MOD 3 - Cell Injury Flashcards Preview

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Flashcards in MOD 3 - Cell Injury Deck (44):
1

in cellular adaptation, increased cellular activity = ?

hyperplasia/hypertrophy

2

in cellular adaptation, decreased cellular activity = ?

atrophy

3

in cellular adaptation, change in cell morphology = ?

metaplasia

4

what are the 9 common aetiology of cell injury

physical trauma, oxygen availability, chemical agents, infectious organisms, irradiation, others - immunological, lack of essential nutrient/vitamin, genetic disorders, ageing

5

what are the 2 main causes of physical trauma?

mechanical trauma - disruption of cells & thrombosis leading to ischaemia, extremes of temperature - heat denatruration of proteins, ice crystals, fever

6

what are the 2 main causes of oxygen availability ?

hypoxia/anoxia - reduction or loss of oxygen delivered to cells often caused by ischaemia, reoxygenation - reprefusion - can generate oxygen free radical which can lead to further cell death ie reprefusion injury

7

what are some of the common chemical agents which can cause cell injury

alcohol, tobacco smoke, drugs, poisons, environmental, occupational

8

what are the common mechanism which infectious organisms cause cell injury

bacterila toxi - exotoxins & endotoxins, hijacking of cell machinery by viral infection - cell lysis, collateral damage by inflammation.

9

what happen to the level of Ca2+ should mitochondria is damaged as part of cell injury

ATP drop - Na pump deactivate - Ca2+ influx along with H2O, Na - cell swell

10

what happen to the level of pH should mitochondria should fail

ATP drop - glycolysis increase (anaerobic production of ATP - lactic acid) - pH drops - nuclear chromatin clumping

11

what happens to the level of protein synthesis should mitochondria should fail

ATP drops - ribosomes detachment - decreased protein synthesis - lipid deposition within the cell (steatosis) (usually exported accompanied by exportation of protein) ie fatty change / cloudy swelling

12

what is a free radical?

it is a highly reactive ions/molecules with single unpaired electron in outer orbital eg oxygen free radicals

13

what does free radical do to proteins and nucleic acids & cel membrane?

chain reaction with the cell membrane to produce more free radical, damages proteins and nucleic acid - causing apoptosis

14

how is free radical detoxified

by superoxide dismutase and antioxidants eg vitamins A, C&E

15

what does superoxide do in our body?

bacterial killing by neutrophils and macrophages depends on superoxide (another reaction used by the body to produce free radical for its own good)

16

what happens when cell membrane is defective?

loss of membrane barriers leads to break down in metabolite gradients - increased Ca2+ which activates a number of enzymes eg ATPase (ATP depletion), prtoeases (break down membrane& cytoskeletal proteins), endonuclease (responsible for DNA fragmentation)

17

what is necrosis?

cll death as a result of lethal cell injury - passive process

18

what will necrosis incite?

inflammatory reaction

19

what are the subtypes of necrosis?

coagulative (most common), caseous (only happen in TB), Colliquative (only happen in brain), gangree (wet and dry subtype), fat & fibrinoid

20

state a description of coagulative necrosis

denaturation of intracytoplasmic proteins which then turn the tissue firm and slightly swollen and in normal setting tissue will have retention of microscopic architecture but protein within the dead cells can leak into blood stream

21

what is common condition for coagulative necrosis?

ischaemic injury (except in brain)

22

what is colliquative necrosis

it is necrotic neural tissue which is subject to total liquefaction and the site is eventually marked by a cyst

23

what is caseous necrosis characteristic of?

TB infection

24

what is caseous necrosis like?

cheese like - cellular detail destroyed then surrounded by granulomatous inflammation, no cellular structure can be identified

25

what is the difference between apoptosis and necrosis?

in apoptosis, cell membrane remain intact and no inflammation reaction and necrosis is the total opposite

26

what is gangrenous necrosis?

it is necrosis with putrefaction of the tissue (sometimes due to infection of certain bacteria such as clostridia) which will appear as black due to the deposition of iron sulphide from degraded haemoglobin

27

example of 'wet' gangrene?

complication of appenditis, intestinal necrosis - clostridia common in bowel

28

example of 'dry' gangrene

usually seen in toes etc as results of gradual arterial or small vessels obstruction in cases of diabetes or atherosclerosis

29

does apoptosis require energy to be carried out?

yes - active process

30

what is the enzyme which is responsible for carrying out apoptosis?

effector caspases

31

what are the 2 enzymes which activates caspases

AIF (apoptosis initiating factor) & cytochrome C

32

where are AIF & cytochrome C normally sequester?

in mitochondria

33

what enzyme normally sequester caspases and what normally down-regulate it?

Bcl-2 which is normally sequester by p53.

34

what can cause extrinsic pathway to commence?

inflammation

35

what can cause intrinsic pathway to commence?

radiation & damages to DNA

36

which one of the necrosis and apoptosis will affect multiple cells?

necrosis

37

which one of the necrosis and apoptosis will cause reduced size cells?

apoptosis

38

what happens to the nucleus of the cells which underwent necrosis?

pyknosis - karyorrhexis - karyolysis

39

which one of the necrosis and apoptosis will have intact plasma membrane?

apoptosis

40

which one of the necrosis and apoptosis will have intact cellular contents?

apoptosis

41

which one of the necrosis and apoptosis will cause adjacent inflammation

necrosis

42

what is pyknosis

process which cause cell nucleus to thicken into a dense mass which occurs when cells die

43

what is karyorrhexis

fragmentation of cell nucleus

44

what is karyolysis

breakdown of cell nucleus occuring during necrosis