Fat, cholesterol and artherosclerosis Flashcards

(63 cards)

1
Q

What is a heart attack/myocardial infarction?

A

When blood supply is blocked to the heart and tissue dies

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

What is a stroke?

A

When blood flow to the brain is blocked and tissue dies

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

What is the Dotter procedure?

A

A percutaneous coronary intervention (gauze to open the blood vessel)

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

How are proteins called that transport lipids through the blood?

A

Lipoproteins

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

What do lipoproteins consist of?

A
  • Proteins
  • Phospholipids
  • Neutral fat (triglycerides. cholesterol, cholesterolesters)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which lipoprotein has the most triglycerides and cholesterol ester?

A

Chylomicrons

Side 11

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

Which lipoprotein has the most free cholesterol?

A

LDL (Low density lipoprotein)

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

Atherosclerotic plaque is rich in?

A

cholesterol

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

List the structures of an artery from outside to lumen

A
  1. Adventitia
  2. External elastic lamina
  3. Tunica media
  4. Internal elastic lamina
  5. Subintimal extracellular space
  6. Endothelial cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When macrophages take up oxidized LDL they form…?

A

Foam cells

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

Which receptors on macrophages take up and mediate oxidized LDL?

A

LOX-1 and CD36

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When the fibrous cap of a vessel is destabalized by inflammatory cells what is the effect of that?

A

Formation of a Thrombus

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

What is atherosclerosis?

A

Accumulation of fat/cholesterol in arterial intima causing inflammation or/and rupture

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

What can an atherosclerotic plaque with thrombus develop into?

A
  • Healed fissure with buried thrombus
  • Mural intraluminar thrombus
  • Occlusive thrombus

An occlusive thrombus can develop into a healed fissure but a healed fis

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

What is reversed cholesterol transport?

A

Excess cholesterol is being removed from peripheral tissues and delivered to the liver by HDL

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

Which effect does heterozygocity of ApoAI have on event-free survival?

A

Over the years, the people who havent had serious complications decline more than people with other alleles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is an effect of low HDL-c, independent of the fact that LDL-c may also be low?

A

Cardiovascular disease risk increasaes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which lifestyle factors decrease HDL-c levels?

A
  • Testosterone
  • Smoking
  • Obesity
  • Anabolic steroids (to increase muscle mass) and anti-epileptics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which factors increase HDL-c levels?

A
  • Alcohol consumption
  • Physical activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is a better marker for CVD than cholesterol in women?

A

CRP (produced as acute phase response)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why is CRP a better marker for CVD in women?

A

Because half of CV events occur withour hyperlipidemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is metabolic syndrome?

A

Combination of obesity, cholesterol levels, hypertension and high BMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does adipose tissue release that are key factors in metabolic syndrom signalling?

A

Interleukins and TNF-alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does interleukin 6 and TNF-alpha cause?

A
  • Hypertension
  • More glucose production
  • More VLDL production
  • Less HDL cholesterol
  • More adipose tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
When does oxidative stress increase in the mitochondria?
When fatty acids increase
26
Is high or low CRP in women bad?
High
27
Steps of the forward cholesterol transport:
1. VLDL 2. IDL 3. LDL 4. Peripheral tissues
28
Cholesterol is a precursor for?
* Bile acids * Steroid hormones
29
Which enzyme extract cholesterol from food?
Cholesterol esterase
30
Which lipoproteins are released after a meal produced by epithelial cells?
Chylomicrons
31
How much % of plasma cholesterol is made by the liver
80%
32
Which metabolites lead to acetyl CoA?
* Pyruvate * Ethanol * Acetoacetate * Fatty acids
33
What is the precursor metabolite of cholesterol?
Acetyl CoA
34
From which metabolite to which substance is cholesterol synthesis fully comitted?
From Acetyl CoA to mevalonate
35
Cholesterol synthesis uses how many ATP?
3 ATP
36
Which compound that is produced in PPP stimulates cholesterol production?
NADPH
37
Via which lipoprotein are carbohysrates and proteins transported from the liver to produce cholesterol and fatty acids?
VLDL
38
What does LDL receptor deficiency lead to?
Very high plasma cholesterol levels and accumulation of cholesterol in tissues
39
How are LDL particles normally taken up?
Via clathrin coated pit endocytosed when binding to LDL receptor
40
Which hormone regulates cholesterol synthesis?
Insulin
41
What are statins?
Cholesterol lowering drugs
42
To what extent does simvastatin reduce risk for myocardial infarct?
30%
43
How can cholesterol synthesis be inhibited in order for HMG-coa not to bind to HMG CoA reductase?
Competitive inhibitor
44
What is HMG CoA reductase regarding cholesterol?
Rate limiting step to cholesterol
45
What happens to cholesterol levels when HMG CoA is inhibited competitively?
Km increases, lower affinity, less cholesterol produced
46
Does simvastatin have a high or low affinity to HMG CoA reductase?
High
47
Why do statins work?
They have higher affinity for enzymes than natural substrates
48
What are omega 3 and 6 the precursors of?
arachidonic acid
49
What derive from arachidonic acid and are short lived local signalling molecules?
Eicosanoids (C20)
50
What are examples of eicosanoids?
* Prostaglandins * leukotrienes * Thromboxanes * Lipoxins
51
What do eicosanoids mostly cause?
Constriction, contraction, aggregation of plasma factors (immune cells and platelets)
52
What substances decrease prostaglandins?
* Glucocorticoids * Aspirin
53
which enzyme converts arachidonic acid to prostaglandins?
Cyclooxygenase
54
Which enzyme does aspirin inhibit?
Cyclooxygenase | decreases production of prostaglandins
55
What do pain killers cause physiologically?
Stomach ulcers and intestinal bleedings
56
What does COX 1 do?
* Protects stomach/intestine * Mucus
57
What does COX 2 do?
Inflammation
58
To reduce information, which COX enzyme needs to be inhibited?
COX 2
59
What is important when inhibiting COX 2?
Choosing the right dose so the drug does not have a high affinity to COX 1 too
60
What is the function of leukotrienes?
Inflammation and pain
61
Function of thromboxanes?
Thrombosis and platelets
62
Function prostacyclin? | Produced by COX 1
Vascular dilation
63
Which cyclooxygenase causes most problems when there is alot of omega 3 and 6?
COX 2