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Block 9 Week 2 > Anti-Hyperlipidemic Drugs and Problems- Duan > Flashcards

Anti-Hyperlipidemic Drugs and Problems- Duan Flashcards

1
Q

What does hypothyroidism do to your lipids? Lipoproteins?

A

Increased cholesterol
Increased TG
Increased LDL
Increased VLDL

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2
Q

What do oral contraceptives do to your lipids? Lipoproteins?

A

Increase TG
Increased VLDL
Decrease HDL

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3
Q

What are the four primary lioprotein disorders?

A

Primary chylomicronemia
Familial hypertrigycleridemia
Familial combined hyperlipoproteinemia
Familia dysbetalipoproteinemia

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4
Q

What happens in primary chylomicronemia?

A

LPL or Cofactory deficincy causing increase in chylomicrons and VLDL

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5
Q

What happens in familial hypertriglyceridemia?

A

Increase VLDL, +/- chylomicrons

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6
Q

What happens in familial combined hyperlipoproteinemia?

A

Increase VLDL or Increase LDL or both

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7
Q

What happens in familial dysbetalipoproteinemia?

A

Increase VLDL remnants and chylomicron remnants

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8
Q

What does mutations in LDL receptors cause?

A

Familial hypercholesterolemia via lack of receptor synthetsisi or impaired function of receptors (most common is impaired function)

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9
Q

What happens if you are heterozygous (1 in 500) for familial hypercholesterolemia?
What happens if you are homozygous for familial hypercholesterolemia (1 in 1,000,000)?

A 
Hetero: Serum cholesterol often up to 2x normal
~5 % have MI before age 60
Homo: Serum cholesterol high
Signs of CVD at an early age
Most have an MI by age 20
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10
Q

In diabetes what happens to your lipids? LP?

A

Increase TG
Increase VLDL
Decreased HDL

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11
Q

In alcoholism what happens to your lipids? LP?

A

Increase TG
Increase VLDL
Increased chylomicrons

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12
Q

In liver disease what happens to your lipids? LP?

A

Increase TG
Increase VLDL
Increased chylomicrons

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13
Q

In hypothyroidism what happens to your lipids? LP?

A

Increase TG
Increase Cholesterol
Increase VLDL
Increase LDL

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14
Q

In oral contraceptives what happens to your lipids? LP?

A

Increase TG
Increase VLDL
Decrease HDL

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15
Q

In nephrotic syndrome what happens to your lipids? LP?

A

Increase TG
Increase Cholesterol
Increase VLDL
Increase LDL

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16
Q

In protease inhibitors (HIV) what happens to your lipids? LP?

A

Increase TG
Increase Cholesterol
Increase VLDL

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17
Q

In Isotretinoin (acne) what happens to your lipids? LP?

A

Increase TG
Increase Cholesterol
Increase VLDL
Decrease HDL

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18
Q

Which type of diabetes causes a risk for CVD?

Why?

A

Both
Insulin increases transcript of LPL and removal of TGs and decreases VLDL
THEREFORE if you lose insuli you have decrease LPL ad increase VLDL and high blood sugar, prtoeins and lipids that becme glycate and increase risk of atherogenesis

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19
Q

In atherosclerosis what happens to LDL?

What can protect you against these effects?

A

it gets oxiized and causes oxidation of Apo B-100 glycation.

HDL-> acts as antioxidant

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20
Q

Explain what happens to LDL during atherosclerosis?

A

LDL goes from arterial lumen to arterial wall-> LDL gets oxidized and taken up by scavenger receptors especially on macrophages which makes cholesterol accumulate in them and converts them into foam cells-> die and become part of plaque

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21
Q

Therapeutic intervention in atherogenic heart disaese focuses on lowering plasma LDL through diet and meds. How do statins work?

A

block cholesterol production and increase expression of LDL receptor on liver which will remove LDL in circulation

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22
Q

Why is vit E good?

A

it is an antioxidant that helps prevent oxidation of LDL

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23
Q

Explain the progresssive process of becoming a atherosclerotic plaque and then causing serious CV complications

A

normal-> fatty streak-> fibrous plaque-> occlusive atherosclerotic plaque (angina, claudication)-> plaque rupture/fissure and thrombosis-> complications

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24
Q

What are the drug therapies for hyperlipidemia?

