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Bleeding Disorders Flashcards

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1
Q

What is meant by induced and spontaneous bleeding?

A

Spontaneous bleeding has no obvious cause

Induced bleeding is caused by trauma or surgery

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2
Q

What is the difference between major and minor bleeding?

A

Major involves significant blood loss - this is more than one pint of blood

Minor involves mild bleeding and it may not need treatment

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3
Q

What are the interventions which may be used to treat major bleeds?

A
  1. plasma concentrates to reconstitute clotting factors
  2. platelet concentrates
  3. coagulation factor concentrates
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4
Q

What may be internal causes of major bleeding?

A
  1. haemophilia
  2. aneurysm rupture
  3. drug-induced
  4. gastrointestinal bleeds
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5
Q

What are the 5 triggers of induced major bleeding?

A
  1. trauma
  2. surgery
  3. sepsis
  4. aneurysm rupture
  5. drugs such as anticoagulants and aspirin
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6
Q

What is disseminated intravascular coagulation (DIC)?

A

A condition in which small blood clots develop throughout the bloodstream

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7
Q

Why does DIC lead to excessive bleeding?

A

The formation of small blood clots depletes platelets and clotting factors

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8
Q

How does disseminated intravascular coagulation begin?

A

If the immune system cannot deal with an infection, it will become systemic and bloodborne

This means it will affect the entire body

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9
Q

What happens in response to a bloodborne infection?

A

Tissue factor is released in response to cytokines that are released in response to infection

TF binds with FVIIa to form the extrinsic tenase complex

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10
Q

What is the role of the extrinsic tenase complex in DIC?

A

It activated FIX and FX to FIXa and FXa

This leads to the common coagulation pathway and formation of thrombin and fibrin

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11
Q

What happens if disseminated intravascular coagulation is untreated?

A

It can lead to multiple organ failure

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12
Q

What is used to treat disseminated intravascular coagulation?

A

Plasma and platelet concentrates to keep platelets and clotting factors at their normal level

The underlying infection must be treated

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13
Q

What is an abdominal aortic aneurysm (AAA)?

A

The progressive dilation of the abdominal aorta inferior to the renal and above the iliac arteries

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14
Q

Which group of people is AAA most common in?

Why is is a risk?

A

Most common in men > 60

There is a high risk of rupture if the aneurysm becomes too large

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15
Q

What is AAA rupture associated with?

A

Major internal bleeding and a 50% mortality rate

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16
Q

When will the aorta be operated on in an AAA?

A

The normal diameter of the aorta is 2 cm

If the diameter of the aorta is over 5cm, then elective surgery is performed to correct this

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17
Q

What are the 3 main causes of spontaneous bleeding and how severe is the bleeding they cause?

A
  1. vitamin K deficiency (mild to severe)
  2. coagulation factor deficiency or haemophilia (severe)
  3. thrombocytopenia (mild)
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18
Q

What is the role of Vitamin K in coagulation?

A

Vitamin K modifies coagulation factors by post-translational modification

This is essential for their function as it forms Vitamin K-dependent clotting factor complexes

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19
Q

what are the 6 Vitamin K dependent clotting factors?

A
  1. FVII
  2. FIX
  3. FX
  4. prothrombin
  5. protein c
  6. protein s
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20
Q

What are protein C and S?

A

They are anticoagulant proteins

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21
Q

What is the post-translational modification performed by vitamin K?

How does this affect the molecule?

A

Glutamic acid (Glu) residues are transformed to gamma-carboxyglutamic acid (Gla)

Gla residues become increasingly negatively charged so that they can bind to calcium

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22
Q

What do Gla residues bind to?

A

Gla binds to Ca2+

In turn, Ca2+ binds to negatively charged phospholipids provided by activated platelets

Calcium acts as a bridge between Gla and the surface of the platelet

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23
Q

Under what conditions will Vitamin K dependent enzyme complexes work efficiently?

A

Only when they are bound to a negatively charged surface (i.e. activated platelets)

This occurs via Ca2+ and Gla-domains

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24
Q

What is Vitamin K a cofactor for?

