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Haematology > Haemostasis And Bleeding Disorders > Flashcards

Haemostasis And Bleeding Disorders Flashcards

1
Q

What are the 3 key steps to haemostasis?

A
  1. vasoconstriction (decreases pressure downstream and so helps limit bleeding)
  2. primary haemostasis- platelet plug forms in seconds to minutes, its fragile but may control bleeding
  3. secondary haemostatic plug forms as fibrin filaments stabilise the platelet plug- 30 mins
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2
Q

What activates platelets to stick together to form the primary plug?

A
  • Collagen surfaces - tissue factor (within extravascular areas)
  • ADP (released from other platelets to amplify response)
  • Thromboxane A2 (also released by other platelets)
  • thrombin
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3
Q

Describe the process of a primary plug forming

A
  • damage to endothilium
  • basement membrane exposed
  • platelets bind to von willebrand factor in the subendothilial basement membrane
  • they secrete ADP, thromboxane A2 ect which causes more platelets to aggregate and initiates clotting cascade
  • platelets crosslink as they aggregate
  • clotting cascade has started to produce fibrinogen which helps cross link them
  • platelets swell and change shape into sticky spheres
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4
Q

How does aspirin decrease platelet aggregation?

A
  • it irreversibly inactivates cyclooxygenase so thromoxane A2 cannot be produced
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5
Q

describe how the extrinsic and intrinsic pathway are initiated

A

intrinsic pathway: activated by abnormal surfaces that are negatively charged (bind via carboxyglutamate residues) (platelets not needed) eg collagen or glass (von willebrand releases factor 8 to help activate it)
extrinsic: activated by damaged cells near area of injury and platelets, this is through tissue factor release

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6
Q

How does warfarin work?

A

inhibits vitamin K production so clotting factors cannot be localised - it is also teratogenic

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7
Q

how does heparin work?

A

it is a co factor for antithrombin 3 so prevents clotting

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8
Q

How does the clotting cascade lead to a secondary plug?

A
  • both pathways lead to prothrombin being activated to thrombin and this cleaving fibrinogen to fibrin
  • fibrin acts as a mesh within the platelet plug to stabilise it
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9
Q

What factors oppose clotting to ensure it is not out of hand?

A

Protein C, S and antithrombin 3 are all released as the clot is being formed to ensure it is not excessive, these oppose the formation of fibrin by inhibiting certain areas of the clotting cascade.
Also dilution of clotting factors and fibrin degradation products

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10
Q

What enzyme is responsible for fibrinoylsis? what activates it

A

plasmin

activated by streptokinase, tissue plasminogen activator (activated by high fibrin levels) and urokinase

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11
Q

When can streptokinase be used therapeutically?

A
  • can only be given once (its antigenic)

- will dissolve emboli and thromboemboli

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12
Q

Why is thrombosis risk high 7-10 days post surgery?

A

fibrinolytic activity remains low

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13
Q

What can be detected by blood and is produced as a result of a lots of fibrinolysis?

A

D- Dimers

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14
Q

What does the APTT (partial thromboplastin time) tell you?

A

The time taken for blood to clot by the intrinsic pathway (factors 12,9,10 and 8 and von willebrand factor)

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15
Q

What does the PT measure?

A

the prothrombin time

The time taken for extrinsic pathway- factor 7

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16
Q

If PT and APTT are abnormal, what factors could be faulty?

A

factors 5,10, prothrombin and fibrinogen

17
Q

What is the INR?

A

the same as the PT but normalised to account for different lab techniques

18
Q

Why should you be careful putting someone on warfarin on antibiotics?

A

antibiotics enhance warfarins ability (less clotting)

19
Q

What are the general signs of someone with a bleeding disorder?

A
  • recurrent bruising of muscle and skin
  • Joint pain and deformity (from bleed)
  • prolonged bleeding from dental extraction
  • prolonged bleeding generally from cuts ect
  • intracerebral haemorrhage
  • recurrent nose bleeds
20
Q

What 4 things can go wrong to cause bleeding disorders?

A
  • too much clotting
  • too much bleeding:
    • coagulation defects
    • vessel wall defects
    • platelets too low or broken
21
Q

What inherited disorders of coagulation are there?

