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Path- Haem Qs laz > Haemostasis and Bleeding Disorders > Flashcards

Haemostasis and Bleeding Disorders Flashcards

1
Q
  1. List some pro-coagulant factors in the body.
A

Platelets
Endothelium
vWF
Coagulation cascade

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2
Q
  1. List some anti-coagulant factors in the body.
A

Fibrinolysis
Anti-thrombins
Protein C/S
Tissue factor pathway inhibitor

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3
Q
  1. Which three responses are stimulated by vessel injury?
A 
Vasoconstriction 
Platelet activation (forms primary haemostatic plug)
Activation of the coagulation cascade
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4
Q
  1. What are the components of blood clot formation?
A

Vascular endothelium
Platelets
Coagulation factors
White blood cells

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5
Q
  1. What are the two main functions of the endothelium?
A

Synthesis of prostacyclin, vWF, plasminogen activators and thrombomodulin

Maintain barrier between blood and pro-coagulant subendothelial structures

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6
Q
  1. How many platelets are produced by each megakaryocyte?
A

4000

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7
Q
  1. What is the life span of platelets?
A

10 days

NOTE: this is important because it means that the effect of antiplatelet drugs lasts for 10 days after stopping the drug

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8
Q
  1. What are glycoproteins?
A

Cell surface proteins through which platelets can interact with the endothelium, vWF and other platelets

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9
Q
  1. What do dense granules contain?
A

Energy stores (ATP and ADP)

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10
Q
  1. Which features of platelets enable them to massively expand their surface area?
A

Open cannalicular system and microtubules and actomyosin

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11
Q
  1. What are the two ways in which platelets can adhere to sub-endothelial structures?
A

DIRECTLY – via GlpIa

INDIRECTLY – via binding of GlpIb to vWF (this is MORE IMPORTANT)

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12
Q
  1. Which factors, released by platelets after adhesion, promote platelet aggregation?
A

ADP

Thromboxane A2

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13
Q
  1. How do platelets bind to each other?
A

GlpIIb/IIIa

It also binds to fibrinogen via this receptor

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14
Q
  1. Describe the effects of aspirin and other NSAIDs on the arachidonic acid pathway.
A

Aspirin is an irreversible COX inhibitor

Other NSAIDs reversibly inhibit COX

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15
Q
  1. What is the rate-limiting step for fibrin formation?
A

Factor 10a

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16
Q
  1. What are the effects of thrombin?
A

Activates fibrinogen
Activates platelets
Activates profactors (factor 5 and 8)
Activates zymogens (factor 7, 11 and 13)

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17
Q
  1. Name the complex that is responsible for activating prothrombin to thrombin.
A

Prothrombinase complex

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18
Q
  1. Outline the initiation phase of the clotting cascade.
A

Damage to the endothelium results in exposure of tissue factor which binds to factor 7 and activates it to factor 7a

The tissue factor-factor 7a complex then activates factors 9 and 10

Factor 10a binds to factor 5a resulting in the first step of the coagulation cascade

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19
Q
  1. Outline the amplification phase of the clotting cascade.
A

Activated factors 5 and 10 will result in the production of a small amount of thrombin

This thrombin will activate platelets

Thrombin will also activate factor 11 which activates factor 9

Thrombin also activates factor 8 and recruits more factor 5a

Factors 5a, 8a and 9a will bind to the activated platelet

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20
Q
  1. Outline the propagation phase of the clotting cascade.
A

Activated factors 5, 8 and 9 will recruit factor 10a
This results in the generation of a large amount of thrombin (thrombin burst)

This enables the formation of a stable fibrin clot

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21
Q
  1. Why is the prothrombinase complex important?
A

It allows activation of prothrombin at a much faster rate

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22
Q
  1. What is required for adequate production/absorption of vitamin K?
A

Bacteria in the gut produce vitamin K

It is fat-soluble so bile is needed for vitamin K to be absorbed

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23
Q
  1. What is the most common cause of vitamin K deficiency?
A

Warfarin

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24
Q
  1. Name two factors that convert plasminogen to plasmin.
A

Tissue plasminogen activator

Urokinase

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25
Q
  1. Name a factor that inhibits the factors mentioned in question 24.
A

Plasminogen activator inhibitor 1 and 2

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26
Q
  1. Name two factors that directly inhibit plasmin.
A

Alpha-2 antiplasmin

Alpha-2 macroglobulin

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27
Q
  1. What is the role of thrombin-activatable fibrinolysis inhibitor (TAFI)?
A

Inhibitor of fibrin breakdown

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28
Q
  1. Describe the action of antithrombins.
A

Bind to thrombin in a 1:1 ratio and this complex is excreted in the urine

29
Q
  1. How many types of antithrombin are there?
A

Five (antithrombin-III is the most active)

30
Q
  1. What is the most thrombogenic hereditary condition?
A

Antithrombin deficiency

31
Q
  1. Outline the role of protein C and protein S.
A

Trace amounts of thrombin generated at the start of the clotting cascade activate thrombomodulin

This allows protein C to bind to thrombomodulin through the endothelial protein C receptor

Protein C is then fully activated in the presence of protein S

Fully activated protein C will inactivate factors 5a and 8a

32
Q
  1. Why does Factor V Leiden cause a prothrombotic state?
A

The factor 5a will be resistant to breakdown by protein C

33
Q
  1. State two causes of activated protein C resistance.
A

Mutated factor 5 (e.g. factor V Leiden)

High levels of factor 8

34
Q
  1. What is the role of tissue factor pathway inhibitor?
A

TFPI neutralises the tissue factor-factor 7a complex once it has initiated the clotting cascade

