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Jar Specimen Pathology: Tuberculosis, Ovarian Cyst, and Fibroid/Leiomyoma

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1. TUBERCULOSIS

What is a "Jar Specimen" in TB?

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Gross Examination

Key gross phrase: "White, cheesy, crumbly material" - this is caseous necrosis. Robbins states that dystrophic calcification is common in caseous necrosis of TB, and "sometimes a tuberculous lymph node is almost entirely converted to radiopaque stone." - Robbins & Kumar Basic Pathology

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Histological Findings

• Caseating epithelioid granulomas: central amorphous eosinophilic necrosis surrounded by epithelioid macrophages, Langhans giant cells (nuclei arranged in horseshoe/peripheral pattern), lymphocytes, and fibroblasts
• Langhans giant cells: multinucleated, nuclei arranged peripherally in a horseshoe/arc pattern (distinguishable from foreign body giant cells where nuclei are scattered)
• Type IV hypersensitivity mediated inflammatory response
• Special stains: Ziehl-Neelsen (ZN) stain / Kinyoun's acid-fast stain - shows acid-fast bacilli (AFB) as slender red rods on blue background; Auramine-rhodamine (fluorescent) stain for screening

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Specimen Types and Site-Specific Notes

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2. OVARIAN CYST

Types of Ovarian Cysts - Gross Pathology

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A. Functional / Physiological Cysts

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B. Neoplastic Cysts - Benign

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Gross Examination Protocol for Jar Specimen

1. Weigh and measure - three dimensions
2. Note outer surface - smooth/bosselated, adhesions, intact/ruptured
3. Open over a sink - note contents (clear/serous, mucoid, blood/chocolate, sebaceous/hair)
4. Unilocular vs. multilocular - number and size of locules
5. Internal lining - smooth vs. papillary excrescences (papillary projections = suspicious for malignancy)
6. Wall thickness - thin and uniform (benign) vs. thick and irregular (suspicious)
7. Solid areas - any solid component must be extensively sampled (rule out malignancy)

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Malignant Features (Red Flags on Gross)

• Solid areas within the cyst
• Papillary excrescences on internal or external surface
• Thickened, irregular wall
• Bilateral involvement
• Necrosis or hemorrhage
• Psammoma bodies (gritty, sandy deposits) - serous cystadenocarcinoma

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3. FIBROID / UTERINE LEIOMYOMA

What is It?

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Gross Examination - Key Features

Key gross finding: White, firm, whorled fascicles on cut surface. The tumor shells out from the surrounding myometrium. - Pathology Outlines - Leiomyoma

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Degenerative Changes in Fibroids (Jar Specimen)

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Histological Findings

• Intersecting fascicles of spindle cells (smooth muscle)
• Cells have cigar-shaped/blunt-ended nuclei with eosinophilic cytoplasm
• Absent or minimal atypia
• Rare mitoses (< 5 per 10 HPF)
• Thick-walled blood vessels
• IHC: positive for desmin, SMA (smooth muscle actin), h-caldesmon, ER, PR

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Distinguishing Fibroid from Leiomyosarcoma (Malignant Rule-Out)

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Quick Comparison Summary

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Jar Specimen Pathology: Atherosclerosis (Aorta) & Micronodular Cirrhosis

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HOW TO PRESENT A JAR SPECIMEN IN A VIVA (General Format)

"Sir/Ma'am, this specimen is from the _____ [organ]. It measures approximately _____ . On external surface / cut surface, I can see _____ . Based on these gross findings, my diagnosis is _____ . This is caused by _____ . The complications include _____ ."

"SOLID C"

• S - Size and Shape
• O - Organ identification
• L - Lesion description (location, number, extent)
• I - Internal/cut surface findings
• D - Diagnosis
• C - Cause + Complications

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PART 1: ATHEROSCLEROSIS - AORTA

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How to Present This Specimen

"Sir, this is a specimen of the aorta - identified by its large caliber, thick muscular wall, and tubular structure. It has been opened longitudinally to display the intimal surface. On the intimal (inner) surface, I can see yellowish flat streaks (early lesion), raised white/pearly fibrous plaques with irregular edges (intermediate lesion), and areas of ulceration, calcification, and thrombus formation (complicated lesion). The plaques are most prominent around the ostia of branch vessels and in the abdominal segment. Based on these findings, my diagnosis is Atherosclerosis of the aorta with complicated plaques."

