Effect on injury on cells (W10) Flashcards

1
Q

causes of cell injury

A

lack of O2
physical agents (temp, psi, electricity, radiation)
chemicals and drugs
infectious agents
immune reactions
genetic defects
nutrition

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2
Q

reversible cell injury features?

A

rapid changes
swelling due to loss of ion/fluid homeostasis
fat accumulation (steatosis)

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3
Q

when does reversible cell injury become irreversable

A

if experiences persistent injury - no defined ‘point of no return’

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4
Q

fatty change histology?

A

large pale spaces - fat globules

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5
Q

2 types of cell death

A

apoptosis and necrosis

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6
Q

apoptosis overview?

A

membrane stays in tact
energy spent from own cell
apoptotic bodies spread off from cell
phagocytosis of cell and fragments

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7
Q

apoptosis 2 stages

A

intrinsic
extrinsic (signal from outside cell - YOU MUST KILL YOURSELF!!!)

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8
Q

apoptosis - extrinsic regulation

A

receptor ligand interactions
leads to series of intracellular protein-protein interactions
activates initiator caspase 8

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9
Q

apoptosis - intrinsic pathway?

A

less BCL2 (anti-apoptotic proteins), more BAX and BAK (pro-apoptotic proteins)
this allows leakage of cytochrome C and SMAC out mitochondria
these lead to activation of caspase 9

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10
Q

initiator caspase for intrinsic apoptosis pathway

A

caspase 9

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11
Q

normal intrinsic pathway before apoptosis

A

growth factors cause transcription of more anti-apoptotic (BCL-2) proteins, outnumbering pro-apoptotic proteins therefore keeping cell alive

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12
Q

initiator caspase for extrinsic apoptosis pathway

A

activates initiator caspase 8

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13
Q

what do active initiator caspases act on in apoptosis? what does this cause?

A

activate executioner caspases (‘cut’ off inhibitory part) which then disassemble the cell

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14
Q

what is autophagy

A

recycling and turnover of cytoplasmic cell constituents

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15
Q

what regulates autophagy

A

autophagy-related genes (ATGs)

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16
Q

what is autophagy a response to

A

extra/intracellular stress

17
Q

autophagy summary?

A

intracellular constituents get packages into autophagosomes which fuse with lysosomes containing enzymes that degrade the components, then the original building blocks are released back into the cytoplasm and are reused

18
Q

necrosis summary?

A

cell loses membrane integrity falls apart, contents outside cell cause inflammation. neutrophils are attracted to the area and cause more damage to other cells

19
Q

what does necrosis look like in histology

A

pink blobs, nuclei not in cells, no properly defined cells

20
Q

types of necrosis

A

coagulative
liquefactive
caseous
gangrenous (dry)
fat

21
Q

coagulative necrosis? histology?

A

cell proteins denature (due to lack of blood supply?)
cells lose nuclei and stain more deeply. ghost outlines of cells.

22
Q

liquefactive necrosis?

A

histology - tissue dissolves into mush, different causes:

inflammation (neutrophils destroy tissue)
bacteria into area of coagulative necrosis (pus, melted mushy tissue, smelly)
lipid rich tissue (eg in brain - cells don’t leave outlines, also go mushy)

23
Q

caseous necrosis?

A

histology - ragged mess, ‘cottage cheese’. cell death you see in the middle of a TB caused granuloma

24
Q

what is a granuloma

A

formed when immune cells clump together and create tiny nodules at the site of infection. the body’s way of containing an area of infection to stop it spreading

25
Q

what is caseous necrosis caused by

A

TB
mycobacterial infection

26
Q

dry gangrene?

A

extreme coagulative necrosis due to slowly developing vascular occlusion

27
Q

fat necrosis?

A

degradation of fatty tissue by lipases, forming chalky deposits

28
Q

necroptosis?

A

virus stops apoptosis, organism can cause organised necrosis to destroy cell as apoptosis cannot occur.

29
Q

earliest changes apoptosis vs necrosis?

A

apoptosis - cell shrinking
necrosis - cell swelling

30
Q

vesicles differences apoptosis vs necrosis?

A

apoptosis - formation of membrane enclosed vesicles
necrosis - no vesicle formation, lysis

31
Q

termination apoptosis vs necrosis?

A

apoptosis - continued fragmentation into smaller bodies
necrosis - complete lysis

32
Q

apoptosis vs necrosis regulation

A

apoptosis - tightly controlled
necrosis - loss of homeostatic regulation

33
Q

energy requirement apoptosis vs necrosis?

A

apoptosis - energy dependant
necrosis - passive

34
Q

DNA differences apoptosis vs necrosis?

A

apoptosis - non-random fragmentation prior to apoptotic body formation
necrosis - random fragmentation after cell lysis