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97 Cards in this Set

  • Front
  • Back
vascular pathology results in disease via what two primary mechanisms
narrowing or stenosis of vessels or weakening of vessel walls leading to dilation or rupture
ratio of wall thickness to artery size
arteries always have thicker walls than veins, arterial wall thickness diminishes as the vessel becomes smaller, but the ratio is maintained
what separates the intima from the media in arteries
internal elastic lamina
where do the smooth muscles of the media receive nourishment from
vessel lumen
where do smooth muscles of outer parts of the media recieve nourishment from
vasa vasorum
outer limit of the media is characterized by what
external elastic lamina
three classifications of arteries
large elastic, medium sized muscular, and small arteries/ arterioles
what happens to elastic arteries with age
lose elasticity and the vessel expands less readily when under pressure
what is unique about the construction of a capillary
endothelium but no media
metabolically active tissues have what concentration of capillaries
blood from capillaries flows into what
postcapillary venules
what is unique about postcapillary venules
where inflammation and vascular leakage and leukocyte exudation occur
vein wall compared to artery
larger diameter, thinner and less organized walls
fun fact: veins are easily penetrated by tumors and inflammatory processed because of thin walls
dat shit cray
important relationship between lymphatics and pathlogy
pathway for disease dissemination throug transport of bacteria or tumor cells through body
de novo formation of new blood vessels during embryogenesis
formation of new vessels in the mature organism
formation of collateral vessels due to occlusions
developmental or berry anyurisms
cerebral vessels where ruptures can cause severe bleeds
arteriovenous fistulas
where a small direct connection between an artery and a vein bypass intervening capillaries
fibromuscular dysplasia
focal irregular thickeninf of the walls of medium and large arteries
how can tight junctions between loosen
hemodynamic factors (HBP), or vasoactive agents (histamine)
what is the process by which intact endothelial cells can express different functions depending on their pathophysiolgical stimuli
endothelial activation
enothelial cell produced relaxing factor
endothelial cell produced contracting factor
endothelial dysfunction
altered phenotype that impaird vasoreactivity or induces a thrombogenic surface
endothelial dysfunction caused by histamine is unique because
it is reversible
smooth muscle cell growth promoters
PDGF, endothelin 1, thrombin, fibroblast growth factor, IFN y and IL-1
smooth muscle cell growth inhibitors
heparan sulfates, nitric oxide and TGF-B
what stimulates thickening of vascular vessels
vascular injury
what is the newly healing endothelium called
what is the typical response of a vessel to intimal injury
intimal thickening
how are the phenotype of neointimal cells differ from those of intimal cells
neointimal cells do not contract, but have the ability to divide
where are neointimal cells derived from
circulating precursor cells
recurrent vascular injury results in what
a severe thickening of the vascular walls
sustained diastolic BP greater than what is associated with increased risk for atherosclerosis
sustained systolic BP greater than what is associated with increased risk for atherosclerosis
what is one of the major risk factors for hypertension
most common form of hypertension
essential hypertension (essentially idiopathic since there is no real direct cause for it)
most pathologic form of hypertension
accelerated or malignant hypertention - (systolic over 200, diastolic over 120)
sodium intake has a direct relationship with that
blood pressure variation
how to vessels locally protect against tissue hypofusion
autoregulation of constriction and dilation
how does the renin-angiotensin system regulate blood pressure
angiotensin II raises blood pressure by increase of peripheral pressure and blood volume
how does kidney counterbalance vasopressor actions of angiotensin
producing vascular relaxing agents (NO, prostaglandins)
what are natriuretic factors
secreted by atrial and ventricular myocardium in response to volume expansion, induces salt loss and consequently diuresis as well
what specific channel regulates the reabsorption pathway for Na+ with angiotensin and tenin
single gene disorders that affect hypertension
anything that increases aldosterone synthesis
liddle syndrome
mutation in distal endothelial NA receptor that causes a tubular increase in sodium reabsorption
what is one of the most common pathways for the presense of essential hypertension
reduced renal sodium excretion
what is most likely the cause of essential hypertension
results from interactions of mutations or several environmental influences that influence blood pressure
renovascular hypertension
rental artery stenosis causes reduced GFR, more renin release, salt absorption, leads to increased blood volume
hyaline arteriosclerosis
plasma protein leake across weakened endothelial layer that leads to smooth muscle synthesis
hyperplastic arteriosclerosis
occurs in malignant hypertension, characterized by laminated thickening of vascular walls with vessel wall necrosis
affects small arteries and arterioles, can cause down stream ischemia
what are calcific deposits in people older than 50 that may turn to bone but are usually not pathogenic
mockenberg medial sclerosis
intimal lesions that protrude into the vessel lumen via plaques
structure of atherosclerotic plaque
raised lesion with a soft core of lipid covered by a white fibrous cap
fun fact: western life styles increase incidences of of heart disease
stop eating cheeseburgers you fat morons
three major risk factors for atherosclerosis
age, gender, genetics
what ages do instances of MI increase
40 to 60
how does gender relate to MI
premenopausal women are least at risk, postmenopausal women instances of MI actually increase compared to equally matched men
what is the most significant independent factor for MI
high levels of LDL in blood stream
what can raise plasma blood cholesterol levels
high dietary intake of cholesterol and saturated fats
polyunsaturated fats?