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Gross Examination - Atherosclerosis Stages

Stage 1: Fatty Streak (Early/Reversible)

Stage 2: Fibrous Plaque (Intermediate)

Robbins: "Atheromatous plaques are raised lesions composed of soft friable (grumous) lipid cores covered by fibrous caps." - Robbins & Kumar Basic Pathology

Stage 3: Complicated Plaque (Advanced/Dangerous)

The abdominal aorta lacks vasa vasorum below L2, making medial ischemia more likely - predisposing to abdominal aortic aneurysm (AAA). - Rosen's Emergency Medicine

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Histological Findings

• Intimal thickening with foam cells (lipid-laden macrophages) - PAS positive
• Fibrous cap: smooth muscle cells, macrophages, lymphocytes, connective tissue
• Necrotic/atheromatous core: cholesterol clefts (empty needle-shaped spaces in paraffin sections), necrotic debris, calcification
• Vulnerable plaque: thin cap, large lipid core, dense macrophage infiltration (prone to rupture)
• Stable plaque: thick fibrous cap, minimal lipid, little inflammation

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Viva Questions & Answers - Atherosclerosis

A: Abdominal aorta (most severely affected) > coronary arteries > popliteal artery > internal carotid arteries. Upper extremity vessels are typically spared.

A: The atheroma (fibrofatty plaque) - a raised intimal lesion with a soft, grumous lipid core covered by a fibrous cap.

A (Mnemonic: "HHOSD" - or use the classic 4):

• H - Hypercholesterolaemia (especially raised LDL)
• H - Hypertension
• S - Smoking
• D - Diabetes mellitus Additional: Male sex, age, obesity, family history, homocysteinaemia

A: A lipid-laden macrophage in the arterial intima. LDL enters the intima through dysfunctional endothelium, gets oxidised (ox-LDL), and is engulfed by macrophages via scavenger receptors (not LDL receptors). These macrophages become bloated with lipid droplets = foam cells.

Mnemonic: "TIACE"

• T - Thrombosis (on ulcerated plaque)
• I - Ischemia/Infarction (MI, stroke, limb ischemia)
• A - Aneurysm (especially AAA)
• C - Calcification / Cholesterol emboli
• E - Embolism (atheroemboli)

A: Monckeberg's medial calcific sclerosis affects the media (not intima) of muscular arteries in elderly. Calcification occurs without lipid or inflammation. Does NOT narrow the lumen (so no ischemia). Seen on X-ray as "pipe-stem" or "eggshell" calcification of vessel wall.

A: Eccentric narrowing of lumen; the intima shows a raised white/yellow plaque; the plaque has a soft, cheesy lipid core with cholesterol clefts; a fibrous cap of pale collagen overlies the core; calcification may be present as chalky deposits.

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Mnemonic: Atherosclerosis Risk Factors

"ABCDE SHIP"

• A - Age (advancing)
• B - Blood pressure (hypertension)
• C - Cholesterol (hyperlipidaemia)
• D - Diabetes
• E - Exercise (lack of)
• S - Smoking
• H - Heredity/family history
• I - Inflammation (CRP, homocysteine)
• P - Physical inactivity/obesity

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PART 2: MICRONODULAR CIRRHOSIS (LIVER)

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How to Present This Specimen

"Sir, this is a specimen of the liver - identified by its wedge shape, smooth capsule (Glisson's capsule), and brown/tan colour. The liver appears shrunken and firm (compared to normal). On the external surface, the capsule shows multiple small nodular elevations - like a 'hobnail' pattern - uniformly distributed. On the cut surface, the entire parenchyma is replaced by multiple small uniform nodules each less than 3 mm in diameter, separated by thin fibrous septa (white connective tissue bands). No normal lobular architecture is visible. The nodules are greenish-yellow (suggesting fatty change/jaundice). Based on these findings, my diagnosis is Micronodular Cirrhosis of the liver, most likely of alcoholic (Laennec's) cirrhosis etiology."

