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CVM II > Vascular Part I - Robbins > Flashcards

Vascular Part I - Robbins Flashcards

1
Q

What are berry aneurysms? Where are they typically found?

A

Outpouchings in cerebral vessels due to congenital wall weakness
2% of population
Rupture can cause fatal subarachnoid hemorrhage
Typically found in the Circle of Willis

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2
Q

What are berry aneurysms usually associated with?

A

Autosomal dominant polycystic disease 10-15%

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3
Q

What are arteriovenous fistulas? How do they arise?

A

abnormal connection between artery and vein (bypass capillaries)
Most commonly a developmental defect, but may arise secondary to inflammation, trauma, rupture

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4
Q

What can arteriovenous fistulas lead to?

A

Rupture and hemorrhage
Large enough, it can create significant left-to-right vascular shunting, with increased venous return that leads to high-output cardiac failure

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5
Q

What is fibromuscular dysplasia?

A

Focal thickening of intima and media of medium to large muscular arteries due to hyperplasia and fibrosis, resulting in stenosis

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6
Q

What stimui can induce change in endothelial cell function, leading to an activated state?

A 
Turbulent blood flow
HTN
complement, bacterial products, lipid products, glycation end products (diabetes)
Viruses 
Hypoxia, acidosis 
Tobacco smoke
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7
Q

What is the activated state of the endothelium

A

Increased expression of procoagulants, adhesion, proinflammatory factors, vasoactive factors, GFs
Factors that can cause SMC contraction and/or proliferation and matrix synthesis

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8
Q

Endothelial dysfunction often characterized by….

A

Procoagulation
Proinflammation
Smooth muscle stimulation

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9
Q

What is neointima?

A

Injured endothelium and underlying vessel wall “heal” by stimulating SMC ingrowth and ECM production, leading to intimal thickening

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10
Q

What is the stereotypical response to vascular injury?

A

With loss of endothelial cells or prolonged dysfunction, intimal thickening occurs

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11
Q

What is intimal thickening?

A

SMC from media migrate to intima, where they proliferate and elaborate ECM

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12
Q

Untreated hypertension can lead to what?

A

vessel and end-organ damage

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13
Q

What can untreated hypotension lead to?

A

inadequate organ perfusion

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14
Q

What is HTN a risk factor for?

A 
Atherosclerosis
Aortic dissection 
HTN heart disease
Stroke
HTN renal disease
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15
Q

How often is HTN essential?

A

90-95%

Most people with HTN have idiopathic or essential HTN

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16
Q

What is secondary HTN usually caused by?

A

Renal (acute glomerulonephritis, CRD, polycystic D, RAS, RAFD, vasculitis, renin-producing tumors) or endocrine disorder (adrenocortical hyperfunction, exogenous hormones, pheochromocytoma, hyper/hypo thyroidism, pregnancy)

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17
Q

What are the risk factors for essential HTN?

A 
High sodium intake
Obesity
Stress
Smoking
Physical inactivity
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18
Q

BP = ?

A

CO x Peripheral resistance

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19
Q

What are the humoral constrictors of peripheral vasculature?

A 
Angiotensin II 
Catecholamines
Thromboxane
Leukotrienes
Endothelin
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20
Q

what are the humora dilators of vasculature?

A

PGs, kinins, NO

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21
Q

What is blood volume and vascular tone modified and maintained by?

A

Renin-angiotensin-aldosterone system

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22
Q

Mutations in what enzymes that influence aldosterone synthesis leads to increased aldosterone production?

A

11-beta hydroxylase, 17 alpha hydroxylase

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23
Q

What is Liddle syndrome?

A

Mutation in renal epithelial Na channel protein leading to increased sodium resorption

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24
Q

What accelerates the development of atherosclerosis and also causes arteriolar structural changes that potentiate aortic dissection and cerebrovascular hemorrhage?

A

HTN

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25
Q

What happens with Hyaline arteriolosclerosis?

A 
Increae sm m matrix synthesis 
Plasma protein leakage across damaged endothelium 
Homogenous pink (hyaline) thickening of the vessel wall, with luminal narrowing
Plasma proteins traversed activated endothelium is the source of hyaline
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26
Q

What is hyperplastic arteriolosclerosis?

A

Occurs in sever HTN
SMC form concentric lamellations (‘onion skinning’ - reduplicated BM and SMC proliferation) with resultant luminal narrowing
Associated with necrotizing arteriolitis

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27
Q

What are the three patterns of arteriosclerosis?

