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YEAR 5: Haematology > Haem: Coagulation Pt.3 > Flashcards

Haem: Coagulation Pt.3 Flashcards

1
Q

What can cause immune-mediated thrombocytopaenia?

A
  • Idiopathic
  • Drug-induced (e.g. quinine, rifampicin)
  • Connective tissue disorder (e.g. SLE)
  • Lymphoproliferative disease
  • Sarcoidosis
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2
Q

List two non-immune mediated conditions that cause thrombocytopaenia.

A

DIC

MAHA

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3
Q

Describe the pathophysiology of ITP.

A
  • Autoantibodies are generated against platelets
  • Platelets are tagged by autoantibodies and then destroyed by the reticuloendothelial system (liver, spleen, bone marrow)
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4
Q

What are the main differences between acute and chronic ITP?

A

Acute:

  • Mainly children
  • Usually there is a preceding infection
  • Abrupt onset of symptoms
  • Lasts 2-6 weeks
  • Spontaneously resolves

Chronic:

  • Mainly occurs in adults
  • More common in females
  • Can be abrupt or indolent
  • Does not resolve spontaneously
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5
Q

How is ITP treated?

A

Mainly with steroids and IVIG based on the platelet count

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6
Q

Give some examples of causes of thrombocytopaenia that can be diagnosed by blood film.

A
  • Vitamin B12 deficiency
  • Acute leukamia
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7
Q

What clotting study abnormality would be seen in Haemophilia?

A

Prolonged APTT

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8
Q

Outline the clinical features of haemophilia.

A
  • Haemarthroses (MOST COMMON)
  • Soft tissue haematomas (e.g. shortened tendons, muscle atrophy)
  • Prolonged bleeding after surgery/dental extractions

NOTE: haemophilia A and B are clinically indistinguishable

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9
Q

What is a typical lesion seen in coagulation factor disorders?

A

Ecchymoses

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10
Q

What is the most common coagulation disorder? What is its inheritance pattern?

A
  • Von Willebrand disease
  • Autosomal dominant - type 1 and 2
  • Autosomal recessive - type 3
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11
Q

What is the main clinical feature in von Willebrand disease?

A

Mucocutaneous bleeding

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12
Q

Outline the classification of von Willebrand disease.

A
  • Type 1 - partial quantitative deficiency
  • Type 2 - qualitative deficiency
  • Type 3 - complete quantitative deficiency
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13
Q

Describe the relationship between vWF and factor 8.

A
  • Binding of factor 8 to vWF protects factor 8 from being destroyed

NOTE: type 3 vWD has a very similar phenotype to haemophilia A (because absent vWF leads to low factor 8)

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14
Q

Describe the expected laboratory test results for the three types of von Willebrand disease.

A
  • Type 1 - low antigen, low activity, normal multimer (decreased size)
  • Type 2 - normal antigen, low activity, normal multimer (structurally abnormal)
  • Type 3 - very low antigen, very low activity, absent multimer
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15
Q

Name a source of vitamin K.

A
  • Green vegetables
  • Vitamin K is synthesised by intestinal flora
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16
Q

What is vitamin K required for?

A
  • Synthesis of factors 2, 7, 9 and 10
  • Synthesis of protein C, S and Z
17
Q

List some causes of vitamin K deficiency.

A
  • Malnutrition
  • Biliary obstruction
  • Malabsorption
  • Antibiotic therapy
18
Q

Outline the pathophysiology of DIC.

A
  • Release of thromboplastic material into the circulation causes widespread activation of coagulation and fibrinolysis
  • This results in increased vascular deposition of fibrin, which leads to thrombosis of small and mid-size vessels with organ failure
  • Depletion of platelets and coagulation factors leads to bleeding
19
Q

List some causes of DIC.

A
  • Sepsis (MOST COMMON)
  • Trauma (e.g. fat embolism)
  • Obstetric complications (e.g. amniotic fluid embolism)
  • Malignancy
  • Vascular disorders
  • Reaction to toxin
  • Immunological (e.g. transplant rejection)
20
Q

Describe the typical clotting study results in DIC.

A
  • Prolonged APTT, PT, TT
  • Decreased fibrinogen
  • Increased FDP
  • Decreased platelets
  • Schistocytes (due to shearing of red blood cells as it passes through a fibrin mesh)
21
Q

Outline the treatment of DIC.

A
  • Treat underlying disorder
  • Anticoagulation with heparin
  • Platelet transfusion
  • FFP
  • Coagulation inhibitor concentrate
22
Q

Describe how liver disease leads to bleeding disorders.

A
  1. Decreased synthesis of clotting factors 2, 7, 9, 10, 11 and fibrinogen
  2. Dietary vitamin K deficiency
  3. Dysfibrogenaemia
  4. Enhanced haemolysis (decreased alpha-2 antiplasmin)
  5. DIC
  6. Thrombocytopaenia due to hypersplenism
23
Q

Outline the treatment of:

  1. Prolonged PT/APTT
  2. Low fibrinogen
  3. DIC
A
  1. Prolonged PT/APTT
    • ​​Oral vitamin K
    • FFP infusion
  2. Low fibrinogen
    • ​​Cryoprecipitate
  3. DIC​​
    • ​​Replacement therapy
24
Q

What is the management of vitamin K deficiency due to warfarin overdose based on?

A

INR

NOTE: warfarin is reversed by giving vitamin K (oral or IV). If severe, FFP or PCC could be given.

25
Q

What is PCC?

A

Prothrombin complex concentrate (contains vitamin K-dependent clotting factors)

YEAR 5: Haematology (37 decks)

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