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Gross Examination - Micronodular Cirrhosis

Key quote: "Grossly, a cirrhotic liver appears nodular, 'hobnailed' on the external surface and nodular on the cut surface. The liver is usually indurated, shrunken, and yellowish-tan." - Luc University Medical Education

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Micronodular vs. Macronodular Cirrhosis

Note: Mixed (macro + micronodular) patterns are common, especially in alcoholic cirrhosis. - Pathology Outlines - Cirrhosis

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Definition of Cirrhosis (Must Know for Viva)

Cirrhosis = Diffuse hepatic fibrosis + Regenerative nodules + Distortion of normal lobular architecture

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Histological Findings

• Hepatic parenchyma replaced by regenerative nodules (islands of hepatocytes surrounded by fibrous tissue)
• Bridging fibrosis connecting portal tracts to central veins and portal tract to portal tract
• Mallory bodies (hyaline inclusions in hepatocytes) - especially in alcoholic cirrhosis
• Fatty change (macrovesicular steatosis) - prominent in alcoholic and NASH cirrhosis
• Perivenular and pericellular fibrosis - characteristic of alcoholic cirrhosis (chicken-wire pattern on trichrome stain)
• Trichrome stain (Masson's) highlights fibrosis in blue/green

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Causes of Micronodular Cirrhosis

Mnemonic: "WATCH WB" (causes of micronodular / Laennec's-type)

• W - Wine/Alcohol (most common cause worldwide)
• A - AFLD/NAFLD (non-alcoholic)
• T - Total parenteral nutrition (TPN)
• C - Cardiac cirrhosis (right heart failure - nutmeg liver)
• H - Haemochromatosis
• W - Wilson's disease
• B - Biliary obstruction (primary/secondary biliary cirrhosis)

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Complications of Cirrhosis

Mnemonic: "PHASE"

• P - Portal hypertension (ascites, varices, splenomegaly, caput medusae)
• H - Hepatic encephalopathy
• A - Ascites (3rd most common cause of exudate ascites)
• S - Spontaneous bacterial peritonitis (SBP)
• E - Esophageal varices (bleeding) + HCC (hepatocellular carcinoma)

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Viva Questions & Answers - Micronodular Cirrhosis

A: Cirrhosis is a diffuse hepatic process characterized by fibrosis and conversion of normal liver architecture into structurally abnormal nodules (regenerative nodules). All three features - diffuse fibrosis, regenerating nodules, and architectural distortion - must be present.

A: Micronodular = nodules < 3 mm, uniform, thin septa - caused by alcohol, metabolic disease. Macronodular = nodules > 3 mm, irregular, thick septa - caused by viral hepatitis B and C (post-necrotic cirrhosis).

A: It is alcoholic (micronodular) cirrhosis, named after Rene Laennec (who also invented the stethoscope). Characterized by small uniform nodules, fatty change, Mallory bodies, and perivenular/pericellular fibrosis.

A: Transient elastography (FibroScan) - measures liver stiffness as a surrogate of fibrosis. Also: serum markers (APRI score, FIB-4 index), imaging (ultrasound showing nodular surface, ascites, splenomegaly). Biopsy using Vim-Silverman needle (if needed).

A: Normal portal pressure = 5-10 mmHg. In cirrhosis, HVPG (hepatic venous pressure gradient) rises. Complications appear at:

• 10 mmHg: varices begin to form

• 12 mmHg: variceal bleeding risk

A: The external capsular surface shows multiple small nodular elevations separated by fibrous depressions, resembling the pattern of hobnail boots (studded leather boots). This is the classic gross description of cirrhosis seen on the liver surface.

