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NSG 120 Midterm Exam – Pathophysiology | Herzing University | Complete Study Guide

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This document contains a comprehensive study guide for the NSG 120 Midterm Exam in Pathophysiology at Herzing University. It covers foundational pathophysiology concepts, cellular processes, disease mechanisms, inflammation, immune responses, and alterations in normal body function. The material is structured to support focused review and preparation for the NSG 120 midterm examination.

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NSG 120 Midterm Exam - Pathophysiology
Complete Study Guide (Herzing University)
• SECTION 1: CELLULAR ADAPTATION, INJURY & DEATH (Q1–Q15)

Q1: A weightlifter's biceps enlarge after months of resistance training. At the cellular level,
this adaptation is defined as:

A. Hyperplasia—increased cell number

B. Hypertrophy—increased cell size

C. Metaplasia—replacement of one cell type by another

D. Dysplasia—disordered cell maturation

Correct Answer: B

Rationale: Skeletal muscle responds to increased workload by enlarging existing fibers
(hypertrophy) because muscle cells have limited ability to divide. Hyperplasia (A) occurs only
in mitotically capable tissues.

Q2: During lactation, breast tissue enlarges primarily through an increase in the number of
glandular cells. This process is:

A. Hypertrophy

B. Atrophy

C. Hyperplasia

D. Apoptosis

Correct Answer: C

Rationale: Estrogen and progesterone stimulation during pregnancy drives glandular cell
division (hyperplasia) in preparation for milk production. Hypertrophy (A) also contributes,
but the question specifies increased cell NUMBER.

Q3: A patient's arm is immobilized in a cast for 6 weeks. After removal, the arm appears
thinner due to reduced muscle cell size. This change is:

A. Hypertrophy from overuse

B. Atrophy from disuse

,C. Metaplasia from pressure

D. Dysplasia from ischemia

Correct Answer: B

Rationale: Disuse atrophy is a decrease in cell size from reduced workload, denervation, or
immobilization and is reversible with activity. It does not involve cell death or replacement of
cell types.

Q4: A 40-year smoker's tracheal biopsy shows ciliated columnar epithelium replaced by
stratified squamous epithelium. This reversible protective change is:

A. Dysplasia

B. Metaplasia

C. Hyperplasia

D. Necrosis

Correct Answer: B

Rationale: Chronic irritation from smoke converts the fragile ciliated columnar epithelium to
tougher squamous epithelium (metaplasia). It remains reversible if the irritant is removed but
increases vulnerability if it progresses to dysplasia.

Q5: A pathologist examining cervical tissue notes cells with enlarged, hyperchromatic nuclei
and loss of the normal orderly maturation from basal to surface layer, but the basement
membrane is intact. The best interpretation is:

A. Benign metaplasia requiring no follow-up

B. Dysplasia—a precancerous change

C. Physiologic hypertrophy

D. Coagulative necrosis

Correct Answer: B

Rationale: Disorderly maturation with nuclear atypia confined above an intact basement
membrane defines dysplasia, which is precancerous and requires surveillance. Metaplasia (A)
shows orderly replacement without atypia.

Q6: Which is an example of PATHOLOGIC hyperplasia?

A. Endometrial thickening during a normal menstrual cycle

,B. Callus formation on the palms with manual labor

C. Endometrial thickening from prolonged unopposed estrogen stimulation

D. Breast enlargement during puberty

Correct Answer: C

Rationale: Unopposed estrogen stimulation drives abnormal endometrial proliferation—a
pathologic hyperplasia that increases endometrial cancer risk. Options A, B, and D are normal
physiologic responses to hormonal or mechanical stimuli.

Q7: Necrosis is best defined as:

A. Programmed, energy-dependent cell suicide

B. Unregulated cell death from injury, with membrane rupture and inflammation

C. An ordered developmental process removing vestigial structures

D. Reversible shrinkage of the cytoplasm

Correct Answer: B

Rationale: Necrosis is accidental, uncontrolled cell death from ischemia, toxins, or trauma,
featuring ATP failure, membrane disruption, and an inflammatory response. Programmed,
non-inflammatory death (A, C) describes apoptosis.

Q8: A cytotoxic T lymphocyte recognizes a virally infected cell and triggers its orderly self-
destruction, which the neighboring tissue tolerates without inflammation. This mechanism is:

A. Necrosis

B. Apoptosis

C. Caseous degeneration

D. Gangrene

Correct Answer: B

Rationale: Virus-infected cells are eliminated by apoptosis—caspase-mediated, energy-
dependent death with cell shrinkage and apoptotic body formation that does not provoke
inflammation. Necrosis (A) would spill contents and inflame surrounding tissue.

Q9: Which feature is common to BOTH apoptosis and necrosis?

A. An inflammatory infiltrate surrounding the dead cells

, B. Eventual loss of membrane integrity and cell death

C. Requirement for intact ATP stores

D. Rounded, shrunken cell morphology with intact membranes

Correct Answer: B

Rationale: Both processes end in cell death, though by different routes. Inflammation (A)
occurs only with necrosis; ATP dependence (C) and membrane integrity (D) characterize only
apoptosis—late in necrosis membranes do rupture, which is why B is correct.

Q10: A patient at high altitude has reduced arterial oxygen content but normal blood flow.
This state is best described as:

A. Ischemia

B. Hypoxia without ischemia

C. Anoxia with infarction

D. Hyperperfusion

Correct Answer: B

Rationale: Hypoxia is reduced oxygen supply to tissues (here from low inspired oxygen) and
can occur with intact perfusion, as in anemia or high altitude. Ischemia (A) is reduced blood
flow, which also deprives tissues of nutrients and impairs waste removal.

Q11: An overdose of acetaminophen overwhelms hepatic glutathione, allowing a toxic
metabolite to generate free radicals that destroy hepatocytes. This illustrates injury by:

A. Osmotic imbalance

B. Free radical (chemical) injury

C. Hypothermic damage

D. Antibody-mediated attack

Correct Answer: B

Rationale: Acetaminophen's metabolite NAPQI produces reactive oxygen species that
peroxidize membrane lipids—classic free radical (chemical) injury, causing centrilobular
hepatic necrosis. N-acetylcysteine is the antidote because it replenishes glutathione.

Q12: Cellular swelling (hydropic change) in reversible injury results primarily from:

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