A

Arteriolosclerosis: downstream ischemia
Muckeberg medial sclerosis: medial calcification in muscular aa; older
Atherosclerosis

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28
Q

What does the fibrous cap of atherosclerotic plaque contain?

A

SMC, Mo, Foam cells, lymphocytes,collagen, elastin, proteoglycans, neovascularization

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29
Q

What are atherosclerotic lesions?

A

Elevated intimal-based plaques composed of lipids, proliferating SMC, inflammatory cells and increased ECM

30
Q

What is the pathology of atherosclerosis/

A

Mechanically obstructing flow
Plaque rupture leading to vessel thrombosis
Weakening of underlying vessel wall, leading to aneurysm formation

31
Q

What are the constitutional risk factors of atherosclerosis?

A

Family history: most significant independent risk factor
Age: 40-60
Gender: age-matched males, postmenopausal women

32
Q

What are the major modifiable risk factors of atherosclerosis

A

Hyperlipidemia (LDL)
HTN: increase risk of ischemic heart disease by 60%
Smoking: doubles death rate of ischemic HD
DM: doubles risk of MI, hypercholesterolemia

33
Q

What are the other (less common) modifiable risk factors of atherosclerosis?

A

inflammation: present at all stages of atherosclerosis development; CRP
Hyperhomocystinemia: low folate or vitamin B12 or hereditary homocystinuria
Metabolic syndrome: central obesity, HTN, glucose intolerance, dyslipidemia, and systemic proinflammatory state

34
Q

What is lipoprotein A?

A

altered form of LDL, elevated lvls confer increased risk of atherosclerosis independent of LDL lvls

35
Q

what is the pathogenesis of atherosclerosis?

A

Chronic injury and dysfunction of endothelium, leads to chronic inflammation and attempts to repair tissue
Increase endothelial perm, WBC and platelet adhesion and coagulation
Mo activation, SMC recruitment
Mo and SMC engulf lipid
SMC proliferation, collagen and ECM deposition, Extracellular lipid

36
Q

Where do most atherosclerotic plaques occur and why?

A

do not occur randomly in vessels, does not occur everywhere
Most lesions occur at openings of exiting vessels, branch points, posterior abdominal aorta
Due to flow disturbances normally seen in these locations

37
Q

What does the increase of LDLs in atherosclerosis cause?

A

Increase local oxygen free radical formation
LDLs oxidized and become toxic to EC and SMCs
Mo ingest LDL causing formation of foam cells -> proinflammatory Mo activation
Fatty streaks
Lipids in plaques are predominately choleterol and cholesterol esters

38
Q

How is inflammation involved in pathogenesis of atherosclerosis?

A

Accumulation of cholesterol crystals wi Mo is recognized by inflammasome, which leads to IL-1 secretion
More Mo and T cell recruitment
Further activaiton of endothelial cells
GFs stimulate SMC to migrate to intima and proliferate

39
Q

What happens after an atheromatous plaque is formed?

A

over time, the soft fibrofatty plaque becomes covered with a fibrous cap (dense collagen fibers)
Center becomes necrotic, contains lipid, debris, foam cells and thrombus, surrounded by a zone of inflammatory and SMCs

40
Q

Describe how unstable plaques are formed

A

Activated inflammatory cells cause medial SMC apoptosis and increase ECM degradation leading to instability

41
Q

What are the common sites of involvement with atherosclerosis?
Name in decreasing order of frequency/severity

A 
Abdominal aorta
Coronary arteries 
Popliteal arteries 
Internal carotid arteries
Circle of WIllis
42
Q

What are the complications of atherosclerotic plaques?

A

Rupture and ulceration - may lead to thrombosis
Hemorrhage and embolism - may follow plaque rupture
Aneurysm formation

43
Q

At what point does a stenosis become a critical stenosis?

A

70% occluded

44
Q

What are the consequences of atherosclerosis?

A

Stenosis of arterial lumen

Acute plaque change (erosion, ulceration, rupture -> occlude artery; or hemorrhage that can expand volume)

45
Q

What are some causes of plaque rupture ?

A

Fibrous cap continually degraded and resynthesized. Inflammation can accelerate fibrous cap degradation and weaken it
Physical stresses - change in BP and vasoconstriction

46
Q

Describe vulnerable plaques?

