pharm test 2 lipid lowering meds

what are modifiable risk factors for people with CAD

smoking cigs, obesity, HTN, hyeprlipidemia

triglycerides are oxidized to generate energy for

muscle contraction and metabolic rxns

what are non modifiable risk factors of Coronary heart disease

male sex, fhx premature CHD, age

other diseases that are risk equivalents to CHD

DM, aortic aneurysms, CAD

CHD mortality decreases ____ for every ____ reduction in serum cholesterol

15%, 10%

this lipoprotein particle transports dietary lipids from intestines to adipose tissue and liver. they’re created when cholesterol and Tg are emulsified in the intestines, and transport Tg to fat tissue and cholesterol to the liver.

chylomicrons

this lipoprotein is made in liver from Tg, cholesterol, phospholipids, and protein. they also deliver Tg to fat tissue like chylomicrons. they eventually turn into IDL and LDL which hold more cholesterol.

VLDL

this lipoprotein takes cholesterol to peripheral tissues to go into cell membrane, sterols, and steroids. Binds to certain LDL receptors in plasma membrane and contribute to atherosclerosis. mostly cholesterol

LDL

this lipoprotein helps VLDL deliver tg to fat tissue, prevent atherosclerosis, inhibits clotting and platelet aggregation and oxidative damage to vessels. you want it to be high. mostly protein

HDL

this lipoprotein is highly associated with CAD. Niacin lowers this while all other drugs don’t

lipoprotein a

what medicine lowers lipoprotein a

Niacin

why can people with low LDL still have cardiac events

bc of lipoprotein a

why do people have hi LDL

genetics or environmental factors, endocrine abnormalities (DM, hypothyroidism). Can be elevated by meds like thiazide diuretics, BB

how does framingham risk score help people wanting to take meds

it estimates the 10 yr risk of a heart attack using info like a persons age, sex, TC, HDL, smoking, SBP

what is the goal for high risk pts who have CHD or similar dz

have an LDL under 100, an LDL under 70 in high risk pts

what ldl do moderate risk (10-20%) pts want

less than 130, if higher than start drug therapy. optimally less than 100

what ldl do low risk (<10%) pts want

drugs given if LDL is greater than 160. stick to lifestyle changes firstly before drugs

lifestyle changes can be

diet changes, weight management, exercise. <200mg cholesterol intake

the most important drug for tx of hypercholesterolemia

HMG-CoA reductase inhibitors aka statins

these drugs lower blood cholesterol levels, prevent CAD and dec mortality. they also improve vascular endothelial function and dec inflammation. they can also protect against OP and some ca

statins

mechanism of action of statins

they competitively inhibit HMG-CoA reductase which then dec cholesterol creation. inc of hepatic LDL receptors happens which inc hepatic uptake of LDL so less LDL is in blood. they also dec serum Tg but not enough to tx it.

these statins are inactive prodrugs that have to be converted to their active metabolite in the liver. they also cross the BBB and cause sleep problems in some pts

Lovastatin and simvastatin

this statin must be taken with an evening meal to allow for absorption

lovastatin

what statins are most potent and have the best effect on triglycerides. they also have longer half lives and can be taken at any time of the day.

rosuvastatin most potent following is atorvastatin.

adverse events of statins

GI issues like cramps, constipation/diarrhea, heartburn, can raise LFTs, hepatitis, serious is rhabdomyolysis. myopathy

pt presents taking statin but complains of myalgias but you check ck levels and they’re nl. what happened

statin induced myopathy. stop the statin then find another one. can turn to myositis which then turns into rhabdo.

what is a severe complication of statins and what occurs during it

rhabdo, myoglobin into circulation that enters the kidneys leading to acute renal failure with CK levels reeeaaally hi. dark/brown colored urine

pt presents with dark colored urine what do you do

send to ER stop statin and give IV fluids until CK and renal function is normal

how to monitor if pt is taking statin

be careful for muscle cramps and if your urine is abnormally dark. if you give abx that dec filtration of the statin levels can inc in blodo and rhabdo can happen

risk factors for taking statins

age, female, renal/hepatic dz, hypothyroid, using drugs that inhibit statin break down

hi dose simvastatin is assoc with what adverse effect

myopathy and rhabdo

reasons to stop a statin

if myopathy is dx or if really hi CK.

how do you tx a pt when rhabdo is suspected 

stop drug and IV fluids to keep renal function

drug interactions of atorvastatin lovastatin and simvastatin

bc metabolized by CYP3A4 inhibitors, plasma conc inc by inhibitors like erythromycin, itraconazole, and ritonavir

drug interactions of pitavastatin pravastatin and rosuvastatin

bc they are excreted unchanged plasma conc is NOT inc by CYP3A4 inhibitors

what are the drug interactions of fluvastatin

metabolized by CYP2C9 so plasma levels can inc from inhibitors like NSAIDs

how do statins affect other drugs

by CYP enzymes. can inc warfarin bc it inhibits its metabolism. be careful taking statins, fibric acid derivatives, and niacin together bc all causes myopathy

bile acid binding resins are

Cholestyramine, colestipol, colesevelam

how do bile acid binding resins dec cholesterol

resins bind to bile acid and drop chloride. less bile is cycling now so liver makes more from cholesterol. inc LDL receptors and serum LDL dec as more cholesterol goes to liver

adverse events of bile acid binding resins

constipation, fecal impaction, other GI sx. prevented by taking meds with a full glass of water. can irritate perianal area and skin rash.

