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NR 507 Exam 3 Actual Exam V3 | NR 507 Advanced Pathophysiology (NR507 Exam 3) [PDF] | Chamberlain University

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NR 507 Exam 3 Actual Exam V3 | NR 507 Advanced Pathophysiology (NR507 Exam 3) [PDF] | Chamberlain University

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NR 507 Exam 3 Actual Exam V3 | NR 507 Advanced Pathophysiology
(NR507 Exam 3) [PDF] | Chamberlain University
1. A patient presents with extreme thirst, polyuria, and a very low urine specific gravity
following a head injury. Serum sodium is 152 mEq/L. Which pathophysiological mechanism
most likely explains these findings?
A. Excessive secretion of antidiuretic hormone (ADH) leading to water retention.

B. Insensitivity of the distal renal tubules to antidiuretic hormone (ADH).

C. Damage to the posterior pituitary leading to a deficiency in ADH production.

D. An overproduction of aldosterone causing excess sodium and water excretion.
Answer: C
Rationale: This clinical scenario describes Central Diabetes Insipidus, which often follows
neurosurgery or head trauma. The lack of ADH prevents the kidneys from reabsorbing
water, leading to dilute urine and hypernatremia. Treatment usually involves replacement
with desmopressin to restore water balance.

2. A 55-year-old male with chronic alcoholism presents with abdominal distension and
yellowing of the sclera. Laboratory results show elevated AST, ALT, and ammonia levels.
Which mechanism is primarily responsible for the development of ascites in this patient?
A. Portal hypertension and decreased synthesis of serum albumin by the liver.

B. Increased capillary oncotic pressure due to excessive protein intake.

C. Decreased hydrostatic pressure in the mesenteric veins.

D. Overproduction of bile leading to leakage into the peritoneal cavity.
Answer: A
Rationale: In cirrhosis, portal hypertension increases the hydrostatic pressure in the
abdominal vessels. Concurrently, the diseased liver produces less albumin, lowering the
plasma oncotic pressure. These two factors together force fluid out of the vasculature and
into the peritoneal space, creating ascites.

3. A patient with Type 1 Diabetes Mellitus presents with Kussmaul respirations, fruity breath,
and a blood glucose of 450 mg/dL. An arterial blood gas (ABG) is performed. Which acid-base
imbalance is expected?
A. Metabolic alkalosis with respiratory compensation.

B. Metabolic acidosis with an increased anion gap.

C. Metabolic acidosis with a decreased anion gap.

,D. Respiratory acidosis with renal compensation.

Answer: B
Rationale: Diabetic Ketoacidosis (DKA) results in the accumulation of ketoacids, which are
unmeasured anions that increase the anion gap. Kussmaul respirations are the body’s
compensatory mechanism to blow off CO2 and raise the pH. This reflects a metabolic
acidosis caused by the exhaustion of bicarbonate buffering capacity.

4. Which of the following findings is most characteristic of Nephrotic Syndrome,
distinguishing it from Nephritic Syndrome?
A. Acute decrease in glomerular filtration rate (GFR).

B. Presence of red blood cell casts in the urine sediment.

C. Hypertension due to sodium and water retention.

D. Massive proteinuria exceeding 3.5 grams per day.

Answer: D
Rationale: Nephrotic syndrome is defined by heavy proteinuria, which occurs due to
increased glomerular permeability to proteins. While edema and hypoalbuminemia are
present, the massive loss of protein is the hallmark sign. In contrast, nephritic syndrome is
characterized more by inflammation, hematuria, and RBC casts.

5. A patient with chronic kidney disease (CKD) presents with a serum potassium of 6.8 mEq/L.
Which physiological consequence is the greatest concern for this patient?
A. Cardiac arrhythmias due to a decreased resting membrane potential.

B. Increased risk of seizure activity due to neuronal hyper-excitability.

C. Hypoventilation due to skeletal muscle weakness.

D. Paralytic ileus resulting from smooth muscle relaxation.
Answer: A
Rationale: Hyperkalemia reduces the concentration gradient of potassium across the cell
membrane, making the resting membrane potential less negative. This makes myocardial
cells more excitable initially, but eventually leads to impaired repolarization and life-
threatening arrhythmias. Management in CKD is critical as the kidneys are the primary
route for potassium excretion.

6. A 30-year-old female presents with weight loss, heat intolerance, and a visible enlargement
in the neck. Her TSH is low, and her free T4 is high. What is the most likely underlying cause?
A. Autoimmune destruction of the thyroid gland.

B. Dietary iodine deficiency leading to goiter formation.

, C. A benign pituitary tumor secreting excessive TSH.

D. Antibodies mimicking TSH and stimulating the thyroid receptors.
Answer: D
Rationale: The patient displays symptoms of Graves’ Disease, the most common cause of
hyperthyroidism. In this condition, thyroid-stimulating immunoglobulins (TSI) bind to TSH
receptors, triggering excessive hormone production. Because of the negative feedback loop,
high levels of T3 and T4 suppress the secretion of TSH from the pituitary.

7. In the Renin-Angiotensin-Aldosterone System (RAAS), what is the direct effect of
Angiotensin II on the systemic vasculature?
A. Potent vasoconstriction to increase systemic blood pressure.

B. Vasodilation to improve renal perfusion.

C. Inhibition of aldosterone release from the adrenal cortex.

D. Stimulation of the kidneys to excrete sodium.
Answer: A
Rationale: Angiotensin II is a powerful vasoconstrictor that acts on the smooth muscle of
arterioles to increase peripheral resistance. It also stimulates the adrenal cortex to release
aldosterone, which promotes sodium and water retention. These mechanisms collectively
work to restore blood pressure and fluid volume.

8. A patient with hyperparathyroidism is at increased risk for which of the following?
A. Hypocalcemia and tetany.

B. Positive Chvostek and Trousseau signs.

C. Pathological bone fractures and renal calculi.
D. Increased neuromuscular excitability.

Answer: C
Rationale: Excessive Parathyroid Hormone (PTH) causes increased bone resorption,
releasing calcium into the blood. This can lead to weakened bones (fractures) and high
levels of calcium in the urine, which precipitate as kidney stones (calculi). Hypercalcemia
generally decreases neuromuscular excitability, unlike hypocalcemia.

9. Which statement best describes the pathophysiology of Crohn’s disease as opposed to
Ulcerative Colitis?
A. Inflammation is limited to the mucosal layer of the colon.

B. It involves transmural inflammation and ‘skip lesions’ throughout the GI tract.

C. The disease typically begins in the rectum and moves proximally.

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