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Here are your comprehensive CVS Pharmacology notes at MBBS level, sourced from Lippincott Illustrated Reviews: Pharmacology and Katzung's Basic & Clinical Pharmacology.

CVS Pharmacology - MBBS Notes

1. ANTIARRHYTHMIC DRUGS

Background

Arrhythmias arise from:

Abnormal automaticity - ectopic pacemaker sites fire faster than SA node
Abnormal conduction - reentry circuits (require unidirectional block + slow conduction)

Key concept - Vaughan-Williams Classification organises drugs by their predominant action on the cardiac action potential.

Proarrhythmic risk: Many antiarrhythmics can CAUSE arrhythmias. K+ channel blockade prolongs QT interval → risk of torsades de pointes (TdP). IV magnesium sulfate is the drug of choice for TdP.

Class I - Sodium Channel Blockers

Block fast Na+ channels → slow Phase 0 depolarization

Subclass	Mechanism	Drugs	Key Adverse Effects
IA	Slows Phase 0; prolongs repolarization	Quinidine, Procainamide, Disopyramide	QT prolongation, TdP, anticholinergic effects
IB	Shortens Phase 3 repolarization	Lidocaine, Mexiletine	CNS toxicity (tremor, seizures), confusion
IC	Markedly slows Phase 0; minimal effect on repolarization	Flecainide, Propafenone	Proarrhythmic - AVOID in structural heart disease

Drug-specific notes:

Quinidine - Cinchonism (tinnitus, blurred vision, headache, psychosis), hemolytic anemia
Procainamide - Lupus-like syndrome, hypotension
Disopyramide - Strong anticholinergic (urinary retention, dry mouth); AVOID in elderly
Lidocaine - IV only; for ventricular arrhythmias (VT/VF); no effect on atrial tissue
Mexiletine - Oral lidocaine analogue; nausea/vomiting
Flecainide - Maintain sinus rhythm in AF/flutter (NO structural heart disease); CYP2D6 metabolised
Propafenone - Atrial arrhythmias; weak β-blocking effect; AVOID in asthma

Class II - Beta-Blockers

Diminish Phase 4 depolarization → depress automaticity, prolong AV conduction, decrease HR and contractility

Uses: Tachyarrhythmias from sympathetic excess, atrial flutter/fibrillation, AV nodal reentrant tachycardia, post-MI ventricular arrhythmias

Drug	Selectivity	Notes
Metoprolol	β1-selective	Most widely used cardiac arrhythmia agent; reduced bronchospasm risk
Propranolol	Non-selective	Also used in thyrotoxicosis, migraine, essential tremor
Esmolol	β1-selective	IV only; ultra-short acting; used in acute settings
Atenolol	β1-selective	Oral; renal elimination

Adverse effects: Bradycardia, fatigue, sleep disturbance, depression, blunted hypoglycemia awareness; bronchospasm in asthmatics (non-selective agents)

Class III - Potassium Channel Blockers

Block K+ channels → prolong repolarization (Phase 3) → prolong QT interval

Drug	Key Features
Amiodarone	Multiple channel blocker (I, II, III, IV activity); most effective antiarrhythmic; very long half-life (40-55 days)
Sotalol	Also has β-blocking activity; requires QT monitoring; can be outpatient-initiated with monitoring
Dofetilide	Pure K+ blocker; requires inpatient QT monitoring for initiation
Dronedarone	Amiodarone analogue WITHOUT iodine moiety; AVOID in severe/permanent AF with heart failure

Amiodarone toxicity (PYTILS mnemonic):

Pulmonary fibrosis (most serious)
Hypothyroidism or hyperthyroidism (contains iodine)
Liver toxicity (hepatotoxicity)
Blue-grey skin discoloration (photosensitivity)
Corneal microdeposits (usually asymptomatic)
Peripheral neuropathy
Teratogen - AVOID in pregnancy

Note: Cinchonism is NOT an amiodarone adverse effect (it belongs to quinidine).

Class IV - Non-Dihydropyridine Calcium Channel Blockers

Block L-type Ca2+ channels in SA/AV node → slow conduction, increase refractoriness

Drug	Uses
Verapamil	SVT, rate control in AF; AVOID with β-blockers (additive AV block)
Diltiazem	SVT, AF rate control

Contraindicated in accessory pathway tachycardias (e.g., WPW) and in combination with IV β-blockers.

Other Antiarrhythmics

Drug	Mechanism	Use
Adenosine	Opens K+ channels → hyperpolarizes AV node	Drug of choice for acute SVT; very short half-life (~10 sec)
Digoxin	Na+/K+ ATPase inhibitor; vagotonic effect	Rate control in AF; NOT for acute use
Magnesium sulfate	Stabilises membranes	Drug of choice for Torsades de Pointes
Ranolazine	Late Na+ current inhibitor	Antiarrhythmic + antianginal; prolongs QT

2. ANTIANGINAL DRUGS

Pathophysiology: Angina = imbalance between myocardial O2 supply and demand.

