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NR 507 Final Exam Actual Exam V2 | NR 507 Advanced Pathophysiology (NR507 Final Exam) [PDF] | Chamberlain University

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NR 507 Final Exam Actual Exam V2 | NR 507 Advanced Pathophysiology (NR507 Final Exam) [PDF] | Chamberlain University

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NR 507 Final Exam Actual Exam V2 | NR 507 Advanced
Pathophysiology (NR507 Final Exam) [PDF] | Chamberlain University
1. A 65-year-old male with a history of chronic hypertension presents with dyspnea on
exertion and an ejection fraction of 35%. Which compensatory mechanism is primarily
responsible for the ventricular remodeling observed in this patient?
A. Chronic elevation of Angiotensin II and Aldosterone

B. Activation of the parasympathetic nervous system

C. Decreased secretion of B-type natriuretic peptide

D. Downregulation of the renin-angiotensin-aldosterone system
Answer: A
Rationale: Angiotensin II acts as a potent growth factor for myocardial cells, leading to
hypertrophic changes and maladaptive remodeling. Aldosterone contributes by promoting
collagen deposition and myocardial fibrosis. Over time, these structural changes reduce
ventricular compliance and further impair systolic function.

2. A patient with Stage 4 Chronic Kidney Disease (CKD) presents with a hemoglobin of 8.2
g/dL. What is the fundamental pathophysiological cause of this anemia?
A. Chronic gastrointestinal blood loss due to uremia

B. Inadequate production of erythropoietin by peritubular fibroblasts

C. Shortened life span of red blood cells in a toxic environment

D. Iron deficiency due to impaired absorption in the duodenum
Answer: B
Rationale: The kidneys are the primary site of erythropoietin (EPO) production in
response to hypoxia. In advanced CKD, the loss of functional renal mass includes the loss of
EPO-producing cells. This deficiency leads to a normocytic, normochromic anemia due to
reduced bone marrow stimulation.

3. During an acute asthma exacerbation, a patient experiences significant air trapping. What
is the physiological consequence of this hyperinflation on the pulmonary vasculature?
A. Increased pulmonary capillary blood flow

B. Compression of alveolar capillaries and increased pulmonary vascular resistance

C. Decreased right ventricular afterload

D. Vasodilation of the pulmonary arteries in response to hypercapnia

,Answer: B
Rationale: Hyperinflation of the alveoli causes mechanical compression of the surrounding
pulmonary capillaries. This increases pulmonary vascular resistance and elevates the
workload of the right ventricle. Additionally, localized hypoxia in poorly ventilated areas
triggers hypoxic pulmonary vasoconstriction, further increasing resistance.

4. A 45-year-old female presents with fatigue, weight gain, and cold intolerance. Lab results
show an elevated TSH and low T4. Which condition is most likely responsible for these
findings?
A. Graves’ disease

B. Pituitary adenoma

C. Secondary hypothyroidism

D. Hashimoto thyroiditis

Answer: D
Rationale: Hashimoto thyroiditis is an autoimmune disorder where T-cell mediated
destruction of the thyroid gland occurs. The elevated TSH reflects the pituitary’s attempt to
stimulate a failing thyroid gland that cannot produce enough T4. This is the most common
cause of primary hypothyroidism in iodine-sufficient regions.

5. In the early stages of septic shock, why does the patient often exhibit a ‘warm’ phase with
flushed skin?
A. Massive vasoconstriction triggered by catecholamines

B. Significant increase in systemic vascular resistance (SVR)

C. Pro-inflammatory cytokines causing widespread vasodilation

D. Redistribution of blood to the visceral organs

Answer: C
Rationale: Sepsis triggers the release of nitric oxide and other inflammatory mediators
that cause profound peripheral vasodilation. This leads to decreased systemic vascular
resistance and a hyperdynamic state where the skin feels warm and appears flushed. As the
shock progresses and cardiac output fails, the patient enters the ‘cold’ or hypodynamic
phase.

6. A patient is diagnosed with metabolic acidosis. How does the respiratory system
immediately attempt to compensate for this acid-base imbalance?
A. Hypoventilation to retain carbon dioxide

B. Increasing the secretion of bicarbonate in the lungs

C. Hyperventilation to decrease the partial pressure of arterial CO2

, D. Decreasing the rate and depth of respirations

Answer: C
Rationale: Peripheral and central chemoreceptors sense the drop in pH and stimulate the
respiratory center. Hyperventilation (Kussmaul respirations) occurs to blow off CO2, which
reduces the carbonic acid level in the blood. This rapid compensation helps shift the pH
back toward the normal range but does not fix the underlying metabolic cause.

7. Which electrolyte abnormality is most commonly associated with the release of
Intracellular components in Tumor Lysis Syndrome?
A. Hypokalemia

B. Hypercalcemia

C. Hyponatremia

D. Hyperuricemia

Answer: D
Rationale: Tumor Lysis Syndrome occurs when large numbers of cancer cells die rapidly,
releasing their contents into the blood. This includes high levels of potassium, phosphorus,
and nucleic acids, which are metabolized into uric acid. Hyperuricemia can lead to acute
renal failure by causing uric acid crystals to precipitate in the renal tubules.

8. A patient with long-standing Type 2 Diabetes Mellitus presents with proteinuria. Which
pathological change in the kidney is most characteristic of diabetic nephropathy?
A. Nodular glomerulosclerosis (Kimmelstiel-Wilson lesions)

B. Thinning of the glomerular basement membrane

C. Acute tubular necrosis

D. Formation of immune complex deposits in the mesangium
Answer: A
Rationale: Chronic hyperglycemia leads to the non-enzymatic glycosylation of proteins
and increased mesangial matrix expansion. Kimmelstiel-Wilson lesions are pathognomonic
nodular deposits of hyaline material in the glomeruli. This process eventually leads to
podocyte damage, basement membrane thickening, and significant proteinuria.

9. A patient suffers from a spinal cord injury at the level of T6. They suddenly develop severe
hypertension, a pounding headache, and bradycardia. What is the suspected
pathophysiology?
A. Neurogenic shock due to loss of sympathetic tone

B. Autonomic dysreflexia caused by uninhibited sympathetic discharge

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