A

Large deformable atheromatous cores, thin fibrous cap, and/or increased inflammatory cell content -> elaboration of MMPs that degrade ECM

47
Q

Describe stable plaques

A

Minimal atheromatous cores and thicker well-collagenized fibrous caps, less inflammation

48
Q

Why can vasoconstriction occur at the location of atherosclerotic plaques?

A

Endothelial dysfunction - loss of nitric oxide production

Or to products elaborated by aggregated platelets or inflammatory cells

49
Q

What is an aneurysm ?

A

a localized abnormal dilation of a blood vessel or the heart

May be congenital or acquired

50
Q

What is a true aneurysm ?

A

Intact but thinned muscular wall at the site of dilation

Bounded by all three vessel wall layers

51
Q

What is a false aneurysm ?

A

Defect through the wall of the vessel or heart, communicating with an extravascular hematoma

52
Q

What is a dissection?

A

blood enters the arterial wall itself, dissecting between the layers

53
Q

Morbidity and death due to aneurysms and dissections are secondary to what?

A

rupture,
impingement on adjacent structures,
occlusion of proximal vessels by extrinsic pressure or superimposed thrombosis
embolism from a mural thrombus

54
Q

When does an aneurysm occur?

A

Whenever the CT of the vascular is weakened - acquired or congenital conditions

55
Q

What can lead to defective vascular wall CT and cause susceptibility to aneurysm?

A

Marfan syndrome: fibrillin synthesi)
Loeys-Dietz syndrom: TGF-b activation (progressive loss of elastic tissue matrix
Ehlers-Danlos: defective collagen II synthesis
Scurvy - vit C deficiency

56
Q

What can cause net degradation of vascular wall CT and lead to aneurysms?

A

Inflammatory conditions like atherosclerosis –> increased MMPs

57
Q

What can cause weakening of vascular wall by ischemic and lead to aneurysms?

A

Atherosclerosis -> inner media
HTN -> outermedia
Tertiary syphilis -> outer media (thoracic aorta)

58
Q

What will lead to cystic medial degeneration?

A

loss of vascular wall elastic tissue

Ineffective elastin synthesis

59
Q

What are the two most important causes of aortic aneurysms ?

A

atherosclerosis and HTN

60
Q

Describe abdominal aortic aneurysms

A 
true aneurysms 
Typically due to atherosclerosis
Covered with mural thrombus
Usually below renal arteries and involve common iliac aa
More freq in men, smokers and 60s
61
Q

What are the complications of AAA?

A

Rupture and hemorrhage
Occlusion of branching aa and downstream ischemia
Embolism
Impingement on another surface

62
Q

What is the rupture risk related to?

A 
Size
Less than 4 cm: negligible 
4-5 cm: 1%
5-6 cm: 11%
greater: 25%
manage surgically
63
Q

describe inflammatory AAAs?

A

5-10% of AAAs
Younger pts
Exuberant transmural lymphoplasmacytic infiltrate and dense periaortic fibrosis
IgG4

64
Q

What are thoracic aortic aneurysms often due to?

A

HTN,

Less commonly - congenital defect in CT synthesis (marfans)

65
Q

Clinical presentation of thoracic aortic aneurysm often due to ….

A

Impingement of lower respiratory tree, esophagus, RLN
Aortic valvular insufficiency
Rupture

66
Q

What are the signs and symptoms of thoracic aortic aneurysm?

A

Dyspnea, dysphagia, cough, vertebral pain

67
Q

Aortic dissection occurs in what type of pts?

A

HTN males, 40-60
Pts with disorder of vessel CT - marfans
Primary risk factor is HTN

68
Q

What is the classic presentation of aortic dissection?

A

Sever chest pain, radiating to the back, between the scapulae
Ascending aorta

69
Q

Why is dissection uncommon in atherosclerosis?

A

Fibrous tissue limits dissection propagation

Any condition with medial scarring

70
Q

Morphology of aortic dissection

A

Cystic medial degeneration; often wo accompanying inflammation

71
Q

Type A dissections

A 
Ascending aorta 
More common 
Higher morbidity and mortality 
Most common cause of death - rupture
Tx: antihypertensive therapy and surgical repair  (early 65-75% survival)
72
Q

Type B dissections

A

Dissection after great vessels, descending aorta

CVM II (4 decks)

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