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pharm exam 2 > drug therapy for dyslipidemia > Flashcards

drug therapy for dyslipidemia Flashcards

1
Q

blood lipids/ blood fats/ blood fatty acids are derived from_______ and found in _____

A

diet and found in body cells, perform essential functions

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2
Q

blood lipids/ blood fats/ blood fatty acids are synthesized at

A

the cellular level by liver and intestine

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3
Q

each lipoprotein contains

A

cholesterol, phospholipid, and triglyceride bound to a protein

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4
Q

what is metabolic syndrome

A

a cluster of conditions that occur together, increasing the risk of heart disease, stroke and type 2 diabetes

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5
Q

s/sx of metabolic syndrome

A

increase waist circumference, increase triglyceride levels (result from excessive dietary proteins and carbohydrates), increase LDL (bad), decrease HDL (healthy), increase BP, increase fasting glucose (r/t insulin resistance), hypertension

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6
Q

for good cholesterol what do you want to see

A

low LDL levels and high HDL levels

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7
Q

metabolic syndrome doubles what

A

risk for cardiovascular disease

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8
Q

dyslipidemia aka hyperlipidemia is

A

increase level of lipids in the blood

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9
Q

a major risk of dyslipidemia is

A

CAD

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10
Q

dyslipidemia/ hyperlipidemia is associated with

A

atherosclerosis, MI and ischemia, CVA, peripheral arterial occlusive disease

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11
Q

primary type of dyslipidemia

A

genetic, familiar

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12
Q

secondary type of dyslipidemia

A

dietary habits; DM, alcoholism, hypothyroidism, obesity, obstructive liver disease

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13
Q

high cholesterol symptoms

A

loose stools, depression, stomach distention, poor appetite, weight gain (central), heart pain, fatigue, aching pain, bumps around eye

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14
Q

total serum cholesterol less than

A

200 is optimal

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15
Q

LDL cholesterol less than

A

100 is optimal

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16
Q

HDL cholesterol higher than

A

60 is optimal

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17
Q

major risk factors that modify LDL goals

A

smoking, hypertension (or on antihypertensive medication), low HDL cholesterol, family history of CHD, age

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18
Q

treatment guidelines for dyslipidemia

A

stop meds that increase blood lipids, start low fat diet, use mediterrean diet, increase dietary intake of soluble fiber, dietary supplements and cholesterol lowering methods, start weight reduction diet, emphasize regular aerobic exercise, stop smoking, postmenopausal hormone replacement therapy

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19
Q

general characteristics of antidyslipidemias

A

decrease blood lipids, prevent/ delay atherosclerotic plaque, promote regression of existing atherosclerotic plaque, reduce morbidity and mortality from cardiovascular disease

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20
Q

mechanism of action of antidyslipidemics

A

alter production (absorption of lipids and lipoproteins) and metabolism (removal of lipids and lipoproteins)

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21
Q

drugs for dyslipidemia

A

hydroxymethylglutaryl-coenzyme A reductase inhibitor (HMG-CoA reeductase inhibitors or statins), bile acid seqestrants, fibrates, cholesterol absorption inhibitors, PCSK9 inhibitors

22
Q

hydroxymethylglutaryl-coenzyme A reductase inhibitor (HMG-CoA reeductase inhibitors or statins) does what

A

decrease cholesterol production = decrease total cholesterol, LDL, VLDL, and triglycerides without reducing HDL (may increase)

23
Q

an example of hydroxymethylglutaryl-coenzyme A reductase inhibitor (HMG-CoA reeductase inhibitors or statins)

A

atorvastatin (lipitor)

24
Q

pharmacokinetics of hydroxymethylglutaryl-coenzyme A reductase inhibitor (HMG-CoA reeductase inhibitors or statins)

A

extensive first pass effect in liver/ food decreases rate/ absorption rate, 80-85% excreted in the stool, the rest is excreted in urine

25
Q

side effects of hydroxymethylglutaryl-coenzyme A reductase inhibitor (HMG-CoA reeductase inhibitors or statins)

A

myalgia, nausea, constipation, diarrhea

26
Q

drug interventions for hydroxymethylglutaryl-coenzyme A reductase inhibitor (HMG-CoA reeductase inhibitors or statins)

A

Mg+ antacids, “azalea” antifungals, some antibiotics, cholestyramine

27
Q

nursing concerns for hydroxymethylglutaryl-coenzyme A reductase inhibitor (HMG-CoA reeductase inhibitors or statins)

