NSG 403 — Advanced Pathophysiology exam
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1. A patient with septic shock develops hypotension, tachycardia,
and elevated serum lactate. Which pathophysiologic process most
directly contributes to the elevated lactate level?
A. Increased hepatic glycogen synthesis
B. Decreased anaerobic metabolism
C. Increased anaerobic glycolysis due to impaired tissue oxygen
utilization
D. Increased renal bicarbonate production
Rationale: In septic shock, systemic inflammation, impaired perfusion,
and cellular dysfunction reduce effective oxygen utilization. Cells
increasingly rely on anaerobic glycolysis, producing excess lactate.
Elevated lactate is therefore an important marker of tissue
hypoperfusion and metabolic stress.
, 2. Which cellular adaptation occurs when a tissue is exposed to
chronic increased workload?
A. Atrophy
B. Metaplasia
C. Dysplasia
D. Hypertrophy
Rationale: Hypertrophy is an increase in cell size caused by increased
functional demand. Cardiac myocytes commonly undergo hypertrophy
in response to chronic pressure overload, such as hypertension.
Hyperplasia involves an increase in cell number rather than cell size.
3. A patient with chronic obstructive pulmonary disease develops
chronic respiratory acidosis. Which compensatory response is
expected?
A. Decreased renal hydrogen ion secretion
B. Decreased bicarbonate reabsorption
C. Increased renal bicarbonate retention
D. Increased respiratory rate as the primary compensation
Rationale: Chronic respiratory acidosis results from persistent carbon
dioxide retention. The kidneys compensate by increasing hydrogen ion
secretion and retaining bicarbonate, thereby helping buffer the excess
,acid. Renal compensation develops more slowly than respiratory
compensation.
4. Which mechanism is primarily responsible for edema associated
with congestive heart failure?
A. Decreased capillary hydrostatic pressure
B. Increased plasma oncotic pressure
C. Increased capillary hydrostatic pressure
D. Increased lymphatic drainage
Rationale: Heart failure increases venous pressure, which raises
capillary hydrostatic pressure. This favors movement of fluid from the
intravascular space into the interstitial space, producing edema.
Reduced cardiac output also activates sodium- and water-retaining
mechanisms that worsen fluid accumulation.
5. A patient with nephrotic syndrome develops generalized edema.
Which abnormality is most directly responsible?
A. Increased serum albumin
B. Increased plasma oncotic pressure
C. Decreased plasma oncotic pressure from hypoalbuminemia
D. Increased erythropoietin production
, Rationale: Nephrotic syndrome causes substantial urinary protein loss,
particularly albumin. Low serum albumin decreases plasma colloid
oncotic pressure, allowing fluid to move into the interstitial space and
causing generalized edema.
6. Which inflammatory mediator is primarily responsible for
vasodilation and increased vascular permeability during acute
inflammation?
A. Erythropoietin
B. Insulin
C. Histamine
D. Albumin
Rationale: Histamine is released primarily by mast cells during acute
inflammation. It causes arteriolar vasodilation and increases venular
permeability, allowing plasma proteins and fluid to enter tissues.
These effects contribute to redness, warmth, swelling, and pain.
7. A patient develops disseminated intravascular coagulation during
severe sepsis. Which pathophysiologic process characterizes DIC?
A. Isolated platelet destruction without coagulation activation
B. Complete absence of clotting factor activation
C. Widespread coagulation activation with consumption of platelets
Questions and Correct Answers (Verified
Answers) Plus Rationale 2027 Q&A| Instant
Download Pdf
1. A patient with septic shock develops hypotension, tachycardia,
and elevated serum lactate. Which pathophysiologic process most
directly contributes to the elevated lactate level?
A. Increased hepatic glycogen synthesis
B. Decreased anaerobic metabolism
C. Increased anaerobic glycolysis due to impaired tissue oxygen
utilization
D. Increased renal bicarbonate production
Rationale: In septic shock, systemic inflammation, impaired perfusion,
and cellular dysfunction reduce effective oxygen utilization. Cells
increasingly rely on anaerobic glycolysis, producing excess lactate.
Elevated lactate is therefore an important marker of tissue
hypoperfusion and metabolic stress.
, 2. Which cellular adaptation occurs when a tissue is exposed to
chronic increased workload?
A. Atrophy
B. Metaplasia
C. Dysplasia
D. Hypertrophy
Rationale: Hypertrophy is an increase in cell size caused by increased
functional demand. Cardiac myocytes commonly undergo hypertrophy
in response to chronic pressure overload, such as hypertension.
Hyperplasia involves an increase in cell number rather than cell size.
3. A patient with chronic obstructive pulmonary disease develops
chronic respiratory acidosis. Which compensatory response is
expected?
A. Decreased renal hydrogen ion secretion
B. Decreased bicarbonate reabsorption
C. Increased renal bicarbonate retention
D. Increased respiratory rate as the primary compensation
Rationale: Chronic respiratory acidosis results from persistent carbon
dioxide retention. The kidneys compensate by increasing hydrogen ion
secretion and retaining bicarbonate, thereby helping buffer the excess
,acid. Renal compensation develops more slowly than respiratory
compensation.
4. Which mechanism is primarily responsible for edema associated
with congestive heart failure?
A. Decreased capillary hydrostatic pressure
B. Increased plasma oncotic pressure
C. Increased capillary hydrostatic pressure
D. Increased lymphatic drainage
Rationale: Heart failure increases venous pressure, which raises
capillary hydrostatic pressure. This favors movement of fluid from the
intravascular space into the interstitial space, producing edema.
Reduced cardiac output also activates sodium- and water-retaining
mechanisms that worsen fluid accumulation.
5. A patient with nephrotic syndrome develops generalized edema.
Which abnormality is most directly responsible?
A. Increased serum albumin
B. Increased plasma oncotic pressure
C. Decreased plasma oncotic pressure from hypoalbuminemia
D. Increased erythropoietin production
, Rationale: Nephrotic syndrome causes substantial urinary protein loss,
particularly albumin. Low serum albumin decreases plasma colloid
oncotic pressure, allowing fluid to move into the interstitial space and
causing generalized edema.
6. Which inflammatory mediator is primarily responsible for
vasodilation and increased vascular permeability during acute
inflammation?
A. Erythropoietin
B. Insulin
C. Histamine
D. Albumin
Rationale: Histamine is released primarily by mast cells during acute
inflammation. It causes arteriolar vasodilation and increases venular
permeability, allowing plasma proteins and fluid to enter tissues.
These effects contribute to redness, warmth, swelling, and pain.
7. A patient develops disseminated intravascular coagulation during
severe sepsis. Which pathophysiologic process characterizes DIC?
A. Isolated platelet destruction without coagulation activation
B. Complete absence of clotting factor activation
C. Widespread coagulation activation with consumption of platelets
