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Pharmacology I > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

2 major sequelea of lipoproteins?

A

acute pancreatitis
athersclerois (leading cause of death in U.S. men and women)

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2
Q

Types of Lipoproteins

A

apolioprotein/apoprotein
chylomicrons
VLDL
IDL
LDL
HDL
LP(a)

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3
Q

what do know about chylomicrons?

A

Fat > muscles, fat cells, liver
the largest lipoprotein
least dense
triglyceride is digested and cholesterol remains.
Cholesterol > liver for metabolism
HIGHEST TRIGLYCERIDE CONTENT

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4
Q

What to know about VLDL?

A

protein, fat, cholesterol

synthesized in the liver

5 different lipoproteins > removal of apoprotein and esterification of cholesterol > IDL and LDL

2nd highest in triglyercerides

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5
Q

what to know about LDL?

A

chiefly cholesterol
only apoprotein it is associated with is apoB-100

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6
Q

what to know about HDL?

A

highest protein/lipid ratio so most dense

“good cholesterol”

carries cholesterol away from tissues to the liver

increased levels decrease risk of CV diesease

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7
Q

what things increase HDL levels?

A

exercise
^ estrogen
alcohol
weight loss
smoking cigarettes

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8
Q

how long to fast before blood draw for lipid levels?

A

10 hours

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9
Q

total cholesterol level

A

<200

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10
Q

LDL level?

A

<130

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11
Q

HDL level in men?

A

> 40

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12
Q

HDL level in women?

A

> 50

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13
Q

triglyceride levels?

A

<120

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14
Q

how do you differentiate the lipoprotein disorders?

A

by the lipoproteins involved

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15
Q

two kinds of primary lipoprotein disorder?

A

primary hypertryglerideemia

primary hypercholesterolemia

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16
Q

Diseases in primary hypertryglercerideemia?

A

primary chylomicronemia

familial hypertryglereridemia
severe
moderate

FAMILILIAL COMBINED HYPERLIPOPROTEINEMIA

familial dysbetalipoproteinemia

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17
Q

diseases in primary hypercholesterolemia?

A

familial hypercholesterolemia

familial ligand deffective apolioprotein B-100

FAMILIAL COMBINED HYPERLIPOPROTEINEMIA

LP(a) hyperlipoproteinemia

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18
Q

2 main things with secondary lipoprotein disordres?

A

must consider 2ndary causes before primary disorders can be diagnosed

lipoprotein abnormality usually resolves if underlying disorder can be treated

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19
Q

lipoprotein disorder treatment

A

dietary measures first

if CAD & PVD start pharmacologic therapy simultaneously.

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20
Q

in which lipoprotein disorders is drug therapy always required?

A

familial hypercholesterolemia

familial hyperlipoproteinemia

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21
Q

how long must weight be stabilized for diet to be sufficient control of lipoprotein disorders?

A

1 month

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22
Q

what three things increase LDL?

A

cholesterol
saturated fat
trans fat

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23
Q

what three things raise triglycerides?

A

^ total fat
alcohol
excess calories

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24
Q

what two things increase VLDL?

A

sucrose
fructose

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25
Q

what route are all statins?

A

PO

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26
Q

Statins are most effective for lowering what?

A

LDL

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27
Q

what do statins do beside lower LDL?

A

decrease oxidative stress
decrease vascular inflammation
^stability of atherosclerotic lesion

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28
Q

when are statins started immediately?

A

post ACS regardless of lipid levels

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29
Q

Are statins used for mono or combo therapy?

A

both

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30
Q

which was the fist statin?

A

Lovastatin (mevacor)

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31
Q

which statin is the most lipophilic?

A

atorvastatin (lipitor)

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32
Q

which statin is the least lipophilic? (most lipophobic)

A

rouvastatin (crestor)

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33
Q

what percentage of statin medications are absorbed?

A

ranges from 45-75%

34
Q

which two statins are inactive lactone pro drugs which are hydrolyzed in the GI tract?

A

lovastatin and simvistatin

35
Q

what is the half life of lovastatin and simvistatin?

A

1-3hr

36
Q

which two statins are flourine containing congeners which are active as given?

A

atrovastatin and rouvastatin

37
Q

all statins are given at night except for?

A

atorvastatin and rouvastatin

38
Q

how are statins metabolised?

A

liver enzymes CPY34A and CYP2C9

39
Q

how are statins excreted?

A

mostly in bile, but 5-20% in urine

40
Q

food increases the absorption of all statins except for?

A

pravastatin

41
Q

Toxicity of statins

A

^serum aminotransferase activity

elevated CK

drug interactions with CYP inducers/inhibitors

myopathy

42
Q

when do do you need to DC statins?

