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Flashcards in cell injury Deck (70):
1

define cell injury

injury to the smallest living unit in the body

2

what 4 factors does maintenance of cellular steady state involve.

1- preservation of genetic integrity
2- normal enzyme content.
3-intact membranes and transmembrane proteins.
4-Adequate supply of substrates and oxygen.

3

it a normal cell is put under stress what change will it undergo

adaptation

4

if a normal cell is put under injurious stimulus then what process will take place

cell injury

5

what 2 forms of cell injury are there

reversible
irreversible

6

is irreversible cell injury takes place what happens to the cell

apoptosis and necrosis.

7

If cells are put under stress due to increased cellular activity they often adapt by undergoing what 2 processes.

hyperplasia
hypertrophy

8

if cell are put under stress due to decreased cellular activity they adapt by undergo in what process

atrophy

9

metaplasia often occurs as a result of increased stress on a cell. what is metaplasia

change in cellular morphology

10

what changes morphologically occur in the cervix at puberty

at puberty the columnar cells replace some squamous cells at the squamouscoloumnar junction

11

What are the injurious stimuli which mean that a cell in unable to adapt and therefore becomes injured.

oxygen availability
physical trauma
chemical agents
infectious organisms
Irradiation
Others- immunological, lack of essential nutrients/vitamin, genetic disorders and ageing.

12

Lack of oxygen delivery to cells is known as

hypoxia

13

no oxygen delivery to cells is known as

anoxia

14

Do loss of oxygen availability result in schema

Yes- if lest to long
No- cell can be reposed if condition causing hypoxia/annoxia is resolved within the given time frame.

15

what are the 2 main causes of physical trauma that cause cell injury

Mechanical trauma- disrupt cell structure, thrombosis, bullet shot through the head cause devascularisation.
Extremes of temperature- heat which denatures proteins and ice crystals.

16

what are the chemical causes which cause cell injury

alcohol, tobacco, drugs, poisons, environmental and occupational.

17

what are the 2 main modes of action of chemical agents in causing cellular injury

simple denaturation
interference with cellular metabolism

18

what are the 2 types of bacterial toxins which result in cell injury

exotoxins.
endotoxins.

19

how do virus cause cell injury

Hijacking of cell machinery
and collateral damage by inflammation.

20

how does irradiation cause cello damage.

e.g. X-rays, radioactive particles
Generation of free radicals and direct damage to macromolecules

21

which parts of the body are very highly sensitive to irradiation

bone marrow, gonads, intestines- parts of the body with high turnover rate

22

which parts of the body are very lowly sensitive to irradiation

uterus, pancreas, adrenal

23

what are the main targets for cell injury

mitochondrial function
membrane integrity and function
protein synthesis
cytoskeleton
genetic apparatus.

24

surplus of what 2 chemicals can cause swelling (known as cloudy swelling) and what symptoms is this associated with.

Na+ and H20 surplus c- associated with hypoxia, but can be due to fever or damage due to toxins.

25

what is the consequence of ribosome detachment

decreased protein synthesis in the mitochondria.

26

what causes decreased pH in injured cells

low glycogen and high lactic acid.
low pH results in less lipids being packaged and hence they build up- fatty change.

27

define a free radical

Highly reactive ions or molecules with single unpaired electron in outer orbital e.g. oxygen free radicals

28

what can cause membrane defects

bacterial toxins, viral proteins, complement, cytolytic lymphocytes, and various physical and chemical agents

29

what detoxifies free radicals

superoxide dismutase and antioxidants.

30

Loss of membrane barriers leads to the loss in what function

maintaining metabolite gradients

31

what enzymes does calcium activate and what is the consequence of this

deleterious effects of calcium increase.

ATPases (thereby hastening ATP depletion),
phospholipases (which cause membrane damage),
proteases (break down membrane and cytoskeletal proteins)
endonucleases (responsible for DNA fragmentation)

32

what are the types of cell death

necrosis
apoptosis.

33

what is necrosis

Cell death as result of lethal cell injury

34

is necrosis a passive or active process

passive

35

does necrosis have a inflammatory process

Yes

36

What are the 5 main forms of necrosis

coagulation- most common
caseous- cheese like
colliquative- liquifies
gangrene- wet bacterial and dry
fat/fibrinoid- fat becomes necrotic when injurged, lysis of necrotic fat releases fatty acids which chelate ca2+

37

when does coagulative encores occur

iscahemia or infarction

38

what bacterial infection causes caseous necrosis occur

TB

39

what organ undergoes colliquative necrosis and why

brain as it has no collagen.

40

what types of proteins are denatured in coagulative necrosis

Denaturation of intracytoplasmic protein

41

does coagulative tissue still have the basic microscopic structure

Yes

42

what happens to the dead cell in coagulative necrosis

become firm and slight swollen

43

what occurs at the site of colliqutive necrosis

cyst

44

does caseous tissue still have the basic microscopic structure

No
Cellular detail destroyed in this area, which is surrounded by granulomatous inflammation.
Dead tissue lacks any structure

45

Does caseous necrosis have granulomatous inflammation around the affected tissue

Yes

46

what causes wet gangrene

bacterial infection

47

what causes dry gangrene

type 2 diabetics- typically in the peripheries

48

define apoptosis

‘Programmed cell death’ or ‘apoptosis’

49

Is apoptosis a passive or active process

active

50

when does physiological apoptosis take place (give examples)

Embryogenesis, Involution, Elimination of self-reacting
lymphocytes

51

when does pathological apoptosis take place (give examples)

DNA/protein damage, Viral infections, Cell killing by cytotoxic T-cells, Chemo/radiotherapy

52

where are Apoptosis initiating factor (AIF) and cytochrome C normally found

inside the mitochondria

53

when Apoptosis initiating factor (AIF) and cytochrome C are relaxed in the cytosol what do they activate

caspases, which are the effector molecules of apoptosis

54

what actives p53, and what is its function

damaged DNA
causes the elimination of damaged cells by apoptosis

55

what does a mutation in p53 cause

unable to eliminate damaged cells by apoptosis, cell accumulate and develop genetic abnormalities and become malignant.

56

what is the function of bcl

sequesters cytochrome C and thus inhibits apoptosis.

57

what can mutations in over expression of bcl result in

tumours gain the ability to proliferate in an uncontrolled way.

58

is necrosis pathological or physiological

pathological

59

is apoptosis pathological of physiological

physicological

60

Is the cell size enlarged of reduced in necrosis

enlarged

61

Is the cell size enlarged of reduced in apoptosis

reduced

62

what happens to the plasma membrane and the contents of a cell in necrosis

plasma membran disruptes an enzyme digestion so they may leak.

63

what happens to the plasma membrane and the contents of a cell in apoptosis

plasma membrane intact cellular contents in tack and may be released into the apoptotic body

64

is there inflammation in necrosis

Yes

65

is there inflammation in apoptosis

No

66

how many cells are affected in apoptosis

1

67

how many cells are affected in necrosis

a group

68

in which subgroup of necrosis do cells lose their nucleus

coagulative

69

what happens to the nuclei in apoptosis

shrink

70

how is a appoptotic body removed

via phagocytosis.