + have a central venous catheter
–– Already on Renal replacement therapy
•• Treatment:- Vancomycin (nephrotoxic) /
Linezolid (cause bone marrow suppression, Lactic –– If no risk factors → monotherapy +
acidosis, peripheral neuropathy) + clindamycin piperacillin and tazobactam , cefepime ,
(increase risk of Clostridium difficile colitis)
Q
meropenem
–– If risk factors present → triple therapy
Pseudomonas aeruginosa (piperacillin & tazobactam, cefepime,
•• It is a typical hospital acquired organism meropenem + Aminoglycosides , Fluoroquinolones
+ Vancomycin)
•• History of Bronchiectasis, cystic fibrosis
* For Making Notes

113
Medicine
Lung abscess •• Halo sign Seen → can be converted into

crescent sign
•• Risk factors
•• Other investigation:- blood test = 1,3 beta D
–– Aspiration due to any cause (low GCS)
glucan +, S. Galactomannan +
Q
•• Features
•• Differential diagnosis of 1,3 beta D Glycan:
–– High grade fever Aspergillus , candida, Pneumocystis carinii
pneumonia, Histoplasmosis, Coccidioidomycosis
–– Foul smelling sputum +/- postural variation
of sputum •• Serum Galactomannan can be false positive in
case of patient taking Amoxicillin- clavulanic
–– D/D for thick wall cavity with air fluid level
acid, piperacillin and tazobactam
= SCC of the lung
•• Treatment:- voriconazole
Q
•• Treatment :- antibiotic regimen:-

–– Ampicillin – sulbactam Allergic broncho pulmonary
–– Piperacillin and tazobactam Aspergillosis
–– Meropenem •• Patient have hypersensitivity reaction
–– Moxifloxacin/ levofloxacin + Metronidazole •• Features:- history of bronchial asthma > cystic
–– Clindamycin fibrosis , worsening of asthma symptoms
•• Blood parameters :- elevated eosinophils ,
ASPERGILLUS LUNG DISEASE elevated IgE (>1000), history of coughing of
brown to black flakes of sputum
Q
•• Chest x-ray → infiltration + Mucus plugging

(finger in glove appearance) +/- central or
peroximal Bronchiectasis
•• To confirm ABPA, blood test – Aspergillus

specific Ab or skin prick test +
•• Treatment: corticosteroid (Prednisolone or

dexamethasone) +/- itraconazole or voriconazole
Aspergilloma
•• Patient have normal immunity PLEURAL DISORDERS
•• Light’s criteria
Q
•• Features:- Asymptomatic
•• Complication:- massive Hemoptysis –– Efficient protein / serum protein: Efficient
protein is > 0.5
•• Monod sign Seen
–– Efficient LDH / serum LDH: Efficient LDH
•• Treatment: surgery > 0.6
–– Efficient LDH > 2/3 of serum LDH
Invasive pulmonary Aspergillosis
(Immunosuppressive patient) –– Any one of these is present, indicates
exudate
•• Features:- fever, shortness of breath ,
hemoptysis , hemodynamic instability
* For Making Notes
114
Etiology Appear WBC RBC pH Glucose Comments

B/L ,
Normal (<1000) cardiomegaly
CHF Clear , straw
, mainly N N N in chest X-ray,
Cirrhosis Yellow colour
lymphocytes Cirrhosis,
portal HTN
Uncomplicated Increased, mainly N / mildly N / Mildly No chest Drain
Turbid Variable
parapneumonic neutrophil reduced reduced requires
Complicated Increased,
Turbid Variable <7.2 <40 mg% Chest drain
parapneumonic mainly neutrophil
Very high (25000
Emphyema Purulent Variable Very low Very low Chest Drain
to 1 lakh)
Gold standard
Increased, mainly Mildly Mildly
Tuberculosis Serosanguinous Variable Diagnosis:
lymphocytes reduced reduced
Pleural biopsy
Mildly Mildly
Malignancy Bloody effusion Increased Increased Cytology
reduced reduced
70 %
Pulmonary
Bloody effusion Increased Increased N N exudate, 30%
embolism
transudate
RA:-
Rheumatoid Mildly extremely low
Turbid Increased N RF + , serology
arthritis/ SLE Reduced SLE:- Mildly
reduced
Left sided
Serosanguinous Variable / effusion,
Pancreatitis Increased N N
or turbid Increased increased
Q
amylase
Left sided
Esophageal Turbid to effusion,
Increased Variable Reduced Reduced
rupture purulent increased
Q
amylase
Other causes –– Diagnosis: effusion hematocrit / blood

•• Urinothorax: transudate hematocrit > 0.5
–– To diagnose, efficient/ creatinine > 1 = •• Chylothorax: exudate

confirm Urinothorax
–– Diagnosis: Triglyceride ≥100 mg% or >55 & if
•• Peritoneal related Pleural effusion:- commonly chylomicrons are detectable in Pleural fluid
Q
have right sided effusion

•• Cardiac causes: post CABG, Dressler’s
–– Diagnosis: efficient/ serum glucose = >1 syndrome → both have left sided effusion
•• Hemothorax: exudate
* For Making Notes

115
Medicine
•• Drugs: have high eosinophils

Q Aspirin hypersensitivity
–– B = bromocriptine
–– A = amiodarone
–– M = methotrexate, methysergide
–– +/- nitrofurantoin Bronchial asthma Nasal polyps

•• Pleurodesis:- obliteration of Pleural
–– EGPA known as Churg Strauss syndrome
–– Agents of Chemical Pleurodesis Triad:- Bronchial asthma
TALC (Increase success)
Tetracycline
Bleomycin
Tension Pneumothorax
Eosinophilia Vasculitis
•• It is a Clinical diagnosis
•• Complaints: Pleuritic chest pain , shortness of Diagnosis Definition of Sign of severe

breath, reduce air entry , Hyper resonant note control exacerbation
on percussion •• Is a •• Symptoms ≤ •• Severe
•• Signs :- hemodynamic instability , low BP , spirometry 2 weeks shortness of
based •• Reliever use breath
evidence of trachea & mediastinal shift
diagnosis is ≤ 2 times •• PEFR cut-off:
•• Treatment:- immediate needle thoracostomy •• FEV1/FVC / week ≤50-60
→ chest drainage (at 2nd ICS in MCL, 5th ICS <0.7 •• Nocturnal •• Pulsus
MAC → preferred)
Q
awaking ≤ 2 paradoxus
•• In X-ray → Hyperleucency, no Broncho / month •• HR >120/min /
Vascular markings, trachea shifted to left side, Use Broncho •• Exacerbation increased RR
right heart border is flat means mediastinum dilator ≤ 1 /year >30/ min
also shifted •• Recheck •• Normal lung •• SpO2 <90%,
ratio after function normal PaCO2 ,
Bronchial asthma 15 minutes •• Good quality increased PaO2
→if it’s ≥ 0.7 of life •• Cyanosis
•• Symptoms:- shortness of breath, cough ,
wheeze •• Satisfaction / altered
mental status/
•• Asthma plus syndrome:- Bronchial
bradycardia /
–– Atopy → allergic rhinitis & Conjunctivitis + asthma
hypotension
atopic Dermatitis + family history + high IgE •• Abdominal
& eosinophils paradox / silent
–– ABPA → worsening asthma chest
–– AERD → over activation of LOX → increased

leukotriene receptor → Triad
Q
* For Making Notes

116
Reversibility Th2 type release

IL4 IL5 IL 13
•• Class •• eosinophils •• Increased

switching blocked by Mucus
Variability Hyper mepolizumab, production
•• block IgE by
reslizumab,
Responsiveness Omlaizumab
Benralizumab
•• Treatment of bronchial asthma: MART

–– IL-4 & IL -13 blocked together by Dupilumab
(maintenance & reliever therapy)
–– TSLP is a protein which stimulates pulmonary
–– Preferred reliever :- LABA + low dose ICS
Q
dendritic cells → block by Tezepelumab
–– Biological: effective if asthma is Th2 type
•• Treatment of acute exacerbation of bronchial asthma

–– Give O2 → target : 90-92%
–– Use Broncho dilators → SABA (Salbutamol/ levo salbutamol) +/- SAMA (ipratropium bromide)
Q
–– Systemic corticosteroid → prednisolone or IV methylprednisolone
–– Adjunctive therapy:- MgSO4 +/- IPPV
COPD
Diagnosis Assess severity Treatment
Post Broncho dilator Gold 1:- ≥ 80% - mild ABCD assessment
FEV1 / FVC < 0.7 Gold 2:- 50-70% - •• Use MMRC scale ≥2 = symptom burden is high
moderate •• Grade of MMRC:-
Gold 3:- 30-49% - 0:- shortness of breath only with mild exercise
severe
Gold 4:- <30% - very 1:- SOB after hurry on level ground or walking on slight uphill
severe 2:- SOB while walking at normal speed
3:- patient able to walk <100 m , develop SOB within few minutes
4:- home bound patient
•• Quality of life :- COPD assessment tool ≥ 10 → poor quality of life
•• Risk :- look for number of exacerbation /year → ≥ 2/ year or ≥ 1/
year → require exacerbation
Q
•• Treatment:- LAMA +/- LABA +/- ICS
(LAMA: Tiotropium, glycopyrrolate, aclidinium, umeclidinium)
(LABA: formeterol, salmeterol) (ultra long acting drugs:-
vilanterol, indacaterol, olodaterol)
Improve quality of life →
•• Stop smoking by giving nicotinic replacement therapy, varanicline,
bupropion
•• *Long term ONotes
For Making 2
therapy to those having long term resting hypoxemia
•• Lung volume reduction surgery
117
Medicine
Diagnosis Assess severity Treatment

Treatment of AECOPD
•• Increase in symptoms + no relief with usual treatment
•• target O2 :- 88-92%
•• BD :- SAMA +/- SABA
•• Systemic corticosteroid
•• If infections present, give Macrolides
•• PPV:- NIPPV > IPPV (indication for BPAP = pH ≤ 7.35 / PaCO2 ≥ 45
mmHg
•• Reduce exacerbation rare:- Roflumilast, chronic Azithromycin
therapy × 1 year
•• Most common cause for exacerbation:-

Emphysema infection
•• Irreversible dilatation of the terminal •• Complications :- high risk Pseudomonas colonization,
respiratory airways → increased static high amyloidosis
compliance , protease- anti protease imbalance
Etiology Clinical Evaluation
•• Characteristics: exercise desaturation due to
Tb :- Sputum or
diffusion limitation , low DLCO , V/Q mismatch
, significant hyperinflation in chest X-ray, Chronic cough, BAL analysis
Chronic infections
avascular regions in lung → transform into bullae persistent ABPA :- IgE ,
( MC is TB, ABPA)
infiltration eosinophils, skin
•• It is a clinical diagnosis → > 3 months / year for
more than 2 years → shunt formation ↔ blue prick test
blotter = cyanosis & heart failure risk + edema Refractory
sinusitis +
Bronchiectasis infertility +
1° ciliary
•• It is an irreversible disease, permanent situs inversus
dyskinesia
dilatation of medial sized bronchus = Kartagener
Q
syndrome
(Dynein mutation)
Chronic &
IgG , IgM, IgA,
Immunodeficiency recurrent
IgF
infections
RA , Sjogren, Arthralgia + other RF , ANCA ,
ANCA issues ANA, ACPA
MC pulmonary
Colonoscopy ,
IBD manifestation =
•• Clinical features: chronic productive cough +/- Q biopsy
Bronchiectasis
hemoptysis
Young , lower
•• Most common cause :- TB Alpha 1 AT lobe Emphysema Alpha 1 AT
•• Most common site :- lower lobe deficiency & lower lobe levels + Genetics
•• Diagnosis:- IOC :- HRCT
Q Bronchiectasis
Right middle lobe
•• Treatment:- supportive – chest physiotherapy,
Anatomic syndrome – in CT
Broncho dilators , drainage
children
* For Making Notes

118
•• William Campbell syndrome:- cartilage defect lumacaftor , Tezacaftor , Elexacaftor (in

→ affects 3rd to 6th order bronchi F508 Deletion, do this triple therapy)
•• Mounier Kuhn syndrome :- smooth muscle & •• DNAase therapy (dornase alpha)
elastin defect
•• Most common cause of exacerbation:- infection
•• Causes of Right middle lobe & left Lingular (Staphylococcus aureus)
lobe bronchiectasis
•• In 1-10 years :- Colonization due to MSSA >
–– In Elderly female → known as Lady windermere H. Influenza
disease due to MAC infection
•• >10-15 years :- due to MRSA , Pseudomonas
aeruginosa, BCC , stenotrophomonas
Q
Cystic fibrosis
•• Defect in CFTR gene on Chromosome 7, AR Indications for Lung transplantation in
pattern
Q
cystic fibrosis patients
•• MC mutation:- F508 Deletion → comes under •• Severely declined lung function → FEV1 <30% ,
type 2 trafficking effect rapidly decrease in FEV1, evidence of Pulmonary
Q
HTN , walking capacity <400 m

Manifestations Features
Rhino - pulmonary Sinusitis , Bronchiectasis
GI Meconium ileus , rectal prolapse ,
EVALUATION OF HEMOPTYSIS
young adults, DIOS
Non massive
GU Infertility , Male :- absence vas ,
•• Most common cause is bronchitis
female :- thick cervical secretion
Metabolic Hyponatremia, hypochloremia, •• Look at chest X-ray → normal = check risk
factors for cancer such as old age & heavy
Metabolic alkalosis , hypokalemia
smoking → if risk factors present = do CT
Other Aquagenic wrinkling, stones ( Gall
chest, if no risk factors → look for bronchitis
bladder, kidney)
•• If bronchitis is present = conservative
Diagnosis treatment for 1-2 weeks → no response → do
CT chest, if bronchitis is not present:- observe
Sweat chloride testing >60
for 4-6 weeks → no improvement→ CT chest
•• Chest x-ray abnormal →

–– Mass lesion / parenchymal disease → CT
chest
–– Infiltrates → antibiotic trial for 1-2 weeks

Genetic testing abnormal
→ no response → CT chest → flexible
2 mutations nasal potential
difference bronchoscopy
should be +
•• Immuno reactive trypsinogen Massive

•• Treatment •• Most common cause is Bronchiectasis (source –
bronchial artery)
•• Supportive +/- disease modifying therapies
→ potentiators = ivacaftor , correctors = •• >400 ml of blood in cough in 1 day or >150 ml
* For Making Notes

119
Medicine
blood in single episode –– Make patient lie in Lateral decubitus (bad

Q
lung down)
•• Treatment :-
–– Endotracheal intubation
–– Patient dies due to asphyxia
–– +/- urgent rigid bronchoscopy
–– ABC + correct coagulopathy
–– +/- angio embolization
APPROACH TO ILD
Known causes Unknown causes Rare but well defined ILD’s
Smoking → Granulomatous ILD •• Pulmonary infiltrates eosinophilia
•• DIP •• Sarcoidosis Causes
Q
•• RB- ILD •• Lofgren syndrome Triad :-
1. AEP
•• Pulmonary Langerhans cell B/L hilar lymphadenopathy BAL eos ≥30
histiocytosis (tennis racket shaped 2. CEP
birbeck granules
Q
3. HES
Drug induced ILD’s
Arthritis, Erythema 4.ABPA
•• methotrexate
Fever nodosum
•• amiodarone 5. Loeffler syndrome → transpulmonary
•• nitrophenytoin •• Herford waldenstrom syndrome
Q
passage of helminths
•• Bleomycin Uveitis Paratoid Enlargement 6.TPE = trapping of microfilia
•• Busulfan
•• cyclophosphamide 7. EGPA
CTD related ILD’s BA

Fever 7th CN palsy
•• NSIP – most common pattern
exception:- RA •• +/- pituitary involvement = CDI

•• +/- skin = lupus pernio
Occupational ILD’s
•• +/- renal involvement = DTA , NDI , stones Eosinophilia Vasculitis
•• Inorganic = known as
•• Cardiac involvement = RCMP , conduction
pneumoconiosis •• Lymphangioleiomyomatosis
blocks
•• Organic → Hypersensitivity –– Defect in TSC gene
•• Liver involvement = Granulomatous
pneumonitis → Thermophilic –– Female > male
hepatitis, neurosarcoidosis
actinomycosis ( farmer’s lung , –– Pregnancy is contraindicated
•• Other = elevation of serum ACE level
Bagassosis , mushroom workers
•• IOC :- biopsy ( EBUS guided biopsy) from –– C/F :- recurrent chylous effusion
lung)
LN of lung with recurrent Pneumothorax
→ Byssinosis = increase risk of COPD –– CT :- Swiss cheese appearance
•• TOC :- corticosteroid
•• Pulmonary Alveolar proteinosis
→ other = grain dust , toxic chemicals Non Granulomatous ILD’s
–– Defective clearance of surfactant
•• IIP:-
–– C/F:- Cough , gummy sputum
Types :-
–– CT:- crazy paving appearance
•• IPF :- at > 50 years →C/F = chronic cough,
–– Treatment:- lung lavage
SOB
On examination: Dry fine end inspiratory
crackles , +/- clubbing, on HRCT = bibasal
subpleural fibrosis +/- Honeycombing +/-
traction Bronchiectasis
Treatment:- TKI :- Nintedanib , TG Beta # :-
pirfenidone ,
•• NSIP * For Making Notes
•• COP (BOOP)
•• AIP
Diagnose of exclusion
120
Hypersensitivity pneumonitis (type 3 (acute), •• CT features :- mosaic pattern, centrilobular

4 (chronic) hypersensitivity reaction) nodules
•• Treatment :- short course steroid
Pneumoconiosis
Q
Silicosis (most common) Asbestosis CWP Berylliosis
Fibrogenicity +++++ ++ Least + ++
Pleural
- ++ - -
involvement
LAN + - + +
ILD +++ + (lower lobe) + +
COPD ++ - + -
Bronchogenic
+ + - +
cancer
Malignant
- + - -
Mesothelioma
•• Anthracosis
Occupational exposure
Increase TB risk , acute •• Normal x-ray,
to beryllium, non
condition can mimic PAP In biopsy, ferruginous asymptomatic
Comments caseating granuloma ,
(Pulmonary Alveolar bodies seen patient, dust cells
dihelium lymphocyte
proteinases) present in LN
proliferation test +
biopsy
Caplan syndrome –– Hormonal Imbalance:- Pregnancy , Early Post

partum period , OCPs
•• Due to pneumoconiosis → develops RA → RA
nodules in upper lobe –– Other:- Cancers, thrombophilia → most
common is factors 5 leiden mutation, most
•• Most commonly associated with Silicosis
Q
common acquired thrombophilia is anti

phospholipid syndrome
VENOUS THROMBOEMBOLISM –– Most common reason for upper limb DVT:
•• Virchow’s Triad central venous catheter
Stasis of blood flow –– Work up:
Suspicious VTE
Endothelial Injury hypercoagulopathy
•• Risk factors:
–– Immobilization ≥ 3 days within 3 months or
long flight travels (6-8 hours) Q
* For Making Notes

121
Medicine
•• Treatment of VTE:- Anti coagulation (heparin - Idiopathic pulmonary

warfarin < DOACs artery HTN
BMPR2 Mutation
Q
•• Deep vein thrombosis Familial pulmonary

artery HTN
•• Pulmonary embolism:-
–– Unexplained SOB +/- pleuritic chest pain
–– Unstable pulmonary embolism treatment:- Associated pulmonary artery HTN → crest
systemic thrombolysis, IVC filters given syndrome
when anticoagulants are contraindicated Others
–– Duration of anticoagulation therapy :- 3-6 ○○ MPAP 20
months
○○ Normal PVR >3 wu
–– Saddle pulmonary embolism
○○ Normal pulmonary capillary
–– ECG :- most common – sinus Tachycardia
Treatment:- vaso dilators
–– Other :- RV dysfunction → T Inversion in V1-
Test:- vaso reactivity testing → + → CCB ,
V4, S1Q3T3
Q
If (-) → combo = ambrisentan + Tadalafil

