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TU/IOM - General Surgery B - XXVIII B Th. (2083/03)

Bachelor Level / MBBS 3rd Phase, 5th Year

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GROUP "A" - GENERAL SURGERY (48 Marks)

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Q1. Classify the complication (wound redness/warmth/pain after appendectomy on day 4). Describe the factors responsible. [3+5=8]

Classification of the Complication (3 marks)

• Clean-contaminated (Class II) wound - GI tract opened under controlled conditions.
• If perforated appendix: Dirty/infected (Class IV).

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Factors Responsible for SSI (5 marks)

1. Age - Extremes of age impair immune response
2. Nutritional status - Malnutrition, hypoalbuminaemia reduce healing
3. Diabetes mellitus - Impaired neutrophil function, poor tissue perfusion
4. Obesity - Poor vascularity of adipose tissue, increased dead space
5. Immunosuppression - Steroids, chemotherapy, HIV
6. Remote infection - Pre-existing infection elsewhere
7. Smoking - Impairs tissue oxygenation, vasoconstriction

1. Duration of surgery - >2 hours significantly increases risk
2. Type of wound - Contaminated > clean wound
3. Inadequate skin preparation / antisepsis
4. Breach in aseptic technique - Glove puncture, inadequate draping
5. Excessive use of diathermy - Creates tissue necrosis/dead space
6. Poor haemostasis - Haematoma formation provides culture medium
7. Use of drains - Act as conduit for retrograde infection
8. Bowel preparation - Inadequate preparation increases contamination

1. Virulence of organism - In appendicitis: E. coli, Bacteroides, Klebsiella
2. Inoculum size
3. Antibiotic resistance
4. Inadequate antibiotic prophylaxis - Wrong choice, timing, or dose

1. Theatre air contamination - Inadequate laminar flow
2. Length of pre-operative hospital stay - Colonization with hospital flora
3. Hair removal - Shaving (vs clipping) increases risk

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Q2. Define Necrotizing Fasciitis. Describe its clinical features and management. [2+6=8]

Definition (2 marks)

• Type I (Polymicrobial/synergistic) - Mixed aerobic + anaerobic organisms; most common (80-90%); occurs in diabetics, immunocompromised, perineal/abdominal region
• Type II (Monomicrobial) - Group A Streptococcus (Streptococcal gangrene); younger healthier patients; limbs
• Type III - Gram-negative monomicrobial (Clostridial/marine organisms)
• Fournier's gangrene - NF of perineum/genitalia

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Clinical Features (3 marks)

• Erythema, swelling, warmth - indistinguishable from cellulitis
• Pain out of proportion to local signs - hallmark finding
• Fever, tachycardia - systemic sepsis

• Skin becomes dusky, violaceous, then grey-black (skin necrosis)
• Blistering / bullae containing serous/haemorrhagic fluid
• Skin anaesthesia - destruction of cutaneous nerves
• Crepitus on palpation (gas-forming organisms - 50% of cases)
• Rapid spread along fascial planes ("spreading hands of death")

• Skin gangrene with frank necrosis
• Septic shock - hypotension, tachycardia, altered consciousness
• Multi-organ failure - renal failure, DIC, ARDS

• CRP >150 mg/L (+4), WBC >25 x 10⁹/L (+2), Hb <11 g/dL (+2), Na <135 (+2), Creatinine >141 (+2), Glucose >10 (+1)
• Score ≥6: High risk for NF

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Management (3 marks)

• IV access, fluid resuscitation, oxygen
• Foley catheter, monitor urine output
• ICU admission

• Blood: CBC, RFT, LFT, coagulation profile, blood cultures, LRINEC score
• Imaging: X-ray (gas in soft tissue), CT scan (gas tracking along fascial planes - "dirty fascia" sign) - gold standard imaging
• Frozen section biopsy for histological confirmation

• Wide radical debridement - the most important step
  • Excise all necrotic tissue until healthy bleeding tissue margins
  • "Finger test" - if fascia separates easily from muscle without bleeding = NF
• Second-look surgery at 24-48 hours - re-exploration mandatory
• Repeated debridement until infection controlled
• Wound left open - packed with antiseptic gauze
• Amputation may be required for limb NF
• Fournier's: orchiectomy rarely needed (testes have separate blood supply)

• Type I: Broad-spectrum - Piperacillin-tazobactam + Metronidazole + Aminoglycoside
• Type II: Penicillin G + Clindamycin (inhibits toxin production)
• Clindamycin is important for streptococcal NF - inhibits M-protein and exotoxin synthesis

