Blood Vessels, Part 1 Flashcards
What makes up the intima?
1 layer of endothelial cells.
What is the internal elastic lamina?
It demarcates the intima from the media.
How are A/V oriented in the media?
As are well organized in layers of smooth muscle, while veins are haphazard.
Features of elastic arteries (3)
High elastin content allows expansion during systole, and recoil during diastole.
Propels blood toward organs.
Less compliant w/ age -> increased systolic BP
How is muscle oriented in muscular arteries?
What does this allow them to do?
Circumferentially.
It allows the arteries to contract (constriction) and relax (dilation).
What is the “principal point of physiologic resistance to blood flow”?
Arterioles
What is the formula for resistance?
R = nL/r^4
What is the adventitia?
It is external to the media and usually separated from media by wide external elastic lamina.
What is vasa vasorum?
“Vessels of the vessels”.
What supplies O2 to outer media of large arteries?
Small arterioles
Large elastic, medium-sized muscular arteries, arterioles examples:
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.
3 features of capillaries
Diameter of an RBC
No media
Have pericytes
Resemble small muscle cells.
What causes an aneurysm?
An underlying defect in the media of the vessel.
2 main features of an AVM
Arteriovenous shunting: arteries -> veins w/o intervening capillaries.
Tangle, worm-like vascular channels w/ pulsatile A/V shunting with high BF.
How can large or multiple AVMs lead to cardiac failure?
They may shunt blood from arterial to venous circulation and force the heart to pump additional volume -> high output cardiac failure.
Fibromuscular dysplasia cause:
A focal irregular thickening in medium and large muscular arteries.
Usually arise during development, but can be from trauma.
Berry aneuryms (4)
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.
1/3 of ruptures of a saccular (berry) aneurysm is associated w/:
Increased intracranial pressure -> straining at stool or sexual orgasm.
How many patients die w/ first rupture of a berry aneurysm?
~25-50%
Repeat bleeding is common in survivors.
Mycotic aneurysms can originate from: (3)
Embolization of a septic embolus (usually from infective endocarditis).
An extension of an adjacent suppurative process.
Circulating organisms directly infecting the arterial wall.
What population is most likely to have fibromuscular dysplasia?
Young women. First degree relatives have increased incidence.
What can medial and intimal hyplasia lead to?
Luminal stenosis (example of fibromuscular dysplasia)
What causes renovascular HTN?
Fibromuscular dysplasia of renal as.
What is a classic finding on angiography in fibromuscular dysplasia?
“String of beads” due to attenuation of adjacent media (can develop aneurysms that may rupture).
3 functions of endothelial cells
Nonthrombogenic surface - maintains blood in fluid state.
Modulate SM tone.
Metabolize hormones, regulate inflammation, affect growth of other cell types.
What can occur as a result of endothelial dysfunction?
Proinflammatory and prothrombotic states ensue -> thrombus formation, atherosclerosis, vascular lesions of HTN.
4 features of vascular SM cells
Able to proliferate.
Synthesize collagen, elastin and proteoglycans.
Elaborate GFs and cytokines.
Vasconstriction/dilation.
Intimal thickening is the…
Stereotypical response of a vessel wall to any insult.
How does intimal thickening occur?
Endothelial cell dysfunction/loss –> +SM cell recruitment and proliferation and associated matrix synthesis.
What BP is associated w/ increased risk of atherosclerosis?
Sustained 139/89.
What leads to Secondary HTN?
Underlying renal or adrenal DZ (primary aldosteronism, Cushing syndrome, pheochromacytoma).
What causes HTN secondary to renal a. stenosis?
Increased production of renin from the ischemic kidney. A bruit can often be heard on auscultation of the kidneys.
Essential HTN risk factors
Prevalence and vulnerability increase w/ age.
AAs have highest risk.
What do untreated HTN pts. most often die from?
1/2 from ischemic heart DZ or CHF.
1/3 from stroke.
Malignant HTN
Rapid increase BP -> death within 1-2 years
Pt. usually has underlying essential HTN.
HTN causes degenerative changes in…
The walls of large and medium arteries and can lead to aortic dissection and/or cerebrovascular hemorrhage.
2 types of small blood vessel DZ
Hyaline arteriosclerosis
Hyperplastic arteriosclerosis
Hyaline arteriosclerosis (3)
Increased muscle matrix synthesis.
Plasma protein leakage across damaged endothelium.
Hyaline (pink) thickening of the vessel wall -> luminal narrowing.
What happens in nephrosclerosis due to chronic HTN?