35
Q
  1. List some genetic defects that cause excessive bleeding.
A

Platelet abnormalities
Vessel wall abnormalities
Clotting factor deficiencies
Excess clot breakdown

36
Q
  1. List some acquired defects that cause excessive bleeding.
A 
Liver disease 
Vitamin K deficiency 
Autoimmune diseases (platelet destruction)
Trauma 
Anti-coagulants/anti-platelets
37
Q
  1. List some genetic defects that cause excessive thrombosis.
A

Clotting factor inhibitor deficiencies

Decreased fibrinolysis

38
Q
  1. List the types of disorders of haemostasis.
A

Vascular disorders (e.g. scurvy)
Platelet disorders
Coagulation disorders
Mixed disorders (e.g. DIC)

39
Q
  1. What is the difference between immediate and delayed bleeding with regards to the underlying pathological process?
A

Immediate – issue with the primary haemostatic plug (platelets, endothelium, vWF)
Delayed – issue with the coagulation cascade

40
Q
  1. Describe the key clinical differences between platelet disorders and coagulation factor disorders.
A

Platelet disorders
• Bleeding from skin and mucous membranes
• Petechiae
• Small, superficial ecchymoses
• Bleeding after cuts and scratches
• Bleeding immediately after surgery/trauma
• Usually mild

Coagulation factor disorders 
•	Bleeding into soft tissues, joints and muscles 
•	No Petechiae
•	Large, deep ecchymoses
•	Haemarthroses
•	No bleeding from cuts and scratches 
•	Delayed bleeding from surgery or trauma 
•	Often SEVERE
41
Q
  1. When is treatment for platelet disorders required?
A

Platelet count < 30 x 109/L (this is associated with spontaneous haemorrhage)

42
Q
  1. Why is it important to look at platelets under the microscope in thrombocytopaenia?
A

To check whether it is pseudothrombocytopaenia (platelets clump together giving an erroneously low result)
Also allows identification of other abnormalities (e.g. Grey platelet syndrome – large platelets)

43
Q
  1. What can cause a decrease in platelet number?
A

Decreased production
Decreased survival (ITP)
Increased consumption (DIC)
Dilution

44
Q
  1. What can cause defective platelet function?
A

Acquired (e.g. aspirin)
Congenital (e.g. thrombasthenia)
Cardiopulmonary bypass

45
Q
  1. What can cause immune-mediated thrombocytopaenia?
A 
Idiopathic
Drug-induced (e.g. quinine, rifampicin)
Connective tissue disorder (e.g. SLE)
Lymphoproliferative disease 
Sarcoidosis
46
Q
  1. List two non-immune mediated conditions that cause thrombocytopaenia.
A

DIC

MAHA

47
Q
  1. 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)

48
Q
  1. 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
49
Q
  1. How is ITP treated?
A

Mainly with steroids and IVIG based on the platelet count

50
Q
  1. Give some examples of causes of thrombocytopaenia that can be diagnosed by blood film.
A

Vitamin B12 deficiency

Acute leukaemia

51
Q
  1. What clotting study abnormality would be seen in Haemophilia?
A

Prolonged APTT (A normal PT with an abnormal aPTT means that the defect lies within the intrinsic pathway)

52
Q
  1. 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

53
Q
  1. What is a typical lesion seen in coagulation factor disorders?
A

Ecchymoses

54
Q
  1. 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

Type 1 – partial quantitative deficiency
Type 2 – qualitative deficiency
Type 3 – complete quantitative deficiency

55
Q
  1. What is the main clinical feature in von Willebrand disease?
A

Mucocutaneous bleeding

56
Q
  1. Outline the classification of von Willebrand disease.
A

Type 1 – partial quantitative deficiency
Type 2 – qualitative deficiency
Type 3 – complete quantitative deficiency

57
Q
  1. 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)

58
Q
  1. Describe the expected laboratory test results for the three types of von Willebrand disease.
A

Type 1 – low antigen, low activity, normal multimer
Type 2 – normal antigen, low activity, normal multimer
Type 3 – very low antigen, very low activity, absent multimer

59
Q
  1. Name a source of vitamin K.
A

Green vegetables

Vitamin K is synthesised by intestinal flora

60
Q
  1. What is vitamin K required for?
A

Synthesis of factors 2, 7, 9 and 10

Synthesis of protein C, S and Z

61
Q
  1. List some causes of vitamin K deficiency.
A

Malnutrition
Biliary obstruction
Malabsorption
Antibiotic therapy

62
Q
  1. 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

63
Q
  1. 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)

64
Q
  1. Describe the typical clotting study results in DIC.
A

Prolonged APTT (intrinsic pathway) and PT (extrinsic pathway)
Prolonged TT
Decreased fibrinogen
Increased FDP
Decreased platelets
Schistocytes (due to shearing of red blood cells as it passes through a fibrin mesh)

65
Q
  1. Outline the treatment of DIC.
A 
Treat underlying disorder 
Anticoagulation with heparin
Platelet transfusion 
FFP 
Coagulation inhibitor concentrate
66
Q
  1. Describe how liver disease leads to bleeding disorders.
A

Decreased synthesis of clotting factors 2, 7, 9, 10, 11 and fibrinogen
Dietary vitamin K deficiency
Dysfibrogenaemia
Enhanced haemolysis (decreased alpha-2 antiplasmin)
DIC
Thrombocytopaenia due to hypersplenism

67
Q
  1. Outline the treatment of:
    a. Prolonged PT/APTT

b. Low fibrinogen
c. DIC

A

a. Oral vitamin K
FFP infusion

b. Cryoprecipitate
c. Replacement therapy

68
Q
  1. 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

69
Q
  1. What is PCC?
A

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

Path- Haem Qs laz (4 decks)

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