vessel pathology Flashcards
large aa
aka elastic
aorta, its large brr, and pulmonary aa
medium sized aa
aka muscular
other brr of aorta
small aa
< 2mm in diameter
vasa vasorum
small aa that feed medium and large aa
in outer 1/2-2/3 medulla
arterioles
20-100um
w/in substance of tissues and organs
veins
venous valves in extremities large diameter large lumen 2/3 of all the blood is in vv thin less well organized walls
post capillary venules
site of leukocyte exudation and vascular leakage
capillaries
approximately he diameter of red blood cell or larger
endothelial cell lining (no media)
surrounded by pericytes
rapid exchange of diffusible substances
lymphatics
endothelial cell lining (no media)
valves in larger lymph vessels
endothelial cells
contain weibel palade bodies
junctions normally impermeable to large molecules
weibel-palade bodies
membrane bound storage organelles that contain vWF
anticoagulant, antithrombotic, fribrinolytics from endothelium
prostacyclin
thrombomodulin
heparin-like molecules
plasminoen activator
prothrombotics from endothelium
vWF
TF
Plasminogen activator inhibitor
modulators of blood flow from endothelium
vasoconstrictors (endothelin, ace)
vasodilators (NO, prostacyclin)
regulators of inflammation and immunity from endothelium
IL1, IL6, chemokines
adhesion molecules( VCAM-1, ICAM, E-selectin, P-selectin)
histocompatilibility Ags
regulators of cell growth from endothelium
stimulators (PDGF, CSF, FGF)
inhibitors (heparin, TGFbeta)
other functions of endothelium
maintenance of permeability
oxidation of LDL
vascular smooth mm
vasoconstriction and dilation
GFs and cytokines
migrate to intima and proliferate following injury
synthesize collagen, elastin, and proteoglycans
can have phagocytic activity
berry aneurysms
aka congenital or berry
2% of autopsies
most in circle of willis
saccular type aneurysm in aa
arteriovenous fistulas
rare abnormal communications btwn aa and vv
most congenital, some produces
short-circuit blood and caue heart to pump additional volume
accelerated HTN
end organ damage
malignant HTN
accelerated plus papilledema
renal causes of HTN
acute glomerulonephritis chronic renal disease polycystic disease renal aa stenosis renal vasculitis renin-producing tumor
endocrine causes of HTN
cushings primary aldosteronism congenital adrenal hyperpalsia licorice exogenous hormones pheochromocytoma acromegaly hypo/hyper thyroidism pregnancy
CV causes of HTN
coarctation of aorta polyarteritis nodosa increased intravascular volume increased CO rigidity of aorta
neurologic causes of HTN
phychogenic
increased intracranial pressure
sleep apnea
acute stress, inducing surgery
liddle syndrome
moderatly severe salt sensitive HTN due to increased distal tubular reabsorption of NA due to over reaction to aldosterone stimulation
3 patterns of arteriosceloris
monckeberg medial cacific scleriosis
arterioloscerosis
atherosclerosis
monckeberg medial calcific sclerosis
in mm aa w/no vessel lumen narrowing and ossify
arteriolosclerosis
in small aa and arterioles
hyaline arterolosclerosis or hyperplastic arterioloscerlosis
hyaline arteriolosclerosis
protein deposition (hyalinized) seen in aging, DM, benign nephrosclerosis, HTN
hyperplastic arterilosclerosis
cell death
onion skinning
+/- necrotizing arteriolitis
seen in malignant HTN
non modifiable risk factors for atherosclerosis
genetics
family Hx
increasing age
male gender
modifiable risk factors for atherosclerosis
hyperlipidemia HTN cigarette smoking DM inflammation
metabolic syndrome
obesity, dyslipedemia, HTn, and insulin resistance
can also have hypercoagulability and inflammatory state
class II LDLR mutations
most common
receptor protein transport form ER to golgi impaired due to abnormal protein folding
lipoprotein a
associated w/higher risk of coronary and cerebrovascular disease
elevated plasminogen activator inhibitor 1
strong predictor of risk for major atherosclerotic events
acute phase reactant
synthesized primarily by the liver
opsonizes bacteria and activating C’
predicts the risk of MI, stroke, peripheral arterial disease, and sudden cardiac death
lowering CRP itself does not decrease risk
smoking cessation, weight loss, statins, and exercise all reduce CRP
infections which may contribute to atherosclerosis
chlamydia pneumoniae, herpesvirus, and cytomegalovirus
COX 1 inhibitors
aspirin
preferentially inhibits COX1 at low doses
blocks thromboxane and increases prostacyclins
COX2 inhibitors
NSAIDS
blocks prostacyclins and increases thromboxanes
abdominal aneurysms
atherosclerosis
M>F, smokers, 50+
thoracic aneurysms
HTN
other causes of aneurysms
marfans, loeys-dietz, ehlers-danos, scurvey, trauma, congenital defects, syphiils and vasculitides
mycotic aneuysms
infections
from embolization of spetic embolus (infective endocarditis)
from extension of adjacent suppurative process
from circulating organisms infecting arterial wall
true aneuysms
bounded by arterial wall component or myocardium
sacular aneurysm
appears rounded
fusiform aneurysm
ivolvoes long segment of a and is not rounded
false aneurysm
aka pedudoaneurysm
hematoma secondary to trasmural rupture
inflamatory abdominal aortic aneurysm
5-10%
rich in lymphocytes, plasma cells, and macrophages
often giant cells
cause uncertain, usually occur at younger age
mycotic abdominal aortic aneurysms
atherosclerotic AAA that have become infected
salmonella gastroenteritis
risk of rupture
6cm 25%
greater then 5cm surgically repaired
obliterative endarteritis
tertiary stage of syphilis (leus) involces vasa vasorum (arterioles) of thoracic aorta
syphilitic aortits
obliterative endarteritis of vasa -> ischemic injury of media -> loss of medial elastic fibuers and mm cells
can lead to aneurysmal dilation -> aortic valve imcompetence
tree-barking appearance
aortic dissection
> 90% men
40-60% w/HTN
arteriolosclerosis -> smooth m loss
in younger people may be CT disorder (marfans, ehlers-danlos, scurvey)
can be iatrogenic
rarely associated w/pregnancy
occasionally secondary to vasa vasorum rupture
Debakey I
begins in ascending aorta and extends into descending aorta