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20/11/2025



Clinical Uses of Vitamin B12

Treats B12 Deficiency (Main Use)

• Pernicious anemia
• Gastric bypass, gastrectomy
• Crohn’s (terminal ileum disease)
• Vegan diet
• Elderly poor intake
• Drugs: Metformin, PPIs

Fixes Neurological Problems Due to Low B12
• Numbness & tingling
• Loss of balance
• Memory issues
• Subacute combined degeneration (posterior column + corticospinal damage)

Corrects Megaloblastic Anemia
• Macrocytic anemia
• Hypersegmented neutrophils
• Prevents irreversible nerve damage

Lowers Homocysteine
• Used with Folate + B6
• Helps reduce thrombosis risk in high homocysteine levels

Antidote

Hydroxocobalamin = Treatment for Cyanide Poisoning
• Binds cyanide → safe excretion
• Fast, safe, and effective

Special Groups Who Often Need It
• Pregnant women with deficiency
• Elderly
• Vegans
• Long-term Metformin users
• Chronic alcohol use

Anticoagulation in Thrombocytopenia(UFH, LMWH, DOACs)Platelets < 10,000/µLAbsolute contraindication• Hold ALL anticoagu...
20/11/2025



Anticoagulation in Thrombocytopenia

(UFH, LMWH, DOACs)

Platelets < 10,000/µL

Absolute contraindication
• Hold ALL anticoagulation
• Extremely high risk of spontaneous intracranial & mucosal bleeding.
• Use mechanical DVT prophylaxis only.

Platelets < 20,000–25,000/µL

Hold therapeutic anticoagulation
• Even prophylactic anticoagulation is generally avoided unless:
• Patient has extremely high thrombosis risk
• Hematology approves short-term use

Platelets 25,000–50,000/µL

Reduced-dose anticoagulation is often used
Treatment of VTE / AF stroke prevention:
• Prophylactic-dose LMWH is preferred.
• Some guidelines allow 50% dose LMWH for acute VTE.
• DOACs typically held (not studied safely in this range).

High-risk situations where anticoagulation MUST continue:
Recent VTE (< 30 days)
Massive PE with RV strain
Mechanical heart valve
LV thrombus

→ Hematology + cardiology decision required.

Platelets > 50,000/µL

Full-dose anticoagulation is generally safe
• LMWH, UFH, and DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) acceptable.
• Most oncology and hematology guidelines use 50,000/µL as threshold for regular anticoagulation.

If bleeding risk is high:
Use LMWH instead of DOACs.

Platelets > 100,000/µL

Safe for all anticoagulation
No dose modification required
DVT prophylaxis and therapeutic doses fully acceptable.

Special Cases

1. Mechanical Heart Valve

• Try to keep platelets > 50,000/µL with transfusions.
• If < 50k, consider UFH infusion with careful monitoring.

2. Cancer-Associated Thrombosis (CAT)

• LMWH preferred when platelets < 50k.
• DOACs ok if platelets ≥ 50k and no GI bleeding risk.

3. ITP (Immune Thrombocytopenia)

• Anticoagulation can be used even with platelets 30–50k after steroids/IVIG increase count.

19/11/2025



When to Hold Aspirin & Clopidogrel in Patient with Thrombocytopenia

Platelets < 10,000/µL
• Avoid ALL antiplatelet therapy (aspirin + clopidogrel)
• Extremely high risk of spontaneous intracranial and GI bleeding.

Platelets < 30,000/µL
• Hold clopidogrel (P2Y12 inhibitors)
• Hold aspirin unless life-saving (e.g., recent stent thrombosis).
• At this level, antiplatelets significantly increase major bleeding risk.

Platelets 30,000–50,000/µL

General recommendation:
• Aspirin: Can be given only if strongly indicated (e.g., post-PCI, ACS).
• Clopidogrel: Usually avoided; may be used only with hematology + cardiology agreement in critical indications.

Dual antiplatelet therapy (DAPT) → Generally avoided unless life-saving and short-term.

Platelets 50,000–100,000/µL
• Aspirin: Usually safe to continue.
• Clopidogrel: Can be continued if clearly indicated (e.g., recent stent).
• DAPT is acceptable short-term if platelets > 50k and bleeding risk is controlled.

Platelets > 100,000/µL
• Aspirin and clopidogrel both safe
• No need to modify therapy.

