Key Pathological Findings: Gross and Microscopic Disease Features

1. Brain Abscess

• Gross Morphology

  Localized area of liquefactive necrosis filled with yellow pus, surrounded by a thin fibrous capsule and edematous, inflamed brain tissue.

• Pathology

  Caused by hematogenous spread of bacterial infection, direct trauma, or contiguous spread (e.g., from sinuses). Represents focal suppurative inflammation of the brain.

2. Neurinoma (Schwannoma)

• Gross Morphology

  Well-circumscribed, encapsulated globoid mass with a soft, tan “fish-flesh” appearance, often with cysts or hemorrhage. Cut surface may show yellow patches.

• Pathology

  A benign tumor of Schwann cells, often seen in cranial nerves (especially CN VIII) and associated with neurofibromatosis type 2. Grows slowly and may compress adjacent structures.

3. Fibrinous Pericarditis (“Bread and Butter” Pericarditis)

• Gross Morphology

  Shaggy, fibrinous strands covering the epicardial surface; roughened texture with loss of glistening appearance.

• Pathology

  Due to acute inflammation (e.g., viral infection, uremia, myocardial infarction). The fibrin causes a friction rub between the pericardium and epicardium.

4. Ischemic Brain Infarction

• Gross Morphology

  Early stage: soft, swollen brain tissue with blurred gray-white junction. Later: liquefaction forming a cystic cavity with glial scarring.

• Pathology

  Anemic (non-hemorrhagic) infarct, usually from thrombosis or embolism. Neuronal necrosis and gliosis develop over time.

5. Myocardial Scar (Post-Myocardial Infarction)

• Gross Morphology

  Pale or white fibrous tissue replacing myocardium, often involving the anterior left ventricular wall and septum.

• Pathology

  Result of a transmural myocardial infarction with fibrous scar formation over weeks. Indicates permanent loss of viable myocardium.

6. Hypertensive Heart Disease

• Gross Morphology

  Left ventricular hypertrophy with wall thickness >2 cm, small ventricular cavity. May reach 500–1100 g in weight.

• Pathology

  Due to chronic pressure overload from systemic hypertension, leading to concentric hypertrophy and eventual heart failure.

7. Chronic Gastric Ulcer

• Gross Morphology

  Sharply punched-out lesion with a clean base, straight walls, surrounded by inflamed mucosa; no heaped-up margins.

• Pathology

  Chronic mucosal injury from gastric acid and pepsin, often associated with H. pylori or NSAID use. Risk of bleeding, perforation, or obstruction.

9. Acute Pyelonephritis

• Gross Morphology

  • Kidneys are normal or slightly enlarged.

  • Multiple small yellowish abscesses (1–5 mm) with hyperemic halos in the cortex.

  • Purulent exudate in renal pelvis and calyces; abscesses may be radially distributed from calyces to cortex (in ascending infections).

• Pathology

  • Bacterial infection of the kidney (commonly E. coli), either ascending from the lower urinary tract or hematogenous.

  • Represents suppurative inflammation of the renal parenchyma.

10. Renal Infarction and Scar

• Gross Morphology

  Infarcts are wedge-shaped, pale, and sharply demarcated, with the apex pointing toward the medulla and a red zone of hyperemia at the margins. Over time, infarcts heal by fibrosis, forming gray, irregular, sunken cortical scars.

• Pathology

  Caused by arterial occlusion—often embolic from the heart or aorta—the result is ischemic coagulative necrosis of kidney tissue. Chronic infarcts lead to scarring, which may impair renal function if extensive or bilateral.

11. Lobular Pneumonia (Bronchopneumonia)

• Gross Morphology

  Multiple small (1–3 cm) yellow-white foci of consolidation are scattered throughout affected lobes, often centered around bronchioles and separated by normal lung tissue. They may become confluent in severe cases.

• Pathology

  Caused by bacterial pathogens such as Staphylococcus aureus, Klebsiella, or E. coli, bronchopneumonia involves patchy inflammation of airways and alveoli. It is common in debilitated or hospitalized patients and can progress to abscesses or fibrosis.

12. Uterine Leiomyoma

• Gross Morphology

  Firm, round, sharply circumscribed white-gray tumors with a whorled cut surface, often located intramurally, but also subserosal or submucosal. They may be single or multiple and vary greatly in size.

• Pathology

  A benign tumor of smooth muscle cells, often hormonally responsive. Leiomyomas are common in reproductive-age women and can cause menorrhagia, infertility, or mass effect symptoms depending on size and location.

