NURS 6501 Advanced
Pathophysiology (Walden
University) – Midterm & Final
2025, multiple versions,
verified, A+ graded.
Cellular & Systemic Foundations
1. Q: What is the primary difference between hypertrophy and hyperplasia?
A: Hypertrophy is an increase in cell size; hyperplasia is an increase in cell number.
2. Q: Describe the pathophysiologic mechanism of necrosis.
A: Unregulated cell death due to injury (e.g., ischemia, toxins), causing inflammation.
3. Q: How does apoptosis differ from necrosis?
A: Apoptosis is programmed, controlled cell death without inflammation.
4. Q: What role do free radicals play in cellular injury?
A: They cause oxidative stress, damaging lipids, proteins, and DNA.
5. Q: Define metaplasia and give one example.
A: Reversible replacement of one mature cell type by another (e.g., Barrett’s
esophagus).
Fluid, Electrolytes, & Acid-Base
6. Q: What causes third-spacing of fluid?
A: Fluid shifts from intravascular space into interstitial/compartments (e.g., burns, ascites).
7. Q: How does the body compensate for metabolic acidosis?
,A: Hyperventilation (respiratory alkalosis) to blow off CO2.
8. Q: Key sign of hyperkalemia on ECG?
A: Peaked T waves, widened QRS complex.
9. Q: Primary regulator of extracellular fluid osmolality?
A: Antidiuretic hormone (ADH).
10. Q: Effect of respiratory alkalosis on serum calcium?
A: Decreases ionized calcium, leading to potential neuromuscular excitability.
Neuro Pathophysiology
11. Q: What is excitotoxicity in stroke?
A: Excessive glutamate release causing neuronal calcium overload and death.
12. Q: Difference between ischemic and hemorrhagic stroke mechanisms?
A: Ischemic: blocked blood flow; Hemorrhagic: ruptured vessel.
13. Q: Pathophysiology of Alzheimer's disease hallmark findings?
A: Beta-amyloid plaques, neurofibrillary tangles (tau protein), cortical atrophy.
14. Q: Mechanism of multiple sclerosis?
A: Autoimmune demyelination of CNS neurons.
15. Q: What is autonomic dysreflexia?
A: Life-threatening sympathetic overresponse to stimulus below a spinal cord injury (T6 or
above).
Cardiovascular
16. Q: Explain afterload and one condition that increases it.
A: Resistance the heart must pump against; increased by hypertension.
17. Q: Pathophysiology of left-sided heart failure leading to pulmonary edema?
A: Left ventricle fails → increased left atrial pressure → increased pulmonary venous pressure →
fluid leaks into alveoli.
18. Q: What is the underlying mechanism of atherosclerosis?
A: Chronic endothelial injury, inflammation, lipid accumulation, plaque formation.
19. Q: Difference between stable and unstable angina?
A: Stable: predictable, relieved by rest; Unstable: unpredictable, occurs at rest, precursor to MI.
20. Q: How does ventricular remodeling occur post-MI?
A: Structural changes (dilation, hypertrophy, fibrosis) due to compensatory mechanisms.
Pulmonary
21. Q: Key pathophysiology of COPD (emphysema vs. chronic bronchitis)?
A: Emphysema: alveolar destruction; Chronic bronchitis: inflamed airways, excessive mucus.
,22. Q: What is V/Q mismatch?
A: Ventilation-perfusion inequality; low V/Q (shunt) or high V/Q (dead space).
23. Q: Mechanism of pulmonary hypertension in left heart failure?
A: Increased left atrial pressure → backward pressure → pulmonary venous hypertension.
24. Q: Pathophysiology of acute respiratory distress syndrome (ARDS)?
A: Diffuse alveolar damage, increased permeability, non-cardiogenic pulmonary edema.
25. Q: How does cystic fibrosis affect the lungs?
A: Defective CFTR protein → thick mucus → chronic infection and inflammation.
Renal & GU
26. Q: Difference between pre-renal, intra-renal, and post-renal acute kidney injury?
A: Pre-renal: hypoperfusion; Intra-renal: direct kidney damage; Post-renal: urinary tract
obstruction.
27. Q: Mechanism of nephrotic syndrome?
A: Glomerular damage → massive proteinuria, hypoalbuminemia, edema, hyperlipidemia.
28. Q: How does chronic kidney disease cause anemia?
A: Decreased erythropoietin production by kidneys.
29. Q: Pathophysiology of benign prostatic hyperplasia (BPH)?
A: Stromal/epithelial hyperplasia → urethral compression → obstructive symptoms.
30. Q: What is acute tubular necrosis (ATN)?
A: Ischemic or toxic injury to renal tubules, most common intra-renal AKI.
Endocrine
31. Q: Pathophysiological triad of diabetic ketoacidosis (DKA)?
A: Hyperglycemia, metabolic acidosis, ketonemia.
