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PATHOLOGY THEORY EXAMINATION - COMPLETE ANSWERS

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SECTION B

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Q.2 — Breast Tumours (10 Marks)

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A) Classification of Breast Tumours

BREAST TUMOURS
│
├── BENIGN
│   ├── Fibroadenoma (most common benign tumour)
│   ├── Phyllodes tumour (benign variant)
│   ├── Intraductal papilloma
│   ├── Fat necrosis
│   └── Fibrocystic change (not a true tumour)
│
└── MALIGNANT (Carcinoma)
    │
    ├── NON-INVASIVE (In situ)
    │   ├── Ductal Carcinoma In Situ (DCIS) - most common
    │   └── Lobular Carcinoma In Situ (LCIS)
    │
    └── INVASIVE (Infiltrating)
        ├── Invasive Ductal Carcinoma (IDC) - 70-80% of all carcinomas
        │   └── Scirrhous / NOS type
        ├── Invasive Lobular Carcinoma (ILC) - 10-15%
        ├── Medullary Carcinoma
        ├── Mucinous (Colloid) Carcinoma
        ├── Tubular Carcinoma
        ├── Papillary Carcinoma
        ├── Paget's Disease of the nipple
        └── Inflammatory Carcinoma

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B) Risk Factors for Carcinoma Breast

• Early menarche (before 12 years)
• Late menopause (after 55 years)
• Nulliparity / late first pregnancy (after 30 years)
• Prolonged use of oral contraceptives / HRT
• Obesity (especially post-menopausal - adipose tissue produces estrogen)

• BRCA1 mutation - risk of breast + ovarian cancer
• BRCA2 mutation - risk of breast cancer (also in males)
• Family history in first-degree relatives
• Li-Fraumeni syndrome (TP53 mutation)

• Previous benign breast disease with atypia (atypical ductal hyperplasia)
• Radiation exposure to chest
• High fat diet, alcohol consumption
• Previous carcinoma in opposite breast

RISK FACTOR SUMMARY
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
Increased ESTROGEN exposure → KEY MECHANISM
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

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C) Gross Features of Carcinoma Breast (IDC - Scirrhous type)

• Size: Variable, usually 1-5 cm
• Shape: Irregular, stellate (star-shaped)
• Consistency: Hard, stony (rock-like) due to dense fibrous stroma - hence called "scirrhous"
• Cut surface: Grey-white, chalky white streaks (due to calcification)
• Borders: Irregular, ill-defined - infiltrates surrounding fat
• Skin changes: Skin dimpling, nipple retraction (due to fibrosis pulling ligaments of Cooper)
• Peau d'orange: Skin looks like orange peel due to lymphatic obstruction (in inflammatory type)

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D) Microscopic Features of Carcinoma Breast (IDC)

• Malignant ductal epithelial cells arranged in:
  • Cords, nests, and clusters
  • Tubule formation (gland-like structures)
  • Indian-file pattern (in lobular carcinoma - single cells in a line)
• Stroma: Abundant fibrous (desmoplastic) stroma - "hard" consistency
• Nuclear features: Large, pleomorphic nuclei, prominent nucleoli, frequent mitoses
• Necrosis: Comedo necrosis in DCIS (central necrosis within ducts)
• Calcification: Dystrophic calcifications may be present
• Lymphovascular invasion: Common in aggressive tumours
• ER/PR/HER2 status - assessed by immunohistochemistry

DCIS Microscopy:
Malignant cells filling ductal lumen
+ Central comedo necrosis
+ No invasion through basement membrane

IDC Microscopy:
Malignant cells BREAKING THROUGH basement membrane
+ Invading stroma
+ Desmoplastic reaction

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Q.3 — Any Five Clinical Scenarios (5 × 3 = 15 Marks)

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Q3-A: 45-year-old obese female with itching, RUQ colicky pain

• High conjugated bilirubin → problem is AFTER the liver (bile cannot drain)
• Very high ALP → classical of bile duct obstruction
• Mildly elevated AST/ALT → secondary liver cell damage due to back-pressure
• Itching (pruritus) → due to bile salts deposited in skin
• RUQ pain → due to gallstone obstructing CBD
• Obese female → classic risk factor (F, Fat, Forty, Fertile = gallstones)

FLOW: Gallstone blocks CBD → Bile cannot flow → 
Conjugated bilirubin regurgitates into blood → 
Jaundice + Itching + ALP rises markedly

