CVS & Renal – Pharmacology · FCPS Part 1

🫀 What determines blood pressure?

BP = CO × SVR

And:

CO = HR × SV

So we can lower BP by:

↓ Heart rate
↓ Contractility
↓ Blood volume
↓ SVR
↓ RAAS activity

That gives us our drug classes:

Target	Drug classes
↓ Blood volume	Diuretics
↓ HR/contractility	β-blockers
↓ SVR	α₁ blockers, CCBs, vasodilators
↓ Ang II	ACE inhibitors, ARBs
↓ sympathetic activity	α₂ agonists

MASTER DIURETIC TABLE

Class	Site	Target	K⁺	Ca²⁺	Classic use
Acetazolamide	PCT	Carbonic anhydrase	↓	—	Altitude sickness, glaucoma
Mannitol	PCT/descending limb	Osmotic	—	—	⭐ Raised ICP
Loop	Thick ascending limb	NKCC2	↓	↓	⭐ Pulmonary edema
Thiazide	DCT	Na⁺/Cl⁻	↓	↑	⭐ Hypertension
Spironolactone	Collecting duct	Aldosterone receptor	↑	—	HF, hyperaldosteronism
Eplerenone	Collecting duct	Aldosterone receptor	↑	—	HF
Amiloride	Collecting duct	ENaC	↑	—	K⁺ sparing
Triamterene	Collecting duct	ENaC	↑	—	K⁺ sparing

Antihypertensive drugs

Drug class	Mechanism	Important adverse effects
ACE inhibitors	Reduce angiotensin II and aldosterone	Cough, hyperkalemia, angioedema
ARBs	Block AT₁ receptors	Hyperkalemia; less cough than ACE inhibitors
Thiazide diuretics	Inhibit NaCl reabsorption in distal convoluted tubule	Hyponatremia, hypokalemia, hyperuricemia
Loop diuretics	Inhibit NKCC2 in thick ascending limb	Hypokalemia, ototoxicity, volume depletion
Calcium channel blockers	Block L-type calcium channels	Dihydropyridines: edema; verapamil: constipation/bradycardia
β blockers	Reduce sympathetic cardiac effects	Bradycardia, fatigue; bronchospasm with nonselective agents
α₁ blockers	Reduce peripheral vascular resistance	Orthostatic hypotension
Central α₂ agonists	Reduce sympathetic outflow	Sedation, dry mouth; rebound hypertension with abrupt clonidine withdrawal

Common clinical choices

Condition	Common drug groups
Hypertension	ACE inhibitors/ARBs, calcium channel blockers, thiazide-type diuretics
Heart failure with reduced ejection fraction	Evidence-based β blocker, ACE inhibitor/ARB/ARNI, mineralocorticoid receptor antagonist, SGLT2 inhibitor
Hypertension with albuminuric CKD	ACE inhibitor or ARB when appropriate
Pregnancy-related hypertension	Labetalol, nifedipine or methyldopa in appropriate circumstances

Diuretics

ACE vs ARB

	ACE inhibitor	ARB
Example	Lisinopril	Losartan
Target	ACE	AT₁ receptor
↓ Ang II	Yes	Blocks its action
Bradykinin	↑	No major increase
Cough	Yes	Much less
Angioedema	Yes	Much less
Hyperkalemia	Yes	Yes
Creatinine ↑	Yes	Yes
Pregnancy	❌	❌

Class	Site/action	Important adverse effects
Loop — furosemide	NKCC2 inhibition	Hypokalemia, hypocalcemia, volume depletion
Thiazide — hydrochlorothiazide	NaCl cotransporter inhibition	Hypokalemia, hyperuricemia, hyperglycemia
Potassium-sparing — spironolactone	Aldosterone receptor blockade	Hyperkalemia, gynecomastia
Potassium-sparing — amiloride	ENaC blockade	Hyperkalemia
Carbonic anhydrase inhibitor — acetazolamide	Proximal bicarbonate reabsorption inhibition	Metabolic acidosis, renal stones
Osmotic — mannitol	Raises tubular fluid osmolality	Fluid shifts, possible pulmonary edema

Electrolyte memory table

Diuretic	Potassium	Calcium
Loop	Decreases	Urinary calcium increases
Thiazide	Decreases	Urinary calcium decreases
Spironolactone	Increases	No major class-defining effect

MCQ tip: Thiazides reduce urinary calcium excretion; loop diuretics increase it.

Dihydropyridines vs Non Dihydropyridines

	Dihydropyridines	Non-DHP
Examples	Amlodipine, nifedipine	Verapamil, diltiazem
Main target	Blood vessels	Heart
Vasodilation	⭐⭐⭐⭐⭐	Moderate
↓ HR	Minimal/reflex ↑	⭐⭐⭐⭐⭐
↓ contractility	Minimal	⭐⭐⭐⭐⭐
↓ AV conduction	Minimal	⭐⭐⭐⭐⭐
Main use	Hypertension	Arrhythmias, angina

Calcium channel blockers

Drug	Class	Main action	Classic adverse effect
Amlodipine	DHP	Vasodilation	⭐ Peripheral edema
Nifedipine	DHP	Vasodilation	Flushing, edema, gingival enlargement
Verapamil	Non-DHP	↓ HR + AV conduction	⭐ Constipation
Diltiazem	Non-DHP	↓ HR + AV conduction	Bradycardia

