Histopathological changes in common diseases

Histopathological changes in common diseases

Histopathological changes in common diseases

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Cellular Adaptations & Injury - Cells Under Stress

  • Adaptation: Reversible changes in cell size, number, phenotype, or function in response to stress.

    • Atrophy: ↓ cell size/number (e.g., disuse atrophy).
    • Hypertrophy: ↑ cell size (e.g., cardiac hypertrophy).
    • Hyperplasia: ↑ cell number (e.g., benign prostatic hyperplasia).
    • Metaplasia: One adult cell type replaced by another (e.g., Barrett esophagus).
  • Cell Injury: Occurs when stress exceeds adaptive capacity.

    • Reversible: Cellular swelling, membrane blebbing, ↓ ATP production.
    • Irreversible: Severe membrane/mitochondrial damage, Ca²⁺ influx, lysosomal rupture → necrosis/apoptosis.

⭐ The hallmark of irreversible cell injury is massive calcium influx and the mitochondrial permeability transition, which prevents ATP synthesis and releases pro-apoptotic proteins.

Inflammation & Repair - The Body's Repair Crew

  • Cardinal Signs: Rubor (redness), Calor (heat), Tumor (swelling), Dolor (pain), Functio laesa (loss of function).
  • Acute: Rapid onset, short duration. Key cell: Neutrophil.
  • Chronic: Prolonged duration. Key cells: Monocytes/Macrophages, Lymphocytes.
  • Repair Outcomes:
    • Regeneration: Replacement by native tissue; ideal outcome.
    • Scarring (Fibrosis): Collagen deposition when severe damage precludes regeneration.

⭐ Granulation tissue is the hallmark of healing, featuring fibroblasts (depositing type III collagen) and new capillaries. This is later remodeled to a scar with stronger type I collagen.

Wound Healing: Granulation Tissue Formation and Remodeling

Neoplasia & Dysplasia - Good Cells Gone Bad

  • Dysplasia: Disordered, non-neoplastic growth; a prelude to cancer. Potentially reversible.
    • Loss of cell uniformity (pleomorphism) & architectural orientation.
    • Increased nuclear-to-cytoplasmic (N:C) ratio (normal 1:41:1).
    • Nuclear hyperchromasia (darker staining) and clumped chromatin.
  • Neoplasia: Abnormal, autonomous new growth (tumor).
    • Benign: Well-differentiated, localized, does not metastasize.
    • Malignant: Invades, destroys, and metastasizes. Shows poor differentiation (anaplasia).

Anaplasia is the hallmark of malignancy. It signifies a complete lack of differentiation, with bizarre, pleomorphic cells and atypical, giant tumor cells.

Cervical Intraepithelial Neoplasia (CIN) Histology

Vascular & Organ Pathology - System-Specific Snapshots

  • Heart (Myocardial Infarction): Progression from coagulative necrosis and wavy fibers (4-24h) to neutrophil infiltration (1-3d), followed by macrophage-led debris removal and granulation tissue (3-14d).
  • Kidney (Diabetic Nephropathy): Kimmelstiel-Wilson lesions (nodular glomerulosclerosis), hyaline arteriolosclerosis (especially efferent arteriole), and thickened glomerular basement membranes. Kimmelstiel-Wilson Lesions in Diabetic Nephropathy
  • Liver (Cirrhosis): Diffuse process with bridging fibrous septa, regenerative parenchymal nodules, and disruption of the entire liver architecture.
  • Lung (ARDS): Diffuse alveolar damage (DAD) is the hallmark, showing hyaline membrane formation lining alveolar ducts and spaces.

⭐ In ARDS, the characteristic hyaline membranes are composed of fibrin-rich edema fluid mixed with the cytoplasmic and lipid remnants of necrotic epithelial cells.

High‑Yield Points - ⚡ Biggest Takeaways

  • Myocardial infarction shows coagulative necrosis, then neutrophil infiltration, followed by macrophages.
  • Alzheimer's disease: Extracellular amyloid-β plaques and intracellular neurofibrillary tangles (hyperphosphorylated tau).
  • Parkinson's disease: Lewy bodies (eosinophilic inclusions) in the substantia nigra.
  • Cirrhosis: Regenerative hepatocyte nodules separated by bands of bridging fibrosis.
  • Barrett's esophagus: Intestinal metaplasia of esophageal mucosa with goblet cells.
  • Celiac disease: Villous atrophy, crypt hyperplasia, and increased intraepithelial lymphocytes.
  • Koilocytes are pathognomonic for HPV, showing perinuclear halos.

Practice Questions: Histopathological changes in common diseases

Test your understanding with these related questions

A 78-year-old man dies suddenly from complications of acute kidney failure. An autopsy is performed and microscopic evaluation of the kidneys shows pale, swollen cells in the proximal convoluted tubules. Microscopic evaluation of the liver shows similar findings. Which of the following is the most likely underlying mechanism of these findings?

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Flashcards: Histopathological changes in common diseases

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In lymph nodes, _____ follicles are dense and dormant

TAP TO REVEAL ANSWER

In lymph nodes, _____ follicles are dense and dormant

primary

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