Dyslipidemia

Question 1

MOA HMG-CoA reductase inhibitors (stations)

Answer 1

-Inhibits HMG-CoA reductase enzyme that converts HMG-CoA into precursor of cholesterol

-Liver senses low cholesterol so it will synthesize more LDL receptors resulting in uptake of LDL

-Stops VLDL secretion, resulting in decrease TG levels

Question 2

Key notes of statins

Answer 2

-First line, all secondary prevention of CVD, primary prevention of CVD in high risk

-S/E: increase CK, myalgia, reversible increased transaminase, rare myopathy, rnhabdomylosis, rare peripheral neuropathy

-Start low, and titrate slow
-Administer in the evening
-Check ALT at least once at 3 months
-Check CK if myalgia develops
-Pravastatin least drug interaction as NOT metabolized through CYP450

Question 3

Contraindications to statins

Answer 3

-Active liver disease, high alcohol consumption, pregnancy

Question 4

MOA ezetimibe

Answer 4

-Decrease intestinal cholesterol absorption
-less hepatic cholesterol stores

Question 5

Key notes ezetimibe

Answer 5

-Add on therapy
-Station and ezetimibe in CKD to reduce CVD events

-S/E: well tolerated generally, rare myopathy, rnhabdomylosis, hepatitis, acute pancreatitis, thrombocytopenia

-low drug interactions

Question 6

Contraindications to ezetimibe

Answer 6

-moderate-severe hepatic impairment

-Statins, ezetimibe, PCSK9 inhibitors should be STOPPED 1 month before stopping contraception

Question 7

MOA Fibrates

Answer 7

-Enhanced LDL receptor expression in liver and decreased synthesis of TG

Question 8

MOA of PCSK9 inhibitors
Key notes

Answer 8

-increase LDL excretion

-For very high risk patients, patients with familial hypercholesterolemia or secondary CV prevention
-Where statins has not worked
-Single dose given as injections every 2 weeks