A

evening administration r/t cholesterol synthesis occurs at this time of day; avoid grapefruit & pomegranate juice, red yeast rice, vitamin B; monitor Liver function test, rnhabdomylosis(severe muscle Ramos, cola colored urine, fatigue), educate on importance of diet and exercise

28
Q

what are bile acid sequestrants

A

Binds bile acids in the intestinal lumen = bile acids excreted via stool= prevents recirculation to liver = stimulates increase bile acid synthesis from cholesterol in liver = increases cholesterol to liver = lowers serum LDL

29
Q

example of bile acid sequestrants

A

cholestyramine

30
Q

pharmacokinetic of bile acid sequestrants

A

not absorbed with oral administration. excreted unchanged in stool/ decrease LDL within a week of use and max levels will maximize in one month

31
Q

side effects of bile acid sequestrants

A

GI fullness, flatulence, constipation/ diarrhea r/t no systemic absorption

32
Q

nursing concerns of bile acid sequestrants

A

decrease absorption of many drugs (dig, folic acid, propranolol, thiazide diuretics, thyroid hormone, warfarin)

33
Q

what are fibrates

A

increase oxidation of fatty acids in liver and muscle tissue = decrease hepatic production of triglycerides, VLDL, and increase HDL

34
Q

example medications of fibrates

A

fenofibrate, gemfibrozil

35
Q

pharmacokinetics of fibrates

A

oral administration/ highly protein bound, peak 6-8 hrs, liver metabolism, urinary excretion

36
Q

side effects of fibrates

A

GI discomfort, diarrhea, RF gallstones (not for pts with preexisting/ PMH of gallbladder disease)

37
Q

nursing concerns for fibrates

A

Nursing: Can enhance effects of warfarin (increasing RF bleeding), increase RF myopathies or rhabdomyolysis with statins, decrease effects of bile sequestrant RX; gemfibrozil must be taken on an empty stomach (30 minutes before a meal)

38
Q

cholesterol absorption inhibitor

A

Inhibit absorption of cholesterol in the small intestines & decreases delivery of intestinal cholesterol to the liver = reduced hepatic cholesterol stores , increasing cholesterol clearance from the blood

39
Q

example medication of cholesterol absorption inhibitor

A

ezetimibe

40
Q

pharmacokinetics of cholesterol absorption inhibitor

A

protein bound, metabolized in small intestines and liver/excreted in stool. Peak effect I n4-12 hours

41
Q

side effects of cholesterol absorption inhibitor

A

HA, diarrhea, nausea

42
Q

nursing concerns for cholesterol absorption inhibitor

A

Educate on diet and lifestyle changes with this medication, can be used as monotherapy or in conjunction with a statin;
Pregnancy category C: not recommended for use

43
Q

PCSK9 inhibitors

A

Antibody that inactivates protein in liver that regulates the lifespan of cholesterol, promoting modulation of the receptors = prolonging receptor activity = promoting clearance of cholesterol = can have a 60-70% reduction in LDL
-Used in patients with familial hypercholesterolemia with max statin dose, lifestyle changes with continued elevated LDL

44
Q

example medication of PCSK9 inhibitor

A

alirocumab

45
Q

pharmacokinetics of PCSK9 inhibitor

A

SubQ every 2-4 weeks/doses vary, 3-7 day max serum concentrations

46
Q

side effects of PCSK9 inhibitor

A

Appears well tolerated/ can see injection site reactions, itching, nasopharyngitis, muscle pain

47
Q

miscellaneous dyslipidemics are

A

niacin and omega 3 fatty acids

48
Q

what does niacin (vitamin B) do

A

boost levels of “healthy” HDL cholesterol and lowertriglycerides modestly lowers “lousy” LDL cholesterol

49
Q

side effects of niacin

A

facial flushing, stomach upset (take with food), diarrhea, can raise blood sugar

50
Q

contraindications of niacin

A

Liver issues, stomach ulcers, changes to glucose levels, muscle damage, low blood pressure, heart rhythm changes, and other issues

51
Q

examples of omega 3 fatty acids

A

omega 3 acid ethyl esters & omega 3 carboxylic acids

52
Q

combination drug therapy for dyslipidemia is

A

Advicor(extended release niacin & lovastatin) & simmer(simvastatin and niacin)

pharm exam 2 (8 decks)

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