1
HESI Pathophysiology Test Bank 2025–2026 | 120
Verified Questions & Answers | 100% Correct, Real
Exam-Based, Guaranteed Pass
1. A patient with left-sided heart failure presents with pulmonary
crackles and dyspnea on exertion. What pathophysiological mechanism
is most responsible for these symptoms?
A. Systemic venous congestion
B. Decreased pulmonary vascular resistance
C. Blood backup into the pulmonary circulation
D. Coronary artery obstruction
Correct Answer: C. Blood backup into the pulmonary circulation
Rationale:
In left-sided heart failure, the left ventricle loses its ability to effectively
, 2
pump blood forward into systemic circulation. As a result, blood begins to
back up into the left atrium and subsequently into the pulmonary veins and
capillaries. This increase in pulmonary venous pressure leads to transudation
of fluid into the alveolar spaces, causing pulmonary edema. The patient may
experience dyspnea (especially on exertion), orthopnea, and auscultated
crackles in the lungs. This is a hallmark of left-sided heart failure. Option A
refers to right-sided heart failure, which causes systemic (not pulmonary)
congestion. Decreased pulmonary vascular resistance (B) would actually
reduce, not worsen, symptoms. D (coronary artery obstruction) can cause
myocardial infarction but is not the direct cause of pulmonary congestion in
this context.
2. A patient with chronic kidney disease (CKD) develops anemia. Which
pathophysiologic mechanism explains this condition?
A. Hemolysis due to uremic toxins
B. Decreased erythropoietin production
C. Iron malabsorption in the gut
D. Chronic blood loss through the urinary tract
Correct Answer: B. Decreased erythropoietin production
Rationale:
The kidneys play a critical role in the production of erythropoietin, a
hormone that stimulates the bone marrow to produce red blood cells. In
chronic kidney disease, especially in end-stage renal failure, the damaged
renal parenchyma is unable to secrete adequate erythropoietin. This results
in a normocytic, normochromic anemia due to decreased red blood cell
, 3
production. Although uremic toxins (A) and GI iron issues (C) may
contribute minimally, they are not the primary cause. Chronic urinary blood
loss (D) is not typical in CKD unless concurrent pathology exists. Thus,
decreased erythropoietin synthesis is the most direct and central mechanism
of CKD-related anemia.
3. A diabetic patient experiences polyuria, polydipsia, and polyphagia.
These classic symptoms are primarily caused by which pathophysiologic
process?
A. Cellular insulin hypersensitivity
B. Osmotic diuresis due to hyperglycemia
C. Decreased renin-angiotensin activity
D. Autoimmune beta-cell stimulation
Correct Answer: B. Osmotic diuresis due to hyperglycemia
Rationale:
In uncontrolled diabetes mellitus, elevated blood glucose exceeds the renal
threshold for glucose reabsorption, leading to glucosuria. The presence of
glucose in the urine increases the osmotic pressure in the renal tubules,
preventing water reabsorption and causing increased urinary output — a
process known as osmotic diuresis. This leads to dehydration, triggering
compensatory polydipsia (increased thirst). Meanwhile, the lack of cellular
glucose uptake (due to insulin deficiency or resistance) signals the body to
increase hunger, resulting in polyphagia. Cellular insulin hypersensitivity
(A) does not cause these symptoms. Option C is unrelated, and D is
, 4
incorrect — autoimmune destruction, not stimulation, is characteristic of
Type 1 diabetes.
4. Which physiologic change most contributes to the development of
ascites in a patient with cirrhosis?
A. Portal hypertension and hypoalbuminemia
B. Bile duct obstruction
C. Increased glomerular filtration rate
D. Excess aldosterone degradation
Correct Answer: A. Portal hypertension and hypoalbuminemia
Rationale:
In cirrhosis, liver scarring impairs blood flow through the portal vein,
leading to portal hypertension. This increases hydrostatic pressure in the
splanchnic circulation, pushing fluid into the peritoneal cavity.
Simultaneously, the liver’s reduced capacity to synthesize albumin results in
hypoalbuminemia, lowering plasma oncotic pressure. The combined effects
of increased hydrostatic pressure and decreased oncotic pressure favor fluid
leakage and accumulation in the abdomen — a process known as ascites.
Bile duct obstruction (B) contributes to jaundice, not ascites. An increased
GFR (C) would promote diuresis, not fluid retention. D is incorrect —
cirrhosis actually decreases aldosterone metabolism, leading to its buildup
and fluid retention.
