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biochemistry > Fat, cholesterol and artherosclerosis > Flashcards

Fat, cholesterol and artherosclerosis Flashcards

1
Q

What is a heart attack/myocardial infarction?

A

When blood supply is blocked to the heart and tissue dies

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2
Q

What is a stroke?

A

When blood flow to the brain is blocked and tissue dies

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3
Q

What is the Dotter procedure?

A

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

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4
Q

How are proteins called that transport lipids through the blood?

A

Lipoproteins

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5
Q

What do lipoproteins consist of?

A
  • Proteins
  • Phospholipids
  • Neutral fat (triglycerides. cholesterol, cholesterolesters)
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6
Q

Which lipoprotein has the most triglycerides and cholesterol ester?

A

Chylomicrons

Side 11

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7
Q

Which lipoprotein has the most free cholesterol?

A

LDL (Low density lipoprotein)

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8
Q

Atherosclerotic plaque is rich in?

A

cholesterol

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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
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10
Q

When macrophages take up oxidized LDL they form…?

A

Foam cells

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11
Q

Which receptors on macrophages take up and mediate oxidized LDL?

A

LOX-1 and CD36

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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

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13
Q

What is atherosclerosis?

A

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

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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

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15
Q

What is reversed cholesterol transport?

A

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

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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

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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

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18
Q

Which lifestyle factors decrease HDL-c levels?

A
  • Testosterone
  • Smoking
  • Obesity
  • Anabolic steroids (to increase muscle mass) and anti-epileptics
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19
Q

Which factors increase HDL-c levels?

A
  • Alcohol consumption
  • Physical activity
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20
Q

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

A

CRP (produced as acute phase response)

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21
Q

Why is CRP a better marker for CVD in women?

A

Because half of CV events occur withour hyperlipidemia

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22
Q

What is metabolic syndrome?

A

Combination of obesity, cholesterol levels, hypertension and high BMI

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23
Q

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

A

Interleukins and TNF-alpha

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24
Q

What does interleukin 6 and TNF-alpha cause?

A
  • Hypertension
  • More glucose production
  • More VLDL production
  • Less HDL cholesterol
  • More adipose tissue
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25
Q

When does oxidative stress increase in the mitochondria?

A

When fatty acids increase

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26
Q

Is high or low CRP in women bad?

A

High

27
Q

Steps of the forward cholesterol transport:

A
  1. VLDL
  2. IDL
  3. LDL
  4. Peripheral tissues
28
Q

Cholesterol is a precursor for?

A
  • Bile acids
  • Steroid hormones
29
Q

Which enzyme extract cholesterol from food?

A

Cholesterol esterase

30
Q

Which lipoproteins are released after a meal produced by epithelial cells?

A

Chylomicrons

31
Q

How much % of plasma cholesterol is made by the liver

A

80%

32
Q

Which metabolites lead to acetyl CoA?

A
  • Pyruvate
  • Ethanol
  • Acetoacetate
  • Fatty acids
33
Q

What is the precursor metabolite of cholesterol?

A

Acetyl CoA

34
Q

From which metabolite to which substance is cholesterol synthesis fully comitted?

A

From Acetyl CoA to mevalonate

35
Q

Cholesterol synthesis uses how many ATP?

A

3 ATP

36
Q

Which compound that is produced in PPP stimulates cholesterol production?

A

NADPH

37
Q

Via which lipoprotein are carbohysrates and proteins transported from the liver to produce cholesterol and fatty acids?

A

VLDL

38
Q

What does LDL receptor deficiency lead to?

A

Very high plasma cholesterol levels and accumulation of cholesterol in tissues

39
Q

How are LDL particles normally taken up?

A

Via clathrin coated pit endocytosed when binding to LDL receptor

40
Q

Which hormone regulates cholesterol synthesis?

A

Insulin

41
Q

What are statins?

A

Cholesterol lowering drugs

42
Q

To what extent does simvastatin reduce risk for myocardial infarct?

A

30%

43
Q

How can cholesterol synthesis be inhibited in order for HMG-coa not to bind to HMG CoA reductase?

A

Competitive inhibitor

44
Q

What is HMG CoA reductase regarding cholesterol?

A

Rate limiting step to cholesterol

45
Q

What happens to cholesterol levels when HMG CoA is inhibited competitively?

A

Km increases, lower affinity, less cholesterol produced

46
Q

Does simvastatin have a high or low affinity to HMG CoA reductase?

A

High

47
Q

Why do statins work?

A

They have higher affinity for enzymes than natural substrates

48
Q

What are omega 3 and 6 the precursors of?

A

arachidonic acid

49
Q

What derive from arachidonic acid and are short lived local signalling molecules?

A

Eicosanoids (C20)

50
Q

What are examples of eicosanoids?

A
  • Prostaglandins
  • leukotrienes
  • Thromboxanes
  • Lipoxins
51
Q

What do eicosanoids mostly cause?

A

Constriction, contraction, aggregation of plasma factors (immune cells and platelets)

52
Q

What substances decrease prostaglandins?

A
  • Glucocorticoids
  • Aspirin
53
Q

which enzyme converts arachidonic acid to prostaglandins?

A

Cyclooxygenase

54
Q

Which enzyme does aspirin inhibit?

A

Cyclooxygenase

decreases production of prostaglandins

55
Q

What do pain killers cause physiologically?

A

Stomach ulcers and intestinal bleedings

56
Q

What does COX 1 do?

A
  • Protects stomach/intestine
  • Mucus
57
Q

What does COX 2 do?

A

Inflammation

58
Q

To reduce information, which COX enzyme needs to be inhibited?

A

COX 2

59
Q

What is important when inhibiting COX 2?

A

Choosing the right dose so the drug does not have a high affinity to COX 1 too

60
Q

What is the function of leukotrienes?

A

Inflammation and pain

61
Q

Function of thromboxanes?

A

Thrombosis and platelets

62
Q

Function prostacyclin?

Produced by COX 1

A

Vascular dilation

63
Q

Which cyclooxygenase causes most problems when there is alot of omega 3 and 6?

A

COX 2

biochemistry (13 decks)

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