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Q3-B: 55-year-old male with chest pain, ST elevation and T-wave inversion

TIME AFTER MI ONSET
│
0 hours ─── Symptoms begin (chest pain, sweating)
│
1-3 hours ── Myoglobin rises (EARLIEST to rise, NOT cardiac specific)
│
3-6 hours ── Troponin I / Troponin T rises (EARLIEST specific marker)
│             CK-MB starts rising
│
12-24 hrs ── Troponin peaks
│             CK-MB peaks
│             LDH starts rising
│
24-48 hrs ── CK-MB returns to normal
│
3-7 days ─── Troponin T remains elevated (useful for LATE diagnosis)
│             LDH peaks
│
7-14 days ── LDH returns to normal
│
14 days ──── Troponin I returns to normal

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Q3-C: 14-year-old male, swelling around knee, X-ray shows destructive metaphyseal tumour with sunburst appearance

• Large, bulky tumour arising in metaphysis of distal femur / proximal tibia
• Cut surface: grey-white to tan, gritty (due to bone formation)
• Areas of haemorrhage and necrosis
• Codman's triangle: Periosteum is lifted by tumour → reactive bone forms a triangular shell at edges (seen on X-ray)
• Tumour breaks through cortex into soft tissue
• Sunburst appearance on X-ray = tumour bone growing perpendicular to shaft through periosteum

• Malignant spindle-shaped osteoblasts (stromal cells)
• Direct production of osteoid / tumour bone by malignant cells (ESSENTIAL for diagnosis)
• High nuclear pleomorphism, frequent mitoses, atypical mitoses
• Areas of cartilage may be present (chondroblastic osteosarcoma)
• Fibroblastic areas also present
• Necrosis common
• Tumour invades surrounding soft tissue

KEY DIAGNOSTIC FEATURE = Malignant cells producing OSTEOID directly

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Q3-D: 40-year-old male with epigastric pain relieved by food, no vomiting or weight loss

NORMAL BALANCE:
Aggressive factors ←→ Defensive factors
(acid, pepsin)         (mucus, bicarbonate, 
                        prostaglandins)

IN PEPTIC ULCER:
Aggressive > Defensive → MUCOSAL BREAKDOWN

1. H. pylori infection (most important cause - 90% of duodenal ulcers)
   • H. pylori colonizes gastric antrum
   • Produces urease → splits urea to ammonia → damages mucosa
   • Causes antral gastritis → decreases somatostatin → increased gastrin → increased acid production
   • Produces vacuolating toxin (VacA) and CagA → damages epithelium
2. Increased acid production:
   • H. pylori → antral gastritis → ↑ gastrin → ↑ HCl
   • Increased parietal cell mass
   • Rapid gastric emptying → acid load in duodenum
3. Decreased mucosal defense:
   • NSAID use → inhibits COX → decreased prostaglandins → decreased mucus & bicarbonate
   • H. pylori disrupts mucus layer
4. Pain relieved by food = because food buffers the acid (typical of duodenal ulcer)
   • (Gastric ulcer pain is typically worse after eating)

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Q3-E: 6-year-old male child with massive proteinuria, hypoalbuminemia, generalized oedema, hyperlipidaemia

CAUSES
├── PRIMARY (Renal disease)
│   ├── Minimal Change Disease (MCD) - MOST COMMON in children (90%)
│   ├── Focal Segmental Glomerulosclerosis (FSGS)
│   ├── Membranous Nephropathy (most common in adults)
│   └── Membranoproliferative GN (MPGN)
│
└── SECONDARY (Systemic disease)
    ├── Diabetes Mellitus (Diabetic nephropathy)
    ├── Systemic Lupus Erythematosus (SLE)
    ├── Amyloidosis
    ├── Infections (Malaria, Hepatitis B/C, HIV)
    └── Drugs (Gold, Penicillamine, NSAIDs)

• Most common cause of nephrotic syndrome in children
• Responds well to steroids

Loss of negative charge on GBM (podocyte damage)
        ↓
Massive PROTEINURIA (>3.5 g/day)
        ↓
Low plasma proteins (Hypoalbuminemia)
        ↓
Low oncotic pressure → fluid leaks into interstitium
        ↓
GENERALIZED OEDEMA (pitting oedema, ascites, pleural effusion)
        ↓
Compensatory: ↑ lipoprotein synthesis by liver
        ↓
HYPERLIPIDAEMIA + LIPIDURIA

