Cell death

1. Which of the following is the hallmark of cell death?

A) Nuclear condensation
B) Cellular proliferation
C) Mitochondrial rupture
D) Cytoplasmic swelling
E) Increased ATP production

2. Which of the following types of necrosis is characterized by the softening of tissue due to
enzymatic lysis?
A) Coagulative necrosis
B) Liquefactive necrosis
C) Fat necrosis
D) Caseous necrosis
E) Gangrenous necrosis

3. In which tissue does coagulative necrosis typically occur?

A) Liver
B) Brain
C) Heart
D) Lung
E) Skin

4. Which type of necrosis is most commonly associated with ischemic infarction?

A) Coagulative necrosis
B) Liquefactive necrosis
C) Caseous necrosis
D) Fat necrosis
E) Fibrinoid necrosis

5. What is the appearance of tissue affected by caseous necrosis?

A) Mummified and dry
B) Soft and friable, resembling cottage cheese
C) Liquefied and watery
D) Chalky white with calcium deposits
E) Pale with preserved structure

6. What characterizes fat necrosis?

A) Presence of granulomatous inflammation
B) Presence of chalky-white deposits in adipose tissue
C) Mummification of tissue
D) Rapid liquefaction of the tissue
E) Formation of abscesses

7. Which of the following is typically associated with dry gangrene?

A) Infected tissue
B) Mummified appearance
C) Liquefactive changes
D) Wedge-shaped infarction
E) Greenish discoloration

8. What is the result of saponification in fat necrosis?

A) Formation of fibrosis
B) Conversion of fat to chalky-white deposits
C) Liquefaction of fat cells
D) Formation of abscesses
E) Calcium deposition on viable tissue

9. What is a defining feature of fibrinoid necrosis?

A) Necrosis of muscle tissue
B) Bright pink staining of the blood vessel wall
C) Necrosis of adipose tissue
D) Formation of granulomas
E) Sudden death of large tissue areas

10. Which of the following tissues undergoes liquefactive necrosis after infarction?
A) Brain
B) Heart
C) Liver
D) Kidney
E) Muscle

11. What is the key process that occurs during apoptosis?

A) Cellular swelling
B) Activation of caspases
C) Pyknosis
D) Vasodilation
E) Massive inflammation

12. Which of the following is NOT typically seen in apoptosis?

A) Nucleus fragmentation
B) Cytoplasmic shrinkage
C) Inflammatory response
D) Formation of apoptotic bodies
E) Cell shrinkage

13. Which enzyme is responsible for DNA fragmentation during apoptosis?

A) Caspase-1
B) Caspase-3
C) Endonuclease
D) Proteinase K
E) Telomerase
14. Which of the following is true about intrinsic apoptosis signaling?
A) Involves activation of TNF receptors
B) Involves cytochrome c release from mitochondria
C) Involves perforin release by cytotoxic T cells
D) Does not require ATP
E) Involves external signals only

15. Which of the following initiates the extrinsic apoptotic pathway?

A) Caspase activation by proteases
B) DNA damage
C) FAS ligand binding to the FAS receptor
D) Cytochrome c release
E) Decreased hormonal stimulation

16. What is the function of caspases in apoptosis?

A) Increase mitochondrial function
B) Break down the cytoskeleton and DNA
C) Induce cell swelling
D) Stimulate inflammation
E) Inactivate proteases

17. What is the main feature of apoptotic cells during microscopy?

A) Enlarged nucleus
B) Disrupted plasma membrane
C) Eosinophilic cytoplasm
D) Increased cell volume
E) Nuclear enlargement

18. Which of the following is an example of apoptosis occurring in the immune system?
A) Virally infected cells killed by CD8+ T cells
B) Cells dying due to ischemic injury
C) Brain cells undergoing liquefactive necrosis
D) Gangrenous tissue in the lower limb
E) Granulomas in tuberculosis

19. Which of the following describes the morphology of coagulative necrosis?

A) Soft, with tissue liquefaction
B) Wedge-shaped, pale, and firm
C) Mummified tissue
D) Cottage cheese-like appearance
E) Chalky-white deposits

