Pathology of Vessels Flashcards
what are the mechanisms of edema formation (4)
- vascular permeability increased
- intravascular hydrostatic pressure increased
- intravascular oncotic pressure decreased
- lymphatic drainage decreased
how does increased vascular permeability increased
inflammation or immunologic stimuli
mediators (histamine, bradykinin, leukotrines)
endothelial cell contraction then retraction
fluid into interstitial space
how does intravascular oncotic pressure lead to edema formation
oncotic pressure = colloid osmotic pressure (interchangable)
if protein levels low the fluid will leak out into surrounding tissues
what causes hydrostatic pressure to increase
blood pressure increase
or
decreased venous return
how does renin potentiate edema
- water and/or blood leaves blood vessels
- decreased blood volume or drop in blood pressure
- kidneys secrete renin
- stimulates production of angiotensin by the liver
- ultimately results in the constriction of blood vessels and increased blood pressure
- increased hydrostatic pressure
- potentiates edema
what other disease can cause edema
congestive heart failure
what maintains oncotic pressure
protein loss
albumin mainly
if albumin level is decreased than fluid can leak out vessels because of decreased oncotic pressure
what are the causes of protein lack/loss (leading to decrease in oncotic pressure)
- lack of albumin (hypoalbuminemia)
- failure of albumin production (liver failure –> cirrhosis)
- loss of albumin (intestinal malabsorption –> Johnes, IBD; renal failure –> nephrotic syndrome (glomeruli cannot reabsorb protein and will be lost in urine); parasitic infection –> severe abdominal blood loss)
how does lack of albumin lead to edema
- liver damage (non-functional, decreased size)
- decreased albumin production
- hypoproteinemia
- decreased oncotic pressure
- edema
how does loss of albumin cause edema
1. albumin loss
- johne’s –> thickening of lamina propria in intestine –> macrophages, not absorbing protein back into circulation
- nephrotic syndrome –> dilated tubules filled with protein –> leaking –> not grabbing protein and lots in urine
- heamonchus worm –> edema in jaw
2. hypoproteinemia
3. decreased oncotic pressure
4. edema
what are disruption of normal circulation
- torsion
- rupture
- vascular thickening
- vasculitis
- thrombosis
what 3 things need to occur in order to form a blood clot
- endothelial cells need to be healthy
- blood needs to be right consistency
- normal blood flow
what is vascular torsion and what does it cause
- low pressure vessels collapose after torsion occurs
- blood can flow in but not out
- congestion
- necrosis
what is shown here
vascular torsion
what are causes of arterial rupture
- traumatic (common)
- spontaneous (uncommon) –> racehorses may be underlying degeneration
what is shown here
aortic rupture
tear in aorta
what are causes of equine sudden death
- horse kicked
- dark red blood in thoracic cavity –> huge blood clot around heart (ruptured heart or blood vessel)
- ruptured aorta
what is petechia
pinpoint hemorrhages
what is purpura
medium sized hemorrhages
what is ecchymoses
large hemorrhages (>1cm)
what are hematomas
localized, extravascular collection of blood
what is hemothorax
free blood in the thorax
what is guttural pouch mycosis
fungal plaque –> erroding through normal tissues –> important vessels near (carotid) and can start erroding through these walls
how does arterioscleorsis occur
proliferation of medial smooth muscle and fibrosis of the intima (+/- mineralization)
–> narrowing of lumen with loss of elasticity
ex. aorta in cow with Johne’s multiple mineralized plaques
how does hypothyroidism and diabetes mellitus cause atherosclerosis
depression of lipid metabolism –> accumulation of plasma lipids
deposition of fibro-fatty plaques (deposits of lipid, fibrous tissue and calcium in vessel walls)
damage to endothelium leads to thrombosis (virchow’s triad)
settles into blood vessels –> cholesterol clefts –> granulomatous inflammation
how does feline infectious peritonitis and pyogranulomatous vasculitis lead to infarction
infarction because pyogranulomatous inflammation (pus, neutrophils and macrophages)
commonly seen in kidneys, gut and abdominal and chest cavity, sometimes brain
what is an example of bacterial vasculitis
omphalophlebitis (navel-ill)
umbilical vein: affected
inflammation of umbilical vein gets into heart and then to systemic circulation –> present with polyarthritis of joints
what is an example of parasitic vasculitis
angiostrongylus vasorum
green and yellow lesions in lung (eosinophils)
larvae and eggs in the lung
draw a flow chart explaining how virchow’s triad leads to a thrombus
what is saddle thrombi in cats and what is it associated with and what do they present with
feline aortic thromboembolism
ventricle thickens –> atrium dilates because blood gathers here –> distention –> might throw a clot into systemic circulation –> causes problem when decrease in lumen size when aorta splits (iliac arteries)
associated with hypertrophic cardiomyopathy
cold back feet, blue, collapsed, act fast
what is an example of thrombosis and occlusion in arterial circulation
mesenteric arteritis in horses
strongylus vulgaris
inflammation and thrombosis due to migrating larvae (L4)
commonly seen in cranial mesenteric artery –> no blood flow –> undergoes ischemia, infarction, necrosis
presents as colic
what is shown here
portal vein thrombosis
accessory portal circulation due to venous occlusion
what is vena caval syndrome in dogs
secondary to heartworm infection, neoplasia (heart base tumour –> blood can’t get past)
venous congestion, pleural effusion
what is vena caval syndrome in cattle
secondary to hepatic abscesses
hepatic venous congestion, pulmonary thromboembolism
what is the pathology when caudal vena cava thrombosis ruptures
can rupture
embolic arteritis and aneurysm
causes hemoptysis (cough blood)