Goals of therapy: Reduce HR, preload, afterload, or increase coronary blood flow.

A. Nitrates

Mechanism: Metabolised to nitric oxide (NO) → activates guanylyl cyclase → ↑ cGMP → smooth muscle relaxation → venodilation (primarily) + arterial dilation

Reduces preload (venodilation) and afterload at higher doses
Net effect: reduces myocardial O2 demand
Also dilates coronary vessels → useful in vasospastic (Prinzmetal) angina

Drug	Route	Onset	Duration
Nitroglycerin (GTN)	Sublingual tablet/spray	1-3 min	30-60 min
Nitroglycerin	IV infusion	Immediate	During infusion
Nitroglycerin	Transdermal patch	30-60 min	8-12 hr (wear 12h, remove 12h)
Isosorbide dinitrate	Oral	15-30 min	4-6 hr
Isosorbide mononitrate	Oral	~30 min	6-8 hr

Adverse effects:

Headache (most common)
Postural hypotension, facial flushing, reflex tachycardia
Tolerance develops rapidly → provide nitrate-free interval of 10-12 hours (usually overnight; remove patch at night)
CONTRAINDICATED with PDE5 inhibitors (sildenafil, tadalafil) - dangerous hypotension
Exception: In variant angina, nitrate-free interval should be in the afternoon (not overnight), as attacks cluster in early morning

B. Beta-Blockers (for Angina)

Mechanism: ↓ HR, ↓ contractility → reduce myocardial O2 demand

Preferred in stable angina, post-MI
β1-selective agents preferred: atenolol, metoprolol
AVOID agents with ISA (e.g., pindolol) in angina
AVOID in vasospastic (Prinzmetal) angina - can worsen coronary spasm

C. Calcium Channel Blockers (for Angina)

Dihydropyridines (amlodipine, nifedipine, felodipine):

Primarily vasodilate peripheral arteries → reduce afterload
Reflex tachycardia with short-acting agents (especially nifedipine)
Adverse: peripheral oedema, flushing, headache
Drug of choice for Prinzmetal/vasospastic angina

Non-dihydropyridines (verapamil, diltiazem):

Reduce HR and contractility + vasodilate
AVOID combining with β-blockers (additive bradycardia/heart block)

D. Ranolazine

Mechanism: Inhibits late Na+ current (late INa) → reduces intracellular Na+ and Ca2+ overload → improves diastolic function and O2 supply-demand balance

Used when other antianginals have failed
Prolongs QT interval - avoid with other QT-prolonging drugs
Metabolised by CYP3A + CYP2D6; substrate of P-glycoprotein
Notable: antianginal effect less pronounced in women

3. DRUGS FOR HEART FAILURE

Key Drugs:

Drug Class	Examples	Mechanism	Role in HF
ACE Inhibitors	Enalapril, Lisinopril, Ramipril	Block ACE → ↓ Angiotensin II → ↓ vasoconstriction, ↓ aldosterone	First-line; reduce mortality; reduce preload + afterload
ARBs	Losartan, Valsartan, Candesartan	Block AT1 receptor	Use if ACE-I not tolerated (e.g., cough)
Beta-Blockers	Carvedilol, Metoprolol succinate, Bisoprolol	↓ sympathetic activation	Reduce mortality in HFrEF; START low, go slow
Mineralocorticoid Antagonists	Spironolactone, Eplerenone	Block aldosterone receptor → ↓ Na/H2O retention	Reduce mortality; risk of hyperkalemia
SGLT2 Inhibitors	Empagliflozin, Dapagliflozin	Glucose/sodium excretion; reduce preload	Reduce HF hospitalisation and mortality
ARNI	Sacubitril/Valsartan (Entresto)	Neprilysin inhibitor + ARB → ↑ natriuretic peptides	Superior to ACE-I in HFrEF
Diuretics	Furosemide (loop), Thiazides	Reduce fluid overload	Symptom relief (NOT mortality benefit)
Digoxin	Digoxin	Na+/K+ ATPase inhibition → ↑ intracellular Ca2+ → positive inotropy + vagotonic → slows AV conduction	Symptomatic benefit in AF + HF; narrow therapeutic index
Ivabradine	Ivabradine	If channel blocker → ↓ HR	HFrEF with HR >70 on max beta-blocker
Nitrates + Hydralazine		Vasodilation	For patients intolerant of ACE-I/ARB (especially African-American patients)

Digoxin toxicity signs:

Nausea, vomiting, anorexia
Visual disturbances (yellow-green halos)
Arrhythmias (bradycardia, heart block, VT)
Precipitated by: hypokalemia, hypomagnesemia, hypercalcemia, renal impairment, hypothyroidism
Treatment: Digoxin-specific antibody fragments (Fab); correct electrolytes

