Apoptosis and necrosis

Question 1

Programmed destruction of cells during embryogenesis

Answer 1

Apoptosis

Question 2

Hormone dependent involution

Answer 2

Apoptosis

Question 3

In endometrium during menstrual cycle

Answer 3

Hormone dependent involution
Physiological
Apoptosis

Question 4

Prostate atrophy after castration

Answer 4

Pathological hormone dependent involution

Apoptosis

Question 5

Cell deletion in proliferating tissues e.g. cell death in tumors

Answer 5

Apoptosis

Question 6

deletion of autoreactive T-lymphocytes in thymus

Answer 6

Immune cell death apoptosis

Question 7

cell death induced by cytotoxic T cells

Answer 7

Immune cell death apoptosis

Question 8

mild heat, radiation, cytotoxic treatment.

Answer 8

Mild injurious stimuli apoptosis

Question 9

Alzheimer disease

Answer 9

Death of neurons in disease processes ,apoptosis

Question 10

Enzymes which are present in the cytoplasm and are key players in apoptosis

Found in an inactive form in the cytoplasm.

Answer 10

Caspases

Question 11

Caspases name meaning

Answer 11

They are called Caspases from C; from Cysteine active site, “asp”; from cleavage after aspartic acid residue.

Question 12

signaling of these caspases results in commitment of cells to apoptotic cell death. These are found in certain cell types.

Answer 12

Initiators

Question 13

these are proteases which bring about the structural degradation of the cells to give the classical morphology. They are present in all cell types.

Answer 13

Effectors

Question 14

BCL-2 / BCL-XL

Answer 14

suppress apoptosis

Question 15

Bax / Bad

Answer 15

Enhance apoptosis

Question 16

protects from apoptosis by stabilizing the mitochondrial membrane, thus preventing increase permeability, by binding and sequestering cytochrome-C, and stabilizing proteins like the Apaf, thus preventing its activation.

Answer 16

Bcl-2

Question 17

Mitochondrial damage mechanism of apoptosis

Answer 17

Stimuli like toxins, or signalling will open permeability transition pore complex (PTPC), or mega channels, which will release material mainly cytochrome-C from the mitochondria to cytosol.
Cytochrome-C will bind to Apaf “pro-apoptotic protease-activating factor” and activate effector caspases

Question 18

intrinsic or extrinsic triggers to induce apoptosis like low ATP and high ROS

Answer 18

Signaling

Question 19

Apoptosis execution

Answer 19

by caspases that activate cytoplasmic endonuclease and proteases that degrade cytoskeletal & nuclear proteins which results in breakdown of cytoskeleton and fragmentation of nuclear chromatin.

Question 20

Apoptosis Control and integration

Answer 20

by the BCL-2 family that can either inhibit or promote cell death.

Question 21

Removal of dead cells

Answer 21

the formation of apoptotic bodies containing various intracellular organelles; they express new ligands that mediate phagocytic cell binding and uptake

Question 22

Apoptosis morphology

Answer 22

Single cells or groups of cells
Cells show intensely eosinophilic cytoplasm and condensed pyknotic nucleus
Cells are not surrounded by inflammatory cells
Rapidly removed by fragmentation and engulfment by cells

Question 23

Pyknosis

Answer 23

increased basophilia due to shrinkage of the nucleus

Question 24

chromatin 
clumping
organellar 
swelling
membrane 
damage 
Enzymatic digestion and leakage of cellular contents

Answer 24

Necrosis

Question 25

chromatin 
condensation
chromatin 
fragmentation
cytoplasmic 
budding

Answer 25

Apoptosis

Question 26

Intact membrane ; altered structure, especially orientation of lipids
What type of death?

Answer 26

Apoptosis

Question 27

Cellular contents Intact; may be released in apoptotic bodies

Answer 27

Apoptosis

Question 28

may be pathologic after some forms of cell injury, especially DNA damage

Answer 28

Apoptosis

Question 29

Apoptosis nuclear change

Answer 29

Fragmentation into nucleosome size fragments

Question 30

death of cells with preservation of the basic structural outlines of the cells for days
Protein denaturation overcomes enzymatic digestion
Seen in most organs after hypoxia/ischemia except brain

Answer 30

Coagulative necrosis

Question 31

necrosis with complete digestion of the cells and destruction of the normal architecture
Enzymatic digestion overcomes the denaturation

Answer 31

Liquefactive necrosis

Question 32

hypoxic/ischemic injury of the brain

What necrosis is it?

Answer 32

Liquefactive necrosis

Question 33

bacterial/fungal infection, with accumulation of WBCs and release of enzymes

Answer 33

Liquefactive necrosis

Question 34

cyst formation at the site of previous necrosis due

brain injury due to hemorrhage

Answer 34

Liquefactive necrosis

Question 35

Special type of necrosis, seen with tuberculous infection
the tissue architecture is completely obliterated
Grossly:
cheesy white appearance to the necrotic focus Microscopically:
the necrotic focus is composed of structure-less amorphous granular debris

Answer 35

Caseous necrosis

Question 36

Special type of necrosis with focal areas of fat destruction
Seen with acute pancreatitis, due to release of enzymes from the injured pancreas
Grossly:
fat saponification: visible white chalky areas
Microscopically:
shadows of cells with calcification

Answer 36

Fatty necrosis

Question 37

Gangrenous necrosis

Answer 37

ischemic coagulative necrosis (Dry gangrene: frequently of a limb)
When there is superimposed infection with a liquefactive component, the lesion is called “wet gangrene”