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Y3 HAEMATOLOGY > Bleeding and Thrombosis > Flashcards

Bleeding and Thrombosis Flashcards

1
Q

List causes of failure of platelet plug formation (failure of primary haemostasis)

A

Vascular disease
Low platelet count (thrombocytopenia)
Impaired platelet function
Von Willbrand Factor disease

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2
Q

What is the main vascular cause of failed primary haemostasis?

A

ACQUIRED: Vasculitis e.g. Henoch-Schonlein purpura

Others include heridatory causes e.g. Marfans

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3
Q

What is the commonest cause of primary haemostatic failure?

A

Thrombocytopaenia (usually acquired)

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4
Q

Thrombocytopenia can be due to what 2 factors?

A

Reduced platelet production (marrow disorder)

Increased platelet destruction

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5
Q

List the main causes of platelet destruction

A

Coagulopathy (DIC)
Autoimmunity (immune thrombocytopaenic purpura)
Hypersplenism (liver disease)

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6
Q

What is the main cause of a platelet functional deficit?

A

HERIDATORY: vWF deficiency

Other include acquired causes (NSAIDs, renal failure, aspirin)

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7
Q

Von Willebrand Factor deficiency is mainly hereditary and follows what inheritance pattern?

A

Autosomal dominant, typically producing a mild disease

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8
Q

In what two groups of patients should you be suspicious of vWF deficiency?

A

Women with menorrhagia

Patients who bleed excessively after surgery

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9
Q

List causes of failure of fibrin clot formation (failure of secondary haemostasis)

A

Multiple clotting factor deficiency

Single clotting factor deficiency

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10
Q

List causes of multiple clotting factor deficiency. What would a clotting screen look like?

A 
DIC
Liver failure
Vitamin K deficiency
Warfarin therapy
Prolonged PT time and aPTT
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11
Q

What is the main cause of single clotting factor deficiency?

A

Haemophilia

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12
Q

Which clotting factors are carboxylated (activated) by vitamin K?

A

II
VII
IX
X

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13
Q

Why is vitamin K important for function of clotting factors?

A

Allows for clotting factor to aggregate at platelet plug: need a negative charge (carboxylation of glutamic acid) as Ca at plug is positive

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14
Q

List causes of vitamin K deficiency

A

Poor dietary intake
Malabsorption (absorbed at upper intestine)
Obstructive jaundice (requires bile salt for absorption)
Antagonists (warfarin)
Haemorrhagic disease of newborn

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15
Q

What is disseminated intravascular coagulation (DIC)?

A

Excessive and inappropriate activation of the haemostatic system, causing depletion of all clotting factors leading to microvascular thrombus formation

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16
Q

What are the main signs of DIC?

A

Abdominal bruising/purpura

Generalised bleeding

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17
Q

What is included in a coagulation screen for haemostasis?

A

Platelet count
Prothrombin time
APT time
D-dimer

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18
Q

List the main causes of DIC

A

Sepsis
Obstetric emergencies
Malignancy
Hypovolaemic shock

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19
Q

How is DIC treated?

A

Treat underlying cause

Replace clotting factors - platelet transfusions, plasma transfusions (FFP), fibrinogen replacement

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20
Q

What is haemophilia? What pattern of inheritance does it follow?

A

X-linked heridatory disorder with abnormal prolonged bleeding episodically at one or few sites

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21
Q

What are the two types of haemophilia? Which is more common?

A 
Haemophilia A (VIII deficiency)
Haemophilia B (IX deficiency)
A is more common than B
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22
Q

Where does bleeding usually occur in haemophilia?

A

Ankles, knees (haemarthroses)
Soft tissue bleeds (bruising in toddlers)
Prolonged bleeding after dental extraction or surgery

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23
Q

Is haemophilia a disorder of primary or secondary haemostasis?

A

Secondary haemostasis

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24
Q

Prothrombin time is usually normal in a haemophiliac. True/False?

A

True

Isolated prolonged APT time

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25
Q

What is the main cause of arterial thrombosis?

A

Atherosclerosis

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26
Q

How is atherosclerosis treated?

A

Antiplatelet (aspirin)

Modify risk factors for atherosclerosis

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27
Q

Venous thrombosis is caused by Virchow’s triad. List the components of this triad

A

Hypercoagulability
Vessel wall damage (valves)
Stasis of blood flow

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28
Q

How is venous thrombosis treated?