A
  • HMG-Coa Reducatase inhibitors (statins)
  • Bile-acid Binding resins
  • Nicotinic Acid
  • Fibrates
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25
Q

What are the 6 statins?

A 
Lovastatin
Simvastatin
Pravastatin
Fluvastatin
Atorvastatin
Rosuvastatin
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26
Q

What is the mechanism of action of HMG-CoA reductase inhibitors?

A

inhibits HMG-CoA reductase
leads to a decrease in cholesterol synthesis
increased synthesis of hepatic LDL receptors
increased uptake of LDL
(decrease TG and LDL, increase in HDL)

27
Q

What are the clinical uses of statins?

A
  • Widely prescribed for lowering LDL
  • Heterozygous form of familial hypercholesterolemia
  • Ssecondary hypercholesterolemia caused by diabetes mellitus.
28
Q

How should you give statins if you have really high LDL levels

A

Combined with bile acid-binding resins or ezetimibe results in greater additive effects with up to a 50% reduction in LDL levels.

29
Q

What are some other effects of statins?

A
  • Osteoporosis (stimulates osteoblasts)
  • anti-inflammatory (regression of atherosclersis, multiple sclerosis, asthma)
  • decreases hsCRP (high-sensitivity C reactive protein)
30
Q

What are the SEs of statins?

A
  • Headache
  • photosensitivity
  • MYALGA (muscle aching) or MYOPATHY (disease of muscle tissue) CUZ grapefruit interferes with metabolism in liver

low incidence of liver damage

31
Q

What are the interactions associated with statins?

A

Cleared by P450A (CYP3A4) used by:
cyclosporin, erythromycin, ketaconazole, niacin, fibrates, St Johns wort, dihydropyridine Ca2+channel blockers & GRAPEFRUIT JUICE.

32
Q

Statins can result in increased levels of what three drugs?

A

oral contraceptives, digoxin, warfarin

33
Q

Do statins decrease the rate of coronary events in women?

A

Yes :) but not as much as men

34
Q

Will Coenzyme Q10 (ubiquinone) supplementation decrease myalgia in patients taking statins?

A

Yes :)

35
Q

What are the three bile-acid binding resins?

A

Cholestyramine, Colestipol, Colesevelam

36
Q

What is the MOA of Bile-acid binding resins?

A

Anion exchange resin that binds bile acids in the intestine leading to an increased fecal excretion of bile acid.

37
Q

Why are Bile-acid binding resins so amazing at their job?

A

because they are hydrophoboic AND unaffected by digestive enzymes so they remain unchanged in the GI tract and not absorbed

38
Q

What will BABRs result in?

A

increased production of LDL receptors and increased activity of HMG-CoA reductase
(decrease LDL fo sho)

39
Q

What are the clinical uses of BABRs?

A
  • Pnts with elevated concentrations of LDL

- Have an additive effect in lowering LDL cholesterol with nicotinic acid and statins

40
Q

What are the SEs of BABRs?

A

GI problems, nausea, indigestion and constipation are common.

Steatorrhea may occur at high doses (excess fat in the stools).

Absorption of vitamins A, D, E and K and folic acid may be impaired

May cause hyperchloremic acidosis, since often given as chloride form of anion exchange resin

41
Q

What are the interactions of BABR?

A

Cholestyramine binds other drugs, including:

  • chlorothiazide
  • anticoagulants
  • digitalis
  • furosemide
  • niacin
  • statins
42
Q

What is the MOA of niacin?

A

Inhibits VLDL secretion which leads to decreased LDL through multiple mechanisms to reduce apoB-containing lipoprotein (VLDL, IDL, LDL) synthesis

43
Q

What is the overall effect of niacin?

A
  • decrease TG
  • decrease LDL (slower 10-15% can increase to 50% when addd with BABR)
  • increase HDL
44
Q

What are the clinical uses of niacin?

A

Useful in treating most forms of hyperlipoproteinemias EXCEPT familial lipoprotein lipase deficiency

  • Drug of choice for severe hypertrigylceridemia associated with elevated chylomicrons
  • in combo with BABR or Statins
  • prolonged tx results in regression of xanthomas (yelow papule containing lipids)
45
Q

What are the SEs of nicotinic acid?

how do you lessen the effects of cutaneous flush and itching?

