Al-Mehdi: Drugs affecting metabolism Flashcards
essential component of cell membranes and functions as a precursor to fat-soluble vitamins and steroid hormones
cholesterol
cholesterol sources in adults
bile acids
diet
sloughed intestinal cells
synthesis
composed of 3 fatty acids attached to glycerol molecule
triglycerides
require apolipoproteins for transport
TG and cholesterol
TG: 10,650
TC: 1102
eruptive xanthoma (sever hypertriglyceridemia)
TG: 6,000
TC: 760
untreated DM
eruptive xanthoma (severe hypertriglyceridemia)
long chain fatty acids brought into intestine through _____
CD36
cholesterol brought into intestine through _____
NPC1L1
bile salts brought into terminal ileum and back to hepatocyte through what
ASBT
chylomicron apo proteins
ApoB48
chylomicron remnant apoproteins
ApoB48 and ApoE
VLDL apo proteins
ApoB100
___ and ___ (Gs) activate hormone sensitive lipase (HSL) to breakdown TG in adipocyte
beta3, Glucagon
TG in hepatocyte is made into VLDL through what
MTTP
made mostly of cholesterol
LDL
made of cholesterol and TG (mostly TGs)
VLDL and chylomicrons
non-atherogenic lipoproteins
HDL and chylomicron
ATP Citrate Lyase inhibitor
(prevents availability of acetyl-CoA in cytoplasm); inhibits FA and cholesterol synthesis
BEMPEDOIC ACID
block HMG-CoA reductase
ultimately lead to hepatocytes upregulating LDL receptors to bring in LDL from blood
-STATINS
PCSK9 inhibitors (LDL receptors not being degraded)
INCLISIRAN
EVOLOCUMAB
binds and prevents recycling of bile salts back to hepatocytes (prevents recycling of major cholesterol source)
CHOLESTYRAMINE
blocks NPC1L1
(prevents cholesterol uptake)
EZETIMIBE
blocks MTTP
(microsomal triglyceride transfer protein in the liver)
LOMITAPIDE
(targets apoB mRNA in the liver and reduces synthesis of apoB100 protein)
MIPOMERSEN
fat from fish that reduces triglyceride synthesis and increases fatty acid metabolism (decreases liver secretion of VLDL)
omega-3-acid ethyl ester
binds Gi receptor on adipocyte and blocks HSL from breaking down TG
(prevents reveres cholesterol transport)
NIACIN
blocks ANGPTL3 that allows LPL to function (reduce hypertriglyceridemia)
EVINACUMAB
blocks ApoCIII and allows LPL to function (reduce hypertriglyceridemia)
VOLANSORCEN
PPARa agonists
(increase FA metabolism; decrease liver secretion of VLDL, increased HDL and LPL)
fibrates (FENOFIBRATE and GEMFIBROZIL)
1st line drug to use for hypercholesterolemia
-STATINS
SE of this drug is rhabdomyolysis and myoglobinuria
-STATINS
CI in pregnancy
-STATINS
2nd line add on to Rx hypercholesterolemia
EZETIMIBE (inhibits NPC1L1)
SE of this drug is diarrhea
EZETIMIBE
3rd line add on to treat hypercholesterolemia
PCSK9 inhibitors (EVOLOCUMAB and INCLISIRAN)
3rd or 4th line drug to treat hypercholesterolemia
bile acid sequestrants (CHOLESTYRAMINE and COLESEVELAM)
these 2 drugs increases LDL receptors
increases VLDL (bad)
reduces HbA1c
CHOLESTYRAMINE
COLESEVELAM
1st line drug to treat hypertriglyceridemia
moderate/high intensity statins (Atorvastatin and Rosuvastatin)
1st-2nd line to treat hypertriglyceridemia
omega-3-acid ethyl ester
used for patients with TG>500
SE myositis and cholelithiasis
Rx hypertriglyceridemia
fibrates (FENOFIBRATE and GEMFIBROZIL)
LDL-C > 190 mg/dL
hypercholesterolemia
TG>500 mg/dL
severe hypertriglyceridemia
what to do if all the medicine fails to reduce TG or cholesterol levels
remove LDL from patients plasma (LDL Apheresis)
process that happens in intestinal epithelial cells that converts Apo gene into ApoB100 and ApoB48 (not nonsense mutation b/c it is meant to happen)
RNA Editing