–– Echocardiogram: RV dysfunction + prostanoids
Prostacyclin receptor agonist is a prodrug
PULMONARY HTN
Prostacyclin antagonist:- epoprostenol ,
•• MPAP ≥ 20 mmHg
Q
treprostinil, iloprost
•• Gold standard:- swan ganz catheter or
pulmonary artery catheter
•• 5 Types of Pulmonary HTN according to WHO
–– Type 1 :- pulmonary artery HTN → problem
is in the small pulmonary arterioles
* For Making Notes

NEPHROLOGY
ABG ANALYSIS Q
–– Chronic = Expected HCO3 = 24+ (PaCO2 –
40 /10 × 4)
Normal values
•• For Respiratory alkalosis
•• pH = 7.36- 7.44 (7.4)
–– Acute = expected HCO3 = 24 – (40- PaCO2
•• PaO2 = 75-100 mmHg (<60= critical) /10 × 2)
•• PaCO2 = 36-44 mmHg (40) –– Chronic = expected HCO3 = 24 – ( 40 -
•• Na = 136-144 mEq/L
+ PaCO2 /10 × 5)
•• K+ = 3.5-5 mEq /L Step 3: find anion gap (mainly in patient

•• Cl = 95-105 mEq /L
- with Metabolic acidosis)
•• HCO3- = 22-28 mEq/L •• Anion gap >12 = high anion gap Metabolic
acidosis
Q
•• Anion gap = <12

–– Causes:
•• A-a gradient = PAO2 - PaO2
G = glycol
•• PAO2 = [ 713 × FiO2 ] - PaCO2 / 0.8
O = oxoproline (APAP)
Step 1: 1° disorders L = L- Lactic acidosis (most common form)
pH HCO3 PaCO2 Interpretation D = D - Lactic acidosis (seen in short
↓ ↓ ↓Comp. Metabolic acidosis bowel syndrome)
↑ ↑ ↑Comp. Metabolic alkalosis M = methanol
↓ ↑Comp. ↑ Respiratory acidosis A = aspirin
↑ ↓Comp. ↓ Respiratory alkalosis R = renal failure
•• In Respiratory acidosis → HCO3 <30 = acute
-
K = ketoacidosis (due to diabetes ,
(pH abnormal), >30 chronic (pH normal) starvation , alcohol)
•• In Respiratory alkalosis → HCO3- >20 = acute –– Find delta: delta ratio = delta anion gap /
(pH abnormal), <20 = chronic (pH normal) delta HCO3- anion gap -12 / 24 - HCO3-
–– If ratio is <1 = means patient is having high
Step 2: expected compensation + associated Normal anion gap Metabolic
•• For Metabolic acidosis = Winter’s formula
Q acidosis
–– Expected PaCO2 = (1.5 × S.HCO3) + 8 –– If ratio is 1-2 = patient is having uncomplicated

high anion gap Metabolic acidosis
•• For Metabolic alkalosis =
–– If ratio is >2 = means patient is having high
–– Expected PaCO2 = (0.7× S. HCO3) + 20 + associated normal anion gap Metabolic
•• For Respiratory acidosis alkalosis
–– Acute = expected HCO3 = 24 + (PaCO2 – •• Anion gap <12 = normal anion gap Metabolic
acidosis
40/10 ×1)
125
Medicine
–– Causes Etiology :- Etiology :-

•• Drugs (Aminoglycosides) •• Drugs (Lithium,
U = ureteral diversion •• Heavy metals , Demeclocycline,
•• Tenofovir (TDF ( high amphotericin B)
R = renal tubular acidosis
risk of nephrotoxicity, •• any conditions
A = Addison’s disease amyloidosis) & TAF which produces
(produrg)) → leads to hypercalcemia
D = diarrhea + other GI Causes like FANCONI syndrome •• connective tissue
pancreatic Causes, fistula, d Lactic disorders
acidosis, ammonium chloride poisoning •• Vascular disease
•• amyloidosis
•• Look for urinary anion gap = (UNa+k) – Ucl
•• medullary sponge
•• Gap is decreased / negative in case of : kidney (recurrent
stone formation ,
–– Diarrhea recurrent UTI)
–– Pancreatic fistula
–– Proximal RTA •• Bicarbonate deficit calculated by :- 0.3 × body
•• Gap is positive / increased in case of: weight × (24 – S. HCO3)
–– Distal RTA
Optional steps
–– Addison’s disease
•• Check for A-a gradient
Proximal RTA Distal RTA
•• Check osmolal gap In poisoned patient + high
Type 2 RTA Type 1 RTA
anion gap Metabolic acidosis
Normal BP , creatinine , Normal BP, creatinine ,
functions functions –– Gap >10 = toxic alcohol → methanol, ethylene
Bicarbonaturia - glycol, propylene glycol
FANCONI syndrome Nephrocalcinosis due to –– Gap <10 = salicylate poisoning → high anion
Triad: lower urinary citrate gap Metabolic acidosis + respiratory alkalosis
Glycosuria
•• Osmolal gap = actual S. Osmolality – calculated
S. Osmolality
= 2(Na) + BUN / 2.8 + glucose /18 +
Phosphaturia aminoaciduria
ethanol/4
Urinary pH < 5.5 Urinary pH > 5.5
Bicarbonate replacement Bicarbonate replacement ABG analysis – sample
therapy dose :- ≥ 5 mmol/ therapy dose :- 1-3
kg/day → worsens the mmol/kg/day → correct
•• A 24 year old pregnant lady (30 weeks) has been
hypokalemia the hypokalemia diagnosed with pneumonia. She is currently
receiving high flow oxygen with an FiO2 of 0.5.
ABG –
* For Making Notes

126
•• HTN + BPH : alpha blockers

•• HTN + migraine : beta blockers ( propranolol)
•• HTN + osteoporosis : thiazide
•• Isolated systolic hypertension: thiazide /
calcium channel blockers
Hypertensive emergencies Q
Clinical Timeliness & 1st line

presentation target BP treatment
Malignant •• In 1st 1 hour =
hypertension reduce BP by
Hypertensive 25% Labetalol ,
encephalopathy •• In 2-6 hours Nicardipine
= target
160/100-110
mmHg
•• Slowly reduce
BP in 24-48
hours
HYPERTENSION – DRUG CHOICES AKI
•• Black , elderly or obese : diuretics ( thiazide Acute ischemic •• If lytic Labetalol,
like diuretics- Metolazone , indapamide , stroke candidate :- Nicardipine
chlorthalidone) target <125/110
•• HTN + LVH : ACE - , ARB - mmHg
•• If not lytic
•• HTN + CAD : A + C ( if angina :- beta blockers
+/- Nitrates ) candidate
:- target
•• HTN + MI : beta blockers (ACE or ARB
<220/120
inhibitors also used)
Acute Target BP :- 140-
•• HTN + HF : angiotensin receptor neprilysin Hemorrhagic 180 mmHg
inhibitor > A +/- beta b + mineralocorticoid stroke
receptors antagonist (spironolactone,
ACS Target SBP :- <140 Beta blockers +/-
eplerenone)
mmHg nitroglycerin
•• HTN + tachyarrhythmia : beta blockers , Acute Target SBP :- <140 Nitroglyceri or
verapamil / diltiazem pulmonary mmHg nitroprusside
•• HTN + Aortic Aneurysm: beta blockers (in edema
marfan syndrome = ARBs) Acute Ao Target SBP :- <120 IV beta blockers
•• HTN + prior stroke : diuretics + ACE / ARB emergencies mmHg / HR <60/ (labetalol)
inhibitors min
Pregnancy Target SBP :- <140 Labetalol,
•• HTN + DM : ACE / ARB inhibitors
related mmHg Nicardipine
•• HTN + CKD : if proteinuria = ACE / ARB +/- MgSO4, +/-
inhibitors, if edema present = diuretics delivery
* For Making Notes

127
Medicine
Approach to monogenic HTN

•• Renin → if increase → not monogenic (ex:- renal artery stenosis)
•• Renin → if decrease
Monogenic HTN
Aldosterone →
Increase
familial Hyper aldosteronism → corticosteroid response

Yes
Familial Hyper aldosteronism type 1 ( Glucocorticoids)
MRA respiratory
No Yes
Liddle syndrome CAH

AD AR
Gordon syndrome syndrome of apparent mineralocorticoid excess
•• Liddle syndrome:- gain of function of mutation Urinary sediments

in ENaC gene
–– Features – hypertension, hypokalemia ,
Metabolic alkalosis
Q
–– Treatment - Amiloride
•• Gordon syndrome: mutation in WNK 1/4 , KLH3,
COL3 gene
–– Features :- hypertension, hyperkalemia ,
Normal anion gap Metabolic acidosis
–– excess function of thiazide sensitive sodium
chloride transporter in DCT
–– Treatment:- thiazide
•• CAH (congenital Adrenal hyperplasia) :- 11 OH
deficiency & 17 OH deficiency
–– Increase Deoxycorticosterone
–– Difference between CAH & SAME = check
DOC : cortisol ratio = ratio is high in this
disease
•• SAME :- mutation in 11 beta HSD2 deficiency→
have role in converting cortisol to cortisone
–– DOC : cortisol ratio is low
–– Acquired condition :- Licorice→ Inhibits 11 •• Hyaline cast :- increase in dehydration in
beta HSD2
Q
patient having concentrated urine
* For Making Notes

128
•• RBC cast :- Glomerulonephritis, vasculitis •• Calcium oxalate crystal:- dehydrated envelope

•• Old fat bodies :- tubular epithelial cells which -shaped & monohydrate – dumbbell-shaped
are loaded with fat •• Uric acid crystal:- rhomboid & rosette-shaped
•• Fatty cast :- Old fat bodies arranged in the – polychromatophilic in polarized microscope
form of cast, seen in Nephrotic syndrome •• Cysteine crystal:- hexagonal in shape
–– Check old fat bodies & fatty cast under •• Indinavir crystal :- rectangular plates – have
polarized microscope :- the cholesterol
needle/ feathery appearance
esters appears as Maltese cross
•• Methotrexate crystal :- clumped appearance
•• Granular muddy brown cast :- seen in acute
tubular necrosis
Q
•• Sulfa crystal :- shocks of wheat appearance
•• WBC cast : acute interstitial necrosis > acute •• Ciprofloxacin crystal
tubular necrosis > acute glomerulo nephritis >
•• Acyclovir crystal:- needle-shaped
Q
Pyelonephritis
GLOMERULAR DISORDER
•• AKI :- kidney injury that occurs within in hours
to days
–– AKI + RBC cast = acute glomerulonephritis
•• CKD :- occurs in months to years
•• RPRF :- Occurs within weeks
–– S. Creatinine doubles within 6 weeks
•• Triad of any nephritic syndrome :-
Hematuria (RBC cast)
•• Calcium phosphate crystal:- Asymmetric Rods HTN AKI
* For Making Notes

129
Medicine
•• Treatment of ANCA :- –– HSP :- low dose corticosteroid

–– High dose of corticosteroid (1g of –– PSGN :- self limiting disease
methylprednisolone ) + cyclophosphamide / –– SLE :- Immunosuppressant
Rituximab + plasma exchange
Nephrotic syndrome
•• Treatment of good pasture syndrome :-
•• Proteinuria (>3.5 g/day) + edema + hypoalbuminemia
–– Corticosteroid, Cyclophosphamide +/- plasma (<3.5 g/dl) + hyper coagulopathy + lipiduria +
exchange Hyperlipidemia + increased risk of pneumonia
Q
•• Treatment of type 2 AGN / RPGN

–– IgA nephropathy :- conservative or if high
creatinine proteinuria, give corticosteroid
* For Making Notes

130
Etiology MCD MGN FSGS MPGN Nodular GS

Child , massive Young
proteinuria, acute concussions,
onset edema , Subacute
1° presentation Male, black Rare Rare
Normal BP, edema , massive
S. Creatinine, proteinuria, C3
Normal urine normal
•Infectious
causes :- HBV
HIV ,
/HCV/ HIV/
hypertension,
Toxoplasmosis, HCV, cryo , Diabetes –
morbid obesity
2° causes Lymphomas syphilis, etc. malaria , IE , Kimmelstiel Wilson
, sickle cell
•CTD related:- shunt nephritis lesion, amyloidosis
disease, reflex
SLE, RA
nephropathy
•Cancers :- colon
cancer
Drug causes NSAIDs Fold / d- penicillin Heroin - -
Thick basement
Q
membrane ,
Thick basement splitting of
membrane basement
without Vascular membrane, tram
Light microscopy changes, Normal Focal segmental track appearance
Biopsy findings
is normal cellularity, epi sclerosis , / double contour
Membranous appearance , no
spike, sub epi Membranous
Q
epithelial deposits spike , sub
endothelial
deposits
Corticosteroid > Immuno - Immuno –
Treatment - -
biopsy suppressant suppressant
•• Treatment of Steroid dependent Nephrotic AKI

syndrome :- Cyclophosphamide/ Rituximab
•• Treatment of steroid resistant Nephrotic
syndrome:- Cyclosporine
* For Making Notes

131
Medicine
Post Renal AKI Difference between contrast induced

•• Occur due to obstruction nephropathy & atheroembolic disease
•• IOC :- imaging → B/L hydroureteronephrosis CIN Atheroembolic
disease
•• Bladder Neck Obstruction due to stone, foley’s
Timing 1st 2 days 4 day
obstruction, prostate cancer
Increased S. Early Late
–– Treatment:- Foley’s > storage pubic catheter
Creatinine
•• Ureteral obstruction due to stone, Retro Asymptomatic, Surgery :- for blue
Peritoneal fibrosis, bulky Retro Peritoneal normal C3 cyanotic toes &
lymph nodes
livedo reticularis &
–– Treatment:- ureteroscopy +/- double j Amaurosis fugax
stenting or percutaneous nephrostomy
Low C3 level
Pre renal AKI Biopsy Vacuoles Clear needle like
spaces in vessels
•• Due to low perfusion to the kidney
Prevention IV fluids - NS
•• Reduced effective arterial blood volume
→ absolute causes (hemorrhage, vomiting,
Diarrhea) & relative causes (edema in case of Galadium contrast :-
heart failure, Cirrhosis •• Creatinine clearance is <30 → nephrogenic
•• Altered local perfusion associated with ACE / systemic fibrosis
ARB inhibitors, NSAIDs
•• Example of Large vessels problem :- renal
Pre renal AKI vs ATN
artery stenosis Parameter Presently AKI ATN
Urine Bland Active- muddy
•• Treatment:- treat the underlying cause &
optimize hemodynamic brown cast
Urine S.G ↑↑ >1.020 ↓↓ <1.010
Intrinsic renal AKI Urine Na <20 >40
(mmol/L)
•• Due to problem of interstitial nephron Q
FE NA <1% >2%
•• Vascular :- atheroembolic disease
Q
↓ ↑
•• Problem in tubule :- acute tubular necrosis (toxic FE UREA <35% ↓ >50% ↑
– Aminoglycosides, Vancomycin & ischemic), Urine Osm >500 ↑ <350 ↓
contrast induced nephropathy , pigments- free (mOsm / kg)
Hb (in intravascular hemolysis) & free myoglobin
Urine Cr/ plasma >40 ↑ <10 ↓
(in rhabdomyolysis), Crystal deposition
Q
Cr
Plasma BUN / Cr >20 ↑ <15 ↓
Indications for dialysis in AKI
A: acidosis (refractory) •• ↑FE NA
in pre renal :- in case of more salt in
E: electrolytes imbalance (refractory hyperkalemia) diet, volume resuscitation, receiving diuretics,
I: intoxication
AKI or CKD
O: overload of volume (refractory pulmonary edema) •• ↓FENA deposit in ATN :- in case of vaso
U: uremic Complications (uremic pericarditis, uremic constriction- free Hb, Myoglobin , contrast , low
encephalopathy, uremic bleeding) salt diet, heart failure, Cirrhosis
* For Making Notes

132
CKD & TRANSPLANT –– Target Hb :- 10-11g%
GFR stage GFR (mL / Goals of treatment –– Most common complication :- HTN
min/1.73 m2) •• CKD mineral bone disease / renal osteo
I ≥ 90 Address the risk dystrophy :- high PTH due to low Ca & high PO4
factors & slow down
progression –– Treatment: calcium & vitamin D supplements,
phosphorus binders – non calcium based →
II 60-89 Estimate progression
& slow it down
sevelamer
III a 45-59 Treat Complications –– Cinacalcet, parathyroidectomy can also be

III b 30-44 Treat Complications used
IV 15-29 Prepare patient for •• Calciphylaxis:
renal replacement
therapy –– Treatment:- stop all vitamins D & Ca
supplements, warfarin (give IV vit K) →
V <15 Dialysis 3 times/week
switch to Apixaban +/- Ab +/- surgical
Most common cause of death in CKD is cardiovascular debridement
diseases
•• Kidney transplant:
•• Peripheral neuropathy is the most common
neurological disease in CKD –– Target CMV
•• Urine albumin : creatinine ratio –– Target acute transplant rejection:- modified
–– A1 stage <30 BANNF criteria
–– A2 = 30-299 Acute cellular rejection treatment:

methylprednisolone + ATG anti
–– A3 = >300
thymocyte globulin
Ab mediated rejection - C4D+
Q
○○ Treatment:- methylprednisolone,
Rituximab + plasma exchange
○○ Calcinurin inhibitor → can lroduce
thrombotic microangiopathy after
transplant , tacrolimus → lead to new
onset diabetes after transplant
•• Anemia of CKD:- IV Fe → erythroid stimulating

agent (epoetin alpha, darbepoetin alpha,
methoxy PEG eopetin beta)
Q
* For Making Notes

133
Medicine
� BKV nephropathy → late ureteric PKD 1

Strictures
•• Chromosome 16
○○ Triad
•• Most common (85%)
PCR +
•• Poor prognosis
•• Early onset renal disease
•• Clinical features - Large palpable cystic kidney
(multiple cysts present)
–– Most common complication:- HTN → give ACE
inhibitors
Decoy cells in urine
Q
biopsy :- BKV IHC +
–– Most common cardiac issue :- mitral valve
•• Target Cancers:- most common is skin cancer → prolapse (asymptomatic) , neurological
SCC/ BCC / Melanoma/ Kaposi sarcoma
issue:- berry Aneurysm → Results in Sub
–– Post transplant lympho proliferative disorder: Arachnoid hemorrhage
EBV related
–– Most common extra renal site for cysts :-
–– Prophylaxis: valganciclovir liver
–– Monitor: CMV PCR –– IOC :- USG
–– Treatment of disseminated infections :- IV –– Modified ravine criteria use for check
ganciclovir (DHPG)
family history
–– Gold standard for diagnosis:- biopsy (owls –– Treatment:- Tolvaptan , mtor inhibitors :-
eye kind of inclusion bodies)
Q
Sirolimus , everolimus
ADPKD PKD 2
•• Chromosome 14
•• Less common (15%)
•• Good Prognosis
SODIUM DISORDERS
•• Formula of S. Osm :- 2 (Na) + BUN / 2.8 + GLU
/ 18
Q
•• Complete penetrance , family history +++

•• Both PKD 1 & 2 have problem with Cilia
* For Making Notes

134
Treatment of hyponatremia •• In chronic condition :- correct <4-6 mEq/L / day
•• If severe symptoms present like coma, seizure •• If over correction done, it may lead to Osmotic
→ 3% NaCl demyelination syndrome
•• If no severe symptoms → –– Clinical features:- quadriparesis +/- bulbar

palsy
–– Hypovolemic: NS (0.9% Nacl)
–– Treatment:- re lower the S. Na by
–– Euvolemic: increased U. Osm → fluid
desmopresssin
restrictions +/- vaptans , if U. Osm low →
•• Sodium deficit calculation
Q
fluid restrictions with Psychiatric counseling,
if patient have low solute → give solute (NS) TBW × (desired Na – actual S. Na)
–– Hypervolemia:- fluid restrictions +/- loop •• Hyponatremia:- free water deficit calculation -
diuretics
S. Na - 140/140 × TBW
•• In acute condition :- correct only < 8-12 mEq /
L/day
* For Making Notes

