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Haematology & immunology > Haemostasis Overview > Flashcards

Haemostasis Overview Flashcards

1
Q

Definition of haemostasis

A

Mechanism which the body maintains blood in a fluid state within blood vessels
Upon injury the body can arrest bleeding with a blood clot
How the clot is removed after healing

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2
Q

In vivo it’s a balance between…

A

Not bleeding und not clotting

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3
Q

What is required for normal haemostasis?

A

Normal blood vessels (vasculature)
Number of functional platelets
Produce fibrin via the ‘coagulation cascade’
Normal fibrinolysis system
Levels of natural anticoagulants

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4
Q

Primary haemostasis

A

Occurs initially the formation of a platelet aggregate, Within 5 minutes of bleeding

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5
Q

Secondary haemostasis

A

Formation of stable fibrin clot within 10 minutes of bleeding

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6
Q

Primary haemostasis

A

Platelet adhesion
Platelet activation
Platelet aggregation

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7
Q

Definition of a platelet

A

Anucleated cell fragment derived from bone marrow MK’s
150-400 x 109/litre
7.7 -11.2 fl
Lifespan of 10 days 30% sequestered in spleen
They circulate as quiescent cells surveying integrity of vascularture
Undergo explosive activation upon vessel wall damage

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8
Q

Normal platelets are circles

A

A nuclear platelets are small red dots

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9
Q

What happens when a blood vessel is disrupted?

A

Collaged fibres and smooth muscle is exposed to blood. Platelets are attracted to this area, then attach to collages fibres by Von Willebrand factor (vWF). Platelets are activated = change shape, release granular contence = attracts further platelets

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10
Q

Blood can still flow through blood vessel

A

Surface for secondary hemostasis

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11
Q

Platelet adhesion

A

Exposior of collagen initiates binding of VWF which also binds to glycol protein 1b complex /IX/V
Locks platets to sight of injury = no blood clot in head

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12
Q

von Willebrand factor

A

Proteins synthesized by mega karyocytes (mks) and endothelial cells
Found in plasma, platelets, endothelial cells, subendothelium
Largest multimers = most effective in Haemostasis
260 kD
Undergoes conformational charge = can bind to Gp 1b

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13
Q

Primary haemostasis

A

Exposure of collagen fibres attract VWF and they bind. Then attracts platelets which bind to GPIb-IX receptor-complex
Release granular contents.
glycoproteins
vWF
fibrinogen
coagulation factors
ADP
serotonin
calcium

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14
Q

Secondary homeostasis

A

Blood forms a stable clot

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15
Q

What is a clot made from?

A

Mesh of fibrin and platelets which form a haemostatic plug at sight of injury in vessel wall

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16
Q

Coagulation

A

Process by which fibrin is produced

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17
Q

Fibrinolysis

A

Process by which fibrin is broken down

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18
Q

Coagulation factors - labile plasma proteins which are activated to become these proteins…

A

Serine proteases- hydrolyse peptide bonds - II, VII, IX, X
Cofactors- tissue factor, V, VIII
Transglutaminase- XIII

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19
Q

Coagulation Cascade

A

When 1 factor is activated, it acts on a factor further down the system = activation of that factor till thrombin is produced = converts fibrinogen to fibrin

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20
Q

Intrinsic pathway

A

Activated by, contact factors
Things which are exposed when blood vessels are disrupted

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21
Q

Extrinsic pathway

A

Damaged tissue release tissue factors = directly activates factor VII
= small amounts of thrombin produced

22
Q

Cell based model of haemostasis

A

Initiation
Amplification
Propagation
Generates thrombin burst = haemostatic fibrin clot

23
Q

Initiation phase

A

Tissue factor bearing cells
Binds to factor VII a = promotes activation of factor X to Xa in conjunction with cofactor V which converts prothrombin to thrombin
Factor IX is activated by tissue factor VII complex to produce small amounts of activated factor IX

24
Q

Amplification

A

Thrombin produced activates further platelets, + releases factor VIII from its vWF complex. It’s bound to surface of platelets which combines with factor IX which was released in initial stage.

25
Q

Propagation

A

Thrombin and activated platelets utilise factor IX to activate factor XI which acts of facto IIX = produces burst of thrombin

26
Q

Clot formation

A

Once Fribrinogen has been converted to the fibrin monomer by the action of thrombin, these monomers polymerise with hydrogen bonding, but this fibrin polymer is still an unstable polymer, and it needs the action factor 13 to cross-link these fibrin polymers to cross linked fibrin to give an insoluble fibrin that will combine with a platelets to form a stable fibrin platelet clot

27
Q

Fibrinogen - fibrin monomer - fibrin polymer - cross-linked fibrin

A

Fibrinopeptide release 2. Hydrogen bonding
3.Transamidase bonding

28
Q

What is fibrinolysis?