19/11/2025

A 58-year-old man with hypertension and dyslipidaemia presents with acute-onset central chest pain radiating to the left arm at 7:00 AM. ECG shows ST-segment elevation in the anterior leads. You recall that myocardial infarctions are more common in the early morning hours.

Which of the following physiological changes most strongly explains the increased incidence of myocardial infarction in the morning?

A. Increased parasympathetic activity leading to bradycardia during the early morning
B. Peak cortisol levels causing enhanced nocturnal fibrinolysis
C. Early morning surge in catecholamines causing increased shear stress on coronary plaques
D. Reduced platelet activity and decreased sensitivity to ADP in early morning
E. Circadian-related drop in blood viscosity between 6–10 AM

19/11/2025

Diagnostic Criteria for Congestive Hepatopathy

1. Clinical Criteria
• Evidence of right-sided heart failure:
• Elevated JVP
• Peripheral edema
• Hepatomegaly (tender, smooth)
• Ascites (high-protein)
• Symptoms of chronic congestion:
• Early satiety, abdominal discomfort
• Fatigue

2. Laboratory Findings

Typical pattern = mild cholestatic + mild hepatocellular elevation
• AST/ALT: mild elevation (usually < 2–3× ULN)
• Bilirubin: mild to moderate elevation (usually indirect + direct)
• Alkaline phosphatase: normal to mildly increased
• GGT: often elevated
• Albumin: may be low in chronic disease
• INR: may increase in chronic passive congestion

Clues suggestive of acute cardiogenic liver injury:
• Sudden AST/ALT > 10× ULN
• Rise after hypotensive episode or acute RHF

3. Imaging Criteria

Ultrasound Findings
• Hepatomegaly
• Dilated IVC (> 2.3 cm)
• Dilated hepatic veins
• Loss of normal hepatic vein respiratory variation
• Hepatic vein Doppler: reversed systolic flow or “saw-tooth pattern”
• Portal vein pulsatility (in severe cases)

CT/MRI Findings
• Heterogeneous (“mosaic”) hepatic enhancement
• Early enhancement near central zones
• Delayed enhancement of peripheral zones
• Enlarged IVC & hepatic veins

4. Hemodynamic Criteria

(Usually via right-heart catheterization or combined hepatic venous pressure gradient)
• Elevated right atrial pressure
• Elevated hepatic venous pressure
• HVPG < 6 mmHg
• Important: Unlike cirrhosis, congestive hepatopathy has normal or mildly elevated HVPG.

This helps distinguish congestive hepatopathy (normal HVPG) vs. cardiac cirrhosis (may have elevated HVPG as fibrosis develops).

5. Histological Criteria (if biopsy needed)
• Sinusoidal dilation and congestion
• Centrilobular (zone 3) hepatocyte atrophy
• Centrilobular fibrosis → bridging fibrosis in chronic cases
•. Reverse lobulation” in severe long-standing
• Minimal inflammation

Biopsy is usually reserved for unclear cases or transplant decision-making.

19/11/2025

Why MI Happens More in the Morning

Most myocardial infarctions (MIs) occur in the early morning hours (around 6 AM–12 PM) because of normal circadian (biological clock) changes that increase cardiac stress and thrombosis risk.

1. Catecholamine Surge (↑ Sympathetic Tone)
• Early morning rise in epinephrine and norepinephrine
• → ↑ Heart rate
• → ↑ Blood pressure
• → ↑ Myocardial oxygen demand
• → ↑ Shear stress → plaque rupture

This is the single most important mechanism.

2. Morning Hypercoagulability

Blood becomes more pro-thrombotic in the morning:
• ↑ Platelet aggregability
• ↑ Plasminogen activator inhibitor-1 (PAI-1) → ↓ fibrinolysis
• ↑ Viscosity

This makes any ruptured plaque more likely to form an occlusive clot.

3. Cortisol Peak

Cortisol rises sharply around 6–8 AM:
• ↑ Blood pressure
• ↑ Glucose → worsens endothelial function
• ↑ Inflammatory activity in plaques

Contributes to plaque instability.

4. Circadian Variation in Vascular Tone
• Morning: increased vasoconstriction and reduced endothelial nitric oxide
• → Higher coronary tone
• → More prone to coronary spasm + decreased perfusion

5. Increased Platelet “Stickiness”

Platelets are more active in the morning:
• ↑ Expression of glycoprotein receptors
• ↑ Sensitivity to ADP and thromboxane A2

This increases the risk of thrombus formation after plaque rupture.

