50 Multiple Choice Questions | MCQ Quiz | OmpathStudy Kenya

Question 1

Which of the following best describes physiologic hypertrophy?

Accepted Answer

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.

Question 2

Barrett esophagus is an example of

Accepted Answer

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.

Question 3

Which cellular adaptation is reversible upon removal of the stimulus?

Accepted Answer

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. ---

Question 4

Endometrial hyperplasia is primarily caused by

Accepted Answer

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. ---

Question 5

The decrease in cell size seen in atrophy is primarily due to

Accepted Answer

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

Question 6

Which is the most common cause of cell injury in clinical medicine?

Accepted Answer

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. ---

Question 7

The earliest ultrastructural change in reversible cell injury is

Accepted Answer

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. ---

Question 8

Free radical injury is most commonly caused by

Accepted Answer

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. ---

Question 9

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

Accepted Answer

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

Question 10

Calcium accumulation in injured cells leads to

Accepted Answer

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

Question 11

The hallmark of irreversible cell injury is

Accepted Answer

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. ---

Question 12

Cellular swelling results from

Accepted Answer

Enhanced oxidative phosphorylation — 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. ---

Question 13

Fatty change (steatosis) is most commonly seen in

Accepted Answer

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. ---

Question 14

Which microscopic change indicates irreversible injury?

Accepted Answer

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. ---

Question 15

Hydropic degeneration is characterized by

Accepted Answer

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

Question 16

Coagulative necrosis is characterized by

Accepted Answer

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. ---

Question 17

Liquefactive necrosis is typical of

Accepted Answer

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. ---

Question 18

Caseous necrosis is most characteristically seen in

Accepted Answer

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. ---

Question 19

Fat necrosis typically occurs in

Accepted Answer

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. ---

Question 20

Fibrinoid necrosis is seen in

Accepted Answer

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. ---

Question 21

Gangrenous necrosis refers to

Accepted Answer

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

Question 22

Apoptosis differs from necrosis in that

Accepted Answer

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. ---

Question 23

The morphologic hallmark of apoptosis is

Accepted Answer

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. ---

Question 24

Which pathway initiates apoptosis through death receptors?

Accepted Answer

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. ---

Question 25

The intrinsic pathway of apoptosis is regulated by

Accepted Answer

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. ---

Question 26

Cytochrome c is released from mitochondria during apoptosis and activates

Accepted Answer

Caspase-9 — Cytochrome c released from mitochondria binds to Apaf-1 (apoptotic protease activating factor-1) forming the apoptosome, which activates caspase-9, the initiator caspase of the intrinsic pathway. ---

Question 27

Apoptotic bodies are removed by

Accepted Answer

Phagocytes without inflammation — Apoptotic bodies are rapidly recognized and phagocytosed by macrophages and neighboring cells without eliciting inflammation. This is due to externalization of phosphatidylserine on the outer membrane. ---

Question 28

Physiologic apoptosis occurs in

Accepted Answer

Embryonic development — Physiologic apoptosis is essential in embryonic development (digit formation, neural development), normal tissue turnover, elimination of immune cells after immune response, and hormone-dependent involution. ---

Question 29

Which tumor suppressor gene can trigger apoptosis in response to DNA damage?

Accepted Answer

p53 — p53 is activated by DNA damage and can induce cell cycle arrest for repair or trigger apoptosis if damage is irreparable. It acts as the "guardian of the genome" and induces pro-apoptotic proteins like Bax. ---

Question 30

Caspases are

Accepted Answer

Proteolytic enzymes — Caspases are cysteine proteases that cleave proteins at aspartic acid residues. They exist as inactive pro-caspases and are activated during apoptosis to execute cell death by cleaving key cellular proteins. --- ## SECTION 6: INTRACELLULAR ACCUMULATIONS

Question 31

Lipofuscin is

Accepted Answer

An aging pigment — Lipofuscin is a yellow-brown "wear and tear" pigment that accumulates in aging or atrophic cells. It represents indigestible material from lipid peroxidation and is considered a marker of aging but is harmless. ---

Question 32

Hemosiderin accumulation is seen in

Accepted Answer

Iron overload — Hemosiderin is an iron-containing pigment formed from breakdown of hemoglobin. It accumulates locally (bruises) or systemically (hemochromatosis, multiple transfusions). It appears golden-yellow to brown and stains blue with Prussian blue. ---

Question 33

Primary hemochromatosis is caused by

Accepted Answer

Genetic defect in iron metabolism — Primary (hereditary) hemochromatosis is an autosomal recessive disorder causing excessive iron absorption from the gut due to mutations in the HFE gene. It leads to iron deposition in liver, pancreas, heart, and skin. ---

Question 34

Anthracosis refers to

Accepted Answer

Carbon pigment in lungs — Anthracosis is the accumulation of carbon particles (from air pollution or smoking) in the lungs and lymph nodes. It is extremely common in urban dwellers and smokers but usually asymptomatic. ---

Question 35

Glycogen accumulation is seen in

Accepted Answer

All of the above — Glycogen can accumulate in glycogen storage diseases (genetic enzyme defects), diabetes mellitus (especially in renal tubular cells and hepatocytes), and with corticosteroid use. It appears as clear vacuoles that are PAS-positive. ---

