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CPR Exam 1 > Blood Vessels Pt. 1 > Flashcards

Blood Vessels Pt. 1 Flashcards

1
Q

What are the three concentric layers of a blood vessel?

A
  1. Intima (single layer endothelium)
  2. Media (smooth muscle layers)
  3. Adventitia (most external, has vasa vasorum)
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2
Q

In arterioles, what is resistance proportional to?

A

resistance to fluid flow is inversely proportional to fourth power of the diameter

-> this affects BP

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3
Q

Where are valves located?

A

in veins only

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4
Q

What is an aneurysm?

A
  • localized abnormal dilation of BV or heart
  • develop over time due to underlying defect in the MEDIA of the vessel

NOTE: they occur at branching points

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5
Q

What is an arteriovenous malformation (AVM)?

A
  • tangled, worm-like vascular channels with prominent pulsatile arteriovenous shunting, high blood flow
  • large or multiple AVMs may shunt blood from arterial to venous circulation (withOUT intervening capillaries), forcing heart to pump additional volume leading to high-output cardiac failure
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6
Q

What is arteriovenous shunting?

A

arteries -> veins without intervening capillaries

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7
Q

What is fibromuscular dysplasia?

A
  • focal irregular thickening in medium and large muscular arteries (renal, carotid, splanchnic and vertebral vessels)
  • usually developmental defect, but can arise from trauma
  • renovascular HTN d/t fibromuscular dysplasia of renal arteries
    • increased incidence in YOUNG WOMEN
    • string of beads appearance
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8
Q

What is a Berry aneurysm?

A
  • happens in the circle of Willis, most commonly found in anterior circulation (90% saccular found near major branch points)
  • “worst headache of my life”
  • most frequent cause of clinically significant subarachnoid hemorrhage
  • 25-50% die with first rupture
  • repeat bleeding common in survivors
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9
Q

What is a mycotic aneurysm?

A

can originate from:

  • embolization of septic embolus, (usually as complication of infective endocarditis)
  • an extension of an adjacent suppurative process (pneumonia or other infection)
  • circulating organisms directly infecting the arterial wall

NOTE: this is the one they worry about when you go to the dentist

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10
Q

How do endothelial cells respond to injury?

A
  • northrombogenic surface: maintain blood in fluid state
  • modulate smooth muscle tone
  • metabolize hormones (angiotensin), regulate inflammation, affect growth of other cell types
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11
Q

How do endothelial cells respond to injury?

A
  • alteration in phenotype, proinflammatory and prothrombogenic
  • initiation of thrombus formation, atherosclerosis and vascular lesions of HTN
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12
Q

How do vascular smooth muscle cells respond to injury?

A
  • normal vascular repair and atherosclerosis**
  • ability to proliferate
  • synthesize collagen, elastin and proteoglycans
  • elaborate growth factors and cytokines
  • vasoconstriction/dilation
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13
Q

What is intimal thickening?

A
  • 1st response, associated with endothelial cell dysfunction, stimulates smooth muscle
  • neointimal smooth muscle cells are motile, undergo cell division, acquire new biosynthetic capabilities
  • healing response results in intimal thickening that never goes away, may impede blood flow
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14
Q

What is secondary HTN?

A

underlying renal or adrenal disease, approx 5% of population

  • primary aldosteronism, Cushings, pheochromocytoma
  • HTN secondary to renal artery stenosis caused by increased production of renin
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15
Q

What is essential HTN?

A

idiopathic, approx 90-95% of population

  • prevalence increases with age, African Americans at increased risk
  • cardiac hypertrophy and heart failure, multi-infarct dementia and renal failure
  • untreated HTN pts, half die of ischemic heart dz, CHF, or stroke
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16
Q

What is malignant HTN?

A

approx 5% rapid increase in BP -> death within 1-2 years

  • systolic BP >200, diastolic >120
  • severe HTN, renal failure, retinal hemorrhage, papilledema
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17
Q

What are the neurologic causes of HTN she wants us to know?

A

sleep apnea, acute stress (including surgery)

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18
Q

What is blood pressure a function of?

A

cardiac output and peripheral vascular resistance

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19
Q

How do you measure cardiac output?

A

HR x SV

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20
Q

What is vascular resistance?

A

regulated at level or arterioles, influenced by neural and hormonal inputs

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21
Q

What does Angiotensin converting enzyme (ACE) do?

A

Cleaves Angiotensin 1 -> angiotensin 2

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22
Q

What does renin do?

A

Cleaves angiotensinogen -> angiotensin 1

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23
Q

What does atrial natriuretic peptide (ANP) do?

A

causes sodium excretion/diuresis, as well as vasodilation -> lowers BP

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24
Q

What is hyaline arteriosclerosis?