4. ANTIHYPERTENSIVE DRUGS

Classification by Mechanism

Class	Drugs	Key Notes
Thiazide diuretics	Hydrochlorothiazide, Chlorthalidone	First-line in most guidelines; cause hypokalemia, hyperglycemia, hyperuricemia
ACE Inhibitors	Lisinopril, Enalapril, Ramipril	First-line; contraindicated in pregnancy; cause dry cough (bradykinin accumulation)
ARBs	Losartan, Valsartan, Irbesartan	Better tolerated than ACE-I (no cough); contraindicated in pregnancy
Dihydropyridine CCBs	Amlodipine, Nifedipine	Effective + safe in elderly; useful if atherosclerotic angina coexists
Non-DHP CCBs	Verapamil, Diltiazem	Also rate-control in AF
Beta-Blockers	Metoprolol, Atenolol, Bisoprolol	Less preferred as monotherapy unless heart failure or post-MI
Alpha1-blockers	Prazosin, Doxazosin	Used in BPH + hypertension; risk of first-dose hypotension
Central alpha2 agonists	Methyldopa, Clonidine	Methyldopa: drug of choice in pregnancy
Direct vasodilators	Hydralazine, Minoxidil	Reserved for refractory cases; cause reflex tachycardia

Special situations:

Pregnancy: Methyldopa (safest), labetalol, nifedipine; AVOID ACE-I/ARBs (teratogenic)
Diabetes + HT: ACE-I or ARB (renoprotective)
HT + HF: ACE-I/ARB + beta-blocker + spironolactone
HT + asthma: AVOID beta-blockers; prefer CCBs
Isolated systolic HT in elderly: Thiazides or CCBs; beware of orthostatic hypotension
HT emergency: IV labetalol, IV nitroprusside, IV hydralazine (in pregnancy)

5. LIPID-LOWERING DRUGS

Class	Drugs	Mechanism	Primary Effect	Key ADRs
Statins (HMG-CoA reductase inhibitors)	Atorvastatin, Rosuvastatin, Simvastatin	Inhibit rate-limiting step of cholesterol synthesis → ↑ LDL receptors	↓↓ LDL (primary)	Myopathy/rhabdomyolysis, hepatotoxicity; AVOID in pregnancy
Fibrates	Fenofibrate, Gemfibrozil	Activate PPAR-α → ↑ LPL → ↑ TG clearance	↓↓ TG, ↑ HDL	Myopathy (especially with statins), gallstones
Niacin (Nicotinic acid)	Niacin	Inhibits VLDL synthesis in liver; inhibits lipolysis in adipose	↓ TG, ↓ LDL, ↑↑ HDL	Flushing (↓ with aspirin pretreatment), hyperglycemia, hyperuricemia, hepatotoxicity
Bile acid sequestrants	Cholestyramine, Colesevelam	Bind bile acids in gut → ↑ conversion of cholesterol to bile acids	↓ LDL	Constipation, bloating; impair absorption of fat-soluble vitamins and many drugs
Ezetimibe	Ezetimibe	Blocks NPC1L1 transporter → ↓ cholesterol absorption in intestine	↓ LDL	Generally well tolerated; modest effect alone
PCSK9 inhibitors	Alirocumab, Evolocumab	Monoclonal Ab → inhibit PCSK9 → prevent LDL receptor degradation → ↑ LDL uptake	↓↓↓ LDL	Injection site reactions; expensive
Omega-3 fatty acids	Icosapentaenoic acid (EPA)	Reduce hepatic VLDL production	↓ TG	Fish odour, GI upset

Statin important notes:

Most important drug class for cardiovascular risk reduction
Risk of myopathy increases with: high doses, renal failure, hypothyroidism, CYP3A4 inhibitors (e.g., azole antifungals, macrolides, grapefruit juice)
Simvastatin + gemfibrozil = high myopathy risk combination
Monitor: CK (if symptomatic), LFTs (baseline)

6. ANTICOAGULANTS & ANTIPLATELET DRUGS

Antiplatelet Drugs

Drug	Mechanism	Uses
Aspirin	Irreversibly inhibits COX-1 → ↓ TXA2 → ↓ platelet aggregation	ACS, secondary prevention of MI/stroke
Clopidogrel	ADP receptor (P2Y12) blocker (irreversible); prodrug requiring CYP2C19 activation	ACS, post-PCI (with aspirin = DAPT); less effective in poor CYP2C19 metabolisers
Ticagrelor	P2Y12 blocker (reversible); NOT a prodrug	ACS; dyspnoea as adverse effect
Prasugrel	P2Y12 blocker (irreversible prodrug); more potent than clopidogrel	ACS with PCI; AVOID in history of stroke/TIA or age >75
Abciximab, Tirofiban, Eptifibatide	GP IIb/IIIa receptor antagonists	IV; high-risk PCI
Dipyridamole	↑ cAMP in platelets (PDE inhibitor + adenosine uptake inhibitor)	Secondary stroke prevention (with aspirin)

