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
side effects of hydroxymethylglutaryl-coenzyme A reductase inhibitor (HMG-CoA reeductase inhibitors or statins)
myalgia, nausea, constipation, diarrhea
26
drug interventions for hydroxymethylglutaryl-coenzyme A reductase inhibitor (HMG-CoA reeductase inhibitors or statins)
Mg+ antacids, "azalea" antifungals, some antibiotics, cholestyramine
27
nursing concerns for hydroxymethylglutaryl-coenzyme A reductase inhibitor (HMG-CoA reeductase inhibitors or statins)
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
what are bile acid sequestrants
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
example of bile acid sequestrants
cholestyramine
30
pharmacokinetic of bile acid sequestrants
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
side effects of bile acid sequestrants
GI fullness, flatulence, constipation/ diarrhea r/t no systemic absorption
32
nursing concerns of bile acid sequestrants
decrease absorption of many drugs (dig, folic acid, propranolol, thiazide diuretics, thyroid hormone, warfarin)
33
what are fibrates
increase oxidation of fatty acids in liver and muscle tissue = decrease hepatic production of triglycerides, VLDL, and increase HDL
34
example medications of fibrates
fenofibrate, gemfibrozil
35
pharmacokinetics of fibrates
oral administration/ highly protein bound, peak 6-8 hrs, liver metabolism, urinary excretion
36
side effects of fibrates
GI discomfort, diarrhea, RF gallstones (not for pts with preexisting/ PMH of gallbladder disease)
37
nursing concerns for fibrates
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
cholesterol absorption inhibitor
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
example medication of cholesterol absorption inhibitor
ezetimibe
40
pharmacokinetics of cholesterol absorption inhibitor
protein bound, metabolized in small intestines and liver/excreted in stool. Peak effect I n4-12 hours
41
side effects of cholesterol absorption inhibitor
HA, diarrhea, nausea
42
nursing concerns for cholesterol absorption inhibitor
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
PCSK9 inhibitors
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
example medication of PCSK9 inhibitor
alirocumab
45
pharmacokinetics of PCSK9 inhibitor
SubQ every 2-4 weeks/doses vary, 3-7 day max serum concentrations
46
side effects of PCSK9 inhibitor
Appears well tolerated/ can see injection site reactions, itching, nasopharyngitis, muscle pain
47
miscellaneous dyslipidemics are
niacin and omega 3 fatty acids
48
what does niacin (vitamin B) do
boost levels of “healthy” HDL cholesterol and lower triglycerides modestly lowers “lousy” LDL cholesterol  
49
side effects of niacin
facial flushing, stomach upset (take with food), diarrhea, can raise blood sugar
50
contraindications of niacin
Liver issues, stomach ulcers, changes to glucose levels, muscle damage, low blood pressure, heart rhythm changes, and other issues
51
examples of omega 3 fatty acids
omega 3 acid ethyl esters & omega 3 carboxylic acids
52
combination drug therapy for dyslipidemia is
Advicor(extended release niacin & lovastatin) & simmer(simvastatin and niacin)