NR 507 WEEK 2 STUDY GUIDE EDAPT ANEMIA
ADVANCED PATHOPHYSIOLOGY
(CHAMBERLAIN UNIVERSITY)
NR 507 WEEK 2 STUDY GUIDE
EDAPT ANEMIA ADVANCED
PATHOPHYSIOLOGY
NR 507 WEEK 2 STUDY GUIDE EDAPT ANEMIA
,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)
,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).
, 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
ADVANCED PATHOPHYSIOLOGY
(CHAMBERLAIN UNIVERSITY)
NR 507 WEEK 2 STUDY GUIDE
EDAPT ANEMIA ADVANCED
PATHOPHYSIOLOGY
NR 507 WEEK 2 STUDY GUIDE EDAPT ANEMIA
,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)
,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).
, 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
