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TOPIC-WISE PHARMACOLOGY ANSWERS

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TOPIC 1: ANTIHYPERTENSIVE DRUGS

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1A. Beta-Blockers: Propranolol vs Atenolol (Compare pharmacological effects)

• Reduce cardiac output (negative chronotropy + inotropy)
• Inhibit renin secretion from JG cells (reducing Angiotensin II and aldosterone)
• Central sympatholytic effect (propranolol more)
• Reduction in peripheral vascular resistance (long-term)

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1B. Antihypertensive Action of Propranolol

1. Reduces cardiac output - block β1 receptors on heart → decreased heart rate and force of contraction
2. Inhibits renin release - block β1 receptors on JG cells of kidney → less Angiotensin II → less vasoconstriction and aldosterone
3. Central action - reduces sympathetic outflow (especially propranolol due to lipophilicity)
4. Presynaptic β2 blockade - reduces norepinephrine release
5. Long-term: reset baroreceptors, reduce TPR

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1C. Antihypertensive Action of Captopril / Lisinopril (ACE Inhibitors)

• Inhibit Angiotensin Converting Enzyme (ACE/kininase II)
• ACE normally converts Angiotensin I → Angiotensin II (potent vasoconstrictor) and inactivates bradykinin
• ACE inhibition → ↓Angiotensin II → vasodilation + ↓aldosterone → Na/water retention decreases
• Bradykinin accumulation → vasodilation + prostaglandin release

• Reduce TPR (arterial + venous dilation)
• Reduce preload and afterload → useful in heart failure
• Renoprotective (reduce glomerular filtration pressure)
• No reflex tachycardia

• Dry, persistent cough (bradykinin accumulation - most common)
• Angioedema (rare but dangerous)
• Hyperkalemia
• First-dose hypotension
• Teratogenic (contraindicated in pregnancy)
• Renal failure in bilateral renal artery stenosis

• Reduces preload and afterload
• Prevents cardiac remodeling
• Reduces mortality in CCF
• Combined with diuretics and digoxin

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1D. Antihypertensive Action of Amlodipine (Calcium Channel Blockers)

• Blocks L-type voltage-gated Ca²+ channels in vascular smooth muscle and myocardium
• Reduces intracellular Ca²+ → smooth muscle relaxation → vasodilation
• Primarily acts on peripheral arterioles → reduces TPR → lowers BP

• Dihydropyridine class (vascular selective)
• Long half-life (35-50 hrs) - once daily dosing
• No significant negative chronotropy/inotropy
• No reflex tachycardia (unlike nifedipine)

• Peripheral edema (ankle edema - most common)
• Flushing, headache
• Gingival hyperplasia
• Reflex tachycardia (mild)

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1E. Prazosin - Antihypertensive Action & Other Uses

• Selective α1-adrenergic receptor blocker
• Blocks post-synaptic α1 receptors on arterioles and veins
• Reduces TPR → lowers BP
• Does NOT block pre-synaptic α2 receptors → no reflex tachycardia (unlike non-selective alpha blockers)

• Benign prostatic hyperplasia (BPH) - relaxes urethral smooth muscle
• Pheochromocytoma
• Raynaud's disease
• Congestive heart failure (reduces afterload)

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1F. Antihypertensive Action of Thiazide & Prevention of Hypokalemia

• Inhibit Na-Cl cotransporter (NCC) in early distal tubule
• Initially: reduce blood volume → ↓CO
• Long-term: reduce TPR (unknown exact mechanism, possibly Ca²+ channel effect)

• Increased Na+ delivery to collecting duct → aldosterone-mediated K+ and H+ secretion → K+ loss in urine

• K+ supplements (oral KCl)
• K+ sparing diuretics (spironolactone, amiloride, triamterene)
• Diet rich in K+ (fruits, vegetables)
• Use of ACE inhibitors with thiazide (synergistic antihypertensive + opposing K+ effects)

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1G. Antihypertensives Safe in Bronchial Asthma

• Calcium channel blockers (Amlodipine, Nifedipine) - FIRST CHOICE
• ACE inhibitors / ARBs (but ACE inhibitors can cause cough - use ARBs preferably)
• Alpha-blockers (Prazosin, Doxazosin)
• Diuretics (Thiazides, Furosemide)
• Methyldopa
• Cardioselective β1 blockers (Atenolol, Metoprolol) - use with caution, not first-line

