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MODULE 2.2: THE FOUNDATIONS OF BIOETHICS

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Q1. Describe and discuss the role of Non-Maleficence as a guiding principle in patient care (5 Marks)

1. Avoiding harm: The physician must not perform procedures or prescribe drugs that cause more harm than benefit. Example: not prescribing a nephrotoxic drug to a patient with renal failure unnecessarily.
2. Risk-benefit analysis: Every clinical intervention carries some risk. Non-maleficence requires that the potential benefits must outweigh the potential harms.
3. Negligence vs. harm: Non-maleficence distinguishes between intentional harm, negligent harm (failure to exercise due care), and unavoidable side effects of treatment.
4. Doctrine of Double Effect: Some treatments intended to do good may have unavoidable harmful side effects (e.g., chemotherapy causing immunosuppression). This is ethically permissible if:
   • The action itself is good or neutral
   • The harmful effect is not the means to the good effect
   • The intention is to achieve the good effect
   • The good effect outweighs the bad
5. Clinical examples:
   • Avoiding polypharmacy in elderly patients
   • Not performing unnecessary surgeries
   • Proper informed consent before high-risk procedures
   • Monitoring for adverse drug reactions

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Q2. Describe and discuss the role of Autonomy and Shared Responsibility as a guiding principle in patient care (5 Marks)

1. The patient must have the capacity to decide (be mentally competent)
2. The decision must be voluntary (free from undue pressure)
3. The patient must be adequately informed

• Before any procedure or drug therapy, the physician must explain the diagnosis, proposed treatment, alternatives, risks, and expected outcomes.
• The patient has the right to refuse treatment even if the physician disagrees.

• Modern patient care is not paternalistic ("doctor knows best") but collaborative.
• The physician provides expertise and options; the patient provides values and preferences.
• Together, they arrive at a mutually acceptable management plan.
• This is especially relevant in chronic diseases (e.g., diabetes, hypertension) where lifestyle changes and long-term medications require patient cooperation.

• When the patient lacks capacity (unconscious, severe psychiatric illness) - surrogate decision-makers or next of kin step in.
• When patient's decision harms others (e.g., refusing isolation for a communicable disease).
• In emergencies, implied consent overrides autonomy temporarily.

• Prescription adherence improves when patients are involved in treatment decisions.
• Empowers patients to manage their own health.

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Q3. Describe and discuss the role of Beneficence as a guiding principle in patient care (5 Marks)

1. Prevent harm to the patient
2. Remove existing harm
3. Actively promote the patient's welfare
4. Prioritize the patient's best interest above personal gain

• Beneficence = do good
• Non-maleficence = avoid harm
• Both are complementary - every clinical decision must maximize benefit while minimizing harm.

• Strong paternalism: overriding patient's autonomous choices "for their own good" - generally not ethically justified.
• Weak paternalism: acting for good when patient lacks decision-making capacity - generally accepted.

• Prescribing evidence-based medications for the correct indication
• Counseling patients about healthy lifestyle
• Vaccinations and preventive medicine
• Honest communication about prognosis to allow informed decisions

• Rational drug therapy - right drug, right dose, right route, right duration
• Choosing a more effective drug even if it has mild side effects when the disease risk is high

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Q4. Describe and discuss the role of a Physician in the Health Care System (5 Marks)

1. Clinician (Care Provider)

• Diagnose illness and prescribe appropriate treatment
• Monitor patient progress and manage complications
• Provide acute, chronic, and preventive care

2. Communicator

• Establish effective doctor-patient relationships
• Explain diagnoses and treatment plans clearly
• Obtain informed consent
• Deliver bad news with sensitivity (breaking bad news)

3. Collaborator

• Work in interdisciplinary teams (nurses, pharmacists, physiotherapists, social workers)
• Coordinate care across specialties and levels of the healthcare system

4. Health Advocate

• Promote community health and disease prevention
• Identify and address social determinants of health (poverty, nutrition, sanitation)
• Advocate for marginalized and vulnerable populations

5. Manager and Leader

• Manage healthcare resources responsibly
• Allocate resources equitably (distributive justice)
• Lead quality improvement initiatives

6. Scholar and Lifelong Learner

• Stay updated with current evidence-based medicine
• Contribute to research and medical education
• Teach junior colleagues and medical students

7. Professional (Role Model)

• Uphold medical ethics: confidentiality, integrity, honesty
• Maintain patient trust and professional boundaries
• Follow the code of medical ethics (MCI/NMC guidelines)

8. Gatekeeper of the Health System

• Appropriate referrals to specialists
• Rational prescribing to reduce drug resistance and costs
• Prevent unnecessary hospitalization

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Q5. Describe and discuss the role of Justice as a guiding principle in patient care (5 Marks)

1. Egalitarian - equal share for all
2. Utilitarian - maximum benefit for maximum number
3. Need-based - sicker patients get priority
4. Contribution-based - those who contributed more (e.g., taxpayers) get more

1. Non-discrimination: Treat all patients equally regardless of caste, religion, gender, socioeconomic status, or sexual orientation.
2. Resource allocation: Decisions about ICU beds, ventilators, organs for transplant - made on clinical need, not social worth.
3. Triage: In emergencies, prioritizing those who will benefit most from immediate care.
4. Equity vs. Equality: Equity means giving more to those who need more (not treating everyone identically).

• Macro justice - national health policy, insurance coverage, healthcare budgets
• Micro justice - individual clinical decisions about resource use for a specific patient

• Special obligations exist toward the poor, elderly, children, prisoners, and mentally ill.
• Research ethics demands that vulnerable populations not be exploited.

• Generic vs. brand drug prescribing to make medicines affordable and accessible
• Rational prescribing avoids wastage of limited healthcare resources
• Ensuring essential medicines are available at all levels of care (WHO Essential Medicines List)

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Summary Table - Four Pillars of Bioethics (Beauchamp & Childress)

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ACSR GOVT MEDICAL COLLEGE, NELLORE

Pharmacology - First Internal Examination

Date: 23-02-2026 | Total: 100 Marks

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ESSAY QUESTIONS (1×10 = 10 Marks each)

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Q1. A 48-year-old man with Type-2 Diabetes Mellitus is newly diagnosed with Hypertension (BP 150/96 mmHg). Urine examination shows microalbuminuria.

a) What is the preferred drug? (2M)

• They reduce intraglomerular pressure and decrease proteinuria/microalbuminuria - nephroprotective in diabetic nephropathy.
• They delay progression to overt diabetic nephropathy.
• If ACE inhibitors are not tolerated (due to cough), ARBs (e.g., Losartan, Telmisartan) are the alternative.