• Hyperbaric oxygen therapy - enhances neutrophil killing, inhibits anaerobes (where available)
• Nutritional support - early enteral/parenteral nutrition
• Wound coverage - split-thickness skin grafts/flaps once infection cleared
• IVIG - for streptococcal toxic shock syndrome

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Q3. Describe the stages of wound healing. Discuss the factors that affect wound healing. [4+4=8]

Stages of Wound Healing (4 marks)

• Vascular injury → vasoconstriction (thromboxane A2, endothelin)
• Platelet aggregation + activation → platelet plug
• Coagulation cascade → fibrin clot formation
• Fibrin clot acts as scaffold for subsequent healing
• Platelets release growth factors: PDGF, TGF-β, EGF
• Role of PDGF: key signal initiating wound healing by attracting neutrophils and macrophages

• Vasodilation - histamine, prostaglandins (PGE2), serotonin
• Cardinal signs: rubor, calor, dolor, tumor, functio laesa
• Neutrophils (peak Day 1-2): phagocytosis of bacteria and debris, release of proteases and ROS
• Macrophages (peak Day 2-4): "master cells of healing" - phagocytose debris, secrete growth factors (VEGF, FGF, TGF-β, IL-1), orchestrate subsequent phases
• Monocytes from blood → tissue macrophages

1. Re-epithelialization: Keratinocytes migrate from wound edges and dermal appendages; complete within 24-48 hours in primary closure. Growth factors: EGF, KGF
2. Granulation tissue formation: Fibroblasts migrate, proliferate; synthesize Type III collagen, proteoglycans, fibronectin. Angiogenesis (VEGF-driven) forms "beefy red" granulation tissue
3. Wound contraction: Myofibroblasts (specialized fibroblasts with α-smooth muscle actin) contract wound by up to 80% of original size (important in open wounds)

• Type III collagen replaced by Type I collagen (organized along stress lines)
• Collagen cross-linking by lysyl oxidase - increased tensile strength
• Scar matures: becomes pale, flat, pliable
• Tensile strength at Day 7: ~10%; Day 21: ~50%; Day 42: ~80%; never >80% of original skin
• Excess remodelling → hypertrophic scar / keloid
• Deficient remodelling → chronic wound

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Factors Affecting Wound Healing (4 marks)

• Protein deficiency: impairs collagen synthesis, immune function
• Vitamin C (ascorbic acid) deficiency: impairs collagen hydroxylation (hydroxylation of proline/lysine) → wound dehiscence (scurvy)
• Vitamin A deficiency: impairs epithelialization
• Zinc deficiency: impairs DNA synthesis, collagen synthesis, reduces tensile strength
• Iron: required for prolyl hydroxylase activity

• Diabetes mellitus: impairs neutrophil function, reduced VEGF, neuropathy, microangiopathy
• Jaundice: impairs fibroblast function, bilirubin inhibits collagen synthesis
• Renal failure: uraemia impairs all phases
• Hypothyroidism: reduced metabolic rate, impaired collagen synthesis

• Corticosteroids: most important drug affecting healing - inhibit inflammation, fibroblast proliferation, angiogenesis, epithelialization; reduce collagen synthesis; Vit A (topical) can reverse this
• Cytotoxic drugs / chemotherapy: impair cell proliferation
• NSAIDs: impair platelet aggregation and early inflammation

• Elderly: reduced cell proliferation, decreased growth factor production, impaired immune response, skin atrophy

• O2 tension critical for collagen synthesis and bacterial killing
• PaO2 <40 mmHg severely impairs healing

• Poor vascularity of adipose tissue, increased wound tension, dead space

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Q4. Classify surgical drains. Enumerate the advantages and disadvantages of each type. [2+3+3=8]

Classification of Surgical Drains (2 marks)

1. Open drains: Corrugated rubber/latex drain (Penrose drain), gauze wick
2. Closed passive drains: tube drain connected to a bag (underwater seal)

1. Low-pressure closed suction: Redivac drain, Blake drain (perforated tube)
2. High-pressure suction: Not preferred in surgery
3. Sump drains: Double lumen - one for drainage, one allows air in

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Advantages and Disadvantages (3+3 marks)

• Advantages: decompresses biliary system, allows cholangiography, maintains CBD patency
• Disadvantages: bile leak if removed prematurely, electrolyte imbalance from bile loss