Beta Blockers

Drug	Receptor action	High-yield association
Propranolol	β₁ + β₂	⭐ Migraine, tremor, hyperthyroidism
Metoprolol	β₁ selective	⭐ Heart disease/HF
Atenolol	β₁ selective	Hypertension
Bisoprolol	β₁ selective	⭐ HFrEF
Carvedilol	β₁ + β₂ + α₁	⭐ HFrEF
Labetalol	β₁ + β₂ + α₁	⭐ Pregnancy hypertension
Esmolol	β₁ selective	⭐ Very short acting
Timolol	β₁ + β₂	⭐ Glaucoma

Alpha Blockers

Drug	Mechanism	Classic association
Prazosin	α₁ blocker	First-dose orthostatic hypotension
Tamsulosin	α₁A blocker	⭐ BPH
Clonidine	Central α₂ agonist	Rebound HTN if stopped abruptly
Methyldopa	Central α₂ agonist	⭐ Pregnancy
Hydralazine	Direct arteriolar vasodilator	⭐ Drug-induced lupus
Minoxidil	K⁺ channel opener	⭐ Hypertrichosis
Nitroprusside	NO donor	⭐ Hypertensive emergency + cyanide toxicity

ANTIANGINAL

Drug	Main mechanism	Key association
Nitroglycerin	NO → ↑cGMP → venodilation	⭐ Acute angina
Isosorbide dinitrate	NO donor	Chronic angina
β-blockers	↓ HR + ↓ contractility	⭐ Stable angina
Amlodipine	Vasodilation	Angina + HTN
Verapamil	↓ HR + contractility	Angina
Diltiazem	↓ HR + vasodilation	Angina
Ranolazine	↓ late Na⁺ current	⭐ QT prolongation

HEART FAILURE TABLE

Drug/class	Main action	Major association
ACE inhibitors	↓ Ang II	↓ remodeling, mortality benefit
Sacubitril/valsartan	↑ natriuretic peptides + ↓ Ang II	⭐ ARNI
β-blockers	↓ sympathetic effects	⭐ HFrEF survival
Spironolactone/eplerenone	↓ aldosterone	⭐ Hyperkalemia
SGLT2 inhibitors	↑ glucose/Na⁺ excretion	⭐ HFrEF
Furosemide	Powerful diuresis	⭐ Pulmonary edema/congestion
Digoxin	↑ contractility + ↑ vagal tone	⭐ Toxicity/AF
Ivabradine	↓ SA node If current	↓ HR
Hydralazine + nitrate	↓ afterload + preload	Selected HFrEF

Anti Arrhymic

Class	Main target	Important drugs	Key association
IA	Na⁺ + K⁺	Quinidine, procainamide	QT ↑
IB	Na⁺	Lidocaine	Ventricular arrhythmias
IC	Na⁺	Flecainide, propafenone	Strong conduction slowing
II	β-blockers	Metoprolol, esmolol	↓ AV conduction
III	K⁺	Amiodarone, sotalol	QT ↑
IV	Ca²⁺	Verapamil, diltiazem	↓ AV conduction

ANTITHROMBOTIC TABLE

Drug	Target	Monitoring	Antidote/reversal
Aspirin	COX-1 → ↓ TXA₂	—	—
Clopidogrel	P2Y12	—	—
Ticagrelor	P2Y12	—	—
Heparin	↑ Antithrombin → IIa/Xa	aPTT	Protamine
Enoxaparin	↑ Antithrombin → Xa>IIa	Usually none routinely	Protamine partial
Warfarin	↓ Vit K-dependent factors	PT/INR	Vitamin K/PCC
Dabigatran	IIa	—	Idarucizumab
Apixaban	Xa	—	Andexanet alfa / PCC depending on setting
Rivaroxaban	Xa	—	Andexanet alfa / PCC depending on setting

Anticoagulants and antiplatelet drugs

Feature	Heparin	Warfarin	Aspirin
Drug class	Anticoagulant	Anticoagulant	Antiplatelet
Mechanism	Enhances antithrombin → inhibits thrombin and Xa	Inhibits vitamin K recycling → decreases functional II, VII, IX, X	Irreversibly inhibits platelet COX-1 → ↓ TXA₂
Route	UFH IV; LMWH usually SC	Oral	Oral
Onset	Rapid with UFH	Delayed; full effect takes several days	Platelet effect begins within hours
Monitoring	aPTT for UFH; anti-Xa in selected situations	PT/INR	No routine coagulation monitoring
Reversal / management	Protamine reverses UFH; partially reverses LMWH	Vitamin K; PCC for urgent reversal, with other measures as indicated	No specific antidote; platelet transfusion may be considered in selected severe bleeding
Major association	HIT	Skin necrosis, teratogenicity	GI bleeding; Reye syndrome association in children

Heparin-induced thrombocytopenia (HIT) is important because it causes thrombocytopenia with a paradoxically increased risk of thrombosis.

Warfarin pearl: Early reduction in protein C can contribute to a transient procoagulant state, explaining the risk of skin necrosis.

Dental relevance

Low-dose aspirin is often continued for routine dental procedures; stopping antiplatelet therapy without medical advice can increase thrombotic risk.
For patients on warfarin, assess INR and procedure-specific bleeding risk rather than stopping treatment automatically.
Patients taking anticoagulants or with liver disease may require coordination with the treating clinician.
Local haemostatic measures include pressure, suturing, haemostatic materials and tranexamic acid where appropriate.