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b) Classify Antihypertensive Drugs (4M)

1. Thiazides - Hydrochlorothiazide, Chlorthalidone
2. Loop diuretics - Furosemide
3. K+-sparing - Spironolactone, Amiloride

1. Beta blockers - Atenolol, Metoprolol, Propranolol
2. Alpha1 blockers - Prazosin, Doxazosin
3. Alpha + Beta blockers - Labetalol, Carvedilol
4. Central sympatholytics - Methyldopa, Clonidine
5. Ganglionic blockers - Trimethaphan (obsolete)
6. Adrenergic neuron blockers - Guanethidine (obsolete)

1. Dihydropyridines - Amlodipine, Nifedipine, Felodipine
2. Phenylalkylamines - Verapamil
3. Benzothiazepines - Diltiazem

1. ACE Inhibitors - Enalapril, Ramipril, Lisinopril
2. Angiotensin II (AT1) Receptor Blockers (ARBs) - Losartan, Telmisartan, Valsartan
3. Direct Renin Inhibitor - Aliskiren
4. Aldosterone antagonist - Eplerenone

1. Arteriolar - Hydralazine, Minoxidil, Diazoxide
2. Arteriolar + Venular - Sodium Nitroprusside

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c) Write the mechanism of action, therapeutic uses, and adverse effects of ACE Inhibitors (4M)

• ACE (Angiotensin Converting Enzyme) normally converts Angiotensin I → Angiotensin II.
• ACE inhibitors block this enzyme.
• Result: ↓ Angiotensin II → vasodilation + ↓ aldosterone → ↓ Na/water retention → ↓ BP.
• Also prevent breakdown of bradykinin → vasodilation, but also causes cough (via substance P and prostaglandins).

1. Hypertension - especially in diabetic patients with microalbuminuria
2. Congestive Heart Failure (CHF) - reduce preload and afterload
3. Post-MI - reduce ventricular remodeling
4. Diabetic nephropathy - reduce proteinuria, slow progression
5. Chronic kidney disease
6. Hypertensive urgency

1. Dry persistent cough - most common (due to bradykinin accumulation) - class effect
2. Hyperkalemia - due to ↓ aldosterone
3. First-dose hypotension - especially with diuretics
4. Angioedema - rare but life-threatening (bradykinin-mediated)
5. Fetotoxicity - contraindicated in pregnancy (2nd, 3rd trimester) - causes renal agenesis, oligohydramnios
6. Acute renal failure - in bilateral renal artery stenosis
7. Taste disturbance - especially Captopril (contains -SH group)
8. Rash, leukopenia (Captopril)

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Q2. A 30-year-old farmer is brought to emergency with excessive salivation, sweating, vomiting, abdominal cramps, difficulty breathing after spraying insecticides. Pulse 52/min, BP 90/60 mmHg, pinpoint pupil (miosis), bronchospasm.

a) What is the likely diagnosis? (1M)

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b) Write the treatment of Organophosphate Poisoning (4M)

• Muscarinic: Salivation, Lacrimation, Urination, Defecation, GI cramps, Emesis, Bradycardia, Bronchospasm, Miosis
• Nicotinic: Muscle fasciculations, weakness, paralysis
• CNS: Anxiety, seizures, coma

• Remove contaminated clothing, wash skin with soap and water, eye irrigation.

• Atropine 2-4 mg IV, repeated every 5-10 minutes until secretions dry up (drying of secretions = end point, NOT pupil dilation).
• Dose may go up to 20-100 mg in severe poisoning.
• Counteracts only muscarinic effects.

• Dose: 1-2 g IV slowly over 15-30 min, then infusion.
• Mechanism: Reactivates inhibited acetylcholinesterase by breaking the OP-AChE bond (if given early, before "aging" occurs).
• Counteracts both muscarinic AND nicotinic effects.
• Must be given within 24-48 hours (before aging of the enzyme).

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SHORT NOTES (11×5 = 55 Marks)

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2. Define Teratogenicity with examples

1. Interference with folic acid metabolism (methotrexate, trimethoprim)
2. Androgen-like effect
3. Inhibition of enzymes
4. Direct DNA damage

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3. Write the difference between First Order Kinetics and Zero Order Kinetics

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4. Therapeutic uses and adverse effects of Beta Blockers

1. Hypertension - first-line, especially in young patients, post-MI
2. Angina pectoris - reduce myocardial oxygen demand (↓HR, ↓contractility)
3. Cardiac arrhythmias - SVT, AF, atrial flutter (rate control), post-MI arrhythmias
4. Myocardial infarction - reduce infarct size, prevent reinfarction
5. Congestive Heart Failure - carvedilol, metoprolol (in stable CHF, reduce mortality)
6. Hyperthyroidism - control tachycardia and tremors (propranolol)
7. Phaeochromocytoma - (after alpha blockade) to control tachycardia
8. Migraine prophylaxis - propranolol
9. Essential tremor - propranolol
10. Anxiety (situational/performance anxiety) - propranolol
11. Glaucoma - timolol eye drops (↓ aqueous humor production)
12. Portal hypertension - propranolol (to reduce variceal bleeding)

1. Cardiovascular: Bradycardia, heart block, hypotension, worsening of CHF (if initiated in decompensated state)
2. Respiratory: Bronchoconstriction - dangerous in asthmatics (avoid non-selective β-blockers)
3. CNS: Fatigue, lethargy, depression, sleep disturbances, nightmares (especially propranolol - lipid soluble)
4. Metabolic:
   • Masking of hypoglycemia symptoms (except sweating) in diabetics
   • ↑ Triglycerides, ↓ HDL
5. Peripheral vascular: Cold extremities, worsening of Raynaud's disease, intermittent claudication
6. Sexual dysfunction: Impotence
7. Withdrawal syndrome: Abrupt discontinuation → rebound hypertension, angina, MI (taper gradually)

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6. Transdermal Drug Delivery System

1. Backing layer (impermeable - polyester foil)
2. Drug reservoir or matrix
3. Rate-controlling membrane (polymer)
4. Adhesive layer
5. Release liner (removed before application)

1. Avoids first-pass hepatic metabolism
2. Sustained, controlled drug release - once daily or weekly dosing
3. Non-invasive - painless
4. Easy to remove if adverse effect occurs
5. Improved patient compliance
6. Avoids GI degradation
7. Stable plasma levels (no peaks and troughs)

1. Only lipid-soluble, low molecular weight drugs can penetrate
2. Skin irritation, allergic contact dermatitis
3. Slow onset of action
4. Limited dose that can be delivered
5. Lag time before achieving therapeutic levels

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7. Define Bioavailability. Write the factors affecting Bioavailability.

