Blood Vessels Pt. 1 Flashcards
1
Q
What are the three concentric layers of a blood vessel?
A
- Intima (single layer endothelium)
- Media (smooth muscle layers)
- Adventitia (most external, has vasa vasorum)
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
3
Q
Where are valves located?
A
in veins only
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
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
6
Q
What is arteriovenous shunting?
A
arteries -> veins without intervening capillaries
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
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
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
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
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
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
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
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
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
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
17
Q
What are the neurologic causes of HTN she wants us to know?
A
sleep apnea, acute stress (including surgery)
18
Q
What is blood pressure a function of?
A
cardiac output and peripheral vascular resistance
19
Q
How do you measure cardiac output?
A
HR x SV
20
Q
What is vascular resistance?
A
regulated at level or arterioles, influenced by neural and hormonal inputs
21
Q
What does Angiotensin converting enzyme (ACE) do?
A
Cleaves Angiotensin 1 -> angiotensin 2
22
Q
What does renin do?
A
Cleaves angiotensinogen -> angiotensin 1
23
Q
What does atrial natriuretic peptide (ANP) do?
A
causes sodium excretion/diuresis, as well as vasodilation -> lowers BP
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
25
What is hyperplastic arteriosclerosis?
- 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
26
What is often described as having a flea bitten appearance?
malignant HTN, numerous variegated hemorrhages in the kidney capsule
27
What is arteriosclerosis?
hardening of the arteries
- arterial wall thickening, loss of elasticity
- small arteries and arterioles, may cause downstream ischemic injury
28
What is Monckeberg medial sclerosis?
>50 years old, calcification of muscular arteries, internal elastic memberane involved, NO lumen narrowing, NO clinical significance
29
What is the most important/frequent clinically important pattern of atherosclerosis?
"gruel" and "hardening"
30
What is atherosclerosis?
underlies the pathogenesis of coronary (MI), cerebral (stroke) and peripheral vascular disease
- extremely common (approx half of all deaths)
31
What is atheroma? and what is it also called?
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
What is the effect of estrogen on atherosclerosis?
premenopausal women are somewhat protected is estrogen started early in menopause, otherwise no benefit
33
What is a major risk factor for atherosclerosis?
hypercholesterolemia, even in the absence of other factors is sufficient to initiate lesion development
34
What is metabolic syndrome?
associated with central obesity
| - insulin resistance, HTN, dyslipidemia (increase in LDL), hypercoagulability and pro-inflammatory state
35
What are the 4 nonmodifiable risk factors of atherosclerosis?
1. genetic abnormalities
2. family history
3. increasing age
4. male gender
36
What are the 5 modifiable risk factors for atherosclerosis?
1. hyperlipidemia
2. HTN
3. cigarette smoking
4. diabetes (incidence of MI 2x higher)
5. inflammation
37
How does C-reactive protein predict cardiovascular risk?
the higher levels of CRP, the higher the percent of 10 year risk
38
Where do most lesions tend to occur in the endothelium?
at openings of exiting vessels, branch points, posterior abdominal aorta
- due to flow disturbances normally seen in these locations
Aka: hemodynamic turbulence
39
Where do circulating lipids accumulate?
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
What does accumulation of cholesterol crystals in macrophages lead to?
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
What growth factors are implicated in smooth muscle cell proliferation?
Platelet derived growth factor, macrophages, endothelial cells, fibroblast growth factor, transforming growth-factor-a (TGFa)
42
What happens to a soft, fibrofatty plaque over time?
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
What are the major complications of atherosclerotic plaques?
- rupture and ulceration (may lead to thrombus)
- hemorrhage (may follow plaque rupture)
- embolism (may follow plaque rupture)
- aneurysm formation
44
What is critical stenosis?
when the lumen of the affected vessel reaches approx 70% occlusion, may lead to chronic ischemia of myocardium, bowel, brain or extremities
45
What is acute plaque change?
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
What is am emboli composed of?
fat droplets, nitrogen bubbles, atherosclerotic debris (cholesterol emboli), tumor fragments, bone marrow, or foreign bodies
47
What can plaque inflammation cause?
it can accelerate fibrous cap degeneration and inhibit its resynthesis, thus decreasing collagen in the cap and weakening it
48
What is a true aneurysm?
Aka saccular, is an intact, but thinned muscular wall at the site of dilation
49
What is a false aneurysm?
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
When do you see an arterial dissection?
it arises when blood enters a defect in the arterial wall and tunnels between its layers
- are often, but not always aneurysmal
51
What are the three important topics of aneurysm pathogenesis?
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
What is obliterative endarteritis?
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
What is cystic medial degeneration?
loss of vascular wall elastic tissue, or ineffective elastin synthesis whihc leads to disrupted and disorganized elastin filaments and increased ground substance (proteoglycans)
54
What is cystic medial degeneration the final common result of?
ischemic medial damage and Marfan syndrome
55
What are the two most important causes of aortic aneurysms?
atherosclerosis and HTN
56
What typically causes an abdominal aortic aneurysm?
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
What are the characteristics of an AAA?
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
What are some complications of an AAA?
- rupture and hemorrhage
- occlusion of branching arteries and downstream ischemia
- embolism
- impingement on another structure
59
What is the AAA rupture risk if greater than 6cm?
25%, rupture risk is related to size
60
What causes a thoracic aortic aneurysm?
HTN, or less commonly congenital defect in connective tissue synthesis (Marfans)
61
What is inheritance pattern of Marfans?
AD, genetic disorder resulting in defective synthesis of fibrillin FBN1 gene, that leads to abnormal TGFb activity that weakens elastic tissue
62
What is the clinical presentation of a thoracic aortic aneurysm?
impingement of
- lower respiratory tree
- esophagus
- recurrent laryngeal nerves
- aortic valve insufficiency
- rupture
63
When do you see an aortic dissection?
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
What is the primary risk factor for an aortic dissection?
HTN
65
***What is the classic presentation of an aortic dissection?
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
What is the pathogenesis of an aortic dissection?
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
What happens with a dissection ruptures through the adventitia?
massive hemorrhage or cardiac tamponade (hemorrhage in pericardial sac)
68
What happens if a dissecting hematoma reenters the lumen of the aorta through a second distal intimal tea,?
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
What is a type A dissection?
involving the ascending aorta, is more common and associated with higher morbidity and mortality
70
What is the most common cause of death for dissections?
rupture
71
How do you treat Type A dissections?
antihypertensive therapy and surgical repair
72
What is the Stanford classification?
scheme divides dissections into type A and B
| Type A involves ascending aorta, Type B does not
