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MELS302 > Coagulation Cascade > Flashcards

Coagulation Cascade Flashcards

1
Q

Where does the coagulation cascade happen

A

On the surface of activated platelets

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2
Q

How to measure the extrinsic pathway

A

Prothrombin time
International normalised ratio

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3
Q

What triggers the extrinsic pathway

A

Tissue injury
Tissue factor is released from the tissue

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4
Q

Main two components of the extrinsic pathway

A

Tissue factor and factor VII

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5
Q

Common pathway factors

A

X and V

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6
Q

Intrinsic pathway factor

A

XII, XI, IX, VIII

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7
Q

How is the intrinsic pathway measured

A

APTT
Activated partial thromboplastin time

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8
Q

What does the intrinsic pathway have a role in

A

Infection and inflammation

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9
Q

What does the common pathway do

A

Converts prothrombin to thrombin
Then thrombin converts fibrinogen to fibrin

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10
Q

Where is tissue factor found

A

It is a receptor found on fibroblasts and SMC and injured macrophages and monocytes

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11
Q

First part of the extrinsic pathway

A

Injury exposes TF
Complex made with VII activated, Ca and phospholipids on the cell which exposed TF

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12
Q

What does the TF-VIIa complex activate

A

IX and X
This activates the common pathway

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13
Q

What starts the intrinsic pathway

A

Contact activation with negatively charged surfaces

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14
Q

What does contact activation happen on

A

Collagen
Prosthetic valves/glass or plastic tubes

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15
Q

What factors make up contact activation

A

XII, PreK, HMWK this makes a complex

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16
Q

What factor does contact activation activate

A

The XII/PreK/HMWK complex activates XI this forms kallikrein and bradykinin formation and helps activate IX in the common pathway

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17
Q

What happens when you get deficiencies under XII and XI in the intrinsic pathway

A

No bleeding but prolongs lab results as the extrinsic pathway can still feed the common pathway

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18
Q

What makes the tenase complex

A

IX, VIII, Ca and phospholipids

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19
Q

What activated the final common pathway

A

Prothrombinase

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20
Q

What makes up prothrombinase

A

Xa,Va, calcium and phospholipids

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21
Q

What does prothrombinase do

A

It activates prothrombin to thrombin
Which will convert fibrinogen to fibrin

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22
Q

How does thrombin convert fibrinogen to fibrin

A

By activating FXIII with calcium
This cross links fibrin making it stronger

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23
Q

What provides positive feedback in the common pathway

A

Thrombin
Activates factors X, VIII, XI

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24
Q

In vivo coagulation - 3 overlapping stages

A

Initiation: continuous low level activation of TF pathway on cells with TF
Amplification: everything comes together and is activated
Propagation: reactions on the surface of activated platelets

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25
Q

What happens to platelets during initiation

A

No platelets or vWF yet so no coagulation until there is an injury

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26
Q

What happens in the initiation coagulation phase

A

TF and VII bind on cells with TF
Low level activation of tenase and prothrombinase so getting ready for cell injury but not enough thrombin is made for a clot to happen

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27
Q

Purpose of initiation

A

To get ready for tissue injury
Generating low levels of thrombin
No injury yet

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28
Q

What happens in the amplification phase

A

Injury happens
Platelets and vWF come in
Platelets are activated from the low level thrombin from initiation and collagen 
Thrombin activates X, VIII, XI too

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29
Q

What happens in the propagation phase

A

Reactions happen on the surface of activated platelets
More tenase is made and more prothrombinase so you get more thrombin being made for the thrombin burst

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30
Q

What happens in a thrombin burst

A

Fibrinogen cleaved to fibrin
XIII activated to stabilise clot
Positive feedback on V,VIII,XI
Stops fibrinolysis

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31
Q

What happens if you don’t have enough thrombin

A

Fibrin strands are thin and weak
Fibrinolysis breaks it down easily through tissue movement

