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How does LDL lead to CVD?
increased levels lead to issues
What are the optimum levels of LDL?
greater than 50 mg/dL
What are the risk levels of LDL?
less than 40 mg/dL
What is the biggest prediction of CVD?
LDL:HDL ratio
What is the optimum ratio LDL:HDL?
<2.5:1
What is Familial Hypercholesterolemia (FH)?
an autosomal dominant disorder resulting in increased LDL levels
What is the genetic cause of FH?
mutation decreasing LDL uptake
What are the possible mutations that lead to FH?
LDL-receptor, LDL-R associated proteins, apoB-100 gene
What are most cases of FH caused by?
mutation in LDL-receptor
Which genotypes are affected by FH?
heterozyg. and homozyg.
What is the frequency of FH among heterozyg.?
1:250
What are the serum LDL levels associated with heterozyg. FH?
320-500 mg/dL
What are the results of having heterozyg. FH?
increased incident CVD, development of fatty deposits (xanthomas) in age 30+
What are xanthomas?
fatty deposits
When do men and women with heterozyg FH have a heart attack?
85% of men by 60 and women by 70
What is the frequency of FH among homozyg.?
1:1000000
What are the serum LDL levels in homozyg. FH?
greater than 600 mg/dL
What are the results of homozyg. FH?
fatty deposits in childhood and if untreated can have heart attack by 30
Which genotype of FH is more severe?
homozygous
What are the treatments for FH?
alter diet and lifestyle
take Statin
liver transplant
filter out fats in blood
What is statin?
a drug used to treat FH that blocks and inhibits HMG-CoA reductase and therefore blocks de novo synthesis
Is statin effective is treating both types of FH?
not effective in treating homozygous FH
What type of enzyme competitor is mevastatin?
competitive with HMG CoA reductase