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Pathology > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

What vessels does atherosclerosis most commonly occur in?

A

Large arteries, not veins

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2
Q

Where especially can atherosclerosis occur in arteries?

A

At bifurcations where there is turbulent flow

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3
Q

What type of a disease is atherosclerosis?

A

A type of chronic inflammation which shows many features of wound repair

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4
Q

Where do atheromas form?

A

Within the intima layer of arteries

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5
Q

What is the first stage of atherosclerosis?

A

Accumulation of LDL and the inflammation of the arterial wall is the first stage of atherosclerosis.

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6
Q

How does atherogenesis first arise?

A

Qualitative changes in the inner arterial surface.

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7
Q

What are the changes to the endothelium which promote atherogenesis?

A

Endothelial cells of the inner layer normally oppose white blood cell attachment, but as they dysfunction, endothelial cells express adhesion molecules.

Permeability increases

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8
Q

What happens after WBC adhere to the intima?

A

WBC migration into the intima.
5. Inside the intima, monocytes mature and transform into macrophages that uptake the LDL particles to yield foam cells.

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9
Q

What changes facilitate LDL to migrate into the intima?

A

Both the composition of the extracellular matrix beneath the endothelium and the changes in endothelial permeability

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10
Q

How does cholesterol enter the intima?

A

Carried by LDL

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11
Q

What changes happen inside the newly invaded intima?

A

Monocytes mature and transform into macrophages that uptake the LDL particles to yield foam cells.

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12
Q

What are foam cells?

A

Macrophages which have uptaken LDL

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13
Q

What changes are there to SMC in the growing atheroma?

A

Smooth muscle cells are transferred from the middle layer of the arterial wall into the tunica intima. Proliferate

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14
Q

What happens eventually to make SMC and macrophages?

A

The smooth muscle cells and macrophages die in advanced lesions by apoptosis.

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15
Q

What makes up the necrotic core of the atheroma?

A

Dead SMCs and macrophages

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16
Q

How can an advanced plaque develop?

A

Development of intra-plaque microvessels from the adventitia

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17
Q

What causes the pathology associated with plaques?

A

Plaques generally cause stenosis and limit blood flow, which can lead to tissue ischemia.

Fibrous cap of a plaque can rupture,

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18
Q

What happens when the fibrous cap of a plaque ruptures?

A

Blood coagulation components come into contact with the thrombogenic plaque and produce thrombi.

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19
Q

What is the role of endothelial cells?

A

Provide a smooth, anti-thrombogenic surface for blood flow

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20
Q

What vasodilators does the endothelium secrete?

A

Nitric oxide (EDRF), Prostaglandin I2 (PGI2) aka prostacyclin

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21
Q

What vasoconstrictors does the endothelium secrete?

A

Endothelin, Angiotensin II

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22
Q

What antithrombotic factors does the endothelium secrete?

A

Tissue plasminogen activator (tPA), Prostaglandin I2 (PGI2)

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23
Q

What prothrombotic factors does the endothelium secrete?

A

Thombonxane A2, plasminogen activator inhibitor

24
Q

What is the role of smooth muscle cells in the artery?

A

Provide muscular arteries with their elasticity

Mediate vasodilation and vasoconstriction

Play a key role in regulating blood pressure

25
Q

What induces SMC apoptosis in vulnerable plaques?

A

Macrophage-induced SMC apoptosis seen in vulnerable plaques

26
Q

What do SMC secrete in stable plaques?

A

Secrete elastin and collagens in stable plaques

27
Q

What secretes important SMC growth factors?

A

Platelets (e.g PDGF)

28
Q

What vasoactive mediators do SMC secrete?

A

5-HT, TxA2

29
Q

Platelet lifespan

A

8-10 days in the circulation

30
Q

What marker is associated with foam cells?

A

CD68

31
Q

What receptors promote LDL uptake by macrophages?

A

Scavenger receptors

32
Q

What do macrophages secrete in atherosclerosis?

A

Inflammatory mediators (IL-1, TNF-a)

Growth factors (M-CSF, PDGF, FGF)

33
Q

Why do macrophages have a role in plaque rupture?

A

Secrete MMPs important in breaking down the fibrous cap

34
Q

What wider immune cells promote atherosclerosis

A

CD4 cells

35
Q

How do DCs activate CD4 cells in atherosclerosis?

