• Wrong document? Swap it for free
  • Written by students who passed
  • Immediately available after payment
  • Read online or as PDF
Sell
Where do you study
Your language
Document preview thumbnail
Preview 3 out of 16 pages
Exam (elaborations)

NURS611 Advanced Pathophysiology 2025/2026 – Verified Exam Questions with Expert Explanations

Document preview thumbnail
Preview 3 out of 16 pages

NURS611 Advanced Pathophysiology 2025/2026 – Verified Exam Questions with Expert Explanations

Content preview

NURS611 Advanced Pathophysiology
2025/2026 – Verified Exam Questions
with Expert Explanations

Cellular and Tissue Pathophysiology
1. What is the primary mechanism of cellular injury in hypoxia?
a. Increased ATP production
b. Oxidative stress from reactive oxygen species
c. Impaired sodium-potassium pump function
d. Excessive calcium influx
Answer: b. Oxidative stress from reactive oxygen species
Rationale: Hypoxia leads to reduced ATP production due to impaired oxidative
phosphorylation, causing an accumulation of reactive oxygen species (ROS). ROS
damage cellular components like lipids, proteins, and DNA, leading to cellular injury.
2. A patient with severe burns develops tissue necrosis. What is the primary cause?
a. Ischemic injury
b. Thermal protein denaturation
c. Hypoxic mitochondrial failure
d. Free radical-mediated damage
Answer: b. Thermal protein denaturation
Rationale: Severe burns cause direct thermal injury, leading to protein denaturation and
disruption of cellular structures, resulting in necrosis.
3. Which cellular adaptation is most likely in a patient with chronic hypertension?
a. Atrophy
b. Hypertrophy
c. Metaplasia
d. Dysplasia
Answer: b. Hypertrophy
Rationale: Chronic hypertension increases cardiac workload, causing cardiac muscle
cells to undergo hypertrophy to compensate for the increased demand.
4. What is the hallmark of apoptosis compared to necrosis?
a. Cellular swelling
b. Inflammatory response
c. Controlled cell death
d. Loss of membrane integrity
Answer: c. Controlled cell death
Rationale: Apoptosis is a programmed, controlled process of cell death that does not
trigger inflammation, unlike necrosis, which involves uncontrolled cell death and
membrane rupture.
5. A patient with chronic smoking develops squamous metaplasia in the bronchial
epithelium. What does this indicate?
a. Irreversible cellular damage
b. Reversible adaptation to stress

, c. Malignant transformation
d. Necrotic tissue formation
Answer: b. Reversible adaptation to stress
Rationale: Squamous metaplasia is a reversible adaptive response where bronchial
columnar epithelium transforms into squamous epithelium due to chronic irritation from
smoking.




Inflammation and Immune Responses
6. Which mediator is primarily responsible for the vasodilation in acute inflammation?
a. Histamine
b. Prostaglandins
c. Leukotrienes
d. Cytokines
Answer: a. Histamine
Rationale: Histamine, released by mast cells, is the primary mediator of vasodilation in
the early phase of acute inflammation, increasing blood flow to the affected area.
7. A patient with systemic lupus erythematosus (SLE) presents with a butterfly rash.
What is the underlying mechanism?
a. Immune complex deposition
b. Direct cytotoxic T-cell attack
c. Type I hypersensitivity reaction
d. Delayed hypersensitivity response
Answer: a. Immune complex deposition
Rationale: SLE involves type III hypersensitivity, where immune complexes deposit in
tissues like the skin, triggering inflammation and the characteristic butterfly rash.
8. Which cytokine is most associated with chronic inflammation in rheumatoid
arthritis?
a. IL-1
b. TNF-α
c. IL-6
d. IFN-γ
Answer: b. TNF-α
Rationale: TNF-α drives chronic inflammation in rheumatoid arthritis by promoting
synovial inflammation and cartilage destruction.
9. What is the primary clinical manifestation of anaphylaxis?
a. Localized edema
b. Systemic vasodilation and hypotension
c. Chronic joint pain
d. Delayed skin rash
Answer: b. Systemic vasodilation and hypotension
Rationale: Anaphylaxis, a type I hypersensitivity reaction, causes widespread histamine
release, leading to systemic vasodilation, hypotension, and potentially life-threatening
shock.
10. A patient with a recent transplant develops graft rejection. What type of
hypersensitivity is most likely involved?
a. Type I
b. Type II

, c. Type III
d. Type IV
Answer: d. Type IV
Rationale: Transplant rejection is primarily a type IV (delayed) hypersensitivity reaction
mediated by T-cells recognizing foreign antigens on the graft.




Genetic and Congenital Disorders
11. A couple is counseled about the risk of cystic fibrosis in their child. The husband is a
carrier, and the wife has the disease. What is the chance their child will have cystic
fibrosis?
a. 25%
b. 50%
c. 75%
d. 100%
Answer: b. 50%
Rationale: Cystic fibrosis is an autosomal recessive disorder. The wife, having the
disease, is homozygous recessive (aa). The husband, a carrier, is heterozygous (Aa).
Their child has a 50% chance of inheriting the recessive allele from each parent (aa).
12. What is the primary defect in cystic fibrosis?
a. Defective sodium-potassium pump
b. CFTR gene mutation
c. Mitochondrial DNA mutation
d. X-linked gene defect
Answer: b. CFTR gene mutation
Rationale: Cystic fibrosis results from mutations in the CFTR gene, impairing chloride
transport and leading to thick mucus production and organ dysfunction.
13. A patient with Down syndrome is at increased risk for which condition?
a. Alzheimer’s disease
b. Type 2 diabetes
c. Rheumatoid arthritis
d. Chronic kidney disease
Answer: a. Alzheimer’s disease
Rationale: Down syndrome (trisomy 21) increases the risk of early-onset Alzheimer’s
disease due to the overexpression of amyloid precursor protein on chromosome 21.
14. Which genetic disorder is characterized by a trinucleotide repeat expansion?
a. Sickle cell anemia
b. Fragile X syndrome
c. Hemophilia A
d. Thalassemia
Answer: b. Fragile X syndrome
Rationale: Fragile X syndrome results from a CGG trinucleotide repeat expansion in the
FMR1 gene, leading to intellectual disability and characteristic physical features.
15. What is the clinical significance of a point mutation in sickle cell anemia?
a. Increased oxygen affinity of hemoglobin
b. Altered hemoglobin structure causing sickling
c. Reduced red blood cell production
d. Impaired iron metabolism

Document information

Uploaded on
September 15, 2025
Number of pages
16
Written in
2025/2026
Type
Exam (elaborations)
Contains
Questions & answers
$17.50

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.
TutorRicks
3.6
(54)
Sold
401
Followers
53
Items
2994
Last sold
3 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