lower plasma cholesterol levels
function of statins
lower circulating cholesterol levels by inhibitng HMG-CoA
how does hypertension affect hyperlipidemia
increases it by 60%
how does diabetes mellitus induce hyperlipidemia
glucose cannot be imported into cells, circulates freely in plasma
how does inflammation affect atherosclerosis
inflammation induces CRP - CRP induces loss of thrombogenic layer and induces a prothrombic state
hyperhomosystinemia affect on atherosclerosis
where a low B12 and folic acid level can induce elevated homocystine levels and induce vessel thrombosis
what is the majorly accepted belief on how atherosclerosis forms
response to injury hypothesis
what is the main basis of atherosclerotic plaque development
endothelial injury
importance of hemodynamic disturbances in creation of atherosclerotic plaques
usually form at branch points on blood vessels, where high friction is created
anything that elevates the level of lipds in the blood increases the chances of fatty streak formation in blood vessels
how does increased plasma lipids increase plaque formation
lipids increase local oxygen free radical production, this build up of lipids in the intima causes ingestion of lipids by macrophage scavenger receptors
increase in the amount of scaveneged Lipids in macrophages leads to what
aggregation of foam cells
what two pathologic instances can oxidized ldl produce
induces chemokines for more macrophages and is cytotoxic to endothelium inducing more damage
what is unique about inflammed vascular endothelial cells vs those that are normal
inflammed ones present VICAM 1 on their surface
how is mononucleocyte activation in plaque formation pathologic
initially it is good because it removed lipids, however increased amounts of macrophages recruit more, which induces inflammatory factors, also release ROS
what generates a chronic inflammatory state in growing plaques
t cells
chronic inflammatory state created by t cells induces what
smooth muscle growth proliferation factors
can infections drive vascular damage?
possible, but there is no concrete evidence linking infections to increased atherosclerosis
role of ECM in plaque proliferation
synthesized by recruited smooth muscle cells and stabilizes plaques
PDGF in plaque proliferation
released by platelets, macrophages and proliferating smooth muscle
dynamic lesions consisting od dysfunctional endothelial cells, recruited and proliferating smooth muscle cells and lymphocytes and macrophages,
smooth fibrous cap proliferation
more advanced version of an atheroma that progresses from ECM synthesis
what happens with fibrous cap disruption
degeneration of the underlying media, thrombosis
fatty streaks
lipid filled foamy macrophages that eventually become 1cm or more in length
what differentiates a fatty streak from an atherosclerotic laque
intimal thickening and lipid accumulation
three principle components of an atherosclerotic plaque
1 cells smooth muscle, macrophages and t cells,2 ECM including collagen, elastic fibers and proteoglycans, 3 intracellular and extracellular lipids
what consists of the necrotic core of a plaque
lipids, cellular debris and foam cells
fibrous plaques
consisting entirely of almost nothing but smooth muscle cells and fibrous tissue
eventual fate of atheromas
undergo calcification and make vessel suceptible to rupture, ulceration or erosion
smaller vessel result of atherosclerotic plaques
occlusions, compromising distal circulation
critical stenosis
when a plaque occludes blood flow to cause distal ischemia
types of acute plaque change
rupture fissure, erososion ulceration, hemmorage
plaques that contain thin fibrous caps
vulnerable plaques - likely to rupture easier