• Pressure necrosis
• Erosion into adjacent vessels
• Drain left in (forgotten)
• Pain at drain site
• Fistula formation along drain track
• Prophylactic drains are no longer routinely recommended in clean elective surgery

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Q5. Write short notes on: [4×4=16]

a. Dyselectrolytemia in TURP (Transurethral Resection of Prostate)

• Absorption of 1-2 litres of irrigant → dilutional hyponatraemia
• Normal serum Na = 135-145 mEq/L; TURP syndrome when Na falls below 120 mEq/L
• Osmotic and volume changes cause: cerebral oedema, cardiac failure, haemolysis

• Hyponatraemia (cardinal feature) - dilutional
• Hyperammonaemia - from glycine metabolism (glycine → ammonia)
• Hypomagnesaemia, hypo/hyperkalaemia

• CNS: confusion, restlessness, visual disturbances (glycine inhibits neurotransmission), headache, seizures, coma
• CVS: hypertension (early), hypotension (late), bradycardia, widened QRS/ventricular arrhythmias
• Nausea, vomiting

• Stop surgery as soon as possible
• IV furosemide (frusemide) - promotes free water excretion
• Hypertonic saline (3% NaCl) - for severe symptomatic hyponatraemia (Na <120 + seizures)
  • Rate: correct at maximum 1-2 mEq/L/hour, not more than 10-12 mEq/L/24 hours (risk of osmotic demyelination syndrome/central pontine myelinolysis)
• Treat seizures: benzodiazepines
• Oxygen, monitoring

• Limit operative time <1 hour
• Low irrigant pressure
• Bipolar TURP (saline irrigant - almost eliminates TURP syndrome)
• Regional anaesthesia (can detect early CNS symptoms)

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b. Physiological Changes of CO₂ Pneumoperitoneum

• Cardiac output: decreased by 10-30% due to reduced venous return
• SVR: increased (aortic compression, sympathetic stimulation, vasopressin release)
• Heart rate: may increase (vagal irritation can cause bradycardia)
• Risk of venous stasis → DVT

• Diaphragm elevation → reduced FRC, increased peak airway pressure
• Ventilation-perfusion mismatch → increased PaCO₂
• CO₂ absorption from peritoneum → hypercapnia (if ventilation inadequate)
• Must increase minute ventilation by 15-25% to maintain normocapnia
• Risk of pneumothorax (CO₂ tracking through congenital diaphragmatic defects)

• Hypercarbia: CO₂ absorbed → increased RR, acidosis
• Hormonal: cortisol, ADH, catecholamines, renin-angiotensin all elevated
• Renal: reduced renal blood flow, reduced GFR, oliguria
• Hepatic: reduced portal blood flow
• Venous air embolism (rare but fatal): CO₂ gas enters open vein

• Head-down (Trendelenburg): further increases cardiac filling but worsens respiratory mechanics and increases ICP
• Head-up (Reverse Trendelenburg): for upper GI laparoscopy - impairs venous return more

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c. Enhanced Recovery After Surgery (ERAS)

1. Patient education and counselling - set expectations, reduce anxiety
2. Optimization: treat anaemia, DM, smoking cessation, nutrition
3. Avoidance of prolonged fasting: allow clear fluids up to 2 hours preoperatively; solids up to 6 hours
4. Carbohydrate loading: 400 mL of 12.5% carbohydrate drink 2 hours pre-op → reduces insulin resistance, protein catabolism
5. Avoidance of mechanical bowel preparation (for most colorectal procedures)
6. Multimodal analgesia planning
7. DVT prophylaxis: compression stockings + LMWH from pre-op

1. Minimally invasive surgery (laparoscopic preferred)
2. Short-acting anaesthetic agents (desflurane, propofol TIVA, remifentanil)
3. Avoidance of opioids or use of low doses
4. Goal-directed fluid therapy (GDT) - avoid both hypo and hypervolaemia
5. Normothermia - active warming (Bair Hugger)
6. Nasogastric tube: NOT routinely placed; if placed, remove in recovery
7. Minimise drains - no routine drains

1. Early mobilization - out of bed on Day 0 or Day 1
2. Early oral feeding - liquids Day 0, semi-solids Day 1
3. Multimodal analgesia: paracetamol + NSAIDs + regional blocks (TAP block, epidural); minimize opioids
4. Remove urinary catheter by Day 1
5. Anti-emetics - PONV prophylaxis (ondansetron, dexamethasone)
6. Glucose control - target 6-10 mmol/L

