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NSG 5140 Advanced Pathophysiology Final Exam Review South College (NSG5140) Questions And Well Graded Solutions With Rationales Updated

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Ace your exam with this high-yield study guide for South College NSG 5140 Advanced Pathophysiology. Features expert-verified multiple-choice questions with deep rationales covering cellular injury, DKA mechanisms, cardiovascular dysfunction, renal failure anemia, and hypersensitivity. Perfect for graduate-level nursing students looking to master core concepts, identify critical system gaps, and guarantee a passing score on the final exam. Download the ultimate NSG5140 preparation resource now.

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NSG 5140 Advanced Pathophysiology
Final Exam Review South College
(NSG5140) Questions And Well Graded
Solutions With Rationales Updated
2026 2027



Ace your exam with this high-yield study guide for South College NSG 5140 Advanced
Pathophysiology. Features expert-verified multiple-choice questions with deep rationales covering
cellular injury, DKA mechanisms, cardiovascular dysfunction, renal failure anemia, and
hypersensitivity. Perfect for graduate-level nursing students looking to master core concepts,
identify critical system gaps, and guarantee a passing score on the final exam. Download the
ultimate NSG5140 preparation resource now.




1. A patient with long-standing, untreated hypertension shows enlargement of the left
ventricle on an echocardiogram. What cellular adaptation is occurring?
A. Hyperplasia
B. Hypertrophy
C. Metaplasia
D. Dysplasia
Rationale: Hypertrophy is an increase in the size of individual cells, typically
triggered by an increased mechanical workload or stress, such as the heart pumping
against high systemic vascular resistance.
2. A tissue biopsy from a smoker's bronchus reveals that normal ciliated columnar
epithelial cells have been replaced by stratified squamous epithelial cells. What is
this adaptive process?
A. Anaplasia
B. Dysplasia
C. Metaplasia
D. Hyperplasia
Rationale: Metaplasia is the reversible replacement of one mature cell type by
another mature cell type, usually in response to chronic irritation or inflammation, like
cigarette smoke.
3. Which of the following processes is a regulated, programmed cellular death that
avoids spilling intracellular contents into the surrounding tissue, thereby preventing
inflammation?
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, A. Coagulative necrosis
B. Liquefactive necrosis
C. Apoptosis
D. Autolysis
Rationale: Apoptosis is an orderly, energy-dependent, programmed cell death
process where the cell breaks down into apoptotic bodies that are quietly
phagocytosed without triggering an inflammatory response.
4. During ischemic cell injury, what is the primary consequence of the decline in
mitochondrial ATP production?
A. Influx of potassium into the intracellular fluid
B. Failure of the sodium-potassium pump leading to cellular swelling
C. Decreased intracellular calcium concentration
D. Immediate activation of cellular protein synthesis
Rationale: Depleted ATP causes the Na+/K+ ATPase pump to shut down. Sodium
accumulates inside the cell, creating an osmotic gradient that pulls water into the
cytoplasm, resulting in acute cellular swelling.
5. A patient experiences an ischemic stroke. Which type of necrosis is uniquely
characteristic of hypoxic injury to the central nervous system?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Caseous necrosis
D. Fat necrosis
Rationale: Liquefactive necrosis occurs primarily in the brain and central nervous
system because glial cells and neurons contain large amounts of digestive hydrolytic
enzymes and lipids, transforming dead tissue into a liquid mass.
6. What form of necrosis is classically associated with tuberculosis infections in the
lungs, resulting in a soft, cheese-like appearance of the dead tissue?
A. Gangrenous necrosis
B. Liquefactive necrosis
C. Caseous necrosis
D. Coagulative necrosis
Rationale: Caseous necrosis combines elements of coagulative and liquefactive
necrosis. It is a hallmark of Mycobacterium tuberculosis infection, where dead cells
disintegrate but are not completely digested, leaving a crumbly appearance.
7. Breast enlargement during pregnancy due to hormonal stimulation is an example of
which type of cellular adaptation?
A. Pathologic hypertrophy
B. Pathologic hyperplasia
C. Physiologic hypertrophy
D. Physiologic hyperplasia
E. Both C and D
Rationale: Hormonal stimulation during pregnancy causes both an increase in cell
size (hypertrophy) and cell number (hyperplasia) in breast glandular tissue. Both are
physiologic adaptations to support lactation.
8. Free radicals cause cellular injury by damaging which critical intracellular
components?
A. Cell membranes, proteins, and DNA
B. Ribosomes and lysosomal enzymes only
C. Extracellular matrix fibers only
D. Golgi apparatus transport vesicles