32. Q: Difference between type 1 and type 2 diabetes at cellular level?
A: Type 1: autoimmune beta-cell destruction; Type 2: insulin resistance and relative insulin
deficiency.
33. Q: Mechanism of Cushing's syndrome?
A: Chronic excess cortisol (endogenous or exogenous).
34. Q: What causes Graves' disease hyperthyroidism?
A: Autoantibodies (TSI) stimulate TSH receptor, causing overproduction of thyroid hormone.
, 35. Q: How does syndrome of inappropriate ADH (SIADH) cause hyponatremia?
A: Excessive ADH → water retention → dilutional hyponatremia.
Gastrointestinal
36. Q: Pathophysiology of portal hypertension in cirrhosis?
A: Scarring increases resistance in hepatic sinusoids → increased pressure in portal venous
system.
37. Q: Mechanism of peptic ulcer disease (H. pylori vs. NSAIDs)?
A: H. pylori disrupts mucosal defense; NSAIDs inhibit prostaglandins (which protect mucosa).
38. Q: What is hepatic encephalopathy caused by?
A: Buildup of toxins (especially ammonia) due to liver failure, bypassing hepatic detoxification.
39. Q: Difference between Crohn's disease and ulcerative colitis?
A: Crohn's: transmural, anywhere in GI tract; UC: mucosal, limited to colon.
40. Q: How does celiac disease cause malabsorption?
A: Autoimmune response to gluten → villous atrophy in small intestine.
Hematology
41. Q: What is the basic defect in sickle cell disease?
A: Point mutation in beta-globin gene → abnormal hemoglobin S → sickle-shaped RBCs under
stress.
42. Q: Pathophysiology of disseminated intravascular coagulation (DIC)?
A: Widespread activation of coagulation → microthrombi & consumption of clotting
factors/platelets → bleeding.
43. Q: Difference between pernicious anemia and iron deficiency anemia?
A: Pernicious: lack of intrinsic factor → B12 deficiency; Iron deficiency: lack of iron for
hemoglobin synthesis.
44. Q: Mechanism of leukemia vs. lymphoma?
A: Leukemia: cancer of blood/bone marrow cells; Lymphoma: solid tumors of lymphoid tissue.
45. Q: What causes polycythemia vera?
A: Clonal myeloproliferative disorder → overproduction of RBCs.
Immune & Inflammation
46. Q: Describe type I hypersensitivity reaction.
A: IgE-mediated, immediate (e.g., anaphylaxis, allergies).
47. Q: What is autoimmunity?
Pathophysiology (Walden
University) – Midterm & Final
2025, multiple versions,
verified, A+ graded.
Cellular & Systemic Foundations
1. Q: What is the primary difference between hypertrophy and hyperplasia?
A: Hypertrophy is an increase in cell size; hyperplasia is an increase in cell number.
2. Q: Describe the pathophysiologic mechanism of necrosis.
A: Unregulated cell death due to injury (e.g., ischemia, toxins), causing inflammation.
3. Q: How does apoptosis differ from necrosis?
A: Apoptosis is programmed, controlled cell death without inflammation.
4. Q: What role do free radicals play in cellular injury?
A: They cause oxidative stress, damaging lipids, proteins, and DNA.
5. Q: Define metaplasia and give one example.
A: Reversible replacement of one mature cell type by another (e.g., Barrett’s
esophagus).
Fluid, Electrolytes, & Acid-Base
6. Q: What causes third-spacing of fluid?
A: Fluid shifts from intravascular space into interstitial/compartments (e.g., burns, ascites).
7. Q: How does the body compensate for metabolic acidosis?
,A: Hyperventilation (respiratory alkalosis) to blow off CO2.
8. Q: Key sign of hyperkalemia on ECG?
A: Peaked T waves, widened QRS complex.
9. Q: Primary regulator of extracellular fluid osmolality?
A: Antidiuretic hormone (ADH).
10. Q: Effect of respiratory alkalosis on serum calcium?
A: Decreases ionized calcium, leading to potential neuromuscular excitability.
Neuro Pathophysiology
11. Q: What is excitotoxicity in stroke?
A: Excessive glutamate release causing neuronal calcium overload and death.
12. Q: Difference between ischemic and hemorrhagic stroke mechanisms?
A: Ischemic: blocked blood flow; Hemorrhagic: ruptured vessel.
13. Q: Pathophysiology of Alzheimer's disease hallmark findings?
A: Beta-amyloid plaques, neurofibrillary tangles (tau protein), cortical atrophy.
14. Q: Mechanism of multiple sclerosis?
A: Autoimmune demyelination of CNS neurons.
15. Q: What is autonomic dysreflexia?
A: Life-threatening sympathetic overresponse to stimulus below a spinal cord injury (T6 or
above).
Cardiovascular
16. Q: Explain afterload and one condition that increases it.
A: Resistance the heart must pump against; increased by hypertension.
