gross Flashcards
gwarn lad u gowt this YEHA
ros=
reactive oxygen series
highly reactive oxygen– contains free radicals (unpaired electron in orbit) or something that easily become a free radical
what do ros attract
electron (commonly hydrogen)
ros exogenous/ endogenous
exog= uv light, tobacco, drugs endog= oxidative phosphorylation electron transport chain, NADPH
fenton equation
transition metals catalyse
H202 + fe2+ –> fe3+ +
OH(dot/radical) + OH-
haber weiss equation
02 (dot/radical) - (both dot and minus) +H2O2 –> 02 +H20 +OH (dot/free rad)
what ON EARTH is relevant about fucking reactive oxygen series
they are lipid soluble- so have power to infiltrate cells and shit
they cause damage to proteins, lipids, carbohydrates, nucelic acids - dna mutations parkinson diabetes renal failure emphysema
what do we do about pesky ros
antioxidant enzymes and vitamins protect us
resp acidosis causes
hypOventilation, copd
inefficient co2 removal
resp alkalosis causes
hypER ventilation, too much co2 gone
metabolic acidosis causes
hco3 isnt being excreted from kindey enough- so too much is reabsorbed into blood– renal failure
metabolic alkalosis causes
too much hco3 gone, vomitting
resp acidosis levels
highco2
high hco3
resp alkalosis levels
low co2
low hco3
metabolic acidosis levels
low hco3 (to compensate for problem) low co2
metabolic alkalosis levels
high hco3 (kidney reabsorbs more to make up for chunder) high co2
ecg p means
atrial depolarization
ecg qrs means
ventricular depolarization
ecg t means
ventricular repolarizartion
ecg lines up with wiggers how??
qrs spike is at beginning of ventricular pressure rise
p is is at beginning of slow atrial pressure rise, sort of mid ejection as ventricular and aortic pressure peaks
pr interval means
and how long
delay between av node and his-purkinje
120-200msec
st segment means
abnormally elevated when
time between ventricular de and repolarization
elevated in acute injury/infarction
qt interval means
effect of heart rate
time of depolarization plus repolarization
heart rate increase causes qt interval to shorten
ketogenesis : what to what
then what two things does this become
2!!! x acetyl coa (from fatty acid beta oxidation) –> acetoacetate
acetone, beta-hydroxybutyrate
when ketoacidosis
too much ketogenesis
- chronic alcohol abuse - low carbohydrate level stimulates ketogenesis
- diabetics - insulin inhibits, so inadequate dose or increased requirement causes more ketogenesis
- starvation (low carb)
fatty acid oxidation cycle
- what to what
- 4 process
acyl coa –> acyl coa with 2 fewer carbons, and acetyl coa (ketogenesis or krebs)
- oxidation, hydration, oxidation, thyolysis
fatty acid activation: what to what (2 steps)
fatty acid to acyl adenylate (atp needed)
acyl adenylate to acyl coa (acyl coa synthase)
then acyl coa into mitochondria