NSG 530 Advanced Pathophysiology Exam
Questions and Answers
Question 1
A patient presents with wide-set eyes, "parrot beak" nose, low-set ears, and receding
chin. What is the renal manifestation associated with this presentation?
A) Potter syndrome
B) Polycystic kidney disease
C) Infundibular stenosis
D) Megacalycosis
Correct Answer
Potter syndrome
Question 1: A patient with chronic hypertension demonstrates left ventricular
hypertrophy on echocardiogram. Which cellular adaptation BEST explains this
finding?
A. Hyperplasia
B. Metaplasia
C. Hypertrophy
D. Dysplasia
CORRECT ANSWER: C. Hypertrophy
Rationale: Hypertrophy is an increase in cell size in response to increased workload
or stress. In chronic hypertension, the left ventricle undergoes hypertrophy to
compensate for increased afterload. Hyperplasia (A) is an increase in cell number.
Metaplasia (B) is replacement of one differentiated cell type with another. Dysplasia
(D) is abnormal cell growth with loss of differentiation, often precancerous.
Question 2: During the inflammatory response, which chemical mediator is
PRIMARILY responsible for increased vascular permeability and pain?
A. Histamine
B. Bradykinin
C. Prostaglandin E2
D. Leukotriene B4
CORRECT ANSWER: B. Bradykinin
Page 1 of 258
, Rationale: Bradykinin is a potent vasodilator that increases vascular permeability
and directly stimulates pain receptors. Histamine (A) causes early vasodilation and
Page 2 of 258
,permeability but is less associated with pain. Prostaglandin E2 (C) mediates pain and
fever but has less effect on permeability. Leukotriene B4 (D) is primarily chemotactic
for neutrophils.
Question 3: A patient with systemic lupus erythematosus (SLE) develops proteinuria
and elevated serum creatinine. Which pathophysiologic mechanism BEST explains
the renal involvement?
A. Direct bacterial infection of glomeruli
B. Immune complex deposition in glomerular basement membrane
C. Ischemic injury from renal artery stenosis
D. Tubular necrosis from nephrotoxic medications
CORRECT ANSWER: B. Immune complex deposition in glomerular basement
membrane
Rationale: SLE is an autoimmune disease characterized by production of
autoantibodies that form immune complexes. These complexes deposit in
glomeruli, activating complement and causing inflammation (lupus nephritis). This
leads to proteinuria, hematuria, and impaired renal function. Bacterial infection (A),
renal artery stenosis (C), and nephrotoxicity (D) are not primary mechanisms in SLE-
related renal disease.
Question 4: Which statement BEST describes the pathophysiology of type 1
diabetes mellitus?
A. Insulin resistance in peripheral tissues with compensatory hyperinsulinemia
B. Autoimmune destruction of pancreatic beta cells leading to absolute insulin
deficiency
C. Impaired incretin effect with relative insulin deficiency
D. Excess counterregulatory hormones causing insulin antagonism
CORRECT ANSWER: B. Autoimmune destruction of pancreatic beta cells leading
to absolute insulin deficiency
Rationale: Type 1 diabetes results from T-cell-mediated autoimmune destruction of
pancreatic beta cells, causing absolute insulin deficiency. Insulin resistance (A)
characterizes type 2 diabetes. Impaired incretin effect (C) contributes to type 2
pathophysiology. Excess counterregulatory hormones (D) may occur in stress-
induced hyperglycemia but is not the primary mechanism of type 1 diabetes.
Page 3 of 258
, Question 5: A patient with chronic obstructive pulmonary disease (COPD) develops
respiratory acidosis. Which compensatory mechanism would the nurse expect to
observe?
A. Increased renal excretion of bicarbonate
B. Increased renal reabsorption of bicarbonate
C. Hyperventilation to decrease PaCO2
D. Hypoventilation to increase PaO2
CORRECT ANSWER: B. Increased renal reabsorption of bicarbonate
Rationale: In chronic respiratory acidosis, the kidneys compensate by increasing
bicarbonate reabsorption and hydrogen ion excretion to raise serum pH. This
metabolic compensation takes 3-5 days to become fully effective. Increased
bicarbonate excretion (A) would worsen acidosis. Hyperventilation (C) is a
respiratory compensation for metabolic acidosis, not respiratory acidosis.
Hypoventilation (D) would worsen CO2 retention.
Question 6: Which pathophysiologic change is MOST characteristic of heart failure
with reduced ejection fraction (HFrEF)?
A. Increased myocardial contractility with decreased afterload
B. Ventricular remodeling with systolic dysfunction
C. Diastolic filling impairment with preserved contractility
D. Reduced preload with increased cardiac output
CORRECT ANSWER: B. Ventricular remodeling with systolic dysfunction
Rationale: HFrEF is characterized by impaired systolic function due to ventricular
remodeling (dilation, hypertrophy, fibrosis) following myocardial injury. This reduces
ejection fraction (<40%). Diastolic dysfunction with preserved contractility (C)
describes HFpEF. Increased contractility (A) and reduced preload (D) are not
characteristic of HFrEF pathophysiology.
Question 7: A patient with sickle cell disease experiences a vaso-occlusive crisis.
Which molecular event INITIATES the pathophysiologic cascade?
