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Pathology > Haemorrhage and Haemostasis and Thrombosis > Flashcards

Haemorrhage and Haemostasis and Thrombosis Flashcards

1
Q

petachia

A

pinpoint haemorrhages

often on gums, minor vascular damage

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2
Q

ecchymosis

A

up to 2-3cm diameter haemorrhages

more severe or extensive vascular damage

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3
Q

suffusive

A

haemorrhage affecting large areas of tissue - usually contained with in a limb or between muscle bellies

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4
Q

haematoma

A

haemorrhage in focal confined space - usually in dog ears or pig spleen after trauma to vasculature

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5
Q

haemoperitoneum

A

blood in peritoneal cavity

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6
Q

haemothorax

A

blood in thoracic cavity

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7
Q

haemopericardium

A

blood in pericardial sac

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8
Q

aneurysm

A

bulge in artery, due to defect in the wall

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9
Q

arterial aneurysm

A

rare

pigs- aorta rupture, pulmonary artery and coronary artery rupture
horses - artic sinus - sudden death
guinea pigs - associated with vitamin C deficiency

seen in cases of developmental collagen disorders - Ehlers-Danlos/marfan syndrome

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10
Q

endothelial injury

A

minor - small number RBCs escape through gap –> endotoxemia
due to infectious agents (adenovirus), chemical damage (uremic toxins), trapped immune complexes between endothelial cells
may be agonal change

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11
Q

haemostasis

what is it and 4 stages

A

stopping of bleeding needed to stop haemorrhage

4 stages -
1. arteriolar vasoconstriction
2. primary haemostasis - platelet plug
3 secondary haemostasis - addition of fibrin to plug
4. thrombus and antithrombotic event - resolution

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12
Q

primary haemostasis

A

3 stages -
1. adhesion - vWF released by endohelium, acts as bridge between platelet surface receptor and collagen
2. activation - caused by thrombin and ADP, release of thromboxane
3. aggregation - glycoprotein allows binding of fibrinogen

needs vWF, platelets and ADP to work

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13
Q

GPllb defect

A

glanzman’s thrombathenia
affects calcium binding domain of extracellular portion
som dog breeds and horse

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14
Q

defective storage of ADP

A

Chediak-hegashi
cattle, some cats, orca

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15
Q

vWF deficiency

A

affects primary hemostasis

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16
Q

acquired primary hemostasis disorders

A

NSAIDS - COX inhibitors –> less thromboxane –> no platelet aggregation
Uremia - chronic renal failure, toxin build up –> negatively affects platelet function
Idiopathic immune- mediated thrombocytopenia - immune system attacks own platelets

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17
Q

testing primary hemostasis function

A

buccal mucosal bleeding time - see how long a small cut in gums bleeds

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18
Q

secondary hemostasis

A

clotting factors lead to production of fibrin - stabilises platelet plug
intrinsic pathway - factors XI and XII
extrinsic pathway - factor VII
both lead to common pathway - factor X –> thrombin formation –> fibrinogen cleaved to fibrin

needs vitamin K - co-factor - needed for formation of factors II, VII, IX, and X

19
Q

haemophilia A

A

factor VIII deficiency

20
Q

haemophilia B

A

factor IX deficiency

21
Q

acquired disorders of secondary haemostasis

A

liver disease - can’t produce clotting factors
vitamin K deficiency - deficiency in factors II, VII, IX, X - rodenticide poisoning (contains warfarin)

22
Q

testing secondary hemostasis function

A

prothrombin time (PT) - tests extrinsic and common pathways
Activated partial thromboplastin time (APT) - intrinsic and common pathways
(machine - tells you how long it takes to clot)

23
Q

thrombus

A

clot, forms antemortem within a vessel

24
Q

thromboembolism

A

section of thrombus broken off and lodged elsewhere

25
antemortem clot
coagulation of blood within a cavity
26
factors controlling thrombus formation (3)
abnormal blood flow hypercoagulability endothelial injury
27
abnormal blood flow
blood flow should be one direction and smooth abnormal flow caused by: valvular disease heart disease shunts aneurysms hypovolemia local stasis or reduced flow
28
hypercoagulability
too much coagulation (if clotting factors not in balance) caused by: glomerular disease - reduced antithrombin 3 production metabolic disease inflammation platelet activation - eg. neoplasia
29
endothelial injury
endothelial cells responsible for: metabolite diffusion and transport local vasoconstriction and vasodilation coagulation inflammation wound healing and angiogenesis synthesis of vWF
30
disseminated intravascular coagulation (DIC)
diffuse or severe pendothelial damage or platelet activation widespread consumption of clotting facors - consumptive coagulopathy lots of little thrombi caused by: severe acidosis - aggravates endothelial cells endothelial cell injury massive tissue destruction severe inflammation - immune disease, neoplasia, pancreatitis multi organ failure widespread haemorrhage
31
arterial thrombi
less likely to take up whole vessel - can go on quite long with them
32
venous thrombi
slower flowing blood, smaller vessel - usually occludes the vessel
33
post mortem clotting
not adherent to wall of vessel, separates into cells and plasma 'chicken fa clot'
34
infarction
local area or acute ischemia - coagulative necrosis secondary to thrombosis or thromboembolism severity depends on kind of vessel occluded, duration, tissue its in and how good the tissue was before
35
fresh whole blood
only fresh for 6 hours, after that becomes stored whole blood (must be refridgerated)
36
blood products
fresh frozen plasma (FFP) frozen plasma - FFP after one year - split into cryo-precipitate and cryo-supernatant packed red blood cells (PRBC) platelet concentrate
37
benefits - components over whole blood
maximise resources reduced volume transferred minimised immune sensitisation immediately available on site - extended storage extended shelf life platelets and clotting factors become therapeutically useless in whole blood after 24 hours
38
benefits - whole blood
doesn't need processing storage easier - just one storage temperature
39
use of RBCs
FWB or PRBCs FWB - all erythrocytes, hemostatic proteins, plasma proteins, immunoglobulins, antiproteases, and platelets, hemostatic resuscitation, may arrest active haemorrhage in patients with thrombocytopenia PRBCs - all erythrocytes only, used for anemia, used in cases of blood loss or hemostatic resuscitation (in combination with fresh or frozen plasma)
40
use of plasma
FFP - all hemostatic proteins, antiproteases, immunoglobulins, antiproteases, and non labile factors II, V, VII, IX, X, XI, and XII used for DIC, adder bites (immunoglobulins for allergic reaction), consumptive coagulopathy, hemophilia A & B, vWF deficiency, bleeding due to angiosrongylus, acute hemorrhagic shock frozen plasma and cryo-supernatant - source of plasma proteins, immunoglobulins, antiproteases and non-labile factors II, V,VII,IX,X,XI and XII used for haemorrhagic gastroenteritis, rodenticide toxicity, hepatic coagulopathy, hemophilia B, hypoporteinemia, resuscitative IVFT, immunoglobulin transfer (failure of passive transfer), hypoalbuminemia cryo-precipitate - source of non-labile factors I, VIII, XIII, and vWF used for vWF disease, hemophilia A, hypofibrinogenemia
41
use of platelets
platelet concentrate - source of platelets only used for uncontrolled life-threatening hemorrhage, prophylactic treatment in patients with hereditary thrombopathia
42
blood typing
types by erythrocyte antigens - expresses certain antigen then positive for that blood type test for antigen DEA-1
43
cross matching
checking recipient plasma for antibodies against donor erythrocytes incompatibility - haemagglutination should cross match if dog has ever received a transfer or if transfer history is unknown more important for erythrocyte containing products

Pathology (24 decks)

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