Classification of Hyperlipidemia Flashcards

1
Q

Primary: cause

A

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

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2
Q

Primary: symptoms

A

Early stages are asymptomatic. As disease progresses eruptive xanthomas, severe hypertriglyceridemia (>2000), lipemic plasma and lipemia retinalis

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3
Q

Examples of primary hyperlipidemia

A

Familial hypercholesterolemia and familial defective Apo B-100. Familial hypertriglyceridemia, familial combined hyperlipidemia, familial chylomicronemia and familial dysbetalipoproteinemia

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4
Q

Polygenic hypercholesterolemia (aka nonfamilial hypercholesterolemia)

A

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

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5
Q

Familial hypercholesterolemia

A

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

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6
Q

PH: treatment

A

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

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7
Q

Familial hypertriglyceridemia

A

Autosomal dominant disease characterized by high triglycerides (200-500) and normal LDL. Treated with lipid lowering drugs; combined with diet and weight loss

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8
Q

Secondary Hyperlipdemias

A

Associated with primary underlying conditions (obesity HT/LHDL, diabetes HT,HTC, alcohol abuse HT/HHDL, chronic renal insufficiency HTC/HT, and hypothyroidism HTC)

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9
Q

Atherogenic dyslipidemia

A

Found ~ 25% of patients with dyslipidemia and is usually diagnosed on patients with metabolic syndrome

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10
Q

Atherogenic dyslipidemia: etiology

A

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

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11
Q

Atherogenic dyslipidemia: labs

A

Mod to high triglycerides (150-500) result from high fat intake and mobilization from adipose tissue and VLDL secretion by the liver

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12
Q

Atherogenic dyslipidemia: treatment

A

Weight reduction; increased physical activity (stimulates lipoprotein lipase activity); statins to lower VLDL; fibrates to lower triglycerides; antioxidants

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13
Q

Drug induced hyperlipidemia

A

Estrogen therapy: increased triglycerides and increased total cholesterol

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14
Q

Drug induced hyperlipidemia

A

Atypical antipsychotics: increased triglycerides

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15
Q

Drug inducred hyperlipdemia

A

Corticosteroids: increased total cholesterol

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16
Q

Drug induced hyperlipidemia

A

Selective alpha blockers without intrinsic sympathetic activity or alpha-antagonism: increased total cholesterol and decreased HDL

17
Q

Drug induced hyperlipidemia: Thiazides

A

Modest increase in total cholesterol and LDL

18
Q

Secondary hyperlipidemia (elevated triglycerides) can be caused by

A

obesity, diabetes, alcohol abuse, HRT, atypical antipsychotic tx

19
Q

Secondary hyperlipidemia (elevated cholesterol) can be caused by

A

chronic renal failure, hypothyroidism, and typical beta blocker use