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cell injury Flashcards

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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
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.

MOD (19 decks)

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