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73 Cards in this Set

  • Front
  • Back
2 types of cell death
necrosis and apoptosis
does necrosis require ATP?
no
does apoptosis require ATP?
yes
which type of cell death causes inflammatory response?
necrosis
why doesn't apoptosis make inflammatory response?
no loss of membrane integrity/ no release of cell contents
why does necrosis occur?
cell doesn't have time to adapt --> dies
initiators of necrosis
1) ischemia
2) membrane damaging agents
3) mitochondrial poisons
ischemia
restriction of blood supply
ischemia series of events
mitochondria get loss oxygen --> low ATP --> lose ion gradients --> increase Ca++ --> activates lots of -ases

anaerobic glycolysis --> generates lactic acid --> pH drops --> ribosomes stop working
name a mitochondrial poison
cyanide
what does increased cytoplasmic Ca++ do?
activates phospholipases, proteases, endonucleases --> promotes injury
what is the irreversible step of cell injury, making it's death inevitable
loss of IMM integrity
what is a clinical example of ischemia/hypoxia
myocardial infarction (MI)
ischemia-reperfusion injury
the restoration of circulation results in inflammation and oxidative damage
2 pathways of apoptosis
1) death receptor (extrinsic)
2) mitochondrial (intrinsic)
describe death receptor apoptosis pathway
lymphocyte fas ligand --> bind to cell's fas receptor --> forms DISC complex --> cleaves procaspases --> chop up everything
describe mitochondrial (intrinsic) apoptosis pathway
cell notices things are going awry --> increase in BH3 proteins --> attach to BCL2 proteins --> move off Bax/Bac pores --> Cytochrome C escapes --> cleaves procaspases --> chop up everything
transglutaminase
cross-links all the junk that was chopped up in apoptosis caspase thing
phosphatidylserine
usually on cytoplasmic side, but with apoptosis flips to outer, screams "eat me" and alerts neighbors
if you see cytoplasmic blebs...
apoptosis!
when does apoptosis happen in normal physiology
webbing between digits
neuronal remodeling
selecting immune cells
post-pregnancy
ischemic injury can cause
necrosis and apoptosis:
1) no blood --> necrosis
2) some blood --> apoptosis
2 important free radicals
OH
superoxide anion O2-
which is the most damaging of ROS?
OH-
what is a non-FR ROS?
H202
why is H202 dangerous
can diffuse --> spread ROS
some key ROS reactions
O2- --> H202

H202 --> OH- (fenton and haber-weiss)
how do ROS affect proteins?
1) bind S-S together --> affects tertiary structures
2) sticks shit on
3) unfolds
4) splits apart
how do ROS affect lipids?
lipids propagates the oxidation!!
how do ROS affect DNA?
base changes induce apoptosis
how do we eliminate ROS?
1) glutathione
2) vitamine E
3) vitamine C
glutathione
quenches FRs

ratio of GSSG / GSH --> more GSSG = more stress = close to depleting this buffer
what metal helps glutathione?
selenium
vitamin E
quenches lipid FRs
vitamin C role with ROS
replenishes Vitamin E
how do we repair/remove molecs damaged by ROS?
repair = chaperones try to help

remove = if too damaged, chaperones ubiquinate the molec = gets chewed up
UPR response
ER membrane detects lots misfolded proteins --> activates tranx of UPR part of promoters --> turns on protective genes
how directly detect ROS?
Nrf2 pathway
how directly detect hypoxia?
HIF pathway
Nrf2 pathway
normally, Nrf2 bound by Keap --> SH part of keap oxidized --> unbinds --> Nrf2 free to be a tranx factor --> turn on protective genes
HIF pathway
normally, OH onto HIF --> no oxygen --> HIF free to be a tranx factor --> turns on protective genes
how can you tell which cells in petri dish are in mitosis?
rounded up --> because of microtubules breaking down to make spindle
interphase
period between 2 mitoses
H-TdR
radioactive thymidine --> will only incorporate into replicating DNA
what phase do we find when put H-TdR in?
S phase
colchicine
prevents spindle formation --> therefore blocks in mitosis
using H-TdR and colchicine elucidates
G2
which phase of cell cycle has twice the amount of DNA
G2
mitogen
stimulates Go cells to enter G1 and continue cycle
histone synthesis occurs...
only during S phase
histone phosphorylation occurs...
at end of G2
RB protein
regulates progression through restriction point

binds to, and so inhibits, tranx factors that would allow cycle to continue
phosphorylated RB
unbinds from tranx --> cycle go
de-phosphrylated RB
bind to tranx --> cycle stop
MPF
M-phase promoting factor
how do we regulate cell cycle?
cyclins --> CDKs
how can you regulate CDK?
1) phosphorylate it
2) add CKI
3) degrade cyclin
are we the same as yeast re: # of CDKs?
no, we have multiple cyclins and CDKs
regeneration requires
intact tissue scaffold
what are the phases of fibrosis?
1) hemostasis and inflammation
2) angiogenesis and fibrogenesis
3) remodel / scar formation
4) re-epithelialization
tissue repair entails either or both of:
regeneration
scarring (fibrosis)
hemostasis happens how?
clotting = caspases --> factor 10a --> fibrin = scab
function of hemostasis
1) stop bleeding
2) keep microorgs out
3) scaffold for cell migration
PDGF
secreted by platelets

recruit fibroblasts to scene
fibrogenesis
replacing fibrin matrix with connective tissue matrix
what is tissue resulting from fibrogenesis?
granulation tissue (transitional)
what happens in remodel phase of wound repair?
remodel blood vessels and collagen

collagen: 3 --> 1
contracture
scar briding a joint
adhesion
organized exudate bridging serosal surfaces
stricture
circumferetial scar in a tubular structure
keloid/hypertrophic scar
excessive collagen production
fibrotic disorders most often caused by
chronic inflammation
examples of fibrotic disorders
1) cirrhosis
2) pulmonary fibrosis
3) scleroderma