Written by students who passed Immediately available after payment Read online or as PDF Wrong document? Swap it for free 4.6 TrustPilot
logo-home
Document preview thumbnail
Preview 4 out of 87 pages
Exam (elaborations)

NSG 5140 Advanced Pathophysiology Comprehensive Midterm Exam Review - Set 2 200 Multiple-Choice Questions with Answers and Rationales

Document preview thumbnail
Preview 4 out of 87 pages

NSG 5140 Advanced Pathophysiology midterm exam review featuring 400 multiple-choice questions with bolded answers and detailed rationales. Covers cellular adaptation, inflammation, immunity, genetics, fluid/electrolytes, cardiovascular, respiratory, renal, endocrine, GI, neurology, and hematology. Essential study resource for South College graduate nursing students. Master complex pathophysiologic concepts with clinical correlations and evidence-based explanations. Pass your midterm with confidence.

Content preview

1|Page



NSG 5140 Advanced Pathophysiology
Comprehensive Midterm Exam Review - Set
2 200 Multiple-Choice Questions with
Answers and Rationales



SECTION 1: CELLULAR ADAPTATION AND INJURY (Questions 1-
30)




Question 1: A 62-year-old male with chronic hypertension develops left ventricular
hypertrophy. Initially, this adaptation serves to:

A) Increase cardiac output
B) Decrease wall stress
C) Increase myocardial oxygen demand
D) Decrease contractility

Answer: B

Rationale: Concentric LV hypertrophy is an adaptive response to chronic pressure
overload (hypertension). By increasing wall thickness, wall stress is reduced (LaPlace's
law: stress = pressure × radius / (2 × wall thickness)). This maintains cardiac function
initially. Over time, however, it becomes maladaptive with diastolic dysfunction and
increased oxygen demand.




Question 2: A 55-year-old male with chronic alcoholism presents with
hepatomegaly. Liver biopsy shows macrovesicular steatosis. Which mechanism is
primarily responsible?

A) Increased fatty acid oxidation
B) Decreased fatty acid synthesis
C) Accumulation of triglycerides in hepatocytes
D) Increased protein synthesis

,2|Page


Answer: C

Rationale: Alcoholic liver disease causes fatty liver (steatosis) through accumulation of
triglycerides within hepatocytes. Mechanisms include increased fatty acid synthesis,
decreased fatty acid oxidation, impaired lipoprotein export, and increased peripheral
fat mobilization. This is an example of injury due to accumulation of endogenous
substances.




Figure 1: Cellular Adaptation Types

text
┌─────────────────────────────────────────────────────────────────────┐
│ TYPES OF CELLULAR ADAPTATION │
├─────────────────────────────────────────────────────────────────────┤
│ │
│ NORMAL CELL ◄─────────────────────────────────────────────────► │
│ ┌─────────┐ │
│ │ Normal │ │
│ │ Size │ │
│ └─────────┘ │
│ │ │
│ ├───────────────────┬───────────────────┬─────────────────┐ │
│ ▼ ▼ ▼ ▼ │
│ ┌─────────┐ ┌─────────┐ ┌─────────┐ ┌─────────┐│
│ │ ATROPHY │ │HYPERTRO│ │HYPER- │ │METAPLAS││
│ │ Smaller │ │PHY │ │PLASIA │ │IA ││
│ │ Size │ │Larger │ │More │ │Change ││
│ │ │ │Size │ │Cells │ │Type ││
│ └─────────┘ └─────────┘ └─────────┘ └─────────┘│
│ │
│ Atrophy: Decreased cell size (disuse, denervation, ischemia) │
│ Hypertrophy: Increased cell size (workload, hormones) │
│ Hyperplasia: Increased cell number (hormonal, compensatory) │
│ Metaplasia: Change in cell type (chronic irritation) │
└─────────────────────────────────────────────────────────────────────┘

,3|Page


Question 3: A 78-year-old patient with Alzheimer disease has accumulation of
amyloid plaques in the brain. This type of cellular injury is classified as:

A) Hypoxic injury
B) Immunologic injury
C) Accumulation of abnormal substances
D) Physical injury

Answer: C

Rationale: Alzheimer disease is characterized by accumulation of abnormal proteins—
specifically amyloid-beta plaques (extracellular) and neurofibrillary tangles composed
of hyperphosphorylated tau protein (intracellular). This represents injury due to
accumulation of abnormal substances, which includes Parkinson disease (Lewy bodies)
and prion diseases.