Anticoagulants

Drug	Mechanism	Key Points
Heparin (UFH)	Activates antithrombin III → inactivates thrombin (IIa) + Xa	IV/SC; monitored by aPTT; antidote = protamine sulfate; HIT is a complication
LMWH (Enoxaparin, Dalteparin)	Preferentially inhibits Xa	SC; no routine monitoring; safer in pregnancy; antidote = protamine (partial)
Fondaparinux	Selective anti-Xa	SC; no HIT risk; antidote = none
Warfarin	Inhibits Vitamin K epoxide reductase → ↓ factors II, VII, IX, X (+ protein C, S)	Oral; monitored by INR; antidote = Vitamin K (slow) or FFP (fast); many drug/food interactions
Dabigatran	Direct thrombin (IIa) inhibitor	Oral DOAC; antidote = idarucizumab
Rivaroxaban, Apixaban, Edoxaban	Direct Factor Xa inhibitors	Oral DOACs; antidote = andexanet alfa

Heparin-induced thrombocytopenia (HIT):

Paradoxically causes THROMBOSIS (not just low platelets)
Stop all heparin immediately → switch to direct thrombin inhibitor (argatroban, bivalirudin)
Do NOT give warfarin or platelet transfusions initially

Quick Reference - Key Drug Interactions

Combination	Consequence
Nitrates + PDE5 inhibitors (sildenafil)	Severe hypotension - CONTRAINDICATED
Non-DHP CCB + Beta-blocker (IV)	Complete heart block
Statin + CYP3A4 inhibitors (azoles, macrolides)	↑ Myopathy risk
Statin + Gemfibrozil	High myopathy/rhabdomyolysis risk
ACE-I + ARB + spironolactone (triple)	Severe hyperkalemia
Warfarin + NSAIDs	↑ Bleeding risk
Amiodarone + warfarin	↑ INR; warfarin dose must be reduced
Digoxin + hypokalemia	↑ Digoxin toxicity

Memory Aids

Vaughan-Williams Classes: I=Na blocker, II=Beta-blocker, III=K blocker, IV=Ca blocker
Amiodarone toxicity: Think "THYROID, LIVER, LUNGS, SKIN, EYES, NERVES"
Nitrate tolerance: "Wear 12, bare 12"
TdP treatment: "Magnesium is the drug of choice"
HIT management: "Stop heparin, don't transfuse platelets, start direct thrombin inhibitor"
Pregnancy hypertension: "Methyl-dopa is safe for MOMS"
Heart failure quadruple therapy (HFrEF): ACE-I/ARB/ARNI + Beta-blocker + MRA + SGLT2i

Sources: Lippincott Illustrated Reviews: Pharmacology, 7th Ed.; Katzung's Basic and Clinical Pharmacology, 16th Ed.

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🫀 CVS Pharmacology — MBBS Notes

🟥 1. ANTIARRHYTHMIC DRUGS

Arrhythmia causes: Abnormal automaticity OR reentry circuits (unidirectional block + slow conduction)

⚡ Vaughan-Williams Classification

🟧 CLASS I — Sodium Channel Blockers (Phase 0 ↓)

Subclass	Action	Drugs	Key ADRs
IA	Slows Phase 0 + prolongs repolarization	Quinidine, Procainamide, Disopyramide	QT prolongation, TdP, anticholinergic
IB	Shortens Phase 3	Lidocaine, Mexiletine	CNS toxicity: tremor, seizures
IC	Markedly slows Phase 0	Flecainide, Propafenone	Proarrhythmic — AVOID in structural HD

🔶 Quinidine → Cinchonism (tinnitus, blurred vision, headache, psychosis) + hemolytic anaemia 🔶 Procainamide → Lupus-like syndrome, hypotension 🔶 Disopyramide → Strong anticholinergic — AVOID in elderly 🔶 Lidocaine → IV only; ventricular arrhythmias ONLY (no effect on atria) 🔶 Flecainide → Safe ONLY in patients WITHOUT structural heart disease 🔶 Propafenone → Weak β-blocker; AVOID in asthma

🟦 CLASS II — Beta-Blockers (Phase 4 ↓)

Reduce automaticity, prolong AV conduction, decrease HR + contractility

Drug	Selectivity	Notes
Metoprolol	β1	Most used; reduced bronchospasm risk
Propranolol	Non-selective	Also: thyrotoxicosis, migraine, tremor
Esmolol	β1	IV only, ultra-short acting
Atenolol	β1	Oral; renal elimination

💙 Uses: AF/flutter rate control, SVT, post-MI VT prevention 💙 ADRs: Bradycardia, fatigue, depression, blunted hypoglycaemia awareness, bronchospasm

🟪 CLASS III — Potassium Channel Blockers (Phase 3 ↑)

Prolong repolarization → prolong QT interval

Drug	Key Features
Amiodarone	Multi-channel blocker (I+II+III+IV); most effective; t½ = 40-55 days
Sotalol	Also has β-blocking activity; needs QT monitoring
Dofetilide	Pure K+ blocker; inpatient QT monitoring required to start
Dronedarone	Amiodarone analogue WITHOUT iodine; AVOID in severe HF + permanent AF

