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Flashcards in Vascular Pathology 1 Deck (39)
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Berry aneurysms

Typically found in the Circle of Willis

Associated with AD polycystic kidney disease

Rupture can cause fatal subarachnoid hemorrhage


Arteriovenous fistulas

artery --> vein

most commonly a developmental defect, may arise secondary to inflammation, trauma, rupture

may lead to rupture and hemorrhage, or to high-output cardiac failure


Fibromuscular dysplasia

Focal thickening of intima and media of middle to large muscular arteries, resulting in stenosis


Vascular response to injury - endothelial cell activated state

Turbulent blood flow
Complement, bacterial products, lipid products, glycation end products
Hypoxia, acidosis
Components of tobacco smoke

Characterized by expression of:
Adhesion molecules
procoagulants and anticoagulants
vasoactive factors, growth factors


Endothelial dysfunction

prolonged activated state

characterized by:
pro coagulation
pro inflammation
smooth muscle stimulation


Vascular injury

loss of endothelial cells secondary to tissue damage or prolonged endothelial dysfunction

Response: intimal thickening
-smooth muscles cells from the media migrate to the intima, where they proliferate and elaborate ECM
-Intima thickened, potentially affecting blood flow in that vessel

Vascular intimal thickening seen in response to any injury to the vessel, regardless of cause


HTN is a risk factor for:

Atherosclerosis, aortic dissection
Hypertensive heart disease
Hypertensive renal disease


Factors that alter cardiac output

Blood volume - sodium, mineralocorticoids, ANP

Cardiac factors - HR, contractility


Factors impacting peripheral resistance

Humoral factors:
Constrictors: AngII, catecholamines, thromboxane, leukotrienes, endothelin
Dilators: prostaglandins, kinins, NO

Neural factors
Constrictors: alpha-adrenergic
Dilators: beta-adrenergic

Local factors: auto regulation, pH, hypoxia



released by juxtaglomerular cells in afferent arterioles in the kidney in states of low volume or low peripheral resistance, or decreased GFR

Cleaves angiotensinogen to angiotensin I


Angiotensin II

ACE converts angiotensin I to angiotensin II

short lived vasoconstrictor

stimulates adrenal cortex release of aldosterone - renal reabsorption of Na+ and water

Resistance and volume increased, raising BP


Atrial natriuretic peptide

released by myocardial cells in response to volume expansion.

Leads to Na+ excretion and diuresis as well as vasodilation --> lower BP


Hyaline arteriolosclerosis

Increased smooth muscle matrix synthesis

Plasma protein leakage across damaged endothelium

Homogenous pink (hyaline) thickening of the vessel wall, with associated luminal narrowing


Hyperplastic arteriolosclerosis

Occurs in severe hypertension
Smooth muscle cells form concentric lamellations ("onion skinning") with resultant luminal narrowing


Constitutional risk factors for Atherosclerosis

family hx


Modifiable risk factors (major) for Atherosclerosis

Hyperlipidemia (especially LDL)


Minor modifiable risk factors for Atherosclerosis

Metabolic syndrome


Response to injury model for atherosclerosis pathogenesis

chronic injury and/or dysfunction of endothelium, leading to chronic inflammation and attempting to repair the tissue

1) chronic endothelial injury due to: hyperlipidemia, HTN, smoking, homocysteine, hemodynamic factors, toxins, viruses, immune reactions

2) Endothelial dysfunction (increased permeability leukocyte adhesion), monocyte adhesion and emigration

3) macrophage activation, sm.m. recruitment

4) macrophages and sm.m. cells engulf lipid

5) Sm.m. proliferation, collagen and other ECM deposition, extracellular lipid


Fibrofatty atheroma characteristics

Fibrous cap - smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, neovascularization

Necrotic center - cell debris, cholesterol crystals, foam cells, calcium



Hemodynamic turbulence associated with endothelial injury and dysfunction in the pathogenesis of atherosclerosis

◦ Atherosclerosis does not occur randomly in vessels, nor does it occur everywhere uniformly

◦ Most lesions tend to occur at openings of exiting vessels, branch points, posterior abdominal aorta—due to flow disturbances normally seen in these locations


Circulating lipids associated with endothelial injury and dysfunction in the pathogenesis of atherosclerosis

◦ Lipids in atheromatous plaques are predominantly cholesterol and cholesterol esters

◦ Accumulate in the intima, are taken up by macrophages and partially oxidized

◦ This modified LDL further accumulates within macrophages and smooth muscle cells, forming foam cells and a lesion known as a “fatty streak”

◦ This stimulates an inflammatory response to accumulation of this toxic form of LDL


Inflammation in the pathogenesis of atherosclerosis

◦ Accumulation of cholesterol crystals within macrophages is recognized by the inflammasome, which leads to IL-1 secretion

◦ More macrophages and T-lymphocytes are recruited and activated

◦ Inflammatory cytokines further activate endothelial cells, and growth factors stimulate smooth muscle cells to migrate to the intima and proliferate


Smooth muscle proliferation and matrix deposition in the pathogenesis of atherosclerosis

◦ Proliferating smooth muscle cells synthesize extracellular matrix, including collagen

◦ Due to the intimal expansion from foam cells and extracellular lipid, recruited inflammatory and smooth muscle cells and increased ECM, an atheromatous plaque is formed

◦ Over time, a soft fibrofatty plaque becomes covered with a fibrous cap (dense collagen fibers). The center of the plaque is necrotic, containing lipid, debris, foam cells and thrombus, surrounded by a zone of inflammatory and smooth muscle cells.


Atherosclerosis - Common sites of involvement

In decreasing order of frequency/severity of involvement: ◦ Abdominal aorta
◦ Coronary arteries
◦ Popliteal arteries
◦ Internal carotid arteries
◦ Circle of Willis


Complications of atherosclerotic plaques

Rupture and ulceration
◦ May lead to thrombosis

◦ May follow plaque rupture

◦ May follow plaque rupture

Aneurysm formation


Stenosis of the arterial lumen in atherosclerosis

◦ Plaques tend to continually grow because of repeated cycling through the injury-healing process

◦ The lumen of the affected vessel gradually shrinks, eventually leading to ischemia downstream (a point known as critical stenosis – approximately 70% occluded)

◦ This may lead to chronic ischemia of myocardium, bowel, brain, the extremities, etc.


Acute plaque change

An acute thrombus may form over the plaque, occluding the artery. This may occur secondary to
◦ Rupture of the plaque
◦ Erosion or ulceration of the plaque surface

Hemorrhage into the plaque may acutely expand its volume


Factors making some plaques more prone to rupture than others

◦ The fibrous cap is continually being degraded and resynthesized (remodeled)

◦ Increased inflammation in the plaque can accelerate fibrous cap degradation and inhibit its resynthesis, thus reducing the amount of collagen in the cap and weakening it

◦ Physical stresses can cause plaque rupture
-Changes in blood pressure



Localized abnormal dilation of a blood vessel or the heart that may be congenital or acquired


True vs false aneurysm

True: characterized by an intact, but thinned, muscular wall at the site of the dilation

False: defect through the wall of the vessel or heart, communicating with an extravascular hematoma