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NUR 631 PHYSIOLOGY AND PATHOPHYSIOLOGY FINAL EXAM EXAM QUESTIONS AND CORRECT DETAILED ANSWERS A NEW UPDATED VERSION LATEST (VERIFIED ANSWERS) ALREADY GRADED A+

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NUR 631 PHYSIOLOGY AND PATHOPHYSIOLOGY FINAL EXAM EXAM QUESTIONS AND CORRECT DETAILED ANSWERS A NEW UPDATED VERSION LATEST (VERIFIED ANSWERS) ALREADY GRADED A+

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NUR 631 PHYSIOLOGY AND PATHOPHYSIOLOGY
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NUR 631 PHYSIOLOGY AND PATHOPHYSIOLOGY

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NUR 631 PHYSIOLOGY AND PATHOPHYSIOLOGY FINAL
EXAM EXAM QUESTIONS AND CORRECT DETAILED
ANSWERS A NEW UPDATED VERSION LATEST 2026-2027
(VERIFIED ANSWERS) ALREADY GRADED A+



1. A patient with chronic kidney disease has elevated serum phosphate levels. Which
compensatory mechanism is expected to occur?
- A. Increased intestinal calcium absorption
- B. Decreased parathyroid hormone secretion
- C. ***Increased parathyroid hormone secretion***
- D. Decreased bone resorption


Rationale: Hyperphosphatemia directly stimulates parathyroid hormone (PTH) secretion. PTH
lowers serum phosphate by increasing renal excretion and also promotes bone resorption, which
releases calcium and phosphate, but the net renal effect dominates in early compensation.




2.A 55-year-old with heart failure develops hyponatremia. Which pathophysiological
mechanism is most likely responsible?
- A. Excessive water intake without solute intake
- B. ***Increased arginine vasopressin (ADH) secretion***
- C. Cerebral salt wasting syndrome
- D. Primary adrenal insufficiency


Rationale:In heart failure, decreased effective circulating volume stimulates baroreceptors,
leading to non-osmotic ADH secretion. ADH increases water reabsorption, causing dilutional
hyponatremia despite total body sodium normal or increased.

,3.In septic shock, which vascular change contributes most to refractory hypotension?
- A. Decreased capillary permeability
- B. ***Inducible nitric oxide synthase (iNOS)-mediated vasodilation***
- C. α-adrenergic receptor upregulation
- D. Increased systemic vascular resistance


Rationale: Septic shock induces iNOS in vascular smooth muscle, producing excessive nitric
oxide that causes sustained vasodilation. This reduces systemic vascular resistance and leads to
hypotension unresponsive to vasopressors.




4. A patient with type 1 diabetes mellitus has a blood glucose of 600 mg/dL, arterial pH 7.10,
and positive serum ketones. Which finding is expected on respiratory assessment?
- A. Apneustic breathing
- B. ***Kussmaul respirations***
- C. Cheyne-Stokes breathing
- D. Biot’s breathing


Rationale: Kussmaul respirations are deep, rapid breaths that compensate for metabolic acidosis
by increasing alveolar ventilation, lowering PaCO₂. This occurs in diabetic ketoacidosis due to
increased hydrogen ion concentration stimulating central chemoreceptors.




5.A 70-year-old with chronic obstructive pulmonary disease (COPD) has a PaCO₂ of 65 mmHg.
Which acid-base disturbance is primarily present?
- A. Acute metabolic acidosis
- B. ***Chronic respiratory acidosis***
- C. Acute respiratory alkalosis

,- D. Mixed metabolic alkalosis


Rationale:In COPD, airflow obstruction reduces alveolar ventilation, causing CO₂ retention.
Chronic hypercapnia leads to renal bicarbonate retention for compensation, but baseline PaCO₂
remains elevated, defining chronic respiratory acidosis.




6. Which finding is most characteristic of hypovolemic shock?
- A. Widened pulse pressure
- B. ***Narrowed pulse pressure and tachycardia***
- C. Bounding peripheral pulses
- D. Increased central venous pressure


Rationale:Hypovolemia reduces stroke volume, narrowing pulse pressure. Compensatory
tachycardia and peripheral vasoconstriction occur to maintain perfusion, leading to cool,
clammy skin and narrowed pulse pressure.




7. A patient with liver cirrhosis develops ascites. Which primary mechanism drives fluid
accumulation?
- A. Increased plasma oncotic pressure
- B. ***Splanchnic arterial vasodilation and portal hypertension***
- C. Decreased renin-angiotensin-aldosterone system activity
- D. Lymphatic overcirculation


Rationale: Cirrhosis causes portal hypertension and splanchnic vasodilation, reducing effective
arterial blood volume. This activates RAAS and sympathetic nervous system, leading to sodium
and water retention, which accumulates as ascites.

, 8. In anemia of chronic disease, which hepcidin-mediated mechanism causes iron
sequestration?
- A. Increased ferroportin expression on enterocytes
- B. ***Decreased iron release from macrophages and enterocytes***
- C. Enhanced erythropoietin sensitivity
- D. Increased transferrin synthesis


Rationale:Inflammatory cytokines, especially IL-6, stimulate hepcidin production. Hepcidin
binds ferroportin, causing its internalization and degradation, trapping iron in macrophages and
reducing intestinal absorption, leading to functional iron deficiency.




9.Which statement best describes the pathophysiology of type 2 diabetes mellitus?
- A. Autoimmune destruction of pancreatic beta cells
- B. ***Insulin resistance with relative insulin deficiency***
- C. Absolute deficiency of glucagon
- D. Genetic defect in renal glucose transporters


Rationale:Type 2 diabetes is characterized by peripheral insulin resistance (muscle, liver, fat)
and inadequate compensatory insulin secretion from pancreatic beta cells, leading to
hyperglycemia.




10. A patient with small cell lung cancer develops syndrome of inappropriate antidiuretic
hormone (SIADH). Which electrolyte abnormality is expected?
- A. Hypernatremia and hyperosmolality
- B. ***Hyponatremia with low serum osmolality***
- C. Hyperkalemia and hypercalcemia
- D. Hypokalemia with metabolic alkalosis

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Instelling
NUR 631 PHYSIOLOGY AND PATHOPHYSIOLOGY
Vak
NUR 631 PHYSIOLOGY AND PATHOPHYSIOLOGY

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