Necrosis

Question 1

what is the order of the 3 events?

Answer 1

necrosis, inflammation, apoptosis.

Question 2

what is hypoxia/ischemia?

Answer 2

no oxygen cell death

Question 3

physcial/chemical reasons for cell death?

Answer 3

trauma.

Question 4

is cell injury reversible or not?

Answer 4

reversible.

Question 5

is cell death reversible or not?

Answer 5

irreversible.

Question 6

what happens to cell size during n?

Answer 6

enlarged.

Question 7

what happens to cell size during a?

Answer 7

reduced,

Question 8

what happens to nucleus during n?

Answer 8

pyknotic.

Question 9

what happens to nucleus during a?

Answer 9

fragmented.

Question 10

what happens to cell membrane during n?

Answer 10

disrupted.

Question 11

what happens to cell membrane during a?

Answer 11

intact.

Question 12

what happens to cell contents during n?

Answer 12

digested/leakage.

Question 13

what happens to cell contents during a?

Answer 13

intact-ish.

Question 14

what happens to inflammation during n?

Answer 14

subsequent/frequent.

Question 15

what happens to inflammation during a?

Answer 15

none usually.

Question 16

necrosis morphology?

Answer 16

1. pyknosis
2. karyorrhexis
3. karyolysis
4. cytoplasmic changes

Question 17

what is pyknosis?

Answer 17

nuclear shrinkage/DNA condenses.

Question 18

what is karyorrhexis?

Answer 18

fragmentation/nuclear memrbane ruptures.

Question 19

what is karyolysis?

Answer 19

fading/dissolution of chromatin (DNAases RNAases)

Question 20

what cytoplasmic changes occur during necrosis?

Answer 20

increased eosinophilia due to binding of eosin to damaged proteins. cells look darker.

Question 21

what is coagulative n?

Answer 21

• proteins denature and aggregate rather than degrade.
• inflammatory response.
• dead cells/tissue replaced by regeneration

Question 22

what is liquefactive n?

Answer 22

• enzymic digestion of cellular components?

- dissolution of tissue

Question 23

what is caseous n?

Answer 23

• end result of tuberculosis infection.
• inflammatory response initiated/phagocytosis.
• cheese-like debris

Question 24

what is fat n?

Answer 24

• end result of lipases digesting cells.
• acute pancreatitis
• inflammatory response intitiated

Question 25

what is fibrinoid n?

Answer 25

- fibrin accumualtion. | - inflammatory response initiated.

Question 26

what is gangrenous n?

Answer 26

- loss of blood supply to limb - undergoes coagulative necrosis across multiple layers of tissue - inflammatory response initiated.

Question 27

what are the potential mechanisms for cell death?

Answer 27

- loss of atp for energy - loss of mitochondrial function - loss of calcium homeostasis - production of reactive oxygen

Question 28

What are major causes of atp depletion?

Answer 28

-hypoxia/ischemia

Question 29

why does the lack of atp lead to cell death?

Answer 29

- failure of the na/k pump to work - na accumulated - gain of solute is followed by gain of water. - cell swells - anaerobic glycolysis increases, so decrease in pH. - protein synthesis apparatus is damaged.

Question 30

how does lack of calcium homeostasis lead to cell death?

Answer 30

- atp dependant ca2+ pump doesn't work, so influx of ca2+. - activation of ca2+ enzymes. - activation of proteases, lipases (breakdown of cytoskeleton proteins and phospholipid membranes), endonucleases

Question 31

how does production of reactive oxygen species lead to cell death?

Answer 31

-ros attack key molecules when uncontrolled.

Question 32

physiological causes of apoptosis?

Answer 32

serves to eliminate cells that are no longer needed, and to maintain a steady number of various cell populations in tissues.

Question 33

pathological causes of apoptosis?

Answer 33

eliminates cells that are injured beyond repair without eliciting a host reaction, thus limiting collateral tissue damage.

Question 34

what pathways are there for apoptosis?

Answer 34

- extrinsic (death receptor pathway) | - intrinsic (mitochondrial)

Question 35

what activates intrinsic pathway?

Answer 35

- DNA damage (dna damage activates pro-apoptotic factors) - promotes release of cytochrome c from the mitochondria which activates caspase 9 - caspase 3 is at the effector stage of apoptosis (cleavage and inactivation of cell constituents)