NR 283 Pathophysiology Exam 3 Study
Guide Chamberlain University | 2025-2026
Academic Year
📋 How To Use This Guide
This guide is compiled from verified 2025/2026 review materials . Focus on
understanding the pathophysiology (mechanism) behind each disease—this is how
Exam 3 questions are typically structured. Each section includes high-yield concepts
followed by practice questions in the Chamberlain format.
UNIT 1: HEMATOLOGIC DISORDERS
Most heavily tested topic on Exam 3
Red Blood Cell Physiology (Foundation Knowledge)
Concept Key Points
RBC Function Tissue oxygenation via hemoglobin; lifespan = 120 days
Erythropoiesis Production of RBCs in bone marrow
Erythropoietin Hormone produced by kidneys that stimulates RBC production
Hemoglobin Oxygen-carrying protein; each HGB carries 4 O₂ molecules
Anemia: Types & Differentiating Features
,Pernicious Anemia
• Pathophysiology: Autoimmune destruction of gastric parietal cells → lack of
intrinsic factor → cannot absorb Vitamin B12
• Etiology: Gastric surgery, chronic gastritis, genetic autoimmune tendency
• Clinical Manifestations: Weakness, fatigue, paresthesia of
feet/hands (neurologic symptoms distinguish it from other anemias)
• Rationale: B12 is essential for myelin synthesis—neurologic symptoms occur
because of spinal cord demyelination
Folate Deficiency Anemia
• Pathophysiology: Impaired DNA synthesis due to folate deficiency
• Etiology: Alcoholism, malnutrition, pregnancy
• Clinical Manifestations: Cheilosis (fissures at mouth corners), stomatitis, painful
tongue ulcers
• Key Difference from Pernicious: NO neurologic symptoms; NO intrinsic factor
involvement
Iron Deficiency Anemia (Most common anemia)
• Pathophysiology: Insufficient iron → decreased heme synthesis → microcytic
(small), hypochromic (pale) RBCs
• Three Stages:
1. Iron stores depleted (normal RBCs)
2. Iron-deficient RBCs produced (low HGB)
3. HGB-deficient cells enter circulation
• Clinical Manifestations: Fatigue, weakness, SOB; Koilonychias (spoon-shaped,
brittle nails); sore tongue
Sideroblastic Anemia
• Pathophysiology: Problem with heme synthesis → iron present but not utilized
→ iron accumulates in RBC mitochondria (ringed sideroblasts)
• Types: Acquired (idiopathic), Hereditary (males), Reversible (alcohol-induced)
• Complication: Hemosiderosis (iron overload affecting liver, heart)
Sickle Cell Disease
• Pathophysiology: Genetic mutation (autosomal recessive) → abnormal HGB S →
RBCs deform into sickle shape under low O₂ conditions
, • Trigger for Crisis: Hypoxia, dehydration, infection, fever, stress
• Vaso-occlusive Crisis: Sickled cells clog vessels → infarction, pain, organ
damage
• Acute Chest Syndrome: Medical emergency—pulmonary vessel occlusion →
hypoxia → more sickling (positive feedback loop)
Polycythemia
Polycythemia Vera (Primary Absolute Polycythemia)
• Pathophysiology: Genetic alteration of erythrocyte receptor → receptor doesn't
sense adequate RBC count → continuous overproduction of RBCs
• Etiology: Unknown (acquired genetic mutation); JAK2 mutation in most cases
• Pathophysiologic Consequence: Increased blood viscosity (hyperviscosity)—
more cells, same plasma volume
• Clinical Manifestations: Headache, dizziness, hypertension, pruritus after
bathing, ruddy complexion, thrombosis risk
Secondary Polycythemia
• Pathophysiology: Appropriate physiological response to chronic hypoxemia →
increased erythropoietin release
• Etiology: COPD, high altitude, chronic lung disease, cyanotic heart disease
• Example: COPD patient with hypoxemia → erythropoietin ↑ → polycythemia
📝 Exam 3 Practice Questions: Hematology
Question 1
A patient with chronic kidney disease develops anemia. Which mechanism explains this
finding?
• A) Iron deficiency from poor intake
• B) Decreased erythropoietin production
• C) Increased RBC destruction
• D) Vitamin B12 deficiency
Correct Answer: B) Decreased erythropoietin production
Rationale: Erythropoietin is produced by the kidneys. In chronic kidney disease, damaged
kidneys produce insufficient erythropoietin, leading to decreased RBC production in bone
marrow.
