1) This is composed of arteries, veins, capillaries and
lymphatics. The composition of each is similar (differences in
the relative thickness)
3 layers... 1) Intima which is continuous with the endo (fibrous
CT and single endo layer), 2) Media- concentric bands of muscle,
3) Adventitia- stabilises
In normal BV's it is the ENDOTHELIAL cells
which prevent platelet adhesion. Secretes
comps that prevent the CC and act as
vasodialtors (hist)
Vessel damage (endo) prevents this and
initiates the CC!
Haemostasis- four stages, advanced by
the subendothelium exposure
3) Aneurysm and rupture
any outpouching of the arterial wall after reduction in the
wall strength (particularly the aventitia). They are rarely
detected prior to causing death but may show CS's
relating to surouding compression of organs/tissue
Strongylus vulgaris in horses,
idiopathic turkeys and cu deficiency
in pigs
2) Arterial ruptures
Usually follows trauma but ca occur
idiopathically in horses/ dogs
following exercise
Arterial
thrombosis
Virchows triangle- A thrombus is an
intravascular blood clot
Animals commonly develop them due to
an altered blood flow, yet endothelial damage is the main
issue. Common: valvular damage, cardiomyopathies, CHF
which slows the blood
Most arise in the atria- travel to the
coronary (myocardial infarct), iliacs
(saddle) and renal arteries
These are due to an UNDERLYING
issue which needs to be
identified...
Recall the other causes of
thrombo-embolism: Fibrocartilage, gas,
septic endocarditis-
adipose from limb fx, strongylus vulagris nfx
Artherosclerosis...
The deposition of liquid within
the intima of BV, common in ppl
but only found in parrots/
hypothyroid dogs (usually without
CS's)
Calcification
Variety of animals-
Johnes in
cattle- hose pipe aorta. In
others: CKD or choleciferol
toxicity
Fibrinoid Necrosis
This is an uncommon
condition in all except pigs/
chickens due to Se
deficiency.
Dogs and cats can develop this - gastric and oral
BV's are effected due to uraemia (^creatine/urea)
associated with renal faiure.
Infectious Arteritis
BACTERIAL
Erysipelas
This can effect all animals but
particularly pigs and turkeys-
thrombosis + infarction due to vascular
damage. Pigs develop diamond shape
lesions
Diamond skin
lesions
PARASITIC
Strongylus Vulgaris- uncommon in
NZ but ca cause a mesenteric
arteritis- aneurysm/ infarction
Dirofilaria Imminitis
This is rare in NZ but is
found in North America
and Australia, arteritis, CHF
and pulmonary embolism
This is the result of endothelial
damage and can be the result
of various infectious diseases
VIRAL
FIP
This is NOT a Peritonitis, NOR
infectious... Its a vasculitis with only
50% having a peritoneal involvement
In a small # of cats the ubiq FICV will mutate
into FIP, escape the git and enter the
bloodstream causing a generalised
vasculitis. Protein rich fluid enters the body
cavities (including peritoneum)
The endothelial damage causes thrombosis,
infarction. The organs effected depend on
localised area- hepatic + renal most common.
25% have a CNS vasculitis sign only
The PM signs depend on the severity of the
BV damage- wet vs dry. Fibrin accumulates
as multiple white foci (immune complex
mediated)
WET: FNA and cytology will show up N0 and
"scaling" The transudtae that is aspirated is
yellow, turbid, has a low cellular, high
protein content and clots rapidly
DRY: this is a common cause of
death in NZ cats and should be suspected
in any "unknown cause of fever". UBiq
nature of dz makes interpretation difficult.
Biopsy and histo are the only DD
MCF
There are two forms of this; OHV
associated is the one that causes dz in
NZ cattle. In a small % the lymphcyte
suppressors are damaged, allowing
Lymphocytes to cause damage
Generalised vasculitis causes variable signs-
Corneal oedema, GIT upset are the most common.
Oral ulceration, crusting lesions, and at times
ulceration of the C.band