Hyperlipidemia Flashcards by Derrick Obeng

LDL less than ….. is very good

100 mg/dl

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LDL more than ….. is high

200 mg/dl

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HDL less than ……. mg/dl is low

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HDL does not necessarily decrease chances or risks for atherogenesis but low HDL increases risk
True or false

True

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What is the normal TG level

<150mg/dl

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TG greater than 1000mg/dl can cause which condition

Pancreatitis

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Elevated TG levels is only modestly associated with CAD. Little evidence that lowering high levels reduces risk for atherogenesis
True or false

True

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Lowering TG levels is not mostly for treating CAD or lowering risk but rather for lowering risk of what condition

Pancreatitis

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What is hyperlipidemia

Elevated total cholesterol, LDL or TGs
It’s a risk factor for coronary disease and stroke

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What are some lifestyle factors which could increase risk of hyperlipidemia

Sedentary lifestyle
Saturated and trans-fatty acid foods
Lack of fiber

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What is primary hyperlipidemia

The cause of the hyperlipidemia is by elevation of LDLs, TGs and TCs and not any other underlying or secondary cause

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What are some causes of secondary hyperlipidemia

Alcohol
Pregnancy (provides more lipids for the baby)
Beta-blockers
HCTZ (thiazide diuretics)
Thyroid disease
Nephrotic syndrome

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What are the treatments for hyperlipidemia

Recommend lifestyle modification (healthy diet, weight loss, quit smoking)
Statin therapy

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What are the two types of therapy for statins

Moderate-intensity statins
High-intensity statins

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What are some choices for moderate intensity statin therapy

Atorvastatin 10 to 20 mg/day
Rosuvastatin 5 to 10 mg/day
Simvastatin 20 to 40 mg/day

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What are some choices for high intensity statin therapy

Atorvastatin 40 to 80 mg/day
Rosuvastatin 20 to 40 mg/day

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What is the maximum dose for Atorvastatin

80 mg/day

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What is the maximum dose for Rosuvastatin

40 mg/day

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What is the treatment goal for hyperlipidemia

To get the LDL under a 100mg/dL
For patients with known vascular disease, the goal is often to get them under 70mg/dL

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When should you put a patient on a high intensity stain therapy

Patient with CAD, stroke or PAD
Patient with LDL > 190 mg/dL

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When should you put a patient on a moderate or high intensity statin therapy

Diabetics greater than 40 years old
ASCVD risk greater than 7.5% over 10 years

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What are some signs of hyperlipidemia

Most patients have no signs and symptoms
Screen patients with blood tests
Physical findings occur in patients (xanthomas, tendinous xanthoma, corneal arcus) with severe high lipids (they usually have a genetic familial syndrome)

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What are xanthomas

They are plaques of lipid-laden cells
They appear as skin bumps or on eyelids

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What is a tendinous xanthoma

Lipid deposits in tendons
Common in Achilles

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What is a corneal arcus

Lipid deposits in cornea Looks like a ring around the iris

Which familial dyslipidemias are autosomal recessive (AR)

Types I and III

Which familial dyslipidemias are autosomal dominant (AD)

IIa and IV

What is another name for type I dyslipidemia

Hyperchylomicronemia

People with hyperchylomicronemia could have elevated triglycerides greater than ……… mg/dL

1000

What plasma appearance is characteristic of type I dyslipidemia

Milky plasma appearance

What is the main problem people have with type I dyslipidemia

Recurrent pancreatitis Enlarged liver and xanthomas might also be present

What is the mainstay treatment for people with type I dyslipidemia

Very low-fat diet

Type I dyslipidemia is associated with what enzyme dysfunction

LPL (lipoprotein lipase)

There is no apparent risk in which familial dyslipidemia

Type I dyslipidemia

Which is another name for type II dyslipidemia

Familial hypercholesterolemia

In which type of familial dyslipidemia do people have few or zero LDL receptors to pull LDL from plasma into the liver thus leading to very high LDL levels

Type II dyslipidemia *Patient can develop tendinous xanthomas and corneal arcus*

What is the main problem in type II dyslipidemias

Severe atherosclerosis (can have MI in their 20s)