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1H. Losartan - Adverse Effects & Contraindications

• Hyperkalemia
• Hypotension (first dose)
• Renal impairment
• Dizziness
• Fatigue
• Unlike ACE inhibitors: NO DRY COUGH (no bradykinin effect)
• No angioedema (unlike ACE inhibitors)

• Pregnancy (teratogenic - renal tubular dysgenesis, oligohydramnios)
• Bilateral renal artery stenosis
• Hyperkalemia
• Severe renal failure

• Blocks AT1 receptors → reduces vasoconstriction, aldosterone secretion
• Reduces cardiac remodeling
• Used as alternative when ACE inhibitor-induced cough is intolerable

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1I. Drugs Acting on Angiotensin-II Receptor / Antihypertensives Blocking Ca++ Channel

• Losartan, Valsartan, Irbesartan, Olmesartan, Candesartan, Telmisartan

• Dihydropyridines: Amlodipine, Nifedipine, Felodipine, Nicardipine (vascular selective)
• Phenylalkylamines: Verapamil (cardiac + vascular)
• Benzothiazepines: Diltiazem (cardiac + vascular)

• HTN, angina, arrhythmias (verapamil/diltiazem), Raynaud's disease

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1J. Methyldopa - Indications & Side Effects

• Hypertension in pregnancy (DRUG OF CHOICE)
• Hypertensive emergencies

• Sedation, drowsiness
• Positive Coombs test (hemolytic anemia)
• Hepatotoxicity
• Lupus-like syndrome
• Nasal stuffiness
• Postural hypotension
• Sexual dysfunction

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1K. Design Therapeutic Approach to Hypertension

• Salt restriction (<6g/day)
• Weight reduction
• Regular exercise
• Reduce alcohol, quit smoking
• DASH diet

• First-line: Thiazide diuretics, ACE inhibitors, ARBs, CCBs
• Special situations:
  • Diabetes: ACE inhibitor or ARB (renoprotective)
  • Heart failure: ACE inhibitor + beta-blocker + spironolactone
  • Asthma: CCB (avoid beta-blockers)
  • Post-MI: Beta-blocker + ACE inhibitor
  • Pregnancy: Methyldopa, Nifedipine, Hydralazine (avoid ACE inhibitors/ARBs)
  • Black patients: Thiazide or CCB preferred

• Add second, then third agent from different classes
• Resistant HTN: Add spironolactone

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TOPIC 2: ANTIARRHYTHMIC DRUGS

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2A. Verapamil - Antiarrhythmic Effects

• Blocks L-type Ca²+ channels → slows depolarization of SA and AV nodes
• SA node: reduces automaticity (rate of spontaneous depolarization)
• AV node: prolongs refractory period, slows conduction (increases PR interval)

1. SVT (Supraventricular Tachycardia) - drug of choice for paroxysmal SVT
2. Atrial flutter and fibrillation - rate control (slows ventricular response)
3. AV nodal re-entry tachycardia (AVNRT)

• Bradycardia, heart block
• Constipation (most common GI effect)
• Negative inotropy - avoid in heart failure
• Peripheral edema, hypotension
• Contraindication with beta-blockers (additive AV block + negative inotropy)
• Contraindicated in WPW syndrome (can accelerate accessory pathway conduction)

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2B. Digoxin - Role in CCF, Toxicity, Adverse Effects

• Inhibits Na+/K+ ATPase pump on cardiac myocyte membrane
• Raises intracellular Na+ → less Na+/Ca²+ exchange → intracellular Ca²+ rises → increased contractility (positive inotropy)
• Also: Vagomimetic action → slows AV conduction (rate control in AF)

• Increases cardiac output (positive inotropy)
• Slows heart rate (vagal effect)
• Reduces preload (indirectly via improved CO)
• Mainly used when CCF coexists with atrial fibrillation
• Combination: Digoxin + ACE inhibitor + diuretic + spironolactone

• Cardiac: AV block, PAT with block, ventricular extrasystoles, VT, VF, bradycardia, bigeminy
• GI: Nausea, vomiting, anorexia (earliest symptoms)
• CNS: Visual disturbances (yellow-green halos - xanthopsia), confusion, headache
• Precipitating factors for toxicity: Hypokalemia, hypomagnesemia, hypercalcemia, renal failure, hypothyroidism

