Dyslipidemia Flashcards
Atorvastatin
Statin
Competitively inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (a rate-limiting enzyme in cholesterol synthesis). Increase hepatic cholesterol uptake from blood, reduce concentrations of total cholesterol, LDL and triglyceride (modest), and produce a small increase in HDL concentrations.
Fluvastatin
Statin
Competitively inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (a rate-limiting enzyme in cholesterol synthesis). Increase hepatic cholesterol uptake from blood, reduce concentrations of total cholesterol, LDL and triglyceride (modest), and produce a small increase in HDL concentrations.
Pravastatin
Statin
Competitively inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (a rate-limiting enzyme in cholesterol synthesis). Increase hepatic cholesterol uptake from blood, reduce concentrations of total cholesterol, LDL and triglyceride (modest), and produce a small increase in HDL concentrations.
Rosuvastatin
Statin
Competitively inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (a rate-limiting enzyme in cholesterol synthesis). Increase hepatic cholesterol uptake from blood, reduce concentrations of total cholesterol, LDL and triglyceride (modest), and produce a small increase in HDL concentrations.
Simvastatin
Statin
Competitively inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (a rate-limiting enzyme in cholesterol synthesis). Increase hepatic cholesterol uptake from blood, reduce concentrations of total cholesterol, LDL and triglyceride (modest), and produce a small increase in HDL concentrations.
Fenofibrate
Fibrate
Activate peroxisome proliferator-activated nuclear receptors and modulate lipoprotein synthesis and catabolism. They reduce plasma triglyceride, moderately increase HDL and have a variable effect on LDL concentrations.
Gemfibrozil
Fibrate
Activate peroxisome proliferator-activated nuclear receptors and modulate lipoprotein synthesis and catabolism. They reduce plasma triglyceride, moderately increase HDL and have a variable effect on LDL concentrations.
Evolocumab
PCSK9 inhibitor
Bind to proprotein convertase subtilisin/kexin type 9 (PCSK9) and inhibit its activity, increasing LDL clearance from the blood.
Colestyramine
Bile acid binding resin
Binds bile acids in intestinal lumen, preventing reabsorption, and increases bile acid excretion in the faeces. The resulting increased demand for cholesterol for bile acid synthesis increases hepatic LDL uptake and removal from plasma.
In partial biliary tract obstruction, increased bile acid excretion reduces bile acid deposited in dermal tissue, decreasing itch.
Ezetimibe
Reduces absorption of dietary and biliary cholesterol by inhibiting its transport across the intestinal wall. This leads to an increased demand for cholesterol, an increase in LDL uptake and its removal from the plasma.
Nicotinic acid
Mechanism unclear. Probably suppresses fatty acid release from peripheral tissue, especially adipose tissue. In doses >1 g daily, nicotinic acid reduces LDL and triglycerides, increases HDL and uniquely lowers potentially atherogenic lipoprotein(a).