A

Heparin/ warfarin

NOACs

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29
Q

List the main clinical signs of DVT. How is it diagnosed?

A 
Hot limb
Swelling, erythema
Tenderness
Pitting oedema
Usually unilateral
Duplex US
Negative D-dimer
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30
Q

List the main clinical signs of PE. How is it diagnosed?

A 
Pleuritic chest pain
Dyspnoea
Collapse
Haemoptysis
VQ scan if CXR normal, CTPA
Negative D-dimer
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31
Q

What is the risk of a deep vein thrombosis in the leg?

A

Clot can form and end up in pulmonary circulation by passing up IVC, causing pulmonary embolism
Can result in post-thrombotic syndrome (chronic painful and swollen leg)

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32
Q

List risk factors for venous thromboembolism

A 
Age
Obesity
Pregnancy
Oestrogen therapy (OCP)
Trauma/surgery
Malignancy
Infection
Paralysis
Thrombophilia
Antiphospholipid syndrome
Previous DVT/PE
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33
Q

What is a thrombophilia?

A

Familial/acquired disorder of haemostatic mechanism which are likely to predispose to thrombus

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34
Q

What are the main mechanisms of thrombophilia?

A

Increased coagulation activity
Decreased fibrinolytic activity
Decreased anticoagulant activity

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35
Q

What are the main naturally occuring anticoagulants?

A

Serine protease inhibitors (antithrombin)

Protein C and S

36
Q

What is Factor V Leiden?

A

Variant of factor V that cannot be inhibited as effectively - increases risk of venous thrombosis due to less anticoagulation

37
Q

List the main hereditary thrombophilias

A

Factor V Leiden
Antithrombin deficiency
Protein C and S deficiency
Prothrombin mutation

38
Q

List clinical features that owuld make you suspicious of thrombophilia

A

VTE <45yo
Recurrent or unusual VTE
Family history of VTE
Family history of thrombophilia

39
Q

How is thrombophilia managed?

A

Advice on avoiding risk
Short-term prophylaxis
Short-term anticoagulation to treat VTE
Long-term anticoagulation if recurrent events

40
Q

What are the two factors that must be weighed up to decide whether a patient should be put on long-term anticoagulation?

A

Risk of recurrent thrombosis

Risk of serious haemorrhage

41
Q

What is the most important contributor to a risk of recurrent thrombosis?

A

A history of previous thrombosis

42
Q

What is the main acquired thrombophilia?

A

Antiphospholipid syndrome

43
Q

Which antibodies prolong phospholipid coagulation tests?

A

Lupus anticoagulants

44
Q

List clinical features of antiphospholipid syndrome

A

Recurrent thrombosis (arterial, venous)
Recurrent fetal loss
Mild thrombocytopaenia

45
Q

How is antiphospholipid syndrome managed?

A

Antiplatelet (aspirin)

Anticoagulant (warfarin, heparin if pregnant)

46
Q

How does atherosclerosis form?

A

Foamy macrophages rich in cholesterol are attracted to damaged arterial endothelium, forming atherosclerotic cholesterol-rich plaques

47
Q

What are the consequences of unstable atherosclerotic plaques?

A

Can rupture and cause arterial thrombosis/embolism (resulting in unstable angina/MI/stroke)

48
Q

List risk factors for arterial thrombosis

A

Hypertension
Smoking
High cholesterol
Diabetes

49
Q

Explain the process of formation of arterial thrombus

A

ENDOTHELIAL DAMAGE: exposes collagen and vWF
Platelet ADHESION to collagen and vWF at injury site
AGGREGATION of platelets at site of injury
ACTIVATION of platelets as they alter shape to expose more phospholipid on the surface, allowing greater coagulation activation and fibrin production to stabilise clot
SECRETION of granules to stimulate more platelet recruitment and activation forming platelet plug

50
Q

Which chemicals released by platelets encourage platelet aggregation?

A 
Thromboxane A2 (TXA2)
ADP
51
Q

Through which receptors do platelets bind together?

A

GP IIb/IIIa

52
Q

How does aspirin work?

A

Antiplatelet that inhibits COX enzyme causing decreased TXA2 production and thus reduced platelet aggregation

53
Q

List some side effects of aspirin

A

Bleeding

Blocks production of prostaglandins:
GI ulceration
Bronchospasm

54
Q

How does clopidogrel work?

