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pharm 1 > drug therapy for dyslipidemia > Flashcards

drug therapy for dyslipidemia Flashcards

1
Q

where are blood lipids derived from

A

diet

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2
Q

where are blood lipids synthesized

A

at the cellular level by liver and intestine

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3
Q

name 3 lipids

A

-cholesterol
-phosoplipids
-triglycerides

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4
Q

where are lipids found and what do they do

A

found in body cells and they perform essential functions

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5
Q

how are lipids transported

A

-transported in plasma by lipoproteins
-each lipoprotein contains cholesterol, phospholipid, and triglyceride bound to protein

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6
Q

look at this thing

A
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7
Q

what is metabolic syndrome

A

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

doubles the risk of cardiovascular disease

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8
Q

what conditions indicate metabolic syndrome

A
  • increased weight circumference/abdominal obesity
  • increased triglceride levels (result from excessive dietary proteins and carbs)
  • increasesd LDL and decreased HDL
  • increased BP, HTN
  • increased fasting glucose (r/t insulin resistance)
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9
Q

what is the goal with metabolic syndrome

A

prevention or early detection

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10
Q

what is dyslipidemia (aka hyperlipidemia)

A

increased level of lipids in the blood

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11
Q

what are some risk factors associated with having dyslipidemia

A

-major risk factor for CAD
-associated wit atherosclerosis
-many pathophysiologic effects
-MI and ischemia
-CVA
-peripheral arterial occlusive disease

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12
Q

what is the tx goal with dyslipidemia

A

reduce morbidity and mortality

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13
Q

there are two types of dyslipidemia, what are they?

A

-primary
-secondary

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14
Q

describe primary dyslipidemia

A

-genetic, familial
-mutation in LDL receptor

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15
Q

describe secondary dyslipidemia

A

-lifestyle associated
-dietary habits, other diseases
-DM, alcoholism, hyperhtyroidism
-obesity, obstructive liver disease

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16
Q

what are symptoms of high cholesterol

A

-loose stools
-depression
-stomach distention
-poor appetite
-weight gain
-heart pain
-fatigue
-bumps
-aching pain

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17
Q

according to the NCEP treatment guidelines, where should someones total serum cholesterol be?

A

<200

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18
Q

according to the NCEP treatment guidelines, where should someones LDL be

A

<100

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19
Q

according to the NCEP treatment guidelines, where should someones HDL be

A

greater than 60

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20
Q

when determining lipoprotein levels, complete lipoprotein profile should be collected after…

A

12 hour fast

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21
Q

look at this thing

A
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22
Q

what are the NCEP treatment guidelines

A
  • assess for and treat conditions known to increase blood lipids
  • stop meds that increase blood lipids if possible
  • start low fat diet, or maditerranean diet
  • increase dietary intake of soluble fiber
  • dietary supplements and cholesterol lowering methods
  • start weight reduction diet (if pt is overweight or obese)
  • emphasize regular aerobis exercise
  • smoking cessation
  • postmenopausal hormone replacement therapy
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23
Q

name some general characteristics of antidyslipidemics

A

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

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24
Q

describe the mechanism of action of antidyslipidemics

A

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

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25
Q

when is pharmacotherapy for dyslipidemia initiated?

A

when 6 months of dietary/lifestyle changes fail to decrease dyslipidemia to acceptable levels

26
Q

what do HMG-CoA reductase inhibitors or “statins” do?

A

decrease cholesterol production = decrease LDL, VLDL, and triglycerides w/o reducing HDL (may increase)

27
Q

what are some examples of HMG-CoA reductase inhibitors

A

atorvastatin, provastatin, rosuvastatin, simvastatin

28
Q

describe the pharmacokinetics of statins

A

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

29
Q

what are some side effects of statins

A

-myalgias
-nausea
-constipation or diarrhea

30
Q

what are some drugs that interact with statins

A

-Mg+ anatacids
-“azole” antifungals
-some antibiotics
-cholestyramine

31
Q

what are some nursing implications r/t statins

A

-evening or HS administration (2100) bc cholesterol synthesis occurs at this time of day
-avoid grapfruit and pomegranate juice, red yeast rice, vitamin B3 (increase effects)
-monitor liver function tests and assess for signs of rhabdomyolysis (severe msucle cramps, cola coloerd urine, extreme fatigue) ; stop and call physician
-educate on importance of adherance, diet and exercise along with medication for increase success to reach therapy goal

32
Q

should a pregnant person take statins?