• Stop digoxin
• Correct electrolytes (especially K+)
• Atropine for bradycardia
• Anti-digoxin Fab fragments (Digibind) for severe toxicity
• Phenytoin, lidocaine for ventricular arrhythmias

• Digoxin alone has narrow therapeutic index and modest mortality benefit
• Combination with furosemide (reduces volume overload) + ACE inhibitor (reduces afterload + prevents remodeling) + spironolactone (prevents aldosterone-mediated fibrosis) gives synergistic benefit

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2C. Diltiazem - Antianginal & Antiarrhythmic Effects

• Blocks Ca²+ channels → dilates coronary arteries → increases O2 supply
• Dilates peripheral arterioles → reduces afterload → reduces O2 demand
• Negative chronotropy → reduces heart rate → reduces O2 demand

• Similar to verapamil but less potent negative inotropy
• Slows SA and AV node → useful in AF, flutter, SVT for rate control

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TOPIC 3: ANTIANGINAL DRUGS

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3A. How Nitroglycerin/Isosorbide Mononitrate Relieves Anginal Pain

• Converted to nitric oxide (NO) in vascular smooth muscle
• NO activates guanylate cyclase → ↑cGMP → dephosphorylates myosin light chain → smooth muscle relaxation

• Venodilation (major effect): Reduces venous return (preload) → reduces cardiac work → reduces O2 demand
• Arteriolar dilation (at high doses): Reduces afterload
• Coronary artery dilation: Especially collateral vessels and vasospastic segments → increases O2 supply
• Redistribution of blood to ischemic subendocardium

• Oral preparation with 100% bioavailability (no first-pass metabolism)
• Long-acting (half-life ~5 hrs) - used for prophylaxis not acute attacks
• Eccentric dosing (two doses: 7 AM and 2 PM) to prevent nitrate tolerance
• Tolerance: Due to sulfhydryl group depletion and neurohormonal activation - overcome by drug-free interval (8-12 hrs/day)

• Stable angina (chronic prophylaxis)
• Vasospastic angina (Prinzmetal's) - DRUG OF CHOICE along with CCBs
• Unstable angina
• Acute MI (IV nitroglycerin)

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3B. Role of Low Dose Aspirin in IHD

• Irreversibly inhibits COX-1 enzyme in platelets
• Prevents thromboxane A2 (TXA2) synthesis → TXA2 normally causes platelet aggregation and vasoconstriction
• Platelets cannot regenerate COX (no nucleus) → effect lasts platelet lifetime (7-10 days)

• Prevents platelet aggregation on ruptured atherosclerotic plaques
• Reduces risk of acute MI and unstable angina
• Post-MI: reduces reinfarction risk by ~25%
• Secondary prevention: reduces cardiovascular events

• Clopidogrel (P2Y12 ADP receptor blocker) - used when aspirin intolerant
• Ticagrelor, Prasugrel
• Combination: Aspirin + Clopidogrel (dual antiplatelet therapy after ACS/stent)

• Streptokinase, Alteplase (t-PA), Reteplase, Tenecteplase
• Activate plasminogen → plasmin → dissolves fibrin clot
• Used in STEMI within 12 hrs of onset

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3C. Antianginal Effect of Beta-Blockers

• Block β1 receptors on heart → reduce HR, contractility, BP
• Reduce myocardial O2 demand (main effect):
  • ↓Heart rate
  • ↓Myocardial contractility
  • ↓Ventricular wall tension (by reducing BP)
• Increase diastolic filling time → better coronary perfusion

• First-line for stable angina (chronic prophylaxis)
• Post-MI: reduce mortality, prevent reinfarction
• Unstable angina: reduces ischemic episodes

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3D. Antianginal Effect of Calcium Channel Blockers

• Block L-type Ca²+ channels
• Reduce peripheral resistance (afterload) → reduce O2 demand
• Dilate coronary arteries → increase O2 supply
• Verapamil/Diltiazem also reduce heart rate (reduce O2 demand)

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TOPIC 4: ANTIDIABETIC DRUGS

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4A. Insulin - Preparations, Mechanism, Clinical Uses, Adverse Effects

