CARDIOVASCULAR PATHOLOGIES | CORRECT QUESTIONS
AND ANSWERS ~ CHAMBERLAIN UNIVERSITY.
NR507 Midterm Study Guide – Week 2: Hematologic & Cardiovascular
Pathologies
Detailed summary based on McCance S Huether’s Pathophysiology (9th ed.)
HEMATOLOGIC PATHOLOGIES
1. Overview of Red Blood Cell Production
- Erythropoiesis occurs in bone marrow under stimulation by erythropoietin (EPO)
produced by the kidneys in response to hypoxia.
- Requires iron, vitamin B12, folate, and functional bone marrow.
- Mature RBCs lack a nucleus; lifespan ≈ 120 days; removed by macrophages in spleen and
liver.
2. Types of Anemia (based on MCV)
Microcytic (MCV <80 fL)
- Mechanism: Impaired hemoglobin synthesis due to iron deficiency, thalassemia, or chronic
disease.
- Pathophysiology: Inadequate iron → decreased heme production → small, pale
(hypochromic) RBCs.
- Labs: ↓Hgb, ↓Hct, ↓MCV, ↓serum ferritin, ↓serum iron, ↑TIBC, ↓transferrin saturation.
- Risk factors: Poor diet, chronic bleeding (GI, menstruation), pregnancy.
- Treatment: Iron replacement (oral/IV), treat cause of bleeding.
Macrocytic (MCV >100 fL)
- Mechanism: Impaired DNA synthesis from vitamin B12 or folate deficiency → enlarged,
fragile RBCs.
- Pathophysiology: Nucleus maturation delayed relative to cytoplasm.
- Causes: B12 deficiency (pernicious anemia, gastric bypass, malabsorption) or folate
deficiency (malnutrition, alcoholism, pregnancy).
- Labs: ↑MCV, hypersegmented neutrophils; ↓B12 or ↓folate.
- Treatment: Vitamin replacement (IM B12 or oral folate).
Normocytic (MCV 80–100 fL)
, - Mechanism: Decreased RBC production or increased destruction.
- Causes: Acute blood loss, hemolytic anemia, anemia of chronic disease (ACD).
- Labs: Normal MCV; low reticulocyte count if production issue.
- Treatment: Manage underlying cause; EPO-stimulating agents in CKD.