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Q3-F: 48-year-old male, chronic smoker, haemoptysis and weight loss

NORMAL BRONCHIAL EPITHELIUM
(Pseudostratified ciliated columnar epithelium)
        ↓
Repeated exposure to cigarette smoke carcinogens
        ↓
STEP 1: BASAL CELL HYPERPLASIA
(Proliferation of basal cells)
        ↓
STEP 2: SQUAMOUS METAPLASIA
(Columnar cells replaced by squamous cells - reversible if smoking stopped)
        ↓
STEP 3: SQUAMOUS DYSPLASIA
(Nuclear atypia, loss of polarity, abnormal mitoses)
        ↓
STEP 4: CARCINOMA IN SITU (CIS)
(Full thickness dysplasia, basement membrane INTACT)
        ↓
Accumulation of mutations: TP53, RB, KRAS, loss of 3p
        ↓
STEP 5: INVASIVE SQUAMOUS CELL CARCINOMA
(Cells breach basement membrane, invade stroma)
        ↓
Presents with: HAEMOPTYSIS (central tumour erodes vessels)
               Weight loss (cancer cachexia)

• Arises centrally (near bronchi)
• Keratin pearls + intercellular bridges on microscopy
• Cavitation common
• Associated with PTHrP secretion → hypercalcaemia (paraneoplastic)

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Q.4 — Any Four Out of Five (4 × 5 = 20 Marks)

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Q4-A: Renal Function Tests

• Urinalysis: Protein, glucose, casts (RBC casts = glomerulonephritis; WBC casts = pyelonephritis; granular casts = ATN)
• Serum electrolytes: Na, K, HCO3 - hyperkalemia and acidosis in renal failure
• Urine protein: 24-hour urine protein >3.5 g/day = nephrotic range

CKD STAGING BY GFR:
Stage 1: GFR ≥ 90 (normal/increased)
Stage 2: GFR 60-89 (mildly reduced)
Stage 3: GFR 30-59 (moderately reduced)
Stage 4: GFR 15-29 (severely reduced)
Stage 5: GFR <15 (kidney failure/ESRD)

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Q4-B: Etiology and CSF Findings in Pyogenic Meningitis

AGE GROUP        COMMON ORGANISMS
─────────────────────────────────────────────────────
Neonates         Group B Streptococcus (#1)
(0-3 months)     E. coli, Listeria monocytogenes

Infants/Children Neisseria meningitidis (#1)
(3 months - 18y) Streptococcus pneumoniae
                 Haemophilus influenzae (now rare - vaccine)

Adults (18-60y)  Streptococcus pneumoniae (#1)
                 Neisseria meningitidis

Elderly (>60y)   Streptococcus pneumoniae (#1)
                 Listeria monocytogenes
                 Gram-negative bacilli

Immunocompromised Any of above + Listeria + Gram negatives

MEMORY AID for Pyogenic Meningitis CSF:
↑ Pressure
↑ Turbid (cloudy)
↑ Neutrophils
↑ Protein
↓ Glucose

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Q4-C: Malignant Melanoma - Sites, Gross and Microscopic Features

• Skin - most common (anywhere but especially: back in men, legs in women)
• Specific types by site:
  • Superficial spreading melanoma - most common type (70%) - trunk/extremities
  • Nodular melanoma - most aggressive - back, trunk
  • Lentigo maligna melanoma - face (elderly, sun-exposed skin)
  • Acral lentiginous melanoma - palms, soles, subungual (under nails) - most common in dark-skinned individuals
• Other sites: eye (uveal melanoma), mucous membranes, meninges

• Asymmetrical lesion (use ABCDE rule: Asymmetry, Border irregularity, Colour variation, Diameter >6mm, Evolution)
• Colours: brown, black, tan, red, white, pink - variable colours
• Irregular, notched borders
• May ulcerate and bleed
• Nodular type: raised, dome-shaped nodule, deeply pigmented, rapidly growing
• May show satellite lesions
• Thickness (Breslow thickness) measured in mm - most important prognostic factor

