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Blood Disorders > Abnormalities Of Haemostasis > Flashcards

Abnormalities Of Haemostasis Flashcards

1
Q

What substances do we need to form a blood clot

A

Platelets
VWF
Clotting factors: proteases (F2,7,9,10)- these are dependent on vitamin k, and f11. Co factors: f5,8, fibrinogen and factor 13.
White blood cells

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2
Q

What is the primary haemostasis

A

Formation of an initial haemostastis plug that contributes by platelets and VWF

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3
Q

What is the secondary homeostasis

A

Involvment of clotting factors to form a stable clot

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4
Q

What do we need for normal haemostasis

A

Normal vessel wall integrity
Adequate number of platetes and platelets funcitoning properly
Adequate number of clotting factors
Proper function of fibrinolytic pathway- this breaks down blood clots to stop thrombosis

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5
Q

What happens when a blood vessel is injured

A
  1. Localised vasoconstriction at the site of injury
  2. Exposure of collagen from blood vessel starts platelet adhesion to subendothelium of damaged blood vessel (primary haemostasis)
  3. Platelet aggregations/activation, this contributes to thrombus formaiton.
  4. Vasoconstriction and release of tissue factor from the vessel wal activates of coagulation cascade
  5. This cuases insoluble Fibrin formation (scaffol) formation which contributes to thormbus formation
  6. Fibrinolytic degradation of clot once the bleeding has stopped.
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6
Q

What lab test can be used to investiage the haemostatic system

A

Platelet count
Prothrombin count (PT)
Activated partial thromboplastin time (APPT)
Fibrinogen level

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7
Q

What is INR

A

International normalised ratio (pt of the patietn to the mean in the population)

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8
Q

Which particular patients should have their INR checked

A

Warfarin users

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9
Q

What pathway does the PT measure

A

Extrinsic pathway

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10
Q

What pathway does the APPT measure

A

Intrinsic pathway

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11
Q

What are the pathways in the clotting cascade

A
  1. Intrinsic pathway
  2. Extrinsic pathway
  3. Final common pathway
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12
Q

Describe what happens in the extrinsic pathway

A
  1. Releease of tissue factor from vessel wall causes cleavafe of factor 7 to acitvated factor 7
  2. Activated factor 7 cleaves factor 10 to factor 10a
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13
Q

What happens in the intrinsic pathway of the clotting cascade

A
  1. Factor 12 cleaves to form acitvated factor12
  2. Factor 12a cleaves factor 11 to factor 11a
  3. Factor 11a cleaves factor 9 to factor 9a
  4. Factor 9a cleaves factor 10 to factor 10a with factor 8
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14
Q

What happens in the final common pathway in the clotting cascade

A
  1. Both intrinsic and extrinsic pathway lead to the formation of factor 10a
  2. Factor 10a with factor 5 cleaves prothrombin into thrombin
  3. Thrombin cleaves fibrinogen to fibrin
  4. Thrombin also cleaves factor 13 to factor 13 a which in turn cleaves fibrin to form a stable fibrin clot by crosslinking fibrin
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15
Q

What receptors are on the surface of platelets

A

Gp1b receptor

Gp11b/3a receptoro

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16
Q

What does gp1b bind to

A

VWF

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17
Q

What does GP11B/3A bind to and what does it cause

A

Other platelets to cause platelet aggregation

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18
Q

Descirbe what happens in primar haemostasis

A
  1. There is exposed collagen on the damaged vessel wall
  2. VWF binds to the collagen receptors
  3. VWF changes configuration
  4. Platelets bind to WVF via gp1b receptor on platelet surface
  5. Platelet becomes activated and releases their secondary granules to cause platelet activatation and aggegation
  6. Platelets cross link with gp11b/3a receptor and VWF
  7. This forms a platelet clot that occludes the blood vessel
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19
Q

What 2 problems can occur with WVF to cause disease

A
  1. Quantitative deficiency of VWF

3. Qualitative defect of VWF

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20
Q

What are the types of quantitative deficiency of VWF that can occur

A

Type 1: partial

Type 3: complete absence of VWF

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21
Q

What are the types of qualitaitve defect of VWF that can occur i.e there are normal numbers of VWF but the function is abnormal

A

Type 2a: decreased interaction of VWF with platelets to from multimers of VWF (many wvf stuck togehter)
Type 2b: increased affinity of VWF for platelet gp1b
Type 2m: decreased interaction of vwf with platelets- not associated with mutlimers of VWF
Type 2n: decreased affinity of vwf for factor8

22
Q

What are the secondary mediators involved in platelet activation and aggregation

A

Adp
Thrombin
Collagen
Txa2

23
Q

What happens when the platelets release granules

A

The platelets become activated by chaning shape and increase SA to enable them to interact with other clotting factors

24
Q

What are the types of granules platelets have

A

Alpha

Dense

25
Q

What do dense granules release

A

Adp
Calcium
5HT

26
Q

What do alpha granules release

A 
FGN
Factor 8
VWF
Factor 5 
PDGF
27
Q

What are the types of congenital disorders platelets can have

A
  • absence of granules

- abnormality of platelet receptor

28
Q

If there is an absence of alpha granules what does this resultin

A

Grey platelet syndrome

29
Q

If there is an absence of dense granules what does this result in

A

Storage pool disease

30
Q

If there is an absence of GP1B receptor on platelet what does this result in

A

Bernard soulier syndrome

31
Q

If there is an absence of gb11b/3a receptor of platelet what does this result in

A

Glanzmann thrombastenia

32
Q

Which protein cleaves VWF multimers

A

ADAMTS13

33
Q

What happens when VWF mutlimers keep on formin and there is a deficiency of ADAMTS13

A

Thrombosis occurs

34
Q

What is TTP

A

An autoimmune condition with deficiency of ADAMTS13 so VWF mutlimers form and thrombus occurs

35
Q

What is the treatment of TTP

A

Plasma exchange

36
Q

What is the reduction in factor 8 called

A

Haemophillia

37
Q

What is haemophillia

A

X-lined conditon i.e males can have condition and females will be carriers

38
Q

What is the treatment of haemophilia

A

Giving missing clotting factor

Emicizumab

39
Q

What is emicuzumab

A

An antibody that binds to factor 9 and 10 so it stimulates the down cascade independent to factor 8

40
Q

How is fibrin formed

A

Thrombin cleaves fibrinogen to fibrin

41
Q

What is fibrin

A

The scaffold of platelets

42
Q

How does fibrinolysis occur

A

Plasminogen is cleaved by tpa to give plasmin

Plasmin breaks down fibrin to break the blood clot

43
Q

What is a measure of the break down product of fibrinolysis

A

D-dimer

44
Q

What does a d dimer tell us

A

That active coagulation and fibrinolysis has been occuring

45
Q

What drugs can we have to stop fibrinolysis and therefore stabilise blood clots

A

Tranexamic acid

46
Q

How does tranexamic acid work

A

Inactivates plasminogen

47
Q

Who is tranexamic acid given to

A

Patients that are bleeding heavily

48
Q

What is immune thrombocytopenia purpurin

A

A reduction in platelets due to antibodies that are directed against the glycoprotein, gp11b/3a or GP1B

49
Q

What does VWF present as

A

Menorhhagia

50
Q

What does haemophilia a present as clinically

A

Bleeding in the joints and muscles and is common in men

Blood Disorders (9 decks)

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