135
Medicine
POTASSIUM DISORDERS
•• ECG changes:- T Flattening, prominent U wave, ST depression, increased QU interval
Q
•• Approach
* For Making Notes

136
Correction •• Treatment :- 1st → calcium gluconate , STAB

membrane potential
•• 1 mEq /L decline in S. K+ → replace 200 mEq/ L
of K+ from outside –– 2nd → drugs that produces transcellular
shift = IV insulin + 25% Dextrose
•• Infusion rate for peripheral line :- 10 mEq/L,
for central line :- 20 mEq/L (best is femoral –– Beta 2 agonist = salbutamol nebulize
line) –– NaHCO3
•• Dilution :- every 1 L of IV fluids → 40 mEq/L of –– Drugs which reduces total body K+ = loop
K+ (fluid = NS) diuretics, k+ binders (increase GI loss
of potassium) → kayexalate (high risk of
Hyperkalemia colonic necrosis)
•• 90% due to drug-related Causes (ACE , ARB –– Sodium zirconium cyclosilicate
inhibitors , MRAs , ENaC blockers , beta
–– Extra corporal removal → dialysis
blockers, heparin , Cyclosporine, tacrolimus ,
pentamidine etc.) or renal failure •• Digitalis induced hyperkalemia Treatment =
digibind
•• ECG changes:- tall T wave , conduction blocks,
wide q wave , absent p wave , wide QRS →
diastolic cardiac arrest , BBB , short QT
* For Making Notes

RHEUMATOLOGY
RHEUMATOID ARTHRITIS
Boutounniere Deformity
Peri - Articular / Juxta - Articular osteopenia
•• Seropositive chronic inflammatory, symmetric
•• Narrowing of joint space can occur in any
polyarthritis (> 5joints)
arthritis/ arthropathy ,only exception can be
•• Common in females, 30-60 yrs age, females gout & acromegaly related arthropathy.
develop more severe symptoms
•• Extra articular manifestation-
•• Genetic association - HLA DR4
Q
1. Lymphadenopathy (MC)
•• Environmental association – smoking
2. MC malignancy associated with RA- NHL
•• Seropositive - RF +, ACPA +, anti CCP + Ab, anti (DLBCL)
Q
MCV + Ab.
3. MC cardiac manifestation- pericarditis , RCM
•• When ↑↑ titres, severity ↑, ↑risk of extra-
articular involvement. 4. MC pulmonary manifestation is pleuritic, with
exudative pleural effusion with low glucose.
•• Acute - <6 weeks, chronic - >6 weeks
5. MC skin manifestation- subcutaneous nodules,
•• Inflammatory - ↑CRP / ↑ESR
mobile, on extensors, painless
•• Any inflammatory arthritis: Early morning
stiffness for >1 hour, pain ↓ with exercise / 6. MC ocular manifestation- keratoconjunctivits
movement, ↑with rest. sicca/dry eyes → MCC of 2° Sjogren’s
syndrome.
•• It is an Additive arthritis - more & more joints
will keep on adding 7. Late kidney involvement seen in amyloidosis
•• MC joint – MCP joint > PIP joint &wrist joint. (AA type) {early kidney involvement is seen
in SLE} MGN also seen.
•• MC large joint involved – knee joint
8. Pulmonary – RA nodules in upper limb,
•• Spared joint - DIP > thoracolumbar spine associated with pneumoconiosis like silicosis
(RA+pneumoconiosis- Caplan syndrome)
Q
•• Can develop erosions, erosive arthritis.
•• Deformities - Boutounniere, swan neck (hyper 9. MC ILD seen in RA- UIP (all other CTD have
flexion at DIP, hyper - extension at PIP), Z – NSIP as MC ILD)
deformity of thumb
Q
10. Hematological – Anemia (AOCD)

140
11. Felty syndrome- late erosive RA with •• TOC in acute flare - corticosteroids, <2 joints
extremely high titres + massive splenomegaly - intraarticular corticosteroids, >3 joints -
+ neutropenia
systemic corticosteroids. (before starting tx,
–– D/D of felty syndrome - T-cell LGL (CD16+, always r/o joint infection)
Q
CD57+)
–– In case of large joint, do joint aspiration
12. MCC death - CV risk
before starting steroids.
13. Pregnant female- good prognosis
•• Triple Therapy c. Other anti-TNF – used upto 3rd trimester

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

Q
* For Making Notes

141
Medicine
Seronegative Spondyloarthropathies
•• Common features - RF-, ACPA-, ANA -. Peripheral arthritis. Variable association with HLA-B27.
•• Inflammatory back pain, early morning stiffness >1hr that improves with exercise. NSAIDS very useful. Most commonly involved
is thoracolumbar spine (only exception is psoriatic arthopathy). Sacroilitis present. Peripheral arthritis - oligoarticular &
asymmetric, LL > UL. Achilles enthesities. Dactylitis. Sausage shaped digits. MC extra - articular manifestation - Ant. uveitis.
Distinguishing features
Disorder AS PsA ReA EA
Axial 1° peripheral arthritis +/- axial
Disease type Oligoarticular /asymmetric
Sometimes, PsA can mimic RA by involving small joints of upper limb
Males / <40yrs Males =females Males /<40yrs Males =females
Gender/ Mean age (yrs)
>40yrs /<40yrs
Axial involvement, Correlates 100% 20-40% 40-60% 5-20%
with HLAB27
Sacroilitis – 1st Ix to be done Symmetric Asymmetric symmetric
when Sacroilitis is suspected is
XRAY - ankyloses/fusion.
MRI – gold standard. BM
edema.
Peripheral distribution UL>LL UL>LL LL>UL UL>LL
Enthesitis ++ ++ ++ Rare
Dactylitis Rare ++ ++ Rare
Q Q
Ocular Ant uveitis Episcleritis +/-ant uveitis conjunctivitis Rare
Rare Psoriatic skin & nail changes Circinate balanitis, Erythema
(80%) keratoderma nodosum,
Skin
blenorrhagicum Pyoderma
gangrenosum
Q
Shiny corner sign / Pencil in cup DIP deformity Asymmetric No specific
bamboo spine/ dagger syndesmophytes
Imaging
sign/symmetric
syndersmophytes
Q
UL fibrosis Types: •• Arthritis (sterile) h/o IBD
MC valvular disease- 1. asymmetric oligoarticular + conjunctivitis 2 Types
AR 2. symmetric polyarticular (sterile) + urethritis Type 1 –
3. isolated DIP (sterile/non sterile) oligoarticular /
4.psoriatic spondylitis asymmetric
•• Reactive arthritis correlates with
Other features 5.athritis mutilans
occurs as a reaction IBD activity.
to infections -
GIT - shigella /
GU - chlamydia (l2b
serovar)
Treatment: DMARDS -
1. Pain- NSAIDs •• Conventional- no efficacy on axial disease
2. Control- DMARDS •• Target synthetic- can be used for both axial &peripheral if disease is refractory to conventional
3. Apremilast – PDE4i – PsA DMARDs & anti TNF.
Q
4. Antibiotics – doxycycline in •• Biological DMARD - best .
PsA
- Anti-TNFα- infliximab /adalimumab
- Anti IL-17 inhibitor- Secukinumab / Ixekizumab – approved for AS/ PsA
- Anti IL-12/23 inhibitor- Ustekinumab
* For Making Notes
- Anti IL-23 inhibitor- GuselkUmab
142
B/L Symmetric Ankylosis - AS
Pencil in Cup Deformity, Classic of PsA.
CRYSTAL ARTHROPATHIES &

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

nocturnal pain, MC •• Monoarticular
joint involved is 1st / asymmetric
metatarsal jt (k/a
oligoarticular
Psoriatic Nail Changes Acute PODAGRA), initial
•• MC joint involved is
attack is monoarticular
→ later polyarticular Knee / MCP , Wrist
attacks. Can have joint
associated cellulitis.
•• Tophi deposition
seen in Joints (toe
•• Pseudo RA- Early
jt/ finger jt/wrist
morning stiffness
Chronic jt/knee jt.)
•• Pseudo OA- non
Enthesitis - seen in all arthropathies except enteropathic •• Soft Tissue (pinna
inflammatory
arthritis / olecranon bursa/
Achilles)
3H-
Associated Metabolic syndrome / hyperparathyroidism
conditions CKD/HF Hypomanesemia
hemochromatosis
* For Making Notes

143
Medicine
Gout (d/t deposition Pseudogout (d/t HIGH YIELD POINTS

Features of monosodium urate deposition of calcium
crystals) pyrophosphate crystals) •• Rasburicase – approved and used only for tumor
•• MSU
lysis syndrome not chronic gout
•• IOC- joint
•• IOC- joint
aspiration .
•• Pegloticase – can be used for chronic gout, not
aspiration approved for tumor lysis syndrome.
Crystals •• Rhomboid shape,
•• Negatively
birefringent, needle
weakly positive •• C/I of Pegloticase & Rasburicase – G6PD
Q birefringence deficiency
shaped
•• Acute – non specific
•• Chondrocalcinosis
Q •• Uricosurics- Probenecid –organic anion
•• Chronic – Martel transport inhibitor
Imaging •• MC seen in knee
G sign, MSK USG - Benzbromarone - selective uric
joint, wrist joint
double contour seen transporter Selective urate
inhibitor
Lesinurad
Treatment
Acute Gout & Acute Pseudogout:
•• 1st line - NSAIDs +/- Colchicine (for 3-6 Martel G Sign /Ratbite Erosions
months) → ↓recurrence
•• Alternate – corticosteroid / ACTH /anti-IL-1 –
Anakinra < Canakimumab (preferred)
•• s/e of colchicine-
–– GI disturbances, diarrhea mostly
–– Agranulocytosis (dangerous s/e)
Chronic Gout
Double Contour Sign
•• Indications for uric acid lowering therapy: >
2attacks / year / Tophi / EGFR <60 / urolithiasis
•• Allopurinol – purine based XO inhibitor →
allopurinol hypersensitivity syndrome mainly in
HLA B 5801.
•• Febuxostat – non purine XO inhibitor
•• Both Allopurinol , Febuxostat → avoided with
Azathioprine / 6-MP (↑BM suppression)
Q
Chondrocalcinosis (Pseudogout)
* For Making Notes

144
•• Plasma cell / dendritic cell type – linked to

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

•• Mucocutaneous –
•• r/o other disorders
a. Oral /nasal (painless) ulcers
•• It is diagnosis of exclusion.
b. Alopecia ( non scarring)
•• Yamaguchi criteria
c. Skin-
•• Tx: DMARDs , anti IL-1 therapy .
ACLE- malar rash , mainly face
JIA
SCLE- anti Ro antibody, spare face
•• <16 yrs of age
CCLE- DLE , MC face>scalp , scarring type,
•• 3 Types- over time ↑risk of squamous cell cancer
–– Oligoarticular / asymmetric
–– All SLE related skin lesions are
–– Polyarticular / symmetric photosensitive.
–– Systemic JIA – still’s disease •• Serositis can result in pleuritic (associated with
•• +/- Growth affected small pleural effusions ) / pericarditis
•• +/- anterior uveitis •• Major organ development- MCC of death in SLE
is CV risk
•• Serology negative – RF-/ACPA-/ANA-
Hematological Kidney Neuropsychiatric Lungs
•• TOC- DMARDs
Q
1. Anemia (anti 1. Lupus 1. MC- ↓cognition 1. <5% - ILD

SLE erythrocyte Ab)– nephritis (associated (MC- NSIP)
AOCD / warm (anti ds with anti NMDA 2.
type AIHA(IgG) DNA Ab/ receptor Ab/anti endocarditis
– DCT+ anti smith glutamate Ab) – libman
2. Leukopenia / Ab) – MC 2. Headache sach’s
lymphopenia (anti & most 3. Seizures endocarditis
lymphocyte Ab) / severe –sterile
4.Psychosis (anti
thrombocytopenia form is vegetations
ribosomal P ab /
(20 ITP)
Q class IV. 3. RCM – HF
APLA ab)
Wire loop d/t diastolic
5. Vascular
lesions are failure.
complications-
seen in
•• Middle age female in reproductive age group stroke (APLA Ab)
this.
•• Genetic association- early classic complement
pathway deficiency (C1q/ C4/C2). SLE - Antibodies
•• C1q- severe disease, TREX gene associated •• C3/C4 can be used as marker of disease activity.
•• Environmental → EBV / hormonal → estrogen /
•• If low C3/C4- active disease
Q
drugs → procainamide, hydralazine
* For Making Notes

145
Medicine
•• CRP can be normal in active disease, if ↑↑- Anti histone Ab- drug induced SLE. Drugs causing this –
suspect infection in SLE. MD - SHIP
•• ESR – normal M - Minocycline , Methyldopa
Ab Significance D - D- penicillamine
Most sensitive, >98-99%, poor S - sulfonamides
ANA
specificity , >1:80 titres H - hydralazine
Specificity >95%, poor
I - isoniazid, interferons, infliximab
Anti ds DNA sensitivity - 50-70%, correlate
P - Procainamide
to lupus nephritis /vasculitis
Anti histone SLE → mild arthritis / serositis Lupus Nephritis
•• Specific for sjogren
syndrome. Class I – Minimal mesangial Asymptomatic →
•• Seen in SLE-Sjogren Class II- mesangial proliferative
Q
Tx: observe &ACEi
overlap
Anti Ro/La (SSA/ •• SCLE, Photsensitivity, Class III- focal

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

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

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

146
SYSTEMIC SCLEROSIS •• 1° vascular disease, skin thickening is a reaction

to underlying vascular damage and resultant
hypoxia.
•• Every patient has 2° raynaud’s phenomenon

abnormal nail fold capillaroscopy.
•• Female, middle age group
Limited Scleroderma Diffuse Scleroderma

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

Treatment +MAHA (hemolysis / schistocytes) +
•• Skin thickening - Mtx /MMF ↓Platelet + severe AKI + ↑BP
•• ILD – MMF /Tocilizumab /Nintedanib •• PAH (Type 1) - Ambrisentan + Tadalafil +/-
Prostanoids
Q
•• Scleroderma renal crisis – ACEi only
* For Making Notes

147
Medicine
SJOGREN SYNDROME GLANDULAR EXTRAGLANDULAR

•• MC , develop early •• constitutional symptoms
•• Dry eyes →↓quality of •• MSK – Arthralgias /arthritis
life (abnormal sensation) •• ILD- MC NSIP
→ corneal ulceration •• RCM , Conduction block
•• Dry mouth → bad •• Distal RTA
odour/dental caries/
•• Hemat- MC is anemia (AOCD)
dysphagia/taste
•• Monoclonal gammopathy
•• Dyspareunia
-20%→↑risk of lymphomas
•• Dry skin- xerosis
•• MC cancer- NHL (Maltoma)
•• b/l parotid enlargement
•• Peripheral neuropathy (small
(symmetric & painless)
fibre) → Ix with skin biopsy
Ix: Triad
1.Serology –
1° Sjogren syndrome-
•• Idiopathic •• Anti Ro (SSA) - specific
Q
•• Female, 40-50 yrs of age

•• MC ANA + (>95%) non specific
•• Extraglandular manifestation - CD4 T cell
infilteration 2.Dry mouth- sialometry
•• Dry eyes - schirmer test
2° Sjogren syndrome-
3. Labial biopsy – focus score >1/4mm2
•• Some associated disease.
•• Treatment – Conservative &supportive
•• MCc- RA
•• Dry eyes- CMC ,cyclosporine eye drops
•• Dry mouth - pilocarpine
INFLAMMATORY MYOSITIS
Features DM PM sIBM NAM
Females>males, 30-40yrs age , Female>males, 30-40 Female>males, Any age
Epidemiology Males, >50 yrs
Can affect children also yrs age
Skin +/- proximal weakness Both proximal(MC
•• if only skin is involved – affected – quadriceps)
k/a Amyopathic DM (anti Proximal muscle +distal (long finger
Clinical Proximal muscle weakness
CADM 140/MDA5 Ab) weaknesss flexors) muscle
•• abnormal nail fold weakness + associated
capillaroscopy neuropathy
CPK ↑↑(>50X) ↑↑ (>50X) Normal/mild↑(<10X) Mildly ↑(<10X)

•• Anti SRP Ab (NAM
+cardiac involvement)
Anti NXP2 Ab •• Anti mup44 Ab, •• Anti HMG CoA
Q
Ab Anti TIF18(P155/140)Ab Anti Jo-1 Ab •• Anti 5’cytonucleotide reductase Ab
Q
Anti mi2 Ab Ab •• Anti 200/100 AG Ab
•• Both are associated
with statin exposure
* For Making Notes Inflammation less, No inflammation.

Peri-fascicular/peri fascial Endomysial inflammation
Biopsy inclusion body seen → β Necrosis , macrophage
inflammation(CD4) (CD8)
amyloid infiltration
Response to CS yes yes No yes
148
•• Anti amino acyl tRNAsynthetase Ab

–– Histidyl = anti Jo-1 (MC synthetase antibody)
Q
SYNTHETASE SYNDROME
1. Fever
2. Raynaud’s
3. Myositis (polymyositis)
Holster Sign
4. ILD
5. Mechanic’s hands
•• Malignancy + myositis → can be associated with
polymyositis or dermatomyositis. Anti TIF-1ϒ
(p155/140)
V Sign
Heliotrope Rash
Mechanic’s Hands
RAYNAUD’S PHENOMENON
Shawl Sign
Triphasic Response. Pallor-Cyanosis-Reperfusion

Gottron Rash
* For Making Notes

149
Medicine
1° Raynaud - MC (>70—80%) 2° Raynaud (<10-20%)

Vessel wall Functionally abnormal Structurally abnormal
•• CTD (SLE/RA)
•• PAD(Buerger’s)
Etiologies idiopathic
•• Hematological
•• Drugs- ergot compound/cocaine
Epidemiology Females, 20-40 yrs of age Females, >30yrs age
Clinical Mildly symmetric, no tissue injured Severely asymmetric, thumb
Auto Ab No present (CTD related)
Nailfold Normal Abnormal (dilation & tortuosity seen)
Mild- moderate- CCB like nitrates
Moderate- severe- PDE5-
Treatment
Digit threatening- prostanoids
Recurrent /refractory – digital sympathectomy
VASCULITIS
Large Vessels Medium Vessels Small Vessels
Feature
TAKAYASU GCA PAN AAV IC
Female ,<40yrs Females , >50yrs, Variable, middle aged HSP, males, <20 yrs, Cryoglobulinemia-
Epidemiology Caucasians Variable variable
Asians 5-10% are HBV+
•• Microaneurysms
•• Infarcts to
Renal artery kidney.
stenosis / •• ++GN → Hematuria, RBC casts/ HTN/AKI
Renal renovasular rare •• HTN,↑S.
•• RPGN
hypertension Creatinine
•• Hematuria,
•• No RBC casts
Pulmonary rare - rare common Cryo >HSP (rare)
PN Rare/uncommon + + +
+
GI rare + + ( HSP> CRYO)
microneursym
+→palpable
purpura
Skin Rare none + + Raynauds
phenomenon,
PLT count
normal
Granulomas Yes no Yes, except MPA No
TRIAD-
MC artery involved
Wegener’s granulomas- Skin - palpable
is superficial
ENT involvement, pulmonary purpura –
temporal artery,
renal syndrome (MCc of death). common in LL/
temporal Q
MC artery C-ANCA + butts
Headache (MC), jaw
involved is Churg strauss syndrome +
claudication (2nd Q
subclavian HBS Ag+ , Testicular (EGPA) - bronchial asthma. MCC GI – abdominal
Others MC)
artery, arm pain, involvement of death is cardiac involvement. pain, +/-
ESR↑↑
pulseless radial P-ANCA + bleeding
Q Ophthalmic artery-
artery MPA - present with pulmonary +
artery AION , * For Making Notes immune syndrome, no ENT / Arthralgia
Blindness
no eosinophilia/ no bronchial +/- renal- IgA
IOC- Temporal Q
asthma. P-ANCA+ mesangial
artery bx
deposits
TOC-
Treatment HSP- NSAID’S
corticosteroids
150
BEHCET’S DISEASE KAWASAKI DISEASE

