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CPR II Exam #1 > Blood Vessels, Part 1 > Flashcards

Blood Vessels, Part 1 Flashcards

1
Q

What makes up the intima?

A

1 layer of endothelial cells.

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2
Q

What is the internal elastic lamina?

A

It demarcates the intima from the media.

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3
Q

How are A/V oriented in the media?

A

As are well organized in layers of smooth muscle, while veins are haphazard.

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4
Q

Features of elastic arteries (3)

A

High elastin content allows expansion during systole, and recoil during diastole.
Propels blood toward organs.
Less compliant w/ age -> increased systolic BP

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5
Q

How is muscle oriented in muscular arteries?

What does this allow them to do?

A

Circumferentially.

It allows the arteries to contract (constriction) and relax (dilation).

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6
Q

What is the “principal point of physiologic resistance to blood flow”?

A

Arterioles

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7
Q

What is the formula for resistance?

A

R = nL/r^4

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8
Q

What is the adventitia?

A

It is external to the media and usually separated from media by wide external elastic lamina.

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9
Q

What is vasa vasorum?

A

“Vessels of the vessels”.

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10
Q

What supplies O2 to outer media of large arteries?

A

Small arterioles

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11
Q

Large elastic, medium-sized muscular arteries, arterioles examples:

A

Large elastic: aorta and its major branches -> common carotid, iliac, pulmonary As.
Medium-sized muscular: smaller branches of aorta -> coronary and renal.
Arterioles: within tissues and organs.

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12
Q

3 features of capillaries

A

Diameter of an RBC
No media
Have pericytes

Resemble small muscle cells.

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13
Q

What causes an aneurysm?

A

An underlying defect in the media of the vessel.

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14
Q

2 main features of an AVM

A

Arteriovenous shunting: arteries -> veins w/o intervening capillaries.
Tangle, worm-like vascular channels w/ pulsatile A/V shunting with high BF.

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15
Q

How can large or multiple AVMs lead to cardiac failure?

A

They may shunt blood from arterial to venous circulation and force the heart to pump additional volume -> high output cardiac failure.

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16
Q

Fibromuscular dysplasia cause:

A

A focal irregular thickening in medium and large muscular arteries.

Usually arise during development, but can be from trauma.

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17
Q

Berry aneuryms (4)

A

Occurs in Circle of Willis.
Presents as a horrible headache.
Usually found near major branch points of anterior circulation.
Most common cause of subarachnoid hemorrhage.

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18
Q

1/3 of ruptures of a saccular (berry) aneurysm is associated w/:

A

Increased intracranial pressure -> straining at stool or sexual orgasm.

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19
Q

How many patients die w/ first rupture of a berry aneurysm?

A

~25-50%

Repeat bleeding is common in survivors.

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20
Q

Mycotic aneurysms can originate from: (3)

A

Embolization of a septic embolus (usually from infective endocarditis).

An extension of an adjacent suppurative process.

Circulating organisms directly infecting the arterial wall.

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21
Q

What population is most likely to have fibromuscular dysplasia?

A

Young women. First degree relatives have increased incidence.

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22
Q

What can medial and intimal hyplasia lead to?

A

Luminal stenosis (example of fibromuscular dysplasia)

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23
Q

What causes renovascular HTN?

A

Fibromuscular dysplasia of renal as.

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24
Q

What is a classic finding on angiography in fibromuscular dysplasia?

A

“String of beads” due to attenuation of adjacent media (can develop aneurysms that may rupture).

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25
Q

3 functions of endothelial cells

A

Nonthrombogenic surface - maintains blood in fluid state.

Modulate SM tone.

Metabolize hormones, regulate inflammation, affect growth of other cell types.

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26
Q

What can occur as a result of endothelial dysfunction?

A

Proinflammatory and prothrombotic states ensue -> thrombus formation, atherosclerosis, vascular lesions of HTN.

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27
Q

4 features of vascular SM cells

A

Able to proliferate.

Synthesize collagen, elastin and proteoglycans.

Elaborate GFs and cytokines.

Vasconstriction/dilation.

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28
Q

Intimal thickening is the…

A

Stereotypical response of a vessel wall to any insult.

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29
Q

How does intimal thickening occur?

A

Endothelial cell dysfunction/loss –> +SM cell recruitment and proliferation and associated matrix synthesis.

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30
Q

What BP is associated w/ increased risk of atherosclerosis?

A

Sustained 139/89.

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31
Q

What leads to Secondary HTN?

A

Underlying renal or adrenal DZ (primary aldosteronism, Cushing syndrome, pheochromacytoma).