20. Which is the defining characteristic of wet gangrene?

A) Mummification of tissue
B) Infection superimposed on necrosis
C) Liquefactive necrosis without inflammation
D) Granulomatous inflammation
E) Dry, non-inflammatory tissue death

21. Which of the following enzymes plays a role in the proteolytic breakdown of the
cytoskeleton in apoptosis?
A) Caspase-9
B) Caspase-3
C) Caspase-6
D) Caspase-7
E) Caspase-8

22. In the intrinsic pathway of apoptosis, the release of cytochrome c from mitochondria
activates which of the following?
A) Perforins
B) Caspase-8
C) Caspase-3
D) FAS receptor
E) Granzyme

23. Which of the following conditions is associated with fat necrosis?

A) Malignant hypertension
B) Trauma to the breast
C) Brain infarction
D) Pancreatic infarction
E) Tuberculosis

24. Which of the following best describes the tissue appearance in fat necrosis?
A) Soft, cottage cheese-like
B) Chalky-white with calcium deposition
C) Pale with preserved architecture
D) Liquefied and watery
E) Greenish and infected

25. Which of the following best describes the role of CD8+ T cells in apoptosis?
A) Inhibit viral replication
B) Destroy virally infected cells via perforin and granzyme
C) Induce necrosis of cancer cells
D) Activate TNF receptor pathways
E) Release cytokines to promote inflammation

26. In what way is fibrinoid necrosis most commonly characterized in histology?

A) Pink-staining deposits of fibrin in the vessel wall
B) Granulomatous formation within the tissues
C) Mummified appearance of necrotic tissue
D) Saponification of adipose tissue
E) Necrosis of liver cells

27. What is the characteristic feature of liquefactive necrosis in the brain?

A) Mummification of tissue
B) Formation of a cystic cavity
C) Fragmentation of neuronal cells
D) Pink staining of the tissue
E) Granulomatous response

28. What role does Bcl-2 play in the mitochondrial pathway of apoptosis?
A) Activates caspase-9
B) Prevents cytochrome c release from mitochondria
C) Inhibits perforin release
D) Activates the FAS receptor
E) Stimulates pro-apoptotic factors

29. The formation of apoptotic bodies is a characteristic feature of which process?

A) Necrosis
B) Apoptosis
C) Inflammation
D) Hypertrophy
E) Hyperplasia

30. Which of the following is true regarding the extrinsic pathway of apoptosis?
A) Involves release of cytochrome c
B) Does not require receptor-ligand interactions
C) FAS receptor binding initiates caspase activation
D) Activation occurs only in cells with damaged DNA
E) Requires the presence of granzyme

31. What is the role of p53 in cell death?

A) Promotes survival by inhibiting apoptosis
B) Induces apoptosis by activating Bax and Bak
C) Prevents cytochrome c release from mitochondria
D) Stimulates necrosis in response to hypoxia
E) Inhibits caspase activation

32. Which of the following is the initiating factor in intrinsic apoptosis?

A) Fas ligand binding
B) Tumor necrosis factor (TNF) receptor activation
C) DNA damage or cellular stress
D) Perforin and granzyme release
E) Bacterial toxin presence

33. How does granzyme B induce apoptosis in target cells?

A) Activates the extrinsic apoptotic pathway
B) Directly activates executioner caspases
C) Stimulates mitochondrial cytochrome c release
D) Forms pores in the cell membrane
E) Triggers a necrotic pathway
34. In ischemic injury, what is the primary molecular event that leads to necrosis?
A) Decrease in ATP production
B) Increase in mitochondrial membrane potential
C) Activation of caspases
D) DNA repair mechanisms
E) Upregulation of Bcl-2 proteins

35. What distinguishes necroptosis from apoptosis?

A) Absence of caspase involvement
B) Cellular shrinkage
C) Formation of apoptotic bodies
D) Absence of mitochondrial involvement
E) Induction of inflammation