•• HLA B51 •• Medium vessel vasculitis
Q
•• Recurrent oral apthous ulcers •• Coronary artery aneurysm

Q
•• Recurrent genital apthous ulcers- male : scrotum •• Children <5yrs, males, Asians
> shaft of penis
•• Gold standard Ix - Coronary angiography
•• Females: labia
•• Monitor disease - ECHO
•• Skin – erythema nodosum
•• Tx: IV Ig + aspirin
Q
•• Eyes- posterior uveitis >anterior uveitis,

F - fever, > 5days
hypopyon formation
E - enathems
•• Pathergy positivity
B - bulbar conjunctivitis (sterile)
•• Superficial thrombophlebitis +DVT
R - rash- groin /perianal
•• Arthritis /fever
I - internal organ involvement : coronary artery
•• CNS – brainstem involvement
involvement → aneurysm → AF/MI → death
L - Lymphadenopathy
E - extremity changes
* For Making Notes

HEMATOONCOLOGY
antibodies develop.
APPROACH TO TRANSFUSION 3. TTI –Transfusion transmitted infections
REACTION
•• Bacterial contamination – Platelets: RDP > SDP
•• Any transfusion reaction, any grade, severity → → gram positive bacteria
transfusion should be stopped. –– PRBC: → gram negative rods
•• MCC Post transfusion hepatitis – HBV
4. TRALI – Transfusion related acute lung injury
•• Onset within < 6hrsQ
•• Allo antibodies of donor attack WBCs of
recipient → attacked WBCs get clogged in
pulmonary capillaries → cytokines released →
Exudate release → ARDS like picture
•• MCC of transfusion related death.
TRALI TACO
•• SOB, Crepitations - •• SOB, crepitations – B/L,
1. AHTR - Acute hemolytic transfusion reaction B/L, diffuse diffuse
•• It is d/t ABO mismatch •• B/L lung infilterate on •• B/L lung infilterate on
Xray Xray.
•• Symptoms -
•• It is d/t non •• It is d/t cardiogenic
–– In conscious patient - burning pain along the cardiogenic pulmonary pulmonary edema
vein/iv line edema •• It is d/t volume overload
–– In comatose patients - bleeding & oozing •• Symptoms - fever •• Risk factor - h/o
from puncture sites d/t DIC because it is a immune overload state like CKD,
–– Fever reaction HF
–– ↓BP/↑HR –– ↓BP/↑HR •• Symptoms - no fever
–– AKI -↑ S.Creatinine /flank pain –– Normal JVP –– Normal BP/↑HR
–– Intravascular hemolysis - ↑LDH/↓S. –– Normal BNP –– ↑JVP
Haptoglobin /hemoglobinuria •• Treatment – no –– ↑BNP
–– DCT /DAT +ve response to diuretics Treatment - diuretics
2. FNHTR - Febrile non hemolytic transfusion 5. Minor Allergic reaction
reactionQ
•• Causes urticaria & itching.
•• No signs of hemolysis
•• Symptoms - fever/chills. •• Stop the transfusion for 10-15 mins and resume
once urticaria settles down.
•• Cause - WBCs of donor reacting with allo
antibodies of recipient. •• Tx: antihistamine
•• Treatment - analgesic 6. Anaphylaxis
•• Prevention – leukodepletion filterQ •• Causes: urticarial, wheeze/SOB, stridor and ↓BP.
•• More regular the transfusion, more the allo
154
•• Tx: antihistamine /dexamethasone/ epinephrine •• C/F: thrombocytopenia, bruises, superficial

(1mg in 1:1000 I.M.) bleeding, petechiae
•• If recurrent anaphylactic reactions occur, •• Tx: IV Ig (urgent Tx), corticosteroids show
always r/o IgA deficiency. affect after 1-2 weeks.
DELAYED REACTION •• HPA1a Antigen is also responsible for

FNAIT (fetal & neonatal allo immune
1. DHTR – delayed hemolytic transfusion reaction
thrombocytopenia)
•• Similar to AHTR, but less severe
3. TA-GVHD
•• ↓Hb, Intravascular hemolysis → ↑LDH/↓
S.Haptoglobin /hemoglobinuria •• In recent bone marrow transplant/ SCID,
the recipient will not have any sort of immune
•• DCT /DAT +ve
system to mount a immune response against
•• It occurs d/t minor antigens → Duffy Ag, donor T cells → donor T cells attack recipient’s
KIDDO Ag‘s anamnestic response stem cells in bone marrow & results in profound
•• Tx: supportive BM suppression.
2. PTP – post transfusion purpura •• Prevention: with irradiated blood products.
•• Causes: Antibodies against platelet antigen
HPA1a Ag in the subsequent transfusions. INTEGRATED APPROACH TO ANEMIA
•• Presents with delayed thrombocytopenia after
(↓HB)
5-7 days of transfusion.
* For Making Notes

155
Medicine
•• Drugs like antibiotics – ceftriaxone/piperacillin/ –– Ferric carboxymaltose( FCM)

cefotetan can induce warm type HA. –– Ferrumoxitol
I. Microcytic –– Isomaltosidase - max. concentration of iron
1. IDA •• IV iron is safe in renal diseases & pregnancy.
•• MCC of iron deficiency •• Reticulocyte index <2
•• Cause - blood loss •• Response to iron supplementation –
•• C/F - subjective features → fatigue, pica, –– Earliest - subjective improvement (within 12-
koilonychia, platynychia, angular cheilitis 24hrs)
•• Plummer Vinson syndrome - IDA + esophageal –– Fatigue will improve, pica will improve.
webs + dysphagia: premalignant condition - –– Koilonychia will take 3- 6 months to improve

↑risk of squamous cell cancer –– Hematological change – BM → erythroid
•• Dx: earliest - ↓S. FerritinQ hyperplasia (48hrs)
•• Transferrin saturation = Fe/TIBC <18 –– On P/S - ↑reticulocyte Hb on smear →

reticulocytosis
•• S. transferrin /log ferritin >2
2. AOCD - Anemia of chronic diseases
•• Hepcidin ↓↓
•• Any inflammation can result in ACOD.
•• Mentzer index = MCV/RBC >13
•• S.Ferritin ↑
•• Gold standard for dx: BM Aspiration. Stained
•• Transferrin saturation = Fe/ TIBC >18%
using Prussian blue.
•• S. transferrin /log Ferritin < 2
•• TOC: Iron supplementation – oral or IV
•• TOC: erythropoietin
•• Indications for IV iron - pregnancy /intolerance
•• Reticulocyte index < 2
to oral iron
3. Β- thalassemia minor
•• Oral iron - 1st choice → MC S/E of oral iron →
GI S/E •• Incidental finding, Asymptomatic
•• Mildly ↓Hb, ↓ MCV

•• Formulations - Fe gluconate (lowest iron content)
/Fe SO4 / Fe fumarate (highest content of iron) •• Mentzer index = MCV/RBC <13
•• IV iron formulation - •• Normal Fe indices
–– IV iron gluconate •• NESTROFT can be used as screening test for
–– LMW Dextran thalassemia in areas of high prevalence.
–– Iron sucrose •• Hb electrophoresis - HbA2 (α2δ2 ) >3.5%Q
* For Making Notes

156
Β thalassemia Α- thalassemia
•• Never present at fetal life or birth •• Can present at birth
•• Take 6- 12 months to manifest •• Classification
•• Classification - –– 1α - asymptomatic/ normal smear
–– Thalassemia major – –– 2α-
Symptomatic + transfusion dependent. Asymptomatic
Need regular transfusion → iron Mild ↓Hb + microcytosis (Hb electrophoresis is normal)
overload therefore iron chelators used –– 3α-
- IV deferoxamine / p/o deferiprone / α thalassemia intermedia
p/o deferasirox
Symptomatic at birth itself
Target Hb >10g/dl (ensure adequate
Severe microcytosis
growth in children)
Moderate – severe anemia (7- 9gm/dl), splenomegaly
Reticulocyte index <2
β4 tetramers - HbH disease, can be detected in Hb
–– Thalassemia intermedia –
electrophoresis, smear seen as golf ball.
Symptomatic but not transfusion
–– 4α-
dependent.
Behave as thalassemia major in utero.
Reticulocyte < 2
ϒ4 tetramer formation in fetal life itself, a/k/a Hb Barts.
–– Thalassemia minor -
Can be detected in Hb electrophoresis.
Asymptomatic + mild ↓ Hb +
Death in uterus without intrauterine transfusion.
microcytosis Reticulocyte index >2
Reason of death - severe anemia → cardiac collapse →
hydrops
4. Sideroblastic anemia II. Normocytic Anemia

•• Iron cannot be utilized due to defective Extravascular hemolysis Intavascular hemolysis
porphyrin synthesis. •• Destruction of RBCs in •• Destruction of RBCs in
•• ↑S.Ferritin, ↑Transferrin saturation (Fe/TIBC) spleen blood vessel, rouleax
>50- 60%, reticulocyte index <2 •• Jaundice formation /agglutination
•• BM aspiration – ringed sideroblasts (RBC •• On P/S - spherocytes •• Hemoglobinuria
precursors with iron accumulation in the form •• Cold HA results in
•• Warm HA results in
of mitochondria) are seen.Q
extravascular hemolysis intravascular hemolysis
•• 2 conditions where ringed Sideroblastic are •• Avoid cold exposure
•• Tx: corticosteroids
seen -
treat main causes
–– Sideroblastic anemia + Splenectomy in
•• Rituximab helpful
–– Refractory anemia with ringed sideroblasts refractory in waldenstrom
(MDS) macroglobulinemia
•• Causes: DCT –ve: Non immune mediated HA
–– Hereditary causes – ALA synthase defect
–– Pyridoxine deficiency – dietary /isoniazid/
chronic alcohol/lead poisoning
•• Tx: Pyridoxine
–– Chelators like succimer /dimercaprol.
* For Making Notes

157
Medicine
1. Thrombotic microangiopathy •• Patient has h/o exposure to causes →

present with ↓Hb, ↑LDH , Hemoglobinuria,
•• Triad – MAHA + thrombocytopenia + End organ ↓S.Haptoglobin (intravascular hemolysis)
damage (Renal /CNS)
•• P/S - Heinz bodies (seen only in vital stains like
2. PNH new methylene blue)
•• Acquired PIG-A gene defect in stem cell –– Blister/Bite cells (seen in routine stains like
wright giemsa stain)
•• PIG-A defect → ↓GPI anchors → ↓CD55
(DAF)/CD59 (MIRL) expressionQ •• Tx - supportive treatment
•• Triad - Nocturnal hemoglobinuria + Pancytopenia 4. Hereditary spherocytosis

with classic cellular marrow + Thrombosis (MCC
•• MC defect – Ankyrin defectQ
of death)
•• Family h/o anemia / h/o gallstones/ jaundice /
•• Infections – 2nd MCC of death d/t pancytopenia
cholecystectomy
•• IOC - flow cytometry (FLAER)Q •• Patient presents with anemia + P/S →
•• TOC - allogenic stem cell transplantation spherocytes (DCT –ve)
•• 1st line of Tx - Eculizumab (Anti C5 Mab) / •• Spherocytes also seen in warm type AIHA, r/o
Ravulizumab (Anti C5 Mab)Q with DCT.
–– S/E - ↑risk of fulminant meningococcal •• Extravascular hemolysis (spleen) - jaundice

infection / ↑risk of pigmented gallstones / chronic leg
ulcers /splenomegaly
–– ↓ intravascular hemolysis
•• Screening - OFT → ↑ fragility of spherocytes
–– No effect on extravascular hemolysis / ↑MCHC
3. G6PD deficiency •• AGLT (Acidified glycerol lysis test) - ↑sensitivity
•• Mc enzyme deficiency in the world •• IOC - Flowcytometry (EMA binding)Q

•• TOC - splenectomy
•• ↓NADPH → ↓glutathione in RBC → ↑risk of
damage by oxidative stress –– Indications - transfusion dependent
•• Causes – drugs: → Primaquine, ciprofloxacin,
sulfonamides, uricase, IV methylene blue,
doxorubicin, nitrofurantoin /DKA/ infections /
Diet → fava beans
* For Making Notes

158
5. Sickle cell disease - •• Tx -
•• Single point mutation that changes CAG –– Transfusions

sequence that code for glutamate at β6 position Exchange transfusion –
to CTG sequence that codes for valine at β6
position. ○○ Indication: acute chest syndrome
&acute stroke
•• Clinical features -
○○ Goal: to keep HbS <30%
–– Anemia (P/S → Drepanocytes, normal MCV)
Simple transfusion –
–– Vaso-occlusion – pain, Dactylitis
○○ Indication: splenic sequestration
•• More common in children, a/k/a hand foot
syndrome ○○ Goal: Hb = 9-10gm%
–– Sequestration crisis - –– Drugs like crizanlizumab - anti P selectin
monoclonal antibody
Acute chest syndrome - pneumonia -
like presentation, present with B/L Voxelotor – inhibit HbS polymerizationQ
crepitations, infilterates in CXR, SOB, → •• Reticulocytic Index <2 %
TOC - exchange transfusion + antibiotics
•• Aplastic anemia
Splenic sequestration – present with
sudden anemia & massive splenomegaly, –– P/S - Pancytopenia
seen in 2-3yrs of age. Older children have –– BM aspiration – hypocellularity (↑↑fat)
autosplenectomy d/t repeated splenic
infarcts by 4-5yrs of age → ↑risk of –– Classified into –
infections Inherited form – Fanconi anemia
Organism associated with osteomyelitis in ○○ Young patients, manifest as BM ↓,
sickle cell disease patients is Salmonella. present as aplastic anemia
–– Others –
○○ Numerous skeletal malformations
Stroke – incidentally diagnosed
○○ ↑risk of cancer
Priapism – teens/young
○○ Screening Ix - DEB (Diepoxybutane) /
Pulmonary hypertension MMC (Mitomycin C test) tests
Chronic leg ulcers ○○ Confirmatory test – genetic testing
Renal papillary necrosis – hematuria, Acquired form - 1° & 2°
↓urine osmolarity
○○ 1° – young adults , present with
•• IOC - Hb electrophoresisQ
aplastic anemia, TOC - Allogenic
–– HbSS – 75-95% HbS, <2% HbF, 0% HbA SCT (best match – matched sibling
–– HbAS (sickle cell trait) - donor): 1st line therapy – triple therapy
→ immunosuppressive drugs like
Asymptomatic normally
Horse ATG + calcineurin inhibitors
In pregnancy/major surgery/ high altitude like Tacrolimus/ Cyclosporine +
→ renal papillary necrosis Eltrombopag
○○ Mc symptom - hematuria ○○ 2° – MC is drugs – chemotherapy (dose
40% HbS, 60% HbA, no sickle cell in smear dependent) /antibiotics/antithyroid
drugs /colchicine idio-syncratic
* For Making Notes

159
Medicine
III. Macrocytic Anemia

Megaloblastic anemia
Bald tongue d/t atrophy of papilla, seen in IDA, B12

def. anemia (beefy red tongue)
B12 deficiency
•• Neurological changes – Axonal peripheral
neuropathy, SACD, psychiatric changes &
dementia
•• Neurological changes precede anemia
•• Occurs in vegans
•• Patients can have ↑MMA (methyl malonyl acid),
↑HomocysteineQ
•• Knuckle hyperpigmentation
Koilonychia - IDA
Folate deficiency
•• No neurological manifestations
•• Occurs in animal meat eaters mainly (green
leafy vegetable deficiency)Q
Myelodysplastic syndrome (MDS)

•• ↑risk of AML – Old age + pancytopenias (MC-
macrocytic anemia)
•• P/S - dysplastic cells +/- blasts.
•• BM aspiration – cellular marrow + dysplastic
cells +/- blasts Knuckle hyperpigme ntation - B12 deficiency
•• Tx – allogenic stem cell transplantation (if fit +
high risk patient)
–– Hypomethylating agents (unfit /low risk
patient) inhibit DNA methyl transferase
(DNMT)
–– Eg - Azacitidine & Decitabine
–– Lenalidomide – TOC for isolated 5q deletion : Bite cells Blister cells
females with thrombocytosis
* For Making Notes
160
G6PD deficiency
• Basophilic stippling retained Sickle cell disease- drepanocytes in P/SQ

RNA fragments in RBCs seen in
• Cabot rings d/t retention of ineffective INTEGRATED APPROACH TO
arginine rich mitotic spindle erythropoiesisQ THROMBOCYTOPENIA
–– Coarse basophilic stippling - lead poisoning &
Sideroblastic anemia
–– Fine basophilic stippling – megaloblastic
anemia (B12 def./FA def.)
Thrombocytopenia – Clumped pseudo thrombocytopenia
Ringed sideroblasts seen in sideroblastic anemia, MDS

of refractory anemia with ringed sideroblasts
Golf ball inclusion seen in HbH disease (3α gene deletion)
* For Making Notes

161
Medicine
1. 2° ITP •• Causes
•• Causes – –– Gold salts/ Procainamide / Sulfonamides/
Vancomycin /Heparin
–– Autoimmune conditions ,Eg- SLE /APS
–– Heparin induced thrombocytopenia (HIT)-
–– Infections – HIV/ HCV
2 types - Type 1 & Type 2 HIT
2. DITP
* For Making Notes

162
Type 1 HIT Type 2 HIT

•• Non immune mediated •• Most important , associated with thrombosis , a/k/a HITTS
•• Timing – occurs in 1st 2-3 days itself •• Immune mediatedQ
•• Symptoms – thrombocytopenia (platelet count >1 lakh •• Timing of thrombocytopenia - D5-D10 (if patient is not exposed to
with ↓ <50%) Heparin in last 3 months), if patient is exposed to Heparin in last 3
months, then reaction can occur in 1st 24hrs itselfQ
•• Risk - UFH > LMWH
•• Symptoms – moderate thrombocytopenia (platelet count < 1 lakh with ↓
by >50%) & venous thromboembolic manifestations.
•• Diagnosis –
–– IOC - HIT Ab (antibody directed against platelet factor 4-Heparin complex)
4T Scoring system-
–– 0-3 score - low probability
HIT Ab testing done only in
–– 4-5 score - intermediate probability
intermediate & high risk
–– 6-8 score - high clinical probability
4T scoring parameters-
–– Degree/severity of thrombocytopenia
–– Timing of events
–– Thrombosis
–– Other causes
Titres of HIT Ab –
–– If ≥ 1.5 optical density – HIT
–– If 0.6- 1.4 optical density – confirm HIT on basis of SRA & HIPA
–– If <0.6 optical density – r/o HIT
•• Treatment-
–– Stop all form of Heparin lifelong /Warfarin
–– Start alternative anticoagulant, continue for 1-2 months, if any evidence for thrombosis then continue or
3-6months.
–– Alternative anticoagulant of choice – Argatroban /Fondaparinux / Danaparaoid /DOAC
–– Warfarin can be started once platelet count >1.5.
3. 1° ITP –– Late Tx (>3 months)- Rituximab (anti

CD 20Mab) , splenectomy (done only in
•• Diagnosis of exclusion refractory cases)
•• No splenomegaly –– Newer drugs -
•• Clinical features - young /middle aged females Thrombopoietin receptor agonist, Eg-
•• P/S - isolated thrombocytopenia +/- giant Eltrombopag, Avatrombopag
platelets +/- Immature platelet fraction >6-7% TPO mimetic- Romoplostim
•• BM aspiration – normal megakaryopoiesis Fostamanitib (SYK inhibitor – spleen
•• Treatment - early tx & late tx tyrosine kinase inhibitor)
–– Early Tx (<3months) – cortisocosteroids + Rilzabrutinib (BTK inhibitor – bruton
IVIG +/- Platelet concentrate & Tranexamic tyrosine kinase inhibitor)
acid if patient bleeding
* For Making Notes