• IV administration: Bioavailability = 100% (F = 1)
• Oral administration: F < 1 due to incomplete absorption and first-pass metabolism

1. Absolute bioavailability - compared to IV route
2. Relative bioavailability - compared to another oral formulation

1. Physicochemical properties - lipid solubility, pKa, molecular size
2. Formulation - particle size, crystal form, excipients
3. Dissolution rate - rate at which drug dissolves in GI fluid
4. Chemical stability - degradation in GI tract

1. First-pass metabolism (hepatic) - most important
   • Drug absorbed from gut → portal vein → liver → metabolized before reaching systemic circulation
   • High first-pass drugs: Propranolol, Lidocaine, Morphine, GTN, Aspirin
2. GI motility - increased motility (diarrhea) → ↓ absorption; decreased motility → ↑ absorption
3. pH - gastric pH affects ionization and absorption
4. GI surface area - reduced in GI disease
5. Splanchnic blood flow
6. Food - may enhance or reduce (e.g., fatty food increases griseofulvin absorption)

1. Chelation - tetracyclines + calcium/iron → ↓ absorption
2. Enzyme induction - rifampicin, phenobarbitone → ↑ first-pass → ↓ bioavailability
3. P-glycoprotein efflux

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8. Describe and discuss the role of Autonomy and Shared Responsibility as a guiding principle in patient care

• Physician provides expertise; patient provides values and preferences.
• Collaborative management planning, especially in chronic diseases.
• Informed consent is its practical expression.
• Improves adherence and patient outcomes.

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9. Write short notes on Calcium Channel Blockers

• Vasodilation of arterioles → ↓ BP (all CCBs)
• ↓ Heart rate (Verapamil > Diltiazem > DHPs)
• ↓ Conduction through AV node (Verapamil, Diltiazem)
• ↓ Myocardial contractility (negative inotropy)

1. Hypertension - Amlodipine (drug of choice in elderly, isolated systolic HTN)
2. Angina - stable angina (all), vasospastic/Prinzmetal's angina (DHPs preferred)
3. Supraventricular tachyarrhythmias (SVT, AF) - Verapamil, Diltiazem
4. Raynaud's phenomenon - Nifedipine
5. Hypertrophic cardiomyopathy - Verapamil
6. Migraine prophylaxis - Verapamil
7. Subarachnoid hemorrhage (cerebral vasospasm) - Nimodipine

1. DHPs: Flushing, headache, ankle edema, reflex tachycardia (nifedipine)
2. Verapamil: Constipation (most common), bradycardia, AV block, hypotension
3. Diltiazem: Bradycardia, AV block
4. Gingival hyperplasia (Nifedipine)
5. Negative inotropy - worsen heart failure (avoid Verapamil in CHF)

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10. Enumerate the Phases of Clinical Trials with examples

• Phase 0: Microdosing studies - sub-therapeutic doses in humans
• Adaptive trials: Modifications during trial based on interim results

• Phase III required for Drug Regulatory Authority (CDSCO in India / FDA in USA) approval
• Phase IV detects rare ADRs missed in Phase III (e.g., COX-2 inhibitors → cardiovascular events found in Phase IV)

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11. A 38-year-old male presents with retrosternal chest pain on exertion for 6 months. Physician prescribes sublingual Nitro-glycerine for acute attacks.

a) Write the mechanism of action and adverse effects of Nitrates (3M)

• GTN is converted to nitric oxide (NO) in vascular smooth muscle
• NO activates guanylyl cyclase → ↑ cGMP → activation of cGMP-dependent protein kinase → dephosphorylation of myosin light chain → smooth muscle relaxation → vasodilation
• Primarily dilates veins (venodilation) → ↓ preload → ↓ myocardial O₂ demand
• At higher doses → arteriolar dilation → ↓ afterload
• Coronary vasodilation → relieves vasospasm

1. Throbbing headache (commonest - due to cerebral vasodilation)
2. Flushing and dizziness
3. Postural hypotension (syncope) - especially with first dose
4. Reflex tachycardia (due to hypotension - mediated by baroreceptor)
5. Methemoglobinemia - at very high doses
6. Tolerance - see below

b) Add a note on Nitrate Tolerance (2M)

• Defined as the loss of hemodynamic and antianginal effects of nitrates with continuous or prolonged administration.
• Develops within 24-48 hours of continuous therapy.

1. Sulfhydryl (-SH) depletion in vascular smooth muscle - needed for NO generation
2. Neurohormonal activation - reflex ↑ catecholamines, angiotensin II, vasopressin
3. Superoxide anion generation → inactivates NO
4. Upregulation of phosphodiesterase

• Eccentric (asymmetric) dosing: provide a 8-12 hour nitrate-free interval (usually overnight when angina is least likely)
• Isosorbide dinitrate: 8 am and 2 pm (not at night)
• Isosorbide mononitrate: given once daily in morning (sustained release)
• N-acetylcysteine (replenishes -SH groups)

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12. Differences between Physostigmine and Neostigmine. Why is Neostigmine preferred for treatment of Myasthenia Gravis?

1. Does not cross BBB → no CNS toxicity (no seizures, coma)
2. Has dual mechanism - AChE inhibition + direct nicotinic receptor action → more effective at NMJ
3. Available in oral form for chronic use
4. Longer duration of action (2-4 hours) allows sustained muscle strength
5. Safer profile for long-term use

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VERY SHORT NOTES (5×3 = 15 Marks)

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13. Explain why Oral Contraceptives are contraindicated along with Rifampicin

• Rifampicin accelerates the hepatic metabolism of ethinyl estradiol and progestins in OCPs.
• This leads to drastically ↓ plasma levels of the contraceptive hormones → contraceptive failure (breakthrough pregnancies).