36. What is the characteristic histologic appearance of liquefactive necrosis?

A) Well-preserved architecture with eosinophilic cytoplasm
B) Complete digestion of cells into a viscous mass
C) Chalky deposits of calcium
D) Wedge-shaped areas of ischemia
E) Mummified tissue with black discoloration

37. Which of the following triggers the mitochondrial pathway of apoptosis?

A) TNF receptor binding
B) Granzyme B release
C) DNA damage causing p53 activation
D) FAS ligand binding to FAS receptor
E) Increased glucose uptake

38. Which molecule is primarily responsible for forming apoptotic bodies?

A) Caspase-8
B) Caspase-3
C) TNF-α
D) FAS ligand
E) Bax protein

39. In apoptosis, phosphatidylserine is translocated to which part of the cell?

A) Nuclear membrane
B) Mitochondrial matrix
C) Inner leaflet of the plasma membrane
D) Outer leaflet of the plasma membrane
E) Cytosol
40. Which of the following best describes pyroptosis?
A) Caspase-independent cell death
B) Inflammatory form of programmed cell death
C) Necrosis induced by infection
D) Caspase-mediated DNA fragmentation
E) Autophagy-mediated cell survival

41. What is the key difference between autophagy and apoptosis?

A) Autophagy leads to inflammation, while apoptosis does not
B) Autophagy is a survival mechanism, whereas apoptosis is a death mechanism
C) Autophagy involves caspase activation, whereas apoptosis does not
D) Autophagy is triggered by TNF receptor binding
E) Apoptosis always involves mitochondrial membrane breakdown

42. Which of the following molecules directly inhibits apoptosis by preventing cytochrome c
release?
A) Bax
B) Bak
C) Bcl-2
D) Caspase-9
E) APAF-1

43. The death-inducing signaling complex (DISC) is associated with which pathway?
A) Intrinsic apoptosis
B) Necroptosis
C) Extrinsic apoptosis
D) Pyroptosis
E) Autophagy

44. Which of the following processes results in karyorrhexis?

A) Necrosis
B) Apoptosis
C) Cellular swelling
D) Inflammation
E) Hypertrophy

45. What is the role of Smac/DIABLO in apoptosis?

A) Activates caspase-9 directly
B) Inhibits caspase activity
C) Promotes apoptosis by inhibiting IAP (inhibitor of apoptosis proteins)
D) Prevents mitochondrial cytochrome c release
E) Stimulates inflammation

46. Which of the following occurs during the resolution of apoptosis?

A) Release of inflammatory cytokines
B) Phagocytosis of apoptotic bodies
C) Formation of granulomas
D) Deposition of calcium salts
E) Necrotic tissue liquefaction

47. What is the morphological hallmark of apoptosis?

A) Cytoplasmic swelling
B) Mitochondrial rupture
C) Nuclear pyknosis and fragmentation
D) Preservation of plasma membrane integrity
E) Eosinophilic cytoplasm

48. Which signaling molecule is essential for caspase activation in the extrinsic pathway?
A) FADD (Fas-associated death domain)
B) Cytochrome c
C) Bcl-2
D) Smac/DIABLO
E) Caspase-9

49. What is a defining feature of apoptosis compared to necrosis?

A) Induces inflammation
B) Cellular swelling
C) Controlled and energy-dependent process
D) Random DNA degradation
E) Loss of plasma membrane integrity

50. Which of the following is NOT involved in necroptosis?

A) Receptor-interacting protein kinase (RIPK1 and RIPK3)
B) Caspase activation
C) Mixed lineage kinase domain-like pseudokinase (MLKL)
D) Phosphorylation of MLKL
E) Inflammatory cytokine release

51. Which of the following proteins acts as an apoptosome in the intrinsic pathway?
A) APAF-1
B) Bcl-2
C) Bax
D) Cytochrome c
E) Caspase-3

52. How does saponification contribute to fat necrosis?

A) By enzymatically digesting triglycerides
B) By forming calcium soaps in necrotic tissue
C) By triggering the release of free fatty acids
D) By inducing cell swelling and rupture
E) By inhibiting lipase activity
53. What is the mechanism by which malignant hypertension causes fibrinoid necrosis?
A) Activation of caspases
B) Deposition of immune complexes in vessel walls
C) Increased vascular wall permeability and fibrin deposition
D) Formation of apoptotic bodies
E) Enzymatic lysis of endothelial cells

