Final Exam Prep for NUR 631 Advanced
Physiology and Pathophysiology Final
Exam Questions and Correct Answers
with Rationales/ NUR 631 Final Exam
Prep MOST RECENT (GRADED A+)
Domain 1: Cellular Adaptation, Injury, and Neoplasia
Q1: A patient with chronic alcoholism presents with fatigue, anorexia, and
right upper quadrant pain. A liver biopsy reveals hepatocytes with large,
pale-staining cytoplasmic vacuoles that displace the nucleus to the
periphery. Which cellular adaptation is primarily responsible for this finding,
and what is the most significant long-term risk?
A) Hyperplasia; risk of cirrhosis
B) Metaplasia; risk of malignancy
C) Fatty change (steatosis); risk of steatohepatitis and fibrosis
D) Dystrophic calcification; risk of liver failure
Answer: C) Fatty change (steatosis); risk of steatohepatitis and fibrosis
Rationale: The description is classic for fatty change (steatosis), where lipid
vacuoles accumulate in hepatocytes due to toxic/metabolic injury (alcohol).
While steatosis itself is reversible, persistent injury leads
to steatohepatitis (inflammation), which can progress to fibrosis and
ultimately cirrhosis. Hyperplasia (A) is an increase in cell number; metaplasia
(B) is a change in cell type; dystrophic calcification (D) occurs in necrotic
tissue, not alcohol-induced liver injury.
,Domain 2: Fluid, Electrolyte, and Acid-Base Balance
Q2: A patient with severe vomiting for 3 days is admitted with lethargy and
muscle twitching. Arterial blood gas (ABG) reveals: pH 7.50, PaCO2 48
mmHg, HCO3- 36 mEq/L. What is the primary compensatory mechanism
occurring in this patient?
A) Hypoventilation to retain CO2
B) Hyperventilation to blow off CO2
C) Renal excretion of bicarbonate
D) Renal retention of hydrogen ions
Answer: A) Hypoventilation to retain CO2
Rationale: The ABG shows metabolic alkalosis (high pH + high HCO3-). The
lungs compensate by hypoventilating (increasing PaCO2) to buffer the
alkalosis. However, the PaCO2 is 48, which is only a slight increase
(expected compensation is PaCO2 rises 0.7 mmHg for every 1 mEq/L rise in
HCO3-). This indicates partial compensation. The renal compensation
(excreting HCO3-) takes days to occur, not hours.
Domain 3: Neuropathophysiology
Q3: A patient with a new diagnosis of Parkinson’s disease is started on
carbidopa-levodopa. The patient asks why they also need carbidopa. What
is the best pathophysiological explanation?
A) Carbidopa prevents the peripheral breakdown of dopamine, allowing
more levodopa to cross the blood-brain barrier.
B) Carbidopa acts as a direct dopamine agonist in the substantia nigra.
C) Carbidopa prevents the central metabolism of dopamine to DOPAC.
D) Carbidopa stimulates the release of acetylcholine in the striatum.
Answer: A) Carbidopa prevents the peripheral breakdown of
dopamine, allowing more levodopa to cross the blood-brain barrier.
Rationale: Levodopa is the precursor to dopamine. Carbidopa is
,a peripheral decarboxylase inhibitor that does not cross the blood-brain
barrier. It inhibits the enzyme that converts levodopa to
dopamine outside the CNS, which reduces peripheral side effects (nausea)
and increases the amount of levodopa that reaches the brain.
Domain 4: Cardiovascular Pathophysiology
Q4: A 68-year-old with a history of hypertension presents with acute onset
of severe, tearing chest pain radiating to the back. Blood pressure is
160/100 mmHg in the right arm and 100/70 mmHg in the left arm. A CT
angiogram reveals a dissection of the ascending aorta. What is the primary
pathophysiological event that led to this condition, and what is the
immediate goal of treatment?
A) Atherosclerotic plaque rupture; immediate surgical repair
B) Weakening of the medial layer (cystic medial degeneration); immediate
blood pressure reduction (MAP < 105)
C) Inflammation of the vasa vasorum; immediate anticoagulation
D) Calcification of the aortic valve; immediate beta-blockade
Answer: B) Weakening of the medial layer (cystic medial
degeneration); immediate blood pressure reduction (MAP < 105)
Rationale: Aortic dissection is caused by a tear in the intima, allowing
blood to enter the medial layer of the aortic wall. Hypertension accelerates
this by increasing shear stress. The immediate goal for Type A dissections
(ascending aorta) is emergency surgical repair, but the immediate medical
goal before and after surgery is aggressive blood pressure control (reduce
MAP to 100-105 mmHg and heart rate to <60) to prevent propagation of
the dissection.