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14. Rationale of using Adrenaline with Lignocaine

1. Prolonged duration of action: Adrenaline causes vasoconstriction (α1-receptor mediated) at the site of injection → slows systemic absorption of lignocaine → drug remains at the site longer → duration of anesthesia increased from ~45 min to ~90-120 min.
2. Reduced systemic toxicity: Slower absorption → lower peak plasma levels → less risk of CNS and cardiac toxicity.
3. Reduced bleeding: Local vasoconstriction → bloodless operative field (useful in dentistry, surgery).
4. Allows use of lower dose of lignocaine.
5. Hemostasis - reduces intraoperative blood loss.

• End-arteries (digits - fingers/toes, nose, ear, penis) - risk of ischemic gangrene
• Patients on MAO inhibitors
• Hyperthyroidism, cardiac arrhythmias

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15. Succinylcholine Apnoea

• Normally hydrolyzed rapidly by plasma cholinesterase (pseudocholinesterase) → action lasts only 3-5 minutes.

• In patients with genetically deficient or atypical pseudocholinesterase (autosomal recessive trait), succinylcholine is NOT broken down.
• Prolonged neuromuscular blockade occurs → apnoea lasting 2-3 hours instead of 3-5 minutes.

1. Genetic - atypical pseudocholinesterase (dibucaine-resistant form)
2. Acquired deficiency - liver disease, malnutrition, pregnancy, burns, organophosphate poisoning

• Dibucaine Number (DN): Dibucaine normally inhibits 80% of pseudocholinesterase activity (DN = 80). In atypical form, DN is low (20-30).

• Ventilate the patient artificially until spontaneous respiration returns.
• There is NO specific antidote (unlike non-depolarizing NMBs, neostigmine CANNOT reverse it - it may worsen by inhibiting the already low cholinesterase).
• Fresh blood or fresh frozen plasma (contains normal pseudocholinesterase) may be given.

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16. Write the mechanism of action and therapeutic uses of Digoxin

1. Inhibits Na⁺/K⁺-ATPase (Sodium Pump): Digoxin binds and inhibits myocardial Na⁺/K⁺-ATPase pump → ↑ intracellular Na⁺.
2. Positive Inotropy: ↑ Intracellular Na⁺ → reduces activity of Na⁺/Ca²⁺ exchanger (NCX) → ↑ intracellular Ca²⁺ → stored in SR → released during action potential → ↑ cardiac contractility (positive inotropic effect).
3. Negative Chronotropy + Dromotrophy (via vagus):
   • ↑ vagal tone (indirect effect) → ↓ heart rate and ↓ AV conduction velocity
   • Useful in controlling ventricular rate in AF

1. Congestive Heart Failure (CHF) with atrial fibrillation - drug of choice
2. Atrial fibrillation (AF) - ventricular rate control
3. Atrial flutter (can convert to AF first, then control rate)
4. Supraventricular tachycardias (SVT)

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17. Define Evidence Based Medicine (EBM) and its components

1. Best available external clinical evidence (from systematic research)
2. Clinical expertise of the physician
3. Patient values and preferences

1. Ask - formulate a clear clinical question (PICO format)
2. Acquire - search for relevant evidence (PubMed, Cochrane)
3. Appraise - critically evaluate the evidence for validity
4. Apply - apply evidence to the individual patient
5. Assess - evaluate the outcome

• Reduces clinical errors and unjustified variation in practice
• Updates practice with current research
• Improves patient outcomes
• Rational prescribing and cost-effective treatment

• Not all clinical questions have RCT-level evidence
• Rare conditions are under-researched
• Individual patient may differ from trial populations

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Note: All answers are based on KD Tripathi's Essentials of Medical Pharmacology, 9th Edition as per the Dr. NTR University of Health Sciences 2nd year MBBS pharmacology syllabus.

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ACSR GOVT MEDICAL COLLEGE - Pharmacology Paper

Questions Classified by System

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🫀 CARDIOVASCULAR SYSTEM (CVS)

• Q1. A 48-year-old with Type-2 DM newly diagnosed with Hypertension (BP 150/96 mmHg) with microalbuminuria:
• a) What is the preferred drug?
• b) Classify Antihypertensive Drugs
• c) Mechanism of action, therapeutic uses and adverse effects of ACE Inhibitors (Angiotensin Converting Enzyme Inhibitors)

• Q4. Therapeutic uses and adverse effects of Beta Blockers
• Q9. Short notes on Calcium Channel Blockers
• Q11. A 38-year-old male with retrosternal chest pain on exertion - sublingual Nitro-glycerine:
• a) Mechanism of action and adverse effects of Nitrates
• b) Note on Nitrate Tolerance

• Q16. Mechanism of action and therapeutic uses of Digoxin

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🧠 AUTONOMIC NERVOUS SYSTEM (ANS) / NEUROPHARMACOLOGY

• Q2b. Treatment of Organophosphate Poisoning (involves ACh, anticholinesterases, atropine)

• Q12. Differences between Physostigmine and Neostigmine; Why Neostigmine is preferred in Myasthenia Gravis

• Q14. Rationale of using Adrenaline with Lignocaine
• Q15. Succinylcholine Apnoea

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☠️ TOXICOLOGY

• Q2. A 30-year-old farmer with Organophosphate Poisoning (salivation, sweating, vomiting, miosis, bronchospasm):
• a) Likely diagnosis
• b) Treatment of Organophosphate Poisoning

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💊 GENERAL PHARMACOLOGY / PHARMACOKINETICS

• Q3. Difference between First Order Kinetics and Zero Order Kinetics
• Q7. Define Bioavailability; Factors affecting Bioavailability
• Q6. Transdermal Drug Delivery System

• Q13. Why Oral Contraceptives are contraindicated along with Rifampicin (drug interaction - enzyme induction)

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🧬 TERATOLOGY / REPRODUCTIVE PHARMACOLOGY

• Q2. Define Teratogenicity with examples

• Q13. Why Oral Contraceptives are contraindicated with Rifampicin (also belongs here)

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🔬 CLINICAL PHARMACOLOGY / RESEARCH METHODOLOGY

• Q10. Enumerate the Phases of Clinical Trials with examples

• Q17. Define Evidence Based Medicine and its components

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⚕️ AETCOM / BIOETHICS

• Q8. Role of Autonomy and Shared Responsibility as a guiding principle in patient care