A. Oxidative damage to red blood cell membranes
B. Polymerization of hemoglobin S under low oxygen conditions
Page 4 of 258
Questions and Answers
Question 1
A patient presents with wide-set eyes, "parrot beak" nose, low-set ears, and receding
chin. What is the renal manifestation associated with this presentation?
A) Potter syndrome
B) Polycystic kidney disease
C) Infundibular stenosis
D) Megacalycosis
Correct Answer
Potter syndrome
Question 1: A patient with chronic hypertension demonstrates left ventricular
hypertrophy on echocardiogram. Which cellular adaptation BEST explains this
finding?
A. Hyperplasia
B. Metaplasia
C. Hypertrophy
D. Dysplasia
CORRECT ANSWER: C. Hypertrophy
Rationale: Hypertrophy is an increase in cell size in response to increased workload
or stress. In chronic hypertension, the left ventricle undergoes hypertrophy to
compensate for increased afterload. Hyperplasia (A) is an increase in cell number.
Metaplasia (B) is replacement of one differentiated cell type with another. Dysplasia
(D) is abnormal cell growth with loss of differentiation, often precancerous.
Question 2: During the inflammatory response, which chemical mediator is
PRIMARILY responsible for increased vascular permeability and pain?
A. Histamine
B. Bradykinin
C. Prostaglandin E2
D. Leukotriene B4
CORRECT ANSWER: B. Bradykinin
Page 1 of 258
, Rationale: Bradykinin is a potent vasodilator that increases vascular permeability
and directly stimulates pain receptors. Histamine (A) causes early vasodilation and
Page 2 of 258
,permeability but is less associated with pain. Prostaglandin E2 (C) mediates pain and
fever but has less effect on permeability. Leukotriene B4 (D) is primarily chemotactic
for neutrophils.
Question 3: A patient with systemic lupus erythematosus (SLE) develops proteinuria
and elevated serum creatinine. Which pathophysiologic mechanism BEST explains
the renal involvement?
A. Direct bacterial infection of glomeruli
B. Immune complex deposition in glomerular basement membrane
C. Ischemic injury from renal artery stenosis
D. Tubular necrosis from nephrotoxic medications
CORRECT ANSWER: B. Immune complex deposition in glomerular basement
membrane
Rationale: SLE is an autoimmune disease characterized by production of
autoantibodies that form immune complexes. These complexes deposit in
glomeruli, activating complement and causing inflammation (lupus nephritis). This
leads to proteinuria, hematuria, and impaired renal function. Bacterial infection (A),
renal artery stenosis (C), and nephrotoxicity (D) are not primary mechanisms in SLE-
related renal disease.
Question 4: Which statement BEST describes the pathophysiology of type 1
diabetes mellitus?
A. Insulin resistance in peripheral tissues with compensatory hyperinsulinemia
B. Autoimmune destruction of pancreatic beta cells leading to absolute insulin
deficiency
C. Impaired incretin effect with relative insulin deficiency
D. Excess counterregulatory hormones causing insulin antagonism
CORRECT ANSWER: B. Autoimmune destruction of pancreatic beta cells leading
to absolute insulin deficiency
Rationale: Type 1 diabetes results from T-cell-mediated autoimmune destruction of
pancreatic beta cells, causing absolute insulin deficiency. Insulin resistance (A)
characterizes type 2 diabetes. Impaired incretin effect (C) contributes to type 2
pathophysiology. Excess counterregulatory hormones (D) may occur in stress-
induced hyperglycemia but is not the primary mechanism of type 1 diabetes.
Page 3 of 258
, Question 5: A patient with chronic obstructive pulmonary disease (COPD) develops
respiratory acidosis. Which compensatory mechanism would the nurse expect to
observe?
A. Increased renal excretion of bicarbonate
B. Increased renal reabsorption of bicarbonate
C. Hyperventilation to decrease PaCO2
D. Hypoventilation to increase PaO2
CORRECT ANSWER: B. Increased renal reabsorption of bicarbonate
Rationale: In chronic respiratory acidosis, the kidneys compensate by increasing
bicarbonate reabsorption and hydrogen ion excretion to raise serum pH. This
metabolic compensation takes 3-5 days to become fully effective. Increased
bicarbonate excretion (A) would worsen acidosis. Hyperventilation (C) is a
respiratory compensation for metabolic acidosis, not respiratory acidosis.
Hypoventilation (D) would worsen CO2 retention.
Question 6: Which pathophysiologic change is MOST characteristic of heart failure
with reduced ejection fraction (HFrEF)?
A. Increased myocardial contractility with decreased afterload
B. Ventricular remodeling with systolic dysfunction
C. Diastolic filling impairment with preserved contractility
D. Reduced preload with increased cardiac output
CORRECT ANSWER: B. Ventricular remodeling with systolic dysfunction
Rationale: HFrEF is characterized by impaired systolic function due to ventricular
remodeling (dilation, hypertrophy, fibrosis) following myocardial injury. This reduces
ejection fraction (<40%). Diastolic dysfunction with preserved contractility (C)
describes HFpEF. Increased contractility (A) and reduced preload (D) are not
characteristic of HFrEF pathophysiology.
Question 7: A patient with sickle cell disease experiences a vaso-occlusive crisis.
Which molecular event INITIATES the pathophysiologic cascade?
A. Oxidative damage to red blood cell membranes
B. Polymerization of hemoglobin S under low oxygen conditions
Page 4 of 258