A

serious injury, trauma, or major surgery

or

precipitous drop in LDL levels

43
Q

how much can serum aminotransferase activity increase in statin toxicty?

A

up to 3x normal levels

44
Q

in elevated aminotransferase activity from statin toxicity when can you still continue therapy?

A

when the patient is asymptomatic

45
Q

what are symptoms of increased aminotransferase activity from statin toxicity?

A

malasie, anorexia, precipitous drop in LDL (DC immediately)

46
Q

Other names for Niacin?

A

nicotinic Acid or Vit B3

47
Q

what does Niacin do?

A

decrease: LDL, VLDL, LP(a)

^ HDL

48
Q

when medication is the most effective in ^ HDL and also the only agent that can decrease LP (a)?

A

Niacin

49
Q

what happens to Niacin in the body?

A

converted to an amide builder for NAD

50
Q

how is Niacin secreted>

A

unmodifed in urine or as several metabolites

51
Q

Niacin MOA?

A

inhibit VLDL secretion into the blood

decrease production of LDL

^ hepatic clearance of HDL > decreased triglycerides

52
Q

is Niacin used for mono or combo therapy?

A

both

53
Q

When to use Niacin?

A

hypercholesterolemia

severe mixed lipemia incompletely responsive to diet

dysbetalipoproteinemia

hypertriglyeridemia

54
Q

toxicity of niacin?

A

Acanothis Nigricans
Insulin resistance
Atrial arrhythmias
Cutaneous vasodilation
“Eye” Macular edema
Nausea & and pain

55
Q

Name two Fibric Acid derivatives

A

gemfibrozil (lopid)

fenofibrate (tricar)

56
Q

is gemfibrozil (lopid) protein bound?

A

yes

57
Q

how does food affect absorption of gemfibrozil (lopid)?

A

increases its absorption

58
Q

does gemfibrozil (lopid) cross the placenta?

A

yes

59
Q

gemfibrozil (lopid) half life?

A

1.5 hours

60
Q

how is gemfibrozil (lopid) eliminated?

A

70% kidney elimination

61
Q

Describe fenofibrate (tricar)

A

isopropyl ester that is hydrolyzed in the intestine

62
Q

half life of fenofibrate (tricar)?

A

20hrs

63
Q

how is fenofibrate (tricar) eliminated?

A

60% in urine
25% feces

64
Q

MOA of fibric acid derivatives?

A

ligand for nuclear transcription receptor PPAR-alpha

65
Q

physiologic effects of fibric acid derivatives?

A

^oxidation of fatty acids in liver and striated muscle

^lipolysis of lipoprotein triglycerides

decrase VLDL

modest reduction in LDL

mod ^ of HDL secretion

66
Q

when are fibric acid derivatives used?

A

VLDL predominated hypertriglyceridemia

dysbetalipoproteinemia

67
Q

toxicty of firbric acid derivatives?

A

potentiate actions of coumadin and indanedione anticoagulants

^ mypopathy risk with statins

^ risk of cholesterol gall stones (especially women, obese, native americans)

68
Q

when to avoid fibric acid derivatives?

A

hepatic and renal dysfunction

69
Q

where does bile acid come from?

A

metabolite of cholesterol

70
Q

name some bile acid binding resins

A

colestipol

cholestyramine

colesevelam

71
Q

when are bile acid binding resins used?

A

isolated ^ LDL only

if triglyerides ^ > ^ VLDL

72
Q

how do Resins work?

A

bind bile acids in the intestines >

prevent reabsorption > 10x ^ of excretion

73
Q

how often are resins administered?

A

BID or TID with meals

74
Q

which medication class is helpful to decrease pruritis from cholestasis & bile salt accumulation?

A

bile acid binding resins

75
Q

toxicity of resins

A

impairs absorption of other meds (give 1 hr before meal or 2hrs after)

Constipation/bloating so CI in diverticulitis

malabsorption of Vit K, monitor PT in patients taking anticoagulants

76
Q

Name an intestinal sterol absorption inhibitor

A

Ezitimibe

77
Q

MOA of ezitimibe

A

selective inhibition of absorption of cholesterol and phytosterols

78
Q

which transport protein does ezitimibe target?

A

NPC1L1

79
Q

how does ezitimibe effect lipid levels?

A

decrase LDL

minimal ^ HDL

80
Q

half life of ezitimibe

A

22hrs

81
Q

ezitimibe is synergystic with what medications?

A

statins

82
Q

toxicity of ezitimibe?

A

low incidence of reversible hepatic dysfunction

Pharmacology I (16 decks)

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