• Reduces hospital stay by 30-50%
• Reduces complications by 50%
• Reduces costs
• No increase in readmission rates
• Now standard of care for colorectal, upper GI, urology, gynaecology procedures

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d. Mismatch Transfusion (Incompatible Blood Transfusion)

• Recipient anti-A or anti-B IgM antibodies bind to donor RBC antigens
• Complement activation (C1 → C5b-9 membrane attack complex)
• Intravascular haemolysis → free haemoglobin
• Haemoglobinaemia, haemoglobinuria
• DIC (due to red cell stroma activating coagulation cascade)
• Renal tubular necrosis (haemoglobin precipitates in acidic urine)

• Awake patient: fever, chills, loin/back pain, chest tightness, facial flushing
• Under GA (recognized signs):
  • Haemoglobinuria (port wine/cola-coloured urine)
  • Hypotension, tachycardia
  • Oozing from surgical field (DIC)
  • Fever (if not masked)

1. STOP the transfusion immediately
2. Maintain IV access - give saline via new giving set
3. Check: patient identity vs blood bag label
4. Notify blood bank - send blood bag back
5. Send to lab: blood for DAT, repeat crossmatch, FBC, coagulation, U&E, LFT
6. Catheterize - monitor urine output (target >1 mL/kg/hour)
7. Aggressive IV fluids - to maintain renal perfusion
8. Frusemide/mannitol - to force diuresis
9. Sodium bicarbonate - alkalinize urine (prevents haemoglobin precipitation)
10. Treat DIC - FFP, cryoprecipitate, platelets

• Acute tubular necrosis → renal failure
• DIC
• Death (mortality 5-10%)

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GROUP "B" - ANAESTHESIOLOGY (16 Marks)

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Q6. 60-year-old, 55 kg, gastric carcinoma, Hb = 12 g%, planned for Whipple's operation. [2+2=4]

a. Calculate Allowable Blood Loss (ABL)

ABL = EBV × (H_initial - H_trigger) / H_initial

• For 60-year-old male: EBV = 70 mL/kg (standard for adult male)
• EBV = 70 × 55 = 3850 mL

• For a cancer patient undergoing major surgery: Hb = 8 g/dL (Hct ~24%) is typically accepted as the transfusion trigger
• Some use Hct (H_trigger = 21-24% for elective surgery)

• Initial Hb = 12 g/dL → Initial Hct ≈ 36% (Hct ≈ Hb × 3)
• Target minimum Hct = 21% (Hb ≈ 7 g/dL) - for young healthy patients
• For this elderly cancer patient: target Hct = 24% (Hb = 8 g/dL)

ABL = 3850 × (36 - 24) / 36 ABL = 3850 × 12/36 ABL = 3850 × 0.333 ABL ≈ 1283 mL (~1300 mL)

• Up to ABL: replace with crystalloids (3:1 ratio) or colloids (1:1)
• Beyond ABL: transfuse packed RBCs

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b. Intra-operative Fluid Management for Whipple's Operation

• Standard formula: 4 mL/kg/hour for first 10 kg + 2 mL/kg/hour for next 10 kg + 1 mL/kg/hour for remaining
• For 55 kg: = 40 + 20 + 35 = 95 mL/hour maintenance

• If fasted for 8 hours: 8 × 95 = 760 mL
• Replace: 50% in first hour (380 mL), 25% in 2nd hour (190 mL), 25% in 3rd hour (190 mL)
• With ERAS: pre-operative carbohydrate loading reduces the need for large deficit replacement

• Major abdominal surgery: 6-10 mL/kg/hour = 6-10 × 55 = 330-550 mL/hour
• Use balanced crystalloids (Hartmann's/Ringer's lactate) for third-space losses

• Monitor: visual assessment, suction canisters, swabs weighing, cell saver (autotransfusion)
• Up to ABL (~1300 mL): Replace with crystalloid (3:1) or colloid (1:1)
• Beyond ABL: Transfuse PRBC; give FFP and platelets when loss >1-1.5× blood volume

• Use: stroke volume variation (SVV), pulse pressure variation (PPV), oesophageal Doppler
• Avoid both fluid overload (→ anastomotic oedema, pulmonary oedema) and hypovolaemia (→ renal failure, hypoperfusion)
• Target: urine output >0.5 mL/kg/hour, MAP >65 mmHg, CVP guide

