PATHOLOGY MCQs: CELL INJURY, DEATH, AND ADAPTATIONS – 54 MCQs | Kenya MBChB

54 Year 3: General Pathology exam questions on PATHOLOGY MCQs: CELL INJURY, DEATH, AND ADAPTATIONS for medical students. Includes MCQs, answers, explanations an

This MCQ set contains 54 questions on PATHOLOGY MCQs: CELL INJURY, DEATH, AND ADAPTATIONS in the Year 3: General Pathology unit. Each question includes the correct answer and a detailed explanation for active recall and exam preparation.

Q1: Question 1 Which of the following best describes the relationship between etiology and pathogenesis?

  1. A. Etiology explains how disease manifests, while pathogenesis identifies the cause
  2. B. Etiology identifies the initiating cause, while pathogenesis explains the sequence of events leading to disease
  3. C. Both terms are interchangeable in modern pathology
  4. D. Etiology focuses on treatment, while pathogenesis focuses on prevention

Correct answer: B – Etiology identifies the initiating cause, while pathogenesis explains the sequence of events leading to disease

Etiology refers to the cause of disease (genetic or environmental factors), while pathogenesis describes the molecular, biochemical, and cellular events that follow the etiologic agent and lead to the development of disease manifestations.

Q2: A 45-year-old patient presents with chest pain. After 30 minutes of ischemia, the cardiomyocytes show cellular swelling and fat accumulation but maintain intact cell membranes. What stage of cell injury is this?

  1. A. Irreversible injury
  2. B. Necrosis
  3. C. Reversible injury
  4. D. Apoptosis
  5. E. is remove

Correct answer: C – Reversible injury

The key features indicating reversible injury are cellular swelling, fatty change, and intact cell membranes. These changes can be corrected if the damaging stimulus (ischemia) is removed. Irreversible injury would show mitochondrial damage with dense deposits and plasma membrane rupture.

Q3: Question 4 Which of the following represents the earliest morphologic manifestation of almost all forms of cell injury?

  1. A. Nuclear pyknosis
  2. B. Cellular swelling
  3. C. Membrane blebbing
  4. D. Chromatin condensation

Correct answer: B – Cellular swelling

Cellular swelling is the earliest visible sign of cell injury, resulting from failure of the ATP-dependent Na+-K+ pump, leading to sodium and water accumulation inside the cell. This occurs before any nuclear changes or membrane disruption.

Q4: Question 5 A researcher observes cells under electron microscopy 2 hours after ischemic injury. Which finding would indicate the point of no return (irreversibility)?

  1. A. Detachment of ribosomes from endoplasmic reticulum
  2. B. Severe mitochondrial swelling with large amorphous densities
  3. C. Disaggregation of nuclear granular elements
  4. D. Appearance of myelin figures

Correct answer: B – Severe mitochondrial swelling with large amorphous densities

Two phenomena consistently characterize irreversibility: inability to reverse mitochondrial dysfunction and profound membrane disturbances. Severe mitochondrial damage with amorphous densities (calcium and protein precipitates) indicates irreversible injury, while the other options can occur in reversible injury. SECTION 2: CAUSES AND MECHANISMS OF CELL INJURY

Q5: Question 6 Which cause of hypoxia differs from ischemia in that it allows anaerobic glycolysis to continue?

  1. A. Carbon monoxide poisoning
  2. B. Coronary artery occlusion
  3. C. Venous thrombosis
  4. D. Arterial atherosclerotic narrowing
  5. E. , blood flow is reduced, compromising delivery of substrates for glycolysis, making ischemia more injurious than hypoxia alone.

Correct answer: A – Carbon monoxide poisoning

Carbon monoxide poisoning causes hypoxia by reducing oxygen-carrying capacity of blood, but blood flow continues, allowing delivery of glucose for anaerobic glycolysis. In ischemia (b, c, d), blood flow is reduced, compromising delivery of substrates for glycolysis, making ischemia more injurious than hypoxia alone.

Q6: Question 7 A patient with tuberculosis shows areas of lung tissue with a friable, white, "cheese-like" appearance. What type of necrosis is this?

