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Exodontia > Haemostasis: acquired disorders > Flashcards

Haemostasis: acquired disorders Flashcards

1
Q

Acquired vascular bleeding disorders

A

Senile Purpura
Scurvy (Vitamin C deficiency)
Steroid Purpura

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2
Q

Causes of thrombocytopenia

A 
Failure of platelet production
-vit B12 or folate deficiency
-bone marrow infiltration (leukaemia or metastases)
-radiation, cytotoxic therapy
Increased consumption of platelets
-immune thrombocytopenia (ITP)
-disseminated intravascular coagulation (DIC)
-HIV infection
Hypersplenism
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3
Q

Immune thrombocytopenia (ITP): adults

A

-cause usually unclear
chronic
-treat if there is bleeding

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4
Q

Immune thrombocytopenia (ITP): children

A

Usually follows acute infection

Self limiting so usually not treated

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5
Q

Immune thrombocytopenia (ITP): diagnosis

A

Thrombocytopenia
Exclusion of other causes of thrombocytopenia
Bone marrow examination

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6
Q

Immune thrombocytopenia (ITP): treatment

A

Steroids
Intravenous immunoglobulin
Splenectomy
Thrombopoietin receptor analogues

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7
Q

Disseminated intravascular coagulation (DIC)

A

Breakdown of haemostatic balance
Simultaneous bleeding and microvascular thrombosis
Life threatening condition

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8
Q

Disseminated intravascular coagulation (DIC): causes

A

sepsis
obstetric
malignancy

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9
Q

Disseminated intravascular coagulation (DIC): treatment

A

Remove underlying cause

Give plasma and platelets if bleeding

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10
Q

Platelet function abnormalities: acquired

A

Antiplatelet drugs
Renal disease
Liver disease
DIC

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11
Q

Antiplatelet drugs

A

Aspirin
Clopidogrel
Preasugrel

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12
Q

Aspirin as an antiplatelet drugs

A

Inhibits cyclo-oxygenase (platelet enzyme) irreversibly

Act for lifetime of platelet ie 7-10 days

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13
Q

Clopidogrel as an antiplatelet drugs

A

Blocks ADP receptor (on platelet surface) irreversibly

Acts for lifetime of platelet ie 7-10 days

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14
Q

Prasugrel as an antiplatelet drugs

A

Blocks ADP receptor irreversibly
Acts for lifetime of platelet ie 7-10days
More rapid and consistent inhibition than clopidogrel

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15
Q

Renal disease

A 
Increased bleeding
-anaemia
-thrombocytopenia in autoimmune renal disease
-uraemia
-treat with DDAVP and/or dialysis
Increased thrombotic risk
-in nephrotic syndrome
-acquired antithrombin deficiency
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16
Q

Liver disease

A

Site of synthesis of coagulation factors and fibrinogen
Liver disease often associated with bleeding and prolonged prothrombin time
Often more than one cause for bleeding in liver disease

17
Q

Causes of bleeding in liver disease

A

Reduced clotting factors
-due to poor synthesis or vitamin K deficiency
Thrombocytopenia due to hypersplenism
Platelet function defect
Portal hypertension – bleeding from varices
Dysfibrinogenemia
Increased fibrinolysis

18
Q

Vitamin K deficiency

A

Vitamin K necessary for the correct synthesis of coagulation factors II, VII, XI and X.
Vitamin K fat soluble vitamin
-deficiency in malabsorption, esp obstructive jaundice
-all babies born with vit K deficiency so must have it at birth
Manifests as prolonged prothrombin time
Treat with vitamin K
-in malabsorption must be given intravenously

19
Q

Drugs as causes of acquired bleeding disorders

A

Antiplatelet drugs such as Aspirin
-affect platelet function
Anticoagulants such as Heparin and warfarin
-affect coagulation cascade
Steroids make tissues thin and cause bruising and bleeding
Many drugs can affect liver, kidneys and bone marrow

20
Q

Two types of thrombosis

A

In the arterial circulation (eg MI or Stroke):
-high pressure system
-platelet rich
In the venous circulation (eg DVT or PE):
-low pressure system
-fibrin rich

21
Q

Arterial thrombosis treatment

A

Antiplatelet drugs

22
Q

Venous thrombosis treatment

A

Anticoagulant drugs

23
Q

Antiplatelet drugs

A

Aspirin
Clopidogrel
Prasugrel
Ticagrelor

24
Q

Anticoagulants

A 
Intravenous
-unfractionated heparin
Subcutaneous
-low molecular weight heparin
Oral
-warfarin, 
-dabigatran, rivaroxaban, apixaban, edoxaban
25
Q

Oral anticoagulants

A 
Vitamin K antagonists
-96% warfarin in the UK
-4% acenocoumarol
Direct oral anticoagulants
-Dabigatran
-Rivaroxaban
-Apixaban
-Edoxaban
26
Q

Heparin

A

Glycosaminoglycan
Binds to antithrombin and increases its activity
Indirect thrombin inhibitor
Not absorbed from the gut so given iv or sc
Monitor with the APTT test
Given by continuous infusion

27
Q

Low molecular weight heparin

A

Glycosaminoglycan
Binds to antithrombin and increases its activity
Indirect thrombin inhibitor
Not absorbed from the gut so given iv or sc
Monitor with the APTT test
Given by continuous infusion

28
Q

Warfarin: pharmacology

A

Given by mouth completely and rapidly absorbed
99% plasma protein bound
Inhibits the production of factors II, VII, IX, X
Peak effect 3-4 days after starting, and effect still present 4-5 days after stopping
-ie slow on and slow off action

29
Q

Side effects of warfarin

A

Bleeding, embryopathy

30
Q

Warfarin: monitoring

A

Measure the INR (International Normalised Ratio)
Dose of warfarin is based on the INR
Target for first DVT/PE: 2.0-3.0
Frequency of monitoring depends on the stability of the patient’s INR
-eg can be 1 per week up to 1 every 8 weeks.
INR must be measured before surgery

31
Q

The direct oral anticoagulants

A 
Oral
No monitoring
Aiming to replace heparin and warfarin
Standard dosing
No alcohol or food interactions
Very few drug interactions
Short half life (10-15hours)
More expensive than warfarin
32
Q

Advantages of DOACs over warfarin

A

Rapid onset of action
Fixed oral dosing with predictable anticoagulant effect
Low potential for food or alcohol interactions
Low potential for drug interactions
No need for blood monitoring

33
Q

Disadvantages of DOACs over warfarin

A

Renal elimination
No specific antidotes for the Xa inhibitors
Licensed for only specific indications
Recently introduced

Exodontia (21 decks)

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