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32
Q

Does the fibrin clot start strong

A

No, starts weak and strengths with FXIII and clot retraction of platelets

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33
Q

Tube collection in coagulation testing

A

Sodium Citrate tube
Anticoagulant to stop clotting and activation of platelets and factors
9:1 ratio

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34
Q

Sample type for plasma aggregometry

A

Centrifuged PRP plasma rich plasma

35
Q

Sample type for most tests in coagulation

A

Platelet poor plasma

36
Q

Sample problems can arise from

A

Too hot or cold
Incorrect volume
Clot, haemolysis, icterus
Traumatic venepuncture
Prolonged tourniquet leads to increased vWF/factor 8
Delayed testing as half lives
Order of draw
Drug history

37
Q

What pathway is TCT related too

A

Common pathway

38
Q

What is PT sensitive too

A

Deficiency in VII, X, V and lesser II

39
Q

Reagents for prothrombin time

A

Thromboplastin (TF reagent with phospholipids and anti heparin)
CaCl
Buffet

40
Q

What is in thromboplastin

A

Tissue factor reagent
Phospholipids
Anti heparin

41
Q

What is detected in PT

A

Fibrin formation using optical detection or electromechanical detection

42
Q

Clinical factors prolonging PT

A

Reduced vitamin K (liver disease, warfarin/anticoagulants, consumptive coagulopathy)
Thrombin and X inhibitor drugs like dabigatran
RARE factor deficiency - X, B, XII or inhibitor antibodies

43
Q

Technical factors prolonging PT

A

Cold activation of FVII
Clotted sample
Haemolysis
Additive ratio/sample volume
Heparin contamination
Old reagents
Delayed testing

44
Q

Steps of APTT

A
  1. 5 min Incubation of PPP with contact activators like silica or soy
  2. Phospholipids platelet substitute added as these reactions happen on platelets
  3. CaCl added for rapid coagulation
45
Q

What is APTT sensitive too

A

Deficiency of factors V, X, VIII, IX, XI, XII

46
Q

What is in the phospholipid platelet substitution used in APTT

A

Partial thromboplastin
NO TF
Point is to eliminate patient platelet variability
Buffer

47
Q

How is APTT measured

A

Measures fibrin formation
Decrease in optical transmittance/absorbance as clot forms
Electromagnetic detection

48
Q

Clinical factors prolonging APTT

A

Decreased coagulation factors (liver disease, VK deficiency, anticoagulants, consumptive coagulopathy, transfusions, factor deficiency)
Coagulation factors inhibitors (antibodies like in lupus)
CRP higher than 100 interferes

49
Q

Technical factors prolonging APTT

A

Clotted sample
Volume/ additive ratio
Heparin
Haemolysis
Turbidity
Thromboplasin nature
Delay in testing etc

50
Q

TCT method

A

PPP
Thrombin reagent with CaCl and buffer
Start timer and wait for clotting

51
Q

Principle of TCT

A

Add thrombin in excess and see how long it takes for a clot to form
Focusing on fibrinogen and heparin screening

52
Q

What affects TCT

A

Fibrinogen conc
Fibrin degradation products
Heparin (VERY SENSITIVE)
Thrombin inhibitor drugs like dabigatran

53
Q

List three anticoagulants which prolongs APTT

A

Heparin
Warfarin
Dabigatran

54
Q

What tests are performed as a duplicate assay

A

PT
APTT
TCT
FIBRINOGEN

55
Q

Fibrinogen method

A

PPP
4 different assays - we use Clauss

56
Q

What prolongs fibrinogen

A

DIC- consumption of fibrinogen
Liver disease
Fibrin degradation products
Thrombotic therapy
Hypo/dysfibrinogenaemia