Question 36

Cholesterol accumulation in macrophages creates

Accepted Answer

Foam cells — When macrophages accumulate cholesterol, they develop foamy cytoplasm and are called foam cells. These are characteristic of atherosclerotic plaques and xanthomas. --- ## SECTION 7: PATHOLOGIC CALCIFICATION

Question 37

Dystrophic calcification occurs in

Accepted Answer

Normal serum calcium with tissue injury — Dystrophic calcification occurs in damaged or necrotic tissues despite normal serum calcium levels. It is seen in atherosclerotic plaques, damaged heart valves, old tuberculous lesions, and areas of fat necrosis. ---

Question 38

Metastatic calcification occurs in

Accepted Answer

Hypercalcemic states — Metastatic calcification occurs in normal tissues when serum calcium levels are elevated (hypercalcemia). Causes include hyperparathyroidism, vitamin D toxicity, renal failure, and extensive bone destruction from malignancy or Paget disease. ---

Question 39

Metastatic calcification preferentially affects

Accepted Answer

Lungs, kidneys, and gastric mucosa — Metastatic calcification preferentially affects tissues that excrete acid (lungs, kidneys, gastric mucosa) because alkaline pH favors calcium phosphate precipitation. Blood vessels and pulmonary alveolar septa are commonly affected. ---

Question 40

The mechanism of dystrophic calcification involves

Accepted Answer

Binding of calcium to phospholipids in damaged membranes — In dystrophic calcification, calcium binds to phospholipids in damaged cell membranes and forms calcium-phospholipid complexes, which then nucleate further calcium deposition forming hydroxyapatite crystals. --- ## SECTION 8: CELLULAR AGING

Question 41

Cellular aging is associated with

Accepted Answer

Accumulation of damaged macromolecules — Aging is associated with accumulation of damaged proteins, lipids, and DNA due to decreased repair capacity, increased oxidative stress, and impaired protein degradation. Telomeres shorten with each division. ---

Question 42

The Hayflick limit refers to

Accepted Answer

Replicative senescence after limited cell divisions — The Hayflick limit is the finite number of times normal human cells can divide before entering replicative senescence (approximately 50-60 divisions). This is due to progressive telomere shortening with each cell division. ---

Question 43

Werner syndrome is characterized by

Accepted Answer

Premature aging — Werner syndrome is a premature aging syndrome caused by mutations in the WRN gene (DNA helicase). Affected individuals show early onset of age-related diseases including atherosclerosis, cataracts, and malignancies. ---

Question 44

Oxidative stress in aging results from

Accepted Answer

Accumulation of reactive oxygen species — Aging is associated with accumulation of reactive oxygen species (ROS) from mitochondrial respiration and other sources, combined with decreased antioxidant defenses. This causes cumulative damage to cellular components. ---

Question 45

Autophagy in aging

Accepted Answer

Decreases with age — Autophagy (self-eating of cellular components) declines with aging, leading to accumulation of damaged organelles and proteins. Enhancing autophagy has been shown to extend lifespan in experimental models. --- ## SECTION 9: ADVANCED CONCEPTS

Question 46

Ischemia-reperfusion injury is primarily mediated by

Accepted Answer

Free radical production — Paradoxically, restoration of blood flow after ischemia can cause additional injury through production of free radicals (reactive oxygen species), calcium overload, inflammation, and complement activation. This is called reperfusion injury. ---

Question 47

Heat shock proteins function to

Accepted Answer

Repair misfolded proteins — Heat shock proteins (HSPs) are molecular chaperones induced by stress (heat, hypoxia, toxins) that help refold damaged proteins, prevent protein aggregation, and assist in protein degradation, protecting cells from injury. ---

Question 48

Which change distinguishes necroptosis from apoptosis?

Accepted Answer

Caspase-independent cell death with inflammation — Necroptosis is a programmed form of necrosis that is caspase-independent, mediated by RIP1 and RIP3 kinases. Unlike apoptosis, it results in membrane rupture and inflammation, but unlike necrosis, it is regulated. ---

Question 49

Autophagy can protect cells by

Accepted Answer

Removing damaged organelles — Autophagy is a survival mechanism where cells degrade and recycle damaged organelles and proteins through lysosomes. It provides nutrients during starvation and removes damaged components, but excessive autophagy can lead to cell death. ---

Question 50

The unfolded protein response (UPR) in the endoplasmic reticulum

Accepted Answer

Attempts to restore normal function or triggers apoptosis — The UPR is activated when misfolded proteins accumulate in the ER. Initially, it attempts to restore homeostasis by decreasing protein synthesis, increasing chaperone production, and enhancing protein degradation. If unsuccessful, it triggers apoptosis. --- ## Study Tips - Review the mechanisms of each type of cellular adaptation - Understand the key differences between reversible and irreversible injury - Know the distinguishing features of different types of necrosis - Master the intrinsic and extrinsic pathways of apoptosis - Understand the clinical significance of various accumulations - Recognize the differences between dystrophic and metastatic calcification --- End of Questions

50 Multiple Choice Questions | MCQ Quiz | OmpathStudy Kenya

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