54. In the setting of wet gangrene, what process leads to the liquefaction of dead tissues?
A) Coagulation of proteins
B) Infiltration by macrophages
C) Infection with bacterial enzymes
D) Release of mitochondrial cytochrome c
E) Formation of a fibrous capsule

55. In caseous necrosis, the appearance of "cottage cheese-like" tissue is caused by:
A) Deposition of dystrophic calcium
B) Combination of liquefactive and coagulative necrosis
C) Extensive apoptosis of immune cells
D) Formation of granulomas by multinucleated giant cells
E) Ischemic infarction of lymphoid tissue

56. What is the role of the Bcl-2 family proteins in apoptosis?

A) They inhibit apoptosome formation
B) They regulate mitochondrial membrane permeability
C) They degrade cellular proteins during apoptosis
D) They act as death receptors on the cell surface
E) They directly activate caspases

57. During apoptosis, which molecule facilitates DNA fragmentation?

A) APAF-1
B) Granzyme B
C) Endonuclease
D) Caspase-8
E) Tumor necrosis factor

58. Why does apoptosis not elicit an inflammatory response?

A) It does not involve immune cells
B) It occurs without release of cellular contents
C) It prevents activation of cytokine pathways
D) It blocks neutrophil infiltration
E) It does not cause vascular changes

59. What is the histological hallmark of fat necrosis?

A) Multinucleated giant cells
B) Protein coagulation
C) Chalky white deposits
D) Fibrinoid deposition
E) Eosinophilic cytoplasm

60. Which of the following factors differentiates metastatic calcification from dystrophic
calcification?
A) Occurs only in living cells
B) Requires pre-existing tissue necrosis
C) Is driven by hypercalcemia
D) Involves saponification of fats
E) Leads to chalky deposits in necrotic tissue

61. Which enzyme class is responsible for the morphological changes observed in apoptosis?
A) Kinases
B) Proteases
C) Lipases
D) Hydrolases
E) Oxidases

62. What is the sequence of nuclear changes during necrosis?

A) Pyknosis → karyorrhexis → karyolysis
B) Karyolysis → pyknosis → karyorrhexis
C) Pyknosis → karyolysis → karyorrhexis
D) Karyorrhexis → pyknosis → karyolysis
E) Pyknosis → chromatin condensation → nuclear reassembly

63. How does ischemia lead to coagulative necrosis?

A) Formation of apoptotic bodies
B) Preservation of cell shape by protein coagulation
C) Activation of lysosomal enzymes
D) Rapid liquefaction of cellular components
E) Inflammatory infiltration

64. The pink staining observed in fibrinoid necrosis is due to:

A) Calcium deposition
B) Protein leakage, including fibrin
C) Apoptotic body formation
D) Nuclear condensation
E) Coagulation of cytoplasmic proteins

65. In apoptosis, which molecule is released from mitochondria to activate caspases?

A) FADD
B) Cytochrome c
C) Bax
D) TNF-α
E) Perforin
66. What distinguishes karyorrhexis from pyknosis?
A) Karyorrhexis involves chromatin condensation
B) Karyorrhexis is nuclear fragmentation
C) Karyorrhexis occurs before pyknosis
D) Karyorrhexis involves cytoplasmic swelling
E) Karyorrhexis results in protein coagulation

67. Which of the following is true about the extrinsic pathway of apoptosis?
A) It is triggered by DNA damage
B) It involves activation of FAS or TNF receptors
C) It requires mitochondrial cytochrome c release
D) It leads to cell swelling and inflammation
E) It is independent of caspase activation

68. In what clinical context is fibrinoid necrosis most commonly observed?

A) Diabetes mellitus
B) Granulomatous infections
C) Malignant hypertension and vasculitis
D) Severe dehydration
E) Chronic inflammation