  1. A. Coagulative necrosis
  2. B. Liquefactive necrosis
  3. C. Caseous necrosis
  4. D. Fat necrosis

Correct answer: C – Caseous necrosis

Caseous necrosis is characteristic of tuberculous infection, appearing grossly as friable, white, cheese-like material. Microscopically, it shows structureless collection of fragmented cells and granular debris enclosed within a granulomatous inflammatory border.

Q7: Question 8 Why does ischemic injury to the brain result in liquefactive necrosis rather than coagulative necrosis seen in other organs?

  1. A. Brain has more lysosomes than other organs
  2. B. Brain lacks structural proteins that can be denatured
  3. C. Hypoxic death of CNS cells manifests as liquefactive necrosis for unknown reasons
  4. D. Brain has higher lipid content that liquefies easily

Correct answer: C – Hypoxic death of CNS cells manifests as liquefactive necrosis for unknown reasons

For unknown reasons, hypoxic death of cells within the central nervous system often manifests as liquefactive necrosis, which is an exception to the general rule that ischemia causes coagulative necrosis in most organs.

Q8: Question 9 A patient with acute pancreatitis develops chalky-white areas in the peritoneal cavity. What is the mechanism of this pathologic finding?

  1. A. Dystrophic calcification of necrotic tissue
  2. B. Release of pancreatic lipases causing fat necrosis with saponification
  3. C. Liquefactive necrosis of adipose tissue
  4. D. Bacterial infection of peritoneal fat

Correct answer: B – Release of pancreatic lipases causing fat necrosis with saponification

In acute pancreatitis, pancreatic enzymes leak and liquefy fat cell membranes, releasing triglycerides. Pancreatic lipases split these into fatty acids, which combine with calcium to produce grossly visible chalky-white areas (fat saponification), characteristic of fat necrosis.

Q9: Question 10 Which nuclear change in necrosis is characterized by nuclear shrinkage and increased basophilia?

  1. A. Karyolysis
  2. B. Karyorrhexis
  3. C. Pyknosis
  4. D. Chromatolysis

Correct answer: C – Pyknosis

Pyknosis is characterized by nuclear shrinkage and increased basophilia due to chromatin condensation into a dense, shrunken basophilic mass. Karyolysis is fading of chromatin, and karyorrhexis is fragmentation of the pyknotic nucleus. SECTION 3: NECROSIS VS APOPTOSIS

Q10: Question 11 Which feature distinguishes necrosis from apoptosis?

  1. A. DNA fragmentation occurs only in necrosis
  2. B. Necrosis involves cell swelling while apoptosis involves cell shrinkage
  3. C. Caspase activation occurs only in necrosis
  4. D. Membrane-bound fragments form only in necrosis

Correct answer: B – Necrosis involves cell swelling while apoptosis involves cell shrinkage

Necrosis is characterized by cell swelling due to membrane damage and loss of osmotic regulation, while apoptosis involves cell shrinkage with intact membranes. DNA fragmentation occurs in both, but caspase activation is specific to apoptosis, not necrosis.

Q11: Question 12 Why doesn't apoptosis elicit an inflammatory response?

  1. A. Apoptotic cells release anti-inflammatory cytokines
  2. B. The process occurs too rapidly for inflammation to develop
  3. C. Dead cells are rapidly phagocytosed before membrane rupture and content leakage
  4. D. Apoptotic cells express MHC class II molecules that suppress inflammation

Correct answer: C – Dead cells are rapidly phagocytosed before membrane rupture and content leakage

In apoptosis, the plasma membrane remains intact and apoptotic bodies are rapidly phagocytosed by macrophages before contents leak out. This prevents release of cellular contents that would trigger inflammation, unlike necrosis where membrane rupture releases DAMPs.

Q12: Question 13 A pathologist observes cells with intensely eosinophilic cytoplasm, dense chromatin masses at the nuclear periphery, and membrane-bound fragments without adjacent inflammation. What process is occurring?

  1. A. Coagulative necrosis
  2. B. Apoptosis
  3. C. Liquefactive necrosis
  4. D. Reversible injury

Correct answer: B – Apoptosis

The key features of apoptosis are present: cell shrinkage (dense eosinophilic cytoplasm), chromatin condensation at the nuclear membrane periphery, formation of apoptotic bodies (membrane-bound fragments), and absence of inflammation.

