the effects of injury on cells

Question 1

causes of cell injury

Answer 1

lack of oxygen
physical agents - temp, pressure, electricity, radiation
chemical and drugs
infectious agents
immune reactions
genetic defects
nutrition - deficiency, imbalance

Question 2

what happens to a cell at homeostasis when it undergoes stress

Answer 2

adaptation

Question 3

what happens when a cell has an inability to adapt after undergoing stress

Answer 3

cell injury

Question 4

what happens when a cell at homeostasis undergoes injurious stimulus

Answer 4

cell injury

Question 5

is a mild, transient cell injury reversible or irreversible

Answer 5

reversible

Question 6

is a severe, progressive cell injury reversible or irreversible

Answer 6

irreversible

Question 7

what happens if a cell undergoes a reversible injury

Answer 7

returns to homeostasis

Question 8

what happens if a cell undergoes an irreversible cell injury

Answer 8

cell death - either necrosis or apoptosis

Question 9

features of a reversible cell injury

Answer 9

rapid changes
swelling due to loss of ion/fluid homeostasis
fat accumulation - steatosis
irreversible if persistent injury
point of no return - not defines

Question 10

features of apoptosis

Answer 10

‘dropping off’ of petals or leaves
programmed cell death - cell suicide
ordered, regulated process
physiological
pathological

Question 11

2 stages of apoptosis

Answer 11

initiation
execution

Question 12

2 pathways of initiation of apoptosis

Answer 12

intrinsic (mitochondrial pathway) pathway - signal from the inside
extrinsic (death receptor initiated) pathway - signal from the outside

Question 13

anti-apoptotic

Answer 13

prevents apoptosis
promotes cell staying alive

Question 14

result of reduction in exposure to growth factors

Answer 14

shift in balance of anti-apoptotic and praptotic

Question 15

caspases

Answer 15

a family of endoproteases that provide critical links in cell regulatory networks controlling inflammation and cell death

Question 16

initiator apoptotic caspases

Answer 16

pro-domain
large subunit
small subunit
caspases 2, 8 and 9

Question 17

executioner apoptotic caspases

Answer 17

large subunit
small subunit
caspases 3, 6 and 7

Question 18

caspase 8 activation

Answer 18

inactive monomer > dimerization and interchain cleavage > active caspase 8

Question 19

executioner caspase activation

Answer 19

inactive dimer > active initiator caspase > active dimer

Question 20

what does autophagy mean

Answer 20

greek
auto - self
phagy - to eat

Question 21

autophagy

Answer 21

indispensable, regulated, and conserved catabolic process
recycling and turnover of cytoplasmic cell constituents
strictly regulated by autophagy-related genes (ATGs)
response to extra or intracellular stress (nutrient starvation, differentiation, metabolic stress, developmental triggers)

Question 22

types of necrosis

Answer 22

coagulative
liquefactive
caseous
gangrenous (dry)
fat

Question 23

coagulative necrosis

Answer 23

cell proteins denature - ‘ghost’ outlines
cells lose nuclei and stain more deeply

Question 24

ischaemia

Answer 24

hypoxia secondary to reduced blood supply

Question 25

infarction

Answer 25

coagulative necrosis due to ischaemia

Question 26

liquefactive necrosis

Answer 26

cell protein digested - loss of tissue architecture
infiltration by inflammatory cells (neutrophils) - pus
secondary infection by bacteria - wet gangrene
lipid rich tissue

Question 27

caseous necrosis

Answer 27

end result of granulomatous inflammation
granulomas - large aggregates of macrophages - epithelioid and giant cells
macrophages - phagocytes
autoimmune conditions, foreign bodies, mycobacterial infection

Question 28

dry gangrene

Answer 28

coagulative necrosis of extremity due to slowly developing vascular occlusion - e.g. diabetic

Question 29

fat necrosis

Answer 29

degradation of fatty tissue by lipases, forming chalky deposits - e.g. in acute pancreatitis, trauma to fatty tissues

Question 30

necroptosis - programmed/regulated necrosis

Answer 30

imperfect/inaccessible apoptotic machinery under severe cellular stress
caspase independent
swelling of organelles, eventual loss of membrane integrity
organised - final common activation of RIP1 via signalling pathway cascade (TNFRs, TCRs, IFNRs, TLRs)

Question 31

apoptosis - earliest changes, chromatic, vesicles, termination

Answer 31

1. cell shrinking
2. remains in tact, blebbing
3. aggregation at nuclear membrane
4. formation of membrane enclosed vesicles (apoptotic bodies)
5. continued fragmentation into smaller bodies

Question 32

necrosis - earliest changes, membrane, vesicles and termination

Answer 32

1. cell swelling
2. loss of integrity
3. no vesicle formation - lysis
4. complete lysis

Question 33

apoptosis - regulation, energy requirement, DNA and effector mechanisms

Answer 33

1. tightly controlled
2. energy dependent
3. non-random fragmentation prior to apoptotic body formation
4. caspase cascade

Question 34

necrosis - regulation, energy requirement, DNA

Answer 34

1. loss of homeostatic regulation
2. passive, no energy required
3. random fragmentation after cell lysis

Question 35

apoptosis - extent, cause and elicited response

Answer 35

1. localised, individual cells
2. triggered - withdrawal of survival factors or pro-aptotic stimulus
3. no inflammatory response and bystander damage

Question 36

necrosis - extend, cause and elicited response

Answer 36

1. groups of cells - indiscriminate
2. evoked by significant non-physiological disturbance
3. significant inflammatory response and bystander danger