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Cardio Exam 2 > lecture 3 > Flashcards

lecture 3 Flashcards

1
Q

Dyslididemia is a major cause of

A

increased atherogenic risk and atherosclerosis-associated conditions (IHD, CVD, PVD)

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2
Q

lipid lowering is very beneficial for the treatment of

A

CVD

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3
Q

1% reduction in total cholesterol->

A

2% reduction in CHD events

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4
Q

many clinical trials have should that avg dyslipidemic therapy results in

A

30-40% reduction of fatal/non-fatal CHD events & stroke

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5
Q

primary goal of dyslipidemia therapy

A

reduction of LDL levels

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6
Q

comparably important dyslipidemia therapy goals

A
  • elevation in HDL independent of LDL
  • reduced CHD events 20-35% in pts with low HDL & avg LDL
  • reduction of TGs
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7
Q

severe hypertriglyceridemia->

A

(>1000mg/dL)-> pancreatitis

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8
Q

moderate elevation of triglycerides ->

A

(150-400mg/dL)-> part of metabolic syndrome

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9
Q

1% reduction in LDL->

A

1% reduction in CHD events

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10
Q

1% increase in HDL->

A

3% reduction in CHD events

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11
Q

how much cholesterol is biosynthesized in the body daily?

A

~1000mg

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12
Q

cholesterol is important

A
  • synthesis of steroid hormones
  • cell membranes
  • synthesis of bile acids
  • absorption of fats & lipid-soluble vitamins
  • transport of fats from liver to tissues
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13
Q

statins are

A

competitive inhibitors of HMG-CoA reductase-> blocks synthesis of cholesterol

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14
Q

HMG-CoA

A

3-hydroxy-3- methylglutaryl coenzyme A

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15
Q

statins block the conversion of HMG-CoA to

A

mevalonate

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16
Q

blocked synthesis of cholesterol in the liver leads to

A
  • increased synthesis of LDL receptors in hepatocytes
  • increased removal of LDL from blood
  • reduction of LDL levels in plasma
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17
Q

reduction of LDL levels is

A

dose dependent

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18
Q

TG levels >250mg/dL

A

-> 35-45% reduction (with max doses)

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19
Q

TG levels <250mg/dL

A

-> up to 25% reduction

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20
Q

statins also increase HDL levels by

A

~7.5%

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21
Q

how do statins reduce TG levels

A
  1. blocked synthesis of cholesterol in liver-> increased synthesis of LDL receptors in liver-> increased removal of LDL-precursors (IDL & VLDL) from blood-> reduced TG
  2. reduce cholesterol in hepatocytes-> reduced synthesis of VLDL in the liver-> reduced TG
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22
Q

main effect of statins

A

reduction of LDL & improvement of the lipid profile

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23
Q

pleiotropic effects of statins

A
  • improvement of endothelial function & enhanced NO production
  • down-regulation of AT1 receptor expression
  • increased plaque stability by inhibiting vascular SMC proliferation & migration & inhibition of monocyte infiltration into the artery wall
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24
Q

pleiotropic effects of statins are independent of

A

lipid-lowering effects

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25
Q

pleiotropic effects of statins are

A

class specific rather than individual drug specific- effects

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26
Q

NO is a potent

A

vasodilator

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27
Q

down regulation of AT1 receptors leads to

A
  • decreased vasocontriction, increase renin & decrease aldosterone
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28
Q

statins are being considered for use in

A 
arrhythmias
preoperative prophylaxis
CNS autoimmune disease
epilepsy
sepsis
cancer
inflammatory diseases
thyroid disorders
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29
Q

what are the 3 major pleiotropic effects of statins?

A
  • anti-inflammatory effect (reduce C-reactive protein)
  • antioxidant effect (inhibit lipoprotein oxidation & peroxidation)
  • anti-platelet effect (reduce platelet aggregation)
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30
Q

PK of statins

A
  • most have poor bioavailability
  • most have large first pass effect
  • > 70% of statins & metabolites are excreted by liver & eliminated in feces
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31
Q

which statins are prodrugs

A

lovastatin & simvastatin

- need to be metabolized (non-CYP_

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32
Q

which statins are metabolized by CYP3A4

A

atorvastatin, lovastatin & simvastatin

- watch for drug interaction

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33
Q

which statins are not really metabolized by CYP enzymes?