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📊 SUMMARY TABLE

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ACSR Govt Medical College, Nellore - Pharmacology Paper

Questions Divided as per Dr. NTR Health University

Paper 1 & Paper 2 Syllabus

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Official Dr. NTR Health University Division (from UHSAP Handbook):

• Paper I: General Pharmacology + ANS + CNS + CVS + Drugs acting on Renal System
• Paper II: Chemotherapy + Hormones + GIT + Blood + Drugs acting on Uterus + Heavy Metal Poisons + Drugs for Respiratory Diseases

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📘 PAPER I QUESTIONS

Essay Questions

Short Notes (5 Marks)

Very Short Notes (3 Marks)

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📗 PAPER II QUESTIONS

Essay Questions

Short Notes (5 Marks)

Very Short Notes (3 Marks)

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📊 FINAL SUMMARY

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⚠️ Important Note

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Is This the Latest Exam Pattern for 2026? - Dr. NTR Health University

✅ What is CONFIRMED for 2025-2026

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📋 Dr. NTR University - 2nd MBBS Pharmacology University Exam Pattern (2025-2026)

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📝 Theory Paper Structure (80 Marks each paper)

*This matches exactly the format of your internal paper (80+20=100, Essay 1×10, Short 11×5=55, VSN 5×3=15)

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⚠️ Important Updates for 2026 Batch

1. NMC New Curriculum (Competency-Based Medical Education - CBME)

• For the 2019 batch onwards, the NMC introduced CBME regulations.
• Your batch (appearing 2026) follows CBME-based syllabus.
• AETCOM questions are now officially included in the theory paper (1 short note of 5 marks from AETCOM per paper) - which is why your question paper had Q8 (Autonomy/Shared Responsibility).

2. The Syllabus Division Remains the Same

• Paper I: General Pharmacology + ANS + CNS + CVS + Renal
• Paper II: Chemotherapy + Hormones + GIT + Blood + Uterus + Respiratory + Heavy metals/Toxicology

3. MCQ Component is Separate

• The 20 MCQ marks are on an OMR sheet answered in the first 20 minutes - separate from the 80-mark theory booklet.
• Your internal exam paper (80+20=100) follows this same structure.

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📌 Bottom Line

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General Pharmacology - What it Includes (Paper I)

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What is Clinical Pharmacology?

1. Clinical trials - Phase I to IV
2. Evidence Based Medicine (EBM)
3. Pharmacovigilance - monitoring ADRs post-marketing
4. Therapeutic drug monitoring (TDM)
5. Rational prescribing
6. Drug regulatory affairs - CDSCO, FDA approvals
7. Bioavailability and bioequivalence studies
8. Prescription writing

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In the Context of Your Question Paper

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Short Answer

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🎯 PREDICTED QUESTIONS - Pharmacology Paper I Pre-Finals

ACSR Govt Medical College, Nellore | Based on Analysis of Both Internal Papers

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📊 ANALYSIS OF BOTH PREVIOUS PAPERS

First Internal Paper (23-02-2026) - Paper I topics covered:

• CVS: Antihypertensives, ACE inhibitors, Beta blockers, CCBs, Nitrates, Digoxin
• ANS: OP Poisoning, Physostigmine vs Neostigmine, Adrenaline+Lignocaine, Succinylcholine
• Gen Pharmacology: Bioavailability, Kinetics, TDDS, Clinical Trials, EBM

Second Internal Paper (27-04-2026) - Covered (mostly Paper II topics mixed):

• CNS: Phenytoin/Antiepileptics, Opioid overdose, Levodopa+Carbidopa, Benzodiazepines, Triptans
• CVS: Aspirin/Antiplatelet, Heparin vs Warfarin
• Gen Pharma: Paracetamol poisoning, Prostaglandins
• Others: Iron, Diuretics, Asthma steroids, SSRIs

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🔴 PATTERN OBSERVATIONS (Critical)

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🥇 MOST PROBABLE ESSAY QUESTION (1×10 Marks)

TOP PREDICTION - ESSAY:

"A patient presents with Parkinson's disease. A) Why is Levodopa combined with Carbidopa? B) Classify Anti-Parkinsonian drugs. C) Write the mechanism of action, therapeutic uses and adverse effects of Levodopa."

"Classify Diuretics. Write the mechanism of action, therapeutic uses and adverse effects of Furosemide (Loop diuretic)."

"A patient with Generalized Anxiety Disorder is prescribed a Benzodiazepine. A) Why are Benzodiazepines preferred over Barbiturates? B) Classify Sedative-Hypnotics. C) Write the mechanism of action, uses and adverse effects of Diazepam."

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🥈 MOST PROBABLE SHORT NOTES (5 Marks each)

RANK ORDER - SHORT NOTES:

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🥉 MOST PROBABLE VERY SHORT NOTES (3 Marks each)

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📋 COMPLETE PREDICTED PAPER (Most Likely Layout)

ESSAY (1×10 = 10 Marks):
→ Anti-Parkinson's / Diuretics / Antiepileptics (a new one)
  with case-based approach

SHORT NOTES (11×5 = 55 Marks):
→ Drugs used in Glaucoma
→ Treatment of Morphine Poisoning
→ Alpha-adrenergic blockers
→ Pharmacokinetic Drug Interactions
→ Newer Antiepileptics
→ Local Anaesthetics
→ CHF management / Diuretics
→ Adverse Drug Reactions classification
→ Anti-Parkinsonian drugs
→ Sedative-Hypnotics classification
→ AETCOM question (1 from bioethics)

VERY SHORT (5×3 = 15 Marks):
→ Tachyphylaxis/Drug tolerance
→ Flumazenil
→ Half-life significance
→ Atropine contraindicated in Glaucoma
→ Placebo

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⚡ LAST-MINUTE HIGH-YIELD TOPICS TO REVISE TONIGHT

🔥 MUST REVISE (Highest probability):

1. Levodopa - mechanism, carbidopa combination, uses, ADRs
2. Diuretics - classify, Furosemide (loop) mechanism + uses + ADRs
3. Drugs for Glaucoma - Timolol, Pilocarpine, Latanoprost, Acetazolamide
4. Morphine poisoning - features + treatment (Naloxone mechanism)
5. Drug interactions - pharmacokinetic types with examples
6. Alpha blockers - Prazosin, Doxazosin - uses, ADRs
7. Newer antiepileptics - Lamotrigine, Levetiracetam, Gabapentin, Vigabatrin
8. ADR classification - Type A (augmented), Type B (bizarre), Type C, D, E, F with examples
9. Diazepam - mechanism, uses, why preferred over barbiturates
10. Local anaesthetics - Lignocaine mechanism, uses

📌 SECONDARY REVISION:

• Tachyphylaxis vs Tolerance vs Dependence
• Placebo
• Therapeutic Drug Monitoring
• Drug receptor theories (agonist/partial agonist/antagonist)

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⚠️ Disclaimer: These are predictions based on pattern analysis of your two internal papers and standard NTR university question trends. They are NOT guaranteed. Make sure you also quickly revise topics from CVS (in case a question repeats with a twist) and have basic knowledge of all Paper I systems.