• Melanocytes showing marked pleomorphism
• Large cells with abundant cytoplasm containing melanin granules
• Prominent large eosinophilic (red) nucleoli - "owl-eye nucleoli"
• High mitotic rate
• Radial growth phase: tumour spreads horizontally in epidermis
• Vertical growth phase: tumour invades dermis (poor prognosis)
• Pagetoid spread: single melanoma cells scattered in epidermis
• Lymphocytic infiltrate at base
• Clark's levels: measured by depth of invasion (Levels I-V)
• Breslow thickness: measured from granular layer to deepest tumour cell

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Q4-D: Differences between Crohn's Disease and Ulcerative Colitis

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Q4-E: Renal Cell Carcinoma

• Clear cell RCC (most common, 70-80%) - VHL gene mutation
• Papillary RCC (10-15%)
• Chromophobe RCC (5%)
• Collecting duct carcinoma (rare, most aggressive)

• Usually in upper pole of kidney
• Large, solitary, spherical mass
• Cut surface: bright yellow to orange (due to lipid and glycogen in clear cells)
• Areas of haemorrhage, necrosis, cystic change
• Well-demarcated by a pseudocapsule
• May extend into renal vein → IVC → right atrium (tumour thrombus)

• Large cells with clear cytoplasm (lipid and glycogen washed out in processing)
• Cells arranged in sheets, nests, tubules or alveolar pattern
• Prominent vascular stroma (very vascular tumour)
• Small round dark nuclei (low grade) to large pleomorphic nuclei (high grade)
• Thin-walled blood vessels between tumour cells

1. Haematuria (blood in urine)
2. Flank pain
3. Palpable flank mass

• Polycythaemia (ectopic EPO)
• Hypercalcaemia (PTHrP)
• Hypertension (ectopic renin)
• Cushing syndrome (ectopic ACTH)

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Q.5 — Any Three (3 × 5 = 15 Marks)

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Q5-A: Gross and Microscopic Features of Lobar Pneumonia

STAGE 1: CONGESTION (0-24 hrs)
• Gross: Lobe heavy, red, congested, boggy
• Micro: Vascular congestion, oedema fluid in alveoli
         Few bacteria, few neutrophils in alveolar spaces
         Alveolar septa stretched

         ↓

STAGE 2: RED HEPATIZATION (2-3 days)
• Gross: Lobe solid, firm, red, airless - like liver (hepatization)
         Red colour due to RBCs
• Micro: Alveoli packed with NEUTROPHILS, RBCs, and fibrin
         Capillaries congested
         Bacteria present

         ↓

STAGE 3: GREY HEPATIZATION (4-8 days)
• Gross: Lobe still solid/firm but grey-white colour
         Grey colour = RBCs disintegrate, fibrin dominates
• Micro: Alveoli filled with FIBRIN meshwork
         Neutrophils (many dead/disintegrating)
         No RBCs (lysed)
         Macrophages appear

         ↓

STAGE 4: RESOLUTION (8-10 days)
• Gross: Lobe returns to normal appearance
         Softening of exudate
• Micro: Macrophages digest fibrin and debris
         Alveolar architecture restored
         Lung returns to normal (if uncomplicated)

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Q5-B: Leiomyoma Uterus (Fibroid)

UTERINE LEIOMYOMA - LOCATIONS
├── Intramural (most common) - within myometrium
├── Submucosal - under endometrium, projects into uterine cavity
│   → Causes MOST SEVERE menorrhagia + infertility
├── Subserosal - under peritoneum, projects outward
│   → May become pedunculated
└── Cervical - rare
    Broad ligament - rare

• Multiple (multiple fibroids in 75% of cases), well-circumscribed, firm tumours
• Whorled, trabeculated grey-white cut surface
• Clearly demarcated from surrounding myometrium by a pseudocapsule
• Size varies from millimetres to >20 cm
• Hard, rubbery consistency

• Interlacing bundles of smooth muscle cells arranged in whorls
• Cells are spindle-shaped with cigar-shaped (blunt-ended) nuclei
• Uniform, bland nuclei - NO atypia, NO necrosis, NO mitoses (distinguishes from malignant leiomyosarcoma)
• Cells have abundant eosinophilic cytoplasm
• Fibrous connective tissue between bundles
• May show secondary changes: hyaline degeneration (most common), cystic, red (carneous), fatty, calcification, malignant change (rare, <1%)

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Q5-C: Papillary Carcinoma of the Thyroid

• Usually unilateral, single nodule
• Often infiltrative, ill-defined borders (unlike follicular carcinoma)
• May be multifocal (20%)
• Cut surface: grey-white, firm, granular
• Psammoma bodies may be felt as gritty areas
• Foci of calcification
• Cystic change sometimes present
• May spread to cervical lymph nodes early (but prognosis still excellent)

