Pathophysiology · MU Sofia

93. Acute and chronic posthemorrhagic anemia.

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Topic 93 of 168 in the MU Sofia syllabus for Pathophysiology (Medicine, Year 3). The free AceMed note covers it in 1 section, about 253 words (2 min of reading), with 15 flashcards.

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  1. Acute and chronic posthemorrhagic anemia.

Acute and chronic posthemorrhagic anemia.

Anemia resulting from significant blood loss, leading to reduced red blood cell mass and decreased oxygen- carrying capacity.

Classification

I. Acute posthemorrhagic anemia

Etiology

  • Trauma (accidents, injuries).
  • Surgery-related hemorrhage.
  • Gastrointestinal bleeding (e.g., peptic ulcer rupture, variceal bleeding).
  • Ruptured ectopic pregnancy or aneurysm.

Pathogenesis

  1. Immediate blood loss → decreased blood volume → hypovolemia → reduced venous return → decreased cardiac output → hypovolemic shock.
  2. Hemodilution phase (hours after bleeding):
  • Interstitial fluid shifts into circulation to restore volume → hematocrit and hemoglobin decrease.
  1. 3 Erythropoietin stimulation → bone marrow increases RBC production.

Compensatory mechanisms

  • Vasoconstriction (SNS activation) → redirects blood to vital organs.
  • Tachycardia, increased cardiac output.
  • Increased respiratory rate → improves oxygen delivery.
  • Reticulocytosis (after a few days) as marrow responds.

Clinical manifestations

  • Signs of hypovolemia: cold, clammy skin; hypotension; tachycardia; weak pulse.
  • Pallor.
  • Oliguria (low urine output).
  • Dizziness, syncope.
  • If severe: shock, multi- organ failure.

II. Chronic posthemorrhagic anemia

Etiology

  • Gastrointestinal blood loss (most common):
  • Peptic ulcer, colon cancer, hemorrhoids.
  • Heavy menstrual bleeding (menorrhagia).
  • Repeated epistaxis (nosebleeds).
  • Parasitic infestations (hookworm).

Pathogenesis

  1. Repeated small-volume blood loss → gradual iron depletion.
  2. Iron stores exhausted → impaired hemoglobin synthesis → iron deficiency anemia (microcytic, hypochromic).
  3. Slow progression allows better circulatory adaptation.

Compensatory mechanisms

  • Increased erythropoietin → marrow stimulation.
  • Increased iron absorption from gut.
  • Chronic blood redistribution to vital organs.

Clinical manifestations

  • Fatigue, weakness.
  • Pallor.
  • Exertional dyspnea.
  • Pica (craving non- food substances like clay or ice).
  • Koilonychia (spoon-shaped nails), angular cheilitis, glossitis (classic iron deficiency signs).
  • May have occult GI bleeding signs (positive fecal occult blood )..

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