13. Benign Prostatic Hyperplasia (BPH)

• Gross Morphology

  The prostate is enlarged and nodular, particularly in the lateral and median lobes. Obstruction of the urethra may cause bladder wall thickening (trabeculation), hydroureter, and hydronephrosis.

• Pathology

  BPH is caused by dihydrotestosterone-induced proliferation of stromal and glandular tissue. It leads to bladder outlet obstruction, incomplete emptying, urinary stasis, and can predispose to infection and kidney damage.

14. Hemorrhagic Brain Infarction

• Gross Morphology

  Soft, red infarcted areas with punctate hemorrhages and swelling. Severe cases may show midline shift due to edema and mass effect.

• Pathology

  Commonly due to embolic stroke followed by reperfusion, resulting in bleeding into infarcted brain tissue. It contrasts with pale infarcts and is more likely to cause secondary damage from increased intracranial pressure.

15. Heart Atrophy

• Gross Morphology

  The heart is small with thin walls and reduced chamber size. Epicardial fat is depleted, making coronary arteries appear prominent; the myocardium shows a dark brown color.

• Pathology

  Seen in chronic wasting conditions or aging, this atrophy results from myocyte shrinkage and lipofuscin accumulation (“brown atrophy”). It reflects long-term catabolic states and diminished cardiac workload.

16. Brain Hemorrhage (Pontine / Duret Hemorrhage)

• Gross Morphology

  Small, linear or blotchy hemorrhages in the pons; soft, edematous tissue; may cause brainstem compression and midline shift.

• Pathology

  Caused by chronic hypertension or herniation (uncal), leading to tearing of perforating arteries. Rapid onset leads to coma, often fatal.

18. Hyalinosis of the Spleen (“Sugar Iced Spleen”)

• Gross Morphology

  Hard, white-tan plaques on the splenic capsule; looks like icing or porcelain.

• Pathology

  Due to recurrent peritonitis (often in cirrhosis). Chronic inflammation causes fibrosis and hyaline deposition. Benign, found at autopsy.

19. Glioblastoma (GBM)

• Gross Morphology

  Large, variegated brain tumor with necrosis, hemorrhage, cysts; often crosses midline (“butterfly”).

• Pathology

  Grade IV astrocytoma. Highly malignant with pseudopalisading necrosis, vascular proliferation, rapid growth, and poor prognosis.

25. Chronic Aneurysm of the Heart

• Gross Morphology

  Thin-walled outpouching of the left ventricle; wall is fibrotic, pale, and non-contractile; often contains mural thrombus.

• Pathology

  Late complication of transmural myocardial infarction. Scarred wall bulges with systole, which reduces cardiac output and increases thromboembolic risk.

26. Chronic Aneurysm of the Aorta with Thrombosis

• Gross Morphology

  Large, fusiform dilatation of the abdominal aorta, often >5 cm, with mural thrombus inside.

• Pathology

  Due to atherosclerosis weakening the wall. Most common infrarenal. Risk of rupture increases with size (>5–6 cm).

28. Bacterial Endocarditis

• Gross Morphology

  Vegetations on valve cusps (usually mitral or aortic), red-yellow, friable, often destroying tissue; may extend to chordae or myocardium.

• Pathology

  Infection of the endocardium (often by Staphylococcus aureus or Streptococcus viridans). May cause emboli, abscess, or valve insufficiency.

29. Cirrhosis with Ruptured Esophageal Varices

• Gross Morphology

  Nodular liver (macronodular if >3 mm); dilated, dark blue veins in lower esophagus (varices), may show rupture/bleeding.

• Pathology

  Cirrhosis (e.g., from hepatitis or alcohol) leads to portal hypertension, which causes dilation of submucosal esophageal veins, prone to massive hemorrhage.

32. Secondary Pulmonary Tuberculosis – Tuberculoma / Miliary TB

• Gross Morphology

  Multiple small, tan-white nodules (2–4 mm), scattered throughout the lung (miliary pattern).

• Pathology

  Caused by Mycobacterium tuberculosis. Reactivation or poor immune response leads to widespread granulomatous inflammation with caseous necrosis.

33. Carcinoma of the Urinary Bladder

• Gross Morphology

  Flat or papillary tumors, often multiple; soft, white-pink fronds or thickened mucosa.

• Pathology

  Mostly urothelial carcinoma. Common in smokers; presents with painless hematuria. Can be superficial or muscle-invasive, often recurrent.

36. Hydronephrosis with Calculosis

• Gross Morphology

  Dilated renal pelvis and calyces, cortical thinning; stone (calculus) visible in ureter or pelvis.

• Pathology

  Obstruction (often from a ureteric stone) leads to urine backflow, causing pressure atrophy of the kidney. May lead to infection and loss of function if prolonged.