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Haematology > Bleeding & clotting disorders > Flashcards

Bleeding & clotting disorders Flashcards

1
Q

What is thrombocytopaenia

A
  • low platelet count.
  • normal platelet count is between 150 to 450 x 109/L.
  • causes split into problems with production or destruction.
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2
Q

Problems with Production of platelets

A 
Sepsis
B12 or folic acid deficiency
Liver failure causing reduced thrombopoietin production in the liver
Leukaemia
Myelodysplastic syndrome
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3
Q

Problems with destruction of platlets

A
  • Medications
  • Alcohol
  • Immune thrombocytopenic purpura
  • Thrombotic thrombocytopenic purpura
  • Heparin induced thrombocytopenia
  • Haemolytic-uraemic syndrome
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4
Q

What medications can cause the destruction of platelets

A
  • sodium valproate
  • methotrexate
  • isotretinoin
  • antihistamines
  • proton pump inhibitors)
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5
Q

What is the presentation of thrombocytopaenia

A
  • Depends how low the count is
  • Asymptomatic
  • nosebleeds
  • bleeding gums
  • heavy periods
  • easy bruising
  • blood in the urine or stools.
  • Spontaneous intracranial haemorrhage or GI bleeds
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6
Q

differential Diagnosis of Abnormal or Prolonged Bleeding

A
  • Thrombocytopenia (low platelets)
  • Haemophilia A and haemophilia B
  • Von Willebrand Disease
  • Disseminated intravascular coagulation (usually secondary to sepsis)
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7
Q

What is Immune Thrombocytopenia Purpura (ITP) (autoimmune thrombocytopenic purpura, idiopathic thrombocytopenic purpura and primary thrombocytopenic purpura)

A
  • antibodies are created against platelets.

- This causes an immune response against platelets, resulting in the destruction of platelets and a low platelet count.

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8
Q

What are the medical management options of ITP

A

Prednisolone (steroids)
IV immunoglobulins
Rituximab (a monoclonal antibody against B cells)
Splenectomy

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9
Q

What advice should be given to patients with ITP

A
  • Follow up
  • Education about signs of bleeding e.g malaena/persistent headaches
  • Control of menstruation
  • Control of BP
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10
Q

What is Thrombotic Thrombocytopenia Purpura

A
  • microangiopathy: tiny blood clots develop throughout the small vessels of the body using up platelets and causing thrombocytopenia.
  • Problem with ADAMTS13 protein (autoimmune or genetic mutation)
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11
Q

What are the signs of thrombocytopenia Purpura

A
  • thrombocytopenia

- bleeding und er the skin

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12
Q

What does ADAMTS13 do

A
  • inactivates von Willebrand factor and reduces platelet adhesion to vessel walls and clot formation.
  • shortage in this protein leads to von Willebrand factor overactivity and the formation of blood clots in small vessels
  • blood clots in the small vessels break up red blood cells, leading to haemolytic anaemia.
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13
Q

what is the management of Thrombotic thrombocytopaemia purpura

A

Guided by a haematologist, may involve:

  • plasma exchange
  • steroids and rituximab (a monoclonal antibody against B cells).
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14
Q

What is Heparin Induced Thrombocytopenia

A
  • development of antibodies against platelets (PF4 protein) in response to exposure to heparin.
  • These are anti-PF4/heparin antibodies.
  • HIT antibodies bind to platelets and activate clotting mechanisms causing hypercoaguable state
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15
Q

Who might you notice has Heparin Induced Thrombocytopenia

A

A patient on heparin with low platelets but blood clots

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16
Q

What is the diagnosis and management of heparin induced thrombocytopaenia

A
  • testing for the HIT antibodies
  • stopping heparin
  • alternative anticoagulant guided by a specialist.
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17
Q

What is Von Willebrand disease (VWD)

A
  • most common inherited cause of abnormal bleeding (haemophilia).
  • Mostly autosomal dominant.
  • deficiency, absence or malfunctioning of a glycoprotein called von Willebrand factor (VWF).
  • Three types, type 3 most severe
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18
Q

What is the presentaiton of Von Willebrand disease (VWD)

A
  • Bleeding gums with brushing
  • Nose bleeds (epistaxis)
  • Heavy menstrual bleeding (menorrhagia)
  • Heavy bleeding during surgical operations
  • FH
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19
Q

How do you diagnose Von Willebrand disease (VWD)

A
  • history of abnormal bleeding, family history, bleeding assessment tools
  • Coagulation studies
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20
Q

What is the management of Von Willebrand disease (VWD)

A
  • Doesn’t need day to day management, just in case of major bleed or trauma, or in preparation for surgery
  • Desmopressin can be used to stimulates the release of VWF
  • VWF can be infused
  • Factor VIII is often infused along with plasma derived VWF
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21
Q

What is the management of Von Willebrand disease (VWD) in patients with menorrhagia

A 
Tranexamic acid
Mefanamic acid
Norethisterone
Combined oral contraceptive pill
Mirena coil
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22
Q

What deficiency causes haemophillia A

A

deficiency in factor VIII (8)

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23
Q

What deficiency causes haemophillia B (christmas disease)

A

deficiency in factor IX (9)

24
Q

What type of inheritance does haemophillia have

A
  • X linked recessive: all of the X chromosomes need to have the abnormal gene
  • boys only need one abnormal gene
  • Girls need 2 abnormal genes otherwise a carrier
25
Q

What are the main signs and symptoms of haemophillia

A
  • Spontaneous haemorrhage
  • Excessive bleeding into joints (haemoathrosis) and muscles
  • intracranial haemorrhage
  • haematomas
  • cord bleeding in neonates
26
Q

Where are common places for abnormal bleeding

A 
Gums
Gastrointestinal tract
Urinary tract causing haematuria
Retroperitoneal space
Intracranial
Following procedures
27
Q

how do you diagnose haemophilia

A
  • bleeding scores
  • coagulation factor assays
  • genetic testing.
28
Q

How do you manage haemophilia

A
  • Co-ordinated by a specialist

- intravenous infusions of clotting factors (VIII or IX) (in response to bleeding or preventative)

29
Q

What are the complications of intravenous infusions of clotting factors

A

formation of antibodies against the clotting factor resulting in the treatment becoming ineffective.

