Biochemistry Flashcards
1
Q
How do statins work?
A
- statins are HMG CoA reductase inhibitors
- they prevent the formation of de novo cholestrol
- also makes the liver express LDL receptors, to remove from blood
2
Q
Why is LDL bad?
A
- it is the main component of a plaque formation, which can build up in the arterial supply and rupture
3
Q
What are examples of other lipid lowering drugs that are not statins?
A
- PCSK9 Inhibitors
- Fibrates
- Ezetimibe
4
Q
How do PCSK9 inhibitors work
A
- They prevent the break down of LDL receptors on the liver, so more LDL is removed from the blood stream
5
Q
Explain familial hypertension and what to check for?
A
- genetic disorder
- autosomal dominant
- check tendons for xantomata
6
Q
Where is cholestrol synthesised?
A
- in the liver
7
Q
Why is cholestrol packed in lipoproteins?
A
- insoluble in blood
8
Q
Explain a lipoprotein
A
- packages cholestrol
- hydrophobic core (esterfied cholestor and TAGs)
- hydrophillic coat
- apoproteins on coat (identification)
9
Q
What causes blood vessel damage?
A
- smoking
- Increased BP
- Increased lipids
- diabetes
10
Q
What apoprotein is associated with HDL?
A
- ApoA I and ApoA II
11
Q
What apoprotein is associated with LDL?
A
- ApoB 100
12
Q
What apoprotein is associated with VLDL?
A
- ApoB 100
13
Q
What apoprotein is associated with chylomicrons?
A
- ApoB48
14
Q
Where are chylomicrons formed and what is their pathway?
A
- formed in the intestinal cells
- exogenous pathway
15
Q
Where are VLDLs formed and what is their pathway?
A
- formed in the liver
- endogenous pathway
16
Q
Explain the pathway by which LDL is taken up and an artheromatous plaque is formed?
A
- Endothelial injury
- LDL uptake
- OXLDL
- monocytes enter
- develope into macrophages
- macrophages uptake OXLDL
- Become foam cells
- formation of a fatty streak
- inflammatory substances enter
- deposition of collagen and proliferation of smooth muscle