57
Q

Correction studies are done on what

A

APTT and PT

58
Q

When are correctional studies done

A

On a prolonged APTT and PT

59
Q

Correctional study method

A

1:1 mix of normal plasma with patient plasma

60
Q

What happens if plasma is not corrected

A

Clotting time is still prolonged or only partially corrected means inhibitor is present like heparin,antibodies or dabigatran

61
Q

What happens if prolonged times are corrected

A

Patient has a factor deficiency

62
Q

What deficiency is haemophilia A

A

Factor VIII/8
X linked
De novo in 30%

63
Q

What is haemophilia B

A

Christmas Disease
FIX deficiency
X linked

64
Q

Haemophilia bleeding pattern

A

Spontaneous bleeding and bleeding into joints (haemarthrosis)

65
Q

Solutions to joint bleeding in harmony

A

Reconstructive joint surgery as cartilage eroded from constant bleeding leading to narrow joint space

66
Q

Haemophilia treatment depends on what

A

How severely deficient they are in the factor
If only less than 1% factor is there then severe
Above 5 is mild

67
Q

Haemophilia treatment

A

Factor concentrates (specific for each lacking factor)
Fibrinolytic inhibitor (tranexamin acid) = stops clot breakdown
DDAVP if mild haemophilia A

68
Q

What does DDAVP do

A

Boosts endogenous vWF release from EC so more factor 8 too

69
Q

Acquired coagulation disorders

A

Vitamin K deficiency
Liver disease
DIC
Anticoagulants
Factor inhibitor antibodies
Haemo dilution

70
Q

Vitamin K dependent factors

A

II, VII, IX, X
PROTEIN C AND S

71
Q

Vitamin K deficiency presentation

A

Normal platelet and fibrinogen
Prolonged APTT and PT

72
Q

Vitamin K deficiency treated with

A

Vitamin K
24h healed if liver good
If not only partial response

73
Q

Cause of vitamin K deficiency in premature babies

A

Liver not developed

74
Q

Cause of VK deficiency newborns

A

Vitamin K stores exhausted in 2-4 and nutritional issues and sick babie s

75
Q

Vitamin K deficiency in adults caused by

A

Not eating for a week as stores last a few weeks
Antibiotics (stops synthesis as microflora is altered)
Cirrhosis and biliary obstruction as VK is fat soluble
Small bowel obstruction
Malabsorption- pancreatitis coeliac

76
Q

How does liver disease impact coagulation

A

Low TPO= Thrombocytopenia/splenomegaly
Platelet dysfunction
Dysfibrinogenaemia
DIC released thromboplastin in vivo inducing coagulation
Reduced synthesis of coagulation factors, fibrinogen, vitamin K dependence ones are not carboxylated, antithrombin

77
Q

What is DIC

A

Disseminated intravascular coagulation

78
Q

What causes DIC

A

Gram neg sepsis infections
Carcinoma
APML
Placental abruption/amniotic fluid embolus
Widespread damage like hypothermia, snake venom, anaphylaxis

79
Q

What happens in DIC

A

Procoagulation materials released
Consumption of platelets in clotting and fibrin is deposited in microvasculature
Decreased in clotting factors and platelets
More fibrinolysis from thrombin and FDPs so D dimers made

80
Q

Complications of DIC

A

Fibrin deposition in glomeruli
Peripheral gangrene
Widespread purpura - meningococcal Sepsis and DIC

81
Q

DIC diagnosis

A

Bleeding from wounds restarts or increases
Low fibrinogen or falling
PT and APTT prolonged
Thrombocytopenia
Lots of D dimers in plasma/urine
RBC fragments

82
Q

DIC treatment

A

Treat underlying
If bleeding replace deficient factors using fresh frozen plasma/fibrinogen but sometimes this is a bad idea
Heparin to save limbs like in malaria
Protein C concentrate if meningococcal

83
Q

DIC factor deficiency

A

V and VIII

84
Q

Lupus anticoagulants

A

Antibody against proteins for phospholipids
Longer APTT and PT

MELS302 (6 decks)

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