A

nope, pregnancy category X

33
Q

what do bile acid sequestrants do?

A

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

34
Q

give an example of a bile acid sequestrants

A

cholestyramine

35
Q

describe the pharmacokinetics 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

36
Q

what are some side effects of bile acid sequestrants

A

-GI fullness
-flatulence
-constipation
-diarrhea

r/t no systemic absorption

37
Q

what are some side effects of bile acid sequestrants

A

-GI fullness
-flatulence
-constipation
-diarrhea

r/t no systemic absorption

38
Q

what are some nursing implications r/t bile acid sequestrants

A

-decrease absorption of many drugs (digoxin, folic acid, propranolol, thiazide diuretics, warfarin)
-fibers can increase effect
-can prevent absorption of fat soluble vitamins (A,D,E,K)
-give other meds 1 hour before or 4-6 hours after

39
Q

what do fibrates do?

A

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

40
Q

give two examples of fibrates

A

-fenofibrate
-gemfibrozil

41
Q

descirbe the pharmacokinetics of fibrates

A

-oral administration
-highly protien bound
-peak 6-8 hours
-liver metabolism
-urinary excretion

42
Q

what are some side effects of fibrates

A

-GI discomfort
-diarrhea
-risk for gallstones, not for pts with preexisting/PMH of gallbladder disease

43
Q

what are some nursing implications r/t fibrates

A

-can enhance effects of warfarin
-increase risk for myopathies or rhabdomyolysis
-can decrease effects of bile sequestrants
-gamfibrozil must be taken on an empty stomach (30 mins before a meal)

44
Q

what do cholesterol absorption inhibitors do

A

inhibit absorption of cholesterol in small intestines and decrease delivery of intestinal cholesterol to the liver = reduced hepatic cholesterol stores and increasing cholesteral clearance from blood

45
Q

give and example of cholesterol absorption inhibitors

A

ezetimibe

46
Q

describe the pharmacokinetics of cholesterol absorption inhibitors

A

-protein bound
-metabolized in small intestines and liver
-excreted in stool

47
Q

what are some side effects of cholesterol absorption inhibitors

A

HA, diarrhea, nausea

48
Q

what are some nursing implications r/t cholesterol absorption inhibitors

A

-educate on diet and lifestyle changes with this med
-can be uses as monotherapy or in conjunction with a statin
-pregnancy category C: not recommended for use

49
Q

what do PCSK9 inhibitors do

A

antibody that inactivates protein in liver that regulates the lifespan of cholesterol, promoting modulation of the receptors = proloning receptor activity = promoting clearance of cholesterol =** can have a 60-70% reduction in LDL**

50
Q

who are PCSK9 inhibitors used for

A

patients with familial hypercholesterolemia with max statin dose, lifelstyle changes with continued elevated LDL

51
Q

give an example of PCSK9 inhibitors

A

alirocumab

52
Q

describe the pharmacokinetics of PCSK9 inhibitors

A

sub Q every 2-4 weeks/doses vary
3-7 day max serum concentrations

53
Q

what are some side effects of PCSK9 inhibitors

A

-appears well tolerates
-can see injection site reactions
-itching
-nasopharyngitis
-muscle pain

54
Q

what are some nursing implications r/t PCSK9 inhibitors

A

-educate pt onsubq injection process
-schedule follow up 4-8 weeks
-encourage diet and exercise as appropriate to facilitate lipid lowering process

55
Q

what does niacin (vitamin B3) do?

A

boost evels of HDL cholesterol and lowers triglycerides modestly lowers LDL cholesterol

56
Q

what are some side effects of niacin

A
  • facial flushing
  • stomach upset (take with food)
  • diarrhea
  • can raise blood sugar
57
Q

what are some contraindications of niacin

A
  • liver issues
  • stomach ulcers
  • changes to glucose levels
  • muscle damage
  • low blood pressure
  • heart rhythm changes
  • other issues
58
Q

what are two omega 3 fatty acids that are though to help lower serum lipids?

A

-omega 3 acid ethyl esters
-omega 3 carboxylic acids

59
Q

name two combination rx therapies for dyslipidemia

A

-advicor
-simcor

60
Q

what is advicor

A

extended release niacin and lovastatin

niacin dose is variable

61
Q

what is simcor

A

simvastatin and niacin

niacin dose is variable

pharm 1 (29 decks)

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