NURS 6501 ADVANCED PATHOPHYSIOLOGY
WALDEN UNIVERSITY MIDTERM EXAM 2025
ACTUAL EXAM AND PRACTICE EXAM TEST
BANK | ACCURATE AND VERIFIED QUESTIONS
WITH DETAILED ANSWERS | SURE PASS!!! |
GRADED A+
Cellular Biology & Systemic Metabolism
1. Q: What is the primary cellular adaptation seen in the left ventricular myocardium in
response to systemic hypertension?
A: Hypertrophy. The muscle cells increase in size to generate more contractile force
against the increased pressure.
2. Q: A patient with chronic emphysema often develops clubbing of the fingers. What is the
most likely pathophysiologic cause?
A: Chronic tissue hypoxia leading to growth factor release and soft tissue proliferation at
the distal extremities.
3. Q: What is the hallmark biochemical change during cellular ischemia that leads to a
switch from aerobic to anaerobic metabolism?
A: Depletion of ATP and accumulation of lactic acid, leading to a decrease in intracellular
pH (acidosis).
4. Q: Which type of necrosis is characterized by a "cheese-like" appearance and is typical of
tuberculosis?
A: Caseous necrosis.
5. Q: What is the role of free radicals in cellular injury?
A: They cause lipid peroxidation of membranes, protein fragmentation, and DNA
damage, leading to oxidative stress.
Fluids, Electrolytes, and Acid-Base
, 6. Q: A patient with heart failure has increased aldosterone secretion. What is the
expected effect on sodium and potassium levels?
A: Sodium retention (and water) and potassium wasting (hypokalemia).
7. Q: What is the primary mechanism of edema formation in nephrotic syndrome?
A: Loss of plasma proteins (especially albumin) in urine leads to decreased plasma
oncotic pressure, causing fluid shift to the interstitium.
8. Q: In metabolic acidosis, how does the respiratory system attempt to compensate?
A: By increasing the rate and depth of ventilation (Kussmaul respirations) to blow off
more CO2 (a volatile acid).
9. Q: A patient has a serum pH of 7.30, PaCO2 of 60 mm Hg, and HCO3- of 34 mEq/L. What
is the primary acid-base disorder?
A: Respiratory acidosis with metabolic compensation (compensated respiratory
acidosis).
10. Q: What is the most common cause of hypercalcemia in hospitalized patients?
A: Malignancy (e.g., bone metastases, PTHrP secretion).
Immunology and Inflammation
11. Q: What is the primary difference between the innate and adaptive immune responses?
A: Innate immunity is non-specific and provides immediate defense; adaptive immunity
is antigen-specific, has memory, and develops over time.
12. Q: During an acute inflammatory response, what causes vasodilation and increased
vascular permeability?
A: Histamine, bradykinin, and prostaglandins released from mast cells and other
mediators.
13. Q: What type of hypersensitivity reaction is involved in anaphylaxis?
A: Type I (IgE-mediated) hypersensitivity.
14. Q: In systemic lupus erythematosus (SLE), what is the primary mechanism of tissue
damage?
A: Type III hypersensitivity (immune complex deposition) leading to complement
activation and inflammation in vessels and organs.
15. Q: What is the role of helper T-cells (CD4+) in the immune response?
A: They orchestrate the immune response by activating B-cells, cytotoxic T-cells, and
macrophages through cytokine signaling.
, Neuropathophysiology
16. Q: What is the Monroe-Kellie doctrine?
A: It states that the skull is a rigid compartment; the volume of intracranial contents
(brain, blood, CSF) must remain constant. An increase in one must be compensated by a
decrease in another to prevent a rise in intracranial pressure (ICP).
17. Q: What is the primary excitatory neurotransmitter in the brain, and what is its
pathophysiologic role in seizures and neuronal injury?
A: Glutamate. In excess, it causes excitotoxicity via overstimulation of NMDA and AMPA
receptors, leading to calcium influx and cell death.
18. Q: In Parkinson's disease, which neurotransmitter-producing cells degenerate in the
substantia nigra?
A: Dopaminergic neurons.
19. Q: What is the difference between ischemic and hemorrhagic stroke in terms of initial CT
scan findings?
A: Ischemic strokes may not appear immediately on CT (often hypodense after hours).
Hemorrhagic strokes appear as hyperdense (bright white) areas immediately.
20. Q: What is the hallmark pathophysiologic finding in Alzheimer's disease?
A: Extracellular amyloid-beta plaques and intracellular neurofibrillary tangles composed
of hyperphosphorylated tau protein.
Cardiovascular Pathophysiology
21. Q: Describe the pathogenesis of atherosclerosis, starting with endothelial injury.
A: Endothelial injury → inflammation and LDL accumulation in intima → macrophage
uptake forming foam cells → fatty streak → fibrous plaque → complicated plaque
(rupture, thrombosis).
22. Q: What is the primary compensatory mechanism in the early stages of heart failure
with reduced ejection fraction (HFrEF)?
A: Activation of the sympathetic nervous system (increased heart rate, contractility) and
the renin-angiotensin-aldosterone system (RAAS) to maintain cardiac output.
23. Q: Differentiate between stable angina and unstable angina.
A: Stable angina: predictable chest pain with exertion, relieved by rest/nitrates, due to
fixed coronary stenosis. Unstable angina: pain at rest, increasing in frequency/severity,
due to ruptured plaque with non-occlusive thrombus.
