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VINAYAKA MISSION'S — GENERAL SURGERY FINAL YEAR IA-2

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ESSAY QUESTIONS

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Q1. 60-year-old male, non-healing ulcer left buccal mucosa + hard ipsilateral neck swelling

Probable Diagnosis: Carcinoma of the Buccal Mucosa (Squamous Cell Carcinoma — Oral Cavity)

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Etiopathogenesis

• Loss of heterozygosity at 3p, 9p (p16), 17p (p53)
• Overexpression of epidermal growth factor receptor (EGFR)
• Field cancerization: entire oral mucosa exposed to carcinogens → multifocal disease

1. Local: Infiltrates buccinator, pterygoid muscles, mandible (bone invasion), skin
2. Lymphatic: To submandibular (Level I), upper jugular (Level II) nodes — N2 bilateral involvement in advanced disease
3. Haematogenous: Rare at presentation; lungs most common distant site

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Clinical Features

• Non-healing ulcer >3 weeks in buccal mucosa
• Pain (otalgia — referred via auriculotemporal nerve, V3)
• Trismus (invasion of pterygoid muscles — poor prognostic sign)
• Difficulty in chewing, altered speech
• Weight loss, dysphagia (advanced disease)
• History of tobacco/betel nut use

• Ulcer: Irregular, indurated edges; raised, everted margins; hard base; floor covered with slough/necrotic tissue; bleeds on touch
• Surrounding mucosa: Leukoplakia, erythroplakia, submucous fibrosis may be present
• TNM assessment: Size (T), bone involvement, trismus

• Hard consistency (stony hard, non-tender)
• Ipsilateral submandibular (Level I) or upper deep cervical (Level II) most common
• Fixed = extracapsular spread (N3)
• Bilateral nodes suggest advanced disease

• Skin fixity, cutaneous fistula
• Mandibular involvement (panoramic X-ray shows "moth-eaten" bone)
• Trismus <3 cm = T4 disease

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Staging (AJCC 8th ed — Oral Cavity SCC)

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Investigations

1. Incisional biopsy (gold standard) — HPE confirms SCC; note degree of differentiation
2. Fine needle aspiration cytology (FNAC) of neck node

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Management

Surgical (Mainstay for operable disease)

• Wide local excision — at least 1.5–2 cm clear margins (confirmed by frozen section intraoperatively)
• Composite resection (commando/pull-through) — if mandible involved: wide excision + marginal or segmental mandibulectomy
• Reconstruction:
  • Small defects: Primary closure
  • Medium: Pectoralis major myocutaneous flap (PMMF) — workhorse flap
  • Large/complex: Free radial forearm flap, anterolateral thigh (ALT) free flap

• Elective neck dissection (END): Indicated if DOI >4 mm (even N0 clinically) due to high occult nodal metastasis rate
• Therapeutic neck dissection: For clinically positive nodes (N+)
• Type: Selective (Levels I–III) for elective; Modified radical neck dissection (MRND) for N+; Radical neck dissection if structures involved

Radiation Therapy

• Post-operative radiotherapy (PORT): Indications — positive/close margins, perineural invasion, lymphovascular invasion, multiple nodes, extranodal extension, T3/T4 disease
• Dose: 60–66 Gy in 30–33 fractions
• Concurrent cisplatin with PORT if high-risk features (positive margins, extranodal extension)

Chemotherapy

• Cisplatin-based concurrent chemoradiotherapy for unresectable or recurrent disease
• Induction chemotherapy (TPF: docetaxel-cisplatin-5FU) for organ preservation or downstaging
• Cetuximab (anti-EGFR) for platinum-ineligible patients

Palliative

• Analgesics (WHO ladder), nutritional support (NG tube, PEG), tracheostomy for airway compromise

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Q2. 58-year-old chronic smoker, cramp pain in right calf on walking, relieved by rest

Probable Diagnosis: Peripheral Arterial Disease (PAD) — Intermittent Claudication