17. Q: Pathophysiology of left-sided heart failure leading to pulmonary edema?
A: Left ventricle fails → increased left atrial pressure → increased pulmonary venous pressure →
fluid leaks into alveoli.
18. Q: What is the underlying mechanism of atherosclerosis?
A: Chronic endothelial injury, inflammation, lipid accumulation, plaque formation.
19. Q: Difference between stable and unstable angina?
A: Stable: predictable, relieved by rest; Unstable: unpredictable, occurs at rest, precursor to MI.
20. Q: How does ventricular remodeling occur post-MI?
A: Structural changes (dilation, hypertrophy, fibrosis) due to compensatory mechanisms.
Pulmonary
21. Q: Key pathophysiology of COPD (emphysema vs. chronic bronchitis)?
A: Emphysema: alveolar destruction; Chronic bronchitis: inflamed airways, excessive mucus.
,22. Q: What is V/Q mismatch?
A: Ventilation-perfusion inequality; low V/Q (shunt) or high V/Q (dead space).
23. Q: Mechanism of pulmonary hypertension in left heart failure?
A: Increased left atrial pressure → backward pressure → pulmonary venous hypertension.
24. Q: Pathophysiology of acute respiratory distress syndrome (ARDS)?
A: Diffuse alveolar damage, increased permeability, non-cardiogenic pulmonary edema.
25. Q: How does cystic fibrosis affect the lungs?
A: Defective CFTR protein → thick mucus → chronic infection and inflammation.
Renal & GU
26. Q: Difference between pre-renal, intra-renal, and post-renal acute kidney injury?
A: Pre-renal: hypoperfusion; Intra-renal: direct kidney damage; Post-renal: urinary tract
obstruction.
27. Q: Mechanism of nephrotic syndrome?
A: Glomerular damage → massive proteinuria, hypoalbuminemia, edema, hyperlipidemia.
28. Q: How does chronic kidney disease cause anemia?
A: Decreased erythropoietin production by kidneys.
29. Q: Pathophysiology of benign prostatic hyperplasia (BPH)?
A: Stromal/epithelial hyperplasia → urethral compression → obstructive symptoms.
30. Q: What is acute tubular necrosis (ATN)?
A: Ischemic or toxic injury to renal tubules, most common intra-renal AKI.
Endocrine
31. Q: Pathophysiological triad of diabetic ketoacidosis (DKA)?
A: Hyperglycemia, metabolic acidosis, ketonemia.
32. Q: Difference between type 1 and type 2 diabetes at cellular level?
A: Type 1: autoimmune beta-cell destruction; Type 2: insulin resistance and relative insulin
deficiency.
33. Q: Mechanism of Cushing's syndrome?
A: Chronic excess cortisol (endogenous or exogenous).
34. Q: What causes Graves' disease hyperthyroidism?
A: Autoantibodies (TSI) stimulate TSH receptor, causing overproduction of thyroid hormone.
, 35. Q: How does syndrome of inappropriate ADH (SIADH) cause hyponatremia?
A: Excessive ADH → water retention → dilutional hyponatremia.
Gastrointestinal
36. Q: Pathophysiology of portal hypertension in cirrhosis?
A: Scarring increases resistance in hepatic sinusoids → increased pressure in portal venous
system.
37. Q: Mechanism of peptic ulcer disease (H. pylori vs. NSAIDs)?
A: H. pylori disrupts mucosal defense; NSAIDs inhibit prostaglandins (which protect mucosa).
38. Q: What is hepatic encephalopathy caused by?
A: Buildup of toxins (especially ammonia) due to liver failure, bypassing hepatic detoxification.
39. Q: Difference between Crohn's disease and ulcerative colitis?
A: Crohn's: transmural, anywhere in GI tract; UC: mucosal, limited to colon.
40. Q: How does celiac disease cause malabsorption?
A: Autoimmune response to gluten → villous atrophy in small intestine.
Hematology
41. Q: What is the basic defect in sickle cell disease?
A: Point mutation in beta-globin gene → abnormal hemoglobin S → sickle-shaped RBCs under
stress.
42. Q: Pathophysiology of disseminated intravascular coagulation (DIC)?
A: Widespread activation of coagulation → microthrombi & consumption of clotting
factors/platelets → bleeding.
43. Q: Difference between pernicious anemia and iron deficiency anemia?
A: Pernicious: lack of intrinsic factor → B12 deficiency; Iron deficiency: lack of iron for
hemoglobin synthesis.
44. Q: Mechanism of leukemia vs. lymphoma?
A: Leukemia: cancer of blood/bone marrow cells; Lymphoma: solid tumors of lymphoid tissue.
45. Q: What causes polycythemia vera?
A: Clonal myeloproliferative disorder → overproduction of RBCs.
Immune & Inflammation
46. Q: Describe type I hypersensitivity reaction.
A: IgE-mediated, immediate (e.g., anaphylaxis, allergies).
47. Q: What is autoimmunity?