69. Which of the following is an example of apoptosis in physiological conditions?

A) Formation of an abscess
B) Endometrial shedding during the menstrual cycle
C) Liquefaction of brain infarction
D) Formation of a granuloma
E) Deposition of amyloid proteins

70. What type of necrosis is typical in acute pancreatitis?

A) Coagulative necrosis
B) Liquefactive necrosis
C) Fat necrosis
D) Fibrinoid necrosis
E) Gangrenous necrosis

71. Which of the following is NOT a characteristic of coagulative necrosis?

A) Cell architecture is preserved.
B) Nucleus undergoes karyorrhexis.
C) It occurs in ischemic infarctions of the brain.
D) Proteins coagulate, maintaining organ structure.
E) It results in firm, pale tissue.

72. How does dystrophic calcification differ from metastatic calcification?

A) It only occurs in the setting of hypercalcemia.
B) It involves necrotic tissues as a nidus.
C) It affects normal, non-damaged tissues.
D) It is unrelated to serum calcium levels.
E) It is seen in conditions like hyperparathyroidism.

73. In liquefactive necrosis, what mediates the breakdown of tissue?

A) Decreased oxygen levels
B) Lysosomal enzyme activation
C) Formation of apoptotic bodies
D) Calcium deposition
E) Caspase activation

74. What is the appearance of a tissue undergoing caseous necrosis?

A) Firm and wedge-shaped
B) Yellow and chalky
C) Soft, friable, and cheese-like
D) Pink with fibrin deposits
E) Pale with intact cell outlines

75. Which feature of apoptosis is most responsible for its lack of inflammation?
A) DNA fragmentation
B) Cellular shrinkage
C) Formation of apoptotic bodies
D) Caspase activation
E) Activation of macrophages

76. What is the defining microscopic feature of fibrinoid necrosis?

A) Granuloma formation
B) Pink-staining vessel walls
C) Intact nuclei with eosinophilic cytoplasm
D) Cottage cheese-like appearance
E) Chalky white calcifications

77. What causes the chalky-white appearance of fat necrosis?

A) Coagulation of proteins
B) Deposition of calcium soaps
C) Infiltration of inflammatory cells
D) Formation of granulomas
E) Lysis of adipose cells

78. Which of the following does NOT activate caspases in apoptosis?

A) Cytochrome c release
B) DNA fragmentation
C) TNF binding to its receptor
D) Perforin-mediated pore formation
E) FAS ligand binding to CD95
79. Why does infarction in the brain result in liquefactive necrosis instead of coagulative
necrosis?
A) Microglial cells release proteolytic enzymes.
B) Ischemia is less severe in the brain.
C) Caspase activation is inhibited.
D) Neurons undergo faster apoptosis.
E) Blood re-entry causes liquefaction.

80. Which pathway is most involved in CD8+ T-cell-mediated apoptosis?

A) Intrinsic mitochondrial pathway
B) Extrinsic receptor-ligand pathway
C) Perforin-granzyme pathway
D) Caspase-independent pathway
E) Fibrinoid necrosis pathway

81. Which cellular process is inhibited by Bcl-2 proteins during apoptosis?

A) Mitochondrial cytochrome c release
B) FAS receptor activation
C) TNF-mediated signaling
D) DNA endonuclease activity
E) Caspase activation

82. What microscopic feature differentiates apoptosis from necrosis?

A) Chromatin condensation
B) Cytoplasmic eosinophilia
C) Lack of inflammation
D) Nuclear fragmentation
E) Swollen mitochondria

83. What clinical condition is most associated with fibrinoid necrosis?

A) Tuberculosis
B) Malignant hypertension
C) Acute pancreatitis
D) Brain infarction
E) Myocardial ischemia

84. In gangrenous necrosis, "wet gangrene" results from:

A) Coagulative necrosis alone
B) Secondary bacterial infection
C) Mummification of tissue
D) Absence of inflammation
E) Calcium deposition

85. What cellular component is targeted by endonucleases during apoptosis?

A) Plasma membrane
B) Mitochondrial outer membrane
C) Cytoskeleton
D) Nuclear DNA
E) Lysosomal enzymes