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Etiopathogenesis

1. Endothelial injury → triggered by smoking, hypertension, hyperlipidaemia, diabetes, oxidative stress
2. Lipid infiltration → LDL oxidized and taken up by macrophages → foam cells → fatty streak
3. Smooth muscle cell migration from media to intima → fibrous cap formation
4. Progressive plaque growth → stenosis → reduced luminal diameter
5. When stenosis >50% → hemodynamic significance → reduced distal blood flow
6. At rest, collateral circulation compensates; during exercise, oxygen demand increases, supply cannot match → ischemic pain (claudication)
7. Muscle metabolites (lactate, H+, adenosine) accumulate → stimulate nociceptors → pain
8. Pain resolves within 1–5 minutes of rest as metabolites clear

• Smoking (single most important modifiable risk factor; 4-fold increase)
• Diabetes mellitus (tibial vessels predominant; severe disease)
• Hypertension
• Dyslipidaemia (elevated LDL)
• Age >50, Male sex
• Chronic kidney disease
• Family history

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Clinical Features

• Claudication distance: Distance at which calf cramp/pain begins (reproducible)
• Relief: Complete relief within 1–5 minutes of standing still (differentiates from neurogenic claudication which requires sitting/flexion)
• Affected limb: Right calf → right superficial femoral artery or popliteal stenosis likely
• No rest pain or ulceration (not critical limb ischemia — yet)
• History of smoking, possible diabetes, hypertension

1. Pallor — on elevation (Buerger's angle <20° indicates severe ischemia)
2. Pulselessness — reduced/absent popliteal, dorsalis pedis, posterior tibial pulses on right
3. Pain — reproducible claudication
4. Paraesthesia — in advanced disease
5. Paralysis — in acute limb ischemia
6. Perishing cold — limb cooler than contralateral

• Buerger's test: Elevation blanching → dependent rubor (reactive hyperaemia)
• Capillary refill >3 seconds
• Venous guttering on elevation
• Skin: thin, shiny, hairless; toenail thickening (dystrophy)
• Bruits over iliac/femoral arteries

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Investigations

1. Ankle-Brachial Index (ABI) — gold standard screening
   • Normal: 0.9–1.3
   • Claudication: 0.6–0.9
   • Rest pain: 0.3–0.6
   • Tissue loss: <0.3

   • 1.3 = non-compressible vessels (calcified — in diabetics)

2. Duplex Doppler ultrasound — location, degree of stenosis, triphasic/biphasic/monophasic waveform
3. Treadmill exercise test — objective claudication distance measurement, post-exercise ABI drop confirms PAD
4. CT Angiography (CTA) — imaging of choice pre-intervention; maps entire aortoiliac-infrainguinal tree
5. MR Angiography (MRA) — no contrast hazard; preferred in CKD
6. Digital Subtraction Angiography (DSA) — gold standard for intervention planning (both diagnostic + therapeutic)

• FBC, fasting glucose, HbA1c, lipid profile, renal function
• ECG, echo (co-existing CAD common — 30–50% have significant CAD)

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Management

1. Risk Factor Modification (Medical — ESSENTIAL in all patients)

• Smoking cessation: Single most important intervention — slows progression, reduces amputation risk
• Antiplatelet therapy: Aspirin 75–100 mg/day or Clopidogrel 75 mg/day (preferred in PAD per CAPRIE trial)
• Statin therapy: Atorvastatin 40–80 mg — reduces cardiovascular events AND improves claudication
• Antihypertensives: ACE inhibitors preferred (HOPE trial); β-blockers no longer contraindicated in mild PAD
• Diabetic control: HbA1c <7%
• Anticoagulation: Only if thrombotic events/AF

2. Supervised Exercise Programme (SEP)

• Most effective non-invasive treatment for claudication
• 30–45 minutes, 3×/week for ≥3 months
• Walk to near-maximum pain, rest, repeat
• Improves claudication distance by 100–150% via collateral development and metabolic adaptation

3. Pharmacotherapy

• Cilostazol (phosphodiesterase-3 inhibitor) — vasodilation + antiplatelet; improves walking distance by ~40%; contraindicated in heart failure
• Naftidrofuryl (5-HT2 antagonist) — second-line
• Pentoxifylline — modest benefit