🔷 Amiodarone Toxicity — "THYROID, LUNGS, LIVER, SKIN, EYES, NERVES"

Pulmonary fibrosis (most serious)
Hypo/hyperthyroidism (has iodine)
Hepatotoxicity
Blue-grey skin + photosensitivity
Corneal microdeposits
Peripheral neuropathy
TERATOGEN — avoid in pregnancy

❗ Cinchonism = Quinidine — NOT amiodarone

🟩 CLASS IV — Non-DHP Calcium Channel Blockers

Block L-type Ca²⁺ in SA/AV node → slow conduction, increase refractoriness

Drug	Uses
Verapamil	SVT, AF rate control
Diltiazem	SVT, AF rate control

💚 AVOID combining with IV beta-blockers (complete heart block) 💚 AVOID in WPW syndrome

⬜ Other Antiarrhythmics

Drug	Mechanism	Use
Adenosine	Opens K+ channels → hyperpolarises AV node	DOC for acute SVT; t½ ~10 sec
Digoxin	Na+/K+ ATPase inhibitor; vagotonic	Rate control in AF + HF
Magnesium sulfate	Membrane stabiliser	DOC for Torsades de Pointes (TdP)
Ranolazine	Late Na+ current inhibitor	Antiarrhythmic + antianginal

🟨 2. ANTIANGINAL DRUGS

Angina = Myocardial O₂ demand > supply Goal: ↓ HR, ↓ preload, ↓ afterload → ↓ O₂ demand; OR ↑ coronary blood flow

💛 A. Nitrates

Mechanism: NO → ↑ cGMP → smooth muscle relaxation → venodilation (preload ↓) + arterial dilation at high doses

Drug	Route	Onset	Duration
Nitroglycerin (GTN)	Sublingual	1-3 min	30-60 min
Nitroglycerin	IV	Immediate	During infusion
Nitroglycerin	Transdermal patch	30-60 min	12 hr (wear)
Isosorbide dinitrate	Oral	15-30 min	4-6 hr
Isosorbide mononitrate	Oral	30 min	6-8 hr

🟡 ADRs: Headache (most common), flushing, postural hypotension, reflex tachycardia 🟡 Tolerance: Provide nitrate-free interval 10-12 hrs (usually overnight) 🟡 Patch rule: "Wear 12 hours, bare 12 hours" ⛔ CONTRAINDICATED with PDE5 inhibitors (sildenafil, tadalafil) — severe hypotension ⚠️ Variant/Prinzmetal angina: Nitrate-free interval in AFTERNOON, not overnight

💛 B. Beta-Blockers (Antianginal)

Reduce HR + contractility → ↓ myocardial O₂ demand
Preferred in stable angina + post-MI
β1-selective preferred: Atenolol, metoprolol
AVOID agents with ISA (pindolol) — don't reduce resting HR
⛔ AVOID in Prinzmetal angina — worsen coronary spasm

💛 C. Calcium Channel Blockers (Antianginal)

Dihydropyridines (DHP): Amlodipine, Nifedipine, Felodipine

Peripheral arterial vasodilation → ↓ afterload
Short-acting (nifedipine) → reflex tachycardia
ADRs: Peripheral oedema, flushing, headache
✅ Drug of choice for Prinzmetal/vasospastic angina

Non-DHP: Verapamil, Diltiazem

↓ HR + contractility + vasodilation
⛔ AVOID combining with beta-blockers

💛 D. Ranolazine

Inhibits late Na+ current → ↓ intracellular Na+ and Ca²+ → improves diastolic function
Use when other antianginals have failed
Prolongs QT — avoid with other QT-prolonging drugs
Metabolised by CYP3A + CYP2D6
Antianginal effect less pronounced in women

🟦 3. DRUGS FOR HEART FAILURE

Drug Class	Examples	Mechanism	Notes
ACE Inhibitors	Enalapril, Lisinopril, Ramipril	↓ Ang II → ↓ vasoconstriction + aldosterone	First-line; reduce mortality; cough (bradykinin)
ARBs	Losartan, Valsartan	Block AT1 receptor	Use if ACE-I not tolerated
Beta-Blockers	Carvedilol, Metoprolol succinate, Bisoprolol	↓ sympathetic activation	Reduce mortality in HFrEF; start low, go slow
MRA	Spironolactone, Eplerenone	Block aldosterone	Reduce mortality; risk of hyperkalemia
SGLT2i	Empagliflozin, Dapagliflozin	Natriuresis + other cardioprotective effects	Reduce HF hospitalisation + mortality
ARNI	Sacubitril/Valsartan	Neprilysin inhibitor + ARB → ↑ natriuretic peptides	Superior to ACE-I in HFrEF
Loop diuretics	Furosemide	↓ fluid overload	Symptom relief only — NO mortality benefit
Digoxin	Digoxin	Na+/K+ ATPase inhibition → +inotropy + vagotonic	Narrow TI; symptomatic benefit in AF + HF
Ivabradine	Ivabradine	If channel blocker → ↓ HR	HFrEF + HR >70 despite max beta-blocker
Nitrates + Hydralazine		Venodilation + arterial dilation	When ACE-I/ARB not tolerated