163
Medicine
Thrombotic microangiopathy (TMA) •• 1° TMA – HUS/TTP

•• 2° TMA-
–– Drug (calcineurin inhibitor like cyclosporine,
tacrolimus/ antiplatelet drugs like
Ticlopidine, Clopidogrel/ Bevacizumab)
–– HELLP syndrome /SRC (scleroderma renal
crisis) / malignant HTN
HUS TTP
•• Cause - endothelial injury •• Cause - Platelet trapping (ADAMST13 defect) → large
•• Can be due to Shiga toxin (EHEC, O157:H7 or O104: VWF multimers are going to persist in circulation →
H4) or complement dysregulation VWF & platelets occlude in microvasculature
Shiga toxin - •• Can be congenital (1/3rd cases, a/k/a Upshaw schulman
–– Children <5yrs, bloody diarrhea disease) or acquired (mc, 2/3rd of cases are d/t
–– a/k/a classical HUS D+ or typical HUS antibodies)
–– Triad - MAHA + ↓platelet (less severe) + AKI (more •• TTP is common in 3rd trimester pregnancy.
severe) •• Triad – MAHA + ↓Platelets (more severe) +
–– Treatment – conservative treatment Neurological (seizure/altered mental status)
No antibiotics. Platelets transfusions are C/I. •• +/- fever +/- AKI (less severe ) → Pentad
•• Complement dysregulation – here defect is in •• IOC – ADAMST13 testingQ

alternate complement pathway •• TOC- Plasma exchange
–– Eg - Loss of function mutation of CFH /CFI /CD-46 •• Newer drug – Caplacizumab (anti VWF Mab)
→ loss of inhibition of alternate complement pathway
→ endothelial injury
Or
Gain of function → mutation of C3/CFB → overactivation
of endothelial complement pathway → endothelial injury
–– a/k/a HUS D -ve /atypical HUS
–– Not associated with bloody diarrhea
–– TOC- Eculizumab +/- Plasma exchange
* For Making Notes

164
OTHER BLEEDING DISORDERS

vWD Other hereditary bleeding disorders
•• Mc inherited bleeding disorder, >85% Q
•• Bernard Soulier syndrome –
•• Function of VWF- –– AR , defective GpIb-IXQ
–– Carry factor 8 & stabilize it so that t1/2 of –– ↓Platelet adhesion
factor 8 ↑ –– P/S - thrombocytopenia & giant platelets
–– It acts as platelet glue, binds to platelet –– Ix - flow cytometry / ↓ RIPA
GpIb – IX receptor on one side & •• Glanzmann thrombasthenia -
subendothelial collagen on other side,
–– AR, defect in GpIIb/IIIaQ
increasing platelet adhesion.
•• 3 types of VWD - –– ↓platelet aggregation
–– Type 1 - AD, MC, >85% cases → partial –– P/S - normal platelet count /no giant platelets
quantitative defect
–– Ix - normal RIPA/ defective aggregation to all other
–– Type 2 - qualitative defect.
agonist ADP, Collagen , Epinephrine.
2A (AD), 2B(AD), 2M (AD), 2N (AR)
•• Gray platelet syndrome –
–– Type 3- AR, complete quantitative defect
–– Defect in NBEAL2 gene defect
•• Type 2 & Type 3 can present like Hemophilias
•• Clinical features- –– Absent α granules
–– Bleeding – Dental/ ENT –– P/S - giant platelets & thrombocytopenia
•• Ix-
–– Myelofibrosis, splenomegaly
–– CBC- normal platelet in all types except 2B.
–– In E/M, absent α granules
–– PT/INR – normal
•• Hermansky pudlak syndrome
–– aPTT- mild ↑( mild ↓ in Factor VIII)
–– Multiple genes implicated
–– ↓ RIPA or ↓R:Co assay except Type 2B
(RIPA ↑) –– P/S - normal, normal platelet count & no giant platelets
–– Type 2N – everything normal except factor –– C/F - pulmonary fibrosis , oculo-cutaneous albinism
VIII levels (↓↓) –– On Electron microscopy - absent δ granules
•• Tx- –– Platelet aggregation – absent 2° wave with ADP (1° wave is
–– Type 1 VWD - DDAVP - ↑release of VWF intact)
from endothelial cells •• Chediak-Higashi syndrome
–– Defect in LYST geneQ
–– Triad – defective neutrophils function with neutropenia {P/S
- giant azurophillic granules} + oculo-cutaneous albinism +
peripheral neuropathy + defective granular release
–– P/S - normal platelet count, no giant platelets
COAGULATION DISORDERS d/t intron 22 inversion

•• Mc inherited coagulation disorder is Hemophilia –– Hemophilia B - Factor IX deficiency / ~20%
cases
•• Types of hemophilias-
–– Hemophilia C - Factor XI deficiency
–– Hemophilia A
Factor VIII deficiencyQ
mc / ~80% cases
* For Making Notes
165
Medicine
–– In Minor bleeds like Hemarthroses /minor

surgery, maintain factor levels at 40-50%
Factor VIII dose - 25units/kg
Factor IX dose – 50units/kg
–– Newer drugs – Emicizumab (Bispecific
antibody) approved for Hemophilia AQ
Hemarthroses, mc joint involved is knee joint
Clotting factor inhibitor : Antibody against

factor VIII – TOC is recombinant Factor
VII A >FEIBA (activated Prothrombin
Hemophilic arthopathy – destruction of knee jointQ complex)
Clinical features Factor XI deficiency- AR

•• Patient can have limb spanning ecchymosis •• ↑↑↑aPTT (correct with mixing )
•• Delayed bleeding is characteristic of like •• Clinical features- present as slow oozing from
Hemophilias. mucous membrane after ENT/GU procedures
•• Intramuscular hematomas •• Tx – FFP
Ix Factor XII deficiency

•• ↑↑aPTTt (correct with mixing)
•• CBC- normal platelet count
•• No bleeding
•• PT/INR- normal
•• aPTT- ↑↑↑ : corrects with mixing Factor XIII deficiency
↓ Factor VIII/ IX levels •• aPTT normal
•• Delayed bleeding (clot stability poor here)
•• Tx: recombinant factor concentrate VIII/IX.
•• Eg - delayed umbilical cord stump bleeding
•• Dose - •• Gold standard Ix - Factor XIII assay
–– In acute bleeds (major ICH /major surgery), •• Ix - clot lysis test
maintain factor levels at 80-100 %
–– Mix clot with 5m urea → if clot dissolves
Factor VIII dose- 50 units /kg within next 24hrs
Factor IX- 100 units/kg –– MCA test
* For Making Notes

166
Overview Of Acute Leukemias

AML ALL
•• Elderly, 60-70yrs •• Children
•• Leukostasis (d/t very high WBC count ,these WBCs can •• Can present as lymphoma also
plug the capillaries of vital organs) •• Present with lymphadenopathy → mc lymph node
–– CNS- altered mental status, seizure involved is mediastinal → can cause SVC syndrome &
hepatosplenomegaly
–– Pulmonary – SOB /Pulmonary infiltration /B/L
•• Bony/lumbar pain
crepitations
•• Tumor lysis syndrome
–– Visual – blurring of vision d/t plugging of retinal
•• CNS & testicles symptoms might arise once blasts
arteriole
are cleared in periphery.
–– TOC of leukostasis – induction Chemotherapy
•• All patients have to undergo LP & intrathecal
↓ If delayed chemotherapy is must.
•• Flow cytometry – Pre B-ALL & Pre T-ALL
Tx - hydroxyurea /leukapheresis
–– Precursor identification → CD34 /TdT+
•• DIC → APL (AML-M3)Q
•• Chloroma → granulocytic sarcomas –– B-Cell → CD19+
–– Can occur in skin (leukemia cutis)/ brain/bones/ oral –– T-Cell → CD3+

cavity (gingival infiltration /gingival hyperplasia) Most of the T-cell tumors will have NOTCH
–– Risk factors - mutation
•• Child:
Young
–– t(12;21) & ETV6/RUNX1Q
t(8;21)
–– Favorable prognosis
M4/M5 (monocytoid variants)
–– Hyperdiploidy (blasts have >50 chromosome)
•• Diagnosis –
•• Infant:
–– Blasts ≥ 20% (peripheral blood /BM)
–– T(4;11) – AFF1-MLL gene
–– Exception –
–– Unfavorable prognosis
Core binding leukemias-
–– Hypodiploidy
→ t(8;21) AML-M2 → RUNX1-RUNX1T1 gene
Poor prognostic markers-
→ t(16;16) inv 16-AML-M4E0 → CBFB-MYH11 gene
•• Philadelphia + ,t(9;22) BCR-ABL
APL - t(15;17) →PML-Rara fusionQ
•• t(4;11) –AFF1-MLL gene
Excellent prognosis
Poor prognostic markers- •• t(1;19)- TCF3-PBX1 gene
•• Philadelphia +ve – t(9;22) → BCR-ABL •• Hypodiploidy (<44 chromosome in blasts)
•• t(6;9) → DEK-NUP214 gene •• Complex karyotypic abnormality
•• t(3;3) inv 3 →GATA-MECOM •• ETP (early T-cell phenotype)/ MRD (minimal residual
disease after chemotherapy)
•• MDS like – loss of chr 5/7/17 OR deletion of parts of
chr like 5q /7q deletion •• Boys , infants ( <1yr)
•• Complex karyotype - ≥ 3 changes •• Adults
•• Molecular changes - FLT3 mutation + NPM-1 wild type •• B-Cell ALL in adults & T-Cell ALL in adults
mutation → poor prognosis
* For Making Notes

167
Medicine
Independent prognostic markers- •• Tx: - V D P A regimen

•• Age >60/70 yrs – V- Vincristine
•• If ECOG ≥ 3
– D- Daunorubicin
•• Treatment related acute AML –
– P- Prednisolone
–– H/o of prior exposure to alkylating agents /radiation therapy /
– A- Peglycated Asparaginase
DNA topoisomerase II inhibitors.
+ intrathecal chemotherapy Ara-C &
–– 5q/7q deletion (MDS like changes) is seen after 5-7yrs of
Methotrexate
exposure to alkylating agents/ radiation therapy And >2-3 yrs
–– Newer drugs –
after exposure to DNA topoisomerase II inhibitors.
Blinatumomab (CD19 bispecific T-Cell
–– MLL (new name – KMT2A) – t(9;11), located on 11q23
engager)
•• Flow cytometry
Inotuzumab ozogamicin (anti CD22
–– Myelod- CD13/33 (CD117/MPO )
IHC- MPO+ve, Mab)
–– Precursor- CD34
–– Monocytoid- CD11b (CD14/15/ 64) SBB+ve ,
–– Erythroid – CD71 / CD 235A NSE+ve
–– Megakaryoid – CD41/CD61 (monocytoid FAB

M4/M5)
PAS+ve
(Granular +erythroid/megakaryoid M6/M7)
–– Auer rods - AML faggot cellsQ

•• Tx: APL (acute promyelocytic leukemia) - ATRA + Arsenic trioxide
–– 25% of cases who are treated with ATRA develop differentiation
syndrome
–– Differentiation Syndrome –
C/F - SOB/ Hypoxemia/pulmonary infiltrate and crepitations
+ altered mental status + hypotension + AKI
TOC - Dexamethasone
•• Tx: Non –APL –
–– If fit (ECOG status < 3/ younger patient) for chemo : 7+3 +/-
Midostaurin
D1-D7 → Cytosine Arabinoside
D1-D3 → Daunorubicin
D8-D21 → Midostaurin, best for FLT3 mutations
–– If unfit for chemo: Hypomethylating agents (Azacitidine/
Decitabine) + venetoclax (Bcl2 inhibitor or BH3 mimetic)
–– Hypomethylating agents are not used in IDH mutations.
IDH1 Mutation – Ivosidenib
IDH 2 Mutation – Enasidenib
Sonic hedgehog inhibitor – Glasdegib
–– Newer drug – Gemtuzumab ozogamicin: MOA - Gemtuzumab is
anti CD33 Mab & delivers toxic drug ozogamicin after binding.
* For Making Notes

168
Down syndrome & ALL –– BM aspiration – BM fibrosis
•• Mc leukemia in down syndrome – ALL (risk is 10 •• Any cancer associated with down syndrome-
- 20% times more in down syndrome) high treatment related mortality
•• Occurs in <10yrs HODGKIN LYMPHOMA

•• B-cell type of ALL •• Young patients
•• CRLF-2 Overexpression /JAK2 mutations •• Present with painless lymphadenopathy,
supradiaphragmatic lymph nodes, MC – cervical
Down syndrome & AML lymphadenopathy, contiguous spread, extranodal
disease at time of presentation rare
•• Acute megakaryotic Leukemia (AML M7) –most
•• Alcohol intake ↑ pain in lymph nodes
specific in down syndromeQ
•• B-symptoms - pel ebstein fever /night sweats,
•• Neonatal – significant weight loss, 10-15% patients may
–– GATA 1 mutation have pruritis
•• NHL - infradiaphragmatic lymph nodes
–– Transient myeloproliferative disorder involvement, extranodal disease common, non
–– Asymptomatic + circulating blasts contiguous spread
(megakaryotic lineage) •• Spleen is considered as nodal disease in HL &
as extranodal in NHL
20%
–– Extranodal sites include Thymus, LN,
Develop Acute megakaryocytic leukemia (AMKL) in
Waldeyer’s ring
<4yrs age
cHL NLPHL
•• 95% cases •• 5% cases
•• Variable prognosis •• Excellent prognosis
•• EBV association ~ 50% •• Rare
•• Histological subtypes •• Variant RS cell /popcorn cells/ Lympho-histiocytic RS
–– Nodular sclerosis type - mc ,females, in Bx- Collagen Cells
bands seen , lacunar RS Cell seen •• CD15/30 -, CD20+
–– Mixed cellularity – EBV association 50-70% , •• Tx: R-CHOP + ISRT +/- Active surveillance
males>female, classic RS cell seen –– Alternative regimen – ABVD
–– Lymphocyte rich type - better prognosis among all –– R - Rituximab (s/e-reactivation of hep B virus)
cHL, EBV association 30-50%, mononuclear RS cell –– C - Cyclophosphamide (s/e – gonadal toxicity/ BM
seen suppression)
–– Lymphocyte poor type – worst prognosis, associated –– H - Hydroxydaunorubicin (s/e- cardiotoxicity)
with HIV, mummified type RS cell seen –– O - Oncovin (s/e- peripheral neuropathy)
•• RS cells – CD15/30+ CD20-
–– P - Prednisone (s/e- bone toxicity)
•• Tx: A B V D +/- Involved site Radiotherapy (ISRT )
–– A -Adriamycin/ doxorubicin(s/e- cardiotoxicity)Q
–– B -Bleomycin
–– V -Vinblastine
–– D -Dacarbazine ( s/e – gonadal toxicity/ BM
suppression / 2nd cancer- MDS & AML)
Brentuximab vedotin (anti CD30 Mab )
Pembrolizumab – immune check inhibitor
* For Making Notes

169
Medicine
•• Prognostic marker- IPS scoring

–– Age >45yrs
–– Male
–– Hb <10.5g/dl
–– S.albumin <4g/dl
–– Stage IV disease/disseminated
–– WBCs count (≥ 15,000)
–– Absolute lymphocyte count < 600/μl
–– DC lymphocyte <8%
Classic RS CellQ
Popcorn RS Cell
•• Diagnosis of any lymphoma- LN Excision Bx >> Trucut Biopsy >>FNAC

•• Staging & follow-up – FDG- PET
An Arbor Staging
* For Making Notes

170
Aggressive B-Cell NHLs

NHL Presentation Clues Possible 1st line Rx
BL •• Endemic BL present with jaw •• HPE - medium cells , starry sky •• Regime
•• Most aggressive mass in children, 100% association appearance •• R-CODOX-M /
with EBV •• Ki67 >95%Q R-IVAC
•• Sporadic BL present with •• Marker- CD10+ •• Intrathecal
Right iliac mass, variable EBV •• Cytogenetic – CMYC overexpression – chemotherapy
associationQ 100% cases d/t ↑risk of CNS
•• HIV Associated BL •• t(8;14) – mcQ dissemination
lymphadenopathyQ
•• t(2;8)
•• t(8;22)
DLBCL Can present as nodal (LAN) / •• HPE - large cells Regime- R-CHOP
•• mc B-cell NHLQ Extranodal (mc site- GIT) •• No starry sky appQ
•• mc aggressive •• Ki67 <95%
B-cell NHL •• Marker –
•• double hit/ triple –– GCB →CD10/Bcl-6
hit DLBCL (worst
–– ABC/non GCB (relatively poor
prognosis) - CMYC
prognosis)→CD10-/MUM1+
overexpression
•• Cytogenetic changes-
+/- Bcl2 +/- Bcl 6
•• Regime - –– CMYC/MLL
EPOCH-R •• No specific cytogenetic marker
MCL •• Lymphadenopathy + GIT •• CD5 +/CD23 - /CD10- Variable

involvement •• HPE- small – medium cells
•• Presents with polyposis •• Cytogenetic –
–– t(11;14) - cyclin D1
–– Cyclin D1 –ve MCL-SOX 11
overexpression
MZL 1. Nodal MZL → lymphadenopathy •• No specific immunophenotypic marker Variable, Eg- If H.pylori
2. Extranodal MZL → MALT •• Diagnosis of exclusion - eradication therapy
lymphoma (depends on site). •• Cytogenetic –
Infections associated – –– mc- trisomy 8
–– H.pylori – gastric maltoma –– t(11;18) – MALT1 gene
–– C.psittaci- orbital malt overexpression
lymphoma –– t(14;18) - MALT1 gene
–– Borrelia- cutaneous malt
lymphoma
–– C.jejuni- S.I malt lymphoma
–– Sjogren syndrome – ass. with
Parotid malt lymphomas &
gastric lymphomas
3. SMZL → splenomegaly +/- LAN,
associated with HCV → villous
lymphocytes in P/S (Hair like
projection seen in pole)
* For Making Notes

171
Medicine

FL •• Mc indolent B-cell lymphoma •• HPE – complete destruction of lymph •• Treatment is based
•• Present with painless peripheral node, follicles seen on grade.
lymphadenopathy •• CD10+ •• Not high grade- R
•• Centrocytic tumor •• Cytogenetic – t(14;18)- Bcl 2 only therapy
•• Centroblast no. tells the grade of overexpressionQ •• Semi-aggressive
the tumor. grade- R2 (Rituximab
+ Lenalidomide )
•• Aggressive tumor –
R-CHOP /EPOCH-R
HCL •• Males >50yrs •• HPE- Hairy cell (circumferential hairy Tx - 1st line : Cladribine /
•• Massive splenomegaly projection) in P/S, TRAP+ FludrabineQ
•• Otherwise aymptomatic •• BM aspiration – fried egg appearanceQ
•• B-symptoms & LAN are rare •• CD103+/ CD123+ / CD11c/ CD25 /
Annexin A1+Q
•• Molecular study - BRAFV600E
mutationQ
CLL/SLL •• Indolent neoplasm •• Incidental finding •• Variable
•• Can transform into aggressive •• Cytopenias – anemia (AIHA ) & •• Indications for
tumor, into DLBCL → Richter’s thrombocytopenia (ITP) treatment –
Transformation @ rate of 5%/year •• Recurrent infections - ↓gamma –– Symptomatic
•• Lots of B-symptoms & cytopenias globulins RAI 3/4 &
•• Difference between CLL & SLL •• Monoclonal gammopathy (5%) Binet c
depends on absolute lymphocyte •• P/S- smudge cells + BMA /LN Bx- small LDT
count(ALC) round blue cells (lymphocyte
–– CLL - if ALC >5000 +/- LAN / •• Immunophenotypic marker - CD5+/ doubling time )
Hepatosplenomegaly (HSM) CD23+ /CD 200+ CD10- Q < 6 months
–– SLL - if ALC < 5000 + LAN +/- •• Cytogenetic marker- Or
HSM –– FAVORABLE MARKERS ALC ↑↑ > 50 % in <2
•• MBL - monoclonal B-cell 13q deletion – mcQ months
lymphocytes, ALC <5000, no LAN, Rb gene deletion Refractory
no HSM
Others- Zap70 - /CD38 /IgVH AIHA /
•• RAI Staging used for CLL (mutated) refractory ITP
patients
–– Unfavorable Markers Massive
–– 0- ↑lymphocytosis splenomegaly
17p deletion
–– 1- LAN Bulky LN
11q deletion (ATM )
–– 2- HSM B-symptoms
IgVH (unmutated)
–– 3- Anemia (present d/t AIHA) TOC–
Zap 70 +
–– 4- Thrombocytopenia –– 1st line BTK
CD38+
•• Binet staging used for SLL inhibitors –
–– Neutral Prognosis – Trisomy 12
patients Ibrutinib
–– Binet A- <3 LN areas Acalabrutinib
–– Binet B- ≥ 3 LN areas –– 2nd line – Bcl 2
–– Binet C- Anemia/ inhibitor
Thrombocytopenia Venetoclax
* For Making Notes