A

Carboxylase enzymes

These are involved in conversion of Glu to Gla

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25
What is the role of gamma-glutamyl carboxylase?
It oxidises vitamin K to a hydroquinone (KH2)
26
What happens to the vitamin K hydroquinone?
It is oxidised into Vitamin K epoxide (KO) during carboxylation of Glu
27
What enzyme will reconvert Vitamin K epoxide into vitamin K?
Vitamin K epoxide reductase (VKOR)
28
What is inhibited by Vitamin K antagonists? How does this work?
They inhibit VKOR Inactive Vitamin K epoxide cannot be recycled back to an active reduced form of vitamin K
29
How do vitamin K antagonists work? What is the consequence of their action?
They are competitive inhibitors that prevent specific glutamic acid residues on prothrombin from being carboxylated The protein does not form the appropriate conformation of thrombin, so fibrin monomers and clots do not form
30
What does dicumarol do?
It causes internal bleeding
31
When may warfarin (dicumarol) be prescribed?
In small doses it is an anticoagulant It inhibits VKOR, so reduces the carboxylation of clotting factors
32
What are the 5 factors that may cause vitamin K deficiency?
1. malnutrition 2. fat malabsorption 3. liver disease (alcoholic cirrhosis) 4. occurs in new-borns 5. overdose of VKAs
33
How are Vitamin K antagonists (VKAs) monitored and why?
By the international normalised ratio (INR) This ensures the levels of anticoagulants to procoagulants remains stable
34
How is a Vitamin K deficiency treated?
Administering Vitamin K Plasma concentrates are given in the short term as Vitamin K administration takes some time to work its effect
35
What is Haemophilia A a deficiency of?
It is a deficiency of FVIII This is a cofactor for FIX in the conversion of FX to FXa in the intrinsic pathway
36
What is Haemophilia B a deficiency of?
It is a deficiency of FIX FIXa converts FX to FXa in the intrinsic pathway
37
What do both Haemophilia A and Haemophilia B have in common?
1. they are X-linked recessive conditions 2. relatively rare 3. if female is a carrier, the male offspring are at risk
38
Why is there insufficient coagulation in haemophilia?
Both FVIII and FIX are important in increasing the amount of thrombin, as they influence the activity of FX Not enough thrombin is produced
39
When is the intrinsic pathway activated?
It is activated by FXII when the blood vessel wall is damaged
40
When is the extrinsic pathway activated?
It is activated by tissue factor when there is trauma to extravascular cells
41
What does prothrombin time (PT) measure? What is its trigger?
It uses tissue factor as a trigger It measures factors in the extrinsic pathway
42
When will PT be prolonged?
FVII deficiency | it is also prolonged in haemophilia, but APTT is not
43
When is PT used?
In the INR monitoring of oral anticoagulants such as warfarin
44
What is normal prothrombin time? What INR reading does this give?
Normal PT is 11 - 13.5 seconds This leads to an INR of 0.8 - 1.1
45
What are both PT and APTT sensitive to?
the common pathway and FV, FX, prothrombin and fibrinogen deficiency
46
What is activated partial prothrombin time used to measure? What is its trigger?
It measures factors in the intrinsic pathway | It uses silica as a trigger this is a negatively charged surface that will activate FXII
47
When will APTT be prolonged?
FVIII, FIX, FXI and FXII deficiency
48
What does it show if both PT and APPT are prolonged?
There is a problem with the common pathway
49
If the mother is a carrier of haemophilia, what is the chance of a son/daughter being affected?
50% chance that the son is affected 50% chance that the daughter is a carrier
50
If the father has haemophilia, what is the chance of a son/daughter being affected?
The son always inherits the unaffected X chromosome from the mother The daughter is an obligatory carrier of haemophilia
51
What is bleeding like in haemophilia?
1. bleeding is severe 2. spontaneous bleeding, particularly into the muscle and joints 3. easy bruising
52
Why is there a significant risk of stroke in haemophilia?
cerebral haemorrhage is common this increases risk of stroke and bleeding into the brain
53
What is the treatment for haemophilia?
Prophylactic treatment is given with recombinant or plasma factor concentrates (either VIII or IX)
54
What types of injections are given for haemophilia A and how often?
Injections of octocog alfa every 48 hours
55
What are the side effects of octacog alfa?
Side effects are uncommon There may be an itchy skin rash at the site of injection
56
