50 Multiple Choice Questions – 50 MCQs | Kenya MBChB

50 Year 3: Endocrine and Metabolic Pathology exam questions on 50 Multiple Choice Questions for medical students. Includes MCQs, answers, explanations and writt

This MCQ set contains 50 questions on 50 Multiple Choice Questions in the Year 3: Endocrine and Metabolic 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 physiologic hypertrophy?

  1. A. Enlargement of skeletal muscle in bodybuilders
  2. B. Cardiac enlargement in hypertension
  3. C. Prostatic enlargement in elderly men
  4. D. Thyroid enlargement in Graves' disease
  5. E. Option B represents pathologic hypertrophy due to increased workload from disease.

Correct answer: A – Enlargement of skeletal muscle in bodybuilders

Physiologic hypertrophy occurs in response to normal stimuli like exercise or hormonal stimulation during pregnancy. Skeletal muscle enlargement with exercise is a classic example. Option B represents pathologic hypertrophy due to increased workload from disease.

Q2: Question 2 Barrett esophagus is an example of

  1. A. Hyperplasia
  2. B. Metaplasia
  3. C. Dysplasia
  4. D. Anaplasia

Correct answer: B – Metaplasia

Barrett esophagus represents metaplasia where normal stratified squamous epithelium is replaced by columnar epithelium with goblet cells in response to chronic acid reflux. This is an adaptive response to chronic injury.

Q3: Question 3 Which cellular adaptation is reversible upon removal of the stimulus?

  1. A. Atrophy
  2. B. Metaplasia
  3. C. Dysplasia
  4. D. All of the above

Correct answer: D – All of the above

All three are potentially reversible if the causative stimulus is removed before irreversible damage occurs. However, dysplasia has a higher risk of progression to cancer if the stimulus persists. ---

Q4: Endometrial hyperplasia is primarily caused by

  1. A. Excessive estrogen stimulation
  2. B. Progesterone excess
  3. C. Testosterone elevation
  4. D. Cortisol deficiency
  5. E. This leads to increased proliferation of endometrial glands and can be a precursor to endometrial carcinom

Correct answer: A – Excessive estrogen stimulation

Endometrial hyperplasia results from unopposed estrogen stimulation without adequate progesterone. This leads to increased proliferation of endometrial glands and can be a precursor to endometrial carcinoma. ---

Q5: Question 5 The decrease in cell size seen in atrophy is primarily due to

  1. A. Increased protein synthesis
  2. B. Decreased protein degradation
  3. C. Increased autophagy and proteasome activity
  4. D. Mitochondrial proliferation
  5. E. This reduces cellular metabolic demands. --- SECTION 2: MECHANISMS OF CELLULAR INJURY

Correct answer: C – Increased autophagy and proteasome activity

Atrophy involves increased degradation of cellular components through the ubiquitin-proteasome pathway and autophagy, leading to decreased cell size. This reduces cellular metabolic demands. --- SECTION 2: MECHANISMS OF CELLULAR INJURY

Q6: Question 6 Which is the most common cause of cell injury in clinical medicine?

  1. A. Immunologic reactions
  2. B. Hypoxia and ischemia
  3. C. Genetic defects
  4. D. Nutritional imbalances

Correct answer: B – Hypoxia and ischemia

Hypoxia and ischemia are the most common causes of cell injury, underlying conditions like myocardial infarction, stroke, and tissue infarcts throughout the body. ---

Q7: Question 7 The earliest ultrastructural change in reversible cell injury is

  1. A. Nuclear pyknosis
  2. B. Mitochondrial swelling
  3. C. Plasma membrane rupture
  4. D. Lysosomal rupture

Correct answer: B – Mitochondrial swelling

Mitochondrial swelling and formation of amorphous densities in the mitochondrial matrix are among the earliest ultrastructural changes in reversible cell injury, reflecting impaired oxidative phosphorylation. ---

Q8: Free radical injury is most commonly caused by

  1. A. Decreased ATP production
  2. B. Lipid peroxidation
  3. C. Protein synthesis inhibition
  4. D. DNA replication errors
  5. E. They also damage proteins and DNA, but lipid peroxidation is the most significant mechanism.