4. Endovascular Intervention

• Percutaneous Transluminal Angioplasty (PTA) ± Stenting:
  • Iliac arteries: Excellent long-term patency (5-year >80%); primary stenting preferred
  • Femoral-popliteal: PTA ± drug-eluting stent (DES); covered stents (Viabahn) for long lesions
  • Infrapopliteal: Balloon angioplasty for critical limb ischaemia

5. Open Surgical Revascularisation

• Aorto-bifemoral bypass graft — aortoiliac disease (PTFE/Dacron; 5-year patency ~80%)
• Femoro-popliteal bypass — above-knee (PTFE or reversed saphenous vein), below-knee (vein preferred)
• Femoro-distal bypass — to tibial/peroneal for limb salvage
• Endarterectomy — for common femoral artery disease (profundoplasty)

6. Amputation

• Last resort for irreversible critical limb ischaemia, wet gangrene, failed revascularisation
• Below-knee amputation (BKA) preferred over above-knee (AKA) for mobility/rehabilitation

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SHORT NOTES

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SN 1. Dermatofibrosarcoma Protuberans (DFSP)

• Pathognomonic translocation: t(17;22) — fusion of COL1A1 (collagen gene) with PDGFB gene → constitutive activation of PDGFRβ → uncontrolled fibroblast proliferation
• May arise at sites of prior trauma, scarring, vaccination

• Slow-growing, painless, indurated plaque or nodule — usually on trunk (50%), proximal extremities (40%), head/neck (10%)
• Three morphological phases:
  1. Patch phase: Atrophic, violaceous/flesh-coloured skin plaque
  2. Plaque phase: Indurated, firm plaque
  3. Nodular phase: Multinodular, protuberant (hence the name), bluish-red, skin stretched taut
• Size: 1–5 cm typically; giant forms >20 cm described
• No regional lymphadenopathy (lymph node metastasis rare <1%)
• Aggressive fibrosarcomatous transformation (FS-DFSP) — 10–20% → higher metastatic potential

1. Excisional/incisional biopsy + HPE
2. Histology: Spindle cells in storiform (cartwheel/pinwheel) pattern; infiltration of subcutaneous fat in characteristic honeycomb/lace-like pattern
3. Immunohistochemistry (IHC): CD34+, Factor XIIIa negative (differentiates from dermatofibroma)
4. FISH or RT-PCR: Detection of COL1A1-PDGFB fusion gene (confirmatory)
5. MRI: Assess deep extent before surgery
6. CT chest for fibrosarcomatous transformation (metastasis screen)

• Wide local excision (WLE): 2–3 cm margins; historically standard; 20–50% local recurrence
• Mohs micrographic surgery (MMS): Treatment of choice — 1% recurrence rate vs 20% for WLE; tissue-sparing; maps all margins
• Imatinib mesylate (Gleevec): PDGFRβ inhibitor; neoadjuvant (to downsize before surgery), adjuvant, or for unresectable/metastatic disease — PDGFB fusion is predictive of response (90% response rate)
• Radiotherapy: Adjuvant if margins positive and re-excision not possible
• Prognosis: Excellent if completely excised; 5-year survival >95%

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SN 2. Cardiac Tamponade

• Normal pericardial fluid: 15–50 mL
• Rapid accumulation (even 150–200 mL) → rises above pericardial compliance threshold → intrapericardial pressure ↑ → diastolic filling impaired → stroke volume ↓ → CO ↓ → compensatory tachycardia → eventually decompensation → obstructive shock

1. Hypotension (reduced CO)
2. Raised JVP (Kussmaul's sign — JVP rises on inspiration) / elevated CVP
3. Muffled/distant heart sounds (fluid insulates sounds)

• Pulsus paradoxus: >10 mmHg fall in SBP with inspiration (pathognomonic); exaggerated ventricular interdependence
• Tachycardia (compensatory)
• Tachypnoea, dyspnoea
• Cold, clammy extremities (shock)
• In chronic: Ewart's sign (dullness at left lung base from lung compression)

