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Pathology > Cell injury > Flashcards

Cell injury Flashcards

1
Q

injury occurs and you can get regeneration or repair; what tissues does this happen in respectfully

A

regeneration-> renewing tissues ( epidermis, GI tract, epithelium, hematopoietic system)
- stable tissues-> compensatory growth of liver and kidneys

repair-> wound -> would helaing or scar formation
-> chronic inflammation -> fibrosis
repair occurs in tissues that can no regenerate themselves

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2
Q

What is the main factor that maintains homeostatis

A

ATP - without enough ATP damage can occur bc calcium gradient is maintained by ATP and so is protein synthesis , secretion and replication

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3
Q

What is a key event in cell death

A

calcium infulx

  • ton of calcium extracellular inside you have little
  • transporters Ca-ATPases and sequestration in the ER via the sarco endoplasmic reticulum
  • if too much calcium gets into the cell then the ATP is decreased, then you get mito damage and ATP drops more and then you get cell death
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4
Q

Elevated intracellular calcium does what>

A
  • poisons mitochondria irreversible
  • inhibit many cellular enzymes
  • activate some lytic enzymes
  • initiate free radical formation
  • high concentrations denature cellular proteins
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5
Q

two pathways where damaged proteins and organelles get removed from the cell

A

the proteasome- > p53, EGFR, cyclins, misfolded proteins

autophagy -> targeting to lysosomal, proteins-microautotphagy, organelles-macroautophagy

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6
Q

proteasome mediated degradation

A

-ubiquitin conjugation- lysine linked covalent modification
-poly ubiquitin -> target for degradation
covalently linked to E1 then the covalent linkage gets transferred to E2 and then to the substrate.

  • very little E1 and E2s but many E3s because they are specific for the targets ( E2 and E3 are a complex together)
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7
Q

Autophagy - micro and macro

A

internal phagocytosis
micro autophagy -> chaperone mediated transport of proteins to the lysosome ( Hsc 70 helps to target proteins to Lamp-2A on the lysosome)

macroautophagy-> double membrane structures form to engulf protein aggregates or organelle fragments and fuse with lysosomes.- p62 sequestosome helps bind the cargo into the autophagosome

  • protects against nutrient deprivation
  • intracellular quality control
  • remodels cellular component to meet changing demands
  • p62 bodies (should go to lysosome but cant get there) appear in multiple pathologies
    - mallory bodies
    - parkinsons and alzheimers
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8
Q

Unfolded protein response

A

activated when you have problems in the ER

Key mediators:
PERK kinase
IREI-alpha
transient ER proteins that get turned on when there is damage to the ER and stop cell growth and protein synthesis - CHOP ( gene gets transcribed) causes apoptosis

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9
Q

Hypoxic injury

A 
following anoxia-cell death occurs at : 
neurons -3-5 min
myocardial cells - 20-30 min
renal tubules cells; 30-60 minutes 
hepatocytes : 1-2 hrs 
skeletal muscles and connective tissue: many hours
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10
Q

effects of hypoxia

A

decrease OX PHOS ->decrease in ATP causes:

  • > decrease in NA pump -> influx Ca, h2o , sodium and potassium -> er swelling, cellular swelling and moss of microvilli, biebs.
  • > increase anaerobic glycolysis-> decrease glycogen, increase lactic acid -> decrease in pH causes clumping of nuclear chromatin
  • > detachment of ribosomes -> decease in protein synthesis and theat leads to lipid deposition
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11
Q

Hypoxic cells produce what

A

pro angiogenic factors to induce neovascularization

Hif-1 alpha -> intracellular protein normally degraded but become stable under hypoxic conditions to increase expression of VEGF

-VEGF-> growth factor that stimulates endothelial cell migration and proliferation

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12
Q

Reperfusion injury

A
  • radicals are formed during ischemia are now combined with oxygen and create more free radicals
  • xanthine dehydrogenase ( gets turned on under hypoxic conditions) cleaved to produce xanthine oxidase and creates uric acid with ROS as by products
  • nitric oxide inducible is turned on during ischemia and NO will react with oxygen with reperfusion and create more free radicals
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13
Q

