Flashcards in Dyslipidemias: Clinical Features and Evaluation Deck (17):
How is LDL calculated?
LDL = total cholesterol – (HDL + triglycerides/5)
The three values on the right side of the equation are measured directly, and VLDL = triglycerides/5.
The average level of LDL in America is _________.
Use of statins and the subsequent lowering of LDL has been shown to ________________.
stabilize atherosclerotic plaques and prevent CVD incidents
True or false: elevated cholesterol is a requirement for development of atherosclerotic plaques.
Familial hypercholesterolemia most often results from ____________.
defects in the LDL receptor
PCSK9 binds to _____________ and leads to its degradation.
the LDL receptor
What is arcus cornealis?
Lipid deposits at the limbis of the cornea due to hypercholesterolemia; can be seen in African Americans without hypercholesterolemia
Tendinous xanthomas can present as _______________.
bumps or thickened tendons
There isn't good enough data to support that having _____________ or ____________ raise CVD risk.
high triglycerides; low HDL
Increased LDL production can result from _____________.
insulin resistance, because the excess insulin stimulates lipogenesis, causing VLDLs to increase (and thus LDLs to increase downstream)
Severe hypertriglyceridemia results from ________________.
defects in lipoprotein lipase and/or overproduction of VLDL
What eight factors go into computing ASCVD risk?
Age (older +)
Gender (men +)
PCSK inhibitors have been theorized to __________.
decrease LDL levels by inhibiting degradation
PCSK gain-of-function mutations have been shown to _____________.
increase serum LDL levels
The two most research-supported genes implicated in hypertriglyceridemia are ___________.
LPL and apoprotein a5
The primary goal in severe hypertriglyceridemia is ____________.
to prevent pancreatitis