1. ECG: Sinus tachycardia; electrical alternans (alternating QRS axis — pathognomonic of large effusion); low voltage complexes; PR depression in pericarditis
2. CXR: Cardiomegaly — "water bottle" or "globular" heart shape (effusion >250 mL); clear lung fields (unlike LVF)
3. Echocardiography (ECHO): Diagnostic gold standard
   • Pericardial effusion
   • RA collapse in systole (earliest sign)
   • RV collapse in diastole (most specific sign of haemodynamic compromise)
   • IVC plethora (non-collapsible on inspiration)
   • Swinging heart motion
4. CT/MRI: Characterise effusion, assess for malignancy
5. Invasive: Right heart catheterization — equalisation of diastolic pressures

• Immediate: Pericardiocentesis (needle drainage) — emergency treatment; subxiphoid approach (Marfan's technique); ECG-guided or echo-guided; aspirate 50 mL may dramatically improve BP
• Surgical:
  • Pericardiotomy/pericardial window — for recurrent effusions; subxiphoid or thoracoscopic (VATS)
  • Pericardiectomy — for constrictive pericarditis (chronic)
• Treat underlying cause (antibiotics, chemotherapy, etc.)
• Do NOT give diuretics or vasodilators (they reduce preload and worsen tamponade)

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SN 3. Deep Vein Thrombosis (DVT)

• Calf DVT (below-knee): Calf pain/tenderness, mild swelling, slight warmth
• Proximal DVT (popliteal, femoral, iliac): More significant swelling, pitting oedema, erythema, distended superficial veins
• Phlegmasia alba dolens ("white painful leg"): Massive DVT causing arterial spasm → white, cold, swollen, painful limb
• Phlegmasia cerulea dolens ("blue painful leg"): Massive DVT occludes venous drainage entirely → venous gangrene; blue, swollen, excruciating pain — limb-threatening
• Homan's sign: Calf pain on forced dorsiflexion — non-specific (only 50% sensitive)
• Moses sign: Calf tenderness on lateral compression
• Pyrexia, tachycardia

1. Wells' DVT Score (pre-test probability):
   • Active cancer (+1), immobility (+1), limb swelling (+1), calf asymmetry >3 cm (+1), pitting oedema (+1), collateral veins (+1), prior DVT (+1), alternative diagnosis as likely (−2)
   • Score ≥2 = high probability
2. D-dimer: High sensitivity (>95%), low specificity; elevated in DVT but also infection, trauma, malignancy; useful to RULE OUT DVT if negative in low/moderate probability
3. Compression Duplex Ultrasonography: Non-invasive; diagnostic gold standard in clinical practice; shows non-compressible vein + absent flow Doppler
4. Venography (ascending phlebography): Gold standard historically; invasive; reserved for equivocal duplex
5. MRI venography: Useful for pelvic/iliac vein thrombosis

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SN 4. Pleomorphic Adenoma of Parotid Gland

• Slow-growing (years), painless swelling in parotid region (pre-auricular or infra-auricular)
• Usually unilateral, solitary
• Rubbery to firm consistency; non-tender
• Mobile (not fixed) initially; bosselated/irregular surface
• Skin not involved; no skin ulceration
• Facial nerve intact (facial nerve palsy = malignancy)
• No pulsation or bruit

1. Malignant transformation → Carcinoma ex pleomorphic adenoma (5–10% with long-standing tumour; rises to 25% after 15 years)
2. Recurrence after inadequate surgery (enucleation) → "seed deposits" of tumour — multinodular recurrence
3. Facial nerve injury during surgery
4. Frey's syndrome (auriculotemporal nerve syndrome) — sweating/flushing over cheek during eating post-parotidectomy; occurs in 40–60%
5. Sialocele, haematoma (post-operative)

1. FNAC — First-line; confirms pleomorphic adenoma (epithelial cells + stromal background); avoids excision for benign lesions; sensitivity ~80–90%
2. MRI — gold standard imaging; shows characteristic intermediate T1/high T2 signal; defines extent, deep lobe involvement, nerve relationship
3. CT scan — if bone involvement suspected
4. Ultrasound — superficial lobe lesions; guides FNAC

• Superficial parotidectomy (standard operation) — removes superficial lobe with tumour, preserving facial nerve; never enucleation (high recurrence)
• Total conservative parotidectomy — if tumour in deep lobe or if uncertain about deep lobe involvement
• Extended parotidectomy ± facial nerve resection — for malignant transformation with nerve involvement
• Radiotherapy — for carcinoma ex pleomorphic adenoma post-operatively