Which familial dyslipidemia is caused by mutations in the apo E gene

Type III Dyslipidemia

What is another name for type III dyslipidemia

Familial dysbetalipoproteinemia

In which familial dyslipidemia are there accumulations of beta lipoproteins

Type III dyslipidemia

Chylomicron remnants and VLDLs are collectively called

Beta lipoproteins

In which familial dyslipidemia are beta lipoproteins poorly cleared by the liver

Type III dyslipidemia

In which familial dyslipidemia are both TC and TG levels elevated (TC elevation usually mild. TC > 300 mg/dL)

Type III dyslipidemia

In which familial dyslipidemia could you have a premature coronary disease

Type III dyslipidemia

What is another name for type IV dyslipidemia

Hypertriglyceridemia

In which familial dyslipidemia is there VLDL overproduction or impaired catabolism of VLDLs

Type IV dyslipidemia

Which familial dyslipidemia is associated with type II diabetes and hypertension

Type IV dyslipidemia

What are some lipid lowering therapies

Statins Niacin Fibrates Absorption blockers Bile acid resins PCSK9 inhibitors Omega-3 fatty acids

Which lipid lowering therapy inhibits HMG CoA reductase

Statins

What are the MOA of statins

Low cholesterol synthesis in the liver which then increase LDL receptors in the liver to pull in plasma cholesterol Major effect: LDL decrease

Mention some statins

Atorvastatin Simvastatin Lovastatin

Which lipid lowering therapy could cause: **Hepatotoxity (rise in AST/ALT)** **Muscle problems**

Statins

What is the **most common** muscle problem associated with statins

Myalgia (patients complain of weakness and soreness but if you measure serum CK levels to look for evidence of muscle damage, it would be normal)

What is a less common but more serious muscle problem associated with statins

Myositis (inflammation of the muscles) (symptoms similar to myalgias, but CK levels are increased in the serum)

What are some statin muscle problems

Myalgias Myositis Rhabdomyolysis

What is a very rare but much more serious statin muscle problem

Rhabdomyolysis (weakness, muscle pain, dark urine from myoglobin spilling into plasma and the urine, serum CK levels very high-1000 or more, acute renal failure -> death) *Rhabdomyolysis rarely occurs just from taking a statin, it usually occurs when someone takes a statin in conjunction with another drug. Eg. Genfibrozil, P450 inhibitors)*

What are the three main statins that are metabolized by the P450 system

Atorvastatin Simvastatin Lovastatin

Mention some statins which are not metabolized by the P450 system

Ravastatin Rosuvastatin

Mention some P450 inhibitors which should not be taken together with some statins

Cyclosporine Macrolide antibiotics Azole antifungal agents HIV protease inhibitors Grapefruit juice

What is the effect of P450 inhibitors on statins

P450 metabolizes statins. Thus, taking a P450 inhibitor would increase plasma levels of statins which could cause myalgias, rhabdomyolysis, etc

Mention one supplement (vitamin) which could be used in the treatment of hyperlipidemia by administering high doses

Niacin *LDL will fall and increases HDL*

Which drug in the treatment of hyperlipidemia could cause **flushing** (stimulates PGs in the skin, face turns red and warm, effect fades with time)

Niacin

What drug could you take to blunt the side effect of flushing by niacin

Aspirin (inhibits prostaglandins)

Which supplement used in the treatment of hyperlipidemia should be avoided in diabetic patients because it leads to hyperglycemia and hyperuricemia (thus can precipitate a gout attack)

Niacin

What is the commonly used drug for patients with high levels of TGs

Fibrates

Give some examples of fibrates

Gemfibrozil Clofibrate Bezafibrate Fenofibrate

Which drug works by activating PPAR-a thus increasing LPL activity leading the liver to break down more fatty acids (fatty acid oxidation)

Fibrates

What kind of fibrate is rather used when a patient is to be on both a statin and dictate together

Fenofibrate Don’t use gemfibrozil

Which drug could raise LFTs thus increase cholesterol gallstones and cause myositis

Fibrates

Mention one cholesterol absorption blocker

Ezetimibe

Which of the lipid curing therapies is highly selective for cholesterol and thus does not affect fat-soluble vitamins and TGs

Cholesterol absorption blockers

Where is the worksite for cholesterol absorption blockers

Intestinal brush border

Why are use of statins picked over absorption blockers

Weak data on hard outcomes (MI, death) for absorption blockers

Which lipid curing drug could cause diarrhea

Absorption blockers