Question 4: During an ischemic event, ATP depletion leads to cellular swelling
primarily through:

A) Failure of the Na⁺/K⁺ ATPase pump
B) Mitochondrial membrane depolarization
C) Increased protein synthesis
D) Activation of lysosomal enzymes

Answer: A

Rationale: ATP is required for the Na⁺/K⁺ ATPase pump to maintain the
electrochemical gradient. When ATP is depleted, the pump fails, causing sodium to
accumulate intracellularly, followed by water influx due to osmotic pressure, resulting
in cellular swelling. This is a hallmark of reversible cell injury.




Question 5: A 35-year-old pregnant female has increased size of her uterine
myometrium. This adaptation is best described as:

A) Hypertrophy
B) Hyperplasia
C) Metaplasia
D) Dysplasia

, 4|Page


Answer: B

Rationale: During pregnancy, the uterine smooth muscle undergoes hyperplasia
(increase in cell number) due to estrogen stimulation. This is a physiologic adaptation.
Hypertrophy (increase in cell size) occurs in cardiac muscle in response to increased
workload, as cardiac myocytes are terminally differentiated and cannot divide.




Question 6: A 65-year-old patient with prostate cancer undergoes androgen
deprivation therapy. The prostate tissue shrinks due to:

A) Hypertrophy
B) Hyperplasia
C) Atrophy
D) Metaplasia

Answer: C

Rationale: Atrophy is the decrease in cell size and organ size due to decreased
workload, loss of hormonal stimulation, or other factors. Androgen deprivation removes
the hormonal stimulus for prostate cell growth, leading to prostate atrophy. This is a
reversible change that can be restored with renewed hormonal stimulation.




Question 7: A 50-year-old patient with chronic hepatitis B infection develops liver
cirrhosis. The mechanism of liver injury involves:

A) Direct hepatocyte destruction by the virus
B) Immune-mediated injury to hepatocytes
C) Accumulation of fat in hepatocytes
D) Genetic mutation in hepatocytes

Answer: B

Rationale: Hepatitis B virus causes liver injury primarily through immune-mediated
mechanisms. The host immune response targets virus-infected hepatocytes, leading to
cell death, inflammation, and eventually fibrosis and cirrhosis. The virus itself does not
directly destroy cells in most cases.

Document information

Uploaded on
August 8, 2026
Number of pages
87
Written in
2026/2027
Type
Exam (elaborations)
Contains
Questions & answers
$25.99

Wrong document? Swap it for free Within 14 days of purchase and before downloading, you can choose a different document. You can simply spend the amount again.
Written by students who passed
Immediately available after payment
Read online or as PDF

Seller avatar
Reputation scores are based on the amount of documents a seller has sold for a fee and the reviews they have received for those documents. There are three levels: Bronze, Silver and Gold. The better the reputation, the more your can rely on the quality of the sellers work.
GradeGlide
3.5
(2)
Sold
12
Followers
2
Items
322
Last sold
4 days ago


Why students choose Stuvia

Created by fellow students, verified by reviews

Quality you can trust: written by students who passed their tests and reviewed by others who've used these notes.

Didn't get what you expected? Choose another document

No worries! You can instantly pick a different document that better fits what you're looking for.

Pay as you like, start learning right away

No subscription, no commitments. Pay the way you're used to via credit card and download your PDF document instantly.

Student with book image

“Bought, downloaded, and aced it. It really can be that simple.”

Alisha Student

Working on your references?

Create accurate citations in APA, MLA and Harvard with our free citation generator.

Working on your references?

Frequently asked questions