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NURS 6501 ADVANCED PATHOPHYSIOLOGY MIDTERM
EXAM 2026/2027 | Latest Comprehensive Assessment |
Verified Q&A | Pass Guaranteed - A+ Graded
Section 1: Cellular Biology & Genetics (Q1-12)
Q1. A 68-year-old male with a 40 pack-year smoking history presents with a lung
mass. Biopsy reveals cells with enlarged, hyperchromatic nuclei, loss of normal
polarity, and increased nuclear-to-cytoplasmic ratio but no invasion through the
basement membrane. This represents:
A. Invasive squamous cell carcinoma
B. Carcinoma in situ [CORRECT]
C. Dysplasia, low grade
D. Metaplasia
A1. Carcinoma in situ is defined by full-thickness cellular atypia with intact basement
membrane—no invasion. Invasive carcinoma would show basement membrane
breach. Dysplasia is partial-thickness atypia, and metaplasia is reversible cell type
change without atypia.
Correct Answer: B
Q2. A patient with chronic alcoholism develops hepatomegaly with fatty
accumulation in hepatocytes. This reversible cellular adaptation is called:
A. Hypertrophy
B. Hyperplasia
C. Steatosis (fatty change) [CORRECT]
D. Dysplasia
A2. Steatosis is the abnormal accumulation of triglycerides in parenchymal cells,
commonly seen in alcohol-induced liver injury. It is reversible with alcohol cessation.
,2
Hypertrophy is increased cell size, hyperplasia is increased cell number, and dysplasia
is disordered growth with atypia.
Correct Answer: C
Q3. A patient suffers cardiac arrest and is resuscitated after 8 minutes. Serum
troponin is elevated. Myocardial cells show eosinophilic cytoplasm, loss of nuclei, and
preserved cellular outlines. This pattern of cell death is:
A. Apoptosis
B. Coagulative necrosis [CORRECT]
C. Liquefactive necrosis
D. Caseous necrosis
A3. Coagulative necrosis is characteristic of ischemic injury in most solid organs
(except brain), featuring denatured proteins that preserve cellular architecture
temporarily. Apoptosis is programmed cell death without inflammation, liquefactive
necrosis occurs in brain infarcts and abscesses, and caseous necrosis is seen in
tuberculosis.
Correct Answer: B
Q4. A patient with severe sepsis develops multi-organ failure. Tissue biopsy shows
cell swelling, mitochondrial damage, and plasma membrane blebbing. The primary
mechanism of this reversible injury is:
A. Karyorrhexis
B. Cellular hypoxia leading to ATP depletion [CORRECT]
C. Activation of caspase cascade
D. Lysosomal enzyme release
A4. Reversible cellular injury from hypoxia initially manifests as ATP depletion
causing ion pump failure, cellular swelling, and organelle dysfunction. Karyorrhexis is
,3
irreversible (nuclear fragmentation), caspase activation defines apoptosis, and
lysosomal enzyme release occurs in irreversible injury.
Correct Answer: B
Q5. A newborn is diagnosed with cystic fibrosis. Both parents are asymptomatic
carriers. This inheritance pattern is:
A. Autosomal dominant
B. Autosomal recessive [CORRECT]
C. X-linked recessive
D. Mitochondrial
A5. Cystic fibrosis is an autosomal recessive disorder caused by CFTR gene mutations
on chromosome 7. Both parents must be carriers (heterozygotes), and offspring have
a 25% chance of expressing the disease. Autosomal dominant requires only one
mutated allele, X-linked affects males predominantly, and mitochondrial inheritance
is maternal.
Correct Answer: B
Q6. A 35-year-old male presents with progressive muscle weakness. Genetic testing
reveals a trinucleotide repeat expansion (CAG) in the HTT gene. His father was
diagnosed at age 42. This pattern demonstrates:
A. Genomic imprinting
B. Anticipation [CORRECT]
C. Variable expressivity
D. Incomplete penetrance
A6. Huntington disease demonstrates anticipation, where trinucleotide repeat
expansions increase in successive generations, causing earlier onset and more severe
disease. Genomic imprinting involves parent-of-origin gene silencing, variable
, 4
expressivity describes differing severity among individuals with the same mutation,
and incomplete penetrance means not all mutation carriers develop the disease.
Correct Answer: B
Q7. A female patient with no family history of hemophilia gives birth to an affected
son. Her father is unaffected. The most likely explanation is:
A. Autosomal dominant new mutation
B. X-linked recessive carrier mother [CORRECT]
C. Autosomal recessive inheritance
D. Mitochondrial inheritance
A7. Hemophilia A and B are X-linked recessive disorders. A carrier mother
(heterozygous for the mutation on one X chromosome) has a 50% chance of
transmitting the affected X to each son. An unaffected father cannot transmit an X-
linked disorder to sons. New mutations are rare compared to inherited carrier status.
Correct Answer: B
Q8. A tumor suppressor gene that, when mutated, contributes to uncontrolled cell
proliferation is:
A. BCL-2
B. RAS
C. TP53 [CORRECT]
D. HER2/neu
A8. TP53 (p53) is the guardian of the genome, a tumor suppressor that arrests the
cell cycle and initiates apoptosis in response to DNA damage. BCL-2 is an anti-
apoptotic oncogene, RAS is a proto-oncogene involved in signal transduction, and
HER2/neu is a growth factor receptor oncogene.
