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Clinical Biomed yr2 > haemostaisis > Flashcards

haemostaisis Flashcards

1
Q

haemostais

A

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

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2
Q

Thrombosis

A

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

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3
Q

bleeding

A

insufficient activation of platlets or coagulation

defects of quanitity or function

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4
Q

what are the 5 steps in haemostasis

A 
vessel spasm
platlet plug formation
coagulation
clot retraction
clot dissolution
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5
Q

outline normal haemstasis

A
  • 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.
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6
Q

vessel spasm

A

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

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7
Q

mediators of vessel spasm

A

thromboxane A2
endothelin
angiotensin

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8
Q

describe platelets

A

small anucleate fragments frrom megakaryocytes

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9
Q

steps in platelet plug formation

A

adhesion, activation, secretion and aggregaton

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10
Q

process of platelt plug formation

A

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
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11
Q

results of the signalling cascase of granules in platlet plug formation

A

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.

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12
Q

platelet agonists

A

collagen and thrombin

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13
Q

weak platler agonists

A

ADP

adrenaline

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14
Q

negative regulation of platelets

A

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

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15
Q

coagulation step of haemostasis

A

fluid blood becomes gelatinous clot

polyermisation of fibrin involved

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16
Q

role of thrombin

A

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

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17
Q

intrinsic pathway of coagulation

A

exposed collagen activated F12

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18
Q

extrinsic pathway

A

damaged tissue released tissue thromboplastin/tissue fctor

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19
Q

clot dissolution

A

fibrinolysis

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20
Q

how does fibrinolysis occur

A

plasminogen converted to plasminwhich disolves the clot

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21
Q

plasminogen

A

activated by thrombin which comes from damaged tissue

is convereted into plasmin which dislves fibrin

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22
Q

what can stop blood in circulation from clotting

A 
inhibition of platelet function by healthy endothelium
inactive clotting factors
blood blow carring away factors
inhibitor factors
fibrinolysis
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23
Q

low factor 8

A

haemophillia

leads to bleeding

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24
Q

arterial thrombosis

A

ltherlosclotic plaques rupture triggering platlers to stick together

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25
Q

venous thrombosis

A

deficiency in inhibitors fr coagulation cascade

found in DVT slow blood allows clotting to be triggered easil

26
Q

primary haemostatis disorder

A

bleeding disorder

platelet plug formation isnt working very well

27
Q

medical name for a bruise

A

haematoma

28
Q

what is a haemoatoma

A

micro or macroscopic tearing of the blood vessels

the leaked blood cells are phagocytosed ad degraded over time

29
Q

blue/red bruise

A

haemoglobin

30
Q

green bruise

A

biliverdin

31
Q

yellow brise

A

billirubin

32
Q

golden bruise

A

hemosiderin

33
Q

3 types of bruise

A

petichiae
purpura
echymoses

34
Q

causes of bleeding defects

A

vascular defects
low plalet numbers
disorders of platelet function
coagulation

35
Q

low platlet numbers

A

thrombocytopenia

36
Q

example of coagulation disorder

A 
heamophilia
results in:
- delayed bleeding
intramuscualr haemotmas
more males
37
Q

exaxmples of primary haemostastic disorders

A

thrombocytopenia
VWD
- petichae, nose bleeds

38
Q

nose bleeds

A

epistaxes

39
Q

signs of a thrombotic disorder

A

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

40
Q

risk factors for haemostastic disorders

A 
age
gender
ethnic
asprin use
warfarin use
previous thrombosis
41
Q

examples of heamostastic investigations

A 
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
Q

examples of easy bleeding

A 
epitaxis
blood in stools
gum bleding
musocal lining bleedings
heavy periods
43
Q

what vacutainer is usedd for a full blood count

A

purple one

contains EDTA

44
Q

what is EDTA

A

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

45
Q

cagulation assay vacutainer

A

blue
sodium citrate
liquid form mops up calcium temportatiliy preventing coagulation

46
Q

prothrombin time

A

INR

47
Q

examples of coagulation assasy

A

prthombin tme
activated partia thromboplastin time
thrombin time

48
Q

blood film

A

used to asses the blood cells down the micoscope

49
Q

PFA

A

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
Q

platelet aggregation studies

A

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
Q

flow cytometry

A

flurestcent Ab to makr thigsn and make them seen

52
Q

serum thromboxane/aprinworks

A

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
Q

efffect of low dose asprin

A

keeps platlers quiet in patienets at risk of arterial thrombosis

54
Q

what part of the coagulation pathway does prothombin time measure?

A

extrinsic pathway

55
Q

prothombin time in patientes on warfarin

A

longer

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

56
Q

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

A

intrinsic pathway`

57
Q

what part of the coagultion assay does thrombin time measure

A

common pathway

58
Q

heparin

A

inhibits thrombin

59
Q

factor assays

A

testing for deficiencies

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

60
Q

inhibition assay

A

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
Q

D-dimer assay

A

these aremade from the breakdown of fibrin

clots mean more D-Dimers

Clinical Biomed yr2 (22 decks)

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