• Crystalloids: Hartmann's / Ringer's Lactate (preferred over normal saline for large volumes - avoids hyperchloraemic acidosis)
• Colloids: Albumin 5% for major losses; avoid synthetic starches (HES) in sepsis/renal failure
• Blood products: PRBC, FFP (1:1 ratio in massive haemorrhage protocol), cryoprecipitate, platelets

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Q7. Depolarizing vs Non-Depolarizing muscle relaxants. Absolute contraindications of succinylcholine. [1+3=4]

Differences: Depolarizing vs Non-Depolarizing (1 mark)

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Absolute Contraindications to Succinylcholine (3 marks)

• Burns - >24 hours after injury until healed (maximum risk at 1-100 days) - upregulation of extrajunctional ACh receptors
• Crush injuries / massive muscle trauma - for same reason
• Denervation injuries (spinal cord injury, paraplegia, hemiplegia) - after 24-48 hours
• Prolonged immobilization - ICU patients
• Muscular dystrophies (especially Duchenne muscular dystrophy) - rhabdomyolysis, hyperkalaemia, cardiac arrest
• Rhabdomyolysis from any cause
• Renal failure with pre-existing hyperkalaemia (K⁺ >5.5 mEq/L)

• Malignant hyperthermia (MH) - succinylcholine is a classic trigger; along with volatile anaesthetics
• Pseudocholinesterase deficiency (relative contraindication - causes prolonged block, not absolute unless symptomatic)

• Open globe injury - succinylcholine raises intraocular pressure by 6-12 mmHg (due to contraction of extraocular muscles) → risk of extrusion of eye contents
• Penetrating eye injury - same reason
• Known hypersensitivity to succinylcholine

1. Burns (>24h) and crush injuries
2. Denervation states (spinal cord injury >24h, hemiplegia)
3. Muscular dystrophies
4. Malignant hyperthermia susceptibility
5. Open globe/penetrating eye injuries
6. Hyperkalaemia (K⁺ >5.5 mEq/L)
7. Myopathies with rhabdomyolysis risk

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Q8. Preoxygenation: a. How it is done, b. Rationale behind it. [2+2=4]

a. How Preoxygenation is Done (2 marks)

• Apply well-fitting face mask (tight seal essential - prevents air entrainment)
• Deliver 100% O₂ via anaesthesia circuit
• Tidal volume breathing for 3-5 minutes - most reliable method
• End-point: End-tidal O₂ concentration ≥90% (or FiO₂ = FEO₂)

1. 4 vital capacity (deep) breaths technique:
   • 4 maximal deep breaths of 100% O₂ in 30 seconds
   • Achieves ~90% of standard 3-minute preoxygenation
   • Useful when rapid sequence induction (RSI) is needed urgently
   • Limitation: Less effective in obese, pregnant, or critically ill patients
2. 8 deep breaths in 60 seconds:
   • Better than 4 VC breaths
   • Used in some RSI protocols
3. High-flow nasal cannula (HFNO / THRIVE):
   • Transnasal Humidified Rapid-Insufflation Ventilator Exchange
   • 70 L/min O₂ via nasal cannula
   • Can maintain SpO₂ during apnoea (apnoeic oxygenation)
   • Particularly useful for anticipated difficult airway

• Tight mask seal - any leak defeats purpose
• Circuit O₂ flush before applying
• Peak flow >10 L/min from circuit to prevent rebreathing

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b. Rationale Behind Preoxygenation (2 marks)

• Healthy adult breathing room air: ~1-2 minutes
• After preoxygenation (100% O₂): ~5-8 minutes
• Obese patient (reduced FRC): ~2-3 minutes even after preoxygenation
• Pregnant patient: ~3-4 minutes (increased O₂ consumption)
• Children: shorter safe apnoea time due to relatively higher O₂ consumption and smaller FRC

• Induction of anaesthesia → apnoea → loss of protective reflexes
• Time needed for: loss of consciousness, checking BVM ventilation, laryngoscopy, intubation = can take 45-90 seconds in ideal conditions, longer if difficult airway
• Preoxygenation provides safety margin for all these steps
• If intubation fails, extended safe time allows rescue oxygenation

• Mask leak (most common failure)
• Obesity (reduced FRC, increased O₂ consumption)
• Pregnancy (same reasons)
• High metabolic states (fever, sepsis)
• Pulmonary disease (V/Q mismatch)

