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CLINICAL PATHOLOGY > Aquired Bleeding Disorders COPY > Flashcards

Aquired Bleeding Disorders COPY Flashcards

1
Q

Give the 6 acquired bleeding disorders?

A

1) Vitamin K deficiency
2) Liver disease
3) Massive transfusion syndrome
4) DIC
5) Iatrogenic
6) Acquired inhibitors

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2
Q

When assessing a patient with a possible bleeding disorder, what 5 things should be examined clinically?

A

1) Patterns of any bruising or other evident haemorrhagic signs
2) Signs of underlying disease
3) Joints
4) Muscles
5) Skin

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3
Q

What are the 3 clotting tests, which part of the clotting cascade does each measure?

A

1) Activated partial thromboplastin time - intrinsic pathway (+common pathway)
2) Prothrombin time - extrinsic pathway (+common pathway)
3) Thrombin clotting time - Thrombin - fibrin

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4
Q

Inhibitors to clotting do exist, if a patient has a prolonged APTT - what test is carried out to tell if this is due to a deficiency or an inhibitor?

A

Repeat the APTT test but this time mix 50:50 with normal plasma
If the APTT time is improved then the problem is a deficiency
If the APTT time is unchanged then the problem is an inhibitor (because this blocks the clotting due to the normal plasma too)

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5
Q

Along with the 3 clotting tests, what is another useful blood test to carry out in patients with defects of haemostasis?

A

Platelet count

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6
Q

Why does a clotting deficiency occur with a massive transfusion?

A

because just transfusing red cell (even if it was whole blood the labile clotting factors would have disappeared anyway) so once you have done the transfusion you have a relative deficiency of red cells

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7
Q

How is the platelet count, PT, APTT and TT altered in liver disease?

A

Platelets low
PT - prolonged
APTT - prolonged
TT - normal

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8
Q

How is the platelet count, PT, APTT and TT altered in DIC?

A

Platelets low
PT - prolonged
APTT - prolonged
TT - grossly prolonged

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9
Q

How is the platelet count, PT, APTT and TT altered in massive transfusion?

A

Platelets low
PT prolonged
APTT prolonged
TT normal

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10
Q

How is the platelet count, PT, APTT and TT altered with oral anticoagulants?

A

Platelets normal
PT grossly prolonged
APTT prolonged
TT normal

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11
Q

How is the platelet count, PT, APTT and TT altered in heparin treatment?

A

Platelets normal
PT mildly prolonged
APTT prolonged
TT prolonged

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12
Q

How is the platelet count, PT, APTT and TT altered with circulating anticoagulant?

A

Platelets normal
PT normal or prolonged
APTT prolonged
TT normal

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13
Q

The intrinsic system is activated by what?

A

Surface contact

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14
Q

The extrinsic system is activated by what?

A

Tissue factor

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15
Q

What is the role of vitamin K in producing coagulation factors?

A

Vitamin K is the co factor for the enzyme gamma glutamyl carboxylase which converts Vit-k dependent clotting factors into active clotting factors

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16
Q

What is the involvement of VKOR in producing clotting factors?

A

As vitamin K acts as a co factor is converted from its reduced form to its oxidised form but needs to be reduced again to perform its function
Vitamin K reductase (VKOR) converts vit K from oxidised back to reduced form thus regenerating it

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17
Q

How does warfarin bring about anticoagulation?

A

It blocks VKOR so it cant regenerate Vit K and leads to a deficiency of Vit K dependent clotting factors

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18
Q

Where are all clotting factors synthesised?

A

In the liver

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19
Q

Vitamin K deficiency leads to deficiencies of which 4 clotting factors?

A

2,7,9,10

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20
Q

Give the 4 causes of vitamin K deficiency?

A

1) Obstructive jaundice
2) Prolonged nutritional deficiency
3) Broad spectrum Abx
4) Neonates - classically 1-7 days)

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21
Q

Liver disease causes what kind of coagulopathy?

A

Cirrhotic coagulopathy

22
Q

How severe is cirrhotic coagulopathy?

A

Have increased risk of severe bleeding from invasive procedures or surgery

23
Q

The liver is essential to maintenance of the levels of which 3 substances involved in haemostasis?

A

1) Coagulation factors
2) Components of fibrinolytic system
3) Naturally occurring anticoagulants

24
Q

What 5 effects of liver disease cause impaired haemostasis?

A

1) Thrombocytopenia
2) Platelet dysfunction (plasmin induced cleavage of surface glycoproteins)
3) Reduced plasma conc of all coagulation factors (except 8)
4) Delayed fibrin monomer polymerisation due to altered fibrinogen glycosylation
5) Excessive plasma activity

25
Q

What is the definition of a massive transfusion?

A

Transfusion of blood volume equal to the patients total blood volume in less than 24 hours or 50% blood volume loss within 24 hours

26
Q

For what 3 reasons do you get haemostatic abnormalities in massive transfusion?

