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Hypercholesteremia and Dyslipidemia > Hypercholesteremia and Dyslipidemia > Flashcards

Hypercholesteremia and Dyslipidemia Flashcards

1
Q

What are the drugs used in the treatment of hypercholesteremia?

A
  • statins
  • nicotinic acid (niacin)
  • bile acid sequestrants
  • fibric acid derivatives
  • inhibitors of cholesterol absorption (ezitimibe)
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2
Q

What are the two surces of lipids?

A
  • Exogenous- what we eat

- Endogenous - body produces itself

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3
Q

Lipid Characterstics

A
  • HDL - the GOOD ones - want high numbers
  • LDL - the BAD ones - want low numbers
  • Tryiglycerides - BAD ones - want low numbers
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4
Q

High HDL

A

Decrease rick of cardiovascular disease

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5
Q

Total cholesterol ( when to start treatment)

A

> 240

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6
Q

LDL (when to start treatment)

A

> 190

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7
Q

HDL (when to start treatment)

A

<40

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8
Q

Triglycerides (when to start treatment)

A

> 500

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9
Q

Modes to reduce lipid levels:

A
  1. Therapeutic lifestyle changes:
    - Improved diet: reduce saturated fat to <200mg/day
    - weight reduction
    - increase physical activity
  2. Medication
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10
Q

How to reduce exogenous sources

A

reduce fat and cholesterol intake

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11
Q

How to reduce endogenous sources

A
  • statins
  • nicotinic acid
  • resins
  • fibric acid derivative
  • inhibitors of cholesterol absorption
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12
Q

What are the mechanisms of statins?

A

-Statins are in competition with HMG-CoA (enzyme that is essential for mevalonate synthesis)
(mevalonate leads to the formation of cholesterol).

Statins are in competition to prevent mevalonate sythesis resulting in decrease of cholesterol synthesis.

Statins also cause upregulation of LDL receptors and will remove more LDL from circulation

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13
Q

Statins Adverse effects

A
  • myopathies, risk of myopathies is increased with other lipid lowering drugs like the fibrates and other drugs that inhibit the activities fo P450 isoenzymess.
  • serum creatin kinase levels are usually elevated 10 times in these patients
  • Avoid fibrates, antibiotics, antifungals, and HIV protease inhibitors
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14
Q

Statins Adverse effects

A

Hepatotoxicity: do not give to liver disease patients, careful with those who drink ETOH heavily, do not give with GRAPEFRUIT juice because it inhibites P450 enzyme

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15
Q

Statins Adverse Effects

A

Do not give in pregnancy, approved for childeren >11 but do not give because they will not take a pill every day for the rest of there life.

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16
Q

Positive effects of statins (FYI)

A
  • endothelial function
  • anit-thrombin
  • anti - inflammatory
  • immunomodulatory
  • vascular cytoprotection
  • anti oxident
  • angiogenesis
  • plaque stability
17
Q

Nicotinic acid Facts

A

-Niacin refers to nicotinc acid and nicotinamide (Vit B3) VIt B3 is required at 15-20mg/day to play vial role in cell meatbolism. Deficiency causes pellagra (dermatitis, insomnia, weakness, confusion, and diarrhea) Nicotinic acid it the treatment for pallegra and also has a lipid lowerin effect with higher concentrations.

18
Q

Nicotinic Acid Facts

A
  • Best agent availiable to increase HDL levels 30-40%
  • Decrease triglyceride levels 35-45%
  • Decrease LDL levels 20-30%
19
Q

Nicotinc Acid adverse effects

A

-dyspesia (heavy gut) , flushing, puritis (can be prevented with aspirin)
-do not give in pregnancy- induced birth defects
-hepatoxycity
-hyperglycemia
-elevates uric acid may reactivate gout
myopathy when used with statins as combo

20
Q

Nicotinic Acid

A

-extended realease minimisis heavy gut felling

requires prescription

21
Q

Bile -Acid seguestrants (Resins)

A
  • oldest and safest lipid lowering agent
  • Max dose can reduce LDL up to 25%
  • Highly positive charged anion exchange resins that bind negatively charged bil acids. (carries transport lipids from gut to liver)
  • Depletes the hepatic cholesterol content and upregulates LDL receptors and increase the triglyceride synthesis
22
Q

Bile Acid (resings) facts

A
  • bind directly and may interfere with absorption of drugs including statins.
  • recommended for patients 11-20 years old and should be given before eating.
23
Q

Fibric Acid Derivatives

A
  • Bind to peroxisome proliferator activate receptors(PPAR) and stimulate oxidation of fatty acids.
  • STRONGEST agent to decrease triglyceride levels
  • PPAR belongs to nuclear receptors superfamily, shown to be a major adipogenic transcription factor
  • Incrreased # of receptors
24
Q

Fibric Acid Derivatives

A
  • Clofibrate 2 grams/day
  • Gemifibrozil 600mg bid
  • Fenofibrate 145-200mg/day
25
Q

Fibric Actid Derivatives recommendations

A
  • patients with -Type III hyperlipoprotenemia
  • severe hypertriglyceridemia
  • Type II diabetes or metabolic syndrome
26
Q

Fibric Acid Adverse effects

A
  • Do not give to children or pregnancy (midgets)
  • n/v
  • increased risk of myopathy
  • headache
27
Q

Fibric Acid Beneficial effects

A
  • Lipid lowering
  • antithrombotic
  • immunomodulation
  • antiinflamatory actions
28
Q

Inhibition of dietary cholesterol uptake: EZETIMIBE

A
  • blocks the function of Niemann Pick C1(NPCIL1)(NPC1L1 manily gets lipids across to the bile acids) protein, a new sterol influx transporter, facilitating cholesterol absorbption. The compensatory increase in the endogenous cholesterol synthesis is prevented by use of statins.
  • Decreases LDL 15-20%
  • combo with statins decrease LDL 30-50%
  • Do not combo with bile acids (they inhibit absorption of ezetimibe)
  • Do not give with pregnancy
29
Q

Vytorin

A

-combo of ezetimibe and statins

30
Q

Ezetimbie Side Effects

A
  • myopathy
  • rhabdomyolysis
  • myalgia
  • hepatitis
  • eczema
  • fatigue
  • headache
31
Q

When to start medication

A
  • advise lifestyle changes first unless they have major risk fo heart disease then start immediately.
  • If no immediate risk advise lifestyle changes and reevaluate in 1month.
32
Q

Risk assessment for lipid disorders

A
  • obtain baseline data (lipid profile)
  • Major risk factors ( smoking, HTN, low HDL, family history, age >45 men, >55 in women
  • test for presence of CHD or equivialants (Diabetes, vascular disease, chronic renal insufficiency)
  • High estrogen level lower LDL - post menopausal women are at risk for higher LDL due to low estrogen

Hypercholesteremia and Dyslipidemia (1 decks)

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