12.5 Management of Coagulopathies & Bleeding Disorders Flashcards

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1
Q

Acute vs long-term goals of antiplatelet therapy

A

Acute: Stop progression of acute thrombus
Long-term: prevent recurrence of CVA, MI etc.

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2
Q

Acetylsalicylic acid is also known as…

A

Aspirin

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3
Q

“Low-Dose Aspirin” is the typical dosage in Australia; how much is it, and how often is it taken?

A
  • 100mg
  • Once daily
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4
Q

Describe the mechanism of aspirin

A

Inhbits COX-1 enzyme, prevents synthesis of Thromboxane A2, which is otherwise used for autocrine platelet activation, thus inhibiting platelet aggregration.

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5
Q

Clopidogrel mechanism

A

IRREVERSIBLY binds to ADP receptor

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6
Q

Ticagrelor mechanism

A

REVERSIBLY binds to ADP receptor

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7
Q

Antiplatelets vs anticoagulants

A

Antiplatelets: stop primary haemostasis
Anticoagulants: stop secondary haemostasis

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8
Q

Acute vs long-term goals of anticoagulant therapy

A

Acute:
- Prevent extension of acute thrombus
- Prevent embolisation
Long-Term:
- Preventing AF-association thromboembolism
- Prevent VTE recurrence

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9
Q

Heparin mechanism

A
  • Binds to antithrombin; makes it up to 1000 times more effective (!)
  • Increased thrombin breakdown -> decreased fibrin production -> decreased coagulation
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10
Q

Warfarin mechanism

A
  • Prevents recycling of vitamin K
  • Depletse Vit-K dependent factors from the coagulation cascade
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11
Q

Which clotting factors are Vitamin-K Dependent

A

2, 7, 9, 10

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12
Q

Targets of LMW vs unfractionated heparin…

A

LMW: Predominantly Factor Xa
Unfractionated: both Xa and antithrombin

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13
Q

Direct acting anticoagulant (DOAC) mechanism

A

Binds to and inhibits factor Xa

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14
Q

Give two examples of Direct acting anticoagulants

A
  • Apixaban
  • Rivaroxaban
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15
Q

Common uses of thrombolysis

A
  • Acute ischaemic stroke
  • Acute MI
  • Acute Limb Ischaemia
  • Massive PE
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16
Q

How do tissue Plasminogen Activators (tPAs) cause fibrinolysis?

A
  • catalyse the activation of plasminogen into plasmin
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17
Q

Give some examples of tPAs

A
  • Tenecteplase
  • Alteplase
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18
Q

How is gene therapy used in Factor IX replacement therapy?

A
  • Viral vector carries gene to liver
  • Cause expression of gene to synthesise protein
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19
Q

Indications for antiplatelets

A

Arterial thrombotic disease:
- Cardio (such as in coronary PCI)
- Cerebrovascular disease
- Peripheral vascular disease
- Pre-eclampsia prevention

20
Q

Contraindications for antiplatelets

A
  • Avtice/recent haemorrhage
  • Upcoming/recent surgery
  • Thrombocytopaenia
21
Q

Side effects of antiplatelets

A
  • Blood loss
  • GI irritation
22
Q

What are three specific side effects associated with ticagrelor

A
  • Dyspnoea
  • Bradycardia
  • Gout
23
Q

Can most procedures be done on aspirin? What about dual platelet therapy?

A
  • MOST (not necessarily all) can be done on aspirin
  • Usually, allow one antiplatelet to wash out of system for 5-7 days before surgery if on dual
24
Q

Which has higher bleeding risk: anticoagulants or antiplatelets?

A

Anticoagulants

25
Q

What advice would you give to a patient who you are prescribing anticoagulants to?

A
  • No contact sports :(
  • High-risk occupations
  • Important to keep doses consistent/don’t miss them
26
Q

Indications for prophylactic vs therapeutic heparin

A

Prophylaxis: VTE prevention
Therapeutic: treatment of VTE, acute arterial events, or mechanical valve prophylaxis

27
Q

Contraindications for heparins

A
  • Active/recent haemorrhage
  • Severe thrombocytopaenia
28
Q

Side effects of heparins

A
  • Heparin-induced thrombocytopaenia syndrome (HIITS)
  • Bleeding; liver enzyme elevation
  • Long term: alopecia, osteoporosis
29
Q

Describe Heparin-Induced Thrombocytopaenia Syndrome

A
  • Antibodies formed against platelets
  • Leads to antibody destruction, and yet HYPERthrombotic state
30
Q

Benefits/limitations of LMW heparin

A

Benefits:
- Subcutaneous (can be used for outpatients)
- Fixed dosage
- No monitoring needed
Limitations:
- Only partially reversible
- Short half life

31
Q

Benefits/limitations of unfractionated heparin

A

Benefits:
- Fully reversible
- Independent of renal function
Limitations:
- IV (so only for inpatients)
- Requires frequent monitoring
- Complex dosing algorithm

32
Q

What are some rare circumstances where a patient requires monitoring for being on LMW heparin

A
  • Obesity
  • Pregnancy
  • Renal impairment
33
Q

Indications for therapeutic vs prophylactic DOACs

A
  • Prophylaxis: VTE prevention
  • Therapeutic: VTE or AF treatment
34
Q

Contraindications for DOACs

A
  • Renal impairment
  • Recent haemorrhage
  • Severe thrombocytopaenia
  • Pregnancy
35
Q

Risks of DOACs

A
  • No reversal agent currently
  • Rivaroxaban also has higher risk of menorrhagia than apixaban
36
Q

Indications for warfarin

A
  • Mechanical heart valve (arterial thrombi prophylaxis)
  • Anticoagulation in renal disease
37
Q

Contraindications for warfarin

A
  • Active/recent haemorrhage
  • Severe thrombocytopaenia
  • Pregnancy
38
Q

Side effects of warfarin

A
  • Bleeding
  • Long-term: alopecia, hepatic dysfunction
39
Q

Importance of diet in warfarin prescription

A

If suddenly changed, vitamin K levels could change, altering drug effectiveness

40
Q

Why do you start enoxaparin when you start warfarin?

A

Because, initially warfarin depletes Protein C before is inhibits vitamin K recycling, creating a prothrombotic state. The enoxaparin prevents this from causing acute thrombotic events.

41
Q

Describe factor replacement therapy in Haemophilia A and Haemophilia B

A

H. A: Recombinant Factor VIII
H. B: Recombinant Factor IX

42
Q

Describe factor replacement therapy for von Willebrand’s Disease

A
  • First, give desmopressin, which increases endothelial release of vWF
  • If not enough, give purified vWF with Factor VIII
43
Q

What is the function of Tran Examic Acid (TXA)?

A
  • Opposes the function of tPA; opposes conversion of plasminogen into plasmin
44
Q

What are some indications for antifibrinolytic therapy?

A
  • GI bleeding
  • Menorrhagia
  • Gum/dental bleeding
  • Epistaxis
45
Q

Describe novel therapy of Haemophilia A

A
  • Synthetic replacement of Factor VIII by using a bi-specific antibody that binds factors IX and X