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🎯 Most Likely Essay Topic in Paper I - Dr. NTR University Exams

The Clear Winner: CVS (Cardiovascular System)

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📊 Historical Essay Topic Frequency - NTR Paper I

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🔥 The #1 Most Repeated Essay in NTR Paper I

"Classify Antihypertensive Drugs + Write mechanism/uses/ADRs of one drug (usually ACE inhibitor, Beta blocker, or CCB)"

• The NTR official handbook sample paper itself uses this as the model essay question: "Classify antihypertensive drugs. Write pharmacological actions, uses and adverse effects of Ramipril"
• Your First Internal (Feb 2026) was: Classify antihypertensives + ACE inhibitors ← it came in your internals because the university itself repeats this pattern
• Antihypertensives = biggest topic in CVS = Paper I = highest weightage

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⚠️ BUT - Since it Already Appeared in Your First Internal...

Option A - Still CVS but different drug:

"Classify Anti-anginal drugs. Write the mechanism of action, uses and adverse effects of Nitrates" OR "A patient has heart failure - Classify drugs used in CHF. Write mechanism/uses/ADRs of Digoxin"

Option B - CNS (2nd most likely for essay):

"A patient presents with epilepsy - Classify Antiepileptic drugs. Write mechanism/uses/ADRs of Phenytoin/Valproate"

• Note: Phenytoin already appeared in Internal 2, so Valproate or Carbamazepine is more likely now

Option C - Diuretics (Dark horse pick):

"Classify Diuretics. Write mechanism/uses/ADRs of Loop diuretics / Furosemide"

• Diuretics bridges CVS + Renal (both Paper I) and has never appeared as essay in your internals

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🎯 FINAL RANKING FOR TOMORROW'S PRE-FINAL ESSAY

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💡 Smart Revision Strategy for Tonight

1. Beta Blockers - Classification of antihypertensives + full beta blocker essay (uses, ADRs already covered in Int 1 - just revise)
2. Valproate / Antiepileptics - Classification + Valproate mechanism/uses/ADRs
3. Furosemide / Diuretics - Classification of diuretics + loop diuretic full answer

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🕐 2-Hour Revision Plan for Tonight

Pharmacology Paper I Pre-Final | ACSR Govt Medical College, Nellore

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⏰ SCHEDULE AT A GLANCE

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🟦 BLOCK 1 (0:05 - 0:55) — BETA BLOCKERS ESSAY

Total: 50 Minutes

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⏱ Minutes 0-10 | CLASSIFICATION (Write it out once)

• "A Met Biso" = Atenolol, Metoprolol, Bisoprolol (cardioselective)
• "Pro Tim Sot" = Propranolol, Timolol, Sotalol (non-selective)

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⏱ Minutes 10-25 | MECHANISM + PHARMACOLOGICAL ACTIONS

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⏱ Minutes 25-40 | THERAPEUTIC USES (The Big List)

1. Hypertension - first-line, especially young patients + post-MI HTN
2. Angina pectoris - ↓ O₂ demand (↓HR + ↓contractility)
3. Myocardial Infarction - reduce infarct size, prevent reinfarction
4. Cardiac Arrhythmias - SVT, AF rate control, ventricular arrhythmias
5. Congestive Heart Failure - Carvedilol, Bisoprolol, Metoprolol (stable CHF only)
6. Hyperthyroidism - control tachycardia, tremors (Propranolol)
7. Glaucoma - Timolol eye drops
8. Migraine prophylaxis - Propranolol
9. Essential tremor - Propranolol
10. Anxiety (situational/performance) - Propranolol
11. Portal hypertension - Propranolol (prevent variceal bleed)
12. Phaeochromocytoma - after alpha blockade

---

⏱ Minutes 40-50 | ADVERSE EFFECTS + CONTRAINDICATIONS

1. Bradycardia, heart block
2. Bronchoconstriction - dangerous in asthma
3. Fatigue, depression, sleep disturbances, nightmares (propranolol - lipid soluble, crosses BBB)
4. Cold extremities, Raynaud's worsening
5. Masking of hypoglycemia in diabetics (except sweating)
6. ↑ Triglycerides, ↓ HDL
7. Sexual dysfunction (impotence)
8. Rebound hypertension/angina on abrupt withdrawal

• Asthma / COPD
• Bradycardia / AV Block (2nd, 3rd degree)
• Cardiogenic shock / decompensated CHF
• Diabetes (poorly controlled)
• Extreme peripheral vascular disease

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🟩 BLOCK 2 (1:00 - 1:50) — ANTIEPILEPTICS ESSAY

Total: 50 Minutes

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⏱ Minutes 0-12 | CLASSIFICATION OF ANTIEPILEPTICS

• Phenytoin, Carbamazepine, Valproate, Phenobarbitone, Lamotrigine, Levetiracetam

• Ethosuximide (drug of choice), Valproate, Clonazepam

• Valproate (drug of choice), Clonazepam, Levetiracetam

• Diazepam IV (first line) → Phenytoin IV → Phenobarbitone IV → General anaesthesia

• Diazepam (rectal/IV), Phenobarbitone (prophylaxis)

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⏱ Minutes 12-30 | FOCUS DRUG: VALPROATE (Most likely - since Phenytoin already appeared)

1. Blocks voltage-gated Na⁺ channels (like phenytoin) - reduces repetitive firing
2. Enhances GABA activity - increases GABA synthesis + inhibits GABA breakdown
3. Blocks T-type Ca²⁺ channels in thalamus - useful in absence seizures