• Binds insulin receptor (tyrosine kinase receptor) on cell surface
• Activates PI3K/Akt pathway → GLUT4 translocation to cell surface
• In liver: promotes glycogen synthesis, inhibits gluconeogenesis, promotes glycolysis
• In muscle: promotes glucose uptake and glycogen synthesis
• In adipose: promotes glucose uptake, lipogenesis, inhibits lipolysis

1. Increases cellular glucose uptake (GLUT4 in muscle/fat)
2. Promotes glycogen synthesis (liver and muscle)
3. Inhibits glycogenolysis
4. Inhibits gluconeogenesis
5. Promotes glycolysis
6. Inhibits lipolysis → less free fatty acids → less gluconeogenesis substrate

• Type 1 DM (mandatory)
• Type 2 DM (when oral agents fail, perioperative, pregnancy)
• Hyperkalemia (drives K+ into cells)
• Diabetic ketoacidosis (DKA)
• Hyperosmolar hyperglycemic state (HHS)
• Nutritional support (with IV dextrose)

• Hypoglycemia (most important) - treat with oral glucose, IV dextrose, glucagon
• Weight gain
• Lipodystrophy at injection sites
• Insulin resistance
• Allergic reactions (rare with human insulin)
• Hypokalemia (shifts K+ intracellularly)

• Mild: Oral glucose (15-20g rapidly absorbed carbs), fruit juice, glucose tablets
• Severe/unconscious: IV 25-50% dextrose (25-50 ml), IM/SC glucagon 1 mg
• Repeated glucose monitoring; identify and treat cause

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4B. Insulin Resistance - Definition & Management

• Reduced cellular response to normal circulating insulin levels
• Pancreas compensates by producing more insulin (hyperinsulinemia)
• When β cells can no longer compensate → T2DM develops

• Receptor defects (reduced number or affinity)
• Post-receptor signaling defects (PI3K/IRS-1 pathway)
• Obesity (excess FFA, adipokines → TNF-α, resistin)
• Chronic hyperglycemia → glucose toxicity

• Weight loss (most important in obese)
• Exercise (improves insulin sensitivity)
• Metformin (first-line drug - reduces hepatic glucose output, improves sensitivity)
• Thiazolidinediones (Pioglitazone, Rosiglitazone) - PPAR-γ agonists → increase GLUT4 expression
• Bariatric surgery (for BMI >35 with diabetes)

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4C. Oral Hypoglycemic Agents - Classification & Mechanisms

• Glibenclamide (Glyburide), Glipizide, Glimepiride
• Mechanism: Block KATP channels on β cells → depolarization → Ca²+ entry → insulin release
• Hypoglycemic effect: Yes (can cause hypoglycemia)
• Require functioning β cells

• Metformin (first-line T2DM)
• Mechanism:
  • Activates AMPK → inhibits hepatic gluconeogenesis (main effect)
  • Increases peripheral insulin sensitivity
  • Reduces intestinal glucose absorption
• Does NOT cause hypoglycemia (euglycemic)
• Does NOT cause weight gain (weight neutral/reduction)
• Other benefits: cardiovascular protection, reduces mortality
• Adverse: Lactic acidosis (rare), GI side effects, B12 deficiency, contraindicated in renal failure

• Pioglitazone, Rosiglitazone
• Mechanism: PPAR-γ agonists → increase insulin receptor expression and sensitivity → increase GLUT4, reduce FFA
• Adverse: Weight gain, edema, heart failure risk, fracture risk, bladder cancer (pioglitazone)

• Acarbose, Voglibose
• Block intestinal α-glucosidase → reduce postprandial glucose rise

• Repaglinide, Nateglinide
• Short-acting, meal-related

• Sitagliptin, Vildagliptin
• Increase GLP-1 → glucose-dependent insulin secretion

• Empagliflozin, Dapagliflozin
• Block renal glucose reabsorption

• Exenatide, Liraglutide

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4D. Sulphonylureas - Hypoglycemic Effects (Glibencamide)

• Stimulate insulin release (primary mechanism)
• May also reduce glucagon secretion
• Increase peripheral insulin sensitivity (secondary)

• Effective when β cells still functional
• Combination with Metformin: Glibencamide (insulin secretion) + Metformin (insulin sensitizer) → complementary mechanisms, additive effect, avoids higher doses of either

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4E. Metformin in Type 2 DM - Other Indications