Guide Chamberlain University | 2025-2026
Academic Year
📋 How To Use This Guide
This guide is compiled from verified 2025/2026 review materials . Focus on
understanding the pathophysiology (mechanism) behind each disease—this is how
Exam 3 questions are typically structured. Each section includes high-yield concepts
followed by practice questions in the Chamberlain format.
UNIT 1: HEMATOLOGIC DISORDERS
Most heavily tested topic on Exam 3
Red Blood Cell Physiology (Foundation Knowledge)
Concept Key Points
RBC Function Tissue oxygenation via hemoglobin; lifespan = 120 days
Erythropoiesis Production of RBCs in bone marrow
Erythropoietin Hormone produced by kidneys that stimulates RBC production
Hemoglobin Oxygen-carrying protein; each HGB carries 4 O₂ molecules
Anemia: Types & Differentiating Features
,Pernicious Anemia
• Pathophysiology: Autoimmune destruction of gastric parietal cells → lack of
intrinsic factor → cannot absorb Vitamin B12
• Etiology: Gastric surgery, chronic gastritis, genetic autoimmune tendency
• Clinical Manifestations: Weakness, fatigue, paresthesia of
feet/hands (neurologic symptoms distinguish it from other anemias)
• Rationale: B12 is essential for myelin synthesis—neurologic symptoms occur
because of spinal cord demyelination
Folate Deficiency Anemia
• Pathophysiology: Impaired DNA synthesis due to folate deficiency
• Etiology: Alcoholism, malnutrition, pregnancy
• Clinical Manifestations: Cheilosis (fissures at mouth corners), stomatitis, painful
tongue ulcers
• Key Difference from Pernicious: NO neurologic symptoms; NO intrinsic factor
involvement
Iron Deficiency Anemia (Most common anemia)
• Pathophysiology: Insufficient iron → decreased heme synthesis → microcytic
(small), hypochromic (pale) RBCs
• Three Stages:
1. Iron stores depleted (normal RBCs)
2. Iron-deficient RBCs produced (low HGB)
3. HGB-deficient cells enter circulation
• Clinical Manifestations: Fatigue, weakness, SOB; Koilonychias (spoon-shaped,
brittle nails); sore tongue
Sideroblastic Anemia
• Pathophysiology: Problem with heme synthesis → iron present but not utilized
→ iron accumulates in RBC mitochondria (ringed sideroblasts)
• Types: Acquired (idiopathic), Hereditary (males), Reversible (alcohol-induced)
• Complication: Hemosiderosis (iron overload affecting liver, heart)
Sickle Cell Disease
• Pathophysiology: Genetic mutation (autosomal recessive) → abnormal HGB S →
RBCs deform into sickle shape under low O₂ conditions
, • Trigger for Crisis: Hypoxia, dehydration, infection, fever, stress
• Vaso-occlusive Crisis: Sickled cells clog vessels → infarction, pain, organ
damage
• Acute Chest Syndrome: Medical emergency—pulmonary vessel occlusion →
hypoxia → more sickling (positive feedback loop)
Polycythemia
Polycythemia Vera (Primary Absolute Polycythemia)
• Pathophysiology: Genetic alteration of erythrocyte receptor → receptor doesn't
sense adequate RBC count → continuous overproduction of RBCs
• Etiology: Unknown (acquired genetic mutation); JAK2 mutation in most cases
• Pathophysiologic Consequence: Increased blood viscosity (hyperviscosity)—
more cells, same plasma volume
• Clinical Manifestations: Headache, dizziness, hypertension, pruritus after
bathing, ruddy complexion, thrombosis risk
Secondary Polycythemia
• Pathophysiology: Appropriate physiological response to chronic hypoxemia →
increased erythropoietin release
• Etiology: COPD, high altitude, chronic lung disease, cyanotic heart disease
• Example: COPD patient with hypoxemia → erythropoietin ↑ → polycythemia
📝 Exam 3 Practice Questions: Hematology
Question 1
A patient with chronic kidney disease develops anemia. Which mechanism explains this
finding?
• A) Iron deficiency from poor intake
• B) Decreased erythropoietin production
• C) Increased RBC destruction
• D) Vitamin B12 deficiency
Correct Answer: B) Decreased erythropoietin production
Rationale: Erythropoietin is produced by the kidneys. In chronic kidney disease, damaged
kidneys produce insufficient erythropoietin, leading to decreased RBC production in bone
marrow.