Domain 5: Pulmonary Pathophysiology
, Q5: A patient with COPD (chronic bronchitis phenotype) has chronic
hypoxemia and hypercapnia. Which of the following best explains the
blunted respiratory drive seen in this patient?
A) Peripheral chemoreceptors become desensitized to low O2.
B) Central chemoreceptors become desensitized to high CO2.
C) The Hering-Breuer reflex is activated, inhibiting inspiration.
D) Ventilation-perfusion (V/Q) mismatch is corrected by pulmonary
vasoconstriction.
Answer: B) Central chemoreceptors become desensitized to high CO2.
Rationale: In chronic hypercapnia (CO2 retainers), the central
chemoreceptors in the medulla become desensitized to elevated CO2/H+
levels. The primary drive to breathe shifts from CO2 to hypoxemia (low O2),
which is sensed by the peripheral chemoreceptors (carotid and aortic
bodies). Giving these patients high-flow oxygen can remove their hypoxic
drive, leading to respiratory depression and apnea.
Domain 6: Renal Pathophysiology
Q6: A patient with diabetic nephropathy develops nephrotic syndrome.
Which of the following findings is most directly responsible for the
generalized edema seen in this patient?
A) Increased hydrostatic pressure in the glomerular capillaries
B) Decreased plasma oncotic pressure due to massive proteinuria
C) Increased aldosterone secretion leading to sodium retention
D) Decreased glomerular filtration rate leading to fluid overload
Answer: B) Decreased plasma oncotic pressure due to massive
proteinuria
Rationale: Nephrotic syndrome is characterized by heavy proteinuria
(>3.5g/day), hypoalbuminemia, and edema. The loss of albumin in the
urine lowers plasma oncotic pressure, which reduces the reabsorption of
fluid from the interstitial space back into the capillaries, leading to
Physiology and Pathophysiology Final
Exam Questions and Correct Answers
with Rationales/ NUR 631 Final Exam
Prep MOST RECENT (GRADED A+)
Domain 1: Cellular Adaptation, Injury, and Neoplasia
Q1: A patient with chronic alcoholism presents with fatigue, anorexia, and
right upper quadrant pain. A liver biopsy reveals hepatocytes with large,
pale-staining cytoplasmic vacuoles that displace the nucleus to the
periphery. Which cellular adaptation is primarily responsible for this finding,
and what is the most significant long-term risk?
A) Hyperplasia; risk of cirrhosis
B) Metaplasia; risk of malignancy
C) Fatty change (steatosis); risk of steatohepatitis and fibrosis
D) Dystrophic calcification; risk of liver failure
Answer: C) Fatty change (steatosis); risk of steatohepatitis and fibrosis
Rationale: The description is classic for fatty change (steatosis), where lipid
vacuoles accumulate in hepatocytes due to toxic/metabolic injury (alcohol).
While steatosis itself is reversible, persistent injury leads
to steatohepatitis (inflammation), which can progress to fibrosis and
ultimately cirrhosis. Hyperplasia (A) is an increase in cell number; metaplasia
(B) is a change in cell type; dystrophic calcification (D) occurs in necrotic
tissue, not alcohol-induced liver injury.
,Domain 2: Fluid, Electrolyte, and Acid-Base Balance
Q2: A patient with severe vomiting for 3 days is admitted with lethargy and
muscle twitching. Arterial blood gas (ABG) reveals: pH 7.50, PaCO2 48
mmHg, HCO3- 36 mEq/L. What is the primary compensatory mechanism
occurring in this patient?
A) Hypoventilation to retain CO2
B) Hyperventilation to blow off CO2
C) Renal excretion of bicarbonate
D) Renal retention of hydrogen ions
Answer: A) Hypoventilation to retain CO2
Rationale: The ABG shows metabolic alkalosis (high pH + high HCO3-). The
lungs compensate by hypoventilating (increasing PaCO2) to buffer the
alkalosis. However, the PaCO2 is 48, which is only a slight increase
(expected compensation is PaCO2 rises 0.7 mmHg for every 1 mEq/L rise in
HCO3-). This indicates partial compensation. The renal compensation
(excreting HCO3-) takes days to occur, not hours.