• Reduces hepatic glucose output (major)
• No hypoglycemia (safe)
• Weight neutral or reduces weight
• Proven cardiovascular outcome benefit (UKPDS)
• Cheap, well-tolerated

• Polycystic ovarian syndrome (PCOS) - reduces insulin resistance, restores menstrual cycle, improves fertility
• Pre-diabetes (prevention of T2DM)
• Obesity management
• Non-alcoholic fatty liver disease (NAFLD)

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4F. Pioglitazone / Rosiglitazone - Hypoglycemic Effect

• Binds PPAR-γ receptors (primarily in adipose tissue, also liver and muscle)
• Regulates gene transcription involved in lipid and glucose metabolism
• Increases GLUT4 expression → improved glucose uptake
• Decreases FFAs → less hepatic gluconeogenesis and improved β-cell function
• Shifts lipid storage from visceral to subcutaneous

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4G. How Does Insulin Lower Blood Glucose (Mechanism)

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TOPIC 5: GLUCOCORTICOIDS

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5A. Anti-inflammatory Action of Glucocorticoids (Hydrocortisone/Dexamethasone)

1. Lipocortin (Annexin A1) induction: Inhibits phospholipase A2 → reduces arachidonic acid → reduces prostaglandins, leukotrienes, thromboxanes
2. Transcription factor inhibition: Inhibit NF-κB → reduces inflammatory cytokines (IL-1, IL-6, TNF-α)
3. Reduce vascular permeability → decrease edema
4. Inhibit leukocyte migration to sites of inflammation
5. Reduce COX-2 expression
6. Suppress T-lymphocyte proliferation (immunosuppressive)
7. Reduce mast cell mediator release

• Decrease T and B lymphocyte function
• Reduce antibody production
• Inhibit phagocytosis
• Used in organ transplant rejection, autoimmune diseases

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5B. Adverse Effects of Long-Term Glucocorticoid Use

• Hyperglycemia (steroid-induced diabetes)
• Hyperlipidemia
• Central obesity (moon face, buffalo hump, centripetal obesity)
• Negative nitrogen balance (muscle wasting)

• Osteoporosis → vertebral fractures
• Avascular necrosis of femoral head
• Myopathy

• Adrenal atrophy → Addisonian crisis on sudden withdrawal
• Growth retardation in children

• Hypertension (Na+/water retention)
• Dyslipidemia

• Peptic ulcer (reduce protective mucus, enhance acid secretion)
• Pancreatitis

• Euphoria, psychosis, insomnia

• Cataracts (posterior subcapsular)
• Glaucoma

• Thinning, striae, easy bruising, impaired wound healing

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5C. Compare Hydrocortisone & Dexamethasone / Hydrocortisone & Betamethasone / Hydrocortisone & Triamcinolone

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5D. Metabolic Effects of Glucocorticoids

• Carbohydrate: Increase gluconeogenesis (↑liver glucose output), decrease peripheral glucose uptake → hyperglycemia
• Protein: Increased catabolism → muscle wasting, negative nitrogen balance
• Fat: Lipolysis (peripheral fat breakdown) but fat redistribution (central deposition) = Cushing's habitus
• Mineral: Na+ retention, K+ loss (aldosterone-like at high doses)
• Calcium: Reduce intestinal Ca²+ absorption, increase renal Ca²+ excretion → osteoporosis
• Immune: Suppress immunity

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TOPIC 6: DIURETICS

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6A. Furosemide - Diuretic Effect & Hypokalemia

• Acts on thick ascending limb of Loop of Henle
• Inhibits Na+K+2Cl- cotransporter (NKCC2)
• Massive Na+, K+, Cl-, water, Ca²+, Mg²+ excretion
• Most potent diuretic

• Increased Na+ delivery to collecting duct → aldosterone activates Na+/K+ exchange → more K+ lost
• Also: Secondary hyperaldosteronism from volume depletion

• Hypokalemia, hyponatremia, hypochloremia
• Metabolic alkalosis (H+ loss)
• Hypomagnesemia, hypocalcemia
• Ototoxicity (especially IV rapid infusion - tinnitus, deafness)
• Hyperuricemia (gout)
• Hyperglycemia
• Hypovolemia, dehydration, postural hypotension
• Azotemia (pre-renal)

• Acute pulmonary edema (first-line emergency)
• CCF, renal edema, hepatic ascites
• Hypercalcemia
• Hypertensive emergencies
• SIADH

