Chapter 20 Flashcards

1
Q

What is responsible for the vast majority of vascular diseases?

A

Atherosclerosis

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2
Q

What are the four modifiable RFs of atherosclerosis?

A

Hyperlipidemia
HTN
DM
Smoking

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3
Q

What is the third leading cause of death in the US?

A

Stroke resulting from cerebrovascular dz

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4
Q

How is dx of carotid artery dz best accomplished?

A

With a combo of duplex ultrasonography and axial imaging (CTA or MRA)

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5
Q

When is carotid endarterectomy of proven benefit?

A

In pts with symptomatic stenosis

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6
Q

What is an alternative to carotid endarterectomy?

A

Endovascular therapy with angioplasty and stenting for high-risk pts

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7
Q

Where is arterial occlusive dz most commonly found?

A

Aortoiliac
Femoropopliteal
Tibioperoneal circulations

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8
Q

Initial tx for arterial occlusive dz

A

Conservation, though revascularization is indicated for pts with crippling claudication or critical limb ischemia

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9
Q

Traditional option for arterial occlusive dz

A

Bypass grafting, though endovascular angioplasty with or without stenting is rapidly emerging as a viable alternative

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10
Q

What remain a major cause of morbidity and mortality?

A

Aneurysms of the aorta, iliac arteries, visceral arteries and peripheral arteries

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11
Q

What is rapidly changing the practice of vascular surgery?

A

Endovascular aneurysm repair

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12
Q

What can cause neurologic, arterial, or venous sx by compression of the brachial plexus, subclavian artery, or subclavian vein?

A

Thoracic outlet syndrome (TOS)

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13
Q

Approach of neurologic TOS

A

Should be approached cautiously, as sx may not improve after surgery
Arterial and venous sx from TOS should prompt surgical resection of the compressing structure.

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14
Q

Surgical tx of mesenteric ischemia

A

Resection of nonviable bowel and revascularization of the remaining intestine

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15
Q

Tx of DVT

A

Anticoagulation and close monitoring for complications

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16
Q

What to do when anticoagulation fails or is contraindicated in DVT

A

Insertion of a vena cava filter dramatically decreases the incidence of pulmonary embolism

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17
Q

How are arteries and veins formed?

A

From endothelium, smooth muscle, and extravascular matrix synthesized by cells in the vessel wall

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18
Q

What are the three layers of arteries and veins?

A

Tunica intima
Tunica media
Tunica adventitia

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19
Q

Tunica intima

A

Lines the luminal surface of the vessel wall and is composed of a thin continuous layer of polygonal endothelial cells overlying subendothelial connective tissue

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20
Q

What do endothelial cells in the tunica intima do?

A

Modulate vascular tone, hemostasis, vessel permeability, and cell proliferation

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21
Q

How do endothelial cells in the tunica intima do what they do?

A

Through the release of vasoactive mediators, anti-inflammaotry cytokines, and antithrombic agents

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22
Q

What covers the endothelial cells of the tunica intima?

A

By a glycocalyx, which is responsible for the anti-thrombogenic properties of the surface

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23
Q

What has been theorized as one of the initiating factors in the development of atherosclerotic lesions?

A

In inflammatory conditions, portions of the glycocalyx coat are lost, leading to the trafficking of leukocytes

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24
Q

Basal lamina

A

Borders endothelial cells on their albuminal surface and forms a boundary separating the endothelium from the underlying intimal structures

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25
Q

How is the basal lamina formed?

A
Formed by:
Glycoproteins
Adhesion molecules such as fibronectin and laminin
Various proteoglycans
Microfibirils of types IV and V collagen
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26
Q

Function of the basal lamina

A

Strengthen the vascular wall through polymer networks of type IV collagen and laminin chains
Regulates numerous functions such as endothelial cell regeneration and vessel permeability

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27
Q

Internal elastic lamina

A

A layer of elastic fibers dividing the subendothelial intima from the tunica media

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28
Q

What do the elastic laminae do?

A

Function as barriers to macromolecule accumulation in the vessel wall

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29
Q

What is the tunica media layer comprised of?

A

Vascular smooth muscle cells, elastic, and collagen separating the internal elastic lamina from the adventitia

30
Q

How are the components of the tunica media layer organized?

A

Arranged with closely packed layers of smooth muscle cells, elastin and collagen fibers surrounded by a basement membrane of laminin, type IV collagen and firbonectins.

31
Q

Tunica adventitia

A

A collection of adipose and other supportive connective tissue that extends from the media to the perivascular connective tissue

32
Q

What is only present in the tunica adventitia?

What does it do?

A

Vasa vasorum

Functions as the blood supply of the vessel wall

33
Q

What is also present in the tunica adventitia?

A

Vasomotor nerve fibers that mediate vasoconstriction and vasodilation via adrenergic alpha and beta receptors, respectively

34
Q

How are arteries classified?

A

Elastic
Distributing
Small

35
Q

What are the largest arteries?

What are examples?

A

Elastic

Aorta and its largest branches, such as the brachiocephalic, common carotid, and common iliac arteries

36
Q

What are the second largest arteries?

Examples?

A

Distributing

Coronary, renal, and hepatic arteries

37
Q

Where are the small arteries contained?

Example?

A

Contained within the substance of organs and tissues

Arterioles

38
Q

Primary function of arterioles

A

Control tissue blood flow and systemic arterial pressure

39
Q

What are the smallest vessels?

