Vascular Diseases in Specific Organs

Brain: Cerebrovascular Disease - CNS Vascular Crises

• Acute neurological deficit from vascular cause (stroke, TIA).
• Types:
  • Ischemic Stroke (~85%): Thrombotic, embolic, lacunar (small vessel disease).
    • Patho: Ischemic core & surrounding penumbra.
  • Hemorrhagic Stroke (~15%):
    • Intracerebral (ICH): e.g., hypertensive bleed (Charcot-Bouchard microaneurysms).
    • Subarachnoid (SAH): e.g., ruptured berry aneurysm ("worst headache").
  • Transient Ischemic Attack (TIA): Symptoms resolve < 24h (typically < 1h), no acute infarction.
• Key risk factors: Hypertension, Diabetes Mellitus, Smoking, Atrial Fibrillation.
• 📌 Mnemonic: FAST (Face, Arms, Speech, Time) for stroke recognition.

⭐ Hypertensive hemorrhages most commonly affect basal ganglia (putamen), pons, thalamus, and cerebellum due to rupture of Charcot-Bouchard microaneurysms.

Kidneys: Renal Vascular Disease - Kidney Vessel Victims

• Hypertensive Nephrosclerosis:
  • Benign: Hyaline arteriolosclerosis (afferent arterioles), fibroelastic hyperplasia (interlobular arteries). Leads to fine, leathery granular cortical surface.
  • Malignant: Fibrinoid necrosis of arterioles, hyperplastic arteriolosclerosis ("onion-skinning"). Petechial hemorrhages on surface ("flea-bitten kidney").
• Renal Artery Stenosis (RAS):
  • Causes: Atherosclerosis (elderly males, ostial); Fibromuscular Dysplasia (FMD) (younger females, "string of beads" appearance).
  • Results in: Renovascular hypertension (↑ renin), ischemic kidney atrophy.
• Thrombotic Microangiopathies (TMAs): e.g., HUS, TTP. Characterized by fibrin thrombi in glomeruli and small vessels.
• Renal Infarcts: Typically wedge-shaped, pale cortical necrosis; usually embolic origin.

⭐ In malignant hypertension, hyperplastic arteriolosclerosis manifests as concentric, laminated thickening of arteriolar walls, often described as "onion-skin" lesions.

Lungs: Pulmonary Vascular Disease - Lung Vessel Logjams

• Pulmonary Embolism (PE): Obstruction of pulmonary arteries.
  • Source: >95% from DVT (Deep Vein Thrombosis).
  • Risk Factors: Virchow's triad (stasis, hypercoagulability, endothelial injury). 📌 Mnemonic: SHE.
  • Types: Saddle (bifurcation), lobar, segmental.
  • Effects: ↑Pulmonary vascular resistance, V/Q mismatch, right heart strain. Infarction uncommon (dual supply).
  • Diagnosis: CT Pulmonary Angiogram (CTPA).
• Pulmonary Hypertension (PHTN): Mean PAP > 20 mmHg at rest.
  • Pathogenesis: Endothelial dysfunction, vasoconstriction, vascular remodeling.
  • Consequences: RV hypertrophy → Cor pulmonale.

  ⭐ Plexiform lesions (tufts of capillary formations) are pathognomonic for severe, long-standing pulmonary hypertension, especially Group 1 PAH.

High‑Yield Points - ⚡ Biggest Takeaways

• Brain: Charcot-Bouchard microaneurysms (hypertension) → intracerebral hemorrhage; Berry aneurysms → subarachnoid hemorrhage.
• Kidney: Hyaline arteriolosclerosis (benign nephrosclerosis); hyperplastic "onion-skin" arteriolosclerosis (malignant hypertension).
• Lungs: Pulmonary hypertension shows plexiform lesions; pulmonary emboli typically from DVT.
• Liver: Budd-Chiari syndrome from hepatic vein thrombosis; portal hypertension causes esophageal varices.
• Retina: Hypertensive retinopathy: AV nicking, cotton-wool spots. Diabetic retinopathy: microaneurysms, neovascularization.
• Spleen: Gamna-Gandy bodies indicate portal hypertension and congestive splenomegaly.