NURS6501 ADVANCED PATHOPHYSIOLOGY
MIDTERM 4 STUDY GUIDE 2026 –
COMPLETE CONCEPT REVIEW & PRACTICE
MATERIALS (LATEST EDITION)
CELLULAR BIOLOGY & ADAPTATION (Q1-20)
1. What is cellular adaptation?
Answer: Reversible structural/functional response to stressors, including atrophy,
hypertrophy, hyperplasia, metaplasia, dysplasia.
2. Differentiate necrosis from apoptosis.
Answer: Necrosis = pathological cell death with inflammation; apoptosis =
programmed, controlled cell death without inflammation.
3. What causes cellular hypoxia?
Answer: Ischemia (reduced blood flow), anemia (reduced O2-carrying capacity),
carbon monoxide poisoning, respiratory disorders.
4. Describe the Warburg effect in cancer cells.
Answer: Cancer cells preferentially use glycolysis for energy even in oxygen
presence (aerobic glycolysis).
5. What is oxidative stress?
Answer: Imbalance between reactive oxygen species (ROS) production and
antioxidant defenses causing cellular damage.
6. Explain the role of ATP in cellular injury.
Answer: ATP depletion → Na+/K+ pump failure → cellular swelling → calcium
influx → enzyme activation → irreversible damage.
,7. Define autophagy.
Answer: Cellular "self-eating" process degrading damaged organelles via
lysosomes for energy during starvation.
8. What are free radicals?
Answer: Unstable molecules with unpaired electrons causing lipid peroxidation,
protein alteration, DNA damage.
9. Describe telomere shortening significance.
Answer: Telomeres shorten with each division; critical shortening triggers cellular
senescence/apoptosis; cancer cells activate telomerase.
10. What is cellular senescence?
Answer: Irreversible cell cycle arrest despite viability, contributing to aging and
tumor suppression.
11. Differentiate hypertrophy vs. hyperplasia.
Answer: Hypertrophy = increased cell size; hyperplasia = increased cell number.
12. What is metaplasia?
Answer: Reversible replacement of one differentiated cell type by another (e.g.,
squamous metaplasia in respiratory epithelium).
13. Define dysplasia.
Answer: Abnormal cell growth with loss of uniformity/organization (precancerous
but reversible).
14. Explain ischemia-reperfusion injury.
Answer: Paradoxical worsening during blood flow restoration due to oxidative
stress, calcium overload, inflammation.
15. What are heat shock proteins?
Answer: Chaperone proteins stabilizing other proteins during cellular stress.
16. Describe mitochondrial role in apoptosis.
Answer: Release cytochrome c → activates caspases → programmed cell death.
,17. What is pyroptosis?
Answer: Inflammatory programmed cell death releasing cytokines, common in
microbial infections.
18. Explain epigenetic changes.
Answer: Heritable gene expression changes without DNA sequence alteration
(methylation, histone modification).
19. What are caspases?
Answer: Protease enzymes executing apoptosis by cleaving cellular proteins.
20. Define cellular edema mechanism.
Answer: ATP depletion → Na+/K+ pump failure → Na+ accumulation → water
influx → swelling.
GENETICS & NEOPLASIA (Q21-40)
21. Differentiate oncogenes vs. tumor suppressor genes.
Answer: Oncogenes = mutated proto-oncogenes promoting growth (e.g., RAS);
tumor suppressors inhibit growth (e.g., p53, RB).
22. Explain Knudson's two-hit hypothesis.
Answer: Both alleles of tumor suppressor gene must be inactivated for cancer
development (hereditary = 1 inherited + 1 somatic).
23. What is BRCA1/2 significance?
Answer: Tumor suppressor genes; mutations increase breast/ovarian cancer risk
via impaired DNA repair.
24. Describe Lynch syndrome.
Answer: Hereditary nonpolyposis colorectal cancer from mismatch repair gene
mutations (MLH1, MSH2).
25. Explain gene penetrance vs. expressivity.
Answer: Penetrance = % with gene who show phenotype; expressivity = variation
in phenotype among those with gene.
, 26. What is angiogenesis in cancer?
Answer: Tumor-induced new blood vessel formation for nutrient
delivery/metastasis (VEGF-mediated).
27. Describe cancer immunoediting.
Answer: Three phases: elimination (immune destruction), equilibrium (immune
control), escape (immune evasion).
28. What are cancer stem cells?
Answer: Self-renewing cells within tumors driving growth, metastasis, and therapy
resistance.
29. Explain epithelial-mesenchymal transition (EMT).
Answer: Epithelial cells lose adhesion, gain migratory properties facilitating
metastasis.
30. Define tumor microenvironment.
Answer: Complex ecosystem including cancer cells, stroma, immune cells,
extracellular matrix influencing progression.
31. What are checkpoint inhibitors in cancer?
Answer: Immunotherapy blocking PD-1/PD-L1 or CTLA-4 to restore T-cell anti-
tumor activity.
32. Describe carcinogenesis stages.
Answer: Initiation (DNA mutation) → promotion (clonal expansion) → progression
(malignant conversion).
33. What is PARP inhibitor mechanism?
Answer: Blocks PARP enzyme → synthetic lethality in BRCA-deficient cancers
(unrepairable DNA damage).
34. Explain chromosomal translocation examples.
Answer: Philadelphia chromosome t(9;22) → BCR-ABL fusion in CML; t(8;14) in
Burkitt lymphoma.