A
  • increase smooth muscle matrix synthesis
  • plasma protein leakage across damaged endothelium
  • homogenous pink (hyaline) thickening of vessel wall -> luminal narrowing
  • in nephrosclerosis d/t chronic HTN, arteriolar narrowing of hyaline arteriosclerosis -> diffuse impairment of renal blood supply
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25
Q

What is hyperplastic arteriosclerosis?

A
  • occurs in severe HTN
  • smooth muscle cells form concentric lamellations (onion skin) -> luminal narrowing
  • in malignant HTN, laminations are accompanied by fibrinoid deposits and vessel wall necrosis (necrotizing arteriolitis), esp in kidney
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26
Q

What is often described as having a flea bitten appearance?

A

malignant HTN, numerous variegated hemorrhages in the kidney capsule

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27
Q

What is arteriosclerosis?

A

hardening of the arteries

  • arterial wall thickening, loss of elasticity
  • small arteries and arterioles, may cause downstream ischemic injury
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28
Q

What is Monckeberg medial sclerosis?

A

> 50 years old, calcification of muscular arteries, internal elastic memberane involved, NO lumen narrowing, NO clinical significance

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29
Q

What is the most important/frequent clinically important pattern of atherosclerosis?

A

“gruel” and “hardening”

30
Q

What is atherosclerosis?

A

underlies the pathogenesis of coronary (MI), cerebral (stroke) and peripheral vascular disease
- extremely common (approx half of all deaths)

31
Q

What is atheroma? and what is it also called?

A

Atheroma = atheromatous = atherosclerotic plaque

  • raised lesion with a soft grumous (chunky, thick) core of lipid covered by a fibrous cap
  • can lead to catastrophic obstructive vascular thrombosis is plaque ruptures
  • can increase diffusion distance from the lumen to the media
32
Q

What is the effect of estrogen on atherosclerosis?

A

premenopausal women are somewhat protected is estrogen started early in menopause, otherwise no benefit

33
Q

What is a major risk factor for atherosclerosis?

A

hypercholesterolemia, even in the absence of other factors is sufficient to initiate lesion development

34
Q

What is metabolic syndrome?

A

associated with central obesity

- insulin resistance, HTN, dyslipidemia (increase in LDL), hypercoagulability and pro-inflammatory state

35
Q

What are the 4 nonmodifiable risk factors of atherosclerosis?

A
  1. genetic abnormalities
  2. family history
  3. increasing age
  4. male gender
36
Q

What are the 5 modifiable risk factors for atherosclerosis?

A
  1. hyperlipidemia
  2. HTN
  3. cigarette smoking
  4. diabetes (incidence of MI 2x higher)
  5. inflammation
37
Q

How does C-reactive protein predict cardiovascular risk?

A

the higher levels of CRP, the higher the percent of 10 year risk

38
Q

Where do most lesions tend to occur in the endothelium?

A

at openings of exiting vessels, branch points, posterior abdominal aorta
- due to flow disturbances normally seen in these locations

Aka: hemodynamic turbulence

39
Q

Where do circulating lipids accumulate?

A

in the intima, and then are taken up by macrophages and partially oxidized
- modified LDL further accumulates within macrophages and smooth muscle cells, forming foam cells** and a lesion known as a fatty streak** -> stimulating inflammatory response

40
Q

What does accumulation of cholesterol crystals in macrophages lead to?

A
  1. they are recognized by the inflammasome, leading to IL-1 secretion
  2. more macrophages and T-lymphocytes are recruits
    - cytokines further activate endothelial cells and growth factors stimulate smooth muscle cells to migrate to the intima
    - aggregations eventually lead to an atheromatous plaque
41
Q

What growth factors are implicated in smooth muscle cell proliferation?

A

Platelet derived growth factor, macrophages, endothelial cells, fibroblast growth factor, transforming growth-factor-a (TGFa)

42
Q

What happens to a soft, fibrofatty plaque over time?

A

it becomes covered with a fibrous cap (dense collagen fibers), with a necrotic center, containing lipid, debris, foam cells and thrombus, surrounded by a **zone of inflammatory and smooth muscle cells

43
Q

What are the major complications of atherosclerotic plaques?

A
  • rupture and ulceration (may lead to thrombus)
  • hemorrhage (may follow plaque rupture)
  • embolism (may follow plaque rupture)
  • aneurysm formation
44
Q

What is critical stenosis?

A

when the lumen of the affected vessel reaches approx 70% occlusion, may lead to chronic ischemia of myocardium, bowel, brain or extremities

45
Q

What is acute plaque change?

A

when an acute thrombus forms over the plaque, occluding the artery

  • it may occur secondary to plaque rupture, erosion or ulceration of plaque surface
  • hemorrhage into the plaque may acutely expand its volume
46
Q

What is am emboli composed of?

