artherosclerosis and lipid metabolism in IHD Flashcards
(38 cards)
function of trigs
energy storage and production
function of choolesterol
- steroid synthesis
- bile acids
- cell membrane
first decade
foam cells > fatty streaks
third decade
intermediate lesion > atheroma
fourth decade
fibrous plaque (fibro atheroma) > rupture
athero is a product of
lifestyle, and then aggravated by genetic factors… NB bc this statement is not reversible
more atherogenic LDL
small dense LDL
FHyperC
- requires intervention from a young age
- single gene defect
leading risk factr that predicts MI
LDL/HDL leves
- smoking is a close second, so pick only when LDL isnt listed
commonest cause of athero world wide
metabolic syndrome
two extremes of athero in SA
- SA black population > socioeconomic status, high prevalance of underlying conditions
- familial hyperC
how do we check LDL levels
lipogram
comparisons of athero across populations
- hugher in SA jews, asiabs and afrikaneers and could be due to lifestyle, genes
is FH rare
no, its not a rare genetic disorder
diagnosis for FH
anything more than 5 mmol/L with a family history = should be concerned
3 ways to spot hypercholesteraemia
- arcus seniles
- xanthelesma
-thickened tendons
whats the target LDL levels for high risk patient
<1.4 mmol/L
specific statin indicated to lower LDL
simvastatin = low intensity, affordable
rule of 6
with each doubling of statin dose, there is 6% reduction in cholesterol
drug inhibitng choesterol absorption
ezetimibe
ezetimibe - 3
- inhibits Niemann Pick C1 like-1 protein
- located in the epithelial brush border
- 20% reduction
residual lipoprotein risk
patient diagnosed late, might not get good reply
therapies for severe HC
- pcsk9 inhibitors
- mAbs
- siRNA
- ANGPTL3 inhibitors
FIRST LINE THERAP Y FOR HYPERCHOLE..
statins + ezetimibe
- but they are not effective in patients with established ASCVD