Q13: Question 14 What is the primary reason that cardiac troponins can be detected in blood 2 hours after myocardial infarction?

  1. A. Increased synthesis by injured myocytes
  2. B. Release through damaged plasma membranes during necrosis
  3. C. Active secretion as a distress signal
  4. D. Conversion from inactive to active form

Correct answer: B – Release through damaged plasma membranes during necrosis

Necrosis involves loss of membrane integrity, leading to leakage of intracellular proteins into the circulation. Cardiac-specific troponins leak out through damaged plasma membranes and serve as biomarkers for myocardial necrosis, detectable well before histologic changes appear.

Q14: Question 15 Which statement about DAMPs (damage-associated molecular patterns) is correct?

  1. A. They are released only by apoptotic cells
  2. B. They include ATP, uric acid, and molecules normally confined within healthy cells
  3. C. They suppress inflammation to promote healing
  4. D. They are synthesized de novo by dying cells
  5. E. They are recognized by receptors on macrophages and trigger inflammation and phagocytosis. SECTION 4: APOPTOSIS MECHANISMS

Correct answer: B – They include ATP, uric acid, and molecules normally confined within healthy cells

DAMPs are normal intracellular molecules (ATP from mitochondria, uric acid from DNA breakdown) that are released during necrosis when membranes rupture. They are recognized by receptors on macrophages and trigger inflammation and phagocytosis. SECTION 4: APOPTOSIS MECHANISMS

Q15: Question 16 Which BCL2 family protein is pro-apoptotic and forms channels in the mitochondrial membrane?

  1. A. BCL2
  2. B. BCL-XL
  3. C. BAX and BAK
  4. D. BID
  5. E. BCL2 and BCL-XL are anti-apoptotic, while BID is a BH3-only sensor protein.

Correct answer: C – BAX and BAK

BAX and BAK are pro-apoptotic proteins with BH1-3 domains that oligomerize and form channels in the outer mitochondrial membrane, allowing cytochrome c leakage. BCL2 and BCL-XL are anti-apoptotic, while BID is a BH3-only sensor protein.

Q16: Question 17 A researcher studying apoptosis blocks the function of APAF-1. Which step of apoptosis will be directly affected?

  1. A. Release of cytochrome c from mitochondria
  2. B. Formation of the apoptosome and activation of caspase-9
  3. C. DNA fragmentation by endonucleases
  4. D. Phosphatidylserine externalization
  5. E.

Correct answer: B – Formation of the apoptosome and activation of caspase-9

APAF-1 (apoptosis-activating factor-1) binds to cytochrome c released from mitochondria to form the apoptosome, which then activates caspase-9. Blocking APAF-1 prevents apoptosome formation and subsequent caspase activation, but doesn't affect upstream events like cytochrome c release.

Q17: Question 18 Which mechanism initiates the extrinsic pathway of apoptosis?

  1. A. DNA damage by radiation
  2. B. Growth factor withdrawal
  3. C. Engagement of death receptors like Fas
  4. D. Mitochondrial damage
  5. E.

Correct answer: C – Engagement of death receptors like Fas

The extrinsic pathway is initiated by death receptor engagement (Fas, TNFR1) by their ligands. This recruits FADD and activates caspase-8. The intrinsic pathway is triggered by DNA damage, growth factor withdrawal, or mitochondrial damage.

Q18: What is the function of BH3-only proteins in apoptosis?

  1. A. They inhibit caspase activation
  2. B. They maintain mitochondrial membrane integrity
  3. C. They act as sensors of cellular stress and activate BAX/BAK
  4. D. They remove apoptotic bodies by phagocytosis
  5. E. are regulated apoptosis initiators that sense cellular stress and damag

Correct answer: C – They act as sensors of cellular stress and activate BAX/BAK

BH3-only proteins (BAD, BIM, BID, Puma, Noxa) are regulated apoptosis initiators that sense cellular stress and damage. When upregulated, they directly activate BAX/BAK to permeabilize mitochondrial membranes and can also neutralize anti-apoptotic BCL2 proteins.

