CVD Flashcards

1
Q

what does atherosclerosis a risk factor for

A

increases risk of heart attack, stroke, peripheral vascular disease + kidney failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where do blockages of blood vessels usually occur at (location)

A

at bifurcations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What artery when blocked is called the widow maker

A

Left coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Below what level of blood cholesterol is ideal (and next best target)

A

ideal- below 3.9mmol

Next best target- 4.7mmol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the path of a VLDL

A

travels to adipocyte and here lipopro lipase disolves the TG so fat goes into cell and LDL is left (filled w cholesterol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the end game of LDL

A

attaches to cells w LDL receptors and cholesterol is taken up to make various things (cell membrane, steriods etc)

But if too much Cholesterol already it will settle on vessel walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do HDLs do

A

picks up ldl to bring back to liver in order to produce bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What apo pro allows LDL to fit on receptors

A

APO B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What apo pros does HDL gives to chylomicrons + VLDL

A

ApocII- activates LPL

APO E- activated LDL receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is familial hypercholesterolemia and what percentage of the pop gets it

A

5%

LDL receptor issue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the pathogenesis of atherosclerotic plaques

A
  • Endothelial damage (lots of oxidation of LDL)
  • platlets form healing dam over injury
  • Monocytes migrate to injury and macrophages take up oxidised LDL cholesterol
  • Eventually die and form foam cells and fibrous plaque forms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how does soluble fibre work

A

Soluble fibre binds to bile and stops it from being reabsorbed
Thus body needs to make new bile thru using cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what does gum guggal do (and what enzyme does it inhibit)

A

Increases LDL clearence by inhibiting 7ahydroxlyase (converts more cholesterol to bile)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Contraindications of gum glugol

A

shouldnt be used with beta blockers/ ca channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the effect of artichoke leaf extract

A

Helps increase bile acid secretion by liver, in turn up regulating LDL cholesterol receptor production in liber

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does homocystein get converted to methionine (+ enzyme)

A

Folic acid picks up methyl group and hands methyle group to b12 via enzyme methionine synthase

17
Q

How to know if you have a polymorphism of the MTHR enzyme

A

normal lvls of folic
Serum B12 normal
high lvls of homocystein

18
Q

high homocystein causes what % of cardiovascular deaths and how many mmol/L is idead

A

10% of all deaths

No higher than 8mmol/L

19
Q

what does CoQ10 deficiency lead to

A

congestive heart failure
hypertension (decreased Nitric oxide release)
Aggrivation of arriythmias

20
Q

What enzyme does statin block that blocks production of cholesterol + also coQ10

A

HMG coa reductase