Arteriolar narrowing of hyaline arteriosclerosis -> diffuse impairment of renal blood supply and glomerular scarring.
Occurs in hyperplastic arteriosclerosis
Hyperplastic arteriolosclerosis
Occurs in severe HTN.
SM cells form concentric lamellations (“onion skinning”)-> luminal narrowing.
Necrotizing arteriolitis of renal vessels
In malignant HTN, laminations are accompanied by…
Fibrinoid deposits and vessel wall necrosis (necrotizing arteriolitis), mostly in the kidney.
180/120
Monckeberg medial sclerosis
> 50 yo.
Calcification of muscular arteries.
Internal elastic membrane is involved.
No narrowing and NO clinical significance.
Countries w/ the highest ischeic heart DZ mortality (3)
- Russia
- US
- Japan
Atheroma = atheromatous = atherosclerotic plaque is…
Raised lesion w/ a soft grumous core of lipid covered by a fibrous cap.
How can an atherosclerotic plaque result in an aneurysm?
It can increase the distance from the lumen to the media and lead to ichemic injury and weakening of the vessel wall -> aneurysm.
Risk factors in atherosclerosis have what kind of effect?
Synergistic
What group seems to be protected against atherosclerosis?
How?
Premenopausal women.
Estrogen has a atheroprotective effect.
What can initiate atherosclerosis in the absence of any other factors?
Hypercholesterolemia
How does hemodynamic turbulence occur in atherosclerosis?
Most lesions occur at openings of existing vessels, branches, posterior abdominal aorta -> turbulence.
What is the role of circulating lipids in atheromatous plaques to create the fatty streak?
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”.
What is the process of inflammation in atherosclerosis? (3)
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.
3 GFs in SM proliferation and matrix deposition
PDGF
Fibroblast GF
TGF-alpha
Most frequent/severe sites of involvement of atherosclerosis (5)
- Abdominal aorta
- Coronary As.
- Popliteal As.
- Internal carotid As.
- Circle of Willis
At what point is critical stenosis?
When approx. 70% of vessel is occluded
How does inflammation affect plaque rupture?
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.
True vs. false aneurysm
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”).
2 major complications of atherosclerotic plaques
Rupture and ulceration -> thrombosis (hemorrhage or embolism may follow the rupture).
Aneurysm formation.
An increase of what enzyme is associated with a net degradation of vascular wall CT leading to an aneurysm?
Increase in matrix metalloproteases (MMP)
Which part of the media becomes ischemic in Atherosclerosis and HTN?
Atherosclerosis - inner media
HTN - outer media
Where does tertiary syphilis occur?
Ischemia of the outer media of the thoracic aorta
What is obliterative endarteritis?
What is it characteristic of?
What does it lead to?
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).
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?
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.
What are the 2 most important causes of aortic aneurysms?
Atherosclerosis and HTN
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)
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.
Rupture risk per year of each size of aneurysm:
<4 cm diameter
4-5 cm
5-6 cm
>6 cm
<4 cm diameter: negligible
4-5 cm: 1%
5-6 cm: 11%
>6 cm: 25%
Thoracic aortic aneurysm is usually due to: (2)
What is the clinical presentation often due to? (3)
HTN, or less commonly Marfan’s syndrome.
Impingement (lower RT, esophagus, recurrent laryngeal ns.), aortic valvular insufficiency, rupture.
Marfan’s syndrome is what inheritance?
What is the major pathology?
AD.
Defective synthesis of FBN1 that leads to aberrant TGF-beta activity that weakens elastic tissue.
How does an aortic dissection occur?
When blood enters a defect in the intima and travels through a tissue plane within layers of the aortic media.
What 2 major age groups does aortic dissection occur?
What is the primary risk factor?
What is the classic presentation?
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.
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?
Via an intimal tear and form an intramural hematoma.
Some degree of cystic medial degeneration.
Ascending aorta, within 10 cm of aortic valve.
What happens when an aortic dissection ruptures through the adventitia? (2)
Massive hemorrhage (into thoracic or abdominal cavities) or carciac tamponade (hemorrhage into pericardial sac).
What is a “double-barreled aorta”?
What us their significance?
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.
What “type” of aortic dissection is most common and associated w/ a higher morbidity and mortality?
How are they treated?
Type A.
Anti-hypertensive therapy and an attempt to surgically repair the intimal tear.
Type A vs. Type B dissections are classified based on:
Stanford classification: type A involve ascending aorta and type B do not involve it.
Most common 4 vessels involved in fibromuscular dysplasia:
Renal a.
Carotid a.
Splanchnic a.
Vertebral a.
Describe the RAAS system:
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.