DIAGNOSTIC FEATURES OF PAPILLARY CARCINOMA:

1. PAPILLARY architecture
   - Papillae with fibrovascular core
   - Lined by 1-2 layers of tumour cells
   (BUT papillary pattern not essential for diagnosis)

2. NUCLEAR FEATURES (MOST IMPORTANT):
   ┌─────────────────────────────────────────┐
   │ • Optically clear ("Orphan Annie eye")  │
   │   nuclei - "ground glass" / empty look  │
   │ • Nuclear grooves (coffee bean nuclei)  │
   │ • Intranuclear cytoplasmic inclusions   │
   └─────────────────────────────────────────┘
   These nuclear features = DIAGNOSTIC hallmark

3. PSAMMOMA BODIES
   - Concentric calcified laminated bodies
   - Present in 40-50% of cases
   - Pathognomonic when combined with papillary features

4. Follicular structures may also be present

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Q5-D: Laboratory Diagnosis of Diabetes Mellitus

DIABETES MELLITUS - LABORATORY DIAGNOSIS
─────────────────────────────────────────────────────────────
Test             Normal      Pre-diabetes    Diabetes
─────────────────────────────────────────────────────────────
Fasting Blood    <100        100-125         ≥ 126 mg/dl
Glucose (FBG)    mg/dl       (IFG)

2-hr Post OGTT   <140        140-199         ≥ 200 mg/dl
(75g glucose)    mg/dl       (IGT)

Random Blood     -           -               ≥ 200 mg/dl
Glucose                                      + symptoms

HbA1c            <5.7%       5.7-6.4%        ≥ 6.5%
─────────────────────────────────────────────────────────────

1. Fasting Blood Glucose (FBG): Patient fasts for 8 hours. ≥126 mg/dl on TWO occasions = DM
2. OGTT (Oral Glucose Tolerance Test): 75g oral glucose given; blood glucose measured at 0, 1, 2 hours. 2-hour value ≥200 = DM. (Gold standard for gestational DM)
3. Random Blood Glucose: Any time of day. ≥200 mg/dl WITH classic symptoms (polyuria, polydipsia, weight loss) = DM
4. HbA1c (Glycated Haemoglobin): Reflects average blood glucose over past 2-3 months. ≥6.5% = DM. Used for monitoring AND diagnosis.
5. Urine Glucose (Glucosuria): Appears when blood glucose >180 mg/dl (renal threshold). Not diagnostic alone but a screening test.
6. Urine Ketones: Positive in DKA (Type 1 DM mainly)
7. C-peptide: Distinguishes Type 1 (low/absent C-peptide) from Type 2 (normal/high C-peptide)
8. Insulin assay: Helpful in research/classification
9. Microalbuminuria (spot urine ACR): 30-300 mg/g = early diabetic nephropathy

MONITORING DM:
HbA1c every 3 months - TARGET <7% (53 mmol/mol)

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Q.6 — Short Notes (4 × 5 = 20 Marks)

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Q6-A: Coal Workers' Pneumoconiosis (CWP)

1. Simple CWP (most common) - coal macules and nodules, usually asymptomatic
2. Complicated CWP / Progressive Massive Fibrosis (PMF) - large fibrotic masses, severe lung damage

Inhalation of coal dust particles (<5 µm reach alveoli)
        ↓
Phagocytosed by ALVEOLAR MACROPHAGES
        ↓
Macrophages cannot digest carbon → accumulate
        ↓
Release: Cytokines (IL-1, TNF), Reactive Oxygen Species
        ↓
FIBROSIS (collagen deposition)
        ↓
COAL MACULES (dust + macrophages around respiratory bronchioles)
        ↓
COAL NODULES (macules + fibrosis)
        ↓
PROGRESSIVE MASSIVE FIBROSIS (PMF) in heavy exposure

• Lungs are black (anthracotic pigmentation)
• Simple CWP: Coal macules (1-2 mm, soft, black) + coal nodules (up to 2 cm, harder) - predominantly in upper lobes
• PMF: Large black fibrotic masses (>2 cm, up to >10 cm) - upper/central lung
• Emphysema around macules (focal emphysema)
• Pleural anthracosis

