Physio 2 - Metabolism 3

drraythe's version from 2015-06-09 01:47

Liver functions

Question Answer
6 summary fxns of liver?(1) protein metabolism (2) carb metabolism (3) fat metabolism (4) blood reservoir (5) defense (kupfer cells) (6) Misc
explain the 4 major "protein metabolism" tasks of the liver(1) deamination of AAs (make into keto-analogues so can go to Krebs) (2) urea formation (NH3 from deamination, turn into UREA to excrete) (3) synth of plasma proteins (4) conversion of AA into other compounds (made from labile protein pool)
describe the two major misc areas of liver fxn(1) STORAGE (vitamins, minerals, trace elements) (2) DETOX/excretion (drugs, hormones, BILIRUBIN, urea)
4 major fxns of liver for fat metabolism?(1) fatty acid synth from excess glc/AA (2) ketogenesis (3) lipid xport (VLDLs) (4) synth of phospholipids, chlosterol, bile acids, etc
6 major points of carb metabolism(1) uptake of blood glc (2) glc storage as glycogen (3) glc release from glycogen (4) convert gal/fru into glc (5) gluconeogenesis out of AAs, lactic acid, pyruvate, propionate, glycerol (6) formation of compounds from krebs cycle intermediates
what is biliruben? where does it come from?main bile pigment, originates from heme breakdown
what is U-BILI? (path etc)Unconjugated biliruben. When biliruben leaves RES (reticulo endothelial system-phagocytic cell shit) cells and binds to albumin (plasma form) aka indirect bili
what is C-BILI?conjugated bilirubin. When unconjugated biliruben is taken up by liver cells (carrier mediated, rate limiting step in HORSES) and is conjugated with glucuronic acid
what is the rate limiting step of bile pigment secretion In what SPECIFIC animal?In horses, the U-bili being TAKEN UP BY LIVER CELLS requires a carrier and is the rate limiting step
what is needed to conjugate u-bili to c-bili?GLUCURONIC ACID
after c-bili is conjugated in the hepatocyte, where does it go?it's secreted into bile ducts, which is the rate limiting step in EVERYTHING EXCEPT HORSES
what is the rate limiting step of bile secretion in all animals EXCEPT horses?when c-bili is secreted into bile ducts
while most of c-bili is secreted into the bile ducts, what happens to a small fraction of it?it is regurgitated into circulation
once the c-bili is in the GI via the bile duct, what happens to it? (converted to what via what which results in what)converted via urobilinogen/ stercobilinogen into urobilin/stercobilin (causes yellow pee and dark color of feces)
which biliruben is normally present in plasma?BOTH u-billi AND c-bili (but there are species diffs)
what is jaundice?yellow pigmentation of skin/ mucosa/ body fluids caused by deposition of biliruben
what are the three types of jaundice?Prehepatic, hepatic, posthepatic
What is elevated in prehepatic jaundice?U-BILI initially, later both forms inc as secretion of C-bili becomes saturated
what is elevated in hepatic jaundice?C-BILI initially (b/o regurg), later u-bili inc as uptake becomes impaired
what is elevated in posthepatic jaundice?C-BILI is VERY dominant, later U-bili can inc from cell damage
what causes prehepatic jaundicecaused by excessive breakdown of Hg (hemolytic disorders, massive internal bleedings, signs of anemia) so biliruben (uncon) production increases beyond capacity for liver for uptake/conjugation
what causes hepatic jaundice?DAMAGE TO LIVER CELLS (inflammation, lipidosis, necrosis) C-bili secretion is initially more impaired (regurg) than U-bili uptake and conjugation (so first C-bili elevated then u-bili inc too)
what causes posthepatic jaundice?caused by OBSTRUCTION OF BILE DUCTS (stones, tumors, intrahepatic cholestasis) so C-bili is regurg into circulation, eventually inc intrahepatic pressure can cause hepatocellular injury
What is of diagnostic value for liver damage?ALT


Question Answer
What is the body's "thermostat"?The hypothalamus which contains a temp. regulatory center with a FIXED SET POINT
how does the hypothalamus know if we are at the right temp, or if we should lose or conserve heat?superficial and deep temp receptors
what are 6 heat losing mechanisms?vasodilation, sweating, panting, b/h, dec basal rate, dec food intake
what are 6 heat conserving mechanisms?vasoconstriction, piloerection, inc metabolic rate, shivering, b/h, inc food intake
what is the def of a fever?rise in the hypothalamic set point
what are the two causes of a fever?pyrogens and compression of hypothalamus (eg: tumors)
what are pyrogens? (specific things)bacterial toxins, protein-breakdown products, cytokines (interleukin I)
what do pyrogens do to the hypothalamus?hey reset the hypothalamic thermostat to a higher value
what can pyrogens induce the formation of? how do we treat this?induce formation of prostaglandin E2, so NSAIDs which inhibit the PG synth are anti-pyretic
what are the three main phases of a fever, in order? what is PGE2 doing during this?"Chill" (PGE2 rise), "Fever", "Crisis" (PGE2 decrease)
describe the chill phasebody is trying to reach a new set point, so it enacts heat conserving mechanisms and you feel cold. PGE2s are rising.
when does the chill phase end?when your body reaches its new set point, now you feel normal again even though you are feverish
describe the crisis phaseNOT A BAD THING! After the removal of the fever inducing factor the set point returns to normal, and the raised body temp now feels hot to you. heat losing mechanisms are initiated
how is a fever good?increases metabolism and circulation, activates defense system, suppresses pathogen replication
what is hyperthermia?when heat loss cannot keep up with heat generation. Body is too hot!
what happens due to the insufficient cooling in hyperthermia? (before 41.5*C/106.7*F)fluid loss --> dehydration --> initial blood pressure drop --> sympathetic response --> vasoconstriction --> disables further heat loss
what happens once the core temp hits 41.5*-42.5*C? (106.7*-108.5*F)impairs cellular fxn --> endothelial damage via hypoxia and protein denaturation --> plasma leakage and hemorrhages --> dizziness, nausea, coma, death (CNS, Kidneys, Liver, GI, mm) (you're over 41? might as well be dead)
what is hypothermia?heat loss greater than heat production.
what temp are heat regulating mechanisms impaired at for hypothermia?29*C (84.2*F) (almost 30 and no regulation in life)
for hypothermia, what temp will cause cardiac arrest?20*C (68*F) (a heart attack at 20 is unheard of)
pathogenesis of frostbite?severe vasoconstriction --> freezing of superficial areas with crystal formation --> permanent tissue damage

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