Function?

A

Capillaries

In tissues, they are the primary site for exchange of oxygen, nutrients, and waste

40
Q

Lymphatics- what are they?

Function?

A

Small, thin-walled structures with an endothelial lining
Function as conduits, which carry extracellular fluids centrally away from tissues for processing in the lymph nodes and eventual return to the vascular system

41
Q

Atherosclerosis

A

A dz whose hallmark is the deposition and accumulation of smooth muscle cells and lipids within the arterial intimaThe source of thromboembolic phenomenon

42
Q

What are the two types of lesions characteristic of late atherosclerosis?

A

Fibrous and complicated plaques

43
Q

Fibrous plaques

A

Consists of a necrotic core, containing foam cells (lipid filled smooth muscle cells or macrophages) and extracellular lipids, covered by a fibrous cap of smooth muscle cells, lymphocytes, and connective tissue

44
Q

Complicated plaques

A

Calcification, ulceration, plaque rupture with subsequent hemorrhage, and thrombosis

45
Q

What can accelerate the process by which a fibrous plaque evolves into a complicated one?

A

HTN

Cigarette smoking

46
Q

What are risk factors for atherosclerosis?

A
Hyperlipidemia
HTN
DM
Tobacco
Age
Gender
FHx
47
Q

Role of LDLs in atherosclerosis

A

Undergo oxidative modification in the bloodstream. The oxidized end products then function as inflammatory mediators, inducing adhesion molecule expression by endothelial cells

48
Q

Role of HDLs in atherosclerosis

A

Exert a protective effect against atherosclerosis because they are involved in transporting cholesterol away from the periphery to the liver for processing and excretion

49
Q

Role of HTN in atherosclerosis

A

The chronic elevation of blood pressure causes endothelial damage, which incites atherogenic inflammatory pathways
Induces increased arterial wall stiffness through the renin-angiotensin-aldosterone system

50
Q

DM is associated with a _____ increase in myocardial infarction and a ______ increase in gangrene of the lower extremities

A

2-fold

8- to 15-fold

51
Q

How DM contributes to atherosclerosis

A

Diabetics have impaired vasodilation due to dysfunction of endothelial nitric oxide synthase and increased production of endothelin I, a potent vasoconstrictor.
Platelet hyperactivity also contributes to decreased microvascular blood flow
Hyperglycemia results in the formation of reactive oxygen species and advanced glycation end products, which promote inflammatory pathways

52
Q

How cigarette smoking contributes to atherosclerosis

A

alters endothelium-mediated vasoreactivity in both the peripheral and coronary circulations by decreasing the availability of nitric oxide
Increases circulating proinflammatory markers

53
Q

Age trends in atherosclerosis

A

The risk for PAD increases 1.5- to 2-fold for every 10-yr increase in age

54
Q

Gender trends in atherosclerosis

A

Women appear to develop CVD 10 yrs later than do men and typically after menopause

55
Q

FHx and atherosclerosis

A

Multifactorial

56
Q

What is the third leading cause of death in the United States?

A

Stoke

57
Q

What percentage of strokes are ischemic and what percentage of strokes are hemorrhagic?

A

87%

13%

58
Q

What is the most common source of emboli in a CVA?

A

Internal carotid artery, followed by cardiac emboli

59
Q

Risk factors of CVA

A
All risk factors for atherosclerosis
Hx of A fib
TIA
Sedentary lifestyle
Excessive alcohol consumption
Obesity
60
Q

Sx of CVA

A

Contralateral weakness or sensory deficit of the face, arm, or leg, or transient ipsilateral blindness (amaurosis fugax)
Aphasia, alexia, anomia
Neglect, visual or sensory extinction, anosognosia, or asomatognosia

61
Q

PE of CVA

A

Carotid bruit may be found

62
Q

Initial carotid studies for CVA

A

Carotid artery duplex ultrasonography (DUS)
Noninvasive and reliable
Estimates the degree of stenosis on the basis of flow velocity
Cannot reliably distinguish very high-grade stenoses from occlusion
Cannot evaluate intracranial portions of the carotid artery system
Highly dependent on technique

63
Q

What is seeing increasing use in the dx of carotid stenosis?

A

Magnetic resonance angiography (MRA)

Tends to overestimate degree of stenosis

64
Q

What is less susceptible to overestimating the degree of carotid stenosis and is more rapid than MRA?

A

CTA

65
Q

What is the criterion standard test for carotid stenosis?

A

Catheter-based DSA

66
Q

Medical management of carotid dz

A

Lowering BP to a target of <140/90 with antihypertensive meds
Quit smoking
Lipid-lowering therapies
Daily aspirin

67
Q

In terms of carotid pathology, what should prompt a CEA?

A

Stenosis >50%

68
Q

When should CEA be considered in asymptomatic pts?

A

When pts have >60% stenosis

69
Q

Where is a carotid endarterectomy incision made?

A

Along the medial border of the sternocleidomastoid muscle or an oblique transverse incision in the neck.

70
Q

Complications of carotid endarterectomy

A

Stroke
MI
Postoperative HTN and/or hemorrhage
Vagus nerve most commonly traumatized

71
Q

When is carotid stenting preferred over CEA?

A

In pts with previous ipsilateral neck surgery or external beam radiotherapy
Medically infirm pts with extremely high perioperative risk, such as those with severe and uncorrectable CAD, CHF, or COPD