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Cardio 2 > Hyperlipidemia Drug DSA > Flashcards

Hyperlipidemia Drug DSA Flashcards

1
Q

HMG-CoA reductase inhibitors

A

aka statins

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2
Q

fibric acid derivatives

A

aka fibrates

fenofibrate

gemfibrozil

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3
Q

bile acid sequestrants

A

aka resins

cholestyramine

colesevelam

colestipol

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4
Q

cholesterol absorption inhibitors

A

ezetimibe

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5
Q

common drug combo

A

simvastatin and ezetimibe

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6
Q

treatment for homozygous familial hypercholesterolemia

A

lomitapide

mipomersen

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7
Q

chylomicron

A

<.94g/mL

1-2proteins

80-95trig

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8
Q

VLDL

A

.94-1.006g/mL

6-10 proteins

55-80 trig

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9
Q

LDL

A

1.006-1.063g/mL

18-22 proteins

5-15 trig

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10
Q

HDL

A

1.063-1.21g/ml

45-55 proteins

5-10 trig

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11
Q

LPL

A

lipoprotein lipase

located on inner surface of capillary endothelial cells of mm and adipose tissue

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12
Q

primary hypertriglyceridemias

A

primary chylomicronemia

familial hypertriglyceridemia

familial combined hyperlipoproteinemia

familial dysbetalipoproteinemia

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13
Q

primary hypercholesterolemia

A

familial hypercholesterolemia

familial ligand-defective apoliproteinemia

familial combined hyperlipoproteinemia

Lp(a) hyperlipoproteinemia

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14
Q

other lipoprotein disorders

A

deficiency of cholesterol 7alpha-hydroxylase

autosomal recessive hypercholesterolemia

mutations in PCSK9 gene

HDL deficencies

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15
Q

HDL deficiencies

A

tangier disease

LCAT deficiency

familial hypoalphalipoproteinemia

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16
Q

secondary hyperlipoproteinemia

A

can be due to common to conditions or drugs such as DM, alcohol ingestion, estrogens, corticosterioids excess, hypopituitarism, acromegaly, resulting in hypertriglyceridemia

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17
Q

other causes of hypercholesterolemia

A

hypothyroidism

anorexia nevosa

early nephrosis

hypopituitarism

corticosteroid excess

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18
Q

CHD or CHD risk equivalents

A

LDL 100mg/dL

LDL at which lifestyle therapy should be initiated >100mg/dL

LDL level at which to consider drug therapy >130mg/dL

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19
Q

2+ risk factors

A

LDL < 130mg/dL

LDL level at which to initiate lifestyle therapy >130

drug therapy >130

drug therapy if risk <10% >160mg

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20
Q

0-1 risk factors

A

LDL <160

LDL at which to initiate lifestyle therapy >160

LDL at which to initiate drug therapy >190

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21
Q

CHD equivalents

A

symptomatic carotid a disease

peripheral arterial disease

abdominal aortic aneurysms

diabetes

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22
Q

total fat

A

20-25%

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23
Q

saturated fat

A

<8% of daily intake

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24
Q

cholesterol

A

<200mg/day

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25
Q

carbohydrates

A

50-60% of total calories

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26
Q

dietary fiber

A

20-30g/day

27
Q

Statins

A

most effective agents in reducing LDL levels and best tolerated class of lipid lowering agents

stuctural analog of HMG-CoA

28
Q

statin pharmacokinetics

A

extensive 1st pass metabolism

plasma half lives ranges from 1-3 hours w/exception of atrovastatin (14hrs) rosuvastatin (19hrs)

primarily excreted in bile

29
Q

statins pharmacodynamics

A

inhibit MHG-CoA reductase, rate limiting enzyme in cholesterol synthesis

30
Q

statin potency

A

rosuvastatin>atorvastatin>>simvastatin>pitavastatin=lovastatin=pravastatin>fluastatin

31
Q

high intensity atorvastatin dosage

A

40-80mg

32
Q

high intensity rousuvastatin dosage

A

20mg

33
Q

statins and liver

A

elevations of serum aminotransferase activity

34
Q

mm and statins

A

creatine kinase activity levels may increase, particularly in patients who have high level o fphysical activity

rhabdomyolysis can occur rarely leading to kidney injury

myopathy can occur w/monotherapy

35
Q

statin drug interactions

A

increased risk of myopahty w/cyclosporine, itraconazole, erythromycin, gemfibrozil, or niacin

increases warfarin levels

should not be used w/inducers phenytoin, friseofulvin

36
Q

statin contraindications

A

pregnancy, lactation, or likely to get pregnant

liver disease

skeletal m myopathy

37
Q

statins in children

A

restricted to those w/homozygous familial hypercholesterolemia and some heterozygous