A

Mechanism the fibrin clot is broken down into smaller fragments for disposal.

most important of these fibrin degradation products is the D-dimer
Diagnosis of DVT deep vein thrombosis
DIC (Disseminated intravascular coagulation)

29
Q

Process of fibrinolysis

A

Plasminogen - plasminogen - fibrin - fibrin degradation products

30
Q

Summary

A

Define coagulation and the process involved in clot formation,
The importance of coagulation factors
What are the stages/pathways involved in coagulation?
How do we best describe what happens in vivo?
Examine the role thrombin plays in secondary haemostasis.
Define fibrinolysis.

31
Q

Laboratory tests

A

Samples must be suitable for parameter being measured
Test system be regulated
Quality control
Results compared to locally established normal ranges

32
Q

Things required for abnormal haemostasis

A

History of abnormal haemostasis
Family history
Preventative screening
Monitoring of anticoagulant therapy

33
Q

Abnormalities =

A

Vasculature
Platelets
Functional fibrin via coagulation cascade
Fibrinolysis
Functional natural anticoagulants

34
Q

Vasculature

A

No specific tests
Imagining techniques
Markers of inflammation e.g. CRP, ESR + vWF

35
Q

Platelets

A

Count number + size using automated blood cell analysers
Check morphology using blood film
Bleeding time
Platelet function analysers PFA
Platelet aggregation tests
Platelet nucleotides

36
Q

Fibrin production

A

Prothrombin time PT
Activated partial thrombophlebitis time APTT
Thrombin time TT
Fibrinogen level Fib

37
Q

Fibrinolysis

A

Clot lysis times
D-diner levels
Plasminogen levels
Alpha -2- antiplasmin levels

38
Q

Natural anticoagulants

A

Function + absolute levels
Protein C, S
Antithrombin
Activated protein C resistance/factor V Leiden

39
Q

PFA-100 platelet function analyser

A

Mimics primary haemostasis

40
Q

Platelet aggregation

A

Centrifuge blood gently to obtain platelet rich plasma
Stirred in a cuvette at 37 oC between a light source and photocell
Addition of agonist = platelet aggregation = platelets clumps = transmission increases + absorbacne decreases
Addition of different agonists at a range of concentration allows detection of certain defects
Agonists bind to their own specific receptors resulting in activation. Shape change, granule release, aggregation

41
Q

Fibrin formation

A

Measures secondary haemostasis
Routine test = coagulation screen (CS)
300-500 daily

42
Q

Screening tests

A

Prothrombin time (PT)
Clotting pathway initiated with damaged tissue
How to make a reagent
Emulsify in a blender !
Wash with chloroform
Sieve !
Dilute in buffer
Standardise

43
Q

Screening tests

A

100ul plasma (in sodium citrate, which binds calcium)

Warm to 37oC

200ul Tissue factor + Phospholipid (to replace platelets removed by centrifugation) + Calcium (removed above)

Time for clot formation

Establish local normal range

44
Q

Screening tests PT abnormal in

A

inherited deficiencies of fibrinogen, prothrombin, FV, FVII, FX
Acquired deficiencies of above
Consumptive - bleeding- over activation- liver disease
Therapeutic - warfarin
Acquired inhibitors to factors

45
Q

Screening tests international normalised ration INR

A

Used to standardise warfarin therapy around world
INR {patients Prothrombin time (seconds)/ control Prothrombin time (seconds)} isi

46
Q

Isi= international sensitivity index

A
47
Q

Screening tests
Activated Partial Thromboplastin Time (aPTT)

A

Demonstration of intrinsic pathway + common pathway
Activated using contact activation
Need source of phospholipid
Need calcium

48
Q

Screening tests aPTT abnormal in

A

Inherited deficiencies
X Acquired deficiencies of above
Consumptive
Bleeding
Over activation (Disseminated Intravascular Coagulation, DIC)
Liver disease
Therapeutic – Heparin
Acquired Inhibitors to factors

49
Q

Thrombin Time (TT)
Screening tests

A

Addition of diluted Bovine Thrombin to neat sample

Direct conversion of Fibrinogen  Fibrin

Abnormal in
Patients with low fibrinogen
Patient with non-functioning fibrinogen
Patients with Inhibitors of Thrombin
Anticoagulant - Heparin

50
Q

Fibrinogen estimation
Screening tests

A

Similar addition of Thrombin (concentrated) to diluted plasma (1:5, 1:10, 1:20)
Time taken to clot = Fibrinogen concentration in the sample
Reported from comparison of standard curve
Oxford range 1.5-4.0 g/l

Abnormal in Inherited fibrinogen deficiency
Acquired deficiency
Bleeding
DIC
Liver disease

51
Q

D-dimer (DD)
Screening tests

A

Breakdown product of clot formation
Only found in cross-linked Fibrin breakdown
Marker of rate of clot formation/breakdown
Reported as ug/l FEU
Oxford <500 ug/l FEU

52
Q

Summmary

A

What body does to prevent blood loss
Understand processes overall
Understand the difference between Primary and Secondary haemostasis
Understand which routine laboratory tests can be used to investigate Haemostasis
Understand test procedures

Haematology & immunology (11 decks)

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