Domain 3: Neuropathophysiology
Q3: A patient with a new diagnosis of Parkinson’s disease is started on
carbidopa-levodopa. The patient asks why they also need carbidopa. What
is the best pathophysiological explanation?
A) Carbidopa prevents the peripheral breakdown of dopamine, allowing
more levodopa to cross the blood-brain barrier.
B) Carbidopa acts as a direct dopamine agonist in the substantia nigra.
C) Carbidopa prevents the central metabolism of dopamine to DOPAC.
D) Carbidopa stimulates the release of acetylcholine in the striatum.
Answer: A) Carbidopa prevents the peripheral breakdown of
dopamine, allowing more levodopa to cross the blood-brain barrier.
Rationale: Levodopa is the precursor to dopamine. Carbidopa is
,a peripheral decarboxylase inhibitor that does not cross the blood-brain
barrier. It inhibits the enzyme that converts levodopa to
dopamine outside the CNS, which reduces peripheral side effects (nausea)
and increases the amount of levodopa that reaches the brain.
Domain 4: Cardiovascular Pathophysiology
Q4: A 68-year-old with a history of hypertension presents with acute onset
of severe, tearing chest pain radiating to the back. Blood pressure is
160/100 mmHg in the right arm and 100/70 mmHg in the left arm. A CT
angiogram reveals a dissection of the ascending aorta. What is the primary
pathophysiological event that led to this condition, and what is the
immediate goal of treatment?
A) Atherosclerotic plaque rupture; immediate surgical repair
B) Weakening of the medial layer (cystic medial degeneration); immediate
blood pressure reduction (MAP < 105)
C) Inflammation of the vasa vasorum; immediate anticoagulation
D) Calcification of the aortic valve; immediate beta-blockade
Answer: B) Weakening of the medial layer (cystic medial
degeneration); immediate blood pressure reduction (MAP < 105)
Rationale: Aortic dissection is caused by a tear in the intima, allowing
blood to enter the medial layer of the aortic wall. Hypertension accelerates
this by increasing shear stress. The immediate goal for Type A dissections
(ascending aorta) is emergency surgical repair, but the immediate medical
goal before and after surgery is aggressive blood pressure control (reduce
MAP to 100-105 mmHg and heart rate to <60) to prevent propagation of
the dissection.
Domain 5: Pulmonary Pathophysiology
, Q5: A patient with COPD (chronic bronchitis phenotype) has chronic
hypoxemia and hypercapnia. Which of the following best explains the
blunted respiratory drive seen in this patient?
A) Peripheral chemoreceptors become desensitized to low O2.
B) Central chemoreceptors become desensitized to high CO2.
C) The Hering-Breuer reflex is activated, inhibiting inspiration.
D) Ventilation-perfusion (V/Q) mismatch is corrected by pulmonary
vasoconstriction.
Answer: B) Central chemoreceptors become desensitized to high CO2.
Rationale: In chronic hypercapnia (CO2 retainers), the central
chemoreceptors in the medulla become desensitized to elevated CO2/H+
levels. The primary drive to breathe shifts from CO2 to hypoxemia (low O2),
which is sensed by the peripheral chemoreceptors (carotid and aortic
bodies). Giving these patients high-flow oxygen can remove their hypoxic
drive, leading to respiratory depression and apnea.
Domain 6: Renal Pathophysiology
Q6: A patient with diabetic nephropathy develops nephrotic syndrome.
Which of the following findings is most directly responsible for the
generalized edema seen in this patient?
A) Increased hydrostatic pressure in the glomerular capillaries
B) Decreased plasma oncotic pressure due to massive proteinuria
C) Increased aldosterone secretion leading to sodium retention
D) Decreased glomerular filtration rate leading to fluid overload
Answer: B) Decreased plasma oncotic pressure due to massive
proteinuria
Rationale: Nephrotic syndrome is characterized by heavy proteinuria
(>3.5g/day), hypoalbuminemia, and edema. The loss of albumin in the
urine lowers plasma oncotic pressure, which reduces the reabsorption of
fluid from the interstitial space back into the capillaries, leading to
