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Flashcards in haemostaisis Deck (61):
1

haemostais

: cessation of bleeding (right place, right time).
ie. At site of injury, when risk of blood loss.
PHYSIOLOGY

2

Thrombosis

inappropriate activation of platelets or coagulation (wrong place, wrong time).

3

bleeding

insufficient activation of platlets or coagulation
defects of quanitity or function

4

what are the 5 steps in haemostasis

vessel spasm
platlet plug formation
coagulation
clot retraction
clot dissolution

5

outline normal haemstasis

- injury to the vessel wall exposes the subendothelium which includes collagens
- circulating platelets come into contact with the collagens they become activated and form a platelet plug.
- Coagulation is the process where fibrin (stringy stuff) is formed to bind all the cells together into a more stable clot.

6

vessel spasm

vessel damaged exposing collagen
pain receptor reflex
releasing meditors of vasoconsriction
reduce blood flow through

7

mediators of vessel spasm

thromboxane A2
endothelin
angiotensin

8

describe platelets

small anucleate fragments frrom megakaryocytes

9

steps in platelet plug formation

adhesion, activation, secretion and aggregaton

10

process of platelt plug formation

At sites of damage the collagens are exposed.
-vWF i bind to both the collagen AND to the GPIb complex on the surface of platelets.
-This isn’t very strong, so just slows the platelet down rather than stopping it.
- The receptor GPVI is then able to bind collagen triggering a signalling cascade

11

results of the signalling cascase of granules in platlet plug formation

The granules are secreted, releasing their contents to further activate nearby platelets.
The fibrinogen is converted from a low affinity state to a high affinity state (more able to bind fibrinogen).
The fibrinogen receptor is now able to bind to fibrinogen, cross-linking platelets together to form a platelet plug.

12

platelet agonists

collagen and thrombin

13

weak platler agonists

ADP
adrenaline

14

negative regulation of platelets

Prostacyclin and NO are produced by healthy endothelium ie at sites where we don’t want platelet activation to occur

15

coagulation step of haemostasis

fluid blood becomes gelatinous clot
polyermisation of fibrin involved

16

role of thrombin

enzyme
catalyses conversion of fibrinogen to fibrin
generated from prothrombin at sites of tissue injury to help with coagulation

17

intrinsic pathway of coagulation

exposed collagen activated F12

18

extrinsic pathway

damaged tissue released tissue thromboplastin/tissue fctor

19

clot dissolution

fibrinolysis

20

how does fibrinolysis occur

plasminogen converted to plasminwhich disolves the clot

21

plasminogen

activated by thrombin which comes from damaged tissue
is convereted into plasmin which dislves fibrin

22

what can stop blood in circulation from clotting

inhibition of platelet function by healthy endothelium
inactive clotting factors
blood blow carring away factors
inhibitor factors
fibrinolysis

23

low factor 8

haemophillia
leads to bleeding

24

arterial thrombosis

ltherlosclotic plaques rupture triggering platlers to stick together

25

venous thrombosis

deficiency in inhibitors fr coagulation cascade
found in DVT slow blood allows clotting to be triggered easil

26

primary haemostatis disorder

bleeding disorder
platelet plug formation isnt working very well

27

medical name for a bruise

haematoma

28

what is a haemoatoma

micro or macroscopic tearing of the blood vessels
the leaked blood cells are phagocytosed ad degraded over time

29

blue/red bruise

haemoglobin

30

green bruise

biliverdin

31

yellow brise

billirubin

32

golden bruise

hemosiderin

33

3 types of bruise

petichiae
purpura
echymoses

34

causes of bleeding defects

vascular defects
low plalet numbers
disorders of platelet function
coagulation

35

low platlet numbers

thrombocytopenia

36

example of coagulation disorder

heamophilia
results in:
- delayed bleeding
intramuscualr haemotmas
more males

37

exaxmples of primary haemostastic disorders

thrombocytopenia
VWD
- petichae, nose bleeds

38

nose bleeds

epistaxes

39

signs of a thrombotic disorder

coronary arties: chest pain
carotis arteires: stoke
deep veins of legs: unilateral leg pain

40

risk factors for haemostastic disorders

age
gender
ethnic
asprin use
warfarin use
previous thrombosis

41

examples of heamostastic investigations

Full blood count (purple vacutainer – EDTA)
Blood film or smear (morphology)
Bleeding time: normal = 3-8min
PFA-100 (replaced bleeding time)
Platelet aggregation studies
Flow cytometry
Serum thromboxane
Aspirinworks (urine test for thromboxane)
Coagulation Assays (blue vacutainer – citrate)
Prothrombin time (INR)
Activated partial thromboplastin time
Thrombin Time
Factor Assays
PCR
D-dimer Assays

42

examples of easy bleeding

epitaxis
blood in stools
gum bleding
musocal lining bleedings
heavy periods

43

what vacutainer is usedd for a full blood count

purple one
contains EDTA

44

what is EDTA

anticoag
powder form so doesnt dilute the blood
binds calcium to stop cogaultion
permanent

45

cagulation assay vacutainer

blue
sodium citrate
liquid form mops up calcium temportatiliy preventing coagulation

46

prothrombin time

INR

47

examples of coagulation assasy

prthombin tme
activated partia thromboplastin time
thrombin time

48

blood film

used to asses the blood cells down the micoscope

49

PFA

platelet function analyser machine
moves blood through capillary tube with collagen in and measure the time it takes for the tube to eet blocked
measures accurately the platelet fuunction

50

platelet aggregation studies

puify platlers and shine light through
if they are active adn stuck together, lots of light through
inaccive, not much through
not used in hopsitals through ay more

51

flow cytometry

flurestcent Ab to makr thigsn and make them seen

52

serum thromboxane/aprinworks

looks at effect of asprin on blood
test used prior to surgery to check if patient has been using it as it might affect their abilty to clot

53

efffect of low dose asprin

keeps platlers quiet in patienets at risk of arterial thrombosis

54

what part of the coagulation pathway does prothombin time measure?

extrinsic pathway

55

prothombin time in patientes on warfarin

longer
warfarin inhibits vit K being cycles and this is needed to make clotting factos so wihout it blood less likely to clot

56

what part of the cogaultion cascad does the activated partial thromboplastin time measure

intrinsic pathway`

57

what part of the coagultion assay does thrombin time measure

common pathway

58

heparin

inhibits thrombin

59

factor assays

testing for deficiencies
take plasma and add in normal plasma dnt he prolonged clotting time should be fixes showing a factor issue

60

inhibition assay

used to asses too much of an inhibitiro
add patients plasma to normal plasma and the clotting time will be longer as stuff it being blocked

61

D-dimer assay

these aremade from the breakdown of fibrin
clots mean more D-Dimers