Pathophysiology · MU Sofia

114. Ischemia and stasis - classification, etiology, pathogenesis, clinical manifestations.

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Topic 114 of 168 in the MU Sofia syllabus for Pathophysiology (Medicine, Year 3). The free AceMed note covers it in 1 section, about 251 words (2 min of reading), with 15 flashcards.

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  1. Ischemia and stasis – classification, etiology, pathogenesis, and clinical manifestations.

Ischemia and stasis – classification, etiology, pathogenesis, and clinical manifestations.

I. Ischemia

Ischemia is a local reduction or complete interruption of blood supply to a tissue, resulting in inadequate delivery of oxygen and nutrients and impaired removal of metabolic waste.

Classification

Etiology

  • Arterial thrombosis or embolism.
  • Severe vasospasm (e.g., Raynaud phenomenon).
  • External compression (e.g., tumor, tight bandage).
  • Atherosclerotic stenosis.
  • Mechanical factors (volvulus or hernia in bowel ischemia).

Pathogenesis

  1. Decreased blood supply → reduced oxygen (hypoxia) and nutrient delivery.
  2. Impaired ATP production → shift to anaerobic glycolysis → lactic acidosis.
  3. Ion pump failure → cell swelling, calcium influx → activation of degradative enzymes.
  4. If prolonged → irreversible cell injury → infarction.

Clinical manifestations

  • Pain (sharp and severe in acute ischemia).
  • Pallor (due to lack of blood).
  • Paresthesias (tingling, numbness).
  • Pulselessness.
  • Poikilothermia (coldness).
  • Paralysis (in severe cases).

Classic "6 Ps" of acute limb ischemia:

II. Stasis

Stasis refers to slowing or stagnation of blood flow in vessels, usually in veins and capillaries.

Classification

Etiology

  • Prolonged immobility (e.g., bed rest, long flights → DVT risk).
  • Chronic heart failure → venous congestion.
  • Varicose veins.
  • External compression of veins (casts, tight dressings).

Pathogenesis

  1. Reduced or stagnant blood flow → increased hydrostatic pressure.
  2. Fluid transudation into interstitium → edema.
  3. Decreased oxygen delivery and impaired removal of metabolic waste → local hypoxia.
  4. Endothelial damage → increased risk of thrombosis (part of Virchow’s triad).

Clinical manifestations

  • Edema (especially in dependent areas, e.g., ankles).
  • Cyanosis (bluish discoloration due to deoxygenated blood pooling).
  • Heavy or aching sensation in legs.
  • Increased risk of skin ulcers and infections (stasis dermatitis).
  • Predisposition to thrombosis.

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