1. Broadest spectrum antiepileptic - used in ALL seizure types
2. Drug of choice for myoclonic seizures
3. Drug of choice for Juvenile myoclonic epilepsy
4. Generalized tonic-clonic seizures
5. Absence seizures (alternative to ethosuximide)
6. Bipolar disorder (mood stabilizer)
7. Migraine prophylaxis

1. Hepatotoxicity - serious, idiosyncratic, especially in children under 2 years
2. Teratogenicity - Neural tube defects (spina bifida) - give folic acid
3. Weight gain - most common
4. GI upset - nausea, vomiting (take with food)
5. Alopecia (hair loss) - reversible
6. Tremors
7. Thrombocytopenia
8. Pancreatitis - rare but serious
9. Hyperammonemia (encephalopathy)

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⏱ Minutes 30-45 | ALSO REVISE: PHENYTOIN (Since it may appear as part of classification question)

• Hirsutism (excess hair)
• Gingival hyperplasia (gum overgrowth) - most characteristic
• Ataxia, nystagmus (dose-related CNS toxicity)
• Lymphadenopathy
• Steven-Johnson syndrome

• Teratogenicity - Fetal hydantoin syndrome
• Megaloblastic anaemia (folate deficiency)
• Zero order kinetics at therapeutic doses - non-linear pharmacokinetics
• Enzyme inducer (CYP450)

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⏱ Minutes 45-50 | NEWER ANTIEPILEPTICS (Short note level)

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🟨 FINAL 10 MINUTES (1:50 - 2:00) — RAPID FIRE REVIEW

Quick recall test - answer mentally without looking:

• Which is DOC in glaucoma? → Timolol
• Why avoid in asthma? → β2 blockade → bronchoconstriction
• Which has α+β action? → Labetalol, Carvedilol
• Which is cardioselective? → Atenolol, Metoprolol, Bisoprolol
• Withdrawal causes? → Rebound HTN/angina

• DOC absence seizures? → Ethosuximide
• DOC myoclonic seizures? → Valproate
• DOC status epilepticus? → Diazepam IV
• Gingival hyperplasia - which drug? → Phenytoin
• Neural tube defects - which drug? → Valproate
• Zero order kinetics drug? → Phenytoin
• Broadest spectrum antiepileptic? → Valproate

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📌 SLEEP & EXAM TIPS

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ESSAY ANSWER 1

Beta Blockers (β-Adrenergic Blocking Drugs)

As per KD Tripathi | 10 Marks

---

INTRODUCTION

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CLASSIFICATION

BETA BLOCKERS
│
├── 1. NON-SELECTIVE (β1 + β2)
│   ├── Without ISA → Propranolol, Timolol, Sotalol, Nadolol
│   └── With ISA    → Pindolol, Oxprenolol
│
├── 2. CARDIOSELECTIVE (β1 only)
│   ├── Without ISA → Atenolol, Metoprolol, Bisoprolol, Esmolol
│   └── With ISA    → Acebutolol, Celiprolol
│
└── 3. α + β BLOCKERS (Mixed)
            └── Labetalol, Carvedilol

ISA = Intrinsic Sympathomimetic Activity (partial agonist property)

---

MECHANISM OF ACTION

Catecholamines (Adrenaline/Noradrenaline)
            ↓
     β1 and β2 Receptors
            ↓
  Beta Blockers COMPETITIVELY BLOCK these receptors
            ↓
    ┌───────────────────────────────┐
    │                               │
  β1 blockade                    β2 blockade
(Heart, Kidney, JGA)         (Bronchi, Blood vessels,
    │                               │  Liver, Uterus)
    ↓                               ↓
↓ HR, ↓ Contractility,        Bronchoconstriction,
↓ AV conduction,              Vasoconstriction,
↓ Renin release               Masking of hypoglycemia

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PHARMACOLOGICAL ACTIONS

---

THERAPEUTIC USES

THERAPEUTIC USES OF BETA BLOCKERS
              │
    ┌─────────┴──────────┐
    │                    │
CARDIOVASCULAR      NON-CARDIOVASCULAR
    │                    │
    ├─ Hypertension       ├─ Glaucoma (Timolol eye drops)
    ├─ Angina pectoris    ├─ Hyperthyroidism
    ├─ MI (post)          ├─ Migraine prophylaxis
    ├─ Arrhythmias        ├─ Essential tremor
    ├─ Heart failure      ├─ Anxiety (situational)
    │  (stable CHF -      └─ Portal hypertension
    │  Carvedilol,
    │  Bisoprolol)
    └─ Phaeochromocytoma
       (after α-blockade)

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ADVERSE EFFECTS

ADVERSE EFFECTS
        │
  ┌─────┴──────────────────────┐
  │                            │
CARDIOVASCULAR           EXTRA-CARDIAC
  │                            │
  ├─ Bradycardia           ├─ Bronchoconstriction (↑ in asthma)
  ├─ Heart block           ├─ Cold extremities
  ├─ Hypotension           ├─ Fatigue, depression (propranolol)
  └─ Worsening CHF         ├─ Nightmares, sleep disturbance
  (decompensated)          ├─ Sexual dysfunction
                           ├─ Masking hypoglycemia (in diabetics)
                           ├─ ↑ TG, ↓ HDL
                           └─ Rebound HTN/angina on
                              abrupt withdrawal

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CONTRAINDICATIONS

CONTRAINDICATIONS
(Mnemonic: ABCDE)

A → Asthma / COPD
B → Bradycardia / AV Block (2nd, 3rd degree)
C → Cardiogenic shock / decompensated CHF
D → Diabetes mellitus (poorly controlled)
E → Extreme peripheral vascular disease
     (Raynaud's, intermittent claudication)

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IMPORTANT DRUG INTERACTIONS

---

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ESSAY ANSWER 2

Antiepileptic Drugs (Antiseizure Drugs)

As per KD Tripathi | 10 Marks

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INTRODUCTION

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CLASSIFICATION

A. Based on Seizure Type

SEIZURE TYPES & DRUGS
          │
  ┌───────┴────────────────────┐
  │                            │
PARTIAL SEIZURES           GENERALIZED SEIZURES
  │                            │
  │                   ┌────────┴─────────────────┐
Simple + Complex       │              │            │
Partial               GTCS         Absence     Myoclonic
  │                    │           (Petit mal)     │
  │              Phenytoin        Ethosuximide   Valproate
  │              Carbamazepine    Valproate      Clonazepam
  │              Valproate        Clonazepam     Levetiracetam
  │              Phenobarbitone
  └──────────────Lamotrigine
                 Levetiracetam