A

1) Due to depletion of platelets and coagulation factors
2) Due to DIC - risk factors are extensive trauma, head injury, prolonged hypertension
3) Due to underlying disease eg. liver or renal drug treatment or surgery

27
Q

How many litres of blood need to be transfused in adults before you see problems with thrombocytopenia?

A

7-8 litres

28
Q

You get coagulation factor depletion due to dilutional effects in massive transfusion, which 3 factors do you mainly see the depletion in?

A

1) Factor 5
2) Factor 8
3) Fibrinogen

29
Q

Why can you get citrate toxicity with massive transfusion, what are its effects?

A

Blood from the blood bank has citrate containing anticoagulants in it
Causes hypothermia in neonates who have increased susceptibility

30
Q

Can get hypocalcaemia with massive transfusion, is the clinically significant?

A

There will be no clinically significant effect on bleeding but may need to treat the hypocalcaemia anyway

31
Q

What is DIC?

A

Inappropriate activation of the clotting system with activation of the fibrinolytic system at the same. Get thrombosis of small vessels which can lead to organ dysfunction and get bleeding due to consumption of platelets and coagulation factors. Can also get microangiopathic haemolysis with it too

32
Q

Give the 5 causes of acute DIC?

A

1) Sepsis
2) Obstetric complications
3) Trauma/ tissue necrosis
4) Acute intravascular haemolysis (eg. ABO incompatibility)
5) Fulminant liver disease

33
Q

Give the 4 causes of chronic DIC?

A

1) Malignancy
2) End stage liver disease
3) Severe localised intravascular coagulation
4) Obstetric - retained dead foetus

34
Q

In a coagulation screen in DIC, how are the 3 times affected?

A

PT - prolonged 70%
APTT - prolonged 50%
TT - usually prolonged

35
Q

What 4 laboratory tests used in investigating DIC?

A

1) FBC and blood film
2) Coagulation screen
3) Fibrinogen concentration
4) FDP or D Dimer

36
Q

Is there a diagnostic test for DIC?

A

No, use the 4 lab tests mentioned previously and a scoring system is sometimes used

37
Q

What is the management of DIC?

A

1) Treat underlying cause: Abx (Sepsis), Obstetric interventions, chemotherapy/tumour resection
2) Supportive treatment

38
Q

What is the supportive treatment used in DIC? 3

A

1) Maintain tissue perfusion
2) Co-ordinate invasive procedures
3) Folic acid and Vit K to support recovery period especially if the illness is prolonged

39
Q

Blood products can be used to treat DIC, their use is determined by bleeding or invasive procedure, what 3 products are given and in what situations?

A

1) Platelets transfusion if platelets 1.5

3) Cryoprecipitate or fibrinogen concentrate if fibrinogen

40
Q

Why could abnormalities of haemostasis present with painful joints?

A

Due to bleeding into joints - haemarthrosis

41
Q

How is dosing of oral anticoagulants controlled?

A

INR measurement

42
Q

INR is the prothrombin ratio, what is the prothrombin ratio?

A

(Patients thrombin time) / (mean normal prothrombin time)

43
Q

Name 3 types of drugs which potentiate warfarin effects?

A

1) Some Abx
2) NSAIDs
3) Corticosteroids

44
Q

Name 5 drugs which antagonise the warfarin effect?

A

1) Cholestyramine
2) Spironolactone
3) Rifampicin
4) Carbamazepine
5) Vitamin K

45
Q

What is the treatment for reversal of warfarin effect in life threatening haemorrhage? 2

A

1) Vitamin K

2) Four factor concentrate (PCC)

46
Q

What is the treatment for reversal of warfarin effect in non-life threatening bleeding? 2

A

1) Withhold warfarin

2) Give Vitamin K

47
Q

Unfractionated heparin antagonises which 2 coagulations factors?

A

1) Thrombin

2) Xa

48
Q

What is the most commonly used assay to monitor anticoagulation with heparin?

A

APTT (activated partial thromboplastin time)

49
Q

What are the 3 alternative assays to APTT in monitoring anticoagulation with unfractionated heparin?

A

1) Heparin level by protamine titration
2) Heparin level by anti-Xa assay
3) Calcium thrombin time

50
Q

Which assay is used in monitoring anticoagulation with low molecular weight heparin? Why is APTT not used?

A

Anti Xa assays must be used

APTT is not sensitive to LMWH

51
Q

In overanticoagulation which drug can be administered to neutralise UFH?

A

Protamine (1mg neutralises 100IU of heparin (max 40mg) but the effects of protamine on LMWH are complex and less predictable)

52
Q

What are the 4 advantages of LMWH over UFH?

A

1) LMWH has a higher ratio of anti-Xa to anti-IIa (thrombin) activity
2) Improved bioavailability
3) Longer half life allowing once daily administration
4) More predictable anti-coagulant response: monitoring is not routinely required

CLINICAL PATHOLOGY (56 decks)

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