172
Indolent T-Cell NHLs

MF •• Mc cutaneous T-cell lymphoma •• Epidermotropic Variable
(CTCL) lymphocytes
•• Skin +/- LAN •• Haloed lymphocytes
•• Patch →scaling lesion →plaque •• Pautrier’s
→erythroderma microabscessQ
SS - leukemic •• present with erythroderma & LAN •• Sezary cells in Variable
transformation of P/ SQ (malignant
mycosis fungoides leukemic cells seen
in circulation that
have characteristic
cerebriform nucleus)
ATCL •• HTLV-1 related Clover leaf like cells CHOP regimen / Mogamulizumab
•• Indolent form to aggressive form (anti-CCR4 Mab)
↓ ↓
•• Skin lesion leukemia + lytic
lesions
ALCL •• LAN + HSM •• ALK +/ CD30+ •• EPOCH
•• ↑risk with female & silicone breast •• Cytogenetic marker- •• Brentuximab vedotin (anti
implants t(2;5) ALK –NPM CD30 Mab)
fusion
Starry sky appearance Hairy cell leukemia - TRAP+
Hairy cell leukemia CLL – Smudge cells
* For Making Notes

173
Medicine
Sezary cell Pautrier microabscess
PLASMA CELL DYSCRASIA

Clonal BMPC M-protein MDE
MGUS- <10% + (<3g/ml) -

•• ↑risk of transformation to SMM
•• M ≥ 1.5g/dlQ
•• Abnormal SFLCR
•• Non IgG MGUS
•• No Tx. Observed
SMM >10%, <60% +/- ( ≥ 3g/ -
•• No Tx. Observed dl)
MM ≥ 10% (50%- IgG / +/- (>3g/ +

•• Tx: 1st line- Triple therapy + Daratumumab (anti CD38 Mab) 20% IgA /20% only dl ) •• Myeloma defining event-
– especially if high risk light chains)
–– SLIMQ –
•• Marker of poor prognosis/ high risk- S - 60% of clonal
1. β2 microglobulin BMPC
2. Cytogenetic markers - t(4;14), t(14;16), t(14;20), 17p deletion LI - Light chains-
(p53deletion), 1q+ kappa/lambda
3. ↑LDH ≥ 2x upper limit (involved/ uninvolved
•• Plasma cell leukemia – if absolute malignant plasma cell in P/S >100 + involved ≥
≥ 500 100mg %)
OR M - Whole body MRI
Differential count ≥ 5% (≥ 2 focal lesions) /
•• Standard triple therapy – Whole body PET
1. Dexamethasone scan
2. Immunomodulator – Lenalidomide /Pomalidomide → ↑CNS –– CRAB – Q
penetration Hypercalcemia
→ if 1 + 2 used together, ↑ risk of thromboembolic manifestations Renal dysfunction
3. Proteasome inhibitors-
Anemia
–– Bortezomib → ↑risk of peripheral neuropathy
Bone Lytic lesions
–– Carfilzomib
–– Ixazomib
•• AKI: causes –
–– ↑↑ S. Creatinine d/t hypercalcemia
–– Cast nephropathy
–– Tx- IVF + chemotherapy – cyBorD regime (Dexamethasone +
Proteasome inhibitor + cyclophosphamide)
Plasmacytoma •• None +/- (0.5g/ +
Types - * For Making
•• Notes
If detectable dl)
1. Solitary bone plasmacytoma- mc, mc site is spine, ↑ risk of clonal BMPC
transformation, ↑ mortality rate - ↑ risk of
2. Solitary extramedullary plasmacytoma – mc sites are head & neck transformation
•• Tx: local RT +/- Surgical excision to MM
174
WM (waldenstrom macroglobulinemia)
•• Lymphoplasmacytoid lymphocytes
•• C/f – old >70yrs age, familial predisposition
•• Cytopenias/ B symptoms /HSM /Cold type

AIHA /Acquired VWD/ peripheral neuropathy
Myeloma cells Lytic lesions - MM
(anti MAG Ab)Q
•• Tx – B-R regime- Bendamustine with Rituximab
•• Alternative to Rituximab – Obinutuzumab
Features WM (waldenstrom MM
macroglobulinemia)
Monoclonal IgMQ IgM rare
Ig
Lytic lesion No CommonQ
HSM/LAN Common Rare
Hyper- ++ (common ) Rare
viscosity
SIg ++ -
CD20 ++ -
CD56 - ++
MYD88 ++ -
Serum Protein Electrophoresis coupled with serum im- mutations

mune fixation t(11;14) - Common,
marker or
standard risk
Important CMPNs
Parameter CML PV ET PMF
CBC WBC ↑↑↑ ↑ Normal ↑/↓
RBC
Normal /↓ ↑↑↑ Normal ↓
Platelets
↑/↓ ↑ ↑↑ ↑/↓
Smear Left shift Normal ↑ Platelets Leukoerythoblastic
pictureQ
LAP score ↓↓ Normal /↑ Normal /↑ Normal /↑
BMAx Cellularity ↑↑ /myeloid ↑↑/trilineage ↑↑/ megakaryoid ↑/↓
hyperplasia
Fibrosis +/- +/- Notes
* For Making +/- ++++
Megakaryocytes Hypolobated Pleomorphic Staghorn Bulbous
Molecular Ph+, t(9;22), BCR-ABLQ JAK-2 mutationQ JAK-2 mutation > JAK-2 > CALR >
V617F > Exon 12 CALR > CMPL CMPL
175
Medicine
Parameter CML PV ET PMF

Clinical Asymptomatic / present •• Vasomotor – erythromelagia / Cytopenias
with cytopenia and Aquagenic pruriritis
B-symptoms +
•• Bleeding (↑ platelet > 15)/thrombosis
(↑WBC)
Splenomegaly Moderate - massive Mild Mild Moderate - massive
Management •• 1st line- TKI Aspirin + phlebotomy Supportive therapy
Imatinib (s/e-edema)
In high risk
NR patients- Ruxolitinib
Target – male : <45% / Newer TKI like
T3151 mutation
–– Female <42% Pacritinib Fedratinib
+
–– Pregnant female <37% Momelotinib
Indication for cytoreductive therapy
Ponatinib
(↑thromboembolic (for ↑ risk)-
manifestations) 1. Age >6oyrs
Other 2nd/3rd gen. TKI 2. H/o thrombosis

Nilotinib/dasatinib(s/e - pleural3. PLT count >15lakhs
effusion) 2nd gen Bosutinib - 3rd For PV-
gen
•• 1 line – HydroxyureaQ
st
•• Triad for dx- ↑

WBCs with left shift
+ BMAx- myeloid
hyperplasia with ↑M:E Not tolerated/ C/I Ruxolitinib (JAK1/2
ratio + Ph+ (FISH & inhibitor)
Karyotyping)Q •• In pregnant women - IFN
•• Follow- up- PCR → For ET-
BCR-ABL mRNA •• 1st line- Hydroxyurea
transcript
•• Alternative- Anagrelide
•• 3 STAGES-
1. Chronic phase - mc
presentation phase,
<10% blasts →
↑platelet / ↑basophilQ
2. Accelerated Phase
- 10-19% → ↓
platelets/↑↑basophils/
≥ 20%
3. Blast phaseQ - ≥ 20%
blasts
2/3rd →myeloid blasts
1/3rd →lymphoid blasts
* For Making Notes

176
CML – leukocytosis + Left shift
Erythromelalagia
FISH – Ph+, BCR-ABL fusion
Tumor marker Cancer Non neoplastic conditions

Hormones
Human chorionic gonadotropin Gestational trophoblastic disease / Pregnancy
gonadal germ cell tumors
Calcitonin Medullary thyroid cancerQ
Catecholamines Pheochromocytoma
Oncofetal antigens
AFP HCC/ Gonadal germ cell tumorsQ Hepatitis / Cirrhosis
CEA Adenocarcinoma colon (Pancreas/ Pancreatitis / Hepatitis /IBD /
Breast) Smoking
Enzymes
Prostatic acid phosphatase Prostate cancer Prostatitis /BNP
Neuron –specific enolase Neuroblastoma /SCLCQ
Lactate dehydrogenase Lymphoma /Ewing sarcoma Hemolysis /MI/ Rhabdomyolysis/
Hepatitis
Tumor associated proteins
Prostate specific antigen Prostate cancers Prostatitis /BNP
Monoclonal immunoglobin MM/ WM MGUS/ infections -HCV
CA-125 Ovary Pregnancy /Menstruation /Peritonitis
CA-19-9 Pancreas/ colon /Breast Pancreatitis /UC
CD30 HL / ALCL
CD25 ATCL /HCL HLH
* For Making Notes

177
Medicine
Syndrome Mechanism Features Cancers

SIADH ↑ADH → ↑H2O reabsorption Euvolemic hyponatriemiaQ SCLC/GI/GU
→ ↓Na ↓S.Na /↑U.Na /
↓S.Osm /↑U.Osm
Cushings ↑ACTH → ↑S.Cortisol Hyperpigmentation/ SCLC /Carcinoid
cushingoid /metabolic
hypokalemia
Hypercalcemia •• PTHrP –mc, >80%Q Polyuria /dehydration +/- ↓ •• SCC (Sq CC)/ RCC
•• Lytic metastasis BP /AKI •• Lytic metastasis – MM/any
•• ↑1, 25 DHCC solid organ tumor
•• Lymphomas
Osteomalacia ↑ FGF23 → ↑PO4 wasting
2-
Bone pain, fractures, Fibromas/ Sarcomas/
hypophosphatemia Hemangiopericytoma
Carcinoid syndrome ↑ serotonin Flushing /diarrhea/ pellagra Carcinoid /MTC (rarely)
/↑ urinary 5HIAA, ↑
S.Chromogranin A.
NICTH ↑IGF2 → hypoglycemia Whipple triad (↓insulin ) HCC/ Mesenchymal tumors
Male feminization ↑β-HCG →↑Aromatase Gynecomastia / Precocious Testicular cancer/ NSCLC
activity in leydig cells → puberty (Large cell cancer)
↑estrogen
Hypothyroidism T3 deiodinase , T4/T3 → ↓T4/T3 ,↑TSH , ↑r T3 Hemangiomas
rT3
Limbic encephalitis Anti HU Ab/ Anti CRMP5 •• Subacute presentation , •• SCLC (anti HU Ab ,
Ab / Anti Ma2 Ab/ Anti psychiatric / behavioural anti CRMP5 Ab, anti
GAD Ab/ Anti amphiphysin changes, with refractory amphiphysin Ab, anti
Ab/ Anti NMDA Ab/ Anti seizures with memory AMPA)
AMPA Ab loss •• Testicular cancer –anti MA
•• MRI- hyperintensities in 2 Ab
B/L medial temporal lobe •• Overian teratoma (anti
•• EEG- Extreme δ brush NMDA Ab)
Cerebellar degeneration Anti Yo Ab /Anti Hu Ab / •• Anti Yo Ab - Breast/Ovary
Anti Ri Ab/ Anti Tr (DNER) cancer
Ab / Anti MGLUR Ab/ Anti •• Anti Hu Ab, Anti Ri Ab-
VGCC Ab SCLC, Anti Tr Ab, Anti
MGLUR Ab-HL, Anti VGCC
Ab-SCLC
Other CNS syndromes Anti amphiphysin Ab /Anti •• Anti amphiphysin Ab /Anti
GAD Ab , Anti AchR Ab Anti GAD Ab – SPS
VGCC Ab •• Anti AchR Ab – Myasthenia
gravis
•• Anti VGCC Ab - LEMS
Polycythemia ↑↑EPO Asymptomatic +/- RCC/HCC /Cerebellar
hyperviscosity features +/- hemangioblastomaQ
thrombosis
* For Making Notes
178
IMPORTANT ONCOLOGIC EMERGENCIES

1. Tumor lysis syndrome
•• d/t hematological cancer → eg – BL/DLBCL
•• Aute leukemia (ALL > AML) → ↑↑ WBCs
•• If LDH ≥ 2x upper limit → high risk
•• C/F-
–– hyperuricemia → MSU crystals → AKI
–– hyperkalemia → Arrythmias
–– hyperphosphatemia
CaPO4 → AKI
–– hypocalcemia
Tetany → seizure
•• Tx – IVF + Rasburicase (C/ in G6PD deficiency) +/- Renal replacement therapy
•• Prevention – IVF + Allopurinol/Rasburicase
•• Urinary alkalinisation to be avoided
2. Epidural spinal cord compression

•• Cancer + back pain → neurological examination → if deficit – Urgent whole spine MRI
•• Tx- dexamethasone
If normal
X-ray spine
Red flag – back pain with coughing

No
Supportive care with analgesic
3. SVC Syndrome
•• d/t compression of SVC by cancer
•• mcc – NSCLCL
•• C/F- edema of face/neck/arms + dilation of chest veins + JVD with pulsations – HJR +/- ↓BP/SOB,
↓spO2 + Headche /altered mental status IOC- CECT chest
* For Making Notes

179
Medicine
Mx- if severe symptoms

Yes
catheter venography 4. Febrile neutropenia – fever + ANC
<500Q
SVC obstruction •• Mcc – gram positive cocci >70% cases
•• TOC – Piptazo
No Balloon angioplasty /stenting of –– Meropenem any 1 +/- cover risk factor
superior VC
–– Cefepime
→ MRSA Cover - ↓BP / ARDS +/- MRSA →
Vancomycin
lx- CECT Tx of cancer
→ Antifungal cover - no resolution of fever
→ Voriconazole/ L-AMB/ Echinocandins
* For Making Notes

182
GASTROINTESTINAL
APPROACH TO DYSPHAGIA
•• Dysphagia - Difficulty in swallowing
•• Odynophagia – painful swallowing
* For Making Notes

183
Medicine
Structural Esophageal Dysphagia –– Barium swallow @ the time of symptoms –

corkscrew appearance
A. Intermittent symptoms
–– Gold std- HRM Manometry, Distal latency
a. Webs – thin tissue (DL) < 4.5 sec
Q
– Causes partial obstruction b. Hypercontractile esophagus (Jackhammer

– Eg- Plummer vinson syndrome → Triad – IDA esophagus)
+ dysphagia + post cricoid esophageal webs –– Dx- Distal contractile integral (DCI) >8000 in
HRM Manometry
Q
b. Ring s – concentric
–– Causes partial obstruction c. Hypertensive esophagus (nutcracker esophagus)
–– Eg- ‘B’ ring (Schatzki ring) → mucosal rings at –– DCI - 5000 -8000, (Its not a disorder now)
squamo-columnar junction.
d. Tx- CCB (Nifedipine), Antispasm, Nitrates
–– Causes intermittent dysphagia ,patient c/o
food impaction B. Progressive symptoms
–– Schatzki rule - if esophageal diameter < a. With GERD
13mm → symptomatic –– DM/Amyloid /Systemic sclerosis (CREST
If >25 mm → asymptomatic Syndrome)
–– Association – chronic GERD /hiatus hernia –– Manometry - ↓peristalsis
–– Tx- Endoscopy dilatation +/- PPI - ↓LES Tone
c. Eosinophillic esophagitis b. Without GERD
–– MCC of dysphagia in world in young adults –– Achalasia cardia - esophageal outflow
–– h/o atopy /bronchial asthma obstruction
–– Dx → Bx shows >15 eosinophils / HPF Idiopathic
–– EGD - Feline esophagus

Q
○○ ↓peristalsis
–– Tx - PPI +/- Corticosteroids (inhaled CS → ○○ ↑LES tone

swallowed) +/- endoscopic dilatation IRP >15mm Hg
B. Progressive symptoms C/F – dysphagia , weight loss +/- aspiration
a. Peptic stricture Ix- Barium swallow findings- bird beak
b. Malignancy appearance
TOC – Endoscopic dilatation → Heller’s
Neuromuscular Esophageal dysphagia myotomy
A. Intermittent symptoms –– Pseudo- achalasia cardia - more common
a. DES EG Junction cancer
–– Premature uncoordinated esophageal IRP >15mmHg
Q
contraction
* For Making Notes

184
Schatzki ring
CMV Esophagitis – immunosuppressed patients
TOC- Ganciclovir
Feline esophagus
Zenker’s diverticulum
Candida esophagitis – curdy white plaques, CorticosteroidsQ /

HIV/ chemotherapy /post-transplant TOC - Fluconazole
Q
DES - cork screw appearance
HSV Esophagitis – vesicles

Q
TOC- Acyclovir
* For Making Notes

185
Medicine
APPROACH TO GERD
Barrett’s esophagus – endoscopic ∆

Achalasia cardia – bird beak appearance
Clinical feature
•• heart burn +/- chest pain +/- refractory
nocturnal coughing
* For Making Notes

186
PUD •• ↑S.Chromogranin A – nonspecific: basal acid

output >15 mEq/hr
•• Causes
–– NSAIDs (↓ PGE2) / H.pylori (Urease) •• H.pylori →
–– Drugs - Corticosteroids /bisphosphonates –– Cag A- MALT lymphomas /gastric carcinoma
–– Viruses - CMV/HSV –– Vac A- PUD (DU >GU
–– ICU – Stress ulcer → risk factors for stress •• Test & treat–
ulcers-
– After 4 weeks of completion of therapy –
•• Mechanical ventilation
>48hrs EGD + RUT – invasive
•• Coagulopathy / severe UBT (↑radiation risk)
thrombocytopenia
Prophylaxis PPI Stool Ag test
•• h/o GI bleeding prior to –– Serology can never be used as test of cure
admission to ICU
–– False testing with these tests- PPI use /
•• High dose corticosteroids
Bismuth use/ Antibiotics
–– Burns → curling ulcer / head injury → –– Tx - quadruple regimes- PPI + (MNZ + AMOX
Cushing’s ulcer + Clarithro)
–– Cancers–
–– Alternative – PPI + (MNZ + TCN + Bismuth)
Gastric cancers
•• Tx - high dose PPI + Surgery (if resectable) +
Lymphoma
octreotide
Gastrinoma (ZES)
Q
•• Triangle of Passaro-
○○ MC – sporadic > familial (MEN 1
syndrome)
○○ clues – multiple ulcers @ unusual
locations
* For Making Notes