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Q9. Write short notes on: [2+2=4]

a. High Quality CPR

• Rate: 100-120 compressions/minute (minimum 100, maximum 120 - higher rates reduce depth)
• Depth: At least 5 cm (2 inches) but not >6 cm (adults); 4 cm child; 1.5 cm infant
• Recoil: Allow complete chest recoil between compressions (do NOT lean on chest)
• Interruptions: Minimize - CPR fraction (chest compression fraction) >80%; pause <10 seconds for pulse check
• Hand position: Heel of hand on lower half of sternum (centre of chest), two-hand technique
• Compression:ventilation ratio: 30:2 (until advanced airway placed); continuous compressions (100-120/min) + 1 breath every 6 seconds once intubated
• Rescuer fatigue: Switch compressors every 2 minutes

• 1 second per breath
• Visible chest rise
• Avoid hyperventilation (gastric distension, increased intrathoracic pressure reduces venous return)
• Bag-mask with 100% O₂ in hospital

• Minimize pre/post-shock pause to <10 seconds
• Resume CPR immediately after shock (don't check pulse)
• CPR quality must continue between shocks

• EtCO₂ (see below) - most important real-time feedback
• Arterial pressure monitoring: target coronary perfusion pressure >15 mmHg
• Clinical: visible chest rise, palpable femoral pulse during compression

• Adrenaline (epinephrine): 1 mg IV every 3-5 minutes
• Amiodarone: 300 mg IV for shockable rhythms after 3rd shock

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b. End-Tidal CO₂ (EtCO₂) Monitor

• Mainstream capnography: sensor placed directly in airway (at ETT)
• Sidestream capnography: gas aspirated from breathing circuit and analysed in machine

• Phase I (AB): dead space gas (no CO₂) - baseline
• Phase II (BC): rising CO₂ - alveolar gas mixing with dead space gas
• Phase III (CD): alveolar plateau - EtCO₂ reading taken at end
• Phase 0 (DE): inspiration - CO₂ falls to zero

1. Confirmation of ETT placement: EtCO₂ >35 mmHg after 6 breaths confirms tracheal intubation (not oesophageal); gold standard for ETT confirmation
2. Monitoring ventilation: Guides respiratory rate/tidal volume adjustments; prevents hyperventilation/hypoventilation
3. CPR quality monitoring: EtCO₂ during CPR reflects cardiac output
   • EtCO₂ <10 mmHg = inadequate compressions; improve quality
   • Sudden rise in EtCO₂ to ≥40 mmHg = ROSC (Return of Spontaneous Circulation) - reliable indicator
4. Detection of pulmonary embolism: Sudden decrease in EtCO₂ (increased dead space)
5. Metabolic monitoring: Elevated EtCO₂ in CO₂ pneumoperitoneum, malignant hyperthermia, metabolic acidosis (compensatory hyperventilation drops EtCO₂)
6. Assessment of sedation: In procedural sedation (capnography detects apnoea before SpO₂ drops)
7. Weaning from ventilator: Trending EtCO₂

• Predicts survival: sustained EtCO₂ <10 mmHg after 20 minutes → poor prognosis
• EtCO₂ >20 mmHg associated with better survival outcomes

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GROUP "C" - DENTAL (16 Marks)

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Q10. Discuss clinical, radiographical, and histological features of Radicular Cyst. [1+1+2=4]

Radicular (Periapical/Dental) Cyst

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Clinical Features (1 mark)

• Age: Most common in 3rd-5th decades
• Sex: Slight male predominance
• Location: Periapical region of any non-vital tooth; maxillary anterior teeth most common, followed by maxillary posterior and mandibular posterior
• Tooth history: Always associated with a non-vital tooth (carious, fractured, history of trauma/deep restoration)
• Symptoms: Usually asymptomatic - discovered on routine X-ray
• Signs when large:
  • Slow-growing, painless swelling of jaw
  • Bony expansion (both buccal and lingual/palatal)
  • Eggshell crackling (crepitus) on palpation when cortex is thin
  • Fluctuant if cystic cavity reached
  • Adjacent teeth may be displaced but rarely devitalized
  • Sinus/fistula if infected (secondary infection makes it painful)

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Radiographical Features (1 mark)

