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Pharm II > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

Hyperlipidemia leads to

A

pancreatitis and atherosclerosis

*atherosclerosis is leading cause of death for both genders in US

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2
Q

what is familial hypercholesterolemia

A

LDL receptor deficiency resulting in increased LDL

*can be heterozygous or homozygous

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3
Q

LDL is increased by

A

cholesterol, sat fat, trans fat

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4
Q

TAG are increased by

A

total fat, alcohol, excess calories

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5
Q

dietary changes should also be the first go to for HTN pt except in pt with

A

coronary or PVD,

family hypercholesterolemia/hyperlipidemia

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6
Q

if on wt. loss regimen, when should you check cholsterol

A

after stabilized wt for 1 mth bc chol levels low during wt loss

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7
Q

what are the bile acid binding resins

A

cholestyramine, colestipol, colesevelam

*note: cholestyramine decreases Digoxin toxicity by decreasing GI absorption

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8
Q

how do bile acid binding resins work

A

they bind bile acids = prevent intestinal reabsorption
this increases LDL receptor expression thus increasing uptake of plasma LDL to make more bile acids.. the decreased LDL will decrease plasma chol

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9
Q

when do you use bile acid binding resins?

A

whenever LDL is high

  • but not effective in HOMOzygous familial hypercholesterolemia bc no functional LDL receptor
  • not effective in hypertrig bc may increase VLDL
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10
Q

When shouldn’t you take bile acid resins

A 
if hypertriglyceridemia (may increase VLDL)
if homozygous familiy hypercholesterolemia
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11
Q

How should you take bile acid resins

A

with meals bc need bile production for effect

*not absorbed

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12
Q

what are the safest hypolipidemics

A

bile acid binding resins bc not absorbed

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13
Q

common side effects of bile acid binding resins include

A
  • *constipation and bloating (hallmark)
  • steatorrhea if pt has cholestasis
  • rare: gallstone formation in obese, hypoprothrombinemia due to vit K malabsorption
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14
Q

bile acid binding resins may impair absorption of ….?

A

certain (acids or fat soluble) drugs such as digitalis, thiazides, statins, tetracycline, thyroxine, ASA

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15
Q

how does niacin (b3) work?

A

lowers plasma VLDL and LDL by INHIBITING VLDL SECRETION
*also inhibits hepatic cholsterologenesis
thus most effective for hyperchol and to increase HDL

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16
Q

indications for Niacin tx

A

increase clearance in LPL path –> dec VLDL
increase HDL (most effective agent)
most effective in hyperchol

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17
Q

Pharmacokinetics of Niacin (absorption, secretion, dosage)

A

ORAL
RENAL EXCRETION
dose in g range

18
Q

Adverse effects of Niacin

A

generally mild but include

  • CUTANEOUS VASODILATION, warm sensation, pruritus, dry skin (PG dependent so take ASA before)
  • Nausea and abdominal discomfort
  • may ^ liver enzymes, **IMPAIRS GLUCOSE TOLERANCE
  • hyperuricemia
  • may cause severe hepatotoxicity
19
Q

How do statins work

A

inhibitors of HMG coA reductase

*analogs of HMG coA reductase intermediate in mevelonate synthesis

20
Q

What do statins do to improve hyperlipidemia

A 
reduce LDL (inhibiting reductase causes increase in LDL receptor affinity) *most effective at reducing LDL
*also decrease TAG, increase HDL
21
Q

other beneficial effects of statins include

A
  • decrease CRP, lipoprotein ox, platelet aggregation
  • increase plaque stability
  • enhance NO production
22
Q

when are statins most effective

A

when LDL is elevated

23
Q

once again.. statins do what?

A 
decrease LDL
Decrease TAG
increase HDL
decrease CRP, lipoprotein ox, platelet aggregation
increase plaque stability, NO production
24
Q

Pharmacokinetics of Statins

A

high first pass
metab by liver, GI excretion
*give at night bc diurnal pattern of chol syn

25
Q

what are some adverse effects of statins

A

increase serum aminotransferase (reversible)

  • may produce liver damage in alcoholics or pt with pre-existing liver problems
  • increase serum creatine kinase in phys activity
  • rhabdo.. myoglobinuria, renal shutdown (rare)
26
Q

when shouldn’t you prescribe statins

A

preg (catX)
active hepatic dz (caution alcoholics, liver dz)
P450 inhibitors increase concentration (grapefruit, macrolide, cyclosporine, verapamil)
P450 activators decrease (phenytoin, barbiturates, rif)
*gemfibrozil inhibits their metab

27
Q

don’t combine statins with

A 
P450 inhibitors (increase statin)
P450 activators (decrease statin)
fibrates (inhibit statin metab)
28
Q

how do fibrates work

A

they are PPAR alpha ligands that UPREGULATE LPL and other genes in FA ox

29
Q

when should you prescribe fibrates

A

increase LPL, increase VLDL catabolism = DECREASE TAG by lowering VLDL
*also decrease chol

30
Q

when are fibrates effective

A

hypertrig

31
Q

adverse effects of fibrates include

A

rashes, GI sx, arrhythmias, hypokalemia, myopathy, increase aminotransferase and alk phos

  • increase CHOLELITHIASIS/GALLSTONES
  • potentiate warfarin action
  • inhibit statin metab
  • may increase LDL in some pt with combined hyperlipidemias
32
Q

MOA of ezetimibe

A

selectively blocks intestinal absorption of CHOL

33
Q

use of ezetimibe

A 
decrease LDL (moderate)
**combine with statin = reduction of LDL up to 25% beyond statin alone
34
Q

how is ezetimibe metab

A

by liver then enterohepatically recirculated

35
Q

adverse effects of ezetimibe

A

none so far

36
Q

HMG CoA reductase effect

A

*decrease LDL, increase HDL, decrease TAG

37
Q

Bil acid binding resins action

A

decrease LDL

38
Q

Fibrate action

A

decrease TAG

39
Q

Niacin action

A

decrease LDL, Increase LDL, decrease TAG

40
Q

if high chol…

A

give cholestyramine, ezetimibe

41
Q

if high TAG

A

give fibrate

42
Q

if high chol and high TAG

A

statin and niacin, ezetimibe

Pharm II (12 decks)

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