WALDEN UNIVERSITY MIDTERM EXAM 2025
ACTUAL EXAM AND PRACTICE EXAM TEST
BANK | ACCURATE AND VERIFIED QUESTIONS
WITH DETAILED ANSWERS | SURE PASS!!! |
GRADED A+
Cellular Biology & Systemic Metabolism
1. Q: What is the primary cellular adaptation seen in the left ventricular myocardium in
response to systemic hypertension?
A: Hypertrophy. The muscle cells increase in size to generate more contractile force
against the increased pressure.
2. Q: A patient with chronic emphysema often develops clubbing of the fingers. What is the
most likely pathophysiologic cause?
A: Chronic tissue hypoxia leading to growth factor release and soft tissue proliferation at
the distal extremities.
3. Q: What is the hallmark biochemical change during cellular ischemia that leads to a
switch from aerobic to anaerobic metabolism?
A: Depletion of ATP and accumulation of lactic acid, leading to a decrease in intracellular
pH (acidosis).
4. Q: Which type of necrosis is characterized by a "cheese-like" appearance and is typical of
tuberculosis?
A: Caseous necrosis.
5. Q: What is the role of free radicals in cellular injury?
A: They cause lipid peroxidation of membranes, protein fragmentation, and DNA
damage, leading to oxidative stress.
Fluids, Electrolytes, and Acid-Base
, 6. Q: A patient with heart failure has increased aldosterone secretion. What is the
expected effect on sodium and potassium levels?
A: Sodium retention (and water) and potassium wasting (hypokalemia).
7. Q: What is the primary mechanism of edema formation in nephrotic syndrome?
A: Loss of plasma proteins (especially albumin) in urine leads to decreased plasma
oncotic pressure, causing fluid shift to the interstitium.
8. Q: In metabolic acidosis, how does the respiratory system attempt to compensate?
A: By increasing the rate and depth of ventilation (Kussmaul respirations) to blow off
more CO2 (a volatile acid).
9. Q: A patient has a serum pH of 7.30, PaCO2 of 60 mm Hg, and HCO3- of 34 mEq/L. What
is the primary acid-base disorder?
A: Respiratory acidosis with metabolic compensation (compensated respiratory
acidosis).
10. Q: What is the most common cause of hypercalcemia in hospitalized patients?
A: Malignancy (e.g., bone metastases, PTHrP secretion).
Immunology and Inflammation
11. Q: What is the primary difference between the innate and adaptive immune responses?
A: Innate immunity is non-specific and provides immediate defense; adaptive immunity
is antigen-specific, has memory, and develops over time.
12. Q: During an acute inflammatory response, what causes vasodilation and increased
vascular permeability?
A: Histamine, bradykinin, and prostaglandins released from mast cells and other
mediators.
13. Q: What type of hypersensitivity reaction is involved in anaphylaxis?
A: Type I (IgE-mediated) hypersensitivity.
14. Q: In systemic lupus erythematosus (SLE), what is the primary mechanism of tissue
damage?
A: Type III hypersensitivity (immune complex deposition) leading to complement
activation and inflammation in vessels and organs.
15. Q: What is the role of helper T-cells (CD4+) in the immune response?
A: They orchestrate the immune response by activating B-cells, cytotoxic T-cells, and
macrophages through cytokine signaling.
, Neuropathophysiology
16. Q: What is the Monroe-Kellie doctrine?
A: It states that the skull is a rigid compartment; the volume of intracranial contents
(brain, blood, CSF) must remain constant. An increase in one must be compensated by a
decrease in another to prevent a rise in intracranial pressure (ICP).
17. Q: What is the primary excitatory neurotransmitter in the brain, and what is its
pathophysiologic role in seizures and neuronal injury?
A: Glutamate. In excess, it causes excitotoxicity via overstimulation of NMDA and AMPA
receptors, leading to calcium influx and cell death.
18. Q: In Parkinson's disease, which neurotransmitter-producing cells degenerate in the
substantia nigra?
A: Dopaminergic neurons.
19. Q: What is the difference between ischemic and hemorrhagic stroke in terms of initial CT
scan findings?
A: Ischemic strokes may not appear immediately on CT (often hypodense after hours).
Hemorrhagic strokes appear as hyperdense (bright white) areas immediately.
20. Q: What is the hallmark pathophysiologic finding in Alzheimer's disease?
A: Extracellular amyloid-beta plaques and intracellular neurofibrillary tangles composed
of hyperphosphorylated tau protein.
Cardiovascular Pathophysiology
21. Q: Describe the pathogenesis of atherosclerosis, starting with endothelial injury.
A: Endothelial injury → inflammation and LDL accumulation in intima → macrophage
uptake forming foam cells → fatty streak → fibrous plaque → complicated plaque
(rupture, thrombosis).
22. Q: What is the primary compensatory mechanism in the early stages of heart failure
with reduced ejection fraction (HFrEF)?
A: Activation of the sympathetic nervous system (increased heart rate, contractility) and
the renin-angiotensin-aldosterone system (RAAS) to maintain cardiac output.
23. Q: Differentiate between stable angina and unstable angina.
A: Stable angina: predictable chest pain with exertion, relieved by rest/nitrates, due to
fixed coronary stenosis. Unstable angina: pain at rest, increasing in frequency/severity,
due to ruptured plaque with non-occlusive thrombus.