HESI Pathophysiology Test Bank 2025–2026 | 120
Verified Questions & Answers | 100% Correct, Real
Exam-Based, Guaranteed Pass
1. A patient with left-sided heart failure presents with pulmonary
crackles and dyspnea on exertion. What pathophysiological mechanism
is most responsible for these symptoms?
A. Systemic venous congestion
B. Decreased pulmonary vascular resistance
C. Blood backup into the pulmonary circulation
D. Coronary artery obstruction
Correct Answer: C. Blood backup into the pulmonary circulation
Rationale:
In left-sided heart failure, the left ventricle loses its ability to effectively
, 2
pump blood forward into systemic circulation. As a result, blood begins to
back up into the left atrium and subsequently into the pulmonary veins and
capillaries. This increase in pulmonary venous pressure leads to transudation
of fluid into the alveolar spaces, causing pulmonary edema. The patient may
experience dyspnea (especially on exertion), orthopnea, and auscultated
crackles in the lungs. This is a hallmark of left-sided heart failure. Option A
refers to right-sided heart failure, which causes systemic (not pulmonary)
congestion. Decreased pulmonary vascular resistance (B) would actually
reduce, not worsen, symptoms. D (coronary artery obstruction) can cause
myocardial infarction but is not the direct cause of pulmonary congestion in
this context.
2. A patient with chronic kidney disease (CKD) develops anemia. Which
pathophysiologic mechanism explains this condition?
A. Hemolysis due to uremic toxins
B. Decreased erythropoietin production
C. Iron malabsorption in the gut
D. Chronic blood loss through the urinary tract
Correct Answer: B. Decreased erythropoietin production
Rationale:
The kidneys play a critical role in the production of erythropoietin, a
hormone that stimulates the bone marrow to produce red blood cells. In
chronic kidney disease, especially in end-stage renal failure, the damaged
renal parenchyma is unable to secrete adequate erythropoietin. This results
in a normocytic, normochromic anemia due to decreased red blood cell
, 3
production. Although uremic toxins (A) and GI iron issues (C) may
contribute minimally, they are not the primary cause. Chronic urinary blood
loss (D) is not typical in CKD unless concurrent pathology exists. Thus,
decreased erythropoietin synthesis is the most direct and central mechanism
of CKD-related anemia.
3. A diabetic patient experiences polyuria, polydipsia, and polyphagia.
These classic symptoms are primarily caused by which pathophysiologic
process?
A. Cellular insulin hypersensitivity
B. Osmotic diuresis due to hyperglycemia
C. Decreased renin-angiotensin activity
D. Autoimmune beta-cell stimulation
Correct Answer: B. Osmotic diuresis due to hyperglycemia
Rationale:
In uncontrolled diabetes mellitus, elevated blood glucose exceeds the renal
threshold for glucose reabsorption, leading to glucosuria. The presence of
glucose in the urine increases the osmotic pressure in the renal tubules,
preventing water reabsorption and causing increased urinary output — a
process known as osmotic diuresis. This leads to dehydration, triggering
compensatory polydipsia (increased thirst). Meanwhile, the lack of cellular
glucose uptake (due to insulin deficiency or resistance) signals the body to
increase hunger, resulting in polyphagia. Cellular insulin hypersensitivity
(A) does not cause these symptoms. Option C is unrelated, and D is
, 4
incorrect — autoimmune destruction, not stimulation, is characteristic of
Type 1 diabetes.
4. Which physiologic change most contributes to the development of
ascites in a patient with cirrhosis?
A. Portal hypertension and hypoalbuminemia
B. Bile duct obstruction
C. Increased glomerular filtration rate
D. Excess aldosterone degradation
Correct Answer: A. Portal hypertension and hypoalbuminemia
Rationale:
In cirrhosis, liver scarring impairs blood flow through the portal vein,
leading to portal hypertension. This increases hydrostatic pressure in the
splanchnic circulation, pushing fluid into the peritoneal cavity.
Simultaneously, the liver’s reduced capacity to synthesize albumin results in
hypoalbuminemia, lowering plasma oncotic pressure. The combined effects
of increased hydrostatic pressure and decreased oncotic pressure favor fluid
leakage and accumulation in the abdomen — a process known as ascites.
Bile duct obstruction (B) contributes to jaundice, not ascites. An increased
GFR (C) would promote diuresis, not fluid retention. D is incorrect —
cirrhosis actually decreases aldosterone metabolism, leading to its buildup
and fluid retention.
