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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
What happens to platelets during initiation
No platelets or vWF yet so no coagulation until there is an injury
26
What happens in the initiation coagulation phase
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
27
Purpose of initiation
To get ready for tissue injury Generating low levels of thrombin No injury yet
28
What happens in the amplification phase
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
29
What happens in the propagation phase
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
30
What happens in a thrombin burst
Fibrinogen cleaved to fibrin XIII activated to stabilise clot Positive feedback on V,VIII,XI Stops fibrinolysis
31
What happens if you don’t have enough thrombin
Fibrin strands are thin and weak Fibrinolysis breaks it down easily through tissue movement
32
Does the fibrin clot start strong
No, starts weak and strengths with FXIII and clot retraction of platelets
33
Tube collection in coagulation testing
Sodium Citrate tube Anticoagulant to stop clotting and activation of platelets and factors 9:1 ratio
34
Sample type for plasma aggregometry
Centrifuged PRP plasma rich plasma
35
Sample type for most tests in coagulation
Platelet poor plasma
36
Sample problems can arise from
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
What pathway is TCT related too
Common pathway
38
What is PT sensitive too
Deficiency in VII, X, V and lesser II
39
Reagents for prothrombin time
Thromboplastin (TF reagent with phospholipids and anti heparin) CaCl Buffet
40
What is in thromboplastin
Tissue factor reagent Phospholipids Anti heparin
41
What is detected in PT
Fibrin formation using optical detection or electromechanical detection
42
Clinical factors prolonging PT
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
Technical factors prolonging PT
Cold activation of FVII Clotted sample Haemolysis Additive ratio/sample volume Heparin contamination Old reagents Delayed testing
44
Steps of APTT
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
What is APTT sensitive too
Deficiency of factors V, X, VIII, IX, XI, XII
46
What is in the phospholipid platelet substitution used in APTT
Partial thromboplastin NO TF Point is to eliminate patient platelet variability Buffer
47
How is APTT measured
Measures fibrin formation Decrease in optical transmittance/absorbance as clot forms Electromagnetic detection
48
Clinical factors prolonging APTT
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
Technical factors prolonging APTT
Clotted sample Volume/ additive ratio Heparin Haemolysis Turbidity Thromboplasin nature Delay in testing etc
50
TCT method
PPP Thrombin reagent with CaCl and buffer Start timer and wait for clotting
51
Principle of TCT
Add thrombin in excess and see how long it takes for a clot to form Focusing on fibrinogen and heparin screening
52
What affects TCT
Fibrinogen conc Fibrin degradation products Heparin (VERY SENSITIVE) Thrombin inhibitor drugs like dabigatran
53
List three anticoagulants which prolongs APTT
Heparin Warfarin Dabigatran
54
What tests are performed as a duplicate assay
PT APTT TCT FIBRINOGEN
55
Fibrinogen method
PPP 4 different assays - we use Clauss
56
What prolongs fibrinogen
DIC- consumption of fibrinogen Liver disease Fibrin degradation products Thrombotic therapy Hypo/dysfibrinogenaemia
57
Correction studies are done on what
APTT and PT
58
When are correctional studies done
On a prolonged APTT and PT
59
Correctional study method
1:1 mix of normal plasma with patient plasma
60
What happens if plasma is not corrected
Clotting time is still prolonged or only partially corrected means inhibitor is present like heparin,antibodies or dabigatran
61
What happens if prolonged times are corrected
Patient has a factor deficiency
62
What deficiency is haemophilia A
Factor VIII/8 X linked De novo in 30%
63
What is haemophilia B
Christmas Disease FIX deficiency X linked
64
Haemophilia bleeding pattern
Spontaneous bleeding and bleeding into joints (haemarthrosis)
65
Solutions to joint bleeding in harmony
Reconstructive joint surgery as cartilage eroded from constant bleeding leading to narrow joint space
66
Haemophilia treatment depends on what
How severely deficient they are in the factor If only less than 1% factor is there then severe Above 5 is mild
67
Haemophilia treatment
Factor concentrates (specific for each lacking factor) Fibrinolytic inhibitor (tranexamin acid) = stops clot breakdown DDAVP if mild haemophilia A
68
What does DDAVP do
Boosts endogenous vWF release from EC so more factor 8 too
69
Acquired coagulation disorders
Vitamin K deficiency Liver disease DIC Anticoagulants Factor inhibitor antibodies Haemo dilution
70
Vitamin K dependent factors
II, VII, IX, X PROTEIN C AND S
71
Vitamin K deficiency presentation
Normal platelet and fibrinogen Prolonged APTT and PT
72
Vitamin K deficiency treated with
Vitamin K 24h healed if liver good If not only partial response
73
Cause of vitamin K deficiency in premature babies
Liver not developed
74
Cause of VK deficiency newborns
Vitamin K stores exhausted in 2-4 and nutritional issues and sick babie s
75
Vitamin K deficiency in adults caused by
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
How does liver disease impact coagulation
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
What is DIC
Disseminated intravascular coagulation
78
What causes DIC
Gram neg sepsis infections Carcinoma APML Placental abruption/amniotic fluid embolus Widespread damage like hypothermia, snake venom, anaphylaxis
79
What happens in DIC
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
Complications of DIC
Fibrin deposition in glomeruli Peripheral gangrene Widespread purpura - meningococcal Sepsis and DIC
81
DIC diagnosis
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
DIC treatment
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
DIC factor deficiency
V and VIII
84
Lupus anticoagulants
Antibody against proteins for phospholipids Longer APTT and PT

MELS302 (6 decks)

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