PATHOPHYSIOLOGY –
SEMESTER EXAM REVIEWER 2025
(PART I)
UNIT 1: BASIC PRINCIPLES OF CELL INJURY AND ADAPTATION
LONG ESSAYS (10 marks)
Q1. What are cellular adaptations? Give examples.
A:
• Definition: Reversible functional/structural changes in response to stress.
• Types & Examples:
o Hypertrophy → ↑ Cell size (e.g., skeletal muscle growth in athletes).
o Hyperplasia → ↑ Cell number (e.g., endometrial hyperplasia).
o Atrophy → ↓ Cell size (e.g., muscle wasting in immobilization).
o Metaplasia → Replacement of one cell type by another (e.g., squamous
metaplasia in smokers).
Q2. Explain the various types of cell injury with examples. Discuss the etiology.
A:
• Types of Injury:
o Reversible → Cell swelling, fatty change.
o Irreversible → Membrane damage, nuclear changes (pyknosis, karyorrhexis,
karyolysis).
• Etiology:
o Hypoxia & Ischemia
o Physical agents (trauma, radiation, temperature)
o Chemical agents/drugs
o Infectious agents (bacteria, viruses)
o Immunological reactions
o Genetic defects
o Nutritional imbalances
Q3. Describe the pathogenesis of reversible cell injury induced by hypoxia/ischemia.
A:
, • ↓ Oxygen → ↓ ATP → Na⁺/K⁺ pump failure → Cellular swelling (hydropic change).
• Anaerobic glycolysis → ↑ Lactic acid → ↓ pH.
• Ribosome detachment → ↓ Protein synthesis.
Q4. Describe the pathogenesis of irreversible cell injury induced by hypoxia/ischemia.
A:
• Severe mitochondrial damage → ATP depletion.
• Lysosomal rupture → Release of enzymes → Autodigestion.
• ↑ Ca²⁺ influx → Enzyme activation (proteases, endonucleases).
• Nuclear changes → Pyknosis, Karyorrhexis, Karyolysis.
Q5. Explain etiology, pathogenesis, and morphology of reversible cell injury.
A:
• Etiology: Hypoxia, toxins, infections, immune reactions.
• Pathogenesis: ↓ ATP → Na⁺/K⁺ pump failure → Cell swelling.
• Morphology: Hydropic swelling, fatty change, plasma membrane blebbing.
Q6. Explain causes, pathogenesis, and morphology of irreversible cell injury.
A:
• Causes: Severe hypoxia, toxins, infections, radiation.
• Pathogenesis: Mitochondrial dysfunction, Ca²⁺ overload, membrane rupture.
• Morphology: Nuclear changes, loss of membrane integrity, necrosis.
SHORT ESSAYS (5 marks)
Q9. What is Cell Injury? Discuss the factors influencing it.
A:
• Definition: State when cell is unable to maintain homeostasis.
• Factors: Type of cell, duration of injury, intensity of stress, metabolic state.
Q10. What are the biochemical intracellular accumulations in cell injury?
A:
, • Lipids (fatty liver)
• Proteins (α1-antitrypsin deficiency)
• Glycogen (glycogen storage diseases)
• Pigments (lipofuscin, melanin, hemosiderin).
Q11. What is Hyperplasia? Differentiate physiological vs. pathological.
A:
• Definition: Increase in cell number.
• Physiological: Hormonal (breast in pregnancy), compensatory (liver regeneration).
• Pathological: Endometrial hyperplasia, psoriasis.
Q12. What is Necrosis? Write the pathogenesis.
A:
• Definition: Irreversible cell death caused by injury.
• Pathogenesis: Loss of ATP, Ca²⁺ influx, enzyme activation → protein denaturation &
enzymatic digestion.
Q13. Principles of pathogenesis of cell injury by agents.
A:
• ATP depletion
• Free radical damage
• Membrane damage
• Calcium influx → enzyme activation
• Mitochondrial damage
Q15. Mechanism of free radical-induced cell injury.
A:
• ROS attack membranes (lipid peroxidation), proteins, DNA.
• Sources: mitochondria, radiation, drugs.
• Neutralized by antioxidants (Vit E, C, glutathione).