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SN 5. Thyroglossal Cyst

• Thyroid gland develops from foramen caecum at the junction of anterior 2/3 and posterior 1/3 of tongue (base of tongue) → descends in midline → passes anterior to/through hyoid bone → reaches final position in neck
• Thyroglossal duct normally obliterates by 7th–10th week; failure to obliterate → thyroglossal cyst, sinus, or fistula

1. Intralingual (at foramen caecum) — rare
2. Subhyoid (most common — 60–65%) — below hyoid bone, above thyroid cartilage
3. Suprahyoid (24%)
4. At the level of hyoid bone (15%)
5. Suprasternal (few percent)
6. Within thyroid (intrathyroidal)

• Usually presents in children <10 years; can present at any age
• Midline neck swelling (or slightly paramedian to the left)
• Moves upward on swallowing AND on protrusion of tongue — pathognomonic (because tract attached to tongue base via hyoid)
• Smooth, spherical, soft to firm, non-tender, transilluminant (if thin-walled)
• Skin not attached (unless infected)
• May become infected → thyroglossal fistula (external opening in midline below hyoid after infection/spontaneous drainage)
• Rarely: thyroglossal cyst carcinoma (1%) — papillary thyroid carcinoma most common; suspect if hard, irregular

1. Ultrasound neck — first-line; confirms cystic nature, locates ectopic thyroid tissue in cyst wall
2. Thyroid scan (Tc-99m) — BEFORE surgery: confirm normal thyroid tissue in normal position (cyst may contain the only thyroid tissue in 1–2% of cases)
3. MRI — complex cysts, suspected carcinoma
4. FNAC — if carcinoma suspected (thick wall, solid component)
5. TFTs — to confirm euthyroid state

• Sistrunk's operation — standard surgery; resects:
  1. The entire cyst
  2. Central portion of body of hyoid bone
  3. Core of tissue from hyoid to foramen caecum (base of tongue)
  • Critical: Hyoid bone central body removal reduces recurrence from 40% to <4%
• If ectopic thyroid is the only functioning thyroid → consider observation or thyroid supplementation
• Infected cyst → antibiotics first, then Sistrunk's after inflammation settles

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SN 6. Retrosternal Goitre

1. Primary (intrathoracic) — rare (<1%); develops from ectopic mediastinal thyroid tissue; has its own blood supply from intrathoracic vessels; no connection to cervical thyroid; harder to approach
2. Secondary (descending/plunging) — majority (>95%); extension of enlarged cervical thyroid into the superior mediastinum; blood supply from inferior thyroid artery; usually anterior mediastinum

• Anterior mediastinal (most common) — between trachea and sternum
• Posterior mediastinal — posterior to trachea/oesophagus; more prone to oesophageal compression

1. Tracheal compression → dyspnoea (especially on lying flat/supine), stridor, recurrent chest infections
2. Oesophageal compression → dysphagia
3. SVC compression → SVC syndrome: facial oedema, suffused conjunctivae, venous distension over chest wall, arm oedema, cyanosis

• Pemberton's sign: Raising both arms above head → facial plethora, cyanosis, JVP rise (tightens thoracic inlet around goitre)
• Hoarseness (recurrent laryngeal nerve compression)
• Horner's syndrome (cervical sympathetic chain involvement)
• Plethoric facies

1. CXR — mediastinal widening; tracheal deviation/compression; superior mediastinal mass
2. CT neck and chest — imaging of choice; maps extent, vascularity, tracheal compression, relation to great vessels; plans surgical approach
3. MRI — better soft tissue detail; useful to distinguish from other mediastinal masses
4. Thyroid isotope scan (Tc-99m) — confirms functioning thyroid tissue in mediastinum
5. TFTs — most are euthyroid; occasionally toxic or hypothyroid
6. PFTs — flow-volume loop shows extrathoracic/intrathoracic obstruction
7. Indirect laryngoscopy — vocal cord mobility pre-operatively