Correct Answer: C
NURS 6501 ADVANCED PATHOPHYSIOLOGY MIDTERM
EXAM 2026/2027 | Latest Comprehensive Assessment |
Verified Q&A | Pass Guaranteed - A+ Graded
Section 1: Cellular Biology & Genetics (Q1-12)
Q1. A 68-year-old male with a 40 pack-year smoking history presents with a lung
mass. Biopsy reveals cells with enlarged, hyperchromatic nuclei, loss of normal
polarity, and increased nuclear-to-cytoplasmic ratio but no invasion through the
basement membrane. This represents:
A. Invasive squamous cell carcinoma
B. Carcinoma in situ [CORRECT]
C. Dysplasia, low grade
D. Metaplasia
A1. Carcinoma in situ is defined by full-thickness cellular atypia with intact basement
membrane—no invasion. Invasive carcinoma would show basement membrane
breach. Dysplasia is partial-thickness atypia, and metaplasia is reversible cell type
change without atypia.
Correct Answer: B
Q2. A patient with chronic alcoholism develops hepatomegaly with fatty
accumulation in hepatocytes. This reversible cellular adaptation is called:
A. Hypertrophy
B. Hyperplasia
C. Steatosis (fatty change) [CORRECT]
D. Dysplasia
A2. Steatosis is the abnormal accumulation of triglycerides in parenchymal cells,
commonly seen in alcohol-induced liver injury. It is reversible with alcohol cessation.
,2
Hypertrophy is increased cell size, hyperplasia is increased cell number, and dysplasia
is disordered growth with atypia.
Correct Answer: C
Q3. A patient suffers cardiac arrest and is resuscitated after 8 minutes. Serum
troponin is elevated. Myocardial cells show eosinophilic cytoplasm, loss of nuclei, and
preserved cellular outlines. This pattern of cell death is:
A. Apoptosis
B. Coagulative necrosis [CORRECT]
C. Liquefactive necrosis
D. Caseous necrosis
A3. Coagulative necrosis is characteristic of ischemic injury in most solid organs
(except brain), featuring denatured proteins that preserve cellular architecture
temporarily. Apoptosis is programmed cell death without inflammation, liquefactive
necrosis occurs in brain infarcts and abscesses, and caseous necrosis is seen in
tuberculosis.
Correct Answer: B
Q4. A patient with severe sepsis develops multi-organ failure. Tissue biopsy shows
cell swelling, mitochondrial damage, and plasma membrane blebbing. The primary
mechanism of this reversible injury is:
A. Karyorrhexis
B. Cellular hypoxia leading to ATP depletion [CORRECT]
C. Activation of caspase cascade
D. Lysosomal enzyme release
A4. Reversible cellular injury from hypoxia initially manifests as ATP depletion
causing ion pump failure, cellular swelling, and organelle dysfunction. Karyorrhexis is
,3
irreversible (nuclear fragmentation), caspase activation defines apoptosis, and
lysosomal enzyme release occurs in irreversible injury.
Correct Answer: B
Q5. A newborn is diagnosed with cystic fibrosis. Both parents are asymptomatic
carriers. This inheritance pattern is:
A. Autosomal dominant
B. Autosomal recessive [CORRECT]
C. X-linked recessive
D. Mitochondrial
A5. Cystic fibrosis is an autosomal recessive disorder caused by CFTR gene mutations
on chromosome 7. Both parents must be carriers (heterozygotes), and offspring have
a 25% chance of expressing the disease. Autosomal dominant requires only one
mutated allele, X-linked affects males predominantly, and mitochondrial inheritance
is maternal.
Correct Answer: B
Q6. A 35-year-old male presents with progressive muscle weakness. Genetic testing
reveals a trinucleotide repeat expansion (CAG) in the HTT gene. His father was
diagnosed at age 42. This pattern demonstrates:
A. Genomic imprinting
B. Anticipation [CORRECT]
C. Variable expressivity
D. Incomplete penetrance
A6. Huntington disease demonstrates anticipation, where trinucleotide repeat
expansions increase in successive generations, causing earlier onset and more severe
disease. Genomic imprinting involves parent-of-origin gene silencing, variable
, 4
expressivity describes differing severity among individuals with the same mutation,
and incomplete penetrance means not all mutation carriers develop the disease.
Correct Answer: B
Q7. A female patient with no family history of hemophilia gives birth to an affected
son. Her father is unaffected. The most likely explanation is:
A. Autosomal dominant new mutation
B. X-linked recessive carrier mother [CORRECT]
C. Autosomal recessive inheritance
D. Mitochondrial inheritance
A7. Hemophilia A and B are X-linked recessive disorders. A carrier mother
(heterozygous for the mutation on one X chromosome) has a 50% chance of
transmitting the affected X to each son. An unaffected father cannot transmit an X-
linked disorder to sons. New mutations are rare compared to inherited carrier status.
Correct Answer: B
Q8. A tumor suppressor gene that, when mutated, contributes to uncontrolled cell
proliferation is:
A. BCL-2
B. RAS
C. TP53 [CORRECT]
D. HER2/neu
A8. TP53 (p53) is the guardian of the genome, a tumor suppressor that arrests the
cell cycle and initiates apoptosis in response to DNA damage. BCL-2 is an anti-
apoptotic oncogene, RAS is a proto-oncogene involved in signal transduction, and
HER2/neu is a growth factor receptor oncogene.
Correct Answer: C
