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Dental Pharmacology Exam 4 > Hyperlipidimia > Flashcards

Hyperlipidimia Flashcards

1
Q

Progression of events in Classic Angina

A
  1. High Cholesterol - no symptoms
  2. Stable Angina - symptoms w/ exertion
  3. Unstable Angina - symptoms increase in frequency and occur at rest
  4. Acute MI - complete occlussion
    * Acute HF/Congestive HF/Cardiac Arrhythmias
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2
Q

Classic angina is the consequence of _______…

A

Atherosclerotic plaque formation in the coronary arteries

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3
Q

What does an atherosclerotic plaque consist of?

A
  1. Cholesterol deposits and cell components

2. Platelets (white thrombi) and fibrin “Cap”

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4
Q

What drugs are used to prevent atherosclerosis in coronary arteries?

A
  • Cholesterol-Reducing Drugs

- Antiplatelet drugs

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5
Q

What diseases is high cholesterol associated w/?

A
  1. Coronary Heart Disease - #1 killer of americans
    * High triglyceride levels also increase the risk of CHD
  2. Stroke
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6
Q

Lipoprotein anatomy

A

Core of nonpolar lipids
Surrounded by protein and polar phospholipids
Carry Cholesterol

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7
Q

Good to bad lipoproteins

A

HDL = good

VLDL and LDL = bad

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8
Q

Normal Lipids Metabolism (6 steps)

A
  1. Chylomicrons
  2. Lipoprotein lipase
  3. VLDL + triglycerides in liver to Circulation
  4. Lipoprotein lipase = IDL -> Liver or LDL
  5. LDL delivers cholesterol to cells by binding to LDL Receptor
  6. HDL is synthesized by liver
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9
Q

Hypertryglyceridemia has increased _____ and some risk for ____ and _____.

A
  1. VLDL
  2. CHD
  3. Pancreatitis
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10
Q

Hypercholesterolemias have increased _____ and high risk for _____.

A
  1. LDL

2. CHD

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11
Q

Primary Hyperlipidemias - how are they determined and what are they a result of?

A
  1. Genetically Determined

2. Hyperlipoproteinemias

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12
Q

Type IIa hypercholesterolemia - what is it?

A

Defect in LDL receptors prevents LDL transfer into liver and extrahepatic cells resulting in increased blood cholesterol available to affect the arteries
PRIMARY HYPERLIPIDIMIA

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13
Q

What are seconary hyperlipidiemias?

A

Secondary to other conditions, such as diabetes, hypothyroidism, increased estrogen… etc…

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14
Q

What is the most common form of hyperlipidia? What are the factors?

A

Multifactorial

  1. Genetic
  2. Lifestyle
  3. Diet
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15
Q

2 Basic strategies of treating hyperlipidimia

A
  1. Decrease amount of lipid entering blood

2. Improve clearance of lipids from the blood

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16
Q

How to decrease amount of lipid entering blood? (3)

A
  1. Low fat, low calorie diets (1st line of defense)
  2. Drugs that reduce lipoprotein Synthesis
  3. Drugs that reduce dietary cholesterol absorption
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17
Q

How to improve the clearance of lipid from the blood (3)

A
  1. For VLDL - involves the enzyme lipoprotein lipase
  2. For LDL- involves LDL receptors: the less cholesterol in the liver, the more LDL receeptors will be synthesized
  3. More LDL Receptors = More effecient removal of LDL from the blood
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18
Q

What drugs are used to treat hypertriglyceridemia? (2)

A
  1. Niacin

2. Fibric Acid Derivatives

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19
Q

What drugs are used to treat hypercholesolemia? (5)

A
  1. Bile-acid binding sequestrants
  2. Statins
  3. Ezetimibe
  4. Niacin
  5. Combo therapy
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20
Q

What is the primary carrier of triglycerides?

A

VLDL

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21
Q

What is the most effective drug at increasing HDL and moderately decreasing LDL?

A

Niacin

22
Q

What are the SE of Niacin?

A

Harmless flushing reaction, pruritis

23
Q

What drug is a fibric acid deriviative? What does it do?

A

Gemfibrozil - most effective drug at reducing VLDL (50%) but minimal effects on LDL and HDL - only for hypertriglyceridemia

24
Q

What are 2 mechanisms that drugs can target to reduce hyperlipidimia: triglycerides?

A
  1. Inhibit VLDL synth in liver (fish oils also do this)

2. Stimulate breakdown of VLDL by lipoprotein lipase in the blood

25
Q

What are the differences between Niacin and FA derivatives in terms of LDL levels?