187
Medicine
Approach To Chronic Diarrhea & Malasborption

Watery
Fatty Inflammatory
Secretory Osmotic Functional
•• Rapid transit/ ↓surface
Multifactorial (gut Malabsorption & Inflammation
Mechanism area Osmotic substance
hypersensitivity) maldigestion →damage
•• Secretagogues
•• Endocrine-
•• Malabsorption-
hyperthyroidism/
structural
carcinoid/MTC/VIPOma/
disease (MC-
ZES Q
•• Laxative abuse sprue) •• Infections
•• Bile acid malabsorption IBS-D
Etiology •• Lactose •• Maldigestion- •• IBD
/villous adenoma/
intolerance pancreatic •• RT/CRC
laxatives (senna/cascara)
insufficiency
/microscopic colitis
& biliary
(c/o diarrhea but gross
insufficiency
appearance is normal)
Osmotic gap <50 >125 50-100 Not required Not required
P/O relation - + variable + -
Nocturnal
+ - - Variable Yes
symptoms
•• 72hr fecal fat >
•• Stool ph <6 Q
7g/dl
Exclude infections → •• H2 breath •• Fecal Q •• fecal calprotectin
•• fecal elastase Q
Testing colonoscopy /biopsy +/- test > 2 ppm calprotectin + colonoscopy
endocrine testing •• colonoscopy
(dx of lactose •• Normal /-ve + Bx
Q +/- EGD +/-
intolerance)
serology
•• Treat underlying cause-
–– Microscopic colitis
- corticosteroids: •• 1st line –
Budesonide antidiarrheals •• Antibiotics
Simple dietary
Tx –– Bile acid – Loperamide Gluten free diet •• Immunosuppresion
review
malabsorption- +/- B.A.S → IBD
cholestyramine +/-Rifaximin
IOC- 75 Se
HCAT scan
Microscopic colitis – Bx lymphocytic colitis: –– Occurs d/t gluten hypersensitivity

> 20 lymphocyte / 100 –– Presents with chronic diarrhea
epithelial cells
Q
–– Extraintestinal –
Collagenous colitis: if
subepithelial collagen band >10
Q 1. IDA / B12 Def / ↓S.calcium
2. Neuropsychiatric- ataxia /seizure
3 causes of chronic diarrhea
3. Dermatitis herpetiformis- blistering /
•• Celiac Disease- pruritis esp in external aspect of elbow,
–– HLADQ2/DQ8
Q
–– Ix- IF → IgA deposition in dermal papilla
* For Making Notes

188
–– Tx- Dapsone –– Caused by T.whipplei

Q
4. Hyposplenism - ↑ risk of infections –– Presents with chronic diarrhea

5. IgA deficiency –– Extraintestinal –
6. Osteoporosis 1. Arthralgia /arthritis – MC
–– Triad – gluten hypersensitivity + serology 2. Neurological – MC → dementia

– anti TTG IgA (most sensitive) / anti –– Oculomastigatory myorhythmia
endomysial IgA (most specific) + EGD
3. Cardiac- myocarditis/ endocarditis /VHD
- ↑intraepithelial lymphocytes /villous
atrophy/ crypt hyperplasia 4. Fever/LAN
–– Severity of disease can be classified using –– Dx - EGD → Bx – PAS + macrophages / PCR
Marsh Classification (best & preferred)
TOC – Gluten free diet . Avoid BROW –– Tx – 1st 2 weeks - IV ceftriaxone / next 2
weeks - TMP-SMX +Streptomycin
Follow-up – Ab become –ve and EGD-
normal •• Abetalipoproteinemia –
Complications – –– AR, MTTP Defect
Q
1. Ulcerative jejunoileitis –– ↓apo B proteins

2. Enteropathy associated T-cell lymphoma –– Triad – P/S – acanthocytes + Neurological -
(EATL) Developmental delay / retinitis pigmentosa /
3. Small intestinal lymphomas ataxia + chronic diarrhea – EGD + Bx – lipid
laden enterocytes
•• Whipple Disease
IBD
Features Ulcerative colitis Crohn’s disease
Risk factor •• IL-10 polymorphism •• Genetic – NOD2 (CARD 15) gene on chr 16
•• HLADR2 •• IL23 R polymorphism
•• Smoking & Appendiectomy ↓ risk •• Smoking /appendiectomy
•• HLADR1
Common site of origin Rectum, MC - rectosigmoid Ileum, MC - ileocolonic
Symptoms Bloody diarrhea +/- tenesmus Abdominal pain +/- diarrhea
Inflammation/ involvement Superficial (mucosa/submucosa) Transmural
Q
Pathology •• Cryptitis /crypt abscess +/- •• Non caseating granulomas
pseudopolyp •• Cobblestone mucosa/ string sign of Kantor
•• Leadpipe colon with featureless
haustrations
Cytokine response Th 2 Th 1/17
Distribution Continuous Discontinuous
Complications Toxic megacolon /hemorrhage Stricture (small bowel obstruction) / abscess /
fistula (DOC- anti TNF therapy) / malabsorption
* For Making Notes

189
Medicine
Extra-intestinal •• >25%
•• Muco-Cutaneous- apthous ulcer/EN/ pyoderma gangrenosum
•• Others- PSC → Cholangiocarcinoma / colonic dysplasia → colorectal cancer if > 8yrs of active
disease
•• MC - Seronegative arthritis → peripheral neuropathy > axial neuropathy /Sacroilitis
•• Gallstones /renal stones – MC oxalate stones
•• Ocular – anterior uveitis > episcleritis
•• Correlate with IBD – T1 Periarthritis /EN/ apthous ulcer /episcleritis
•• Does not correlate with IBD- T2 Peri arthritis /axial /PG/ scleritis/uveitis / PSC
Assessment Truelove & witts criteria CDAI
Tx overview •• Mild – moderate → 5-ASA •• Mild – moderate → p/o – budesonide (EC)
(Sulfasalazine /in india, MC is –– 5- ASA
Q
Mesalamine) •• Moderate-severe → p/o – Prednisolone +
•• Corticosteroid- MMX budesonide Azathioprine /6MP +/- MTX
•• Moderate-severe → p/o prednisolone / •• Severe → IV CS
Azathioprine /6-MP +/- anti TNF
•• Severe → IV Corticosteroids
Anti TNF α – Infliximab /Adalimumab /

NR Certolizumab
CNI •• Newer drugs –
–– Vedolizumab (α4β7 int)
–– Natalizumab (α4 β1 int) → ↑ risk of PML
–– Ustekinumab (anti IL-12/23)
Anti TNF α
•• Anti-TNFα approved to use-
Infliximab /Adalimumab / Golimumab
•• Newer drugs –
- Vedolizumab (α4β7 int)
- Ustekinumab (anti IL-12/23)
- Jakinibs (Tofacitinib /Upadacitinib)
- SIP ϒ + (Ozanimod)
•• Toxic Megacolon –
- Causes – Cl. Difficle
–– UC
–– Colonic diameter > 6cm without any
mechanical obstruction + systemic
signs of toxicity
–– 1st line Tx - IV corticosteroids →
CS response measured by Travis
criteria on D3 of starting of CS
therapy
–– 2nd line - CNI like cyclosporine or
anti - TNF α like infliximab
–– Surgery - total proctocolectomy
with IPAA
* For Making Notes

190
IBS –– Systemic signs (GI Bleeds / fever / wt. loss)
•• Functional bowel disease –– Family h/o GI malignancy
•• Diagnosis of exclusion –– Nocturnal symptoms
•• ROME IV criteria - persistent abdominal pain –– Absolute increase in stool quantity

>/1 week & > 3 months + > 2/3
Q
•• Tx:
–– Pain related to defecation –– all patients advised to avoid FODMAP / high
–– Change in stool frequency gas forming food items
–– Change in stool form or appearance –– Based on Bristol stool chart

•• Red flags-
–– Lab abnormality - ↑CRP /FOBT + / ↓Hb /stool
calprotectin +
IBS-C IBS-D Pain

•• Tx- fiber + laxative •• Tx- •• Tx –
(PEG) –– 1st line - Antidiarrheals- –– 1st line –
•• Drugs- Loperamide – μ agonist antispasmodic
–– Lubiprostone Diphenoxylates- μ agonist Hyoscine /
–– Linaclotide Eluxadoline –μ+δ agonist Dicyclomine
–– 2nd line - Bile acid sequestrants-Cholestyramine TCA/SSRI /SNRI
–– 3rd line – Rifaximin
–– Others-
5HT3 – Ondansetron, Alosetron
Mesentric Ischemia
Cause Features Ix Tx
Q
AE- MCc /h/o A.Fib Acute abdomen pain (out of CECT abdomen Surgical embolectomy
proportion pain) /CTA (alternative- catheter based
thrombolysis)
AT- k/c/o ASCVD •• Acute: acute abdominal Pain CECT abdomen Surgical revascularization
•• Chronic: post prandial pain (alternative- catheter based
thrombolysis +/- angioplasty /
+ weight loss (mesenteric
stenting)
angina)
MVT – hypercoagulable state Vague abdominal pain (subacute) CECT abdomen Anticoagulation
(APLA/PNH /MPS /Factor V +/- diarrhea
leiden mutation)
NOMI- critically ill /high dose Abdominal pain + bloody CECT abdomen Supportive therapy
vasopressor ICU patients +/- diarrhea / Angiogram
Cardiovascular factors
* For Making Notes

191
Medicine
APPROACH TO UGI BLEED
Q
Mallory Weiss tear – Partial tear, MC site cardia, near EGJ
Varices
•• GAVE – gastric antral vascular ectasia, MC

Q site- antrum, can extend to pylorus
Balloon tamponade devices
•• Associated with – SSC
–– ESRD
–– Portal HTN
•• Dieulafoy lesion – dilated submucosal artery

•• ∆ - EUS +/- doppler
•• Usual location – fundus (6cms from EGJ)
* For Making Notes

192
•• Endoscopy (EGD)- <12-24hrs*→ others

Forrest Classification
IA - Spurting - Vascular
IB - slow oozing Dieulafoy
IIA - NBVV (pigment protruberance) AVM Endoscopic treatment
IIB - adherent clot
Q
Angiodysplasia (monotherapy)
IIC - flat pigmented base
Mallory Weiss tear - conservative tx +/-
III - clean ulcer base
endoscopic tx
* For Making Notes
193
Medicine
GAVE – tx- APC (argon plasma coagulation)

–– EGD – Normal (no source found)
Colonoscopy
If normal then → ? small bowel bleed

- Enteroscopy
- Capsule endoscopy
APPROACH TO LGI BLEED

Hematochezia
Diagnosis Features Evaluation & treatment
Angiodysplasia, AVMs Recurrent / painless bleed Colonoscopy ↔ APC +/- SSTR
Q
/ age >60yrs agonist like Lanreotide
Colon cancer Right colorectal cancers → Colonoscopy +/- biopsy
bleed → IDA (FOBT +)
Diverticular bleeding •• Age >50-60yrs + Conservative tx +/- endoscopic tx
painless bleed MC- +/- surgery (colectomy)
right side > left side
Diverticulitis •• Tx - IVF /ABC + p/o Antibiotics
•• → presents with fever / ↑ WBCS / LLQ pain +/- mild - Amox-clav / FQ-MNZ
bloody diarrhea, IOC → CECT •• Severe - IV Antibiotics
•• Colonoscopy to be avoided ↑ perforation risk - Piptaz/ Meropenem
•• Complications – abscess / fistula / free
- 3rd Gen Cephalosporins + MNZ
perforation /obstruction
•• Indications for surgery –
•• Hinchey’ classification
- Undrainable abscess
Diverticulosis
- Free perforation
•• IOC - colonoscopy/sigmoidoscopy
•• Tx – conservative - Failure of medical tx
•• Drain when abscess >4cm
(percutaneous drainage/ surgical
drainage)
Hemorrhoids •• External – itching + pain •• Grade 1-3 → banding + IR
•• Internal – itchy / photocoagulation, ↑fibres in diet
painless •• Symptomatic grade 3/4-
Surgery
* For Making Notes

194
Diagnosis Features Evaluation & treatment

Infectious colitis – h/o consumption of Fever / ↑WBC / ↑CRP +/- •• Tx - antibiotics
contaminated food pain +/- bloody diarrhea •• Avoid antibiotics in EHEC
Pseudomembranous Colitis-
•• cl.difficile
•• h/o antibiotic use – 3rd gen cephalosporin,
clindamycin (max. risk)
•• c/f - watery diarrhea, occasionally bloody
diarrhea +/- systemic symptoms
•• Dx - stool Ag assay
–– Stool GDH
•• Tx
Q
–– Mild To Moderate – Fidaxomycin, oral
vancomycin - 125mg QID
Severe (temp. > 103° F / WBCS >15000 /
S.creatinine >1.5 / ↓BP/ ileus)
Oral /Rectal vancomycin
–– Fulminant - toxic megacolon
P/O vancomycin + IV metronidazole
–– Recurrence – Fidaxomicin vs oral vancomycin
+/- Beclotoxumab (anti toxin B Mab)
If > 3 recurrences → best choice is FMT (fecal
microbiota transplant)
Inflammatory bowel disease MC – UC- bloody diarrhea , Colonoscopy + Bx
tenesmus
Ischemic colitis •• Age >50-60 yrs +/- CV •• Colonoscopy (erythema / edema
risk factors / ulcers) +/- CECT (CTA)
•• Present with cramping •• Tx- Conservative Mx +/- surgery
left lower pain + bloody •• Griffith point >> Sudeck’s
diarrhea point for ischemia
Post-polypectomy bleeding Occurs within 30 days of Tx - endoscopic tx
polypectomy
Acute Pancreatitis
3 criteria, if > 2 out of 3 present, dx – pancreatitis
Abdominal pain >95-98% , epigastric / LUQ radiation, nausea & vomiting
↑enzymes >3x upper normal limit → ↑amylase, ↑lipase (99% sensitivity & 99% specificity)
Imaging –
USG Abdomen to r/o gallstones / CBD dilatation
CECT Abdomen – best Ix for diagnosing & to check for complications - should be done @48-72 hrs
* For Making Notes

195
Medicine
Risk scores
•• Ranson score – for research, has poor
prognostic values
@Admission @ 48Hrs
G - glucose >200mg% C- hypocalcemia <8mg%
A - age >55yrs H - ↓ Hct by >10%
L - LDH >350 O - ↓PaO2 <60mm Hg
A - AST >250 B - base deficit > 4mEq /l
W - WBC >16000 B -↑Bun > 5mg %
S - Sequestered fluid - fluid
loss >6 litres

•• APACHE II
•• BISAP - <24hrs of admission
Q
•• B- BUN > 25
•• I- Impaired Mental status
•• S- SIRS >3 ↑risk
•• A- Age >60yrs
•• P- Pleural effusion
Causes –
•• MCC of pancreatitis is gall stones >alcohol
•• Others – metabolic – Hypertriglyceridemia : h/o of familial hypertriglyceridemia
–– Hypercalcemia (MEN 1)
–– Genetic – PRSS -1
–– Anatomic
–– Post-ERCP
–– Drugs - Didanosine
Tx – supportive therapy – ABC
•• IVF- bolus NS/RL @20ml/kg f/b maintenance dose of 3ml/kg/hr with urine output >0.5-1ml/kg/hr
•• Pain – opioids
•• Correct electrolytes - mainly look for calcium because of calcium sequestration, patient can develop
severe refractory hypercalcemia
* For Making Notes
196
•• Nutrition – early enteral nutrition → Complications

↓complications
•• Metabolic - ↓Ca2+ /↑glucose / +/- ↑TG
•• Specific – antibiotics → started only if infected
collection noticed especially infected necrosis •• Systemic – severe SIRS /ARDS/ DIC/ AKI /
↓BP +shock
•• ERCP - <24hrs (urgent) provided total bilirubin
>5mg% / if sepsis/ cholangitis •• Splanchnic vessel thrombosis - MC vessel
•• Cholecystectomy – in hospital →gallstones + affected in this is splenic vein thrombosis
mild pancreatitis •• Fluid collection
•• Severe hypertriglyceridemia – IV regular

insulin + fibrates + Apheresis
Acute PPC (<4weeks) Walled off PFC (>4wks)
- CECT Scan – unencapsulated - CECT Scan – capsulated
Acute PPC Walled off PFC
Interstitial Necrotizing Interstitial - Pseudocyst Necrotising –walled

off pancreatic necrosis
(WOPN)
•• Homogeneous fluid See if its sterile (no tx required) •• Homogenous fluid Heterogeneous fluid
collection or infection (gram negative rod) collection collection with thick
•• Resolve by 1-2 week, •• Asymptomatic → no tx fibrous capsule
no therapy required •• Symptomatic →
CT guided aspiration –culture + interventions –
antibiotic (pip-tazo /meropenem percutaneous drainage/
/ 3rd gen ceftriaxone + MNZ) +/- endoscopic drainage /
Interventional surgical drainage
Chronic & Autoimmune Pancreatitis –– chronic diarrhea (steatorrhea) because of

pancreatic exocrine insufficiency, Ix- fecal
•• Etiology
elastase
–– T - toxins – MC ethanol
–– Pancreatic diabetes type 3C
–– I - idiopathic
Brittle, ↑hypoglycemia risk
–– G - genetic – CFTR /SPINK1 /CASR / PRSS1
↓DKA risk low
–– A - Autoimmune
Imaging – CECT / ERCP → atrophy /
–– R - recurrent calcification / duct diltation +/- strictures
: Chain of Lakes Appearance
–– O - obstruction
•• Clinical features triad → •• Treatment – supportive (pain control +
pancreatic enzyme replacement therapy +/-
–– chronic abdominal Pain interventions)
* For Making Notes

197
Medicine
Sausage shaped pancreas- autoimmune pancreatitis
Autoimmune Pancreatitis APPROACH TO ALTERED LFTS Q
•• Mass like lesions in pancreas Pattern ALT AST ALP Bilirubin

•• HISORT Criteria
Q
Hepatocellular ↑↑ ↑↑ N/ ↑ N/↑(direct
bilirubin)
1. H - histology → 2 types – type 1 & type 2
Viral hepatitis , ALT>AST , N/ ↑ N / ↑(direct
–– Type 1 –
NASH AST/ALT <1 bilirubin)
Old /Asia > U.S / ↑S. Ig G4 Alcoholic AST >ALT , AST N/↑ N/↑ (direct
On biopsy – lymphoplasmacytic infilterate hepatitis /ALT >2 (deritis bilirubin)
ratio )
+ storiform fibrosis + obliterative
AST <400
phlebitis
Ischemic injury ↑↑↑ ↑↑↑ ↑↑ ↑↑(direct
↑recurrence rates - ALT/LDH <1.5 bilirubin)
–– Type 2- Wilson’s disease ↑ ↑↑ •• ALP/Total bilirubin <4
+ AST/ALT >2.2
Young / Europe > U.S / Normal or mild
•• DCT –ve, hemolysis
Ig G4
Cholestatic N/↑ N/↑ ↑↑ (GGT ↑ (direct
On biopsy- duct centric inflammation ↑↑) bilirubin )
Infiltrative Near normal ↑↑↑ Near normal
↓recurrence rates
- Causes →
2. I - imaging → mass like, sausage shaped granulomatous
pancreas infiltration –
sarcoidosis/TB/
3. S - serology → ↑IgG4 /N
Amyloidosis/
4. O - Other organ involvement abscess /
malignancy
–– Type 1 - have associated cholangiopathy (HCC/mets)
/ Riedel’s thyroiditis / parotid issues/
Muscle injury AST >> ALT Normal Normal
mediastinal or retroperitoneal fibrosis
–– Type 2 – have associated IBD like picture Bone disease Normal Normal ↑↑↑ (GGT Normal
normal)
5. RT- response to therapy → corticosteroids
+/- Mycophenolate mofeti /Azathioprine / Hemolysis – LDH Normal Normal Normal ↑ (indirect
/AST >30 (mild bilirubin)
Rituximab /Cyclophosphamide
↑)
Congenital Normal Normal Normal ↑↑
causes
* For Making Notes