86. Which of the following pathways leads to the activation of caspases during apoptosis?
A) TNF receptor signaling
B) Dystrophic calcification
C) Protein coagulation
D) Neutrophil recruitment
E) Calcium influx

87. Which necrosis type is most likely observed in tuberculosis?

A) Coagulative necrosis
B) Fat necrosis
C) Liquefactive necrosis
D) Caseous necrosis
E) Fibrinoid necrosis

88. How is apoptosis involved in embryogenesis?

A) Formation of inflammatory granulomas
B) Removal of excess cells
C) Promotion of vascular calcifications
D) Deposition of fibrin in tissues
E) Initiation of coagulative necrosis

89. What is the primary mediator of apoptosis via the extrinsic pathway?
A) Granzyme B
B) Bcl-2 proteins
C) Cytochrome c
D) Death receptors
E) Proteolytic enzymes

90. Which necrotic process involves enzymatic lysis of dead cells?

A) Liquefactive necrosis
B) Coagulative necrosis
C) Caseous necrosis
D) Fat necrosis
E) Fibrinoid necrosis

91. Which molecule binds FAS death receptor during apoptosis?

A) Cytochrome c
B) FAS ligand
C) Perforin
D) Granzyme B
E) APAF-1
92. How does cytochrome c trigger caspase activation?
A) By activating the FAS receptor
B) By binding APAF-1 in the cytoplasm
C) By cleaving mitochondrial proteins
D) By inducing DNA fragmentation
E) By releasing proteolytic enzymes

93. What is the typical shape of ischemic infarcts in organs except the brain?
A) Wedge-shaped and pale
B) Rounded and friable
C) Chalky and granular
D) Diffuse and hemorrhagic
E) Soft with calcifications

94. In apoptosis, what is the role of caspases?

A) To break down the cytoskeleton and DNA
B) To deposit calcium in necrotic tissues
C) To promote mitochondrial swelling
D) To initiate inflammation
E) To inhibit cell shrinkage

95. Which organ is an exception to coagulative necrosis in ischemia?

A) Liver
B) Heart
C) Kidney
D) Brain
E) Spleen

96. Which cell type releases perforins in apoptosis?

A) Neutrophils
B) CD4+ T cells
C) CD8+ T cells
D) Macrophages
E) NK cells

97. What defines the progression of dry gangrene to wet gangrene?

A) Chronic ischemia
B) Calcification of tissues
C) Superimposed bacterial infection
D) Absence of neutrophils
E) Coagulative necrosis alone
98. What triggers the intrinsic pathway of apoptosis?
A) FAS ligand binding
B) Cellular injury and DNA damage
C) TNF receptor activation
D) Bacterial infection
E) Neutrophil infiltration

99. What is the predominant mechanism of brain infarction necrosis?

A) Coagulative necrosis
B) Liquefactive necrosis
C) Fibrinoid necrosis
D) Fat necrosis
E) Caseous necrosis

100. What histological finding is characteristic of apoptosis?

A) Pyknosis with inflammation
B) Nuclear karyolysis with macrophage recruitment
C) Eosinophilic cytoplasm and apoptotic bodies
D) Calcium deposits and granular debris
E) Fibrin deposition in tissues

