---

BDS 2nd Year Theory Examination - Complete Answers

Part A (Short Questions)

---

PART B

Q.1 — Drugs for Asthma: Importance of Inhaled Steroids + Treatment (4+3 = 7 marks)

1. Beta-2 agonists:
   • Short-acting (SABA): Salbutamol (albuterol), Terbutaline - used as "relievers"
   • Long-acting (LABA): Salmeterol, Formoterol - used as "controllers"
2. Methylxanthines: Theophylline, Aminophylline
3. Anticholinergics: Ipratropium bromide, Tiotropium

1. Inhaled corticosteroids (ICS): Beclomethasone, Budesonide, Fluticasone
2. Leukotriene receptor antagonists: Montelukast, Zafirlukast
3. Mast cell stabilisers: Sodium cromoglycate, Nedocromil
4. Biologics: Omalizumab (anti-IgE), Mepolizumab (anti-IL-5)

1. Anti-inflammatory action: Suppress airway inflammation by inhibiting synthesis of prostaglandins, leukotrienes, and cytokines; reduce mast cell, eosinophil, and T-lymphocyte activity in airways.
2. Reduce airway hyper-responsiveness: Long-term use decreases bronchial hyper-reactivity.
3. Prevent remodelling: Inhibit structural changes (fibrosis, smooth muscle hypertrophy) that occur with chronic asthma.
4. Reduce exacerbations: Significantly lower frequency and severity of asthma attacks.
5. Improve lung function: Increase FEV1 and peak expiratory flow rate (PEFR) over time.
6. Minimal systemic side effects: Compared to oral steroids, inhaled delivery targets the lung directly - lower doses, fewer systemic effects.
7. Reduce need for rescue bronchodilators: Better day-to-day control.

---

Q.2 — Antiepileptic Drugs: Classify + Mechanism of Phenytoin + Adverse Effects (2+2+3 = 7 marks)

• It binds to the inactivated state of Na+ channels, prolonging their inactivation.
• This reduces the ability of neurons to fire rapidly (limits high-frequency repetitive discharge).
• It does NOT affect normal neuron firing at low frequencies (selective for epileptic foci).
• Additionally, it inhibits Ca2+ influx at nerve terminals and may enhance GABA activity at high doses.

• Nystagmus (earliest sign of toxicity)
• Ataxia (cerebellar signs)
• Diplopia, dizziness, mental confusion

• Gingival hyperplasia (gum overgrowth) - occurs in ~20% of patients; very relevant in dentistry
• Hirsutism (excess hair growth)
• Coarsening of facial features
• Megaloblastic anaemia (folate deficiency)
• Peripheral neuropathy
• Osteomalacia (vitamin D metabolism interference)
• Teratogenicity: Fetal hydantoin syndrome

• Skin rashes (Stevens-Johnson syndrome rarely)
• Hepatotoxicity
• Lupus-like syndrome

---

Q.3 — Short Notes (4x4 = 16 marks)

1. Drug selection: Choose the most effective drug with the least toxicity for the dental indication (e.g., amoxicillin for dental infections, NSAIDs for pain).
2. Minimum effective dose: Use the lowest dose that achieves the therapeutic goal.
3. Route of administration: Local/topical preferred over systemic when possible to minimise systemic side effects (e.g., local anaesthetics, topical antifungals for oral candidiasis).
4. Drug interactions: Assess patient's existing medications (e.g., avoid NSAIDs in patients on anticoagulants; vasoconstrictor caution in patients on tricyclic antidepressants or MAO inhibitors).
5. Patient factors: Consider age, weight, renal/hepatic function, allergies (especially penicillin allergy), pregnancy, and comorbidities.
6. Antibiotic stewardship: Avoid prophylactic antibiotics unless indicated (e.g., infective endocarditis prophylaxis). Do not over-prescribe to prevent resistance.
7. Informed consent: Patient must be informed about drugs, their effects, and alternatives.
8. Emergency drugs: Dentist must keep emergency drugs available - adrenaline (epinephrine) for anaphylaxis, GTN for angina, glucose for hypoglycaemia, diazepam for seizures.