A

rosuvastatin
pravastatin - not at all
pitavastatin

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34
Q

which statins are significantly metabolized by CYP2C9?

A

fluvastatin

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35
Q

which statin has the longest half life

A

pravastatin

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36
Q

inhibitors of CYP3A4

A

grapefruit juice

clarithromycin, erythromycin, itraconazole, ketoconazole, HIV protease inhibitors

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37
Q

inducers of CYP3A4

A

rifampin

efavirenz

38
Q

inhibitor of CYP2C9

A

gemfibrozil

39
Q

increased risk of adverse event risk with clarithromycin and

A

statins NOT metabolized by CYP3A4 (rosuvastatin, pravastatin, or fluvastatin)

40
Q

need for periodic monitoring of liver enzymes when on statins

A

has been REMOVED in 2012

  • elevated liver enzymes resolve spontaneously in most cases
  • routine LFT do not detect or prevent statin-induced heptotoxicity
41
Q

myopathy definition

A

breakdown of muscle fibers

42
Q

myopathy & statins

A
  • major adverse effect, rarely developing to rhabdomylysis

- elevation of creatine-kinase (CK) levels >10 of upper normal limit- indicator of statin-induced rhabdomyolysis

43
Q

cognitive effects of statins

A
  • generally non-serious & reversible, more common >50yo
  • impairment is typically reversed upon discontinuation of statin therapy
  • is NOT dose-dependent
44
Q

hyperglycemia & statins

A
  • clinical evidence for increased blood glucose & HgbA1C levels
  • statin therapy is beneficial in DM
45
Q

thyrotropin (TSH) concentrations & statins

A

may falsely lower serum TSH levels w/out altering thyroid function

46
Q

the risk of adverse effects with statins is proportional to

A

plasma statin concentration

47
Q

caution in statin use with:

A 
drug combinations
hepatic/renal dysfunction
perioperative period
advanced age
multisystem disease
small body size
48
Q

most common interaction with statins

A

gemfibrozil

~38%

49
Q

gemfibrozil

A
  • inhibits uptake of active hydroxyl acid forms of statins into hepatocytes & their glucuronidation-> may double the plasma conc of statins**
  • also inhibits CYP2C9(fluvastatin)
50
Q

main statins

A 
atorvastatin
lovastatin
simvastatin
pravastatin
pitavastatin
fluvastatin
rosuvastatin
51
Q

main ADE

A

hepatotoxicity
myopathy
cognitive effects
decreased TSH levels

52
Q

bile acid sequestrants (resins)

A

cholestyramine
colestipol
colesevlam

53
Q

bile acid sequestrants are not absorbed

A

from the intestines

54
Q

cholesterol is the precursor of

A

bile acids

55
Q

bile acid sequestrants can reduce LDL

A

up to 25%

56
Q

what is usually second line if statin monotherapy is not sufficient?

A

bile acid sequestrants

57
Q

what can be used in 11-20 yo patients?

A

bile acid sequestrants

58
Q

bile acid sequestrant MOA

A
  • resins are highly + and bind - bile acids. being large, they are NOT absorbed in the intestines & are eliminated in feces-> increase hepatic synthesis of bile-acids (cholesterol is used!)-> decreased hepatic cholesterol-> increased LDL receptors & clearance of LDL-> reduced plasma LDL
59
Q

effects of resins on lipid profile

A
  • reduce LDL (max red. in 1-2 wks)
  • reduce cholesterol content in the liver stimulates its biosynthesis by up-regulating HMG-CoA reductase, so combining with statins is very beneficial
  • HYPER-TG: bc of altered bile acid production
  • elevated HDL by 4-5%
60
Q

