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NURS 6501N - Advanced Pathophysiology Actual Final Exam Questions & Verified Answers Walden University | 2026/2027 Latest Update.

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NURS 6501N - Advanced Pathophysiology Actual Final Exam Questions & Verified Answers Walden University | 2026/2027 Latest Update.

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NURS 6501N - Advanced Pathophysiology
Actual Final Exam Questions & Verified
Answers Walden University | 2026/2027
Latest Update.


1. A patient presents with severe, crushing chest pain that radiates to the jaw and left ar
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m. An ECG reveals ST-segment elevation in leads V1-
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V4. Which of the following is the most likely diagnosis?
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A. Unstable Angina
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B. Non-ST Elevation Myocardial Infarction (NSTEMI)
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C. ST-Elevation Myocardial Infarction (STEMI) - Anteroseptal
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D. ST-Elevation Myocardial Infarction (STEMI) - Inferior
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Correct Answer: C hg hg




Rationale: ST-segment elevation in the precordial leads V1-
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V4 indicates an anteroseptal wall MI, typically caused by occlusion of the left anterior descendi
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ng (LAD) coronary artery. Pain radiating to the jaw and left arm is classic for cardiac ischemia.
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Unstable angina (A) and NSTEMI (B) do not present with ST-
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elevation. Inferior STEMI (D) would show changes in leads II, III, and aVF.
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2. A 65-year-
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old patient with a history of heart failure is prescribed furosemide. Which of the followi
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ng electrolyte imbalances is a primary concern with this medication?
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A. Hyperkalemia
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B. Hypernatremia
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C. Hypokalemia
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D. Hypercalcemia
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Correct Answer: C hg hg




Rationale: Furosemide is a loop diuretic that inhibits the Na-K-
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2Cl cotransporter in the thick ascending limb of the loop of Henle. This leads to increased excr
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etion of sodium, chloride, and potassium, often resulting in hypokalemia. Hyperkalemia (A) is a
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concern with potassium-sparing diuretics. Hypernatremia (B) is not a typical side effect.
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,3. A patient with chronic obstructive pulmonary disease (COPD) has chronic hypoxemia.
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This leads to which of the following long-term compensatory mechanisms?
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A. Decreased erythropoietin production
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B. Decreased red blood cell mass
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C. Increased erythropoietin production and secondary polycythemia
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D. Increased oxygen saturation of hemoglobin
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Correct Answer: C hg hg




Rationale: Chronic hypoxemia stimulates the kidneys to produce more erythropoietin, which in
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turn stimulates the bone marrow to increase red blood cell production (secondary polycythemi
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a). This is a compensatory attempt to increase the oxygen-carrying capacity of the blood.
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4. A patient is diagnosed with type 1 diabetes mellitus. The underlying pathophysiology
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involves:
A. Insulin resistance at the cellular level
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B. Autoimmune destruction of pancreatic beta cells
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C. Impaired glucose uptake in skeletal muscle
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D. Deficiency of glucagon
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Correct Answer: B hg hg




Rationale: Type 1 diabetes is an autoimmune disease where the body's immune system attack
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s and destroys the insulin-
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producing beta cells in the pancreas. Insulin resistance (A and C) is the hallmark of type 2 diab
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etes. A deficiency of glucagon (D) is not the cause.
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5. Which of the following best describes the pathophysiology of septic shock?
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A. Massive vasoconstriction leading to hypertension
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B. Decreased cardiac output due to pump failure
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C. Systemic vasodilation, increased capillary permeability, and maldistribution of blood flow
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D. Obstruction of blood flow in the pulmonary vasculature
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Correct Answer: C hg hg




Rationale: Septic shock is characterized by a massive systemic inflammatory response to infecti
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on. This causes widespread vasodilation (decreased systemic vascular resistance), increased capi
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llary permeability (leading to third-
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spacing of fluid), and maldistribution of blood flow, resulting in tissue hypoperfusion and hypot
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ension.