Q19: Question 20 During apoptosis, what signal promotes phagocytosis of apoptotic cells?

  1. A. Expression of MHC class I molecules
  2. B. Release of ATP and inflammatory cytokines
  3. C. Externalization of phosphatidylserine on the outer membrane leaflet
  4. D. Increased expression of adhesion molecules
  5. E. During apoptosis, it flips to the outer surface, where it serves as an "eat me" signal recognized by macrophage receptors, promoting efferocytosis wit

Correct answer: C – Externalization of phosphatidylserine on the outer membrane leaflet

In healthy cells, phosphatidylserine is on the inner leaflet of the plasma membrane. During apoptosis, it flips to the outer surface, where it serves as an "eat me" signal recognized by macrophage receptors, promoting efferocytosis without inflammation.

Q20: Question 21 Which cellular process is impaired in patients with chronic granulomatous disease?

  1. A. Apoptosis of neutrophils
  2. B. Generation of superoxide by leukocytes
  3. C. Phagocytosis of bacteria
  4. D. Chemotaxis toward infection sites

Correct answer: B – Generation of superoxide by leukocytes

Chronic granulomatous disease results from defects in NADPH oxidase, which is required for the respiratory burst that generates superoxide (O2•−) in leukocytes. This impairs their ability to kill phagocytosed microbes, leading to recurrent infections. SECTION 5: OTHER MECHANISMS OF CELL DEATH

Q21: Question 22 What distinguishes necroptosis from classical necrosis?

  1. A. Necroptosis does not involve plasma membrane rupture
  2. B. Necroptosis is a regulated process involving specific signaling pathways
  3. C. Necroptosis occurs only in cancer cells
  4. D. Necroptosis requires caspase activation

Correct answer: B – Necroptosis is a regulated process involving specific signaling pathways

Necroptosis is "programmed necrosis" - it resembles necrosis morphologically but is triggered by defined signaling pathways (RIPK1/RIPK3/MLKL). It is caspase-independent, unlike apoptosis. Classical necrosis is passive cell death from severe injury.

Q22: Question 23 A patient with viral infection shows cell death accompanied by IL-1 release and fever. Which mechanism is most likely?

  1. A. Apoptosis
  2. B. Necroptosis
  3. C. Pyroptosis
  4. D. Ferroptosis

Correct answer: C – Pyroptosis

Pyroptosis is characterized by caspase-1 activation (by the inflammasome in response to microbial products), which cleaves pro-IL-1 to active IL-1 (causing fever - "pyro"). The caspases also cause cell death with inflammatory response, unlike classical apoptosis.

Q23: Question 24 Which protein must be phosphorylated by RIPK3 to execute necroptosis?

  1. A. Caspase-8
  2. B. MLKL
  3. C. FADD
  4. D. BAX

Correct answer: B – MLKL

In necroptosis, RIPK3 phosphorylates MLKL (mixed lineage kinase domain-like protein), which then oligomerizes and translocates to the plasma membrane, causing membrane disruption characteristic of necrotic cell death.

Q24: Question 25 Ferroptosis is characterized by which primary mechanism?

  1. A. Mitochondrial cytochrome c release
  2. B. Unchecked lipid peroxidation of cellular membranes
  3. C. Lysosomal membrane rupture
  4. D. Nuclear DNA fragmentation

Correct answer: B – Unchecked lipid peroxidation of cellular membranes

Ferroptosis occurs when iron or ROS overwhelm glutathione-dependent antioxidant defenses, causing unchecked lipid peroxidation of membranes. This disrupts membrane function and leads to cell death. It's iron-dependent (hence "ferro") and can be prevented by reducing iron levels. SECTION 6: AUTOPHAGY

Q25: Question 26 What is the primary function of autophagy in starved cells?

  1. A. Eliminate neighboring cells to reduce competition
  2. B. Trigger apoptosis to conserve resources
  3. C. Recycle cellular components to generate metabolites and energy
  4. D. Increase protein synthesis

Correct answer: C – Recycle cellular components to generate metabolites and energy

Autophagy is a survival mechanism where cells digest their own contents (organelles, proteins) and recycle the products for energy and metabolite production. In starvation, cells "cannibalize" themselves to survive until nutrients become available again.

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