Classification of Hyperlipidemia Flashcards
Primary: cause
Result from single or multiple genetic mutations that result in increased plasma concentrations of cholesterol, triglycerides, or both and are the result of either increased synthesis or decreased clearance. HDL levels may be lower than normal, either from decreased synthesis or increased clearance
Primary: symptoms
Early stages are asymptomatic. As disease progresses eruptive xanthomas, severe hypertriglyceridemia (>2000), lipemic plasma and lipemia retinalis
Examples of primary hyperlipidemia
Familial hypercholesterolemia and familial defective Apo B-100. Familial hypertriglyceridemia, familial combined hyperlipidemia, familial chylomicronemia and familial dysbetalipoproteinemia
Polygenic hypercholesterolemia (aka nonfamilial hypercholesterolemia)
Is the most common form of hyperlipidemia, with a prevalence of > 25% in the American population. Results from the combination of decreased activity of the LDL receptor and reduction of LDL clearance. This underlying genetic susceptibility becomes apparent with dietary intake of saturated fats, obesity, and sedentary lifestyle. 20% of these patients have Fhx of CHD. Present with mild-to high TC (250-350) and LDL (130-250). Treatment: LCs and lipid lowering drugs
Familial hypercholesterolemia
An autosomal dominant disease responsible for defective LDL receptors that results in either reduction in receptor synthesis or inability of the receptor to bind and/or efficiently remove LDL. Pts typically present with tendon xanthomas, premature MI, elevated TC 275-500 in heterozygotes and 700-1200 in homozygotes; triglycerides 250-500 in heterozygotes and > 500 in homozygotes
PH: treatment
Heterozygotes: TLC and drug tx that combines statins with other drugs that upregulate the LDL receptors (bile acid sequestrants, ezetimibe, or niacin). Due to the H risk of CHD and MI in homozygous patients, they should be treated in specialized medical centers that provide LDL apheresis and liver transplants
Familial hypertriglyceridemia
Autosomal dominant disease characterized by high triglycerides (200-500) and normal LDL. Treated with lipid lowering drugs; combined with diet and weight loss
Secondary Hyperlipdemias
Associated with primary underlying conditions (obesity HT/LHDL, diabetes HT,HTC, alcohol abuse HT/HHDL, chronic renal insufficiency HTC/HT, and hypothyroidism HTC)
Atherogenic dyslipidemia
Found ~ 25% of patients with dyslipidemia and is usually diagnosed on patients with metabolic syndrome
Atherogenic dyslipidemia: etiology
There is increased mobilization of triglycerides and cholesterol from adipose tissue to the circulation. This results in increased concentrations of triglycerides and VLDL rich in Apo C-III. Apo C-III inhibits lipoprotein lipase and prevents extraction of triglycerides from VLDL
Atherogenic dyslipidemia: labs
Mod to high triglycerides (150-500) result from high fat intake and mobilization from adipose tissue and VLDL secretion by the liver
Atherogenic dyslipidemia: treatment
Weight reduction; increased physical activity (stimulates lipoprotein lipase activity); statins to lower VLDL; fibrates to lower triglycerides; antioxidants
Drug induced hyperlipidemia
Estrogen therapy: increased triglycerides and increased total cholesterol
Drug induced hyperlipidemia
Atypical antipsychotics: increased triglycerides
Drug inducred hyperlipdemia
Corticosteroids: increased total cholesterol