,6. In liver failure, why does hyperammonemia occur?
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A. Increased breakdown of proteins by the liver
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B. Failure of the liver to convert ammonia to urea
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C. Decreased renal excretion of ammonia
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D. Increased absorption of ammonia from the GI tract
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Correct Answer: B hg hg




Rationale: The liver's primary role in ammonia metabolism is to convert it into urea via the ure
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a cycle, which is then excreted by the kidneys. In liver failure, this detoxification process is impa
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ired, leading to a buildup of ammonia in the blood (hyperammonemia), which can cross the bl
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ood-brain barrier and cause hepatic encephalopathy.
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7. A patient with a history of peptic ulcer disease develops a sudden onset of severe, sha
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rp abdominal pain. On exam, the abdomen is rigid and board-
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like. Which complication is most likely?
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A. Gastric outlet obstruction
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B. Upper GI bleeding
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C. Perforation
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D. Penetration into the pancreas
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Correct Answer: C hg hg




Rationale: A sudden onset of severe, sharp pain with a rigid, board-
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like abdomen is the classic presentation of a perforated peptic ulcer. This allows gastrointestina
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l contents, including air and acid, to enter the peritoneal cavity, causing a chemical peritonitis t
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hat leads to guarding and rigidity.
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8. The pathophysiological mechanism responsible for the development of atherosclerosis
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begins with:
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A. Plaque rupture and thrombus formation
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B. Smooth muscle cell proliferation in the tunica media
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C. Endothelial injury and dysfunction
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D. Deposition of calcium in the arterial wall
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Correct Answer: C hg hg




Rationale: The initiation of atherosclerosis is widely accepted to be endothelial injury or dysfun
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ction caused by factors like hypertension, hyperlipidemia, smoking, and diabetes. This injury inc
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reases vascular permeability, allowing LDL cholesterol to enter the intima, where it becomes oxi
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dized and triggers an inflammatory response.
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, 9. A patient has a cerebrovascular accident (CVA) affecting the left hemisphere. Which of
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the following deficits is most characteristic?
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A. Left-sided hemiparesis and neglect
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B. Aphasia and right-sided hemiparesis
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C. Ataxia and dysmetria
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D. Bilateral blindness and confusion
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Correct Answer: B hg hg




Rationale: The left hemisphere is dominant for language in most individuals. A stroke in the lef
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t middle cerebral artery territory will typically cause aphasia (difficulty with language) and right-
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sided motor and sensory deficits (right hemiparesis/hemiplegia) because the motor and sensor
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y tracts decussate at the medulla.
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10. Which of the following is the primary mechanism of tissue injury in ischemic stroke?
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A. Excitotoxicity due to glutamate release
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B. Direct physical compression of brain tissue
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C. Formation of an amyloid plaque
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D. Demyelination of neurons
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Correct Answer: A hg hg




Rationale: In ischemic stroke, the lack of oxygen and glucose leads to a failure of the Na+/K+
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ATPase pump, causing depolarization and massive release of the excitatory neurotransmitter gl
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utamate. Glutamate overstimulates NMDA receptors, leading to a lethal influx of calcium into t
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he neuron, initiating a cascade of cell death (excitotoxicity).
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11. A patient with asthma is experiencing an acute exacerbation. Which of the following
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pathophysiological changes is most responsible for the expiratory wheezing? hg hg hg hg hg hg hg hg




A. Constriction of pulmonary arterioles
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B. Narrowing of the airways due to bronchospasm, edema, and mucus
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C. Collapse of the alveoli due to surfactant deficiency
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D. Fluid accumulation in the alveolar spaces
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Correct Answer: B hg hg




Rationale: Wheezing, particularly on expiration, is a hallmark of asthma. It is caused by turbule
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nt airflow through narrowed airways. The narrowing is due to a combination of bronchospasm,
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mucosal edema, and increased mucus production. Airway obstruction is worse during expiratio
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n because positive intrathoracic pressure compresses the airways further.
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