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Flashcards in Hyperlipidemias Deck (44)
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What are lipoproteins made of?

- Have a central core of lipids (triglycerides and cholesterol esters)
- An outer case of phospholipids, free cholesterol and proteins (called apoproteins)


What are the classes of lipoproteins?

(1) Chylomicrons
(2) VLDL
(3) IDL
(4) LDL
(5) HDL
- They all differ in size, density and relative proportion of the core lipids and type of apoproteins-



An increase in plasma lipids in general



An increase in plasma cholesterol, indicated by an increases in LDL (familial, hypothyroidism, corticosteroids)


Hypertriglyceridemia or Hyperlipemia

An increase in triglycerides, indicated by an increase in VLDL (familial, diabetes, centripetal obesity, alcohol use, corticosteroids, estrogens)


Mixed hyperlipidemia

An increase in both cholesterol and triglycerides (LDL & VLDL)


What contributes to increased risk of coronary artery disease?

(1) High LDL cholesterol
(2) Low HDL cholesterol
(3) Hypertriglyceridemia (increased VLDL)


Which lipoproteins are rich in triglycerides? Cholesterol? Apoproteins?

VLDLs, LDL, HDLs respectively


Which lipoproteins are large/small in size?

Chylomicrons very large in size, VLDLs smaller in size than chylomicrons, HDLs very small in size,


What are desirable levels of Total Cholesterol and LDL Cholesterol? Borderline high? High?

(1) Desirable- 240, >160


What are the desirable LDL levels for moderate and high risk patients?

- Moderate risk: LDL <70


What are the 5 classes of Lipid-lowering drugs?

(1) HMG-CoA reductase inhibitors (Statins)
(2) Niacin (Nicotinic acid)
(3) Fibric acid derivatives
(4) Bile acid binding agents
(5) Inhibitors of intestinal sterol absorption


What do you have to make sure of with drugs that alter plasma lipoprotein concentrations?

They may require adjustment of warfarin doses


What are the HMG-CoA Reductase inhibitors?

(1) Lovastatin
(2) Atorvastatin


What drug is the most effective in reducing LDL?

Statins (HMG-CoA reductase inhibitors)


Lovastatin/Atorvastatin- Mechanism of Action

(1) Reduce cholesterol synthesis by inhibition of HMG Co A reductase
(2) Increases LDL receptors (indirect effect), thus increasing the extraction of LDL by the liver and decreasing LDL in the plasma


Statins- Uses

(1) Hypercholesterolemia (increased LDL)
(2) Mixed hyperlipidemia (LDL and VLDL increase)
(3) First line of treatment after M.I.


Statins- Adverse effects

(1) Hepatitis (increase of hepatic enzymes such as serum amino transferase)
(2) Myalgia


When should statins be discontinued?

If serum levels of creatine phosphokinase are elevated of if myopathy occurs (rhabdo, myoglobinuria)


Niacin- Mechanism of Action

(1) Reduces VLDL secretion from liver and in turn, decreases production of LDL
(2) Inhibits lipolysis in adipose tissue, decreasing FFA supply to the liver and VLDL synthesis
(3) Increases VLDL clearance in the plasma by increasing LPL activity
(4) Decreases catabolism of HDL and increases HDL


Niacin- Uses

(1) Useful in mixed hyperlipidemia because of its favorable effects of VLDL, LDL, and HDL
(2) combined with other drugs for hypercholesterolemia and hypertriglyceridemia


Niacin- Adverse Effects

- Useful only in large doses which produce vasodilation
(1) cause skin flushing
(2) pruritis (usually goes away within first few days)
- increase in serum transaminase level, gastric distress, glucose intolerance, and hyperuricemia
- Avoid in liver disease, peptic ulcer, gout, diabetes


What is used with Niacin to reduce adverse effects?

Aspirin (the effects are mediated by prostaglandins)


What are the fibric acid derivatives?

Gemfibrozil and Fenofibrate


Fibric acid derivatives- Mechanism of Action

(1) Decrease triglycerides (VLDL) by stimulation of LPL (hypolysis of VLDL), promote the delivery of FFA to adipose tissue
(2) May decrease VLDL synthesis in the liver


Fibric acid derivatives- Uses

- Used primarily in hypertriglyceridemia (increase in VLDL)
- May be used in mixed hyperlipidemia


Fibric acid derivatives- Adverse Effects

(1) Allergic reactions, myalgia, blood cell deficiencies, hypokalemia, and an increase in serum aminotransferase
(2) Risk of myopathy increases when used with HMG-CoA reductase inhibitors
(3) Moderate increase risk in gallstones
(4) Contraindicated in hepatic or renal dysfunction


T/F Fibric acid derivatives increase effects of warfarin.

TRUE because of it's binding to plasma proteins


What are the bile acid binding agents?

Colestipol, Cholestyramine


Bile acid binding agents- Mechanism of Action

(1) Bind bile acids and prevent their absorption which leads to synthesis of replacement bile acids from cholesterols in the liver
- to obtain more cholesterol for this purpose, the liver increases LDL receptors leading to increased uptake of LDL from the plasma (indirect effect)
(2) May increase triglycerides and cause a small increase in HDL