• Shape: Well-defined, round or oval periapical radiolucency
• Margins: Well-corticated (thin opaque/sclerotic border) - when not infected; if infected, margins become ill-defined and cortication lost
• Location: Centred on the root apex of a non-vital tooth; the apex of the tooth projects INTO the lesion
• Size: Usually <1 cm but may enlarge up to several cm
• Effect on adjacent structures:
  • Displacement (not resorption) of adjacent teeth (except large ones)
  • Root resorption of causative tooth (rare)
  • Displacement of inferior dental canal or floor of maxillary antrum
• Continuity of lamina dura: Lost at the apex of the causative tooth
• OPG shows the relation to root apex clearly

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Histological Features (2 marks)

• Outer fibrous wall: Dense collagenous connective tissue (fibrous capsule)
• Contains: chronic inflammatory cells (lymphocytes, plasma cells, macrophages); Russell bodies (hyaline deposits from plasma cells); cholesterol clefts with foreign body giant cells
• Rushton bodies (hyaline bodies) - pathognomonic of odontogenic cysts; eosinophilic, curvilinear structures thought to be from red cell breakdown or epithelial secretion

• Lined by non-keratinized stratified squamous epithelium
• Derived from epithelial rests of Malassez (remnants of Hertwig's epithelial root sheath)
• Epithelium is irregular and arcaded (rete ridges, spongiosis) when inflamed; when uninflamed becomes flatter/regular
• Mucous cells may be present (mucous metaplasia)
• Ciliated columnar cells occasionally (especially near maxillary sinus)

• Contains cholesterol crystals (due to cell breakdown/haemorrhage)
• Foamy macrophages, RBCs, degenerating cells
• Fluid: straw-coloured, rich in albumin, soluble proteins, cholesterol crystals (gives "shimmering" appearance)
• Protein content >4 g/100 mL (used to distinguish from non-neoplastic cysts)

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Q11. 60-year-old male, 30-year smoking and alcohol history, non-healing ulcer on lateral border of tongue for 6 weeks. Key examination features + investigation for oral SCC. [2+2=4]

Key Examination Features Raising Suspicion of Oral SCC (2 marks)

• Age >40, male, 30-year smoking history, alcohol - all major risk factors (synergistic: 15× increased risk combined)
• Non-healing ulcer >3 weeks on high-risk site (lateral border of tongue = most common site of oral SCC)

1. Ulcer morphology: Irregular, indured, raised and rolled/everted margins (classical SCC)
2. Floor of ulcer: Necrotic, sloughing, may be granular or fungating
3. Surrounding mucosa: Leukoplakia (white patch) or erythroplakia (red patch) - erythroplakia has ~50% chance of malignancy
4. Fixation to underlying tissue - inability to move ulcer independently
5. Induration: Hard, gritty feel (due to desmoplastic reaction)
6. Size: Document in cm

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Investigations (2 marks)

• Incisional biopsy from the edge of the ulcer (not the necrotic centre)
• Histology: well/moderate/poorly differentiated squamous cell carcinoma; keratin pearls, individual cell keratinization, intercellular bridges
• Toluidine blue staining can help identify biopsy site

• FBC, LFT, RFT (pre-treatment baseline)
• HPV testing (p16 immunohistochemistry) - important for oropharyngeal SCC; less relevant for oral cavity

• T: tumour size/depth of invasion
• N: lymph node status (ENE - extranodal extension now key)
• M: distant metastasis
• Depth of invasion (DOI) >4 mm: upstages T category in oral SCC (new in AJCC 8th)

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Q12. Write short notes on: [4×2=8]

a. Sequence of Tooth Loss (Gottlieb's sequence / Deciduous and Permanent)

• First molar and central incisors = age 6
• Lateral incisors = age 7
• First premolars = age 10
• Canines/second premolars = age 11-12
• Second molars = age 12 ("12-year molar")
• Third molars = 18-21 years

• First permanent tooth (lower central incisor / first molar) at age 6 - if extracted, causes drift and arch collapse
• Loss of first permanent molar in children = most detrimental (causes mesial drift, tilting of second molar, supra-eruption of opposing tooth, arch collapse)

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b. Post-Extraction Complications

1. Haemorrhage: Primary - at time of extraction; reactionary - 2-4 hours (as vasoconstriction wears off); secondary - 7-10 days (infection dissolving clot)
2. Swelling and ecchymosis: Normal if minor; excessive if inadequate wound closure
3. Trauma to adjacent structures: Fractured adjacent tooth, instrument slippage
4. Fractured/retained root tip
5. Oro-antral communication (upper posterior extraction - thin sinus floor)
6. Displacement of tooth into sinus, infratemporal fossa, pterygomandibular space
7. Nerve damage: Inferior alveolar nerve (paraesthesia of lip), lingual nerve, mental nerve