SEMESTER EXAM REVIEWER 2025
(PART I)
UNIT 1: BASIC PRINCIPLES OF CELL INJURY AND ADAPTATION
LONG ESSAYS (10 marks)
Q1. What are cellular adaptations? Give examples.
A:
• Definition: Reversible functional/structural changes in response to stress.
• Types & Examples:
o Hypertrophy → ↑ Cell size (e.g., skeletal muscle growth in athletes).
o Hyperplasia → ↑ Cell number (e.g., endometrial hyperplasia).
o Atrophy → ↓ Cell size (e.g., muscle wasting in immobilization).
o Metaplasia → Replacement of one cell type by another (e.g., squamous
metaplasia in smokers).
Q2. Explain the various types of cell injury with examples. Discuss the etiology.
A:
• Types of Injury:
o Reversible → Cell swelling, fatty change.
o Irreversible → Membrane damage, nuclear changes (pyknosis, karyorrhexis,
karyolysis).
• Etiology:
o Hypoxia & Ischemia
o Physical agents (trauma, radiation, temperature)
o Chemical agents/drugs
o Infectious agents (bacteria, viruses)
o Immunological reactions
o Genetic defects
o Nutritional imbalances
Q3. Describe the pathogenesis of reversible cell injury induced by hypoxia/ischemia.
A:
, • ↓ Oxygen → ↓ ATP → Na⁺/K⁺ pump failure → Cellular swelling (hydropic change).
• Anaerobic glycolysis → ↑ Lactic acid → ↓ pH.
• Ribosome detachment → ↓ Protein synthesis.
Q4. Describe the pathogenesis of irreversible cell injury induced by hypoxia/ischemia.
A:
• Severe mitochondrial damage → ATP depletion.
• Lysosomal rupture → Release of enzymes → Autodigestion.
• ↑ Ca²⁺ influx → Enzyme activation (proteases, endonucleases).
• Nuclear changes → Pyknosis, Karyorrhexis, Karyolysis.
Q5. Explain etiology, pathogenesis, and morphology of reversible cell injury.
A:
• Etiology: Hypoxia, toxins, infections, immune reactions.
• Pathogenesis: ↓ ATP → Na⁺/K⁺ pump failure → Cell swelling.
• Morphology: Hydropic swelling, fatty change, plasma membrane blebbing.
Q6. Explain causes, pathogenesis, and morphology of irreversible cell injury.
A:
• Causes: Severe hypoxia, toxins, infections, radiation.
• Pathogenesis: Mitochondrial dysfunction, Ca²⁺ overload, membrane rupture.
• Morphology: Nuclear changes, loss of membrane integrity, necrosis.
SHORT ESSAYS (5 marks)
Q9. What is Cell Injury? Discuss the factors influencing it.
A:
• Definition: State when cell is unable to maintain homeostasis.
• Factors: Type of cell, duration of injury, intensity of stress, metabolic state.
Q10. What are the biochemical intracellular accumulations in cell injury?
A:
, • Lipids (fatty liver)
• Proteins (α1-antitrypsin deficiency)
• Glycogen (glycogen storage diseases)
• Pigments (lipofuscin, melanin, hemosiderin).
Q11. What is Hyperplasia? Differentiate physiological vs. pathological.
A:
• Definition: Increase in cell number.
• Physiological: Hormonal (breast in pregnancy), compensatory (liver regeneration).
• Pathological: Endometrial hyperplasia, psoriasis.
Q12. What is Necrosis? Write the pathogenesis.
A:
• Definition: Irreversible cell death caused by injury.
• Pathogenesis: Loss of ATP, Ca²⁺ influx, enzyme activation → protein denaturation &
enzymatic digestion.
Q13. Principles of pathogenesis of cell injury by agents.
A:
• ATP depletion
• Free radical damage
• Membrane damage
• Calcium influx → enzyme activation
• Mitochondrial damage
Q15. Mechanism of free radical-induced cell injury.
A:
• ROS attack membranes (lipid peroxidation), proteins, DNA.
• Sources: mitochondria, radiation, drugs.
• Neutralized by antioxidants (Vit E, C, glutathione).