MIDTERM 4 STUDY GUIDE 2026 –
COMPLETE CONCEPT REVIEW & PRACTICE
MATERIALS (LATEST EDITION)
CELLULAR BIOLOGY & ADAPTATION (Q1-20)
1. What is cellular adaptation?
Answer: Reversible structural/functional response to stressors, including atrophy,
hypertrophy, hyperplasia, metaplasia, dysplasia.
2. Differentiate necrosis from apoptosis.
Answer: Necrosis = pathological cell death with inflammation; apoptosis =
programmed, controlled cell death without inflammation.
3. What causes cellular hypoxia?
Answer: Ischemia (reduced blood flow), anemia (reduced O2-carrying capacity),
carbon monoxide poisoning, respiratory disorders.
4. Describe the Warburg effect in cancer cells.
Answer: Cancer cells preferentially use glycolysis for energy even in oxygen
presence (aerobic glycolysis).
5. What is oxidative stress?
Answer: Imbalance between reactive oxygen species (ROS) production and
antioxidant defenses causing cellular damage.
6. Explain the role of ATP in cellular injury.
Answer: ATP depletion → Na+/K+ pump failure → cellular swelling → calcium
influx → enzyme activation → irreversible damage.
,7. Define autophagy.
Answer: Cellular "self-eating" process degrading damaged organelles via
lysosomes for energy during starvation.
8. What are free radicals?
Answer: Unstable molecules with unpaired electrons causing lipid peroxidation,
protein alteration, DNA damage.
9. Describe telomere shortening significance.
Answer: Telomeres shorten with each division; critical shortening triggers cellular
senescence/apoptosis; cancer cells activate telomerase.
10. What is cellular senescence?
Answer: Irreversible cell cycle arrest despite viability, contributing to aging and
tumor suppression.
11. Differentiate hypertrophy vs. hyperplasia.
Answer: Hypertrophy = increased cell size; hyperplasia = increased cell number.
12. What is metaplasia?
Answer: Reversible replacement of one differentiated cell type by another (e.g.,
squamous metaplasia in respiratory epithelium).
13. Define dysplasia.
Answer: Abnormal cell growth with loss of uniformity/organization (precancerous
but reversible).
14. Explain ischemia-reperfusion injury.
Answer: Paradoxical worsening during blood flow restoration due to oxidative
stress, calcium overload, inflammation.
15. What are heat shock proteins?
Answer: Chaperone proteins stabilizing other proteins during cellular stress.
16. Describe mitochondrial role in apoptosis.
Answer: Release cytochrome c → activates caspases → programmed cell death.
,17. What is pyroptosis?
Answer: Inflammatory programmed cell death releasing cytokines, common in
microbial infections.
18. Explain epigenetic changes.
Answer: Heritable gene expression changes without DNA sequence alteration
(methylation, histone modification).
19. What are caspases?
Answer: Protease enzymes executing apoptosis by cleaving cellular proteins.
20. Define cellular edema mechanism.
Answer: ATP depletion → Na+/K+ pump failure → Na+ accumulation → water
influx → swelling.
GENETICS & NEOPLASIA (Q21-40)
21. Differentiate oncogenes vs. tumor suppressor genes.
Answer: Oncogenes = mutated proto-oncogenes promoting growth (e.g., RAS);
tumor suppressors inhibit growth (e.g., p53, RB).
22. Explain Knudson's two-hit hypothesis.
Answer: Both alleles of tumor suppressor gene must be inactivated for cancer
development (hereditary = 1 inherited + 1 somatic).
23. What is BRCA1/2 significance?
Answer: Tumor suppressor genes; mutations increase breast/ovarian cancer risk
via impaired DNA repair.
24. Describe Lynch syndrome.
Answer: Hereditary nonpolyposis colorectal cancer from mismatch repair gene
mutations (MLH1, MSH2).
25. Explain gene penetrance vs. expressivity.
Answer: Penetrance = % with gene who show phenotype; expressivity = variation
in phenotype among those with gene.
, 26. What is angiogenesis in cancer?
Answer: Tumor-induced new blood vessel formation for nutrient
delivery/metastasis (VEGF-mediated).
27. Describe cancer immunoediting.
Answer: Three phases: elimination (immune destruction), equilibrium (immune
control), escape (immune evasion).
28. What are cancer stem cells?
Answer: Self-renewing cells within tumors driving growth, metastasis, and therapy
resistance.
29. Explain epithelial-mesenchymal transition (EMT).
Answer: Epithelial cells lose adhesion, gain migratory properties facilitating
metastasis.
30. Define tumor microenvironment.
Answer: Complex ecosystem including cancer cells, stroma, immune cells,
extracellular matrix influencing progression.
31. What are checkpoint inhibitors in cancer?
Answer: Immunotherapy blocking PD-1/PD-L1 or CTLA-4 to restore T-cell anti-
tumor activity.
32. Describe carcinogenesis stages.
Answer: Initiation (DNA mutation) → promotion (clonal expansion) → progression
(malignant conversion).
33. What is PARP inhibitor mechanism?
Answer: Blocks PARP enzyme → synthetic lethality in BRCA-deficient cancers
(unrepairable DNA damage).
34. Explain chromosomal translocation examples.
Answer: Philadelphia chromosome t(9;22) → BCR-ABL fusion in CML; t(8;14) in
Burkitt lymphoma.
