Vascular Disease Flashcards

1
Q

When does atherosclerosis begin?

A

early childhood

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2
Q

What are the stages of atherosclerosis?

A

1) prenatal/early childhood exposures
2) endothelial dysfunction
3) fatty streaks
4) fibrous plaques
5a) occlusive atherosclerotic plaques
5b) plaque rupture & thrombosis

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3
Q

What are fatty streaks?

A

accumulation of lipid (from lipid-laden macrophages and monocytes) and smooth muscle migration into the tunica intima

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4
Q

What happens in the case of:

  • occlusive atherosclerotic plaques
  • plaque rupture & thrombosis
A

occlusive atherosclerotic plaques - luminal obstruction and its associated symptoms of ischemia (angina + claudication)

plaque rupture & thrombosis - causes acute MI, coronary death, stroke

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5
Q

What are the major modifiable + nonmodifiable risk factors for coronary heart disease?

A

nonmodifiable

  • age
  • male
  • family hx

modifiable

  • HTN
  • smoking
  • hypercholesterolemia
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6
Q

What are therapies (Rx + procedural) for coronary heart disease?

A

Rx

  • aspirin
  • b-blockers
  • ACE inhibitors
  • statins

Procedural

  • PCI angioplasty + stent
  • CABG (grafting of arteries/veins)
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7
Q

Which therapy provides the greatest decrease in LDL levels and greatest reduction in coronary mortality?

A

statins

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8
Q

What are the 4 layers of the blood vessel anatomy (out->in)

A

endothelium
intima - contains IEL
media
adventitia - contains EEL + vasa vasorum

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9
Q

What is the difference between hyaline arteriosclerosis and hyperplastic arteriosclerosis?

Which one causes malignant hypertension?

A

hyaline arteriosclerosis - thickening of arteriolar wall due to collagen deposition

hyperplastic arteriosclerosis - thickened concentric smooth muscle layer with thickened basement membrane; AKA malignant HTN

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10
Q

What are the two types of aneurysms?

A

True - when ALL of the layers of the blood vessel are dilated, which results in an increased lumen size. This leads to increased wall stress, which can rupture.

False - when there is a tear of the arterial wall, which creates a collection of blood that is bound externally by adherent extravascular connective tissue (NOT a true dissection).

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11
Q

What are the causes of true dissection? (when ALL of the layers of the blood vessel are dilated)

A

Congenital/genetic disorders
Atherosclerosis
Marfan’s disease
Syphilis

CAMS

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12
Q

In what patients would you expect an abdominal aorta aneurysm?

What would you find on a physical examination?

How would you diagnose it?

What is the treatment?

A

M 40-60yo with chronic HTN
younger patient with CT dz

physical examination: pulsatile epigastric mass + abdominal bruit

Dx: ultrasound

Trmt: surgical repair graft

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13
Q

What is an aortic dissection? What is the difference between a type A and type B dissection?

In what patients is this most common?

A

Occurs when blood enters the vessel wall by breaking through the endothelial/subendothelial intimal layers and causes medial degeneration.

Type A

  • type I - extensive dissection that involves proximal aorta
  • type II - dissection that involves only the proximal aorta

Type B
- dissection that arises AFTER the great vessels (distally)

common in Marfan’s syndrome.

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14
Q

What is vasculitis? What are the 3 main types?

A

inflammation of blood vessels

Types:
Polyarteritis Nodosa (med + small arteries)
Temporal Arteritis (vessels of the head/neck)
Granulmoatous w. Polyangiitis

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15
Q

What is Polyarteritis Nodosa?

What is this common in? Are men more susceptible to this disease compared to women?

A

vasculitis of med+small arteries that result in small aneurysms that resemble beads on a rosary

30% of pts have HepB infection; men are 2x likely to get it than women

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16
Q

What is temporal arteritis?

What is this also known as?

A

damage to blood vessels that supply the head area, particularly the large or medium arteries that branch from the neck and supply the temporal area; cause of vasculitis is unknown

aka giant cell arteritis/Horton’s disease - presence of giant cells in the thick arterial wall

dx: Perinuclear pattern of antineutrophil cytoplasmic antibodies (p-ANCA)

17
Q

What is granulomatosis w. polyangiitis?

What is this also known as?

A

vasculitis of small- and medium-size vessels in many organs that’s caused by an autoimmune attack by an abnormal antibody (ANCA)

aka Wegener’s granulomatosis

dx: ANCAs that react with the enzyme proteinase 3 (cANCA) in neutrophils

18
Q

Which vascular neoplasm is more malignant: hemiangiomas or angiosarcomas?

A

angiosarcomas are malignant endothelial neoplasms which can metastases to distant sites

Hemiangiomas are self-involuting endothelial cells of blood vessels

19
Q

Why may repeated sympathetic activation be atherogenic?

Why might people who have hyper-responsive emotional stimuli be more likely to develop HTN and atherosclerosis?

A

it increases BP + vasoconstriction, which may result in increased endothelial injury

these people have increased stress levels, which may result in an exaggerated catecholamine responses HR and BP in response to emotional stress.

20
Q

Why might cigarette smoking be atherogenic?

A

nicotine can activate the sympathetic ganglia (NN receptors), resulting in increased HR, BP, which may result in increased endothelial injury