A: Intracytoplasmic eosinophilic inclusions in hepatocytes made of aggregated intermediate filaments (cytokeratin 8 and 18). Characteristic of alcoholic hepatitis but can be seen in NASH, Wilson's disease, and primary biliary cholangitis.

A: Once established with dense nodules and portal hypertension, cirrhosis is irreversible. However, less-advanced fibrosis (before cirrhosis) can regress if the causative injury is removed (e.g., alcohol abstinence, antiviral treatment for Hep B/C).

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Quick Comparison Summary

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Master Mnemonic for Cirrhosis Definition

"Cirrhosis = FAN"

• F - Fibrosis (bridging, diffuse)
• A - Architecture distortion (loss of lobular pattern)
• N - Nodules (regenerative)

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JAR SPECIMEN PATHOLOGY - Complete Viva Guide (8 Specimens)

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1. PERFORATED PEPTIC ULCER

How to Present

"Sir, this is a specimen of the stomach (or duodenum) - identified by its rugae pattern, muscular wall, and tubular structure. On the mucosal surface, I can see a well-defined, punched-out ulcer crater on the lesser curvature / first part of duodenum, approximately ___ cm in diameter. The ulcer has clean, sharply cut, vertical walls with no heaped-up margins (unlike malignant ulcers). The base is smooth and clean. There is a perforation - a through-and-through defect extending full thickness of the wall. The surrounding mucosa shows erythema and congestion. My diagnosis is Perforated Peptic Ulcer."

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Gross Findings

Classic distinction: Benign peptic ulcer = punched-out, vertical walls, clean base, no heaped margins | Malignant ulcer = raised/heaped-up, irregular, dirty base, indurated edges - Pathology Outlines - PUD

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Histological Findings (Four Zones - Mnemonic: "NFGG")

N - Necrotic debris (surface zone) F - Fibrinoid necrosis G - Granulation tissue (new capillaries, fibroblasts) G - Grey-white fibrous/scar tissue (base)

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Viva Q&A - Perforated Peptic Ulcer

A: Duodenal - anterior wall of first part of duodenum. Gastric - lesser curvature near incisura angularis.

A: Anterior DU perforates into the peritoneal cavity (free air = pneumoperitoneum). Posterior DU erodes into the gastroduodenal artery causing massive hemorrhage, or penetrates into the pancreas (pain radiates to back).

• H - H. pylori (most common - 95% of DU, 70% of GU)
• N - NSAIDs
• A - Acid hypersecretion (Zollinger-Ellison syndrome)
• S - Smoking, Stress (Cushing's ulcer = head injury; Curling's ulcer = burns)
• P - Prior history

A: Gastrin-secreting tumour (gastrinoma) of pancreas/duodenum causing massive acid hypersecretion and multiple, recurrent, atypical peptic ulcers (post-bulbar duodenum, jejunum). Diagnosed by fasting serum gastrin > 1000 pg/mL.

H-pylori, Acid/NSAIDs, Neoplasm, Drugs (steroids), Stress

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2. BREAST CARCINOMA

How to Present

"Sir, this is a specimen of the breast - identified by the surrounding fatty tissue and breast parenchyma. On cut surface, I can see a firm, irregular, stellate/spiculated mass in the upper outer quadrant, measuring approximately ___ cm. The mass has ill-defined borders, extends into surrounding tissue with a spider-like/stellate appearance due to fibrous strands. The cut surface is grey-white, hard, gritty ('like cutting through unripe pear' or 'cartilaginous feel'). There is skin dimpling/nipple retraction (if present). No capsule is visible. My diagnosis is Invasive Breast Carcinoma (Scirrhous type / Invasive Ductal Carcinoma NOS)."