38
Q

niacin

A

most effective agent for increasing HDL

lowers LDL and VLDL

only lipid lowering agent that significantly reduces Lp(a)

39
Q

niacin chem and pharmacokinetics

A

converted to amide and incorporated into NAD

well absorbed distibuted to amily hepatic, renal, adipose tissue

extensive first pass

excreted in urine

40
Q

Niacin pharmacodynamics

A

inhibits lipolysis of triglycerides in adipose tissue -> fewer circulating FFAs -> lower VLDL -> lower LDL

fibrinogen levels reduces and tissue plasminogen activaotr levels are increased which can reverse some of endothelial cell dysfunction

41
Q

therapeutic uses of niacin

A

often used in combo w/biel acid sequesterant or reductase inhibitor for heterozygous familial hypercholesterolemia and some cases of nephrosis

mixed lipemia incompletely responsive to diet

42
Q

adverse effects of niacin

A

most common side effect is an intense cutaenous flush (aspirin can mitigate this)

pruritis, rashes, dry skin or mucous membranes, acanthosis nigricans

may cuase hepatotoxicity

43
Q

contraindications of niacin

A

hepatic disease or active peptic ulcer

DM -> increased insulin resistance -> elevated insulin -> acanthosis nigricans

44
Q

fibrates pharmacokinetics

A

derivated of fibric acid

well absorbed when taken w/meal, highly bound to serum albumin

gemfibrozil half life = 1.5hrs

fenofibrate half life = 20 hrs

45
Q

fibrates pharmacodynamics

A

acts as agonist ligands for PPARalpha (TF receptor)

when activated increases expression of genes for lipoprotein strucutre and function

VLDL levels decrease LDL levels modestly decrease, HDL increse modestly

46
Q

uses of fibrates

A

hypertriglyceridemia where VLDL predominates

dysbetalipoproteinemia

hypertriclygeridemia due to viral protease inhibitors (HIV)

47
Q

fibrate adverse effects

A

GI

lithiasis, especially gallstones

myositis, myopathy, rhabdomyolysis

48
Q

fibrate drug interactions

A

fibrates potentiate actions of coumarin and indanedione anticoagulants

49
Q

fibrates contraindications

A

hepatic or renal dysfunction

not sure in pregnancy or lactation

biliary tract disease or high risk for gallstones

50
Q

bile acid sequesterants pharmacokinetics

A

insoluble in water

neither absorbed nor metabolically altered by intestine, totally excreted in feces

51
Q

resin pharmacodynamics

A

positively bound substances that bind negatively charged bile salts

increased excretion of bile causes more cholesterol to be converted to bile

decline in hepatic cholesterol causes increase in LDLRs

52
Q

resin uses

A

primary hypercholesterolemia

type IIa or IIb hyperlipidemias

relieve pruitus in patients w/bile salt accumulation

digitalis toxicity

53
Q

adverse effects of resins

A

GI- constipation, nausea, flatulence)

at high does imprai absorption of fat soluble vitamins

54
Q

drug interactions resins

A

impari absorption of

tetracycline

phenobarbital

digoxin

warfarin

pravastatin

flustatin

aspirin

thiazide diuretics

55
Q

resin contraindications

A

diverticulits, preexisting bowel disese, cholestasis

56
Q

cholesterol absorption inhibitors pharmacokinetics

A

highly water insoluble

enters enterohepatic circulation as active compound

excreted in feces 22 hour half life

57
Q

cholesterol absorption pharmacodynamics

A

selectivly inhibits GI absorption of cholesterol and phytosterols

effective even in absence of dietary cholesterol b/c inhbits reabsorption of cholesterol excreted in bile

58
Q

uses of cholesterol absorption inhibitors

A

various causes of elevated cholesterol

59
Q

cholesterol absorption inhibitor contraindicatios

A

don’t combine w/resins b/c resins will inhibit ezetimibe absorption

60
Q

lomitapide

A

directly binds to and inhibits microsomal triglyceride transfer protein which is located in lumen of ER -> prevents assembly of apo-B containing lipoproteins -> decrease LDL

61
Q

lomitapide adverse effects

A

GI, increased liver aminotransferase levels, and hepatic fat accumulation

costs >250,000/yr

62
Q

mipomersen

A

antisense oligonucleotide targets apoB-100 mRNA and disrupts fnx

63
Q

mipomersen adverse effects

A

injection site rxns, flu like symptoms, headache, elevation of liver enzymes, expensive

64
Q
A

Cardio 2 (17 decks)

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