32
Q

What causes HTN secondary to renal a. stenosis?

A

Increased production of renin from the ischemic kidney. A bruit can often be heard on auscultation of the kidneys.

33
Q

Essential HTN risk factors

A

Prevalence and vulnerability increase w/ age.

AAs have highest risk.

34
Q

What do untreated HTN pts. most often die from?

A

1/2 from ischemic heart DZ or CHF.

1/3 from stroke.

35
Q

Malignant HTN

A

Rapid increase BP -> death within 1-2 years

Pt. usually has underlying essential HTN.

36
Q

HTN causes degenerative changes in…

A

The walls of large and medium arteries and can lead to aortic dissection and/or cerebrovascular hemorrhage.

37
Q

2 types of small blood vessel DZ

A

Hyaline arteriosclerosis

Hyperplastic arteriosclerosis

38
Q

Hyaline arteriosclerosis (3)

A

Increased muscle matrix synthesis.
Plasma protein leakage across damaged endothelium.
Hyaline (pink) thickening of the vessel wall -> luminal narrowing.

39
Q

What happens in nephrosclerosis due to chronic HTN?

A

Arteriolar narrowing of hyaline arteriosclerosis -> diffuse impairment of renal blood supply and glomerular scarring.

Occurs in hyperplastic arteriosclerosis

40
Q

Hyperplastic arteriolosclerosis

A

Occurs in severe HTN.
SM cells form concentric lamellations (“onion skinning”)-> luminal narrowing.

Necrotizing arteriolitis of renal vessels

41
Q

In malignant HTN, laminations are accompanied by…

A

Fibrinoid deposits and vessel wall necrosis (necrotizing arteriolitis), mostly in the kidney.

180/120

42
Q

Monckeberg medial sclerosis

A

> 50 yo.
Calcification of muscular arteries.
Internal elastic membrane is involved.
No narrowing and NO clinical significance.

43
Q

Countries w/ the highest ischeic heart DZ mortality (3)

A
  1. Russia
  2. US
  3. Japan
44
Q

Atheroma = atheromatous = atherosclerotic plaque is…

A

Raised lesion w/ a soft grumous core of lipid covered by a fibrous cap.

45
Q

How can an atherosclerotic plaque result in an aneurysm?

A

It can increase the distance from the lumen to the media and lead to ichemic injury and weakening of the vessel wall -> aneurysm.

46
Q

Risk factors in atherosclerosis have what kind of effect?

A

Synergistic

47
Q

What group seems to be protected against atherosclerosis?

How?

A

Premenopausal women.

Estrogen has a atheroprotective effect.

48
Q

What can initiate atherosclerosis in the absence of any other factors?

A

Hypercholesterolemia

49
Q

How does hemodynamic turbulence occur in atherosclerosis?

A

Most lesions occur at openings of existing vessels, branches, posterior abdominal aorta -> turbulence.

50
Q

What is the role of circulating lipids in atheromatous plaques to create the fatty streak?

A

Most are cholesterol and cholesterol esters and accumulate in the intima where they are taken up by Mo and partially oxidized -> LDL.
Modified LDL accumulates in MO and SM cells and lead to foam cells -> “fatty streak”.

51
Q

What is the process of inflammation in atherosclerosis? (3)

A

Accumulation of cholesterol crystals in Mo is recognized by the inflammasome -> IL-1 secretion.
IL-1 -> + Mo and T cells.
Inflammatory cytokines further activate endothelial cells and GFs that stimulate SM cells to migrate into the intima and proliferate.

52
Q

3 GFs in SM proliferation and matrix deposition

A

PDGF
Fibroblast GF
TGF-alpha

53
Q

Most frequent/severe sites of involvement of atherosclerosis (5)

A
  1. Abdominal aorta
  2. Coronary As.
  3. Popliteal As.
  4. Internal carotid As.
  5. Circle of Willis
54
Q

At what point is critical stenosis?

A

When approx. 70% of vessel is occluded

55
Q

How does inflammation affect plaque rupture?

A

The fibrous cap is constantly degraded and resynthesized. Increased inflammation in the plaque can accelerate fibrous cap degredation and inhibit its re-synthesis -> decreasing the collagen content and weakening it.

56
Q

True vs. false aneurysm

A

True - an intact, but thinned muscular wall at the site of dilation.

False - there is a defect through the wall of the vessel, or heart, that communicates with an extravascular hematoma (“pulsating hematoma”).

57
Q

2 major complications of atherosclerotic plaques

A

Rupture and ulceration -> thrombosis (hemorrhage or embolism may follow the rupture).

Aneurysm formation.