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6B. Thiazide - Adverse Effects & Causes

• Hypokalemia (most common electrolyte disturbance)
• Hyperuricemia (gout) - compete for urate secretion
• Hyperglycemia - reduce insulin secretion, increase gluconeogenesis
• Dyslipidemia - increase LDL, triglycerides
• Hyponatremia
• Hypercalcemia (↑Ca²+ reabsorption - beneficial in osteoporosis)
• Impotence
• Allergic reactions (sulfonamide structure)

• Increased distal Na+ delivery → aldosterone-mediated K+ secretion
• Volume depletion → secondary hyperaldosteronism

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6C. Spironolactone - Adverse Effects & Causes

• Blocks mineralocorticoid receptors in collecting duct
• Retains K+ and H2O, excretes Na+

• Hyperkalemia (most dangerous - due to K+ sparing) → especially dangerous with ACE inhibitors
• Gynecomastia (binds androgen receptors - anti-androgenic)
• Menstrual irregularities in women
• Impotence in men
• Metabolic acidosis
• Peptic ulcers
• Rashes

• Hyperkalemia: due to aldosterone blockade → K+ retained
• Gynecomastia: due to anti-androgenic and progestogenic effects on breast tissue

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6D. Low Molecular Weight Heparin (LMWH)

• Binds antithrombin III (ATIII) and potentiates it
• LMWH primarily inhibits Factor Xa (anti-Xa activity)
• Less thrombin (Factor IIa) inhibition compared to unfractionated heparin
• Does NOT require monitoring of APTT (unlike UFH)
• More predictable pharmacokinetics (given SC once/twice daily)

• DVT prevention (prophylaxis) - orthopedic/general surgery patients
• Treatment of DVT and PE
• Unstable angina / NSTEMI
• Prevention of clotting during dialysis
• Bridge therapy when warfarin stopped
• Pregnancy (safe - does not cross placenta)

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TOPIC 7: UTERINE DRUGS

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7A. Oxytocin and Ergometrine - Effects on Uterus

• Induction of labour: Oxytocin preferred (IV infusion, controllable)
• Post-partum hemorrhage: Both used; Syntocinon (oxytocin) + ergometrine = Syntometrine
• Active management of third stage of labour: Oxytocin preferred
• Subinvolution of uterus: Ergometrine
• Abortion: Both

• Hypertension, pre-eclampsia, eclampsia (raises BP)
• Peripheral vascular disease
• NOT used for induction of labour (causes non-physiological contractions)

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7B. Drugs Used in Post-Partum Hemorrhage

1. Oxytocin (IV/IM) - first-line
2. Ergometrine (IM) - causes sustained contraction
3. Syntometrine (oxytocin + ergometrine combination)
4. Carboprost (PGF2α analogue) - for refractory PPH; contraindicated in asthma
5. Misoprostol (PGE1 analogue) - oral/sublingual/rectal
6. Tranexamic acid - antifibrinolytic

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7C. Drugs Affecting Uterine Contractility

• Oxytocin, Ergometrine
• Prostaglandins (Dinoprostone/PGE2, Carboprost/PGF2α, Misoprostol/PGE1)
• High-dose Oxytocin

• β2 agonists: Ritodrine, Terbutaline, Salbutamol (most commonly used)
• Ca²+ channel blockers: Nifedipine (safe, effective)
• Oxytocin antagonist: Atosiban
• Magnesium sulfate (MgSO4)
• Progesterone (cervical ripening prevention)
• NSAIDs: Indomethacin (COX inhibitor → reduces prostaglandins)

• β2 agonists: Activate β2 → increase cAMP → decrease intracellular Ca²+ → muscle relaxation
• Nifedipine: Block Ca²+ entry → relaxation
• MgSO4: Competes with Ca²+ → reduces contractility

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TOPIC 8: CONTRACEPTIVES

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8A. Combined Oral Contraceptive Pill (OCP)

1. Inhibit ovulation (suppress LH surge - main mechanism)
2. Thicken cervical mucus → prevent sperm penetration
3. Alter endometrium → prevent implantation
4. Alter tubal motility

• Contraception
• Dysmenorrhea, menorrhagia
• Endometriosis
• PCOS
• Acne

• Pregnancy
• Thromboembolism history / DVT / PE
• Stroke, IHD
• Breast/uterine cancer
• Uncontrolled hypertension
• Migraine with aura
• Liver disease, jaundice

