1|Page
#PATHOPHYSIOLOGY: THE BIOLOGIC BASIS
FOR DISEASE IN ADULTS AND CHILDREN##
COMPLETE PRACTICE QUESTION BANK – 150+
QUESTIONS WITH ANSWERS & RATIONALES
**Target Audience:** BSN, MSN, DNP, NP, PA, Medical Students
**Textbook Alignment:** McCance & Huether (9th/10th Editions)
**Updated:** 2026-2027 – Includes current understanding of cellular
biology, genetics, immunology, and systemic pathophysiology
## SECTION 1: CELLULAR BIOLOGY & ADAPTATION
**Question 1**
A patient with chronic anemia develops an enlarged heart with thickened
ventricular walls. This cellular adaptation is best described as:
A) Hyperplasia
B) Metaplasia
C) Hypertrophy
D) Dysplasia
**Answer: C – Hypertrophy**
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**Rationale:** Hypertrophy is an increase in cell size leading to organ
enlargement. In chronic anemia, the heart works harder to pump
oxygenated blood, resulting in increased myocyte size (cardiac
hypertrophy). Hyperplasia is increased cell number; metaplasia is one
adult cell type replacing another; dysplasia is disordered cell growth.
---
**Question 2**
A pathologist examines a cervical biopsy and notes cells that vary in size
and shape with hyperchromatic nuclei but no invasion through the
basement membrane. This finding is called:
A) Anaplasia
B) Dysplasia
C) Neoplasia
D) Metaplasia
**Answer: B – Dysplasia**
**Rationale:** Dysplasia is disordered cellular growth characterized by
loss of uniformity, pleomorphism (variation in size/shape), and
hyperchromatic nuclei. Dysplasia is often premalignant but reversible if
the inciting cause is removed. Anaplasia is severe dysplasia with loss of
differentiation (characteristic of malignant tumors).
,3|Page
---
**Question 3**
Reactive oxygen species (free radicals) cause cellular injury primarily
by:
A) Increasing ATP production
B) Lipid peroxidation of cell membranes, protein oxidation, and DNA
damage
C) Activating lysosomal enzymes
D) Decreasing intracellular calcium
**Answer: B – Lipid peroxidation of cell membranes, protein oxidation,
and DNA damage**
**Rationale:** Free radicals (ROS) have unpaired electrons and cause
oxidative stress by damaging cell membranes (lipid peroxidation),
oxidizing proteins (inactivating enzymes), and damaging DNA
(mutations). This contributes to aging, ischemia-reperfusion injury, and
many diseases.
---
**Question 4**
, 4|Page
A cell undergoing necrosis differs from apoptosis in that necrosis is
characterized by:
A) Cell shrinkage and nuclear fragmentation
B) Inflammation in surrounding tissue
C) Phagocytosis of apoptotic bodies by neighboring cells
D) ATP-dependent programmed cell death
**Answer: B – Inflammation in surrounding tissue**
**Rationale:** Necrosis is pathologic cell death caused by injury
(hypoxia, toxins, trauma). It results in cell swelling, membrane rupture,
release of cellular contents, and inflammation. Apoptosis is programmed
cell death (physiologic), with cell shrinkage, nuclear fragmentation, and
no inflammation.
---
**Question 5**
A patient with chronic gastroesophageal reflux disease (GERD) has the
normal squamous epithelium of the lower esophagus replaced by
columnar epithelium. This change is called:
A) Barrett esophagus (metaplasia)
B) Esophageal dysplasia
C) Esophageal carcinoma in situ
#PATHOPHYSIOLOGY: THE BIOLOGIC BASIS
FOR DISEASE IN ADULTS AND CHILDREN##
COMPLETE PRACTICE QUESTION BANK – 150+
QUESTIONS WITH ANSWERS & RATIONALES
**Target Audience:** BSN, MSN, DNP, NP, PA, Medical Students
**Textbook Alignment:** McCance & Huether (9th/10th Editions)
**Updated:** 2026-2027 – Includes current understanding of cellular
biology, genetics, immunology, and systemic pathophysiology
## SECTION 1: CELLULAR BIOLOGY & ADAPTATION
**Question 1**
A patient with chronic anemia develops an enlarged heart with thickened
ventricular walls. This cellular adaptation is best described as:
A) Hyperplasia
B) Metaplasia
C) Hypertrophy
D) Dysplasia
**Answer: C – Hypertrophy**
,2|Page
**Rationale:** Hypertrophy is an increase in cell size leading to organ
enlargement. In chronic anemia, the heart works harder to pump
oxygenated blood, resulting in increased myocyte size (cardiac
hypertrophy). Hyperplasia is increased cell number; metaplasia is one
adult cell type replacing another; dysplasia is disordered cell growth.
---
**Question 2**
A pathologist examines a cervical biopsy and notes cells that vary in size
and shape with hyperchromatic nuclei but no invasion through the
basement membrane. This finding is called:
A) Anaplasia
B) Dysplasia
C) Neoplasia
D) Metaplasia
**Answer: B – Dysplasia**
**Rationale:** Dysplasia is disordered cellular growth characterized by
loss of uniformity, pleomorphism (variation in size/shape), and
hyperchromatic nuclei. Dysplasia is often premalignant but reversible if
the inciting cause is removed. Anaplasia is severe dysplasia with loss of
differentiation (characteristic of malignant tumors).
,3|Page
---
**Question 3**
Reactive oxygen species (free radicals) cause cellular injury primarily
by:
A) Increasing ATP production
B) Lipid peroxidation of cell membranes, protein oxidation, and DNA
damage
C) Activating lysosomal enzymes
D) Decreasing intracellular calcium
**Answer: B – Lipid peroxidation of cell membranes, protein oxidation,
and DNA damage**
**Rationale:** Free radicals (ROS) have unpaired electrons and cause
oxidative stress by damaging cell membranes (lipid peroxidation),
oxidizing proteins (inactivating enzymes), and damaging DNA
(mutations). This contributes to aging, ischemia-reperfusion injury, and
many diseases.
---
**Question 4**
, 4|Page
A cell undergoing necrosis differs from apoptosis in that necrosis is
characterized by:
A) Cell shrinkage and nuclear fragmentation
B) Inflammation in surrounding tissue
C) Phagocytosis of apoptotic bodies by neighboring cells
D) ATP-dependent programmed cell death
**Answer: B – Inflammation in surrounding tissue**
**Rationale:** Necrosis is pathologic cell death caused by injury
(hypoxia, toxins, trauma). It results in cell swelling, membrane rupture,
release of cellular contents, and inflammation. Apoptosis is programmed
cell death (physiologic), with cell shrinkage, nuclear fragmentation, and
no inflammation.
---
**Question 5**
A patient with chronic gastroesophageal reflux disease (GERD) has the
normal squamous epithelium of the lower esophagus replaced by
columnar epithelium. This change is called:
A) Barrett esophagus (metaplasia)
B) Esophageal dysplasia
C) Esophageal carcinoma in situ
