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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
carbohydrates
50-60% of total calories
26
dietary fiber
20-30g/day
27
Statins
most effective agents in reducing LDL levels and best tolerated class of lipid lowering agents stuctural analog of HMG-CoA
28
statin pharmacokinetics
extensive 1st pass metabolism plasma half lives ranges from 1-3 hours w/exception of atrovastatin (14hrs) rosuvastatin (19hrs) primarily excreted in bile
29
statins pharmacodynamics
inhibit MHG-CoA reductase, rate limiting enzyme in cholesterol synthesis
30
statin potency
rosuvastatin\>atorvastatin\>\>simvastatin\>pitavastatin=lovastatin=pravastatin\>fluastatin
31
high intensity atorvastatin dosage
40-80mg
32
high intensity rousuvastatin dosage
20mg
33
statins and liver
elevations of serum aminotransferase activity
34
mm and statins
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
statin drug interactions
increased risk of myopahty w/cyclosporine, itraconazole, erythromycin, gemfibrozil, or niacin increases warfarin levels should not be used w/inducers phenytoin, friseofulvin
36
statin contraindications
pregnancy, lactation, or likely to get pregnant liver disease skeletal m myopathy
37
statins in children
restricted to those w/homozygous familial hypercholesterolemia and some heterozygous
38
niacin
most effective agent for increasing HDL lowers LDL and VLDL only lipid lowering agent that significantly reduces Lp(a)
39
niacin chem and pharmacokinetics
converted to amide and incorporated into NAD well absorbed distibuted to amily hepatic, renal, adipose tissue extensive first pass excreted in urine
40
Niacin pharmacodynamics
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
therapeutic uses of niacin
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
adverse effects of niacin
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
contraindications of niacin
hepatic disease or active peptic ulcer DM -\> increased insulin resistance -\> elevated insulin -\> acanthosis nigricans
44
fibrates pharmacokinetics
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
fibrates pharmacodynamics
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
uses of fibrates
hypertriglyceridemia where VLDL predominates dysbetalipoproteinemia hypertriclygeridemia due to viral protease inhibitors (HIV)
47
fibrate adverse effects
GI lithiasis, especially gallstones myositis, myopathy, rhabdomyolysis
48
fibrate drug interactions
fibrates potentiate actions of coumarin and indanedione anticoagulants
49
fibrates contraindications
hepatic or renal dysfunction not sure in pregnancy or lactation biliary tract disease or high risk for gallstones
50
bile acid sequesterants pharmacokinetics
insoluble in water neither absorbed nor metabolically altered by intestine, totally excreted in feces
51
resin pharmacodynamics
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
resin uses
primary hypercholesterolemia type IIa or IIb hyperlipidemias relieve pruitus in patients w/bile salt accumulation digitalis toxicity
53
adverse effects of resins
GI- constipation, nausea, flatulence) at high does imprai absorption of fat soluble vitamins
54
drug interactions resins
impari absorption of tetracycline phenobarbital digoxin warfarin pravastatin flustatin aspirin thiazide diuretics
55
resin contraindications
diverticulits, preexisting bowel disese, cholestasis
56
cholesterol absorption inhibitors pharmacokinetics
highly water insoluble enters enterohepatic circulation as active compound excreted in feces 22 hour half life
57
cholesterol absorption pharmacodynamics
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
uses of cholesterol absorption inhibitors
various causes of elevated cholesterol
59
cholesterol absorption inhibitor contraindicatios
don't combine w/resins b/c resins will inhibit ezetimibe absorption
60
lomitapide
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
lomitapide adverse effects
GI, increased liver aminotransferase levels, and hepatic fat accumulation costs \>250,000/yr
62
mipomersen
antisense oligonucleotide targets apoB-100 mRNA and disrupts fnx
63
mipomersen adverse effects
injection site rxns, flu like symptoms, headache, elevation of liver enzymes, expensive
64

Cardio 2 (17 decks)

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