cell injury Flashcards

1
Q

define cell injury

A

injury to the smallest living unit in the body

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2
Q

what 4 factors does maintenance of cellular steady state involve.

A

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

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3
Q

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

A

adaptation

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4
Q

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

A

cell injury

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5
Q

what 2 forms of cell injury are there

A

reversible

irreversible

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6
Q

is irreversible cell injury takes place what happens to the cell

A

apoptosis and necrosis.

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7
Q

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

A

hyperplasia

hypertrophy

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8
Q

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

A

atrophy

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9
Q

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

A

change in cellular morphology

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10
Q

what changes morphologically occur in the cervix at puberty

A

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

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11
Q

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

A
oxygen availability
physical trauma
chemical agents
infectious organisms
Irradiation
Others- immunological, lack of essential nutrients/vitamin, genetic disorders and ageing.
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12
Q

Lack of oxygen delivery to cells is known as

A

hypoxia

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13
Q

no oxygen delivery to cells is known as

A

anoxia

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14
Q

Do loss of oxygen availability result in schema

A

Yes- if lest to long

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

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15
Q

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

A

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

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16
Q

what are the chemical causes which cause cell injury

A

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

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17
Q

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

A

simple denaturation

interference with cellular metabolism

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18
Q

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

A

exotoxins.

endotoxins.

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19
Q

how do virus cause cell injury

A

Hijacking of cell machinery

and collateral damage by inflammation.

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20
Q

how does irradiation cause cello damage.

A

e.g. X-rays, radioactive particles

Generation of free radicals and direct damage to macromolecules

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21
Q

which parts of the body are very highly sensitive to irradiation

A

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

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22
Q

which parts of the body are very lowly sensitive to irradiation

A

uterus, pancreas, adrenal

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23
Q

what are the main targets for cell injury

A
mitochondrial function
membrane integrity and function
protein synthesis
cytoskeleton
genetic apparatus.
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24
Q

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

A

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

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25
Q

what is the consequence of ribosome detachment

A

decreased protein synthesis in the mitochondria.

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26
Q

what causes decreased pH in injured cells

A

low glycogen and high lactic acid.

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

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27
Q

define a free radical

A

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

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28
Q

what can cause membrane defects

A

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

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29
Q

what detoxifies free radicals

A

superoxide dismutase and antioxidants.

30
Q

Loss of membrane barriers leads to the loss in what function

A

maintaining metabolite gradients

31
Q

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

A

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
Q

what are the types of cell death

A

necrosis

apoptosis.

33
Q

what is necrosis

A

Cell death as result of lethal cell injury

34
Q

is necrosis a passive or active process

A

passive

35
Q

does necrosis have a inflammatory process

A

Yes

36
Q

What are the 5 main forms of necrosis

A
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
Q

when does coagulative encores occur

A

iscahemia or infarction

38
Q

what bacterial infection causes caseous necrosis occur

A

TB

39
Q

what organ undergoes colliquative necrosis and why

A

brain as it has no collagen.

40
Q

what types of proteins are denatured in coagulative necrosis

A

Denaturation of intracytoplasmic protein

41
Q

does coagulative tissue still have the basic microscopic structure

A

Yes

42
Q

what happens to the dead cell in coagulative necrosis

A

become firm and slight swollen

43
Q

what occurs at the site of colliqutive necrosis

A

cyst

44
Q

does caseous tissue still have the basic microscopic structure

A

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

45
Q

Does caseous necrosis have granulomatous inflammation around the affected tissue

A

Yes

46
Q

what causes wet gangrene

A

bacterial infection

47
Q

what causes dry gangrene

A

type 2 diabetics- typically in the peripheries

48
Q

define apoptosis

A

‘Programmed cell death’ or ‘apoptosis’

49
Q

Is apoptosis a passive or active process

A

active

50
Q

when does physiological apoptosis take place (give examples)

A

Embryogenesis, Involution, Elimination of self-reacting

lymphocytes

51
Q

when does pathological apoptosis take place (give examples)

A

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

52
Q

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

A

inside the mitochondria

53
Q

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

A

caspases, which are the effector molecules of apoptosis

54
Q

what actives p53, and what is its function

A

damaged DNA

causes the elimination of damaged cells by apoptosis

55
Q

what does a mutation in p53 cause

A

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

56
Q

what is the function of bcl

A

sequesters cytochrome C and thus inhibits apoptosis.

57
Q

what can mutations in over expression of bcl result in

A

tumours gain the ability to proliferate in an uncontrolled way.

58
Q

is necrosis pathological or physiological

A

pathological

59
Q

is apoptosis pathological of physiological

A

physicological

60
Q

Is the cell size enlarged of reduced in necrosis

A

enlarged

61
Q

Is the cell size enlarged of reduced in apoptosis

A

reduced

62
Q

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

A

plasma membran disruptes an enzyme digestion so they may leak.

63
Q

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

A

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

64
Q

is there inflammation in necrosis

A

Yes

65
Q

is there inflammation in apoptosis

A

No

66
Q

how many cells are affected in apoptosis

A

1

67
Q

how many cells are affected in necrosis

A

a group

68
Q

in which subgroup of necrosis do cells lose their nucleus

A

coagulative

69
Q

what happens to the nuclei in apoptosis

A

shrink

70
Q

how is a appoptotic body removed

A

via phagocytosis.