WEEK 2 Edapt:
Anemia
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NR 507 Week 2 Study Guide Anemia
Basics of Anemia: A normal hemoglobin level is 12.0–17.0 g/dL (HGB mild 10-12,
Moderate 6-10, Severe below 6)
● Definition: Decreased red blood cells (RBCs) or hemoglobin → reduced oxygen
delivery to tissues.
● Symptoms: Pallor, Fatigue, shortness of breath, increased HR/RR, decreased
BP, Cold intolerance. (Module says); fatigue, pallor, muscle pain, increased
respiratory rate, exertional dyspnea, dizziness, and fainting.
Causes:
Blood Loss (Acute or Chronic): -Menstruation -Trauma -Gastrointestinal lesions
Decreased/Impaired RBC Production:
● Genetic defects: Thalassemia syndrome
● Nutritional deficiencies: B12, folate, iron
● Disease-related: Renal failure, acute leukemia, endocrine disorders
Increased RBC Destruction (Hemolysis):
● Genetic disorders:
o Red cell membrane disorders (e.g., spherocytosis)
o Enzyme deficiencies (e.g., pyruvate kinase deficiency)
o Hemoglobin abnormalities (e.g., thalassemia, sickle cell disease)
● Acquired conditions:
o Antibody-mediated destruction (e.g., Rh disease, transfusion reactions,
autoimmune disorders)
o Infections (e.g., malaria)
o Cardiac traumatic hemolysis (e.g., defective cardiac valves)
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Microcytic Anemia
● Key Features: Small RBCs (low mean corpuscular volume, MCV).
● Causes:
o Iron deficiency anemia: Most common, due to poor diet, chronic
bleeding, or poor iron absorption.
o Thalassemia: Genetic disorders affecting hemoglobin
production.
o Chronic diseases: Impact iron usage.
● Pathophysiology: Decreased hemoglobin synthesis due to iron, copper,
or vitamin B-12 deficiencies.
Macrocytic Anemia:
● Key Features: Large RBCs (MCV > 100 fL).
● Causes:
o Vitamin B-12 or Folate deficiency: Requires intrinsic factor for
absorption; deficiency may cause neurological symptoms.
o Folate deficiency: Needed for DNA synthesis during RBC
production.
● Pathophysiology: Impaired DNA synthesis → enlarged, immature RBC
precursors (megaloblasts).
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Normocytic Anemia
● Key Features: Normal-sized RBCs (MCV 80-99 fL).
● Causes:
o Chronic diseases: Cancer, Inflammation, kidney disease-kidney failure,
hereditary spherocytosis, G6PD deficiency, and paroxysmal nocturnal
hemoglobinuria, disrupted iron metabolism.
o Hemolysis or blood loss: High reticulocyte count indicates active
RBC production.
o Bone marrow disorders: Impaired RBC production.
Hemoglobinopathies
● Sickle Cell Disease:
o Mutation → hemoglobin S (HbS) → sickled RBCs.
o Pathophysiology: Sickled cells break down quickly, leading to anemia.
o Complications: Splenic sequestration, vaso-occlusive crises (pain
and tissue ischemia), chronic anemia.
Edapt.ai Module Questions and images part 1 Anemia
Downloaded by Benjamin Luca ()
Anemia
, lOMoARcPSD|516 483 32
NR 507 Week 2 Study Guide Anemia
Basics of Anemia: A normal hemoglobin level is 12.0–17.0 g/dL (HGB mild 10-12,
Moderate 6-10, Severe below 6)
● Definition: Decreased red blood cells (RBCs) or hemoglobin → reduced oxygen
delivery to tissues.
● Symptoms: Pallor, Fatigue, shortness of breath, increased HR/RR, decreased
BP, Cold intolerance. (Module says); fatigue, pallor, muscle pain, increased
respiratory rate, exertional dyspnea, dizziness, and fainting.
Causes:
Blood Loss (Acute or Chronic): -Menstruation -Trauma -Gastrointestinal lesions
Decreased/Impaired RBC Production:
● Genetic defects: Thalassemia syndrome
● Nutritional deficiencies: B12, folate, iron
● Disease-related: Renal failure, acute leukemia, endocrine disorders
Increased RBC Destruction (Hemolysis):
● Genetic disorders:
o Red cell membrane disorders (e.g., spherocytosis)
o Enzyme deficiencies (e.g., pyruvate kinase deficiency)
o Hemoglobin abnormalities (e.g., thalassemia, sickle cell disease)
● Acquired conditions:
o Antibody-mediated destruction (e.g., Rh disease, transfusion reactions,
autoimmune disorders)
o Infections (e.g., malaria)
o Cardiac traumatic hemolysis (e.g., defective cardiac valves)
Downloaded by Benjamin Luca ()
, lOMoARcPSD|516 483 32
Microcytic Anemia
● Key Features: Small RBCs (low mean corpuscular volume, MCV).
● Causes:
o Iron deficiency anemia: Most common, due to poor diet, chronic
bleeding, or poor iron absorption.
o Thalassemia: Genetic disorders affecting hemoglobin
production.
o Chronic diseases: Impact iron usage.
● Pathophysiology: Decreased hemoglobin synthesis due to iron, copper,
or vitamin B-12 deficiencies.
Macrocytic Anemia:
● Key Features: Large RBCs (MCV > 100 fL).
● Causes:
o Vitamin B-12 or Folate deficiency: Requires intrinsic factor for
absorption; deficiency may cause neurological symptoms.
o Folate deficiency: Needed for DNA synthesis during RBC
production.
● Pathophysiology: Impaired DNA synthesis → enlarged, immature RBC
precursors (megaloblasts).
Downloaded by Benjamin Luca ()
, lOMoARcPSD|516 483 32
Normocytic Anemia
● Key Features: Normal-sized RBCs (MCV 80-99 fL).
● Causes:
o Chronic diseases: Cancer, Inflammation, kidney disease-kidney failure,
hereditary spherocytosis, G6PD deficiency, and paroxysmal nocturnal
hemoglobinuria, disrupted iron metabolism.
o Hemolysis or blood loss: High reticulocyte count indicates active
RBC production.
o Bone marrow disorders: Impaired RBC production.
Hemoglobinopathies
● Sickle Cell Disease:
o Mutation → hemoglobin S (HbS) → sickled RBCs.
o Pathophysiology: Sickled cells break down quickly, leading to anemia.
o Complications: Splenic sequestration, vaso-occlusive crises (pain
and tissue ischemia), chronic anemia.
Edapt.ai Module Questions and images part 1 Anemia
Downloaded by Benjamin Luca ()