• 35 years + smoker

• Nausea, vomiting, breast tenderness
• Weight gain
• Breakthrough bleeding
• Mood changes, depression
• DVT/Thromboembolism (estrogen component)
• Hypertension
• Gallbladder disease
• Increased risk of cervical cancer
• Amenorrhea post-pill

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8B. Progesterone-Only Contraceptive - Advantages Over Combined Pill

• Safe in breastfeeding mothers (no estrogen)
• Safe in hypertension, thromboembolism risk, migraines with aura
• No DVT risk (no estrogen)
• Can be used in diabetes, smokers >35 years
• Safe in cardiac diseases

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8C. Hormonal Contraceptive Preparations & Permanent Methods

• Combined oral pill (OCP)
• Progestogen-only pill (mini-pill)
• Injectable: Depo-medroxyprogesterone acetate (DMPA) - 3 monthly
• Implants: Etonogestrel implant (Nexplanon) - 3 years
• IUD with hormone: Levonorgestrel IUS (Mirena) - 5 years
• Emergency contraception: Levonorgestrel (Plan B), Ulipristal

• Female: Tubectomy (tubal ligation)
• Male: Vasectomy

• Couple has desired family size
• Medical conditions where pregnancy dangerous
• Genetic disorders

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TOPIC 9: IRON PREPARATIONS

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9A. Iron Deficiency Anaemia - Oral and Parenteral Preparations

• Chronic blood loss (menorrhagia, GI bleed - most common)
• Inadequate intake (vegetarian diet)
• Malabsorption (celiac, post-gastrectomy)
• Increased demand (pregnancy, growth)

• Ferrous sulfate (most widely used, cheapest)
• Ferrous gluconate (better tolerated)
• Ferrous fumarate
• Ferric ammonium citrate (for children - liquid)
• Iron-folic acid tablets (prophylaxis in pregnancy)

• Iron dextran (IV/IM)
• Iron sucrose (IV infusion - safer, preferred)
• Ferric carboxymaltose (IV - high dose, single infusion)
• Sodium ferric gluconate

• Intolerance to oral iron
• Malabsorption syndromes
• Non-compliance with oral iron
• Severe anaemia requiring rapid replenishment
• Inflammatory bowel disease (impaired absorption)
• Chronic kidney disease on dialysis

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9B. Justify Iron-Folic Acid in Pregnancy

• Pregnancy increases iron demand (200-600 mg extra)
• Folic acid deficiency causes neural tube defects (anencephaly, spina bifida) - must start periconceptionally
• Government programs provide iron-folic acid tablets to all pregnant women
• Prevention of pregnancy-related iron deficiency anaemia and megaloblastic anaemia

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9C. Treatment of Iron Deficiency Anaemia

• Ferrous sulfate 200 mg TDS (60 mg elemental iron per tablet)
• Given on empty stomach for better absorption (but causes more GI side effects)
• Given with Vitamin C (ascorbic acid) - enhances absorption
• Continue for 3-6 months after Hb normalises (to replenish stores)
• Adverse effects: constipation, nausea, dark stools, abdominal discomfort

• Reticulocytosis peak at 7-10 days (first sign of response)
• Hb rises ~1-2 g/dL per week
• Full normalisation in 4-8 weeks

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TOPIC 10: ANTIHYPERTENSIVES IN SPECIAL SITUATIONS

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10A. Antihypertensives Safe in Diabetes Mellitus

• ACE inhibitors (Captopril, Enalapril) - FIRST CHOICE (renoprotective, reduce microalbuminuria)
• ARBs (Losartan) - if ACE inhibitor not tolerated
• CCBs (Amlodipine)

• Beta-blockers: mask hypoglycemia symptoms, worsen insulin resistance
• Thiazides: hyperglycemia (high dose)

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10B. Antihypertensives in Hypertension with Bronchospasm

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10C. Postural (Orthostatic) Hypotension

• Alpha-blockers (Prazosin - especially first-dose effect)
• Tricyclic antidepressants
• Phenothiazines (Chlorpromazine)
• Nitrates
• Methyldopa
• Levodopa
• Diuretics (volume depletion)
• Calcium channel blockers

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SUMMARY TABLE: HIGH-YIELD EXAM POINTS

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