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Gross Findings

"A typical invasive ductal carcinoma forms an irregular, poorly-defined mass that feels firm or hard and consists of a mixture of white, tan, and pale yellow tissue." - MGH Pathology

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Histological Findings

• Invasive ductal carcinoma (IDC/NST): most common type (80%); ductal cells breaking through basement membrane
• Tubular glands with cellular pleomorphism; enlarged nuclei; mitoses
• Dense desmoplastic (fibrous) stroma = scirrhous reaction
• Graded by Bloom-Richardson-Nottingham grading (tubule formation, nuclear pleomorphism, mitotic count)
• IHC: ER, PR, HER2 status (determines treatment)

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Viva Q&A - Breast Carcinoma

A: A macroscopic description of invasive ductal carcinoma (IDC/NST) characterized by a hard, fibrous, gritty consistency due to dense desmoplastic stromal reaction elicited by the tumour. The Greek word "skirros" means hardness.

• I - Invasive Ductal (NST) - most common (80%)
• D - Ductal carcinoma in situ (DCIS)
• L - Lobular (invasive + in situ)
• M - Medullary
• P - Paget's disease of nipple
• M - Mucinous/Colloid
• M - Metaplastic

A: Intraepidermal spread of ductal carcinoma cells into the nipple epidermis. Appears as eczematous, scaly, crusted lesion of the nipple. Paget cells = large, pale, vacuolated cells with clear halo in nipple epidermis. Almost always associated with underlying DCIS or IDC.

A: "Orange-peel skin" appearance due to dermal lymphatic obstruction by tumour emboli causing skin edema. The hair follicles and sweat glands remain tethered = dimpled appearance like orange peel. Classic in inflammatory breast carcinoma.

A: Upper outer quadrant (50%) - because it has the most glandular tissue (tail of Spence extends into axilla). Mnemonic: "Upper Outer = Most cancer, Most lymph nodes"

A: Tumor cells express estrogen and progesterone receptors = hormone-dependent growth. Responds to anti-oestrogen therapy (tamoxifen, aromatase inhibitors). Better prognosis than ER/PR negative tumors.

Family history, Age/Alcohol, Radiation, Menarche early/Menopause late, Estrogen (exogenous), Reproductive history (nulliparous, late first pregnancy)

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3. CENTRAL TYPE LUNG CANCER

How to Present

"Sir, this is a specimen of the lung - identified by its spongy texture, grey-pink parenchyma, and pleural surface. On cut surface, there is a large grey-white firm mass located centrally near the hilum, arising from a main/lobar bronchus. The mass has irregular, infiltrating borders and appears to obstruct the bronchial lumen. The bronchus proximal to the mass shows thickening and distortion. Distal to the obstruction, there is evidence of obstructive pneumonia/collapse (consolidated grey/yellow tissue). Hilar lymph nodes appear enlarged and matted. My diagnosis is Central type Lung Carcinoma - most likely Squamous Cell Carcinoma (or Small Cell Carcinoma)."

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Gross Findings

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Types of Lung Cancer - Central vs. Peripheral

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Histological Findings - SCC (most common central type)

• Keratinizing: keratin pearls (onion-like concentric rings of keratinized cells), individual cell keratinization
• Non-keratinizing: intercellular bridges (desmosomes) visible
• IHC: p40, p63, CK5/6 positive; TTF-1 negative

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Viva Q&A - Central Lung Cancer

A: Adenocarcinoma (40%+) is the most common overall. Among central tumours, squamous cell carcinoma (30%) and small cell carcinoma (15%) predominate.

A: Small cell carcinoma > squamous cell > adenocarcinoma. Adenocarcinoma is the most common in non-smokers.

• SIADH - Small cell → inappropriate ADH secretion
• ACTH (ectopic) - Small cell → Cushing syndrome
• Calcium (hypercalcaemia) - Squamous cell → PTHrP secretion
• Syndrome of Eaton-Lambert - Small cell → myasthenia-like syndrome (antibodies against presynaptic Ca²⁺ channels)

A: Tumour at the apex of lung causing Pancoast syndrome: shoulder pain + Horner's syndrome (ptosis, miosis, anhidrosis) + brachial plexus involvement (C8/T1 - ulnar nerve). Usually squamous cell carcinoma.

