cell adaptation, cell injury, cell death Flashcards
What are 2 mechanisms cells are injured
inherited
acquired
etiology
what causes disease
pathogensis
how does disease propagate
atrophy
shrinkage of cell size by decrease size and number of cells
what are 5 pathologic causes of atrophy
inadequate nutrition decrease use decrease blood supply change in hormonal level loss nervous innervation to muscles
what are 2 ways atrophy happens in cells
- apoptosis
2. ubiquitin-proteasome pathway
Ubiquitin-proteasome pathway?
Ubiquitin tags
proteosomes- destroyed
autophagy
what are lipofusin?
brown atrophy
increased residual bodies
undigested lipitds
defective ubiquitination may play a role in what
several neurodegenerative diseases
define: hypertrophy
increase in size of cells
No new cells
name 3 things that cause hypertrophy
increase workload
increase functional demand
hormone/growth factor
What causes hypertrophy
increase growth factors (IGF-1)
increase vasoactive agents (ANF)
ANF (atrial natriuetic factor) does what
in cardiac hypertrophy releases ANF to decrease blood volume
define hyperplasia
increase number of cells
3 things that cause hyperplasia
increase functional deman
hormonal stimulus
persistence tissue injury
name 3 situations in which the body will start hyperplasia
- low O2 breathed in
- breast lobules
- infection
Metaplasia
change in cell type
name 2 situations in which metaplasia can happen
Barret’s disease
Vitamin A Deficiency
what happens in vitamin A Deficiency for metaplasia
mucus-secreating epithelium on eye turns into keratinizing epithelium
Why do cells change in metaplasia
better withstand stress
metaplasia is a risk for
cancer
what are 2 mechanisms that can cause irreversible cell injury
necrosis
apoptosis
necrosis
accidental and unregulated cell death
pathological
necrosis is associated with
cell injury from ischemia
what specific cell injuries occur in necrosis
cell membrane rapture
nucleus – pyknosis-karyorrhexis-karyolysis
condensation - fragmentation-dissolution
protein degeneration
coagulative necrosis
necrotic tissue remains firm, nucleus disappears
localized area of coagulative necrosis is called
infarct
what causes necrosis
ischemia in all organs except brain
liquefactive necrosis
where can it occur
enzymatic digestion of dead cells into liquid
brain
what does caseous necrosis look like
cottage-cheese like apperance
caseous is a combination of what kind of necrosises
coagulative and liquefactive
what is fat necrosis
calcium deposition
saponification
free fatty acids join calcium
dystrophic calcification
calcium deposits on dead tissues
fat necrosis
where does one see fibrinoid necrosis
vessel walls in hypertension and Vasculitis
gangrenous necrosis
ischemia of lower limb and GI
wet gangrene
coagulative necrosis with superimposed liquefactive necrosis due to bacterial infections
what is apoptosis
programmed cell death
does apoptosis induce inflammation
no
Apoptosis vs. Necrosis: cell size
A: shrinkage
N: englarged
Apoptosis vs. Necrosis: process of dying
A: fragment nucleosome
N: nucleus-pyknosis-karyorrhexis-karyolysis
Apoptosis vs. Necrosis: plasma membrane
A: intact
N: disrupted
Apoptosis vs. Necrosis: leakage
A: no
N: cellular components
autophagy
starved cell eat its own components in an attempt to reduce nutrient demand to match supply
name 2 pathways in apoptosis
ntrinsic mitochondrial pathway
extrinsic mitochondrial pathway
etrinsic mitochondrial pathway what happens
FAS ligand binds FAS death receptor
TNG binds TNG receptor
Mitochondrial (intrinsic) pathway is triggered by
loss of cell survival signals (BCL2 )
cytochrome c activates protease
etrinsic mitochondrial pathway when does this happen
T lymphocytes
apoptosis results from the activation from what enzyme
caspases
When do the two apoptotic pathways converge
caspase activation
biochemical mechanisms of cell injury, name 4
- reduced ATP production
- loss calcium homeostasis
- disrupt membrane permeability
- free radicals