Correct answer: B – Lipid peroxidation

Free radicals cause cellular injury primarily through lipid peroxidation of membrane lipids, leading to membrane damage. They also damage proteins and DNA, but lipid peroxidation is the most significant mechanism. ---

Q9: Which enzyme protects cells against free radical injury by converting superoxide to hydrogen peroxide?

  1. A. Catalase
  2. B. Glutathione peroxidase
  3. C. Superoxide dismutase
  4. D. Myeloperoxidase
  5. E. converts superoxide radicals (O2-) to hydrogen peroxide (H2O2). Catalase and glutathione peroxidase then convert H2O2 to water.

Correct answer: C – Superoxide dismutase

Superoxide dismutase (SOD) converts superoxide radicals (O2-) to hydrogen peroxide (H2O2). Catalase and glutathione peroxidase then convert H2O2 to water. ---

Q10: Question 10 Calcium accumulation in injured cells leads to

  1. A. Enhanced ATP production
  2. B. Activation of destructive enzymes
  3. C. Increased protein synthesis
  4. D. Stabilization of membranes
  5. E. , and ATPases (deplete ATP), all contributing to cell death. --- SECTION 3: REVERSIBLE VS IRREVERSIBLE INJURY

Correct answer: B – Activation of destructive enzymes

Increased intracellular calcium activates phospholipases (damage membranes), proteases (break down proteins), endonucleases (damage DNA), and ATPases (deplete ATP), all contributing to cell death. --- SECTION 3: REVERSIBLE VS IRREVERSIBLE INJURY

Q11: Question 11 The hallmark of irreversible cell injury is

  1. A. Cellular swelling
  2. B. Fatty change
  3. C. Inability to reverse mitochondrial dysfunction
  4. D. Ribosomal detachment

Correct answer: C – Inability to reverse mitochondrial dysfunction

The point of no return in cell injury is marked by the inability to restore mitochondrial function even after resolution of the original injury. This leads to progressive loss of membrane integrity and cell death. ---

Q12: Question 12 Cellular swelling results from

  1. A. Increased protein synthesis
  2. B. Failure of the Na+/K+ ATPase pump
  3. C. Enhanced oxidative phosphorylation
  4. D. Decreased membrane permeability

Correct answer: B – Failure of the Na+/K+ ATPase pump

Failure of the Na+/K+ ATPase pump due to ATP depletion leads to sodium and water influx into the cell, causing cellular swelling (oncosis). This is a characteristic feature of reversible injury. ---

Q13: Question 13 Fatty change (steatosis) is most commonly seen in

  1. A. Heart
  2. B. Brain
  3. C. Liver
  4. D. Kidney

Correct answer: C – Liver

The liver is most commonly affected by fatty change due to its central role in fat metabolism. Causes include alcohol, toxins, diabetes, obesity, and protein malnutrition. ---

Q14: Question 14 Which microscopic change indicates irreversible injury?

  1. A. Cytoplasmic eosinophilia
  2. B. Nuclear pyknosis
  3. C. Cellular swelling
  4. D. Ribosomal disaggregation

Correct answer: B – Nuclear pyknosis

Nuclear changes (pyknosis, karyorrhexis, karyolysis) are hallmarks of irreversible injury and cell death. Cytoplasmic eosinophilia can occur in reversible injury due to ribosomal detachment. ---

Q15: Question 15 Hydropic degeneration is characterized by

  1. A. Lipid accumulation in cytoplasm
  2. B. Protein aggregates in cytoplasm
  3. C. Water accumulation causing cell swelling
  4. D. Glycogen depletion

Correct answer: C – Water accumulation causing cell swelling

Hydropic degeneration (vacuolar degeneration) refers to the accumulation of water in the cytoplasm causing cellular swelling. It represents an early manifestation of reversible cell injury. --- SECTION 4: TYPES OF NECROSIS

Q16: Question 16 Coagulative necrosis is characterized by

  1. A. Complete loss of tissue architecture
  2. B. Preservation of tissue architecture
  3. C. Liquefaction of tissue
  4. D. Caseous appearance

Correct answer: B – Preservation of tissue architecture

Coagulative necrosis maintains the basic tissue architecture for several days due to denaturation of structural proteins and enzymes. It is the most common type of necrosis and typical of ischemic injury in solid organs. ---