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, Rationale: Free radicals are highly reactive, unstable atoms with unpaired electrons.
They cause oxidative stress, damaging cell membranes via lipid peroxidation,
altering proteins, and causing DNA strand breaks.
9. Which cellular adaptation is characterized by deranged cellular growth with abnormal
variations in size, shape, and organization, and is considered a precursor to
malignancy?
A. Metaplasia
B. Hyperplasia
C. Dysplasia
D. Atrophy
Rationale: Dysplasia represents an abnormal, atypical growth pattern. While it can
be reversible if the stimulus is removed, it is strongly recognized as a pre-cancerous
lesion requiring close surveillance.
10. When a cell undergoes hypoxic injury, what happens to the intracellular pH, and
why?
A. It increases due to bicarbonate retention
B. It increases due to ammonia production
C. It decreases due to anaerobic glycolysis and lactic acid accumulation
D. It remains unchanged due to cytosolic buffering
Rationale: In the absence of oxygen, cells switch from aerobic metabolism to
anaerobic glycolysis to generate ATP. This metabolic pathway produces lactic acid,
which releases hydrogen ions and lowers intracellular pH.
11. An individual with Klinefelter syndrome inherits which of the following chromosomal
compositions?
A. 45, X
B. 47, XY, +21
C. 47, XXY
D. 47, XYY
Rationale: Klinefelter syndrome is a genetic condition occurring in males who
possess an extra X chromosome, resulting in a 47, XXY karyotype, which impacts
testosterone production and fertility.
12. Which genetic term describes a situation where an individual carries a mutant gene
but does not display any clinical manifestations of the disease?
A. Variable expressivity
B. Reduced penetrance
C. Genomic imprinting
D. Autosomal recessive inheritance
Rationale: Penetrance refers to the percentage of individuals with a specific
genotype who express the expected phenotype. Reduced or incomplete penetrance
means some individuals inherit the mutation but never develop the disease.
13. What is the standard inheritance probability for a child to develop an autosomal
recessive disorder if both parents are asymptomatic carriers of the mutated gene?
A. 0%
B. 25%
C. 50%
D. 100%
Rationale: For autosomal recessive conditions, each parent provides one allele. If
both parents are heterozygous carriers (Aa), there is a 25% chance of an offspring
inheriting both mutant alleles (aa) and developing the disease.


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, 14. Which condition is a progressive neurodegenerative disorder inherited in an
autosomal dominant pattern, characterized by chorea and cognitive decline, typically
manifesting in adulthood?
A. Cystic fibrosis
B. Huntington disease
C. Duchenne muscular dystrophy
D. Tay-Sachs disease
Rationale: Huntington disease is an autosomal dominant disorder caused by a CAG
trinucleotide repeat expansion in the HTT gene. Symptoms typically present between
ages 30 and 50.
15. Why are males predominantly affected by X-linked recessive disorders, such as
Hemophilia A?
A. Males produce higher levels of circulating estrogens
B. Males are hemizygous and have only one X chromosome
C. The Y chromosome actively suppresses clotting factor genes
D. X-linked dominant traits cancel out recessive ones in males
Rationale: Males have one X and one Y chromosome (XY). Because they have only
a single copy of X-linked genes, a mutation in that single X chromosome will express
the disease fully, as there is no second X chromosome to carry a normal allele.
16. What term describes the clinical phenomenon where individuals with the exact same
disease-causing genetic mutation exhibit vastly different degrees of severity or
symptoms?
A. Incomplete penetrance
B. Variable expressivity
C. Genetic heterogeneity
D. Codominance
Rationale: Variable expressivity means that a genetic trait is expressed to different
degrees among individuals who carry the gene mutation, ranging from mild
subclinical features to severe illness.
17. Which chromosomal abnormality involves a piece of one chromosome breaking off
and attaching to a completely different, non-homologous chromosome?
A. Inversion
B. Deletion
C. Translocation
D. Nondisjunction
Rationale: Translocation is the interchanging of material between non-homologous
chromosomes. A classic clinical example is the Philadelphia chromosome
(translocation between chromosomes 9 and 22) in chronic myeloid leukemia.
18. What is the underlying chromosomal mechanism responsible for Down syndrome
(Trisomy 21)?
A. Robertsonian translocation
B. Nondisjunction during meiosis
C. Chromosomal inversion in somatic cells
D. Microdeletion of the short arm of chromosome 21
Rationale: Most cases of Down syndrome are caused by chromosomal
nondisjunction during maternal or paternal meiosis, where chromosomes fail to
separate properly, leaving the gamete with an extra copy of chromosome 21.
19. Which genetic disorder is caused by a mutation in the gene encoding fibrillin-1,
leading to skeletal abnormalities, cardiovascular defects like aortic aneurysms, and
ocular lens dislocation?

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