• Surgery is the definitive treatment — due to risk of progressive compression and malignancy (2–3%)
• Approach:
  • Cervical approach alone in >90% — through standard collar incision; most secondary retrosternal goitres can be delivered digitally from mediastinum using "finger fracture" technique
  • Median sternotomy — required if primary retrosternal (own blood supply), very large, malignant, cannot be delivered from above, or posterior mediastinal position
• Pre-operative preparation: Euthyroid state, vocal cord check
• Complications of surgery: Recurrent laryngeal nerve injury (1–2% bilateral = stridor/airway obstruction), hypoparathyroidism, bleeding, SVC injury, tracheomalacia (softened tracheal rings after long compression → tracheal collapse post-extubation)
• Radioiodine (I-131): For non-toxic retrosternal goitre if unfit for surgery; reduces size by 40–60%

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BRIEF ANSWERS

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BA 1. Clinical Features of Hyperthyroidism

• Exophthalmos/proptosis (thyroid eye disease — TED)
• Pretibial myxoedema (infiltrative dermopathy — skin plaques over shin)
• Thyroid acropachy (clubbing)
• Diffuse goitre with bruit

• Warm, moist, smooth skin
• Stare and lid lag (von Graefe's sign)
• Onycholysis (Plummer's nails)
• Thyroid bruit (Graves')
• Tachycardia even at rest
• Broad pulse pressure

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BA 2. Indications of Intercostal Drainage (ICD)

1. Pneumothorax:
   • Tension pneumothorax (immediate needle decompression first, then ICD)
   • Large (>2 cm rim on CXR) spontaneous pneumothorax
   • Secondary spontaneous pneumothorax (any size)
   • Traumatic pneumothorax
   • Persistent/recurrent pneumothorax after aspiration
2. Haemothorax — traumatic; significant (>300 mL)
3. Haemopneumothorax
4. Pleural effusion:
   • Exudative effusion not responding to medical treatment
   • Malignant pleural effusion (symptom relief; pleurodesis)
   • Empyema thoracis (pus in pleural cavity) — free-flowing empyema; fibrinopurulent stage
5. Empyema/Pyothorax — frank pus (frank empyema)
6. Post-operative:
   • After thoracotomy
   • After oesophagectomy
   • After cardiac surgery (mediastinal drains)
7. Chylothorax (thoracic duct injury)

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BA 3. Flail Chest

• The flail segment moves inward during inspiration (paradoxical — opposes normal outward movement) and outward during expiration
• This reduces tidal volume, causes hypoxia
• Main cause of respiratory failure is NOT the paradoxical movement but the underlying pulmonary contusion — alveolar haemorrhage, oedema, reduced compliance
• Splinting due to pain → hypoventilation → atelectasis → pneumonia

• History of severe chest trauma (RTA, crush injury)
• Dyspnoea, tachypnoea, hypoxia (SpO2 low)
• Paradoxical movement of chest wall segment (visible or palpable)
• Tenderness/crepitus over multiple rib fractures
• Associated injuries: pneumothorax, haemothorax, cardiac contusion

• CXR: Multiple rib fractures, pulmonary contusion (ground-glass opacity)
• CT chest: Superior — detects rib fractures, contusion, pneumo/haemothorax precisely
• ABG: Hypoxia, hypercapnia (type II respiratory failure in severe cases)

1. Immediate: Oxygen (high flow), analgesia (pain relief crucial for adequate breathing)
2. Analgesia: IV opioids, intercostal nerve block, epidural analgesia (gold standard for thoracic pain — allows deep breathing)
3. Respiratory support: If SpO2 <90% or PaO2 <60 mmHg → CPAP/BiPAP; intubation + mechanical ventilation (IPPV) if severe respiratory failure — acts as "internal pneumatic stabilisation"
4. Treat associated injuries: ICD for pneumo/haemothorax
5. Surgical rib fixation (ORIF): Now increasingly used for severe flail chest — reduces ICU stay, ventilation duration, and long-term chest deformity
6. Physiotherapy, nutritional support

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BA 4. Clinical Types of Melanoma

• Asymmetry, Border irregularity, Colour variation, Diameter >6 mm, Evolution (change over time)

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BA 5. Smoking Index and Pack Year Index

