T3 L16: Atherogenesis Flashcards

1
Q

In which part of the vessel do atherogenic plaques develop?

A

In the tunica intima of the artery wall

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2
Q

What causes atherogenesis?

A

Migration of cells from the tunica media into the tunica intima and caused by recruitment of leukocytes and deposition of lipid from the blood

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3
Q

What are the 3 components of atherogenic plaques?

A

Cells, matrix components like collagen, and intracellular and extracellular lipids like cholesterol

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4
Q

What 2 effects does NO have on epithelium of vessels?

A

Vasorelaxation and anti-adhesive properties causing recruitment of monocytes and platelets to be inhibited

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5
Q

Which molecules transform monocytes into macrophages?

A

Cytokines like IFN-alpha, TNF-alpha, GM-CSF, and M-CSF secreted by the vascular smooth muscle cells

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6
Q

Which molecules attract monocytes to developing plaques?

A

MCP-1/CCL2, chemokines produced by endothelial cells

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7
Q

What do macrophages produce which can oxidise LDL?

A

ROS

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8
Q

What role do monocytes have in atherogenesis?

A

Transform into macrophages which can generate ROS, produce pro-inflammatory cytokines, and express scavenger receptors

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9
Q

What are remnants of LDL?

A

Smaller lipoproteins

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10
Q

What does oxidised LDL stimulate?

A

stimulates expression of VCAM-1 and MCP-1`

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11
Q

How do macrophages become foam cells?

A

When they constantly phagocytose oxidised LDL

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12
Q

What is oxidised LDL recognised by?

A

Scavenger receptors not LDL receptors

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13
Q

What are vascular smooth muscles cells responsible for?

A

Structure of the vessel wall

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14
Q

Which cells secrete PDGF and TGF-beta?

A

Endothelial cells and macrophages

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15
Q

What role do VSMC’s (Vascular smooth muscle cells) have in atherogenesis?

A

They can differentiate into macrophage-like cells and become foam cells. Activated VSMC’s can synthesise molecules like collagen which deposits in the plaque.

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16
Q

Which 2 types of cells can develop into foam cells?

A

Macrophages and vascular smooth muscle cells

17
Q

What is TGF-beta?

A

Transforming growth factor beta

18
Q

What can cause epithelial dysfunction/injury?

A

Hyperlipidaemia, hypertension, smoking, toxins, haemodynamic factors

19
Q

What is the difference between a stable and ruptured plaque?

A

Stable plaques have a thick fibrous cap, high VSMC, small amounts of lipid, and few inflammatory cells. Ruptured plaques have a thin fibrous cap, low VSMC content, large lipid content, and many inflammatory cells

20
Q

What are the 2 main theories behind atherogenesis?

A

Lipid oxidation and response to injury hypothesis

21
Q

What is familial hypercholesterolaemia?

A

A genetic disorder causing elevated levels of LDL

22
Q

What is the mechanism behind statin action?

A

They are competitive inhibitors of HMG-CoA reductase

23
Q

Lovastatin, Compactin, pravastatin, and simvastatin are types of which statin class?

A

Natural statin

24
Q

Atorvastatin and Fluvastatin are types of which statin class?

A

Synthetic statin

25
What effect does blocking PCSK9 proteins have on cholesterol and why?
Decreased blood cholesterol. PCSK9 proteins degrade LDL receptors so blocking them allows more LDL to enter the liver and therefore leave the blood so it can't build up in vessels