A

fat droplets, nitrogen bubbles, atherosclerotic debris (cholesterol emboli), tumor fragments, bone marrow, or foreign bodies

47
Q

What can plaque inflammation cause?

A

it can accelerate fibrous cap degeneration and inhibit its resynthesis, thus decreasing collagen in the cap and weakening it

48
Q

What is a true aneurysm?

A

Aka saccular, is an intact, but thinned muscular wall at the site of dilation

49
Q

What is a false aneurysm?

A

Aka pseudo-aneurysm, is a defect through the wall of the vessel or heart, communicating with an extravascular hematoma that freely communicates with the intravascular space (aka pulsating hematoma)

50
Q

When do you see an arterial dissection?

A

it arises when blood enters a defect in the arterial wall and tunnels between its layers
- are often, but not always aneurysmal

51
Q

What are the three important topics of aneurysm pathogenesis?

A
  1. defective vascular wall connective tissue (Marfans)
  2. net degradation of vascular wall connective tissue (atherosclerosis/inflammation -> increase matrix metalloprotease)
  3. weakening of the vascular wall by ischemia
    - atherosclerosis: ischemia of inner media
    - HTN: ischemia of outer media
    - ** tertiary syphilis: ischemia of outer media in the THORACIC AORTA (v specific location)
52
Q

What is obliterative endarteritis?

A

characteristic of late-stage syphilis, shows a predilection for small vessels, including those of the vasa vasorum of the thoracic aorta
- leads to ischemic injury of the aortic media and aneurysmal dilation, which sometimes involves the aortic valve annulus (aortic valve regurgitation)

53
Q

What is cystic medial degeneration?

A

loss of vascular wall elastic tissue, or ineffective elastin synthesis whihc leads to disrupted and disorganized elastin filaments and increased ground substance (proteoglycans)

54
Q

What is cystic medial degeneration the final common result of?

A

ischemic medial damage and Marfan syndrome

55
Q

What are the two most important causes of aortic aneurysms?

A

atherosclerosis and HTN

56
Q

What typically causes an abdominal aortic aneurysm?

A

atherosclerosis

  • they occur in the abdominal aorta, usually below the renal arteries, often involve common iliac arteries
  • more frequent in: men, smokers, 6th decade
57
Q

What are the characteristics of an AAA?

A

severe atherosclerosis of the aorta, cover with mural thrombus

  • may be detected as a pulsating mass in the abdomen
  • *** lines of Zahn (layered thrombus) are hallmark
58
Q

What are some complications of an AAA?

A
  • rupture and hemorrhage
  • occlusion of branching arteries and downstream ischemia
  • embolism
  • impingement on another structure
59
Q

What is the AAA rupture risk if greater than 6cm?

A

25%, rupture risk is related to size

60
Q

What causes a thoracic aortic aneurysm?

A

HTN, or less commonly congenital defect in connective tissue synthesis (Marfans)

61
Q

What is inheritance pattern of Marfans?

A

AD, genetic disorder resulting in defective synthesis of fibrillin FBN1 gene, that leads to abnormal TGFb activity that weakens elastic tissue

62
Q

What is the clinical presentation of a thoracic aortic aneurysm?

A

impingement of

  • lower respiratory tree
  • esophagus
  • recurrent laryngeal nerves
  • aortic valve insufficiency
  • rupture
63
Q

When do you see an aortic dissection?

A

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

  • seen in hypertensive males, aged 40-60
  • also seen in younger pts with CT disorders (Marfans)
64
Q

What is the primary risk factor for an aortic dissection?

A

HTN

65
Q

***What is the classic presentation of an aortic dissection?

A

sudden onset of severe chest pain (usually beginning in anterior chest), radiating to the back between the scapulae and moving downward as the dissection progresses

NOTE: can be confused with AMI

66
Q

What is the pathogenesis of an aortic dissection?

A
  1. blood enters via intimal tear, forming hematoma
    - usually some degree of cystic medial degenration
    - most disections arise in ascending aorta, within 10cm of aortic valve
67
Q

What happens with a dissection ruptures through the adventitia?

A

massive hemorrhage or cardiac tamponade (hemorrhage in pericardial sac)

68
Q

What happens if a dissecting hematoma reenters the lumen of the aorta through a second distal intimal tea,?

A

a new false vascular channel aka double-barreled aorta is created
- this averts a fatal extraaortic hemorrhage, and over time can be endothelialized to become recognizable chronic dissection

69
Q

What is a type A dissection?

A

involving the ascending aorta, is more common and associated with higher morbidity and mortality

70
Q

What is the most common cause of death for dissections?

A

rupture

71
Q

How do you treat Type A dissections?

A

antihypertensive therapy and surgical repair

72
Q

What is the Stanford classification?

A

scheme divides dissections into type A and B

Type A involves ascending aorta, Type B does not

CPR Exam 1 (18 decks)

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