• Used in India
• Formula: Smoking Index = Number of cigarettes/bidis smoked per day × Number of years of smoking
• SI ≥300 → significant risk; SI ≥600 → heavy smoker with high COPD/cancer risk
• Example: 15 cigarettes/day × 20 years = SI of 300

• Used internationally (standardised)
• Formula: Pack Years = (Number of cigarettes per day ÷ 20) × Number of years smoked
• 1 pack = 20 cigarettes
• Example: 20 cigarettes/day (1 pack/day) × 30 years = 30 pack years
• 40 pack years = significant threshold for lung cancer risk
• Used for COPD staging, lung cancer screening (LDCT recommended if ≥20 pack years, age 50–80)
• Does not account for depth of inhalation, cigar/pipe smoking

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BA 6. Shionoya's Criteria for Buerger's Disease (Thromboangiitis Obliterans)

1. Smoking history — patient is a smoker (or recent ex-smoker)
2. Onset before age 50 years — affects young men predominantly
3. Infrapopliteal arterial occlusions — involvement of below-knee arteries (tibial, peroneal vessels); may also involve upper limb (radial, ulnar)
4. Upper limb involvement OR phlebitis migrans — superficial migratory thrombophlebitis (hallmark); can affect arms (differentiated from atherosclerosis)
5. Absence of atherosclerotic risk factors other than smoking — no diabetes, hypertension, hyperlipidaemia (to exclude atherosclerosis)

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BA 7. Complications of Varicose Veins

1. Haemorrhage — rupture of varicosity → severe bleeding (especially if standing); may be life-threatening; subdermal haemorrhage
2. Superficial Thrombophlebitis — painful, tender, red, cord-like thrombosed varicosity; risk of proximal extension to deep veins
3. Venous (varicose) Eczema — chronic inflammatory skin change over lower 1/3 of leg; itchy, eczematous, pigmented skin
4. Lipodermatosclerosis — chronic fibrotic change of skin and subcutaneous fat; inverted champagne bottle appearance; precedes ulceration
5. Haemosiderin pigmentation — brown discolouration from haemosiderin deposition (RBC extravasation)
6. Venous/Varicose Ulcer — most serious complication; "gaiter area" (medial malleolus); shallow, large, sloping edges, painless, granulating base, surrounding lipodermatosclerosis; recurrent
7. Atrophie blanche — white sclerotic patches over lipodermatosclerotic skin; avascular
8. Calcification — phleboliths in thrombosed varicosities
9. DVT — extension of thrombophlebitis; or de novo in venous stasis

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BA 8. Premalignant Conditions of Oral Cavity

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BA 9. Complications of Parotidectomy

1. Haemorrhage / haematoma — reactionary haemorrhage most dangerous; may compress airway
2. Airway obstruction (haematoma)

• Temporary palsy (neurapraxia) — 15–25%; recovers within 6 months
• Permanent palsy — 1–3% for benign disease; higher for malignancy
• Features: lagophthalmos, ectropion, inability to close eye → corneal exposure keratitis; drooping of corner of mouth; loss of forehead creases

1. Sialocele — saliva pooling under skin flap; treated by aspiration ± pressure dressing; usually resolves
2. Salivary fistula (if duct not properly ligated) — rare
3. Wound infection

• Aberrant reinnervation of sweat glands by parasympathetic secretomotor fibres (from auriculotemporal nerve)
• Gustatory sweating and flushing over cheek/preauricular area during eating
• Diagnosis: Minor's starch-iodine test (skin turns blue over sweating area when eating)
• Treatment: Botulinum toxin injection (effective); antiperspirant; tympanic neurectomy

1. Tumour recurrence — especially with inadequate margins or after enucleation (for pleomorphic adenoma)
2. Numbness of ear lobe (great auricular nerve division — inevitable in most cases)
3. Trismus — rare; from fibrosis

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BA 10. Stages of Tuberculosis Lymphadenitis

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All answers follow the Sabiston Textbook of Surgery, Bailey & Love's Short Practice of Surgery, and Cummings Otolaryngology content framework, cross-referenced with current surgical practice.

