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CVM II > Vascular Part I - Robbins > Flashcards

Vascular Part I - Robbins Flashcards

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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
What happens with Hyaline arteriolosclerosis?
``` 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 ```
26
What is hyperplastic arteriolosclerosis?
Occurs in sever HTN SMC form concentric lamellations ('onion skinning' - reduplicated BM and SMC proliferation) with resultant luminal narrowing Associated with necrotizing arteriolitis
27
What are the three patterns of arteriosclerosis?
Arteriolosclerosis: downstream ischemia Muckeberg medial sclerosis: medial calcification in muscular aa; older Atherosclerosis
28
What does the fibrous cap of atherosclerotic plaque contain?
SMC, Mo, Foam cells, lymphocytes,collagen, elastin, proteoglycans, neovascularization
29
What are atherosclerotic lesions?
Elevated intimal-based plaques composed of lipids, proliferating SMC, inflammatory cells and increased ECM
30
What is the pathology of atherosclerosis/
Mechanically obstructing flow Plaque rupture leading to vessel thrombosis Weakening of underlying vessel wall, leading to aneurysm formation
31
What are the constitutional risk factors of atherosclerosis?
Family history: most significant independent risk factor Age: 40-60 Gender: age-matched males, postmenopausal women
32
What are the major modifiable risk factors of atherosclerosis
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
What are the other (less common) modifiable risk factors of atherosclerosis?
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
What is lipoprotein A?
altered form of LDL, elevated lvls confer increased risk of atherosclerosis independent of LDL lvls
35
what is the pathogenesis of atherosclerosis?
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
Where do most atherosclerotic plaques occur and why?
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
What does the increase of LDLs in atherosclerosis cause?
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
How is inflammation involved in pathogenesis of atherosclerosis?
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
What happens after an atheromatous plaque is formed?
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
Describe how unstable plaques are formed
Activated inflammatory cells cause medial SMC apoptosis and increase ECM degradation leading to instability
41
What are the common sites of involvement with atherosclerosis? Name in decreasing order of frequency/severity
``` Abdominal aorta Coronary arteries Popliteal arteries Internal carotid arteries Circle of WIllis ```
42
What are the complications of atherosclerotic plaques?
Rupture and ulceration - may lead to thrombosis Hemorrhage and embolism - may follow plaque rupture Aneurysm formation
43
At what point does a stenosis become a critical stenosis?
70% occluded
44
What are the consequences of atherosclerosis?
Stenosis of arterial lumen | Acute plaque change (erosion, ulceration, rupture -> occlude artery; or hemorrhage that can expand volume)
45
What are some causes of plaque rupture ?
Fibrous cap continually degraded and resynthesized. Inflammation can accelerate fibrous cap degradation and weaken it Physical stresses - change in BP and vasoconstriction
46
Describe vulnerable plaques?
Large deformable atheromatous cores, thin fibrous cap, and/or increased inflammatory cell content -> elaboration of MMPs that degrade ECM
47
Describe stable plaques
Minimal atheromatous cores and thicker well-collagenized fibrous caps, less inflammation
48
Why can vasoconstriction occur at the location of atherosclerotic plaques?
Endothelial dysfunction - loss of nitric oxide production | Or to products elaborated by aggregated platelets or inflammatory cells
49
What is an aneurysm ?
a localized abnormal dilation of a blood vessel or the heart | May be congenital or acquired
50
What is a true aneurysm ?
Intact but thinned muscular wall at the site of dilation | Bounded by all three vessel wall layers
51
What is a false aneurysm ?
Defect through the wall of the vessel or heart, communicating with an extravascular hematoma
52
What is a dissection?
blood enters the arterial wall itself, dissecting between the layers
53
Morbidity and death due to aneurysms and dissections are secondary to what?
rupture, impingement on adjacent structures, occlusion of proximal vessels by extrinsic pressure or superimposed thrombosis embolism from a mural thrombus
54
When does an aneurysm occur?
Whenever the CT of the vascular is weakened - acquired or congenital conditions
55
What can lead to defective vascular wall CT and cause susceptibility to aneurysm?
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
What can cause net degradation of vascular wall CT and lead to aneurysms?
Inflammatory conditions like atherosclerosis --> increased MMPs
57
What can cause weakening of vascular wall by ischemic and lead to aneurysms?
Atherosclerosis -> inner media HTN -> outermedia Tertiary syphilis -> outer media (thoracic aorta)
58
What will lead to cystic medial degeneration?
loss of vascular wall elastic tissue | Ineffective elastin synthesis
59
What are the two most important causes of aortic aneurysms ?
atherosclerosis and HTN
60
Describe abdominal aortic aneurysms
``` 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
What are the complications of AAA?
Rupture and hemorrhage Occlusion of branching aa and downstream ischemia Embolism Impingement on another surface
62
What is the rupture risk related to?
``` Size Less than 4 cm: negligible 4-5 cm: 1% 5-6 cm: 11% greater: 25% manage surgically ```
63
describe inflammatory AAAs?
5-10% of AAAs Younger pts Exuberant transmural lymphoplasmacytic infiltrate and dense periaortic fibrosis IgG4
64
What are thoracic aortic aneurysms often due to?
HTN, | Less commonly - congenital defect in CT synthesis (marfans)
65
Clinical presentation of thoracic aortic aneurysm often due to ....
Impingement of lower respiratory tree, esophagus, RLN Aortic valvular insufficiency Rupture
66
What are the signs and symptoms of thoracic aortic aneurysm?
Dyspnea, dysphagia, cough, vertebral pain
67
Aortic dissection occurs in what type of pts?
HTN males, 40-60 Pts with disorder of vessel CT - marfans Primary risk factor is HTN
68
What is the classic presentation of aortic dissection?
Sever chest pain, radiating to the back, between the scapulae Ascending aorta
69
Why is dissection uncommon in atherosclerosis?
Fibrous tissue limits dissection propagation | Any condition with medial scarring
70
Morphology of aortic dissection
Cystic medial degeneration; often wo accompanying inflammation
71
Type A dissections
``` 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
Type B dissections
Dissection after great vessels, descending aorta

CVM II (4 decks)

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