A
  1. Lipoprotein lipase increases LDL
    Niacin produces a net decrease in LDL
    FA Derivatives have no net effect on LDL
26
Q

What drug is a bile acid sequestrant?

A

Colesevelam

27
Q

What does colesevelam do?

A 
Reduce LDL (cholesterol), increase HDL
Prevents bile acid re-absorption, causes greater conversion of cholesterol to bile acids and lower liver cholesterol levels
28
Q

SE of colesevelam?

A

GI (nausea, bloating), reduced absorption of folic acid

29
Q

What are statin drugs?

A

HMG-CoA reductase inhibitors

30
Q

What is a Statin Drug?

A

Atorvastatin (lipitor)

31
Q

What is HMG-CoA redudctase do?

A

Liver enzyme that synthesizes cholesterol

32
Q

What happens to LDL when cholesterol synthesis is reduced?

A

LDL receptors are upregulated, resulting in increased removal of LDL from the blood

33
Q

How well does atorvastatin work?

A

Decrease cardiac events by up to 60% and stroke up to 70%

Modest increases in HDL and decreases in VLDL (less than niacin though)

34
Q

What drug is taken orally before bed?

A

Atorvastatin

35
Q

What is the efficiacy of statins at Low, Medium, and High doses?

A

Low: pravastatin, lovastatin
Medium: simvastatin, pitavastatin
High: atorvastatin rosuvastatin

36
Q

SE of Statins

A

Usually safe w/ mild GI SE

  1. Low liver tox
  2. Memory loss
  3. Diabetes risk
  4. Potential teratogens
  5. Myopathy
    * interacts w/ grapefruit juice
37
Q

What drug can produce myopathy with a risk for Rhabdo?

A

Statins

38
Q

What are the symptoms of a myopathy?

A
  1. Muscle pain
  2. Muscle atrophy
  3. Fatigue
  4. Dark urine
  5. Elevated blood creatine kinase lvls
39
Q

What is rhabdomyolysis?

A

Skeletal muscle cell lysis and release of muscle contents into the circulation, potentially resulting in kidney failure and death

40
Q

Is risk of myopathy and rhabdo related to efficacy?

A

No: lovastatin and simvastatin have higher risk than a atorvastatin/rosuvastatin
*CYP inhibitors increase risk

41
Q

What is the newest approved anti-cholestrol drug? What does it do?

A

Ezetimibe

  1. Inhibits intestinal absorption of dietary cholesterol
  2. Reduces LDL elvels
  3. GI SE
42
Q

What is Vytorin and what was it a part of?

A

Ezetimibe and simvastatin

Part of Enhance study

43
Q

What is the enhance study?

A

Vytorin produced greater reduction in LDL than simvastatin alone
No difference in coronary atherosclerotic plaque formation

44
Q

Implications of enhance study?

A
  1. Vytorin is no more protective vs CHD than statin monotherapy; questions efficacy of ezetimibe
  2. Suggests effectiveness of statsin versus CHD may not only involve reductions in LDL, potential anti-inflammatory effects
45
Q

What is niaspan and what study was it a part of?

A

Niaspan = extended release niacin

Government study examining benefit of adding niaspan to statin

46
Q

Results of AIM high study

A
  1. Niaspan failed to educe risk for Heart Attack vs placebo
  2. Risk for stroke was slightly INCREASED
  3. Benefit of increasing HDL and reducing LDL for prevention of HD and Stroke now in question
47
Q

What does PCSK9 do?

A

Breaks down LDL receptors, deceasing number of receptors that get recycled

  • variants of gene are associated w/ significant alterations in circulating LDL levels
  • Several PCSK9 inhibitors are in development
48
Q

What is Praluent?

A

First FDA approved PCSK9 Inihibitor

49
Q

What does praluent do? When is it prescribed? How is it used?

A

Antibody that binds and inhibits PCSK9
Approved for cases where statins and diet are insufficient
Injected subcutaneously

50
Q

ACC and AHA guidelines for statin treatment

A
  1. Individuals Diagnosed w/ CHD (history of HA, angina, stroke, IA, PAD)
  2. LDL > 190mg/dL
  3. Diabetics 40-75y/o w/o clnical ASCVD and LDL 189mg/DL who have estimated HD risk > 7.5% and 40-75 y/o

Dental Pharmacology Exam 4 (5 decks)

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