A: Central tumour obstructs a bronchus → air resorbed distal to obstruction → atelectasis (collapse) → impaired mucociliary clearance → bacterial superinfection → pneumonitis and consolidation distal to tumour.

Small cell, Adenocarcinoma, Squamous, Adenosquamous, Large cell

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4. MILIARY TB OF LUNG

How to Present

"Sir, this is a specimen of the lung - identified by its pyramidal shape, spongy texture, and pleural surface. On the external (pleural) surface and throughout the cut surface, I can see innumerable tiny, grey-white nodules of uniform size, approximately 1-2 mm in diameter, scattered uniformly throughout both lobes like millet seeds (hence the term miliary). The background lung tissue is congested and dark red. The nodules are firm and slightly gritty on sectioning. My diagnosis is Miliary Tuberculosis of the Lung."

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Gross Findings

"The lungs were deeply congested and throughout both were small millet-seed-sized greyish nodules. Similar nodules were noted in the spleen, liver and kidneys." - University of British Columbia Pathology

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Histological Findings

• Epithelioid granulomas with central caseous necrosis
• Langhans giant cells (horseshoe peripheral nuclei arrangement)
• Lymphocytes, macrophages, fibroblasts at periphery
• ZN (Ziehl-Neelsen) stain - AFB-positive red rods
• No calcification in miliary TB (unlike old healed TB)

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Viva Q&A - Miliary TB

A: A form of disseminated TB resulting from haematogenous spread of Mycobacterium tuberculosis, producing uniform 1-2 mm granulomas throughout organs resembling millet seeds on gross examination. Named after Prosper Louis Landouzy, from the Latin "milium" (millet grain).

A: Rupture of a caseating focus into a blood vessel - either into a pulmonary vein (systemic miliary TB) or pulmonary artery (pulmonary miliary TB), or via the thoracic duct. May also result from eroded lymph node.

A: "LSCK" - Lungs, Spleen, liver (hep-atomegaly), Kidneys, Choroid (eye) - choroidal tubercles on fundoscopy are pathognomonic.

A: Respiratory failure (pulmonary involvement), TB meningitis (from haematogenous seeding of meninges), or sepsis.

Millet seeds, Mycobacterium haematogenous, Multiple organs

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5. BRONCHIECTASIS (& COPD/EMPHYSEMA)

How to Present

Bronchiectasis

"Sir, this is a specimen of the lung - identified by its parenchymal structure and pleural surface. On cut surface, I can see markedly dilated bronchi which can be traced almost to the pleural surface (normally bronchi stop 2 cm from pleura). The dilated bronchi have thick, irregular walls and appear filled with thick, mucopurulent secretions (yellow-green). The types of dilation include saccular (balloon-like), cylindrical (uniform widening), and varicose (irregular). The surrounding parenchyma shows fibrosis and collapse. Honeycomb-like appearance on cut section. My diagnosis is Bronchiectasis."

COPD/Emphysema

"Sir, this is a specimen of the lung - which appears hyperinflated, over-distended and pale. The lung feels soft, voluminous, loss of elasticity - does not collapse normally. On cut surface, I can see enlarged air spaces (bullae/blebs) - abnormal permanent enlargement of air spaces distal to the terminal bronchiole with destruction of alveolar walls, without fibrosis. Upper lobes are more severely affected (centriacinar pattern). My diagnosis is Emphysema (a component of COPD)."

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Gross Findings

Bronchiectasis

Emphysema (COPD)

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Viva Q&A - Bronchiectasis & COPD

A: Permanent, abnormal irreversible dilatation of bronchi and bronchioles due to destruction of bronchial wall components (muscle, cartilage, elastic tissue), usually resulting from necrotizing infection.