💙 HFrEF Quadruple Therapy: ACE-I/ARB/ARNI + Beta-blocker + MRA + SGLT2i

🔵 Digoxin Toxicity

Nausea, vomiting, anorexia
Yellow-green visual halos
Arrhythmias (bradycardia, heart block, VT)
Precipitated by: Hypokalemia ⭐, hypomagnesemia, hypercalcemia, renal failure
Treatment: Digoxin-specific Fab antibodies; correct electrolytes

🟩 4. ANTIHYPERTENSIVE DRUGS

Class	Drugs	Key Notes
Thiazides	HCTZ, Chlorthalidone	First-line; cause hypokalemia, hyperglycemia, hyperuricemia
ACE Inhibitors	Lisinopril, Enalapril	First-line; dry cough; ⛔ pregnancy
ARBs	Losartan, Valsartan	No cough; ⛔ pregnancy
DHP CCBs	Amlodipine, Nifedipine	Effective in elderly + atherosclerotic angina
Non-DHP CCBs	Verapamil, Diltiazem	Rate control in AF too
Beta-Blockers	Metoprolol, Bisoprolol	Less preferred unless HF/post-MI
Alpha1-blockers	Prazosin, Doxazosin	Also useful in BPH; first-dose hypotension
Central α2 agonists	Methyldopa, Clonidine	Methyldopa = DOC in pregnancy
Direct vasodilators	Hydralazine, Minoxidil	Refractory HT; reflex tachycardia

💚 Special Situations

🤰 Pregnancy: Methyldopa, labetalol, nifedipine — ⛔ AVOID ACE-I/ARBs
🩺 Diabetes + HT: ACE-I or ARB (renoprotective)
❤️ HT + HF: ACE-I + beta-blocker + spironolactone
🌬️ HT + asthma: ⛔ AVOID beta-blockers → use CCBs
👴 Elderly isolated systolic HT: Thiazides or CCBs; beware orthostatic hypotension
🚨 HT emergency: IV labetalol, IV nitroprusside, IV hydralazine (in pregnancy)

🟪 5. LIPID-LOWERING DRUGS

Class	Drugs	Mechanism	Primary Effect	Key ADRs
Statins	Atorvastatin, Rosuvastatin	Inhibit HMG-CoA reductase → ↑ LDL receptors	↓↓ LDL	Myopathy/rhabdomyolysis, hepatotoxicity; ⛔ pregnancy
Fibrates	Fenofibrate, Gemfibrozil	PPAR-α activation → ↑ LPL → ↑ TG clearance	↓↓ TG, ↑ HDL	Myopathy (esp. with statins), gallstones
Niacin	Nicotinic acid	Inhibit VLDL synthesis + lipolysis	↓ TG, ↑↑ HDL	Flushing (↓ with aspirin); hyperglycemia, hyperuricemia
Bile acid sequestrants	Cholestyramine, Colesevelam	Bind bile acids → ↑ cholesterol → bile conversion	↓ LDL	Constipation; impair absorption of fat-soluble vitamins
Ezetimibe	Ezetimibe	Block NPC1L1 → ↓ intestinal cholesterol absorption	↓ LDL	Well tolerated; modest effect alone
PCSK9 inhibitors	Alirocumab, Evolocumab	Monoclonal Ab → ↑ LDL receptor availability	↓↓↓ LDL	Injection site reactions

🟣 Statin myopathy risk increases with: High dose, renal failure, hypothyroidism, CYP3A4 inhibitors (azoles, macrolides, grapefruit juice) ⛔ Simvastatin + Gemfibrozil = high rhabdomyolysis risk

🟥 6. ANTIPLATELET & ANTICOAGULANT DRUGS

❤️ Antiplatelets

Drug	Mechanism	Uses
Aspirin	Irreversible COX-1 inhibitor → ↓ TXA2	ACS, MI/stroke secondary prevention
Clopidogrel	P2Y12 (ADP) blocker — irreversible prodrug	ACS, post-PCI (DAPT with aspirin)
Ticagrelor	P2Y12 blocker — reversible, NOT a prodrug	ACS; ADR: dyspnoea
Prasugrel	P2Y12 blocker — irreversible prodrug; more potent	ACS + PCI; ⛔ prior stroke/TIA, age >75
GP IIb/IIIa inhibitors	Abciximab, Tirofiban, Eptifibatide	IV; high-risk PCI
Dipyridamole	↑ cAMP (PDE inhibitor)	Secondary stroke prevention (+ aspirin)