A
  • **intense cutaneous flush and itching
  • GI problems, peptic ulceration
  • vasodilation and postural hypotension (may be increased by anti-htn agents)
  • DO NOT GIVE DURING PREGNANCY unless to treat life threatening pancreatitis due to hypertriglyceridemia

-take an aspirin

46
Q

What are the 2 fibrates?

A

Gemfibrozil, Fenofibrate

47
Q

What is the MOA of fibrates?

What is the overall effect of these?

A

Activates peroxisome proliferator-activated receptors alpha (PPAR)

  • decrease TAGs
  • decrease LDL
  • Increase HDL
  • decrease VLDL
48
Q

Why does PPARs get rid of lipids?

A

it induces transcription of a number of genes that facilitate lipid metabolism

49
Q

Fibrates increase the expression of (blank) to increase the breakdown of FFA

A

acyl coa synthase

50
Q

What are the clinical uses of fibrates?

A
  • reduce VLDL in hypertrigylceridemic pnts who do not respond to diet
  • raises HDL levels
  • lower TAGs in type II diabetes, nephrotic syndrome and uremia
51
Q

What are the SEs of fibrates?

A
  • Gi distress
  • Skin rash,
  • eosinophilia
  • muscoskeletal pain
  • drowsiness
  • blurred vision
  • mild anemia
  • hyperglycemic effect (diabetic pnts may require increase of insulin)
  • Gallstones
  • aggravate renal dysfunction
52
Q

What are the drug interactions for fibrates?

A

Potentiates the effect of oral anticoagulants and other acid drugs by displacing them from albumin

53
Q

What is the MOA of ezetimibe?

A

Selectively inhibits cholesterol absorption in the intestinal lumen at the enterocyte brush border
(no effect on lipid soluble vits or most other lipids)

54
Q

What is the overall effect of exetimibe

A

decrease TAG
decrease LDL (17%)
decrease VLDL
increase HDL (3.5%)

55
Q

What are the clinical uses of ezetimibe?

A
  • Either mono or combo therapy

- Combo therapy with statin or fibrate further decreased LDL

56
Q

What are the possible SEs of Ezetimibe?

A

None detected so far

-Contraindicated in pnts w/ liver disease

57
Q

Is vytorin (ezetimibe + simvastatin) any more effective than simvastatin alone?

A

decreases LDL but little improvement on atherosclerosis compared to statin alone

58
Q

What is the mechanism of action of Orlistat?

What is the overall effect of Orlistat?

A

Inhibits activity of intestinal lipases. A portion of the dietary fat is not ingested and excreted with the feces.
-decrease LDL, decrease TAG

59
Q

What are the clinical uses of Orlistat?

A
  • tx of obesity
  • conjuction with a reduced fat diet
  • daily multivitamin supplements contain vit A, D, E, and K and beta carotene
  • GI disturbances
60
Q

What do omega-3 acid ehtyl esters do?

A
  • lower TAGs
  • reduce postprandia chylomicrons and VLDL
  • thought to reduce production of TG in liver
  • may be anti-inflammatory
61
Q

How should you eat omega 3 if you are without documented CHD?
with CHD?
pnts needing TAGs lowering?

A
  • eat a variety of fish
  • 1 g of EPA and DHA per day
  • 2-4 grams of EPA and DHA per day
62
Q

What are foods rich in omega 3s?

A

-Fish oil
-Walnuts, flax, linseed
Soy
-Margarines – Benecol, Take Control etc.
-Avocado
-Red wine or alcohol?
-Other nuts?
-Fiber
-Fruit & vegetables for antioxidants

63
Q

What is a gallstone solubilizing agent?

What is the MOA of this?

A
  • Ursodial
  • dissoultion of radiolucent gallstones
  • increases concentration at which saturation of cholesterol occurs
64
Q

What are the drug reactions of gallstone solubilizing agents (ursodiol)?

A
  • antacids and BABR may interfere w/ absorption

- estrogens may counteract since they encourage stone formation

Block 9 Week 2 (7 decks)

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