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
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