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5 Cards in this Set

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Clinical Association: Rare Childhood Disease
Laboratory Findings: Increased chylomicron and Triacylglycerol, normal cholesterol and LDL. Standing Chylomicron test - Supranate but no infranate
Type I: Familial Lipoprotein Lipase Deficiency; ApoC-II Deficiency
Pathogenesis: Inability to hydrolyze chylomicrons
Clinical Association:
Autosomal dominant disorder with premature coronary artery disease
Achilles tendon xanthomas are pathognomonic
Acquired causes - diabetes, hypothyroidism, obstructive jaundice, progesterone in birth control pills
Lab Findings:
A - Increased LDL (often >260mg/dL) and cholesterol, normal triacylglycerol
B - Increased LDL, cholesterol, and triacylglycerol
Type II: Familial Hypercholesterolemia
Pathogenesis: Absent or defective LDL receptors
Clinical Association:
Increased risk for coronary artery disease
Hyperuricemia, obesity, diabetes
Lab Findings:
Cholesterol and Triacylglycerol equally increased
Increased chylomicron and IDL remnants
Type III: Familial dysbetalipoproteinemia "remnant disease"
Pathogenesis: Deficiency of apoE; chylomicron and IDL remnant are not metabolized in liver
Clinical Association:
Autosomal Dominant
Most common hyperlipoproteinemia
Increased triacylglycerol begins at puberty
Increased incidence of coronary artery disease and peripheral vascular disease
Acquired causes - alcoholism, diuretics, beta blockers, renal failure
Lab Findings:
Very increased triacylglycerol
Slightly increased cholesterol
Standing chylomicron test - turbid infranate
Decreased HDL (inverse relationship with VLDL)
Type IV: Familial Hyperglyceridemia
Pathogenesis: Decreased catabolism or increased synthesis of VLDL
Clinical Associations:
Particularly common in alcoholics and individuals with diabetic ketoacidosis
Hyperchylomicronemia syndrome -
Abdominal pain, pancreatitis, dyspnea (impaired oxygen exchange), hepatosplenomegaly (fatty change), papules on skin
Lab Findings:
Very increased triacylglycerol
Normal LDL
Standing chylomicron test - supranate and infranate
Type V: Most commonly a familial hypertriglyceridemia with exacerbating factors
Pathogenesis: Combination of type I and type IV mechanisms.