Q17: Question 17 Liquefactive necrosis is typical of

  1. A. Myocardial infarction
  2. B. Renal infarction
  3. C. Brain infarction
  4. D. Splenic infarction

Correct answer: C – Brain infarction

Liquefactive necrosis occurs in brain infarctions due to the high lipid content and abundance of hydrolytic enzymes. It also occurs in bacterial infections due to release of lysosomal enzymes from neutrophils. ---

Q18: Question 18 Caseous necrosis is most characteristically seen in

  1. A. Acute bacterial infection
  2. B. Tuberculosis
  3. C. Viral hepatitis
  4. D. Fungal infection

Correct answer: B – Tuberculosis

Caseous necrosis is characteristic of tuberculosis and some fungal infections. It has a cheese-like (caseous) appearance, combining features of coagulative and liquefactive necrosis. ---

Q19: Fat necrosis typically occurs in

  1. A. Acute pancreatitis
  2. B. Myocardial infarction
  3. C. Cerebral infarction
  4. D. Pulmonary infarction

Correct answer: A – Acute pancreatitis

Fat necrosis occurs when pancreatic enzymes (lipases) are released into the peritoneum in acute pancreatitis, breaking down fat cells. It also occurs in traumatic injury to adipose tissue such as breast tissue. ---

Q20: Question 20 Fibrinoid necrosis is seen in

  1. A. Acute inflammation
  2. B. Chronic inflammation
  3. C. Immune-mediated vascular injury
  4. D. Ischemic injury

Correct answer: C – Immune-mediated vascular injury

Fibrinoid necrosis occurs in blood vessel walls in immune-mediated conditions like vasculitis, malignant hypertension, and autoimmune diseases. It appears as bright pink amorphous material on H&E staining. ---

Q21: Question 21 Gangrenous necrosis refers to

  1. A. A specific type of necrosis
  2. B. Coagulative necrosis with bacterial overgrowth
  3. C. Liquefactive necrosis only
  4. D. Caseous necrosis of extremities

Correct answer: B – Coagulative necrosis with bacterial overgrowth

Gangrene is not a specific type of necrosis but refers to coagulative necrosis of a large area (usually an extremity) with superimposed bacterial infection. Wet gangrene has a liquefactive component. SECTION 5: APOPTOSIS

Q22: Question 22 Apoptosis differs from necrosis in that

  1. A. It causes inflammation
  2. B. It affects groups of cells
  3. C. It is energy-dependent
  4. D. It causes cell swelling

Correct answer: C – It is energy-dependent

Apoptosis is an ATP-dependent active process of programmed cell death affecting single cells without inflammation. Necrosis is passive, affects groups of cells, and causes inflammation. ---

Q23: Question 23 The morphologic hallmark of apoptosis is

  1. A. Cellular swelling
  2. B. Nuclear and cytoplasmic shrinkage
  3. C. Membrane rupture
  4. D. Inflammatory infiltrate

Correct answer: B – Nuclear and cytoplasmic shrinkage

Apoptotic cells show cell shrinkage, chromatin condensation (pyknosis), nuclear fragmentation, and formation of apoptotic bodies. The cell membrane remains intact initially. ---

Q24: Question 24 Which pathway initiates apoptosis through death receptors?

  1. A. Intrinsic pathway
  2. B. Extrinsic pathway
  3. C. Perforin-granzyme pathway
  4. D. Lysosomal pathway

Correct answer: B – Extrinsic pathway

The extrinsic pathway is initiated by binding of death ligands (like FasL, TNF) to death receptors (like Fas, TNFR1) on the cell surface, leading to caspase activation. ---

Q25: Question 25 The intrinsic pathway of apoptosis is regulated by

  1. A. Death receptors
  2. B. Bcl-2 family proteins
  3. C. Caspase-8
  4. D. Fas ligand

Correct answer: B – Bcl-2 family proteins

The intrinsic (mitochondrial) pathway is regulated by the Bcl-2 family of proteins. Pro-apoptotic members (Bax, Bak) promote apoptosis, while anti-apoptotic members (Bcl-2, Bcl-xL) inhibit it. ---

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