A

Dendritic cells enter plaques and are exposed to LDL/oxLDL and activates Tcells via presentation of ApoB.

36
Q

Th1 role in atherogenesis

A

Interferon-g and has pathogenic effects, including less collagen fiber formation, higher expression of major histocompatibility complex class II, enhanced protease and chemokine secretion, upregulation of adhesion molecules, induction of proinflammatory cytokines, and enhanced activation of macrophages and endothelial cells.

37
Q

Th2 role in atherogenesis

A

Involvement of TH2 cells are contradictory, with some showing pro-atherosclerotic effects and others showing protective effects.

38
Q

What plasma components have a role in atherosclerosis?

A

Lipoproteins (LDL, modified LDL, HDL)

Coagulation cascade components

C- Reactive Protein (CRP)

Complement components

Oxidants / anti-oxidants

39
Q

What are lipoproteins?

A

Complex particles that have a central hydrophobic core of non-polar lipids, primarily cholesteryl esters and triglycerides. This hydrophobic core is surrounded by a hydrophilic membrane consisting of phospholipids, free cholesterol, and apolipoproteins.

40
Q

What are lipoproteins in order of density?

A 
Chylomicrons 
Very low density lipoprotein (VLDL) 
Intermediate density lipoprotein (IDL) 
Low density lipoprotein (LDL) 
High density lipoprotein (HDL)
41
Q

What lipoproteins are pro-atherogenic?

A

VLDL, IDL and LDL are pro-atherogenic. HDL is anti-atherogenic (reverse cholesterol transport and anti oxidant properties)

42
Q

What lipoprotein is antiatherogenic

A

HDL

43
Q

Why is HDL antiatherogenic?

A

Mediates reverse cholesterol transport

Important source of anti-oxidants

44
Q

Why are free radicals bad for atherosclerosis?

A

oxLDL is more readily taken up by macrophages (forming foam cells)

45
Q

Relative Risk

A

Relative risk is the ratio of the likelihood of CHD developing in persons with and without a given risk factor

46
Q

Absolute Risk

A

Absolute risk is the probability of developing CHD in a finite period, (e.g. within the next 10 years)

47
Q

Non-modifiable risk factors

A

A personal history of CHD

A family history of CHD

Advanced age

Gender

48
Q

Modifiable risk factors

A

High plasma LDL Cholesterol (>5.2mmol/L)

Hypertension (>140/90mm Hg)

Physical inactivity / Obesity (BMI > 30)

Smoking

Diabetes

49
Q

What is the cause of familial hypercholesterolaemia?

A

Mutations diminish the number of functional LDL receptors in the liver.

As a result, LDL is not endocytosed and converted to cholesterol, and remains high in the plasma.

50
Q

What is an angioplasty?

A

Minimally invasive endovascular procedure used to widen narrowed or obstructed arteries or veins, typically to treat arterial atherosclerosis.

A deflated balloon attached to a catheter (a balloon catheter) is passed over a guide-wire into the narrowed vessel and then inflated to a fixed size.

The balloon forces expansion of the blood vessel and the surrounding muscular wall, allowing an improved blood flow.

A stent may be inserted at the time of ballooning to ensure the vessel remains open, and the balloon is then deflated and withdrawn

51
Q

What is CABG?

A

Surgical procedure to restore normal blood flow to an obstructed coronary artery.

CABG is often indicated when coronary arteries have a 50 to 99 percent obstruction.

Surgery anastomoses conduit vessel which is harvested from the patient and grafted between the aorta and just below the lesion.

52
Q

How do statins work?

A

Reduce cholesterol levels by inhibiting the hepatic enzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase

Increase hepatic LDLR expression

Lower plasma LDL-C, lower plasma TGs, raised plasma HDL

53
Q

How do anti PCSK9 antibodies work?

A

Alirocumab monoclonal antibody can be used to bind to PCSK9 before it can bind to LDL receptors and lead to their sequestering.

54
Q

What is an anti PCSK9 antibody example?

A

Alirocumab

55
Q

What does a PCSK9 gain of function mutation mean?

A

Individual gets atherosclerosis young

56
Q

What does a PCSK9 loss of function mutation mean?

A

Resistance to atherosclerosis

Pathology (21 decks)

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