🔴 Anticoagulants

Drug	Mechanism	Monitoring	Antidote
Heparin (UFH)	Activates antithrombin III → inactivates IIa + Xa	aPTT	Protamine sulfate
LMWH (Enoxaparin)	Preferentially inhibits Xa	Usually none	Protamine (partial)
Fondaparinux	Selective anti-Xa	None	None
Warfarin	Inhibits Vit K epoxide reductase → ↓ II, VII, IX, X	INR	Vit K (slow) or FFP (fast)
Dabigatran	Direct thrombin (IIa) inhibitor	None	Idarucizumab
Rivaroxaban/Apixaban	Direct Factor Xa inhibitors	None	Andexanet alfa

🚨 HIT (Heparin-Induced Thrombocytopenia)

Paradoxical thrombosis (not just low platelets)
Stop ALL heparin immediately
Switch to direct thrombin inhibitor (argatroban, bivalirudin)
⛔ Do NOT give warfarin or platelet transfusions initially

⭐ KEY INTERACTIONS — Red Flag Summary

Combination	Problem
🔴 Nitrates + Sildenafil/Tadalafil	Severe hypotension — CONTRAINDICATED
🔴 Non-DHP CCB + IV Beta-blocker	Complete heart block
🔴 Statin + CYP3A4 inhibitors	↑ Myopathy risk
🔴 Simvastatin + Gemfibrozil	Rhabdomyolysis
🔴 ACE-I + ARB + Spironolactone	Severe hyperkalemia
🔴 Warfarin + NSAIDs	↑ Bleeding
🔴 Amiodarone + Warfarin	↑ INR — reduce warfarin dose
🔴 Digoxin + Hypokalemia	Digoxin toxicity

🧠 Memory Aids

Mnemonic	Meaning
I-II-III-IV	Na blocker / Beta-blocker / K blocker / Ca blocker
"Wear 12, bare 12"	Nitrate tolerance — patch on 12h, off 12h
"Mg for TdP"	Magnesium sulfate is DOC for Torsades de Pointes
"Methyldopa for Moms"	DOC for hypertension in pregnancy
ARNI > ACE-I	Sacubitril/valsartan is superior in HFrEF
HIT = Thrombosis, not just ↓ platelets	Stop heparin, start argatroban
Quad therapy in HFrEF	ARNI + Beta-blocker + MRA + SGLT2i

Sources: Lippincott Illustrated Reviews: Pharmacology, 7th Ed. | Katzung's Basic & Clinical Pharmacology, 16th Ed.

In diagramatic and image form

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Medical study diagram: Vaughan-Williams Antiarrhythmic Drug Classification. Colorful educational poster for MBBS students. Show a cardiac action potential curve with phases 0-4 labeled. Four colored boxes arranged around it: RED box (Class I - Na+ Channel Blockers) listing IA: Quinidine/Procainamide/Disopyramide, IB: Lidocaine/Mexiletine, IC: Flecainide/Propafenone with their mechanisms. BLUE box (Class II - Beta Blockers) listing Metoprolol/Propranolol/Esmolol. PURPLE box (Class III - K+ Channel Blockers) listing Amiodarone/Sotalol/Dofetilide/Dronedarone. GREEN box (Class IV - Ca2+ Channel Blockers) listing Verapamil/Diltiazem. ORANGE box (Others) listing Adenosine/Digoxin/Magnesium. Each box shows mechanism and key adverse effects. Clean white background, bold colored headers, clear medical illustration style.

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Medical study diagram: Antianginal Drugs visual summary poster for MBBS students. Central heart diagram showing coronary arteries. Three main branches radiating out with colored sections: YELLOW section - Nitrates (Nitroglycerin/Isosorbide), mechanism: NO→cGMP→venodilation, reduces preload, adverse effects: headache, tolerance, contraindicated with PDE5 inhibitors, nitrate-free interval 10-12hrs. BLUE section - Beta Blockers (Atenolol/Metoprolol), mechanism: reduce HR and contractility, avoid in Prinzmetal angina. GREEN section - Calcium Channel Blockers showing DHP (Amlodipine/Nifedipine) for vasospastic angina and Non-DHP (Verapamil/Diltiazem). ORANGE box - Ranolazine: late Na+ current inhibitor, last resort drug, prolongs QT. Arrows showing O2 supply vs demand balance. Clean colorful medical poster style.

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Medical study diagram: Heart Failure Drug Treatment poster for MBBS students. Central illustration of a failing heart (dilated, weak). Surrounding it in a circular arrangement with colored drug class boxes with connecting arrows to the heart: BLUE - ACE Inhibitors (Enalapril/Lisinopril/Ramipril): blocks Ang II, reduces preload+afterload, causes cough. CYAN - ARBs (Losartan/Valsartan): use if ACE-I not tolerated. RED - Beta Blockers (Carvedilol/Metoprolol/Bisoprolol): reduce sympathetic activation, start low go slow. PURPLE - MRA/Spironolactone: blocks aldosterone, risk of hyperkalemia. ORANGE - SGLT2 inhibitors (Empagliflozin): reduce hospitalisation. GREEN - ARNI Sacubitril/Valsartan: superior to ACE-I. YELLOW - Furosemide loop diuretic: symptom relief only. BROWN - Digoxin: narrow therapeutic index, watch for toxicity. Bottom banner: HFrEF Quadruple Therapy = ARNI + Beta-blocker + MRA + SGLT2i. Clean colorful educational medical poster.