A

Haemophilia A, B and Von Willebrands disease

22
Q

What is the inheritance pattern of haemophilia A and B?

A

X linked ressesive

23
Q

What is wrong in haemophilia A and B and how do you treat it?

A

A= factor 8
B= factor 9
They can treated with recombinant factor 8/9 and heamophilia A can also be treated with DDAVP

24
Q

What will be the blood test abnormalities in haemophilia A and B?

A
  • in both
  • APTT with be raised
  • PT will be normal
  • platelets and fibrin normal
  • factor 8/9 levels low
25
Q

What is the inheritance pattern and defect in Von willebrand s disease?

A
  • auto dominant
  • defect in vwf receptor defect so less produced
  • This therefor impacts platelet adhesion and factor 8
26
Q

What will be blood test abnormalities in Von willebrand s disease?

A
  • VWF, factor 8 decrease
  • APTT increases
  • PT normal
  • longer bleeding time
  • microcytic anaemia due to bleeding
27
Q

Since the intrinsic pathway is mostly effected in Von willebrands disease, what specific symptoms will it come with?

A
  • associated with platelet associated bleeding from trauma
  • nose and gum bleeds
  • prolonged bleeding after trauma
  • heavy periods
  • bruising
  • joint bleeds more rare
28
Q

What aquired diseases of coagulation defects are there?

A
  • Vit K deficiency (also when on warfarin)
  • liver disease (clotting factors made here)
  • anticoagulants
  • disseminated travascualr coagulopathy
29
Q

What is disseminated intravascular coagulopathy?

A

DIC is a secondary condition to many other diseases which leads to activation of clotting meaning many microthrombi form, using up clotting factors, platelets ect, leading the pt susceptible to excessive bleeding. Also they get a haemolytic anaemia as the micro thrombi damage RBCs

30
Q

What can cause DIC?

A
  • sepsis (gram - bacteria can produce endotoxin which activates it)
  • severe trauma (especially to brain as it contains lots of thromboplastin)
  • extensive burns
  • child birth complication (amniotic fluid embolism)
  • malignancies
  • snake bites
31
Q

What will be blood test results of DIC?

A
  • high FDPs and D dimers
  • raised PT and APTT, low fibrinogen
  • microangiopathic haemolytic anaemia
32
Q

What is the presentation of DIC?

A

Large bruises as venepuncture sites

  • large bruises on legs and sites of trauma
  • bleeding from ears, nose and throat
  • GI and resp bleeding
  • confusion
  • fever
  • pupuric rashes
  • anaemia and thrombi signs (cyanosis, gangrene )
  • haemoatouria
33
Q

How is DIC treated?

A
  • transfuse platelets, fresh frozen plasma (contains clotting factors), cryoprecipitates (contain factor 8, von willebrand factor, fibrinogen ect) if bleeding
  • heparin to prevent microthrombi if no bleeding
  • treat underlying cause
34
Q

Below what platelet count does someone have thrombocytopenia?

A

Less than 100x10^9 g/L

35
Q

Below what platelet count does spontaneous bleeding occur and what are the key signs of thrombocytopenia?

A
  • less than 20x10^9 g/L
  • easy bruising
  • petchiae (small red dots) and purpra (larger red areas)
  • mucosal bleeding
  • severe bleeding after trauma
36
Q

what will be the blood test abnormalities of some one with thrombocytopenia?

A
  • low platelets
  • long bleeding time
  • normal APTT and PT
37
Q

WHAT CAN CAUSE REDUCED PRODUCTION OF PLATELETS ?

A
  • b12/ folate deficiency
  • bone marrow cancer
  • drugs (chemo and antibiotics)
  • viruses (HIV, hepatitis, EBV, CMV)
38
Q

What can cause increased removal of platelets?

A
  • hypersplenism
  • autoimmune destruction (immune thrombocytopenic purpura)
  • DIC
39
Q

What can cause vessel wall defects?

A
  • hereditary diseases (HHT)
  • ehlers danlos and other connective disuse disorders
  • old age
  • steroids
  • infections like meningitis
  • scurvey

Haematology (3 decks)

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