• 3% of routine extractions, 25-30% of mandibular third molars
• Loss of blood clot (lysis) → exposed bone → severe throbbing pain radiating to ear
• Day 2-4 onset; empty socket, no clot, necrotic bone visible, foul odour
• Treatment: irrigation, alvogyl/ZOE pack, analgesics
• Risk factors: smoking, OCP use, traumatic extraction, infection, female sex

1. Surgical site infection: Pain, swelling, pus, trismus
2. Trismus: Infection/haematoma in masticator space, or trauma

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c. Acute Necrotizing Ulcerative Gingivitis (ANUG)

• Fusospirochetal infection: Fusobacterium nucleatum + Borrelia vincentii (Treponema vincentii) - specific synergistic organisms
• Other anaerobes: Prevotella intermedia, Selenomonas, Porphyromonas

• Poor oral hygiene (most important)
• Psychological stress (first described in WWI soldiers - "trench mouth")
• Malnutrition, immunosuppression (HIV/AIDS), smoking
• Pre-existing gingivitis

• Age: Young adults (18-30 years)
• Classic triad:
  1. Necrosis and ulceration of interdental papillae (punched-out craters at papillae tips)
  2. Spontaneous gingival bleeding (touching or spontaneous)
  3. Foul breath (fetor oris) - characteristic fetid odour
• Other features: Pain, metallic taste, excessive salivation
• Grey pseudomembrane over necrotic papillae (sloughs off to leave bleeding surface)
• Fever, lymphadenopathy (submandibular), malaise in severe cases
• Rapid progression if untreated → Cancrum oris/Noma (in severely immunocompromised/malnourished)

1. Local treatment:
   • Gentle debridement with cotton pellets (don't curette in acute phase)
   • Hydrogen peroxide (3%) mouthwash - provides O₂ (inhibits anaerobes)
   • Chlorhexidine 0.12-0.2% mouthwash
   • After acute phase: scaling and root planing
2. Systemic:
   • Metronidazole 400 mg TDS × 5 days - drug of choice (covers anaerobes including spirochetes)
   • Amoxicillin if unresponsive
   • Analgesics (ibuprofen/paracetamol)
3. Supportive: Nutrition, hydration, oral hygiene instruction, smoking cessation
4. Follow-up: Surgical papillae reconstruction if craters remain after healing

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d. Oral Manifestations of HIV Infection

1. Oral Candidiasis (most common oral manifestation)
   • Pseudomembranous candidiasis (thrush): white, removable plaques on buccal mucosa, palate, tongue
   • Erythematous candidiasis: flat, red patches on palate/dorsum of tongue
   • Angular cheilitis: erythema and fissuring at corners of mouth
   • Organism: Candida albicans; treat with fluconazole
2. Oral Hairy Leukoplakia (OHL)
   • White, corrugated/hairy patches on lateral borders of tongue
   • Cannot be removed (unlike candidiasis)
   • Caused by Epstein-Barr virus (EBV)
   • Pathognomonic of HIV if other causes excluded
   • Treat with antiretrovirals
3. HIV-associated periodontal diseases:
   • Linear gingival erythema (LGE): fiery red band at gingival margin despite good hygiene
   • Necrotizing ulcerative periodontitis (NUP): severe NUG extending to periodontal tissues; rapid bone/soft tissue destruction; 6 mm attachment loss in months
4. Kaposi's Sarcoma (KS):
   • Most common HIV-associated oral malignancy
   • Caused by HHV-8 (Human Herpesvirus-8)
   • Flat or raised, bluish-purple to red lesions
   • Most common on hard palate and gingiva
   • Painless unless secondarily infected/ulcerated

• Recurrent aphthous ulcers (major, minor, herpetiform) - more frequent, larger, more painful
• Viral: Herpes simplex (HSV), Herpes zoster, CMV ulcers
• Salivary gland disease: xerostomia, parotid enlargement (lymphoepithelial cysts)
• Thrombocytopenic purpura/petechiae

• Melanotic hyperpigmentation (may be ART-related)
• Non-Hodgkin's lymphoma (NHL) - oral ulcers/masses
• Bacillary angiomatosis

• CD4 >500: mainly aphthous ulcers, OHL
• CD4 200-500: candidiasis, LGE, NUP
• CD4 <200: KS, NHL, disseminated fungal infections

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