• Carbon-laden macrophages in clusters
• Coal nodules: Aggregates of dust-laden macrophages + haphazardly arranged collagen
• PMF: Dense collagen + coal dust pigment + areas of necrosis
• Emphysematous spaces surrounding nodules

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Q6-B: Osteomyelitis

1. Haematogenous spread (most common in children)
   - Bacteria in blood → seeds metaphysis (rich blood supply, sluggish flow)
   
2. Direct spread from contiguous focus
   - Trauma, surgery, bite wounds
   
3. Direct inoculation
   - Open fractures, orthopaedic procedures

• Staphylococcus aureus - most common at ALL ages
• Neonates: Group B Streptococcus, E. coli
• Children: H. influenzae (rare now), S. aureus
• Sickle cell patients: Salmonella (unique)
• Diabetics/immunocompromised: Gram-negatives, fungi

• Bone is red, congested, oedematous
• Pus formation in medullary cavity
• Involucrum: New bone formed by periosteum around dead bone (shell of living bone)
• Sequestrum: Dead devascularized bone fragment (grey-white, separated from living bone)
• Cloaca: Opening in involucrum through which pus discharges
• Sinus tract: Channel through soft tissue/skin for pus drainage

• Acute: Neutrophilic infiltration, necrosis, vascular congestion
• Chronic: Lymphocytes, plasma cells, macrophages, fibrosis, new bone formation, necrotic bone (sequestrum)

SEQUESTRUM → Dead bone
INVOLUCRUM → New bone around it
CLOACA → Hole in involucrum
SINUS TRACT → External drainage pathway

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Q6-C: Seminoma

• Testis enlarged, smooth surface
• Cut surface: Homogeneous, lobulated, grey-white ("cream cheese" appearance)
• Well-defined borders, lobulated by fibrous septa
• No haemorrhage or necrosis (unlike non-seminomatous GCTs)
• Replaces testicular parenchyma
• Tunica albuginea usually intact

CLASSIC APPEARANCE:
• Large, uniform, round cells with:
  - Clear/pale cytoplasm (abundant glycogen - PAS positive)
  - Large central nucleus
  - Prominent nucleoli
  - Well-defined cell borders

• Arranged in SHEETS and LOBULES
  separated by fibrous septa

• Fibrous septa infiltrated by LYMPHOCYTES
  (important diagnostic feature)

• Granulomatous reaction may be present
  (giant cells, histiocytes)

• NO trophoblastic cells, NO yolk sac elements

• Placental ALP (PLAP) - elevated in 90% of cases
• β-hCG - elevated in 15-20% (syncytiotrophoblast cells)
• AFP - NEGATIVE (if AFP raised → not pure seminoma, mixed GCT)
• LDH - non-specific, raised

• Radiosensitive (unlike non-seminomatous GCTs)
• Excellent prognosis even in advanced stages
• Spreads via lymphatics to para-aortic lymph nodes first
• Associated with cryptorchidism (undescended testis)

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Q6-D: Ethical Issues Pertaining to Consent for Surgical Procedures

4 PILLARS OF MEDICAL ETHICS
┌─────────────────┬────────────────────────────────────────────┐
│ Autonomy        │ Patient's right to make own decisions       │
│ Beneficence     │ Act in patient's best interest              │
│ Non-maleficence │ Do no harm                                  │
│ Justice         │ Fair treatment for all patients             │
└─────────────────┴────────────────────────────────────────────┘

1. Disclosure: Doctor must explain:
   • Nature of the diagnosis
   • Nature of the proposed procedure
   • Benefits and risks of the procedure
   • Alternatives available (including doing nothing)
   • Consequences of refusing treatment
2. Comprehension: Patient must understand the information (use appropriate language, translator if needed)
3. Voluntariness: Patient must decide freely - without coercion, pressure or undue influence
4. Competence/Capacity: Patient must have the mental ability to make decisions (age >18 years; no severe mental illness; not under influence of drugs/alcohol)

• Patient not given enough time to decide (rushed consent)
• Consent obtained by junior doctors who may not explain fully
• Language barriers → poor comprehension
• Illiterate patients - verbal consent + thumb impression
• Consent for teaching/photography requires additional consent
• Post-operative complications not disclosed → medicolegal issues

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All answers based on: Robbins & Kumar Basic Pathology, Bailey and Love's Surgery, Fishman's Pulmonary Diseases, and standard MBBS pathology curriculum. Good luck with your exam!