Cell Death

Question 1

Pkynosis

Answer 1

Severe condensation of chromatin

First step of irreversible injury

Question 2

Karyorrhexis [kăr′ē-ō-rĕk′sĭs]

Answer 2

Nuclear fragmentation

Second step of irreversible injury

Question 3

Karyolysis

Answer 3

Nuclear dissolution

Third step of irreversible injury

Question 4

What are the main differences between necrosis and apoptosis

Answer 4

Necrosis

• Grow
• Pyknosis, karyorrhexis, karyolysis
• Cytoplasm leaks, releasing pro-inflammatory factors
• Pathogenic
• Multiple cells

Apoptosis

• Shrink
• No karyolysis
• No leakage/inflammation
• Can be normal
• Individual cells

Question 5

Coagulative necrosis

Answer 5

• Denaturation of proteins
• Normal cell outline
• Eosinophilic cytoplasm
• Due to hypoxia, ischemia, or acute toxicity
• Nuclear death (denaturation slows degradation of proteins but not nucleic acids)
• Grossly: pale tan-gray
• Kidney, liver, and muscle

Question 6

Caseous necrosis

Answer 6

• Complete loss of cellular architecture
• Amorphous (no cell outlines)
• Eosiniphilic blob w/ basophilic nuclear debris (WBCs)
• Surrounded by lymphocytes and macrophages
• Tuberculosis

Question 7

Liquefactive necrosis

Answer 7

• Neutrophils/cell debris in fluid contents of lysed cells (enzyme-mediated)
• Final stage in parenchyma of brain spinal cord (malacia)
• Only type of necrosis in brain
• Pyogenic bacterial infection w/ suppurative (neutrophil-rich) inflammation

Question 8

Enzymatic fat necrosis

Answer 8

• Peripancreatic adipose due to release of lipase from necrotic pancreatic acinar cells
• Micro: lipid-laden macrophages w/ neutrophils (inflammation); adipocytes w/ palely staining cytoplasm (adipocytes should not stain at all b/c lipids are removed)
  basophilic deposits (saponification)
• Macro: firm, nodular, white chalky deposits (= fat saponified w/ Ca)

Question 9

Nutritional fat necrosis (steatitis)

Answer 9

• Carnivores fed fish (hi unsaturated fat, low antioxidants) and vitamin E deficient cows
• Macro: firm, nodular, yellow-brown

Question 10

Idiopathic fat necrosis is found where?

Answer 10

• Mesentery/retroperitoneal tissue of over conditioned cows

- Ventral parietal peritoneum of horses

Question 11

Wet/gas gangrene

Answer 11

• Bacterial infection

Question 12

Dry gangrene

Answer 12

• Decreased blood supply or vascular perfusion
• type of coagulative necrosis
• i.e. frostbite, fescue toxicity

Question 13

Sequelae

Answer 13

Foreign material/bone fragments that resist degradation in the context of necrosis-associated inflammation

Question 14

Initiation phase of intrinsic (mitochondrial) apoptosis

Answer 14

• Mitochondria releases cytochrome c (controlled by BCL2 proteins)
• Cytochrome c binds APAF-1
• APAF-1 activates caspase-9

Question 15

Initiation phase of extrinsic (death receptor-initiated) apoptosis

Answer 15

• Death receptors = TNF family
• Bind pro-caspase-8 (and 10) when bound to ligand
• Multiple receptors congregate: pro-caspase-8 (and 10) activate each other

Question 16

Execution phase of apoptosis

Answer 16

Caspase-3, -6, -7, or -12 induce nuclear fragmentation

Question 17

Why do cells become senescent (non-dividing)?

Answer 17

1) Shortening of the telomeres

2) Tumor suppressor genes

Question 18

What are 4 scenarios in which apoptosis benefits the body?

Answer 18

1) Embryogenesis
2) Hormone dependent involution
3) Turnover
4) Elimination of self-reactive lymphocytes

Question 19

What are 4 causes of aging?

Answer 19

1) DNA damage
2) Cellular senescence
3) Defective protein homeostasis
4) Increased calorie uptake

Question 20

What is p53, what is its function, and what happens when it does not work?

Answer 20

1) Tumor supressor gene
2) Triggers apoptosis of damaged cells
3) Cancer