Cell injury, necrosis and apoptosis Flashcards

1
Q

check out flow chart

A

do it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

def cell injury

A

homeostasis disruption of the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

3 overall causes of cell injury

A
  1. adaptive failure
  2. exposure to damaging stim
  3. intrinsic abnormality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

2 types of possible oxygen deprivation

A
  1. hypoxia - lack of O2 reducing oxidative resp

2. ischemia - def. of circulation reducing oxidative resp and metabolic processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

7 different ways to injure a cell

A
  1. O2 dep
  2. physical agents - trauma, burns
  3. chemical agents - cyanide, asbestos
  4. infectious
  5. immune reactions - autoimmine
  6. genetic abnormalities - DNA damage, chromosomal
  7. nutritional imbalance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are 4 factors that decide if injury is reversible

A
  1. nature of stim
    2, target of stim
  2. intensity/duration
  3. capacity for cells to adapt
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

3 types of irreversible injuries

A
  1. incapacity to gen ATP
  2. loss of menbrane function
  3. damage to DNA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

6 mechanism of cell injury

A
  1. no ATP
  2. mitochonidrial damage - leak pro-apoptotic species
  3. Ca into cell - enzyme cascade
  4. ROS - damages proteins
  5. membrane damage - loss of components and enzyme damage
  6. protein misfolding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

3 probs with loss of ATP

A
  1. Na/K pump down so get swelling of cell
  2. more anaerobic glycolisis - pH drops - clumping of chrmatin
  3. detached ribosomes - lipid depostition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is normal Ca homeostais

A

very low in cytosol and sequestered in ER and mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

3 things that happen when Ca in

A
  1. activates intracellular enzymes - lipase, phosophlipase (membrane), endonuclease (nuleaus)
  2. activates caspases - apop
  3. mitochondrial leakage - H out and apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what happens with ROS

A

react with other compounds to create autocatalyitc reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what defines oxidative stress

A

more ROS being made than removed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

normal and patho ROS reactions

A
  1. normal - inflammatory burt

2. path - reperfusion injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

6 sources of free radicals

A
  1. oxidative phosphorylation
  2. radiant E
  3. inflammation
  4. NO conversion in endothelium
  5. enzymatic transformation of drugs
  6. transition metals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

2 ways to remove free radicals

A
  1. enxymatic - catalase, glutathione peroxidase, superoxide dismutase
  2. non-enzymatic
17
Q

2 non-enzymatic removal methods

A
  1. antioxidants - viatmin A and C( membranes) or C and glutatione (cytosol)
  2. seqquestrants - ferratin…
18
Q

what is important about membrane permiability

A

consistently found in all injurious processes leading to necrosis, BUT NOT APOP

19
Q

3 places where pathological processes occur in membrane leakage

A
  1. mitochond - loss of ATP
  2. cell membrane- osmotc loss and inflammatory trigger
  3. lysosome - cell digestion and triggering of inflammatiokn
20
Q

2 options of DNA damage

A
  1. isolated - apoptosis

2. complex injury - mix of necrosis and apoptosis

21
Q

2 options for accumulation of non-folding proteins

A
  1. isolated - apoptosis

2. complex injury - mix of necrosis and apoptosis

22
Q

def necrosis

A

PATHOLOGICAL state of tissues resulting from IRREVERSIBLE damage with eventual breakdown of membrane leaking and induction of inflammatory response

23
Q

4 cellular features of necrosis

A
  1. coagulation of cytoplasimc proteins - cytoplasmic eosinphilia
  2. coag of DNA - nuclear basophilia
  3. disrupted phospholipids - myelin figures
  4. activates endonucleases - nuclear changes
24
Q

what is clinical utility of membrane leakage

A

can be a useful marker of disease states and timing

25
Q

3 things the tissue morphology is dependent on in necrosis

A
  1. concentration of hydrolytic enzymes
  2. etiology of injury
  3. non-specifics
26
Q

what are 2 options based on amount of enzymes

A
  1. coagulative - intact architecture, hypereosiniphilia, loss of nuc- INFARCT
  2. liquefactive - rapid release of enzymes - CNS - get PUS
27
Q

what are 3 options based on the etiology of disease

A
  1. caseous - TB - cheeselike with granuloma because can’t break down the substance
  2. fibrinoid - vasculitis - immune mediated destruction of the vessel walls
  3. fat necrosis - acute pancreatitis - release of lipase breaks down fat everywhere
28
Q

2 types of gangrene

A
  1. dry - limb that has lost blood supply and is coagulative

2. wet - infected and so get bacteria and neutrophils - pussss

29
Q

def. apoptosis

A

tightly regulated form of cell death without cell breakdown and preserved membrane and no inflammatory response

30
Q

2 types of apoptosis and examples

A
  1. physiologic (maintains steady state) - embryoginesis, tissue atrophy, removale of self-reactive lymphocytes
  2. pathologic - severe DNA damage, misfolded proteins, viral infections
31
Q

2 pathways in apoptosis

A
  1. intrinsic (mitochondrial)

2. extrinisc

32
Q

steps in intrinsic pathways

A

lack of survivale signal on cell membrane>antagonism of BCL-2>activation of cytochrone C in mitochondria>actiaves capsases

33
Q

steps in extrinsic

A

signal from outside cell leads to direct activation of capsases

34
Q

what will be seen on PCR in necro vs. apop

A

apop - ladder pattern because fragmented endonuclease make discrete chops
necrosis - smear because release of DNAases chops DNA whereever

35
Q

what happens in apop

A

cell slowly pulls pieces off and shrink and the peices are phaged

36
Q

***6 features that differentiate necrosis from apoptosis

A
  1. cell size
  2. nuclear morphology
  3. membrane
  4. cellular contents
  5. nearby inflammation
  6. pathologic or physiological
37
Q
  • **features of apoptosis based on
    1. cell size
    2. nuclear morphology
    3. membrane
    4. cellular contents
    5. nearby inflammation
    6. pathologic or physiological
A
  1. cell size - smaller
  2. nuclear morphology - fragmented
  3. membrane - intact
  4. cellular contents - intact and released in vacuoles
  5. nearby inflammation - no
  6. pathologic or physiological - either
38
Q
  • *** features of necrosis based on
    1. cell size
    2. nuclear morphology
    3. membrane
    4. cellular contents
    5. nearby inflammation
    6. pathologic or physiological
A
  1. cell size - larger - swollen
  2. nuclear morphology - karyolisis, nuclear basophilia, myelin figures
  3. membrane - disruted
  4. cellular contents - lyses and may spill out
  5. nearby inflammation - frequent
  6. pathologic or physiological - always patho