B. Classification by Drug Generation

ANTIEPILEPTICS
      │
      ├── OLDER / CLASSICAL
      │       ├── Phenytoin
      │       ├── Phenobarbitone
      │       ├── Carbamazepine
      │       ├── Ethosuximide
      │       └── Valproate (Sodium valproate)
      │
      ├── NEWER (2nd Generation)
      │       ├── Lamotrigine
      │       ├── Gabapentin
      │       ├── Topiramate
      │       ├── Vigabatrin
      │       ├── Oxcarbazepine
      │       └── Levetiracetam
      │
      └── BENZODIAZEPINES (used in epilepsy)
              ├── Diazepam (Status epilepticus - IV)
              ├── Clonazepam
              └── Lorazepam

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MECHANISMS OF ACTION

HOW AEDs WORK
(3 Main Mechanisms)

1. Na⁺ CHANNEL BLOCKADE
   ──────────────────────
   Phenytoin, Carbamazepine, Lamotrigine,
   Oxcarbazepine, Valproate (partial)
         │
         ↓
   Block voltage-gated Na⁺ channels
   in inactivated state
         │
         ↓
   Prevent repetitive high-frequency
   neuronal firing


2. GABA ENHANCEMENT
   ──────────────────
   Phenobarbitone, Benzodiazepines,
   Vigabatrin, Valproate, Gabapentin
         │
         ↓
   ↑ GABA-mediated Cl⁻ influx
   OR inhibit GABA breakdown
         │
         ↓
   Neuronal hyperpolarization
   → reduced excitability


3. Ca²⁺ CHANNEL BLOCKADE
   ────────────────────────
   Ethosuximide, Valproate
         │
         ↓
   Block T-type Ca²⁺ channels
   in thalamic neurons
         │
         ↓
   Suppress thalamocortical
   pacemaker activity
   (prevents absence seizures)

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FOCUS DRUG: SODIUM VALPROATE (Most Important)

Mechanism (TRIPLE action - write all 3):

1. Blocks Na⁺ channels
2. Enhances GABA (inhibits GABA transaminase - the enzyme that breaks down GABA)
3. Blocks T-type Ca²⁺ channels

Why Valproate is Special - BROADEST SPECTRUM:

SODIUM VALPROATE

Broadest spectrum AED
        │
  ┌─────┴────────────────────────┐
  │                              │
SEIZURES                   OTHER USES
  │                              │
  ├─ Generalized TC          ├─ Bipolar disorder
  ├─ Absence seizures        │   (mood stabilizer)
  ├─ Myoclonic (DOC)         └─ Migraine prophylaxis
  ├─ Juvenile myoclonic
  │   epilepsy (DOC)
  └─ Partial seizures

Adverse Effects of Valproate:

ADVERSE EFFECTS OF VALPROATE
(Mnemonic: "WHAT PAN")

W → Weight gain (most common)
H → Hepatotoxicity (serious - monitor LFTs)
A → Alopecia (hair loss - reversible)
T → Teratogenicity (neural tube defects - spina bifida)

P → Pancreatitis (rare but serious)
A → Ammonia ↑ (hyperammonemia)
N → Nausea, vomiting (take with food)

Plus: Tremor, thrombocytopenia

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FOCUS DRUG: PHENYTOIN

Mechanism:

Uses:

1. GTCS (Generalized Tonic-Clonic Seizures) - drug of choice
2. Partial seizures
3. Status epilepticus (IV)
4. Cardiac arrhythmias (digoxin-induced)

Adverse Effects:

ADVERSE EFFECTS OF PHENYTOIN
(Mnemonic: "GASH NMZ")

G → Gingival hyperplasia (most characteristic)
A → Ataxia, nystagmus (cerebellar)
S → Steven-Johnson syndrome
H → Hirsutism (facial hair in women)

N → Neonatal toxicity (teratogenic)
M → Megaloblastic anaemia (folate deficiency)
Z → Zero-order kinetics (nonlinear - toxic at small dose increase)

Plus: Enzyme inducer (reduces OCP efficacy)
      Osteomalacia (vitamin D metabolism)

---

STATUS EPILEPTICUS - TREATMENT FLOWCHART

STATUS EPILEPTICUS
(Seizure > 5 minutes OR 2+ seizures without recovery)
                    │
                    ↓
          ┌─── ABC + IV access ───┐
          │   Oxygen, Monitor     │
          └───────────┬───────────┘
                      │
                      ↓
            STEP 1 (0-5 min)
         Diazepam 10mg IV STAT
         OR Lorazepam 4mg IV
                      │
                 Not controlled?
                      │
                      ↓
            STEP 2 (10-30 min)
         Phenytoin 15-20 mg/kg IV
         (slow infusion - risk of arrhythmia)
                      │
                 Not controlled?
                      │
                      ↓
            STEP 3 (30-60 min)
         Phenobarbitone 20mg/kg IV
                      │
                 Not controlled?
                      │
                      ↓
            STEP 4 (>60 min)
         REFRACTORY STATUS
         General Anaesthesia
         (Thiopentone / Propofol / Midazolam)
         + ICU + EEG monitoring

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NEWER ANTIEPILEPTIC DRUGS (Short Table)

---

DRUG OF CHOICE SUMMARY TABLE

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KEY EXAM POINTS TO REMEMBER

QUICK EXAM MEMORY ANCHORS

Phenytoin   → Gingival hyperplasia + Zero order kinetics
Valproate   → Broadest spectrum + Neural tube defects
Ethosuximide → ONLY for absence seizures
Carbamazepine → Drug of choice for Trigeminal neuralgia
Vigabatrin   → Visual field defects
Gabapentin   → Neuropathic pain
Diazepam    → Status Epilepticus (IV)
Lamotrigine → Safe in pregnancy
Levetiracetam → Fewest drug interactions

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Both these answers cover a full 10-mark essay response. In your exam, write the classification first, then mechanism, uses, and ADRs. Draw the flowcharts wherever possible - examiners give extra credit for neat diagrams. All the best tomorrow! 🍀