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Pharmacology I > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

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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
what route are all statins?
PO
26
Statins are most effective for lowering what?
LDL
27
what do statins do beside lower LDL?
decrease oxidative stress decrease vascular inflammation ^stability of atherosclerotic lesion
28
when are statins started immediately?
post ACS regardless of lipid levels
29
Are statins used for mono or combo therapy?
both
30
which was the fist statin?
Lovastatin (mevacor)
31
which statin is the most lipophilic?
atorvastatin (lipitor)
32
which statin is the least lipophilic? (most lipophobic)
rouvastatin (crestor)
33
what percentage of statin medications are absorbed?
ranges from 45-75%
34
which two statins are inactive lactone pro drugs which are hydrolyzed in the GI tract?
lovastatin and simvistatin
35
what is the half life of lovastatin and simvistatin?
1-3hr
36
which two statins are flourine containing congeners which are active as given?
atrovastatin and rouvastatin
37
all statins are given at night except for?
atorvastatin and rouvastatin
38
how are statins metabolised?
liver enzymes CPY34A and CYP2C9
39
how are statins excreted?
mostly in bile, but 5-20% in urine
40
food increases the absorption of all statins except for?
pravastatin
41
Toxicity of statins
^serum aminotransferase activity elevated CK drug interactions with CYP inducers/inhibitors myopathy
42
when do do you need to DC statins?
serious injury, trauma, or major surgery or precipitous drop in LDL levels
43
how much can serum aminotransferase activity increase in statin toxicty?
up to 3x normal levels
44
in elevated aminotransferase activity from statin toxicity when can you still continue therapy?
when the patient is asymptomatic
45
what are symptoms of increased aminotransferase activity from statin toxicity?
malasie, anorexia, precipitous drop in LDL (DC immediately)
46
Other names for Niacin?
nicotinic Acid or Vit B3
47
what does Niacin do?
decrease: LDL, VLDL, LP(a) ^ HDL
48
when medication is the most effective in ^ HDL and also the only agent that can decrease LP (a)?
Niacin
49
what happens to Niacin in the body?
converted to an amide builder for NAD
50
how is Niacin secreted>
unmodifed in urine or as several metabolites
51
Niacin MOA?
inhibit VLDL secretion into the blood decrease production of LDL ^ hepatic clearance of HDL > decreased triglycerides
52
is Niacin used for mono or combo therapy?
both
53
When to use Niacin?
hypercholesterolemia severe mixed lipemia incompletely responsive to diet dysbetalipoproteinemia hypertriglyeridemia
54
toxicity of niacin?
Acanothis Nigricans Insulin resistance Atrial arrhythmias Cutaneous vasodilation “Eye” Macular edema Nausea & and pain
55
Name two Fibric Acid derivatives
gemfibrozil (lopid) fenofibrate (tricar)
56
is gemfibrozil (lopid) protein bound?
yes
57
how does food affect absorption of gemfibrozil (lopid)?
increases its absorption
58
does gemfibrozil (lopid) cross the placenta?
yes
59
gemfibrozil (lopid) half life?
1.5 hours
60
how is gemfibrozil (lopid) eliminated?
70% kidney elimination
61
Describe fenofibrate (tricar)
isopropyl ester that is hydrolyzed in the intestine
62
half life of fenofibrate (tricar)?
20hrs
63
how is fenofibrate (tricar) eliminated?
60% in urine 25% feces
64
MOA of fibric acid derivatives?
ligand for nuclear transcription receptor PPAR-alpha
65
physiologic effects of fibric acid derivatives?
^oxidation of fatty acids in liver and striated muscle ^lipolysis of lipoprotein triglycerides decrase VLDL modest reduction in LDL mod ^ of HDL secretion
66
when are fibric acid derivatives used?
VLDL predominated hypertriglyceridemia dysbetalipoproteinemia
67
toxicty of firbric acid derivatives?
potentiate actions of coumadin and indanedione anticoagulants ^ mypopathy risk with statins ^ risk of cholesterol gall stones (especially women, obese, native americans)
68
when to avoid fibric acid derivatives?
hepatic and renal dysfunction
69
where does bile acid come from?
metabolite of cholesterol
70
name some bile acid binding resins
colestipol cholestyramine colesevelam
71
when are bile acid binding resins used?
isolated ^ LDL only if triglyerides ^ > ^ VLDL
72
how do Resins work?
bind bile acids in the intestines > prevent reabsorption > 10x ^ of excretion
73
how often are resins administered?
BID or TID with meals
74
which medication class is helpful to decrease pruritis from cholestasis & bile salt accumulation?
bile acid binding resins
75
toxicity of resins
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
Name an intestinal sterol absorption inhibitor
Ezitimibe
77
MOA of ezitimibe
selective inhibition of absorption of cholesterol and phytosterols
78
which transport protein does ezitimibe target?
NPC1L1
79
how does ezitimibe effect lipid levels?
decrase LDL minimal ^ HDL
80
half life of ezitimibe
22hrs
81
ezitimibe is synergystic with what medications?
statins
82
toxicity of ezitimibe?
low incidence of reversible hepatic dysfunction

Pharmacology I (16 decks)

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