Dyslipidemias: Clinical Features and Evaluation Flashcards Preview

MS2 - Digestive, Endocrine, and Metabolic Systems > Dyslipidemias: Clinical Features and Evaluation > Flashcards

Flashcards in Dyslipidemias: Clinical Features and Evaluation Deck (17)
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1
Q

How is LDL calculated?

A

LDL = total cholesterol –(HDL + triglycerides/5)

The three values on the right side of the equation are measured directly, and VLDL = triglycerides/5.

2
Q

The average level of LDL in America is _________.

A

116

3
Q

Use of statins and the subsequent lowering of LDL has been shown to ________________.

A

stabilize atherosclerotic plaques and prevent CVD incidents

4
Q

True or false: elevated cholesterol is a requirement for development of atherosclerotic plaques.

A

False.

5
Q

Familial hypercholesterolemia most often results from ____________.

A

defects in the LDL receptor

6
Q

PCSK9 binds to _____________ and leads to its degradation.

A

the LDL receptor

7
Q

What is arcus cornealis?

A

Lipid deposits at the limbis of the cornea due to hypercholesterolemia; can be seen in African Americans without hypercholesterolemia

8
Q

Tendinous xanthomas can present as _______________.

A

bumps or thickened tendons

9
Q

There isn’t good enough data to support that having _____________ or ____________ raise CVD risk.

A

high triglycerides; low HDL

10
Q

Increased LDL production can result from _____________.

A

insulin resistance, because the excess insulin stimulates lipogenesis, causing VLDLs to increase (and thus LDLs to increase downstream)

11
Q

Severe hypertriglyceridemia results from ________________.

A

defects in lipoprotein lipase and/or overproduction of VLDL

12
Q

What eight factors go into computing ASCVD risk?

A
Age (older +) 
Gender (men +) 
Hypertension 
Diabetes
LDL
Total cholesterol 
Cigarette smoking
13
Q

PCSK inhibitors have been theorized to __________.

A

decrease LDL levels by inhibiting degradation

14
Q

PCSK gain-of-function mutations have been shown to _____________.

A

increase serum LDL levels

15
Q

The two most research-supported genes implicated in hypertriglyceridemia are ___________.

A

LPL and apoprotein a5

16
Q

The primary goal in severe hypertriglyceridemia is ____________.

A

to prevent pancreatitis

17
Q

Dysbetalipoproteinemia results from __________ and leads to ______________.

A

apoE2 phenotype (when the normal is E3 or E4); high triglycerides and low HDL

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