ADE of resins

A

hyper-triglyceridemia

  • can interfere with absorption of other drug: sterols (digitalis), acidic drugs, fat-soluble vitamins
  • may cause constipation (bulky)
61
Q

niacin is a

A

B vitamin & is a precursor of nicotinamide adenine dinucleotide (NAD) & NAD-P

62
Q

niacin is the best agent for

A

increasing HDL (up to 30-40%) in 4-7 days

63
Q

niacin effect on LDL & TGs

A

dec. LDL 20-30%

dec. TG 35-45%

64
Q

niacin MOA

A
  • niacin + specific receptors in adipocytes->reduction of cAMP
  • decreased lipolysis of TG
  • decreased transport of FFA to liver
  • decreased hepatic TG synthesis
  • decreased production of VLDL & reduction of LDL
  • elevation of HDL levels in the result of reduced hepatic clearance of apaA-I
65
Q

niacin PK

A
  • complete absorption
  • at LOW doses: metabolized into nicotinuric acid & excreted in urin
  • HIGH doses: greater amount excreted unchanged
66
Q

Niacin ADE

A 
flushing & associated pruritis
dyspepsia
hepatotoxicity- elevated AST/ALT & hyperglycemia
insulin resistance
- elevated urinc acid->gout
67
Q

sign of niacin toxicity

A

50% or more reduction of LDL

68
Q

fibric acid derivatives

A

clofibrate
gemfibrozil
fenofibrate

69
Q

fibric acid derivatives are

A

PPAR (peroxisome proliferator-activated receptor) alpha agonists

70
Q

fibric acid derivatives MOA

A
  • increase FA oxidation
  • increase lipoprotein lipase synthesis->increase clearance of TG rich lipoproteins
  • decr. expression/synthesis of apoC-III-> incr. clearance of VLDL
  • -> reduced TGs
  • incr expression/synthesis of apoA-I & II-> elevation of HDL
71
Q

effects of fibric acids on lipid profile

A
  • mild hyperTG (<400mg/dL): up to 50% decr in TG, ~15% inc in HDL, LDL unchaged
  • marked hyperTG (400-1000mg/dL): ~50% TG reduction, 10-30% LDL INCREASE
72
Q

fibrates are DOC for treating

A

sever hypertriglyceridemia & chylomicronemia syndrome

- usually used as second choice if statin therapy is not sufficient

73
Q

where are PPAR alpha found

A

abundant in liver and brown adipose cells

74
Q

fibrate PK

A
  • take with food

- strong protein binding

75
Q

fibrate main ADE

A
  • GI
  • rash, myalgia, fatigue, HA, sexual impotency, anemia
  • increased lithogenicity of bile
76
Q

caution in combining fibrates with

A
  • oral anticoagulants- decreased albumin binging-> higher circulating dose of oral anticoagulants
  • statins w/ gemfibrozil: decr hepatic uptake-> higher circulating statins
77
Q

ezetimibe is a

A

dietary cholesterol uptake inhibitor

78
Q

ezetimibe inhibits cholesterol absorption in

A

the small intestines (inhibits its transport) by 54%

79
Q

MOA of ezetimibe

A
  • decr. cholesterol absorption in SI-> decr chylomicron formation-> incr LDL receptors-> incr clearance of LDL
80
Q

ezetimibe effect on lipids

A
  • 15-20% LDL reduction
  • 5% TG reduction
  • 1-2% HDL increase
81
Q

ezetimibe PK

A
  • water INSOLUBLE

- do not admin with bile acid sequestrants

82
Q

main ADE of ezetimibe

A

rare allergic rxns

83
Q

omega-3 acid ethyl esters

A

lovaza

vascepa

84
Q

lovaza

A

aka omacor

- mix of omega 3 acid ethyl esters, mostly EPA & DHA

85
Q

vascepa

A

icosapent

- contains EPA

86
Q

omega 3 acid ethyl esters are used in adjunct to

A

diet to reduce TG

- NOT combined with statins

87
Q

omega 3 acid ethyl esters MOA

A
  • not well understood
  • inhibition of acyl CoA: 1,2- diacylglycerol acyltransferase
  • inc mito & peroxisomal beta- oxidation of lipids in liver cells
  • decr. lipogenisis in liver
  • incr plasma lipoprotein activity
88
Q

omega 3 is mainly used for the treatment of

A

hyperTG (>500mg/dL)

89
Q

lovaza vs vascepa

A
  • lovaza incr LDL

- vascepa decr LDL

90
Q

fish oil

A
  • large doses (1-4g)
  • fish burps
  • risks: mercury & other heavy metals, hypomania/mania
91
Q

novel drug target for dyslipidemic therapy

A

targeting PCSK9

- induces degradation of LDL receptor

Cardio Exam 2 (12 decks)

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