---

• Oral ulcers (aphthous stomatitis): Triamcinolone in orabase (topical)
• Oral lichen planus: Topical/systemic steroids
• Post-extraction swelling: Reduce inflammation
• Pemphigus/pemphigoid: Systemic prednisolone
• Anaphylaxis: Hydrocortisone IV (adjunct to adrenaline)
• Bell's palsy: Prednisolone
• General: Asthma, rheumatoid arthritis, organ transplantation, Addison's disease, nephrotic syndrome

• S - Susceptibility to infections (immunosuppression)
• T - Thin skin, bruising, striae, delayed wound healing
• E - Electrolyte imbalance (Na+ retention, K+ loss - hypokalemia)
• R - Raised blood glucose (steroid-induced diabetes)
• O - Osteoporosis (long-term use)
• I - Increased BP (hypertension), Increased weight (Cushing's syndrome)
• D - Depression/psychosis; also Dyspepsia/peptic ulcer
• S - Suppression of HPA axis (adrenal suppression - abrupt withdrawal causes Addisonian crisis)

---

1. Penicillins: Amoxicillin, Ampicillin, Cloxacillin, Piperacillin
2. Cephalosporins: 1st generation (Cefalexin), 2nd (Cefuroxime), 3rd (Ceftriaxone), 4th (Cefepime), 5th (Ceftaroline)
3. Carbapenems: Imipenem, Meropenem, Ertapenem
4. Monobactams: Aztreonam

• Inhibit transpeptidase enzyme (also called penicillin-binding proteins, PBPs) which cross-links peptidoglycan chains in bacterial cell walls.
• This prevents cell wall synthesis - bacteria undergo osmotic lysis and death.
• They are bactericidal and act on actively dividing bacteria.

• Beta-lactamase enzyme production (cleaves the beta-lactam ring)
• Modified PBPs (e.g., MRSA)
• Reduced outer membrane permeability
• Efflux pumps

• Hypersensitivity reactions (most important - range from rash to anaphylaxis)
• Diarrhoea, nausea, vomiting
• Superinfection (Clostridium difficile colitis with broad-spectrum agents)

---

1. H. pylori eradication (if H. pylori positive):
   • Triple therapy: PPI + Amoxicillin + Clarithromycin for 14 days
   • Quadruple therapy (if resistance): PPI + Bismuth + Metronidazole + Tetracycline
2. Proton Pump Inhibitors (PPIs) - First line:
   • Omeprazole, Pantoprazole, Rabeprazole
   • Mechanism: Irreversibly inhibit H+/K+-ATPase pump in parietal cells
   • Most potent acid suppressants
3. H2 Receptor Antagonists:
   • Ranitidine, Famotidine, Cimetidine
   • Block histamine H2 receptors on parietal cells, reducing acid secretion
4. Antacids:
   • Magnesium hydroxide, Aluminium hydroxide
   • Neutralise gastric acid; provide quick symptomatic relief
5. Mucosal protective agents:
   • Sucralfate: Forms protective coating over ulcer
   • Misoprostol (PGE1 analogue): Stimulates mucus/bicarbonate secretion; used in NSAID-induced ulcers
   • Bismuth: Kills H. pylori, coats ulcer
6. Avoid NSAIDs and smoking cessation.

---

Q.4 — Fill in the Blanks (5x1 = 5 marks)

---

---

Part A (Short/One-line Questions)

---

PART B

Q.1 — Classify Antitubercular Drugs + Mechanism of Action and Adverse Effects of First-Line ATT Drugs (3+2+2 = 7 marks)

• Fluoroquinolones: Levofloxacin, Moxifloxacin
• Injectable agents: Amikacin, Kanamycin, Capreomycin
• Others: Ethionamide, Cycloserine, Para-aminosalicylic acid (PAS), Linezolid, Bedaquiline (newer)

• Isoniazid: Prodrug activated by mycobacterial catalase-peroxidase (KatG) → inhibits InhA (enoyl-ACP reductase) → blocks mycolic acid synthesis → disrupts cell wall
• Rifampicin: Binds beta-subunit of bacterial RNA polymerase → inhibits mRNA transcription → bactericidal
• Pyrazinamide: Converted to pyrazinoic acid → disrupts membrane potential and energy metabolism → bactericidal against dormant/intracellular bacilli
• Ethambutol: Inhibits arabinosyl transferase → prevents polymerisation of arabinogalactan → weakens cell wall → bacteriostatic

• Intensive phase: 2 months HRZE
• Continuation phase: 4 months HR

---

Q.2 — Classify Antiepileptic Drugs + Mechanism of Action and Adverse Effects of Phenytoin (3+2+2 = 7 marks)

• It preferentially binds to the inactivated state of Na+ channels and slows their recovery back to the resting (activatable) state.
• This prolongs the refractory period, limiting the ability of neurons to fire at high frequencies.
• It selectively suppresses epileptic foci (which fire rapidly) without affecting normal neuronal activity at low frequencies.
• Additional actions: inhibits Ca2+ influx at presynaptic terminals; may potentiate GABA at higher concentrations.

