Term
| familia hypechoelsteromeia |
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Definition
| defects in ldl receptors dont endocyotse ldl so it accumulates |
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Term
| ldl uptake and choelsterol homeostasis |
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Definition
| when lots of ldl gets uptaken, hmg coa reducatse goes down, Acat- for choelsterol esterifcaiton goes up, and ldl receptors go down . - so uptake is also decreased . |
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Term
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Definition
| ldl comesi nto cell via recetpors, hmg coa makes choelsetero land ldl is made to choelsterol , choelstero lthen ameks bile acids. Bileaacid depletion upregulates HMG COA and LDL receptor uptake to create mroe bile acids. Adding a reductase inhbiitor further upregulates the ldl re ceptor pathway |
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Term
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Definition
| hmg-coa reductase competitive inhibitors. inhibition of mevaolinic acid formation. |
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Term
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Definition
inhibits choelsterolgenesis. Ireased expression fo ldl receptor and icnreased removal of ldl form blood.
decresed heptaic vldl
can be used in kids with fmailal hhperchoelserolemia |
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Term
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Definition
| short halflifes <4 hours. cleared by CYP |
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Term
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Definition
| women who have pregnant, lactating. dont want ot mess up fetuss ability to develop choelsterol. |
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Term
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Definition
| most efficaous agent for sever hyperchoelsterolemia . mor tg lwoering acvitivy comapredi wth other statins |
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Term
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Definition
| most efficaous agent for sever hyperchoelsterolemia . mor tg lwoering acvitivy comapredi wth other statins |
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Term
| statins adverse effects/toxiccity |
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Definition
elevated ALT levels.
Myopathies- flulike symtpoms- however can leed to rhabdomyolysis -> myoglobinuria-> renal failure and death
cyp3a4 metabolism and contraidnication.
TC genotype is intermediate for myopathies nad CC genotype is very high risk for myopathies due to decreased clearance from plasma |
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Term
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Definition
posivel charged polymers, physically bind bile acids. Inhibit reabosrption, you get increaased syntehsis and secretion. you shoudl cadmisnter with statin, to that hmg coa doenst jsut coregulate.
leads to increase in hetapic tg synthesis |
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Term
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Definition
| take with meals or wont have any effect. for patients with bile salt accumulation, and removal of certain drugs from gut |
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Term
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Definition
| constipation bloating, heartburn adn diarrhea. rare malabospriton of vitamin k (hypporhtimbenamia). malabsorp of folic acidc, and incrased TG syntehsis |
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Term
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Definition
| binds lots of drugs, so make sure to take a certin amoutn of time after resins |
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Term
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Definition
| best agent for icnreasing hdl, lowers triglicerides and ldl as well |
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Term
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Definition
| resutls in decreased mobilziationof ffa into liver. , leading to reduced vldl secrtion. |
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Term
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Definition
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Term
| niacin toxicity/adverseeffects |
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Definition
hepatoxicity. concurent usei wth statin can cause myopathy.
cutaneos vasodilation.
hyperuricemia nad precipiate gout.
blunt th response to insulin. - diabetics.
teratogenic |
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Term
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Definition
| pparalpha activation, which regulates enes that contorl lipid metabolism . Primary effect to reduce plasma TG. litle effect on LDl, sometimes even conversion to ad icreasa.e |
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Term
| fibrates pharmacokientnics |
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Definition
| gemfibrozil coresses placenta. Excretion impariedi n reinal failure. Also excretion impaired in liver |
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Term
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Definition
highly plasma protein bound can dispalce other drugs such as anticoagulatns poetntiating their action.
Myopathy risk on statins (gemfiborizl). Increased choelsterol content of blodo and modesti ncrease of gal lstones. Contraidncaiton wtih renail fialure and hepatic dysfunciton. SHould nto be used bychildren or pregnatn women |
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Term
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Definition
| slelctively inhibitsi ntestinal choelsteraol absorption. Target is NPCL1 transport protein in enterocytes. This decreases intestinal delivery of choelsterol to the liver. Increases expression of Heptaic LDL receptors. |
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Term
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Definition
| circulates enteroheptaically, which limits sytemic exposure |
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Term
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Definition
| possible elvation fo liver enzymes, glucoronidated. |
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