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Medical study diagram: Antihypertensive Drugs classification poster for MBBS students. Large blood pressure gauge in center. Eight colored sections radiating outward like a wheel/pie chart: RED - Thiazides (HCTZ): first line, causes hypokalemia/hyperglycemia/hyperuricemia. BLUE - ACE Inhibitors (Lisinopril): dry cough, avoid in pregnancy. CYAN - ARBs (Losartan): no cough, avoid in pregnancy. GREEN - DHP Calcium Channel Blockers (Amlodipine): good in elderly. ORANGE - Beta Blockers (Metoprolol): avoid in asthma. PURPLE - Alpha blockers (Prazosin): also for BPH, first dose hypotension. PINK - Central alpha2 agonists (Methyldopa): DRUG OF CHOICE IN PREGNANCY. YELLOW - Direct vasodilators (Hydralazine/Minoxidil): refractory cases. Special situations box: pregnancy=methyldopa, diabetes=ACEi/ARB, asthma=CCB, HF=ACEi+BBlocker. Clean colorful medical educational poster style.

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Medical study diagram: Lipid Lowering Drugs and Antiplatelet/Anticoagulant drugs poster for MBBS students. TOP HALF - Lipid lowering: cholesterol biosynthesis pathway with statin blocking HMG-CoA reductase step (labeled red X). Table showing: Statins (Atorvastatin/Rosuvastatin): reduce LDL, myopathy risk. Fibrates (Fenofibrate): reduce TG, increase HDL. Niacin: increase HDL most. Ezetimibe: blocks NPC1L1 in intestine. PCSK9 inhibitors: monoclonal antibodies. BOTTOM HALF - Anticoagulation: coagulation cascade diagram showing intrinsic and extrinsic pathways converging. Color coded drug mechanisms: Heparin/LMWH blocking Factor Xa and IIa via antithrombin. Warfarin blocking Vitamin K factors II VII IX X. Dabigatran direct thrombin inhibitor. Rivaroxaban/Apixaban direct Xa inhibitors. Antiplatelet section: Aspirin blocks COX-1/TXA2. Clopidogrel/Ticagrelor blocks P2Y12 ADP receptor. GP IIb/IIIa inhibitors. Antidotes listed: Protamine for heparin, Vit K/FFP for warfarin, Idarucizumab for dabigatran, Andexanet alfa for Xa inhibitors. Clean educational medical diagram.

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Medical study diagram: Amiodarone Toxicity and Antiarrhythmic Special Notes visual summary for MBBS students. Central large pill/tablet labeled AMIODARONE. Six organ silhouettes around it with red arrows and warning signs showing toxicity: LUNGS (silhouette) - Pulmonary fibrosis (most serious). THYROID (silhouette) - Hypo/Hyperthyroidism (contains iodine). LIVER (silhouette) - Hepatotoxicity. SKIN (silhouette) - Blue-grey discoloration, photosensitivity. EYE (silhouette) - Corneal microdeposits. NERVE (silhouette) - Peripheral neuropathy. PREGNANT WOMAN icon with red X - Teratogen. Bottom section - separate colored boxes: GREEN box: Torsades de Pointes (TdP) = IV Magnesium Sulfate is DOC. BLUE box: Adenosine = DOC for acute SVT, half-life 10 seconds. RED box: Lidocaine = ventricular arrhythmias ONLY (no effect on atria). ORANGE box: Flecainide = ONLY use in patients WITHOUT structural heart disease. Bold colorful medical educational poster style.

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Medical study diagram: CVS Pharmacology Key Drug Interactions and Memory Aids cheat sheet poster for MBBS students. Red danger warning section at top titled DANGEROUS COMBINATIONS with red warning symbols: Nitrates + Sildenafil = Severe Hypotension (CONTRAINDICATED). Non-DHP CCB + IV Beta-blocker = Complete Heart Block. Simvastatin + Gemfibrozil = Rhabdomyolysis. ACEi + ARB + Spironolactone = Severe Hyperkalemia. Amiodarone + Warfarin = Increased INR. Digoxin + Hypokalemia = Digoxin Toxicity. Middle section - MEMORY AIDS with colorful icons: Clock icon: Wear 12, Bare 12 (nitrate tolerance). Magnet icon: Mg for TdP. Baby icon: Methyldopa for Moms (pregnancy hypertension). Four connected boxes: HFrEF Quadruple Therapy = ARNI + Beta-blocker + MRA + SGLT2i. HIT section with warning: Stop heparin, No platelets, Start Argatroban. Bottom: Antidote table: Heparin=Protamine, Warfarin=VitK/FFP, Dabigatran=Idarucizumab, Xa inhibitors=Andexanet alfa. Clean colorful cheat sheet style medical poster.

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