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3.23 > Lecture 9 > Flashcards

Lecture 9 Flashcards

1
Q

Define atheroma

A

The accumulation of intracellular and extracellular lipid in the intima of large and medium sized arteries

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2
Q

How long does atherosclerosis take to develop?

A

Several years

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3
Q

When can atherosclerosis start?

A

As early as infancy and childhood and progresses very slowly during life

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4
Q

The accumulation of what results in the formation of atherosclerosis? (4)

A
  • lipid
  • connective tissue
  • inflammatory cells
  • smooth muscle cells
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5
Q

What does the Greek work atheros mean?

A

Gruel or paste

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6
Q

What does the Greek work sclerosis mean?

A

Hardness

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7
Q

Where can atheromas form? (5)

A
  • Intimal lining of large and medium sized arteries such as the aorta and its branches
  • The coronary arteries
  • The large vessels that supply the brain
  • Carotid arteries
  • Leg arteries
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8
Q

How is atherosclerosis detected?

A
  • Typically asymptomatic
  • Usually found after a heart attack or stroke
  • ## Measure of LDL in blood as a predictor
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9
Q

What are the three layers of the artery?

A
  • Intima
  • Media
  • Adventitia
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10
Q

What layer of the artery contributes most to its mechanical strength?

A

The medial layer

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11
Q

What are the macroscopic features of an atheroma?

A
  • Fatty streak
  • Simple fibrous plaque
  • Complicated plaque
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12
Q

What is a fatty streak?

A

Compromises a slightly elevated zone on the arterial wall caused by accumulation of a small number of lipid laden cells

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13
Q

What is a simple fibrous plaque?

A
  • Lipid accumulated both free and in cells
  • Smooth muscle cells also migrate from the media
  • Fibrosis develops around the lipid and forms a cap over the lesion
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14
Q

What is a compliacated plaque?

A

Ulcers and fissures of the fibrous cap expose plaque contents resulting in thrombosis

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15
Q

What is the development of atherosclerosis initiated by?

A

Endothelial dysfunction

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16
Q

What are the main components of plaque? (3)

A
  • Lipid containing macrophages
  • Extracellular matrix
  • Proliferating smooth muscle cells
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17
Q

Where is cholesterol absorbed?

A

Intestine

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18
Q

Where is cholesterol produced?

A

Liver

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19
Q

What is the daily cholesterol dietary intake?

A

300mg

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20
Q

How much cholesterol is synthesized per day?

A

1 gram

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21
Q

How is cholesterol carried in the blood?

A

Attached to proteins called lipoproteins

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22
Q

What are the two forms of lipoproteins?

A
  • Low density lipoproteins
  • High density lipoproteins
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23
Q

How is LDL removed from the circulation

A
  • By LDL receptor or
  • By scavenger cells such as monocytes or macrophages
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24
Q

How is 70% of LDL removed?

A

By receptor dependent pathway

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25
Q

Where are 75% of LDL receptors located?

A

On hepatocytes

26
Q

Give examples of scavenger cells?

A
  • Monocytes
  • Macrophages
27
Q

What do scavenger cells do?

A

Have receptors that bind LDL that has been oxidized or chemically modified

28
Q

What is the amount of LDL that is removed by the scavenger pathway directly related to?

A

Plasma cholesterol level

29
Q

What causes an increase in the amount of LDL removed by scavenger cells?

A
  • When LDL levels exceed receptor availability
  • When there’s a decrease in LDL receptors
30
Q

How does oxidized LDL form?

A

When LDL particles react with free radicals

31
Q

What causes an increase in oxidized LDL levels?

A
  • Consuming a diet high in trans fats
  • Smoking
  • Poorly controlled diabetes
32
Q

What cells absorb oxidised LDL?

A

Specialised white blood cells - macrophages and T lymphocytes

33
Q

How is a foam cell formed?

A

When macrophages and lymphocytes absorb oxided LDL

34
Q

What causes the plaque to rupture?

A

When the foam cells are not able to process the oxidised LDL and recruit HDL particles to remove the fats

35
Q

What does LDL in the endothelial lining promote the accumulation of in blood vessels?

A
  • White blood cells (lymphocytes)
  • Immune cells (dendritic cells)
  • Inflammatory cells (macrophages)
36
Q

What causes the hardness of the plaques?

A

Platelets which stick to areas of inflammation in the artery

37
Q

What is extra cellular matrix?

A
  • Elastin
  • Collagen
  • Proteoglycans
38
Q

What causes a plaque to grow further?

A

Macrophages release growth factors and recruit smooth muscle cells to the plaque. The smooth muscle cells may proliferate and deposit extracellular matrix in the lesions

39
Q

What forms a cap around a plaque?

A

Smooth muscle cells

40
Q

What is released from necrotic foam cells?

A

Lipids

41
Q

What do lipids form?

A

The lipid core of unstable plaques

42
Q

What does calcium tissue synthesis determine?

A
  • Stiffness
  • Calcium fixation
  • further ulceration of atheromatous plaque
43
Q

What drugs are secondary prevention for atherosclerosis?

A
  • Antiplatelets
  • Statins
  • B blockers
  • Ace inhibitors
44
Q

What drugs are used to control symptoms of atherosclerosis?

A
  • B blockers
  • Calcium antagonists
  • Nitrates
  • Potassium channel openers
  • Ranolazine
45
Q

What surgery can be done for atherosclerosis?

A
  • Bypass
  • PCI
46
Q

What does endothelium damage promote?

A

Thrombus formation

47
Q

What does endothelial damage following blood vessel injury result in?

A
  • Loss of the endothelium anti thrombotic functions
  • Gain of procoagulant function
48
Q

What happens when platelets adhere to exposed subendothelial connective tissue ?

A

Platelets become more spherical and extrude long pseudopods which enhance interaction between adjacent platelets

49
Q

What do platelets membrane glycoproteins contribute to?

A

Platelet adhesion to collagen

50
Q

What allows platelets to bind fibrinogen?

A

Binding of von willebrand factor results in conformational change within platelet glycoproteins allowing them to bind fibrinogen

51
Q

What do adherent platelets release?

A

ADP and thromboxane A2

52
Q

What are ADP and thromboxane A2?

A

Platelet agonists

53
Q

What do ADP and thromboxane A2 do?

A

Activate more platelets and recruit them to the site of vascular injury

54
Q

What is the mechanism of action of aspirin?

A

- Thromboxane A2 is a platelet agonist produced and released by platelets
- Aspirin blocks production of thromboxane A2 by inhibiting platelet enzyme responsible for its synthesis, COX 1

55
Q

How long does the action of aspirin on platelet COX 1 last?

A

It’s permanent, lasting for the life of the platelet

56
Q

How long is the life of a platelet?

A

7-10 days

57
Q

What are the lipid lowering drugs?

A

Statins

58
Q

When is the greatest cholesterol synthesis?

A

During fasting states

59
Q

Which statins have a short half life?

A

Simvastatin

60
Q

When is simvastatin usually given?

A

Before bedtime

3.23 (26 decks)

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