Free Radicals - mediated injury

A
  • single unpaired electron in outer orbital
  • extremely reactive with cellular macromolecules
  • generated in cells : oxidative rxns, radiation, enzymatic metabolism or exogenous chemicals (p450s)
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14
Q

H202

A

produced by superoxide dismutase from 02

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15
Q

what drives hypertrophy

A

calcium influx turns on calcium dependent mechanisms the cascade for hypertrophy is turned on -

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16
Q

hyperplasia

A

chronic irritation leads to hyper proliferation - increased cell division in basal layer
-shift in population dynamic to changes in stem cell compartment

17
Q

Atrophy -types

A

disuse
pressure
hormonal
denervation

18
Q

metaplasia

A

response to - chronic irritation, stress, tissue damage

19
Q

fatty change

A

rapid-acute

due to toxic insult, hypoxia and viral infection

20
Q

response to damage

A

injury/stress->
-> reversible - clearance of damaged proteins/organelles -> adaptation -> hypertrophy/ hyperplasia , increase expression of stress response genes

-> irreversible ( stress mediators p53) -> persistent DNA damage, accumulation of protein aggregates -> necrosis, apoptosis, senescence

21
Q

p53 - activation

A 
p53 is activated by DNA damage and cell stress- 
p53 is regulated by MDM2 
p53->dna binding protein 
-> N-terminal domain for activation 
and tetramerization in the c-terminus
22
Q

necrosis

A

cell lysis
necrotic debris
immune activation

  • cell enlarged , nuclear karyolysis, plasma membrane disruption, cellular contents leak, , enzymatic digestion, scarring, pathologic, increased eosinophilia ( due to loss of rna )
23
Q

apoptosis

A

cell intact
little immune activation

cell shrinks, nuclear pyknosis, plasma membrane intact, apoptotic bodies, clearance by phagocytes, physiologic

24
Q

senescence

A

( irreversible arrest)
cell remains intact
- p53 mediated and p21, cyclins D and E and arrest in G1

immune activation (IL-6)

  • cell remains in situ
  • nuclear changes subtle
  • cell releases cytokines
  • NK cell clearance
25
Q

intrinsic pathway of apoptosis

A

activated via p53 ( phosphorylation) -> activates puma and pro-apoptotic

  • > activates Bcl-2 ->– opens mitochondrial pores and the release of cytochrome C ->binds to APF-1 and activates and bind caspase 9 forming apoptosome -> activates caspases 8,3,6 ,7 ( activated caspases= proteases)
  • cell is dismantles, nuclei become pyknotic and undergo fragmentation
  • create apoptotic bodies <- gets phagocytized
26
Q

extrinsic pathway- apoptosis

A

mediated interaction of TNF alpha with TNFR1 or Fas ligand with Fas receptor
- death domain-> procaspase 8 to activate cysteine protease activity
- caspase 8 can cleave caspases 3 and 7
-caspase 3,6, 7 known as effector caspases
-caspase 8 - facilitate release of cytochrome C from mit
caspase 3 -»> takes apart the cell

27
Q

necrosis

A

classic patterns -
pyknosis ( irreversible condensation of chromatin in the nucleus )
karyorrhexis - (rupture of the cell nucleus in which the chromatin disintegrates into formless granules that are extruded from the cell)
karyolysis (complete dissolution of the chromatin matter of a dying cell due to the activity of DNase)

28
Q

coagulative necrosis

A

architecture of dead tissue is preserved

  • injury denatures structural protein, enzymes and blocks proteolysis, anucleate cells may persist for days or weeks
  • ex : acute MI, vascular occlusion
29
Q

liquefaction necrosis

A

focal bacterial or fungal infection- neutrophils and macrophages degrade necrotic material and infectious organism

  • destruction of cellular architecture
  • (abscess)
30
Q

caseous necrosis

A

collection of fragmented cells and granular debris

  • giant cells ( overstimulated by TGF ) langerhans cell - moon shape
  • ex - TB granuloma
31
Q

gummatous necrosis

A

spirochaetal infections-syphilis

32
Q

Fat necrosis

A

focal area of destruction usually specific to the release of pancreatic lipases

-

33
Q

fibrinoid necrosis

A

deposition of immune complexes and fibrin

  • deposition of immune complexes and fibrin often seen around blood vessels ,pink in H&E

Pathology (12 decks)

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