Hyperlipidemia Flashcards
LDL less than ….. is very good
100 mg/dl
LDL more than ….. is high
200 mg/dl
HDL less than ……. mg/dl is low
45
HDL does not necessarily decrease chances or risks for atherogenesis but low HDL increases risk
True or false
True
What is the normal TG level
<150mg/dl
TG greater than 1000mg/dl can cause which condition
Pancreatitis
Elevated TG levels is only modestly associated with CAD. Little evidence that lowering high levels reduces risk for atherogenesis
True or false
True
Lowering TG levels is not mostly for treating CAD or lowering risk but rather for lowering risk of what condition
Pancreatitis
What is hyperlipidemia
Elevated total cholesterol, LDL or TGs
It’s a risk factor for coronary disease and stroke
What are some lifestyle factors which could increase risk of hyperlipidemia
Sedentary lifestyle
Saturated and trans-fatty acid foods
Lack of fiber
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
What are some causes of secondary hyperlipidemia
Alcohol
Pregnancy (provides more lipids for the baby)
Beta-blockers
HCTZ (thiazide diuretics)
Thyroid disease
Nephrotic syndrome
What are the treatments for hyperlipidemia
Recommend lifestyle modification (healthy diet, weight loss, quit smoking)
Statin therapy
What are the two types of therapy for statins
Moderate-intensity statins
High-intensity statins
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
What are some choices for high intensity statin therapy
Atorvastatin 40 to 80 mg/day
Rosuvastatin 20 to 40 mg/day
What is the maximum dose for Atorvastatin
80 mg/day
What is the maximum dose for Rosuvastatin
40 mg/day
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
When should you put a patient on a high intensity stain therapy
Patient with CAD, stroke or PAD
Patient with LDL > 190 mg/dL
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
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)
What are xanthomas
They are plaques of lipid-laden cells
They appear as skin bumps or on eyelids
What is a tendinous xanthoma
Lipid deposits in tendons
Common in Achilles
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
