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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
Q

antemortem clot

A

coagulation of blood within a cavity

26
Q

factors controlling thrombus formation (3)

A

abnormal blood flow
hypercoagulability
endothelial injury

27
Q

abnormal blood flow

A

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
Q

hypercoagulability

A

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
Q

endothelial injury

A

endothelial cells responsible for:
metabolite diffusion and transport
local vasoconstriction and vasodilation
coagulation
inflammation
wound healing and angiogenesis

synthesis of vWF

30
Q

disseminated intravascular coagulation (DIC)

A

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
Q

arterial thrombi

A

less likely to take up whole vessel - can go on quite long with them

32
Q

venous thrombi

A

slower flowing blood, smaller vessel - usually occludes the vessel

33
Q

post mortem clotting

A

not adherent to wall of vessel, separates into cells and plasma
‘chicken fa clot’

34
Q

infarction

A

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
Q

fresh whole blood

A

only fresh for 6 hours, after that becomes stored whole blood (must be refridgerated)

36
Q

blood products

A

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
Q

benefits - components over whole blood

A

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
Q

benefits - whole blood

A

doesn’t need processing
storage easier - just one storage temperature

39
Q

use of RBCs

A

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
Q

use of plasma

A

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
Q

use of platelets

A

platelet concentrate - source of platelets only

used for uncontrolled life-threatening hemorrhage, prophylactic treatment in patients with hereditary thrombopathia

42
Q

blood typing

A

types by erythrocyte antigens - expresses certain antigen then positive for that blood type

test for antigen DEA-1

43
Q

cross matching

A

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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