A

Antiplatelet that is an ADP receptor antagonist (blocks P2Y1) to reduce platelet aggregation

55
Q

How does dypridamole work?

A

Antiplatelet acting as a phosphodiesterase inhibitor , reducing cAMP - messenger in platelet activation

56
Q

How does abciximab work?

A

Antiplatelet acting as a GPIIb/IIIa inhibitor that prevents aggregation of platelets

57
Q

How is bleeding managed in a patient taking antiplatelets?

A

If serious bleeding reverse with platelet transfusion

Stop antiplatelet agents 7 days prior to elective operations

58
Q

How does atrial fibrillation increase the risk of stroke?

A

Stasis of blood flow (due to irregular heartbeat) causes congealing and clot formation in atrium, which may travel and lodge in the brain

59
Q

Which factors do protein C and S inhibit in the clotting cascade?

A

V
VIII
IX
Xa

60
Q

How does heparin work?

A

Anticoagulant that potentiates action of antithrombin (inhibitor of thrombin) to reduce clotting
Inhibiting thrombin reduces factor VIII/IX that speed up the system

61
Q

How is heparin administered?

A

IV or subcutaneous

62
Q

Which factors are inhibited by unfractionated heparin?

A

Thrombin

Xa

63
Q

Which factors are inhibited by LMW heparin?

A

Xa only (indirectly inhibits thrombin since X is higher in the cascade)

64
Q

Which coagulation test is used to monitor heparin?

A

APT time for unfractionated heparin

Anti-Xa assay for LMW heparin

65
Q

List some side effects of heparin

A

Bleeding
Thrombocytopenia, causing thrombosis (monitor FBC)
Osteoporosis long-term

66
Q

How can the effects of heparin be reversed?

A 
Stop heparin
Protamine sulphate (reverses AT so complete reversal for unfractionated heparin)
67
Q

What is required for vitamin K absorption?

A

Bile salts

68
Q

Which factors are vitamin K -dependent?

A 
II (prothrombin)
VII
IX
X
Protein C and S
69
Q

Where are vitamin K-dependant factors synthesised?

A

Liver

70
Q

How does warfarin work?

A

Anticoagulant acting as an antagonist of vitamin K to cause reduced clotting factor activation (synthesis of non-functional clotting factors II, VII, IX, X)

71
Q

How are patients on warfarin monitored? Why?

A

International Normalised Ratio (corrected PT ratio)

Warfarin has a narrow therapeutic window

72
Q

What is the equation for calculating a patient’s INR?

A

(PT time / mean normal PT time)^ISI

73
Q

How is acute thrombosis in hospital treated - heparin or warfarin?

A

Heparin (works immediately)

74
Q

List adverse effects of warfarin therapy

A

Drug interactions, including alcohol

Bleeding (mild or severe)

75
Q

How can the effects of warfarin be reversed?

A

Omit warfarin dose
Oral vitamin K (6 hours)
Administer clotting factors

76
Q

What are the advantages of newer anticoagulants or NOACs?

A 
Oral and no monitoring required
Less drug interactions
Less bleeding (no antidote for reversal)
77
Q

Give an example of a direct thrombin inhibitor

A

Dabigatran

78
Q

Give an example of an oral Xa inhibitor

A

Rivaroxaban

79
Q

Why are Xa inhibitors preferred over a direct thrombin inhibitor in older patients?

A

Direct thrombin inhibitors are excreted renally

Check U+Es before prescribing

80
Q

What does prothrombin time measure?

A

How long it takes your blood to clot by measuring the activity of the clotting factor prothrombin (II), focusing on the extrinsic pathway (tissue factor related)

81
Q

What does activated partial thromboplastin time measure?

A

How long it takes clotting to occur by measuring the function of the intrinsic pathway (blood vessles)

82
Q

What would an isolated thrombocytopaenia on blood test make you suspicious of?

A

Autoimmine thrombocytopaenic purpura

83
Q

Outline the management of VTE

A 
LMW Heparin or Warfarin
TED stockings
Physiotherapy
Early mobilisation
Intermittent pneumatic compression
84
Q

Warfarin affects the PT time and heparin affects the APT time. True/False?

A

True

85
Q

If the PT time is prolonged and the APT time is normal, which factors are causing the problem?

A

Tissue factor

VIIa

86
Q

If the PT time is normal and the APT time is prolonged, which factors are causing the problem?

A

VIII

IXa

Y3 HAEMATOLOGY (16 decks)

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