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Pharm II > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

what are the 3 major classes of lipoproteins?

A

LDLs
HDLs
very low density lipoproteins (VLDLs)

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2
Q

where is synthesis of lipids greatest?

A

liver

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3
Q

what does the intestinal mucosa secretes?

A

VLDL (TG-rich)

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4
Q

what do triglycerides break down into?

A

FFA + phospholipids (transferred to HDL)

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5
Q

what enzyme breaks down cholesterol?

A

HMG-CoA reductase (rate limiting step)

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6
Q

what type lipidemia is from a single inherited gene defect or caused by combo of genetic and environmental factors

A

primary hyperlipidemia

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7
Q

what type lipidemia is result of generalized metabolic disorders ie., DM, excessive ETOH, hypothyroidism, primary biliary cirrhosis

A

Secondary hyperlipidemia

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8
Q

what is due to dysfunctional or absent LDL receptors and leads to increased LDL (250-450)

A

Familial hypercholesterolemia (FH)

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9
Q

What id due to a decreased LPL activity leading to decreased TG removal. manifests as TG of 200-500

A

Familial hypertriglyceridemia (FHTG)

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10
Q

Defect with increased HDL catabolism. Will have isolated HDL <35.

A

Hypoalphalipoproteinemia

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11
Q

what are 3 drugs that may alter lipid profiles

A 
Thiazide diuretics (increase TGs)
Beta blockers (Increase TGs, decrease HDL) 
OCPs (increase cholesterol and TGs)
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12
Q

what do macrophages due to LDL

A

Oxidize LDL and then take up the LDL creating foam cells which makes the cell surface more adhesive

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13
Q

What does HDL promote?

A

Reverse cholesterol transport

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14
Q

what is Preventing the development of atherosclerosis and cardiovascular disease

A

primary prevention

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15
Q

Prevent the progression of cardiovascular disease and recurrence of cardiovascular events

A

secondary prevention

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16
Q

what is the optimal LDL level?

A

<100

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17
Q

what is the desirable total cholesterol level?

A

<200

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18
Q

what should HDL be between?

A

40-60

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19
Q

what should triglycerides be less than?

A

<150

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20
Q

what should antihyperlipidemic drugs be combined with?

A

diet
exercise
weight reduction

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21
Q

after antihyperlipidemia drugs are started when should you get labs?

A

4-8 weeks after starting therapy

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22
Q

What is the MOA of Niacin?

A

Inhibits mobilization of FFA’s from adipose tissue => results in decreased VLDL synthesis by the liver

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23
Q

therapeutic uses for niacin?

A

mixed hyperlipoporteinemias
increase HDL (most effective)
decrease TG

24
Q

ADRs with niacin

A

Vasodilation –> Flushing, itching, HA
GI- activation of PUD
hepatotoxicity (LFTs 3X ULN) (get LFTs q 6-8 weeks)

25
contraindications w/ niacin
DM (worse glucose tolerance), gout, peptic ulcer | liver dz
26
what is an anithyperlipidemic drug that is a fibrate?
Gemfibrozil (main one) | fenofibrate
27
MOA of gemfibrozil
inhibits lipolysis and increases liporprotein lipase. Decrease serum VLDL and increase HDL
28
what is gemifibrozil approved for?
Lowering TG in patients with hypertriglyceridemia | used for combined increased cholesterol and TG (in combo)
29
ADRs with gemfibrozil
``` GI (most common, decrease with time) myopathy hepatotoxicity neutropenia gallstones and pancreatitis (avoid in high risk patients) ```
30
What are 2 bile acid binding resins?
Cholestyramine | Colestipol
31
MOA of bile acid binding resins
inhibit enterohepatic recycling of bile acids and salts | liver stimulated to convert stores cholesterol to bile acids
32
What do bile acid binding resins lower?
Total cholesterol LDL in dose dependent area (may increase TGs)
33
ADRs of bile acid binding resins
primarily GI | can increase triglycerides
34
what three drugs should you not give w/i 2 hours of bile acid binding resins?
warfarin, thyroid, digoxin
35
Contraindications with bile acid binding resins
Biliary obstruction, fasting TG >500 | relative is fasting TG >200
36
MOA of HMG-COA reductase inhibitors
Competitively inhibit the rate-limiting enzyme (HMG-CoA Reductase) necessary for cholesterol synthesis results in an increase in hepatic LDL receptors
37
effects of HMG-CoA reductase inhibitors
Decrease LDL, TG, increases HDL
38
Other CV benefits with statins
Stabilize atherosclerotic plaques enhance vascular nitric oxide production attenuate inflammation due to vascular injury decrease oxidative stress
39
What drug class also inhibit bone resorption, modulate inflammatory precess in glomerular mesangial.
statins
40
when do statins have their greatest efficacy?
dinner or at bedtime to coincide with peak cholesterol biosynthesis
41
Most common ADRs with statins
HA, myalgias, dyspepsia Hepatotoxicity (LFTs) myopathy and CPk >10 x normal
42
Biggest contraindications with statins
``` grapefruit juice macrolides triazole antifungals fluoroquinolones diltiazem verapamil amoidarone omperzole protease inhibitors ```
43
What does lovastatin due to warfarin?
increases warfarin effects
44
what is a drug that combines Niacin ER and lovastatin?
advicor
45
ADRs with advicor
increased risk of myopathy | monitor LFTs
46
drug that inhibits absorption of choelsterol at the brush border of the small intestine and there is decreased delivery of cholesterol to the liver.
Ezetimbe (cholesterol absorption inhibitor)
47
ADRs with ezetimbe
HA GI arthralgia sinusitis
48
what is simvastatin + ezetimbe
Vytorin
49
when should vytorin be used?
only is other drugs aren't working well enough
50
is there any CV benefit for replacing estrogen for women going into menopause?
No, not recommended to use estrogen to prevent CAD
51
what is fish oil effective at lowering
Triglycerides
52
side effects of lovaza (Rx fish oil drug)
can effect bleeding time (more thinning of blood) may impair insulin secretion GI
53
What does metamucil help lower
LDL
54
What are OTC things that help with hyperlipidemia
Garlic olestra red yeast rice
55
what can moderate alcohol consumption help with
Increase HDL decreased LDL oxidation decreased platelet aggregation

Pharm II (16 decks)

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