30
Q

How is Acute episodes of bleeding or prior to surgery is managed in haemophiliacs

A

Infusions of the affected factor (VIII or IX)
Desmopressin to stimulate the release of von Willebrand Factor
Antifibrinolytics such as tranexamic acid

31
Q

What is Venous thromboembolism (VTE)

A

blood clots (thrombosis) developing in the circulation in response to stagnation of blood and hyper-coagulable states

32
Q

What is a pulmonary embolism

A
  • Once a thrombosis has developed, it can mobilise (embolise) from the deep veins and travel through the right side of the heart and into the lungs where it becomes lodged in the pulmonary arteries.
  • This blocks blood flow to areas of the lungs and is called a pulmonary embolism (PE).
33
Q

Why do some patients with a DVT end up with a stroke

A
  • hole in their heart (ASD) the blood clot can pass through to the left side of the heart and to the systemic circulation.
34
Q

What are the risk factors for VTE

A 
Immobility
Recent surgery
Long haul flights
Pregnancy
Hormone therapy with oestrogen (COCP & HRT)
Malignancy
Polycythaemia
Systemic lupus erythematosus
Thrombophilia
35
Q

What are thrombophillias

A

conditions that predispose patients to developing blood clots

36
Q

What are some examples of thrombophillias

A 
Antiphospholipid syndrome (this is the one to remember for your exams)
Antithrombin deficiency
Protein C or S deficiency
Factor V Leiden
Hyperhomocysteinaemia
Prothombin gene variant
Activated protein C resistance
37
Q

What are contraindications for VTE prophylaxis

A
  • active bleeding

- existing anticoagulation with warfarin or a NOAC

38
Q

What VTE prophylaxis do we use

A
  • low molecular weight heparin such as enoxaparin

- Compression stocking

39
Q

When are compression stockings contraindicated

A

peripheral arterial disease

40
Q

What is the presentation of DVT

A
  • almost always unilateral
  • Calf or leg swelling
  • Dilated superficial veins
  • Tenderness to the calf
  • Oedema
  • Colour changes to the leg
41
Q

What is more likely than a DVT if presentation is bilateral

A
  • chronic venous insufficiency

- HF

42
Q

How do you examine for leg swelling

A

measure the circumference of the calf 10cm below the tibial tuberosity. More than 3cm difference between calves is significant.

43
Q

What is the Wells score

A
  • predicts the risk of a patient presenting with symptoms actually having a DVT or pulmonary embolism
  • takes in to account risk factors such as recent surgery and clinical findings such as unilateral calf swelling 3cm greater than the other leg.
44
Q

What other conditions can cause a raised D dimer

A 
Pneumonia
Malignancy
Heart failure
Surgery
Pregnancy
45
Q

What ivnestigations should be completed if suspecting VTE

A
  • D dimer
  • US doppler (repeat 6-8 days if wells score is likely and D dimer +ve)
  • CT pulmonary angiogram or ventilation–perfusion (VQ) scan.
46
Q

What is the initial management of VTE

A
  • LMWH: Start immediately if delay in getting a scan
  • Switch to long term anticoagulation e.g. warfarin or DOACs
  • Bridge with LMWH until INR stable for 24 hours if warfarin
  • Aim INR 2-3
47
Q

How long should you continue long term anti-coagulation

A
  • 3 months if obvious reversible cause (then review)
  • > 3 months if the cause is unclear, there is recurrent VTE or there is an irreversible underlying cause such as thrombophilia (usually 6 months)
  • 6 months in active cancer (then review)
48
Q

Examples of direct-acting oral anticoagulants

A

apixaban, dabigatran and rivaroxaban.

49
Q

What anti-coagulation is first line in pregnancy or active cancer

A

LMWH

50
Q

What are inferior vena cava filters

A
  • devices inserted into the inferior vena cava designed to filter the blood and catch any blood clots traveling from the venous system towards the heart and lungs.
  • recurrent PEs or if unsuitable for anticoagulation
51
Q

How do you investigate an unprovoked VTE

A

Investigate for possible cancer

  • History and examination
  • Chest X-ray
  • Bloods (FBC, calcium and LFTs)
  • Urine dipstick
  • CT TAP if >40
  • Mammogram >40
  • antiphospholipid antibodies.
52
Q

In patients with a FH or VTE what should you check for

A

Test for hereditary thrombophilias:

  • Factor V Leiden (most common hereditary thrombophilia)
  • Prothrombin G20210A
  • Protein C
  • Protein S
  • Antithrombin
53
Q

What is Budd-Chiari Syndrome

A
  • blood clot (thrombosis) develops in the hepatic vein, blocking the outflow of blood.
  • associated with hyper-coagulable states
  • causes an acute hepatitis.
54
Q

How does Budd-Chiari syndrome present

A

Abdominal pain
Hepatomegaly
Ascites

55
Q

How do you manage Budd-Chiari Syndrome

A
  • anticoagulation (heparin or warfarin)
  • investigating for the underlying cause of hyper-coagulation
  • treating the hepatitis.

Haematology (4 decks)

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