MOD Ch2

Question 1

Anti-apoptotic factors

Answer 1

BCL-2, BCL-XL, MCL-1

Question 2

Pro-apoptotic factors

Answer 2

BAX and BAK

Question 3

Apoptotic sensors

Answer 3

BAD, BIM, BID, PUMA, NOXA

Question 4

Intrinsic apoptotic pathway

Answer 4

Cell injury–> BCL2–> BAX, BAK–> Mitochondria–> Cytochrome C

Question 5

Extrinsic apoptotic pathway

Answer 5

Receptor-ligand [Fas, TNF]–> Adaptor proteins

Question 6

Karyolysis

Answer 6

loss of DNA–> less basophilic

Question 7

Pyknosis

Answer 7

nuclear shrinkage, more basophilia

Question 8

Karyorrhexis

Answer 8

nucleus fragments

Question 9

Coagulative necrosis

Answer 9

Enzymes fail to lyse dead cells. Called an infarct when localized.

Question 10

Liquefactive necrosis

Answer 10

Digestion of cells leads to liquid mass. Caused by hypoxic death in CNS.

Question 11

Gangrenous necrosis

Answer 11

Caused by a necrosed limb. If bacterial infection, liquefaction can lead to wet gangrene.

Question 12

Caseous necrosis

Answer 12

Structureless fragments of lysed cells and granulations. Associate with tuberculosis and granulomas.

Question 13

Fat necrosis

Answer 13

Focal area of fat destruction (often from pancreatic lipases in acute pancreatitis) leading to fat sopanification

Question 14

Fibrinoid

Answer 14

Antigen/Antibody complexes deposited in arterial walls, combined with fibrin.

Question 15

Necroptosis

Answer 15

Triggers: TNFR1, viral RNA and DNA

Depends on: RIP1 and RIP3 signaling

Question 16

Pyroptosis

Answer 16

Cells invaded by microbes–> Caspase 1 activated–> IL-1 activated by cleaving

Question 17

Dystrophic Calcification

Answer 17

In diseased tissues, with normal calcium levels

Question 18

Metastatic Calcification

Answer 18

In normal tissues, with hypercalcemia due to CA2+ metabolism disturbance