• Nystagmus - earliest sign of toxicity
• Ataxia - cerebellar sign
• Diplopia, vertigo, mental confusion

• Gingival hyperplasia (~20% patients) - very important in dental practice
• Hirsutism (excess body/facial hair)
• Coarsening of facial features
• Megaloblastic anaemia (folate deficiency due to impaired absorption)
• Osteomalacia (induces CYP450 → accelerated vitamin D catabolism)
• Peripheral neuropathy

• Fetal hydantoin syndrome: cleft palate, digital anomalies, growth retardation

• Stevens-Johnson syndrome
• Drug-induced lupus
• Hepatotoxicity

---

Q.3 — Short Notes (4×4 = 16 marks)

(i) Mast Cell Stabilisers in Bronchial Asthma

• Stabilise mast cell membranes by blocking chloride channels and preventing Ca2+ entry into mast cells
• Inhibit degranulation of mast cells triggered by allergen-IgE interaction
• Prevent release of mediators: histamine, leukotrienes (LTC4, LTD4), prostaglandins, platelet-activating factor (PAF)
• Also inhibit activation of eosinophils, neutrophils, and macrophages in airways
• Block both early and late phase of allergic bronchoconstriction

• Prophylaxis of mild-to-moderate allergic (extrinsic) asthma - especially in children
• Exercise-induced asthma (taken 15-20 min before exercise)
• Allergic rhinitis, allergic conjunctivitis

• NOT useful for acute attacks (no bronchodilator action)
• Must be taken regularly (4-6 weeks for full effect)
• Very safe - no significant systemic side effects
• Available as inhaler/nebuliser solution

---

(ii) Fluoroquinolones

• 1st generation: Nalidixic acid (urinary infections only)
• 2nd generation: Ciprofloxacin, Norfloxacin, Ofloxacin
• 3rd generation: Levofloxacin, Sparfloxacin
• 4th generation: Moxifloxacin, Gatifloxacin

• Inhibit DNA gyrase (topoisomerase II) and topoisomerase IV enzymes in bacteria
• DNA gyrase introduces negative supercoils to relieve tension during DNA replication
• Inhibition causes double-strand DNA breaks → bactericidal action
• Concentration-dependent killing

• Pericoronitis, aggressive periodontitis (combined with metronidazole)
• Orofacial infections resistant to penicillin

• GI upset (nausea, vomiting, diarrhoea) - most common
• CNS: headache, dizziness, rarely seizures (lower seizure threshold)
• Tendinopathy/tendon rupture (Achilles tendon - especially with steroids)
• Phototoxicity (skin)
• Cartilage damage - contraindicated in children and pregnant women
• QT prolongation (Moxifloxacin)
• C. difficile colitis

---

(iii) Omeprazole

• Prodrug: activated in the acidic environment of the parietal cell canaliculus to a sulfenamide (active form)
• Irreversibly inhibits H+/K+-ATPase (the proton pump) on the luminal surface of gastric parietal cells
• Blocks the final common pathway of acid secretion regardless of the stimulus (histamine, gastrin, acetylcholine)
• Effect lasts 24-48 hours (new pumps must be synthesised for recovery)

• Peptic ulcer disease (gastric and duodenal ulcers)
• H. pylori eradication (part of triple/quadruple therapy)
• GERD (Gastroesophageal Reflux Disease)
• Zollinger-Ellison syndrome
• NSAID-induced ulcer prevention
• Stress ulcer prophylaxis

• Generally well tolerated
• Long-term use: hypomagnesaemia, vitamin B12 deficiency, osteoporosis (reduced Ca2+ absorption), increased risk of C. difficile infection
• Headache, diarrhoea, nausea (short-term)
• Drug interactions: reduces absorption of ketoconazole, iron; reduces efficacy of clopidogrel (via CYP2C19 inhibition)

---

(iv) Chelating Agents

---

Q.4 — Fill in the Blanks (5×1 = 5 marks)

• Adrenaline causes local vasoconstriction → reduces absorption of local anaesthetic into blood → prolongs duration of action and reduces systemic toxicity.

---