92. Anemias - definition, etiology, classification, pathomorphology, pathogenesis, compensatory mechanisms, clinical manifestations.

Anemias - definition, etiology, classification, pathomorphology, pathogenesis, compensatory mechanisms, and clinical manifestations

Anemia is a condition characterized by decreased total red blood cell (RBC) mass, resulting in reduced hemoglobin concentration, hematocrit, and oxygen-carrying capacity of blood.

• WHO definition:
• Hb <13 g/dL in men.
• Hb <12 g/dL in women.

Etiology

1. 1 Decreased RBC production

• Nutritional deficiencies:
• Iron deficiency.
• Vitamin B12 or folate deficiency.
• Bone marrow failure:
• Aplastic anemia.
• Myelodysplastic syndromes.
• Chronic diseases:
• Chronic infections, chronic kidney disease (↓ erythropoietin).

1. 2 Increased RBC destruction (hemolysis)

• Intrinsic defects:
• Membrane defects (hereditary spherocytosis).
• Enzyme defects (G6PD deficiency).
• Hemoglobinopathies (sickle cell anemia, thalassemia).
• Extrinsic factors:
• Autoimmune hemolytic anemia.
• Mechanical trauma (prosthetic valves).

1. 3 Blood loss

• Acute hemorrhage (trauma, surgery).
• Chronic bleeding (GI ulcers, heavy menstruation).

Classification

By morphology (MCV)

By pathogenesis

Pathomorphology

• Bone marrow
• Hypercellularity in hemolytic anemias (erythroid hyperplasia).
• Hypocellularity in aplastic anemia.
• Megaloblastic changes in B12/folate deficiency (large abnormal erythroid precursors).
• Peripheral blood smear
• Microcytosis, hypochromia (iron deficiency).
• Macroovalocytes, hypersegmented neutrophils (megaloblastic anemia).
• Spherocytes (hereditary spherocytosis).
• Schistocytes (fragmented cells, microangiopathic hemolytic anemia).
• Other organs
• Extramedullary hematopoiesis (liver, spleen) in severe chronic anemias.
• Iron overload (secondary hemosiderosis) in chronic hemolysis or multiple transfusions.
• Pathogenesis

1. Reduced oxygen-carrying capacity → tissue hypoxia.
2. Activation of compensatory mechanisms (see below).
3. Depending on cause: iron depletion, ineffective erythropoiesis, or increased RBC destruction.

Compensatory mechanisms

• Increased cardiac output → tachycardia, palpitations.
• Increased erythropoietin production → marrow hyperplasia.
• Redistribution of blood flow → preferential perfusion of vital organs.
• Increased 2,3-BPG in RBCs → enhanced oxygen release to tissues.

Clinical manifestation s

General (due to hypoxia)

• Fatigue, weakness.
• Dyspnea on exertion.
• Dizziness, headache.
• Palpitations.

Skin and mucous membranes

• Pallor (skin, conjunctivae, mucosa).

Cardiovascular

• Tachycardia.
• Flow murmurs.
• Possible heart failure in severe cases.

Specific signs (by type)

• Iron deficiency anemia: koilonychia (spoon nails), glossitis, angular cheilitis, pica.
• Megaloblastic anemia: smooth red tongue, neurological symptoms (paresthesias, ataxia) in B12 deficiency.
• Hemolytic anemia: jaundice, dark urine, splenomegaly.