58
Q

An increase of what enzyme is associated with a net degradation of vascular wall CT leading to an aneurysm?

A

Increase in matrix metalloproteases (MMP)

59
Q

Which part of the media becomes ischemic in Atherosclerosis and HTN?

A

Atherosclerosis - inner media

HTN - outer media

60
Q

Where does tertiary syphilis occur?

A

Ischemia of the outer media of the thoracic aorta

61
Q

What is obliterative endarteritis?

What is it characteristic of?

What does it lead to?

A

It is a predilection for small vessels, including the vasa vasorum or the thoracic aorta.

Characteristic of late-stage syphilis.

Leads to ischemic injury or the aortic media and aneurysmal dilation, and may involve the aortic valve annulus (aortic valve regurg).

62
Q

What causes cystic medial degeneration?

What is the outcome of cystic medial degeneration on a molecular level?

Cystic medial degeneration is a final common result of which main 2 conditions?

A

Loss of vascular wall elastic tissue, or ineffective elastin synthesis.

Disrupted and disorganized elastin filaments and increased ground substance (proteoglycans).

Ischemic medial damage and Marfan syndrome.

63
Q

What are the 2 most important causes of aortic aneurysms?

A

Atherosclerosis and HTN

64
Q

Abdominal aortic aneurysm (AAA) is due to:

Where does it occur?

In what patients is it most common?

What is it characterized by? (2)

How can it be detected?

What are some complications? (4)

A

Atherosclerosis.

Usually below renal as. and often involve the common iliac as.

Men, smokers, 6th decade of life.

Characterized by severe atherosclerosis of aorta, covered in mural thrombus.

Detected as a pulsating mass in the abdomen.

Rupture, hemorrhage, occlusion of branching as. and downstream ischemia.

65
Q

Rupture risk per year of each size of aneurysm:

<4 cm diameter
4-5 cm
5-6 cm
>6 cm

A

<4 cm diameter: negligible
4-5 cm: 1%
5-6 cm: 11%
>6 cm: 25%

66
Q

Thoracic aortic aneurysm is usually due to: (2)

What is the clinical presentation often due to? (3)

A

HTN, or less commonly Marfan’s syndrome.

Impingement (lower RT, esophagus, recurrent laryngeal ns.), aortic valvular insufficiency, rupture.

67
Q

Marfan’s syndrome is what inheritance?

What is the major pathology?

A

AD.

Defective synthesis of FBN1 that leads to aberrant TGF-beta activity that weakens elastic tissue.

68
Q

How does an aortic dissection occur?

A

When blood enters a defect in the intima and travels through a tissue plane within layers of the aortic media.

69
Q

What 2 major age groups does aortic dissection occur?

What is the primary risk factor?

What is the classic presentation?

A

HTN males 40-60
Younger pts. w/ vessel CT DZs (Marfan’s)

HTN.

Sudden onset of severe chest pain (usually beginning anterior) and radiating to the back between scapulae and moves downwards. Can be confused w/ AMI.

70
Q

How does blood enter the aortic wall in an aortic dissection?

It usually occurs in hypertensive pts. w/ some degree of:

Where do most dissections occur?

A

Via an intimal tear and form an intramural hematoma.

Some degree of cystic medial degeneration.

Ascending aorta, within 10 cm of aortic valve.

71
Q

What happens when an aortic dissection ruptures through the adventitia? (2)

A

Massive hemorrhage (into thoracic or abdominal cavities) or carciac tamponade (hemorrhage into pericardial sac).

72
Q

What is a “double-barreled aorta”?

What us their significance?

A

It occurs when the dissecting hematoma re-enters the lumen through a second distal intimal tear and creates a false vascular channel.

It averts a fatal hemorrhage and over time these channels can be endothelialized to become recognizable chronic dissections.

73
Q

What “type” of aortic dissection is most common and associated w/ a higher morbidity and mortality?

How are they treated?

A

Type A.

Anti-hypertensive therapy and an attempt to surgically repair the intimal tear.

74
Q

Type A vs. Type B dissections are classified based on:

A

Stanford classification: type A involve ascending aorta and type B do not involve it.

75
Q

Most common 4 vessels involved in fibromuscular dysplasia:

A

Renal a.
Carotid a.
Splanchnic a.
Vertebral a.

76
Q

Describe the RAAS system:

A

When BP is low, kidneys release renin.
Renin converts Angiotensinogen to Angiotensin I.
Angiotensin I is converted to Angiotensin II via ACE.
Angiotensin II may activate Aldosterone to influence BP.

CPR II Exam #1 (30 decks)

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