- Shuffle
Toggle OnToggle Off
- Alphabetize
Toggle OnToggle Off
- Front First
Toggle OnToggle Off
- Both Sides
Toggle OnToggle Off
Front
How to study your flashcards.
Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key
Up/Down arrow keys: Flip the card between the front and back.down keyup key
H key: Show hint (3rd side).h key
PLAY BUTTON
PLAY BUTTON
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
|
high
|
|
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
|
|
vasculogenesis
|
de novo formation of new blood vessels during embryogenesis
|
|
angiogenesis
|
formation of new vessels in the mature organism
|
|
arteriogenesis
|
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
|
NO
|
|
endothelial cell produced contracting factor
|
endothelin
|
|
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
|
neointima
|
|
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
|
89
|
|
sustained systolic BP greater than what is associated with increased risk for atherosclerosis
|
139
|
|
what is one of the major risk factors for hypertension
|
atherosclerosis
|
|
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
|
ENaC
|
|
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
|
|
arteriosclerosis
|
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
|
|
atherosclerosis
|
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
|
genetics
|
|
hypercholesterolemia
|
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
|
|
dyslipoprotenemias
|
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
|
|
atheroma
|
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
|