• A - Aspiration (foreign body, recurrent)
• B - Bronchial obstruction (tumour, lymph node)
• C - Cystic fibrosis (most common congenital cause); Ciliary dyskinesia (Kartagener's)
• D - Defence impairment (immunodeficiency - hypogammaglobulinemia)
• E - Endobronchial infection (TB, pertussis, measles - post-infectious)
• F - Fibrotic/traction (pulmonary fibrosis pulling on bronchi)

A: Primary ciliary dyskinesia - autosomal recessive defect in dynein arms of cilia. Classic triad: Bronchiectasis + Situs inversus + Sinusitis. Infertility (immotile sperm) in males.

A: Autosomal recessive deficiency of the serine protease inhibitor α1-antitrypsin (α1-AT). Results in unchecked neutrophil elastase activity destroying alveolar walls. Causes panacinar emphysema (lower lobe predominant). Also causes liver disease (hepatitis/cirrhosis from abnormal α1-AT protein accumulation in hepatocytes).

Smoking (most common), Pollution, Infections (recurrent), Noxious gases, Environmental/genetic (α1-AT)

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6. POLYCYSTIC KIDNEY

How to Present

"Sir, this is a specimen of the kidney - identifiable by its bean-shaped structure with renal pelvis and ureter. The kidney is markedly enlarged (well beyond normal 11 cm length), and both the external surface and cut surface are entirely replaced by multiple cysts of varying sizes - ranging from small millimetric cysts to large cysts several centimetres in diameter. The cysts contain clear, straw-coloured fluid (some may be haemorrhagic - brown). No normal renal parenchyma is visible between the cysts. The condition is bilateral. My diagnosis is Polycystic Kidney Disease (Adult type / ADPKD)."

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Gross Findings

"The kidney is markedly enlarged and contains numerous dilated cysts." - Robbins & Kumar Basic Pathology, FIG. 12.23

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ADPKD vs. ARPKD

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Viva Q&A - Polycystic Kidney

A: PKD1 mutation (chromosome 16) in 85% of cases - encodes polycystin-1 (transmembrane receptor involved in cell-cell and cell-matrix interactions). PKD2 mutation (chromosome 4) in 15% - encodes polycystin-2 (Ca2+ channel). Both involve cilia dysfunction in tubular epithelium.

• C - Cyst haemorrhage (flank pain, haematuria)
• H - Hypertension (75% of patients - due to RAAS activation from cyst compression of intrarenal vessels)
• A - Aneurysm (Berry aneurysm in circle of Willis - 10-15%; risk of SAH is cause of death in 15%)
• P - Progression to renal failure (CKD by age 60 in 50%) Additional: Hepatic cysts, UTI/infected cysts, mitral valve prolapse

A: Flank pain or heavy dragging sensation due to enlarged kidneys. Also: haematuria (cyst rupture into collecting system), hypertension, UTI, or palpable abdominal mass.

A: No cure. Symptomatic: BP control (ACE inhibitors/ARBs), infection treatment, pain management. Tolvaptan (vasopressin V2 receptor antagonist) slows cyst growth and progression. Renal replacement therapy (dialysis/transplant) for ESRD.

Berry aneurysm, Aortic regurgitation/MVP, Liver cysts, Kidney failure

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7. COLONIC POLYP

How to Present

"Sir, this is a specimen of a segment of colon - identified by its sacculated (haustrated) wall, taenia coli, and mucosal folds. On the mucosal surface, I can see a polyp - a pedunculated/sessile mass projecting into the lumen, measuring approximately ___ cm, with a stalk (pedunculated) or a broad base (sessile). The surface appears lobulated/frond-like (villous) or smooth/rounded (tubular). The surrounding mucosa is normal. My diagnosis is Adenomatous Polyp (Tubular / Villous / Tubulovillous adenoma) of the colon."

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Types of Colonic Polyps

Neoplastic (Adenomatous) - Important for viva

Non-neoplastic

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Viva Q&A - Colonic Polyp

A: Villous adenoma (40% risk of malignancy). Rule: the more villous = more malignant risk. Also: larger size > 2 cm, sessile, high-grade dysplasia = high risk.