6. Blood Pressure Morning Surge

As the body transitions from sleep to wake:
• ↑ Sympathetic activation
• ↑ Peripheral resistance
• ↑ BP variability

Sudden BP surge can stress vulnerable plaques.

7. REM Sleep–Related Arrhythmias & Demand
• REM sleep is associated with bursts of sympathetic activity.
• Transition from REM → waking can trigger ischemia.

19/11/2025

Gluten-Containing Foods

(Sources of wheat, barley, rye, and contaminated oats)

1. Grains & Flours
• Wheat (all forms)
• Barley
• Rye
• Triticale
• Spelt
• Kamut
• Semolina
• Farina
• Durum wheat
• Bulgur
• Couscous
• Wheat bran / wheat germ
• Malt (barley-based)

2. Breads & Baked Goods
• Regular bread
• Toast
• Buns / rolls
• Croissants
• Cakes
• Muffins
• Donuts
• Pastries
• Cookies
• Pizza crust (regular)
• Pita / naan / chapati / paratha (unless GF)
• Biscuits / crackers

3. Pasta & Noodles
• All wheat pasta
• Egg noodles
• Ramen
• Udon
• Spaghetti / macaroni
• Lasagna sheets
• Vermicelli (if wheat-based)

4. Breakfast Foods
• Most cereals (wheat, malt, barley-containing)
• Granola (often contains gluten)
• Pancakes & waffles (non-GF)
• French toast

5. Snacks
• Pretzels
• Normal chips with wheat flavorings
• Trail mixes with granola
• Wheat crackers
• Cookies & wafers

6. Processed Foods (Hidden Gluten)
• Soy sauce (contains wheat unless GF)
• Salad dressings
• Gravies & sauces (thickened with flour)
• Soups (cream soups, packet soups)
• Marinades
• Processed meats (sausages, meatballs, cold cuts with fillers)
• Veggie burgers (wheat binders)

7. Beverages
• Beer
• Ale
• Malt beverages
• Barley tea (mugicha)

8. Other Sources
• Breaded/fried foods (flour coating)
• Tempura
• Seitan (“wheat meat”)
• Stuffings
• Imitation crab (surimi sometimes contains wheat)
• Energy bars with oats (unless certified gluten-free)

Oats
• Naturally gluten-free
• But often contaminated with wheat during processing
• Only safe if labeled “certified gluten-free oats”

Approach to Treatment of Multiple Myeloma1. Confirm Diagnosis & Risk StratificationBefore treatment: Diagnostic Confirma...
18/11/2025

Approach to Treatment of Multiple Myeloma

1. Confirm Diagnosis & Risk Stratification

Before treatment: Diagnostic Confirmation

• Bone marrow plasma cells ≥10% OR biopsy-proven plasmacytoma
AND at least one CRAB or SLiM feature:
• Calcium > 11 mg/dL
• Renal dysfunction (Cr >2 or eGFR

18/11/2025

Important Adverse Effects of BRAF Inhibitors and MEK Inhibitors

BRAF Inhibitors
• Secondary skin cancers (SCC, keratoacanthoma)
• Photosensitivity (vemurafenib)
• Arthralgia, fatigue

MEK Inhibitors
• Cardiomyopathy (↓ EF)
• Retinal detachment
• Rash, diarrhea

Combo therapy reduces skin toxicity but adds cardiac/ocular monitoring needs.

18/11/2025

Clinical Uses Anti-BRAF Inhibitors

1. Metastatic Melanoma
• First-line if BRAF V600 positive
• Prefer BRAF + MEK combo (better PFS, less cutaneous SCC)

2. Hairy Cell Leukemia
• Vemurafenib used in relapsed/refractory cases

3. BRAF-mutated Colorectal Cancer
• Encorafenib + Cetuximab (targeting EGFR required)

4. Thyroid Cancer (Papillary / Anaplastic)
• Dabrafenib + Trametinib for metastatic or unresectable BRAF-positive disease

5. NSCLC
• Dabrafenib + Trametinib

18/11/2025

Anti-BRAF Inhibitors

Target BRAF V600 mutations in the MAPK pathway.

Approved BRAF Inhibitors
1. Vemurafenib
2. Dabrafenib
3. Encorafenib

BRAF + MEK Combinations

(Used to prevent resistance & reduce paradoxical MAPK activation)
1. Dabrafenib + Trametinib
2. Vemurafenib + Cobimetinib
3. Encorafenib + Binimetinib

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