198
VIRAL HEPATITIS → •• Cholestatic Pattern- look at USG → Biliary

radical dilatation
1. Acute – ALT → 1000’s
2. Chronic – ALT → 50’s/100’s Yes No
Alcoholic Hepatitis NASH
Common for both - Biopsy – steatosis + ballooning +
inflammation +/- fibrosis +/- Mallory hyaline denk body •• ERCP/MRCP causes of Intrahepatic
•• H/o alcohol use •• R/o alcohol & HCV cholestasis - PBC →AMA +ve
•• AST/ALT >2 (AST <400) •• AST/ALT <1
•• D/D-
•• Tx- supportive +/- •• Tx - lifestyle
Corticosteroids + N-acetyl modifications – weight –– PSC
cysteine loss>10%
•• C/I for Corticosteroids – •• Drugs – –– Cholangiocarcinoma
1. Active GI bleed 1. Metformin –– Periampullary cancer

2.Uncontrolled infections 2. GLP1RA – Liraglutide –– Choledocholithiasis
3. Untreated HBV 3. PPAR Agonist-
•• Congenital Pattern – Isolated bilirubin increase
•• Indications for –– ϒ- Pioglitazone
corticosteroids –
without any other changes
–– Α+ϒ- Saroglitazar
1. Maddrey’s DF >32
–– Pan PPAR ( αβϒδ)-
–– Maddrey’s DF = 4.6 *PT
Lanifibranor
(T-C) +TB Direct bilirubin
•• Bariatric surgery Indirect bilirubin
2. MELD > 18
–– UGT1A1 Defect
3. Hepatic encephalopathy
•• To assess response to CS
@1 week - Lille index
Indirect Bilirubin Direct Bilirubin

Q
Criggler Najjar (<10%) Gilbert (>10%) Dubin Johnson Rotor syndrome
Syndrome
TYPE1 (0%) TYPE 2 (<10%) •• Asymptomatic •• MRP2 protein •• OATP1B1/B3
•• 0% Enzyme •• <10% enzyme activity adults defective defect
Q
activity •• TB <20mg% •• TB<4mg% •• Brown black liver •• Asymptomatic
•• TB >20mg% •• Kernicterus absent •• Phenobarbitone •• TB<6mg% •• TB <6mg%
•• Kernicterus •• > 25% ↓bilirubin positive results •• Asymptomatic, •• No pigmentation of
•• phenobarbitone •• Phenobarbitone test in normalization incidental finding liver
test-ve +ve of normal
bilirubin
Progressive Familial Intrahepatic •• Type 3 - MDR 3 defective- GGT ↑

Cholestatsis •• Severe cholestasis, ↑↑ALP, presents in early
childhood → progress to cirrhosis slowly
3 types –
•• No treatment
•• Type 1 - FIC 1 defective
GGT normal
•• Type 2 – BSEP defective
* For Making Notes

199
Medicine
Hepatitis •• Anti HBc Ag- marker of exposure (IgG- chronic

or remote infection / IgM- recent infection)
•• Surface Ag - marker of infection
Q
•• Anti HBs Ag- marker of Immunity

•• E Ag - marker of infectivity
•• HBV DNA Ag- marker of replication, correlate
•• Vertical transmission – risk is 10-30% if mother with risk of complication like cirrhosis/HCC
is e EAg –ve
–– Risk is 70-90% if mother is e EAg +ve HBV Serology-
Diagnosis HBSAg Anti-HBs Anti-HBc HBE-Ag Anti-HBE HBV DNA
Acute Infection + - + (IgM) + - +
Window Period - - + (IgM) - - +
Recovery - + + (IgG) - Variable -
Vaccinated - + - - - -
Chronic HBV, E Ag+ve + - + (IgG) + - +
Chronic HBV E Ag –ve + - + (IgG) - + +
Occult HBV - - + (IgG) - Variable + (low)
Chronic HBV, E Ag +ve

1. If ALT normal / DNA ↑↑ → immunetolerance
phase
2. If ALT > 2 x times normal /DNA ↑ → immune
active phase - ↑risk of cirrhosis
Chronic HBV, E Ag -ve
1. If ALT normal / DNA ↑↑ (<2000) → immune
control phase / inactive carrier
Viral Hepatitis – Natural History &
Management
2. If ALT >2 x times normal /DNA (>2000) {has
precore mutant}} → immune escape phase
– also indicates chronic HBV, EAg –ve with
active hepatitis →↑ risk of progression to
cirrhosis is high
HCV
•• Earliest marker to become detectable in
this are HCV RNA
•• To itdentify whether it’s a acute infection
or chronic infection – redo HCV RNA within
>12-16 weeks
Anti-HCV HCV-RNA
Active HCV + +
Recovery + -
Not exposed - -
* For Making Notes

200
•• Tx - supportive tx Chronic HBV Tx

•• Some patients of acute hepatitis can develop •• Indications for therapy according to APASL
acute fulminant liver (ALF) – risk is <1% & IASL guidelines–
•• ALF -
Q
–– HBV DNA > 2000 IU/ml
–– Immune active phase (HBV E Ag +ve / DNA
–– ALT >10000
> 20,000 /ALT >2 x UNL)
–– TB >1 mg%
–– Immune escape phase (precore mutant –
–– Evidence of liver failure – coagulopathy HBV E Ag-ve / DNA >2K / ALT > 2 x UNL)
(elevated PT / INR) /encephalopathy –– Cirrhosis + DNA > 2000
–– Risk factor – age >40yrs /H/o chronic –– Decompensated cirrhosis
liver disease / pregnant female with Hep E –– Severe extrahepatic manifestations
infection (20% risk and high mortality)
–– Special population – HCC / HCV+ HBV /
–– Supportive Tx. Pregnancy – if DNA >1 million, start tx in
3rd trimester after 24-28weeks, DOC –
–– If it is d/t acute hep. B virus, Tx - antivirals Tenofovir (TDF/TAF)
– Tenofovir /Entecavir
Indications acc. to Harrison
•• Risk of chronicity in HBV infections –
•• Drugs – oral >> parenteral
–– Chronic HBV α 1/age , Eg- –– Oral → Tenofovir – TAF> TDF, TAF is less
neonatal – 90% risk nephrotoxic
TDF - 300mg/day
Infants – 50% risk
TAF - 25mg/day, less nephrotoxic
Children – 20% risk
Entecavir - 0.5-1mg/day
Adults- 1-2% risk Duration of therapy depends on E Ag +/-
•• Risk of chronicity in HCV is >80-85% regardless E Ag +ve → give till seroconversion + 6-12
months as consolidation
of age
E Ag -ve → infinite duration, goal – S. Ag
•• Extrahepatic manifestations with regard to should become -ve
HBV & HCV – –– Parenteral therapy - IFN α
HBV HCV Not much useful in Indians
1. MC – serum sickness in 1. MC – cryo (type 2- Advantage - finite advantage, 48-52 wk
acute HBV mixed)
s/e – flu like reactions
–– MC – GN in chronic 2. GN (MPGN > MN)
HBV (membranous 3. Porphyrea cutanea tarda Chronic HCV Tx
nephropathy (MN > 4.lichen planus •• All patients are to be treated .
MPGN type 1) 5. metabolic syndrome
•• Direct acting antivirals (DAA)
2. PAN 6. sicca syndrome
3. Polyarthritis •• NS5A - → ASVIRS
4. cryo (mixed) –– Ledipasvir / Ombitasvir / Velpatasvir /
Declatasvir / Pibrentasvir
* For Making Notes

201
Medicine
•• NS5B- →BUVIRS •• HDV –

–– Sofosbuvir / Dalasbuvir –– Delta particle
•• NS3-, 4A- → Protease inhibitors –– COINFECTION – acute HBV (anti HBc IgM
+ , HBsAg +) + HDV (anti HDV)
–– Simepravir / Bocepravir / Paritapravir /
Glecapravir –– Outcome – clearance of both of viruses
•• Regimen used in India- Sofosbuvir +Velpatasvir –– SUPERINFECTION – chronic HBV (HBsAg +,
X 12 Weeks ( SVR can be achieved in >95% anti HBC IgG +) + HDV (anti HDV )
of patients in just 12 weeks)
–– Outcome - ↑liver failure / ↑cirrhosis /↑HCC
•• Regimen used in western countries – Glecapravir
+ Pibrentavir X 8weeks Autoimmune Liver Disease
•• MC genotype in India in HCV – 3a → ↑steatosis
,↑fatty infiltration, ↑steatohepatitis
Feature AIH PBC PSC

Gender Female Female Male
Age Middle age Middle age Younger –middle age >85% cases associated
,hypercholesterolemia, with IBD (UC)
xanthomas , associated -↑ risk of cholangiocarcinoma
sicca syndrome
AST & ALT ↑↑ ( >3X ULN) N/ ↑(<3X ULN ) N/ ↑ (<3X ULN)
ALP N/↑ (< 2X ULN) ↑↑(>2X ULN ) ↑↑(>2 X ULN)
Immunoglobulins ↑↑ (IgG > 2X ULN) N/ ↑IgM N/ ↑ (non specific )
Q Q
Autoantibodies •• Type 1(>85%) > Type AMA (M2) + P-ANCA+ (Atypical)
Q
2
•• Type 1- ANA+/SMA+
•• Type 2- Anti LKM-1+/
Anti SLA + Anti SC-1+
Q
Biopsy Interface hepatitis Bile ductopenia /granuloma Periductal - onion skin fibrosis
ERCP/MRCP Not required Normal •• Biliary stricture & dilatation

•• >85% - extrahepatic dilatation ,
abnormal imaging
•• <15% - intrahepatic dilatation, normal
imaging
Rx Corticosteroids + •• UDCA •• ?UDCA
Azathioprine •• 2nd line – liver •• 2nd line – orthotopic liver transplant
transplant
* For Making Notes

202
METABOLIC LIVER DISEASE- •• MRI brain – face of giant panda seen
Wilson Disease
•• AR, ATP7B defect
•• Copper overload in liver and ↑free copper in
circulation
•• C/F-
–– Liver disease –
ALF – ALP/DB <4 + AST/ALT >2.2 + DCT
–ve
KF Ring
Chronic hepatitis – CLD/Cirrhosis
–– Neuropsychiatric – Hemochromatosis
Hepatolenticular degeneration •• AR, 2 types – hereditary form (not seen in
India) & acquired form
Extrapyramidal (wing beating tremor)
•• Hereditary –
–– KF Rings – also seen in cholestatic conditions
Q
–– HFE related – MC
Q
KF rings and neuropsychiatric symptoms

are 98% correlated CD282Y
•• Ix- H63D – associated with ALS
–– S.Ceruloplasmin ↓ (<20mg/dl) → s/o Wilson –– Non HFE –
disease HJV
–– 24hr urine copper ↑ (>100μg/day) → dx of Ferroportin defect
Wilson disease
Transferrin 2 defect
–– S. Cu → total -↓ / free -↑
•• Acquired-
–– Gold std - Liver bx →↑hepatic copper, stain
copper using Rhodamine stain If >250μg/g –– Iron loading anemia (Eg- Thalassemia)
of dry weight of liver → s/o wilson disease –– Chronic regular blood transfusion
•• Disadvantage - can also be seen in chronic –– CLD
cholestatic conditions
•• C/f –
–– Genetic testing can be done in difficult to
–– MC- fatigue/arthralgias
diagnose cases
–– Other manifestations –
•• Tx – chelators – d-penicillamine = Trientine +/
Zinc (maintenance) Liver – cirrhosis → ↑HCC
•• To predict liver transplant requirement – DCM/RCM → HF

NAZER SCORE
Q
Musculoskeletal arthropathy – MC joint
affected is MCP (2nd /3rd ) +/- Wrist
–– Total bilirubin
Endocrine – Testes → Hypogonadism
–– AST
○○ Pituitary → DI
–– PT
○○ Β-Cells → DM
* For Making Notes

203
Medicine
Skin hyperpigmentation (melanin + iron IMPORTANT SCORES

deposition)
–– Triad – Cirrrhosis + Skin Hyperpigmentation Child pugh score Q
+ Dm (Bronze Diabetes) Points

–– ↑risk of infections - Vibrio /Yersinia / Features 1 2 3
Listeria Encephalopathy None Grade 1/2 Grade 3/4
•• Ix- Slight
Severe /
–– TsAT ↑↑ (Fe /TIBC) Ascites None (diuretic
refractory
–– S.Ferritin ↑↑ responsive )
Bilirubin (mg/dl) <2 2-3 >3
–– Gold std – Liver Bx→ ↑Fe
Albumin (g/dl) >3.5 2.8-3.5 <2.8
Prussian blue
PT
–– Genetic testing <4s 4-6 s >6 s
Coagulation (s)
•• Tx- INR <1.7 1.7-2.3 >2.3
–– TOC for hereditary forms- Phlebotomy Score 5-6 → A
–– TOC for acquired forms- chelators Score 7-9 →B ↑Mortality / ↓survival
Score 10-15 → C
Α1AT Deficiency
•• Co-dominant inheritance MELD Score Q
•• Damage to lungs – emphysema (d/t protease ‘’C B I’’

antiprotease imbalance) •• C - creatinine
–– Young /never smoked •• B - bilirubin
–– Lower lobe / Panacinar •• I - INR
–– Family H/O +/- Na+
•• liver (intracellular accumulation of α1 AT in

PELD –
hepatocytes)
•• Albumin
•• Gold std for dx- Genetic testing
•• Bilirubin
•• Specific phenotype resulting in liver problems –
•• INR
Z phenotype
•• +Age <1
•• Tx - α1AT Replacement /supportive therapy
•• +/- growth failure
NAZER index- Wilson disease

•• Bilirubin
•• AST
•• INR
* For Making Notes

204
Ascites & SBP

•• SAAG = S. Albumin – ASC. Albumin
SAAG > 1.1 → Portal HTN SAAG <1.1

Q
TP < 2.5g/dl 1.Sinusoidal cause- Cirrhosis /late budd 1.Nephrotic syndrome

chiari syndrome
2.Myxedema
TP >2.5 g/dl Extra sinusoidal portal HTN (pre-sinusoidal 1. Peritoneal carcinomatosis
/post-sinusoidal)
2. TB
1. Pre - sinusoidal causes
3. Pancreatic ascites
•• Schistosomiasis
•• NCPF → young adult with splenomegaly +/-
4. 20 bacterial peritonitis - Infection →
variceal bleed ascites
•• EHPVD → children → 10-15 yrs of age •• Dx with RUNYON criteria – Ascitic fluid
+ mild splenomegaly +/- variceal bleed / TP >1g%
no liver failure or jaundice / imaging – •• Ascitic LDH > ULN of S.LDH
cavernomatous transformation of portal •• Ascitic glucose <50mg% Vs {spontaneous
vein bacterial peritonitis – Ascites →
2. Post - Sinuoidal Causes- infection}
•• Cardiac problems→ CP 5. Chylous ascites - ↑ triglyceridemia
•• Budd chiari syndrome →
myeloproliferative disorder PNH / 6.Meig syndrome – Triad – ovarian
Hereditary thrombophillias fibromas + ascites + pleural effusions
–– present with tender Hepatomegaly and
ascites
–– enlargement of caudate lobe
•• SOS → Hepatic veno occlusive disease.
Causes -
–– Post – HSCT
–– H/O cytotoxic drug use- Ara-C/Cyc
–– TOC – Defibrotide
Management of Ascites
•• Diuretics + ↓Na+ diet
Spontaneous bacterial peritonitis
•• If PMN >250 in ascitic fluid + C/S +ve
Q
Spironolactone 400Mg + Furosemide •• If PMN >250 in ascitic fluid, but C/S – ve →

160mg culture negative SBP
Refractory ascites •• Tx - Empirical antibiotics –
LVP > 5L + Add Albumin for every 1 –– Ceftriaxone
litre of ascitic fluid removed.
–– Piptazo
•• TIPPS
* For Making Notes

205
Medicine
OTHER COMPLICATIONS OF Hepatic encephalopathy

PORTAL HTN •• Not a complication of portal HTN ,rather
•• Varices prophylaxis complication of liver failure
–– 1o - Propranolol if small varices / serial EVL - •• Precipitants–

if large varices –– ↓K+ / metabolic acidosis
–– 2 - propranolol + Serial EVL
o
–– GI bleeding
HEPATORENAL SYNDROME –– Sepsis (SBP)
•• H/O cirrhosis /portal HTN –– Bendzodiazepines
•• Patient presents with pre-renal AKI –– Hypoxia
•• ∆ of exclusion –– Shunts- TIPSS /surgical shunt
•• Mx – stop all nephrotoxic drugs + withhold all •• Clinical Diagnosis
diuretics + volume expansion
•• Volume expansion – 20%albumin @dose 1g/kg •• Grading – West Haven Classification
infusion - 48hrs •• TOC - 1st line Lactulose + Refaximin
If no response +/- BCAA +/-Probiotics
HRS
Refractory
•• TOC- Terlipressin + NA + Albumin @1g/
kg/day at 100g/day Or Octreotide +
OLT
Midodrine + Albumin
TIPSS /OLT
* For Making Notes

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TABLE OF CONTENT

Subjects Page No.

Medicine Quick Revision Notes 1-205

Surgery Quick Revision Notes 208-297

Pediatrics Quick Revision Notes 300-371

OBG Quick Revision Notes 374-454

ARRHYTHMIAS •• Early biomarkers (rise early & fall early) -

Features suggesting ACS

(Levine’s Sign - retrosternal crushing pain)

•• Acute heart failure (eg- pulmonary edema) cardiac biomarkers (troponins)

Three step protocol for ACS work up b. Imaging:

iii. Coronary angiogram - specially done in

Types of MI •• Rise of troponin to detectable level (time lag is

Troponin dynamics If difference is <20%

Difference of >20% rise can also be used to diagnose

Difference between STEMI & NSTE-

* For Making Notes

STEMI NSTEMI iv. Prasugrel (L.D. 60mg,

↓collateral Extensive collaterals M.D. 10mg/d), Preferred for PCI

3. N - Nitrates → NTG –short acting nitrate, can

* For Making Notes

If patient has h/o heparin induced thrombocytopenia

DEFINITIVE TX- a. PCI centre → <60mins → PPCI (10 PCI )

•• If DTB >120 mins –thrombolyse within next

Reperfusion for all patients i. If yes----do PCI in next 24hrs.

* For Making Notes

Very high risk patient- Absolute Relative

b. Acute heart failure stroke of unknown origin presentation

c. Mechanical complications of •• Intracranial neoplasm, •• Ischemic

d. Ventricular arrhythmias <24hrs •• Ischemic stroke< •• Other intracranial

TIMI risk score (TRS) – 7 components •• Active internal bleeding vascular

>/=3 –intermediate high risk

C/I to thrombolysis : NSTEM-ACS (cause

EXTENSIVE ANTERIOR WALL STEMI:

Sequence of changes in STEMI: Causes of ST Elevation:

Localization of STEMI: (only STEMI can •• TOC- CCB.

a) II/III/aVF – inferior MI – PDA (originate from •• Old >50yr history of stress

ECG 2: 2. Pericardial causes:

3. Conduction causes: LBBB

Dx : II/III / aVF-INFERIOR WALL MI

* For Making Notes

ECG 3: STEMI Pattern:

ECG 4: TYPE B WELLEN’S PATTERN

ECG 5: Arrhythmias – Tachyarrythmias (VT/VF) or

* For Making Notes

2. Cardiogenic shock – MCC of in hospital death. V. Mortality – 85-100%

IV. PCWP - ↑↑, large V waves. Transmural ischemia/stemi

Approach To SIHD (Stable Ischemic i. Patient should be able to exercise

2. Work up for SIHD- a. When patient becomes symptomatic-

(b) Stress ECG AI (Angina Index)-

(c) Indications for exercise ECG-

* For Making Notes

1. Aspirin 2. CABG-only absolute indication is

Ivabradine- bradycardia ,Luminous phenomena

* For Making Notes

Pulmonary HTN eg-

I -, aVF-, aVR+ : Northwest/extreme Axis Hyperkalemia, WPW

Normal axis/ LAFB

+/- eosinophilia •• IOC- CMR