What types of injections are given for haemophilia B and how often?
Injections of nonacog alfa twice a week
57
What are the side effects of nonacog alfa?
Headache, altered taste and swelling at the injection site
58
When may desmopressin be administered?
As an on-demand treatment for haemophilia A It stimulates the production of clotting factors
59
What is the on-demand treatment for haemophilia b?
Injection with nonacog alfa
60
What may make treatment for haemophilia become less effective?
Patients may develop IgG inhibitor against the factor concentrates An antibody binds to FIX or X and acts like FXIII
61
How can IgG inhibitors be treated?
Immune tolerance induction (ITI) This involves daily injections of clotting factors so that the immune system recognises them and stops producing inhibitors
62
What causes Von Willebrand disease?
It is an inherited disorder It is caused by a deficiency of Von Willebrand factor vWF
63
What are the symptoms of Type 1 von Willebrand disease? What is it caused by?
There is a reduced level of vWF in the blood This causes mild bleeding, usually only after injury or surgery
64
What are the symptoms of Type 2 von Willebrand disease? What is it caused by?
The vWF that is present does not function properly Bleeding is more frequent and heavier than type 1
65
What are the symptoms of Type 3 von Willebrand disease? What is it caused by?
There are very low levels of vWF or none at all bleeding from the nose and gut is common, and muscle bleeds occur after injury
66
What causes platelet type von Willebrand disease?
There is a mutation in the gene encoding platelet glycoprotein Iba (GPIba) This is a receptor for vWF
67
What is the main consequence of platelet type von Willebrand disease?
there is excessive and unnecessary platelet-vWF interaction This removes platelets from the circulation and leads to thrombocytopenia
68
What is the primary function of vWF? Where is it found?
It helps platelets to adhere to wound sites It is always in circulation but the levels in the blood increase when it is needed
69
How does vWF influence clotting factors?
It stabilises FVIII, allowing it to have a longer half-life in the blood
70
Where is vWF produced from?
It is produced by endothelial cells in the Weibel-Palade bodies (inner lining of blood vessels) and by megakaryocytes It is then packaged into alpha granules in platelets
71
How does vWF help with platelet aggregation and adhesion?
1. In addition to GPVI binding collagen, GPI will bind vWF 2. vWF will, in turn, bind collagen 3. vWF and fibrinogen will also bind to a(IIb)b(3) which further supports aggregation
72
What are the common bleeds seen in von Willebrand disease?
1. menorrhagia 2. epistaxis 3. bleeding after tooth extractions 4. easy bruising
73
What is menorrhagia?
Abnormally heavy bleeding at menstruation
74
What types of bleeds are seen in more severe cases of vWD?
1. gastrointestinal bleeds 2. petechiae 3. muscular or joint bleeds
75
What is petechiae?
Capillary bleeding in the skin
76
What is the treatment for von Willebrand disease?
1. vWF concentrates 2. desmopressin (type 1 and 2) 3. platelet concentrates
77
How does desmopressin work to treat vWD?
It releases vWF from the endothelium
78
Which clotting factor deficiency does NOT lead to bleeding?
factor 12
79
What is thrombocytopenia?
The loss or dysfunction of platelets, leading to an abnormally low level of platelets in the blood
80
What is a normal human platelet count?
from 150,000 - 450,000 platelets per microlitre of blood
81
How may thrombocytopenia be acquired?
1. leukaemia 2. blood loss 3. disseminated intravascular coagulation 4. drug-induced 5. immune thrombocytopenia purpura (ITP)
82
How may thrombocytopenia be inherited?
1. congenital amegakaryocytic thrombocytopenia (CAMT) 2. faconi's anaemia (haematological malignancy and bone marrow failure) 3. Glanzmann thrombocytopenia 4. Bernard-Soulier syndrome
83
What is Glanzmann thrombocytopenia?
A mutation in a(IIb)b(3)
84
What is Bernard-Soulier syndrome?
A deficiency of GPI
85
How does bleeding in thrombocytopenia vary to haemophilia?
Bleeding is milder than haemophilia It can be severe in the case of CAMT
86
What are the characteristic bleeds seen in thrombocytopenia?
1. easy bruising 2. gum bleeds 3. epistaxis 4. menorrhagia 5. petechiae
87
What are the treatments for thrombocytopenia?
1. corticosteroids are given for ITP 2. platelet transfusions 3. splenectomy
88
What types of thrombocytopenia are treated?
the most severe cases are treated treatment focuses on the underlying cause

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