1|Page
NSG 5003 COMPLETE WEEKLY KNOWLEDGE
CHECK: 201 QUESTIONS & VERIFIED
SOLUTIONS (WEEKS 1-10) – ADVANCED
PATHOPHYSIOLOGY
## Table of Contents
| Week | Topic | Questions | Page |
|------|-------|-----------|------|
| 1 | Cellular Biology & Genetics | 21 | 2 |
| 2 | Immunity & Inflammation | 20 | 12 |
| 3 | Hematologic Function | 20 | 22 |
| 4 | Cardiovascular Pathophysiology | 20 | 32 |
| 5 | Pulmonary Pathophysiology | 20 | 42 |
| 6 | Renal & Urinary Tract Disorders | 20 | 52 |
| 7 | Endocrine & Metabolic Disorders | 20 | 62 |
| 8 | Gastrointestinal & Hepatobiliary | 20 | 72 |
| 9 | Neurologic Disorders | 20 | 82 |
| 10 | Musculoskeletal & Integumentary | 20 | 92 |
| **Total** | | **201** | |
,2|Page
# WEEK 1: Cellular Biology & Genetics
**1.** A 15-year-old male presents with fatigue and pallor. Lab results
show macrocytic anemia. Which cellular adaptation is most likely
occurring in his bone marrow?
A) Hyperplasia
B) Hypertrophy
C) Atrophy
D) Metaplasia
**Answer:** A) Hyperplasia
**Rationale:** Macrocytic anemia (B12/folate deficiency) increases
erythroid precursor proliferation → hyperplasia. Hypertrophy (B) = cell
enlargement. Atrophy (C) = decreased size. Metaplasia (D) = reversible
cell type change.
**Ref:** McCance & Huether, Ch. 4, pp. 92-95.
**2.** Which organelle is responsible for ATP production via oxidative
phosphorylation?
A) Golgi apparatus
B) Ribosome
C) Mitochondrion
D) Lysosome
,3|Page
**Answer:** C) Mitochondrion
**Rationale:** Mitochondria produce ATP. Golgi (A) packages proteins.
Ribosomes (B) synthesize proteins. Lysosomes (D) digest waste.
**3.** A genetic mutation leads to a nonfunctional p53 protein. What is
the most likely consequence?
A) Increased apoptosis
B) Uncontrolled cell division
C) Enhanced DNA repair
D) Decreased angiogenesis
**Answer:** B) Uncontrolled cell division
**Rationale:** p53 is a tumor suppressor; loss of function removes cell
cycle arrest → proliferation.
**4.** Which statement best describes apoptosis?
A) Programmed cell death without inflammation
B) Uncontrolled cell death with inflammation
C) Reversible cell injury
D) Necrosis due to hypoxia
**Answer:** A) Programmed cell death without inflammation
, 4|Page
**Rationale:** Apoptosis is energy-dependent, neat, no inflammation.
Necrosis (B/D) is messy, inflammatory.
**5.** A patient has a mutation in the CFTR gene leading to defective
chloride channels. This is an example of:
A) Trinucleotide repeat disorder
B) Autosomal dominant disorder
C) Autosomal recessive disorder
D) Mitochondrial disorder
**Answer:** C) Autosomal recessive disorder
**Rationale:** Cystic fibrosis is AR. Trinucleotide repeat (A) =
Huntington’s. AD (B) = Huntington’s, Marfan.
**6.** Which cellular process is directly impaired in Leigh syndrome?
A) Glycolysis
B) Oxidative phosphorylation
C) Fatty acid oxidation
D) Gluconeogenesis
**Answer:** B) Oxidative phosphorylation
**Rationale:** Leigh syndrome is a mitochondrial disorder affecting
ATP synthesis.
NSG 5003 COMPLETE WEEKLY KNOWLEDGE
CHECK: 201 QUESTIONS & VERIFIED
SOLUTIONS (WEEKS 1-10) – ADVANCED
PATHOPHYSIOLOGY
## Table of Contents
| Week | Topic | Questions | Page |
|------|-------|-----------|------|
| 1 | Cellular Biology & Genetics | 21 | 2 |
| 2 | Immunity & Inflammation | 20 | 12 |
| 3 | Hematologic Function | 20 | 22 |
| 4 | Cardiovascular Pathophysiology | 20 | 32 |
| 5 | Pulmonary Pathophysiology | 20 | 42 |
| 6 | Renal & Urinary Tract Disorders | 20 | 52 |
| 7 | Endocrine & Metabolic Disorders | 20 | 62 |
| 8 | Gastrointestinal & Hepatobiliary | 20 | 72 |
| 9 | Neurologic Disorders | 20 | 82 |
| 10 | Musculoskeletal & Integumentary | 20 | 92 |
| **Total** | | **201** | |
,2|Page
# WEEK 1: Cellular Biology & Genetics
**1.** A 15-year-old male presents with fatigue and pallor. Lab results
show macrocytic anemia. Which cellular adaptation is most likely
occurring in his bone marrow?
A) Hyperplasia
B) Hypertrophy
C) Atrophy
D) Metaplasia
**Answer:** A) Hyperplasia
**Rationale:** Macrocytic anemia (B12/folate deficiency) increases
erythroid precursor proliferation → hyperplasia. Hypertrophy (B) = cell
enlargement. Atrophy (C) = decreased size. Metaplasia (D) = reversible
cell type change.
**Ref:** McCance & Huether, Ch. 4, pp. 92-95.
**2.** Which organelle is responsible for ATP production via oxidative
phosphorylation?
A) Golgi apparatus
B) Ribosome
C) Mitochondrion
D) Lysosome
,3|Page
**Answer:** C) Mitochondrion
**Rationale:** Mitochondria produce ATP. Golgi (A) packages proteins.
Ribosomes (B) synthesize proteins. Lysosomes (D) digest waste.
**3.** A genetic mutation leads to a nonfunctional p53 protein. What is
the most likely consequence?
A) Increased apoptosis
B) Uncontrolled cell division
C) Enhanced DNA repair
D) Decreased angiogenesis
**Answer:** B) Uncontrolled cell division
**Rationale:** p53 is a tumor suppressor; loss of function removes cell
cycle arrest → proliferation.
**4.** Which statement best describes apoptosis?
A) Programmed cell death without inflammation
B) Uncontrolled cell death with inflammation
C) Reversible cell injury
D) Necrosis due to hypoxia
**Answer:** A) Programmed cell death without inflammation
, 4|Page
**Rationale:** Apoptosis is energy-dependent, neat, no inflammation.
Necrosis (B/D) is messy, inflammatory.
**5.** A patient has a mutation in the CFTR gene leading to defective
chloride channels. This is an example of:
A) Trinucleotide repeat disorder
B) Autosomal dominant disorder
C) Autosomal recessive disorder
D) Mitochondrial disorder
**Answer:** C) Autosomal recessive disorder
**Rationale:** Cystic fibrosis is AR. Trinucleotide repeat (A) =
Huntington’s. AD (B) = Huntington’s, Marfan.
**6.** Which cellular process is directly impaired in Leigh syndrome?
A) Glycolysis
B) Oxidative phosphorylation
C) Fatty acid oxidation
D) Gluconeogenesis
**Answer:** B) Oxidative phosphorylation
**Rationale:** Leigh syndrome is a mitochondrial disorder affecting
ATP synthesis.
