Lipid/Lipoprotein Disorders Flashcards
Dietary/Exogenous Pathway
Chylomicrons carry shit around, become chylomicron remnants and go to liver
Chylomicron 4 Apo Proteins
ApoB48, and chylomicrons also have ApoC II and III, and then chylomicron remnants get ApoE which targets them to liver
Chylomicron composition
A lot of TGs, some cholesterol
Endogenous Pathway
Liver sends out VLDL, which becomes IDL, which gets ApoE so its targeted back to liver (or becomes LDL)
Endogenous Pathway Apo Prot(s)
Has B100, but also has CII and III, and gets ApoE to target to liver
LDL Composition
Lotta cholesterol comparatively
Best Estimate of Artherosclerotic Risk
Non-HDL cholesterol
Change in Fats After Eating
Not huge increase in cholesterol - increase in chylomics, which are mainly TGs so that’s what spikes after meal
Size of Particles w/in a Subclass Importance
Smaller particles in a subclass associated w/ increased risk of CV disease
Familial Hypercholesterolemia
AD mut of B or E or R, inhibiting LDL clearance and presenting at birth
3 Visual Signs of Familial Hypercholesterolemia
Corneal Arcus
Thickened tendons, especially achilles
Xanthoma - cholesterol deposition often around eyes
High Cholesterol Diet Effect
Raises LDL levels by downreg’ing B/E Rs on Liver
3.5 Causes of Increased LDL Production
Familial Combined Hyperlipidemia
Acquired - obesity, nephrotic syndrome
Drugs - thiazides, corticosteroids, progestogens
Hypertriglyceridemia
Lipoprotein Lipase deficiency, enzyme that removes chylomicrons more effectively than it does VLDL. So mild deficiency is just VLDL accumulation, but severe can cause hyperchylomicronemia
4 Signs of Hyperchylomicronemia (3 visual, 1 clinical condition)
Milky serum
Lipemic pattern in eye (retinal vessels)
Eruptive Xanthomas
Acute pancreatitis
Familial Combined Hyperlipidemia
Overproduction of B100 containing particles, so you get lotsa small VLDLs from the liver which become a lot of small LDL
Familial Hypertriglyceridemia
Increased production of VLDL-TG (normal numbers of VLDL particles), but not LDL because not ApoB increase in production
Direct Pathway of HDL Cholesterol Transport
Packaged into HDL3 which then turns into HDL2 to dump its shit into liver
Indirect Pathway of HDL
HDL3 gives cholesterol to VLDL/LDL and receives TG from them
Dislipidemic/Lipid Triad
High TGs and Low HDL are a common combination, and always present w/ increased small, dense LDL
Lp(a)
LDL + Apolipoprotein A which is kinda like a shitty plasminogen protein which doesn’t work but causes a lot more disease or something