A: The stepwise progression from normal epithelium → adenoma → carcinoma over 10-15 years, driven by accumulation of mutations: APC (tumour suppressor) → K-RAS (oncogene) → DCC (deleted in colon cancer) → p53 → carcinoma Mnemonic: "A Killer Damn Problem" = APC, KRAS, DCC, p53

A: Autosomal dominant mutation in APC gene (chromosome 5q21). Hundreds to thousands of colorectal adenomas develop by teenage years; 100% risk of colorectal carcinoma by age 40 if untreated. Treatment = prophylactic colectomy. Gardner's syndrome = FAP + osteomas + desmoid tumours + epidermoid cysts.

A (Mnemonic: "VISA"): Villous component > 75%, Increased size > 2 cm, Sessile base, Atypia (high-grade dysplasia)

A: Ulceration of the surface, haemorrhage, induration at the base, firm/hard consistency, loss of stalk definition, tethering to bowel wall.

Tubular (pedunculated, low risk), Villous (sessile, HIGH risk), Tubulovillous (mixed)

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8. NUTMEG LIVER

How to Present

"Sir, this is a specimen of the liver - identified by its characteristic wedge shape, smooth surface, and brown parenchyma. The liver appears enlarged and firm. On cut surface, I can see a striking mottled pattern of alternating dark red (congested areas) and pale yellow (fatty change areas), resembling the cut surface of a nutmeg kernel - hence the term 'nutmeg liver'. The red areas are centrally located (centrilobular congestion) while the pale yellow zones are in the periphery (periportal fatty hepatocytes). There is NO nodularity (no cirrhosis). My diagnosis is Nutmeg Liver - due to Chronic Passive Venous Congestion (most likely right heart failure)."

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Gross Findings

"The liver was enlarged and tense. The lobular architecture was accentuated by central reddish areas, alternating with slight yellowish zones - the nutmeg liver of chronic venous congestion, caused by chronic right heart failure." - UBC Pathology

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Pathogenesis (Must know)

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Histological Findings

• Centrilobular zone (Zone 3): dilated, congested hepatic veinules; haemorrhagic necrosis; hepatocyte atrophy/loss
• Mid-zone (Zone 2): transitional, partially affected
• Periportal zone (Zone 1): hepatocytes intact, showing macrovesicular fatty change (steatosis)
• Late stage: centrilobular fibrosis → cardiac cirrhosis (rare); trichrome stain shows pericellular/perivenular fibrosis

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Viva Q&A - Nutmeg Liver

A: Chronic passive venous congestion (CPVC), most commonly from right heart failure (RHF). Other causes: constrictive pericarditis, tricuspid stenosis/regurgitation, Budd-Chiari syndrome (hepatic vein thrombosis), inferior vena cava obstruction.

A: Zone 3 (centrilobular) hepatocytes are farthest from the portal triad (blood supply) and are the last to receive oxygen. They are most vulnerable to both hypoxia (from low output) AND congestion (from high backpressure). Zone 1 (periportal) hepatocytes are next to hepatic arterioles and receive the most oxygen.

A: Nutmeg liver = early/reversible stage of CPVC with congestion and necrosis but NO established cirrhosis. Cardiac cirrhosis = late stage of CPVC with fibrosis bridging from centrilobular to centrilobular veins creating a reversed cirrhosis pattern; occurs with longstanding severe congestion.

A: Thrombosis of hepatic veins (or IVC above hepatic veins) causing acute/subacute/chronic hepatic outflow obstruction. Presents with painful hepatomegaly, ascites, and liver failure. Causes: hypercoagulable states (polycythaemia vera most common, pregnancy, OCP), tumour invasion. Gross: similar nutmeg pattern.

A: Dilated, congested central veins (hepatic veinules); perivenular haemorrhage; hepatocyte atrophy and dropout; haemosiderin-laden macrophages (from lysed RBCs).

Right Heart Failure, Hepatic vein (Budd-Chiari), Failure of IVC, Adhesive pericarditis (constrictive), Budd-Chiari, Cardiac tamponade, Dextrocardia complications

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MASTER SUMMARY TABLE