why do you give bile acid binding resins

if you don’t wanna raise statins, tx hypercholesterolemia. doesn’t cause hepatitis or myopathy. tx chronic diarrhea bc of bile acid malabsorption

cholestyramine and colestipol drug interactions

bind to digoxin, thyroxine, warfarin, other drugs, so take 2 hrs before/after taking other meds.

what is good about cholesevelam

doesn’t affect oral bioavailability of digoxin, warfarin, or lovastatin so can be given with other drugs. taken as a solid tablet.

cholestyramine and colestipol are prepared how

powder for mixing w water or juice. cholesty also as chewable bar.

what is ezetimibe

no absorb cholesterol to tx hypercholesterolemia. localizes in brush border to inhibit absorbing of biliary and dietary cholesterol.

if i want to lower LDL a little bit and i don’t ewant to give a statin what do i give

ezetimibe

if i dont wanna give a high dose statin to lower cholesterol what else can i give

simvastatin/atorvastatin + ezetimibe

niacin aka nicotinic acid aka vit b3 is used to tx

hypertriglyceridemia and inc HDL. broadest spectrum of lipid altering effects

how does niacin work

you need a lot of niacin in order for it to be effective. it lowers everything and raises HDL. inhibits creation and secretion of hepatic VLDL.

why do we give niacin

to dec ldl, tris, LP(a) and inc HDL in pts with primary hyperlipidemia and mixed dyslipidemia. sometimes +statin or bile acid sequestrant to dec LDL when one drug isn’t enough. dec risk of pancreatitis in pts with hi tris.

adverse events of niacin

vasodilation = skin flushing, itchy, warm/tingles. Pre-treat with ASA. inc serum transaminases = hepatitis, inc LFTs, worsen peptic ulcer, raise glucose, raises uric acid levels, hyperuricemia

the fibrates are

gemfibrozil and fenofibrate

what does fibrates do

lower tris by effecting an enzyme that speeds the removal of tris from VLDL. dec LDL by inc expression of hepatic LDL receptors that uptake more LDL to dec it in the serum

why do you give fibrates

tx severe hypertriglyceridemia (>500) to prevent pancreatitis. Reduces CHD in pts w inc LDL, dec HDL and inc Tg if lifestyle changes did nothing.

adverse events of fibrates

GI side effects, blood deficiencies and hypersensitivities. also myopathy and rhabdo. combo w statin is avoided. can be given with cholestyramine and colestipol but need to be 2 hrs apart. used for pts with super hi tris.

what is an omega 3

flaxseed, chia, walnut, fatty fish, fish oil. lowers Tg, dec PTL aggregation, dec BP a bit. neuro/cognitive benefits

what is an omega 6

veggie oils, meat, poultry, eggs. needed for growth and development. just enough = dec cholesterol. too much = inflammation

what is the ideal balance of omega 6:omega 3

4:1 or lower

what is the typical western diet of Omega 6: omega 3

15-20:1

what does fish oil do

omega 3s = sudden death by arrhythmias and in pts with CHD. antithrombotic and anti inflammatory effects. omega 6s (seeds, veggie oil, meat) are prothrombotic and proinflammatory w ratio >4:1. 2 servings/wk for pts w no pmhx of CHD and 1 serving/day for pts w CHD.

what can omega 3 acid ethyl esters (lovaza) tx alongside with diet chnages

hi tris which can dec risk of pancreatitis. not as ideal as statins

side effects of omega 3 acid ethyl esters (lovaza)

burping, nausea, GI upset.

Icosapent ethyl (vascepa) is used for what

aka eicosapentaenoic acid (e-epa). First drug approved by FDA to reduce CV risk in pts w hi tris.

what is the difference between Lovaza and Vascepa

Lovaza can inc LDL so its only approved to tx hi tris. not needed to dec CV risk. Vascepa doesn’t inc LDL. approved for hi trisand to dec CV events in statin tx hi risk pts.

PCSK9 inhibitors are

evolocumab and alirocumab. 

what do PCSK9 inhibitors do

destroy LDL in the liver. inc uptake of LDL to dec serum LDL. dec LPa 20-30%.

why do you perscribe PCSK9 inhibitors

when a pt with a statin still has high LPa/cholesterol. or when pt has atherosclerotic cv dz.

adverse events of PCSK9 inhibitors

allergic rxns, +ISRs, inc LFTs

Bempedoic acid is used for what

adenosine triphosphate citrate lyase (ACL) inhibitor. tx heterozygous familial hypercholesterolemia or ASCVD that needs more LDL lowering.

adverse effects of bempedoic acid

hyperuricemia, muscle pain, anemia, and tendon rupture