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Nephrology / Urology MCQ Answers — Detailed Explanations

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Question 1 — 45-year-old male, dysuria, frequency, hazy urine

✅ Answer: C) Urinary Tract Infection (UTI)

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Why C is correct

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Why the other options are wrong

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Question 2 — 30-year-old, recurrent kidney stones, urine pH 5.2

✅ Answer: c) Acidic urine

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Explanation

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Clinical Relevance to Kidney Stones

• Low urine volume
• High purine diet / gout
• Insulin resistance (drives renal ammoniagenesis impairment → acidic urine)

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Why the other options are wrong

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Question 3 — Main indications for renal biopsy

✅ Answer: c) Evaluation of proteinuria, hematuria, and kidney dysfunction

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Indications for Renal Biopsy (Detailed)

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Why the other options are wrong

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Question 4 — 60-year-old diabetic/hypertensive, BUN:Creatinine ratio 25:1

✅ Answer: a) Prerenal cause of acute kidney injury

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Key Diagnostic Values

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Why BUN rises more than creatinine in prerenal states

1. Reduced renal perfusion (from heart failure, hypovolaemia, hypotension, sepsis, renal artery stenosis)
2. Reduced GFR → less filtration of both BUN and creatinine
3. BUT — in prerenal states, tubules are intact and functioning: they reabsorb water avidly (aldosterone + ADH activated)
4. BUN (urea) is passively reabsorbed with water in the proximal tubule and collecting duct → disproportionate rise in serum BUN
5. Creatinine is filtered but NOT reabsorbed → rises more slowly
6. Result: BUN rises faster than creatinine → ratio >20:1

• Upper GI bleeding (blood breakdown → urea load)
• High protein diet
• Corticosteroid therapy (increased protein catabolism)
• Severe catabolic states

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Why the other options are wrong

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Question 5 — 65-year-old, heart failure + CKD, FeNa 2.5%, muddy brown casts, granular casts

✅ Answer: b) Intrinsic renal cause of acute kidney injury

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Interpretation of FeNa 2.5%

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The Pathognomonic Urinary Findings

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Why ATN in this patient?

1. Acute haemodynamic compromise (reduced cardiac output → renal hypoperfusion)
2. Prolonged prerenal state → ischaemic ATN (tubular cell death from ischaemia-reperfusion injury)
3. Or nephrotoxic ATN (contrast, diuretic-induced hypoperfusion, NSAID)

1. Initiation — ischaemic insult; GFR falls
2. Maintenance (oliguric) — GFR remains low; oliguria; lasts 1–2 weeks
3. Recovery (diuretic) — tubular repair; polyuria (tubules can't concentrate yet); risk of hypokalaemia
4. Complete recovery — GFR normalises over weeks-months (may not fully recover in elderly/CKD)

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Important Caveat — Heart Failure Exception

• FEUrea <35% = prerenal
• FEUrea >50% = intrinsic (ATN)

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Why the other options are wrong

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Question 6 — 40-year-old, leg swelling, decreased urine output, WBC casts on microscopy

✅ Answer: a) Acute kidney injury (AKI)

Important note: This question requires careful analysis. WBC casts indicate renal parenchymal origin of WBCs — they are NOT seen in simple UTI (bladder infection). The answer requires understanding what WBC casts specifically indicate.

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What WBC Casts Mean

1. Acute interstitial nephritis (AIN) — most important cause; drug-induced (NSAIDs, antibiotics, PPIs), immune-mediated; WBC (eosinophil-rich) infiltration of interstitium → WBCs shed into tubular lumen → WBC casts
2. Acute pyelonephritis — bacterial invasion of renal parenchyma → renal WBC infiltration → WBC casts; accompanied by fever, flank pain, bacteriuria
3. Lupus nephritis (Class III/IV) — inflammatory cells in tubules
4. ANCA-associated vasculitis — with necrotising GN

• Leg swelling (oedema)
• Decreased urine output (oliguria)
• WBC casts

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Why NOT the other options

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Summary Table — Urine Cast Diagnostic Guide

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Final Answer Summary

Sources: Goldman-Cecil Medicine; Brenner and Rector's The Kidney; Schwartz's Principles of Surgery; Rosen's Emergency Medicine; Miller's Anesthesia.