ANSWERS

1. **A. Nuclear condensation**

2. **B. Liquefactive necrosis**
3. **C. Heart**
4. **A. Coagulative necrosis**
5. **B. Soft and friable, resembling cottage cheese**
6. **B. Presence of chalky-white deposits in adipose tissue**
7. **B. Mummified appearance**
8. **B. Conversion of fat to chalky-white deposits**
9. **B. Bright pink staining of the blood vessel wall**
10. **A. Brain**
11. **B. Activation of caspases**
12. **C. Inflammatory response**
13. **C. Endonuclease**
14. **B. Involves cytochrome c release from mitochondria**
15. **C. FAS ligand binding to the FAS receptor**
16. **B. Break down the cytoskeleton and DNA**
17. **C. Eosinophilic cytoplasm**
18. **A. Virally infected cells killed by CD8+ T cells**
19. **B. Wedge-shaped, pale, and firm**
20. **B. Infection superimposed on necrosis**
21. **B. Caspase-3**
22. **C. Caspase-3**
23. **D. Pancreatic infarction**
24. **B. Chalky-white with calcium deposition**
25. **B. Destroy virally infected cells via perforin and granzyme**
26. **A. Pink-staining deposits of fibrin in the vessel wall**
27. **B. Formation of a cystic cavity**
28. **B. Prevents cytochrome c release from mitochondria**
29. **B. Apoptosis**
30. **C. FAS receptor binding initiates caspase activation**
31. **B. Induces apoptosis by activating Bax and Bak**
32. **C. DNA damage or cellular stress**
33. **B. Directly activates executioner caspases**
34. **A. Decrease in ATP production**
35. **A. Absence of caspase involvement**
36. **B. Complete digestion of cells into a viscous mass**
37. **C. DNA damage causing p53 activation**
38. **B. Caspase-3**
39. **D. Outer leaflet of the plasma membrane**
40. **B. Inflammatory form of programmed cell death**
41. **B. Autophagy is a survival mechanism, whereas apoptosis is a death mechanism**
42. **C. Bcl-2**
43. **C. Extrinsic apoptosis**
44. **A. Necrosis**
45. **C. Promotes apoptosis by inhibiting IAP (inhibitor of apoptosis proteins)**
46. **B. Phagocytosis of apoptotic bodies**
47. **C. Nuclear pyknosis and fragmentation**
48. **A. FADD (Fas-associated death domain)**
49. **C. Controlled and energy-dependent process**
50. **B. Caspase activation**
51. **A. APAF-1**
52. **B. By forming calcium soaps in necrotic tissue**
53. **C. Increased vascular wall permeability and fibrin deposition**
54. **C. Infection with bacterial enzymes**
55. **D. Formation of granulomas by multinucleated giant cells**
56. **B. They regulate mitochondrial membrane permeability**
57. **C. Endonuclease**
58. **B. It occurs without release of cellular contents**
59. **C. Chalky white deposits**
60. **C. Is driven by hypercalcemia**
61. **B. Proteases**
62. **A. Pyknosis → karyorrhexis → karyolysis**
63. **B. Preservation of cell shape by protein coagulation**
64. **B. Protein leakage, including fibrin**
65. **B. Cytochrome c**
66. **B. Karyorrhexis is nuclear fragmentation**
67. **B. It involves activation of FAS or TNF receptors**
68. **C. Malignant hypertension and vasculitis**
69. **B. Endometrial shedding during the menstrual cycle**
70. **C. Fat necrosis**
71. **C. It occurs in ischemic infarctions of the brain**
72. **B. It involves necrotic tissues as a nidus**
73. **B. Lysosomal enzyme activation**
74. **C. Soft, friable, and cheese-like**
75. **C. Formation of apoptotic bodies**
76. **B. Pink-staining vessel walls**
77. **B. Deposition of calcium soaps**
78. **B. DNA fragmentation**
79. **A. Microglial cells release proteolytic enzymes**
80. **C. Perforin-granzyme pathway**
81. **A. Mitochondrial cytochrome c release**
82. **A. Chromatin condensation**
83. **B. Malignant hypertension**
84. **B. Secondary bacterial infection**
85. **D. Nuclear DNA**
86. **A. TNF receptor signaling**
87. **D. Caseous necrosis**
88. **B. Removal of excess cells**
89. **D. Death receptors**
90. **A. Liquefactive necrosis**
91. **B. FAS ligand**
92. **B. By binding APAF-1 in the cytoplasm**
93. **A. Wedge-shaped and pale**
94. **A. To break down the cytoskeleton and DNA**
95. **D. Brain**
96. **C. CD8+ T cells**
97. **C. Superimposed bacterial infection**
98. **B. Cellular injury and DNA damage**
99. **B. Liquefactive necrosis**
100. **C. Eosinophilic cytoplasm and apoptotic bodies**