Inflammation I

Question 1

What is apoptosis?

Answer 1

Programmed cell death requiring ATP (p.212)

Question 2

What are the two pathways of apoptosis?

Answer 2

Intrinsic and extrinsic- both involve activation of cytosolic caspases that mediate cellular breakdown (p.212)

Question 3

How much inflammation is involved in apoptosis?

Answer 3

No significant inflammation (p.212)

Question 4

What characterizes apoptosis?

Answer 4

Characterized by cell shrinkage, nuclear shrinkage (pyknosis) and basophilia, membrane blebbing, nuclear fragmentation (karyorrhexis), and formation of apoptotic bodies which are subsequently phagocytosed (p.212)

Question 5

What is karyorrhexis?

Answer 5

Nuclear fragmentation (p.212)

Question 6

Name three instances where the intrinsic pathway of apoptosis used.

Answer 6

1.) Involved in tissue remodeling in embryogenesis; 2.) Occurs when a growth factor is withdrawn from a proliferating cell population (e.g. decreased IL-2 after a completed immune reaction causes apoptosis of proliferating effector cells); 3.) Occurs after exposure to injurious stimuli (radiation, toxins, hypoxia, etc.) (p.212)

Question 7

What changes lead to increased mitochondria permeability and cytochrome c release in the intrinsic pathway of apoptosis?

Answer 7

Changes in the proportions of anti- and pro- apoptotic factors (p.212)

Question 8

What are the two pathways associated with the extrinsic pathway of apoptosis?

Answer 8

1.) Ligand receptor interactions (Fas ligand binding to Fas CD95); 2.) Immune cell (cytotoxic T cell release of perforin and granzyme B) (p.212)

Question 9

Define necrosis.

Answer 9

The enzymatic degradation and protein denaturation of a cell resulting from exogenous injury. Intracellular components extravate. (p.212)

Question 10

What is the principle difference between apoptosis and necrosis?

Answer 10

Necrosis is an inflammatory process; apoptosis is not (p.212)

Question 11

Name the 6 types of necrosis.

Answer 11

1.) Coagulative; 2.) Liquefactive; 3.) Caseous; 4.) Fatty; 5.) Fibrinoid; 6.) Gangrenous (p.212)

Question 12

Where does coagualtive necrosis occur?

Answer 12

Heart, liver, kidney (p.212)

Question 13

Where does liquefactive necrosis occur?

Answer 13

Brain, bacterial abcesses, pleural effusions (p.212)

Question 14

What are the two types of gangrenous necrosis?

Answer 14

Dry (ischemic coagulative) or wet (with bacteria) (p.212)

Question 15

Where does caseous necrosis occur?

Answer 15

TB, systemic fungi (p.212)

Question 16

Where does fatty necrosis occur?

Answer 16

Peripancreatic fat (p.212)

Question 17

Where does fibrinoid necrosis occur?

Answer 17

Blood vessels (p.212)

Question 18

Where does gangrenous necrosis occur?

Answer 18

Limbs and in the GI tract (p.212)

Question 19

What are the six hallmark signs that cell injury is reversible with oxygen?

Answer 19

1.) decreased ATP synthesis; 2.) cellular swelling (no ATP causes impaired Na/K pump); 3.) Nuclear chromatin clumping; 4.) decreased glycogen; 5.) fatty change; 6.) ribosomal detachment (decreased protein synthesis) (p.213)

Question 20

What are the five hallmark signs that cell injury is irreversible?

Answer 20

1.) Nuclear pyknosis, karyolysis, karyorrhexis; 2.) Calcium influx –> caspase activation; 3.) Plasma membrane damage; 4.) Lysosomal rupture; 5.) Mitochondrial permeability (p.213)

Question 21

What areas of the brain are most susceptible to hypoxia and ischemia/ infarction?

Answer 21

ACA/MCA/PCA boundary areas (p.213)

Question 22

What areas of the heart are most susceptible to hypoxia and ischemia/ infarction?

Answer 22

Subendocardium (LV) (p.213)