Adam Shared "Dyslipidemias" - 5 Picmonics
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Dyslipidemias
Hyperchylomicronemia (Type I Familial Dyslipidemia)
- INHERITANCE
- Autosomal Recessive
- PATHOGENESIS
- Lipoprotein Lipase Deficiency (LPL)
- Altered Apolipoprotein C-II (Apo C-II)
- Lab Findings
- Increased Chylomicrons
- Increased Cholesterol
- Increased Triglycerides
- Symptoms/Findings
- Pancreatitis
- Hepatosplenomegaly
- No Increased Risk for Atherosclerosis
- Eruptive/Pruritic Xanthomas
- Milky White Appearance of Blood When Drawn
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IIa—Familial hypercholesterolemia
- Autosomal dominant
- Absent or defective LDL receptors
- Increased LDL, cholesterol
- Heterozygotes (1:500) have cholesterol ≈ 300mg/dL; homozygotes (very rare) have cholesterol ≈ 700+ mg/dL
- Accelerated atherosclerosis (may have MI before age 20)
- Tendon (Achilles) xanthomas
- Corneal arcus
- Defective ApoB-100
- Xanthelasmas
- Although other body parts have LDL recptors, 70% of LDL is cleared by the liver
- IIb - Familial hypercholesterolemia
- In addition to cholesterol and LDL increase, there is a VLDL increase
III—Dysbetalipoproteinemia FA 17 90
- Autosomal recessive
- Defective ApoE3 and ApoE4
- Increased Chylomicron/VLDL remnants
- Premature atherosclerosis
- Tuberoeruptive xanthomas
- Xanthoma striatum palmare
IV—Hypertriglyceridemia
- Autosomal dominant
- Hepatic overproduction of VLDL
- Increased VLDL, TG
- Hypertriglyceridemia (> 1000 mg/dL) can cause acute pancreatitis because the binding capacity of albumin becomes overwhelmed
- Coronary disease
- ApoA-V
Abetalipoproteinemia
- Autosomal recessive
- Deficiency of apolipoprotein B-48 and B-100
- Malabsorption due to defection chylomicron formation (B-48)
- Absent plasma VLDL and LDL (B-100)
- Low plasma triglyceride
- Enterocytes contain clear or foamy cytoplasm
- Microsomal transfer protein (MTP) is necessary for proper folding of proteins
- Loss of function of MTP
- Fat soluble vitamin deficiency particularly Vitamin E
- Later manifestations: retinitis pigmentosa, spinocerebellar degeneration (vitamin E deficiency), progressive ataxia, acanthocytosis
- Infants present with severe fat malabsorption, steatorrhea, failure to thrive
- Treatment: restriction of long-chain fatty acids, large doses of oral vitamin E
