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ACP > Bleeding and Thrombotic Disorders > Flashcards

Bleeding and Thrombotic Disorders Flashcards

1
Q

Functions of haemostasis

A

Maintain circulation
Coagulation
Fibrinolysis

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2
Q

Sequence of haemostasis

A

Vasoconstriction
Primary, secondary and tertiary haemostasis
- recall coagulation cascade (extrinsic, intrinsic and common pathways)
Fibrinolysis process and inhibitors

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3
Q

Laboratory evaluation of bleeding; interpretation of individual results

A

CBC and blood smear
- why is morphology important
Coagulation
- PT, APTT, TT, D-dimer, fibrinogen assay, mixing test
Platelets
- function test, vWF, bleeding time, function analyser

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4
Q

Clinical features of bleeding disorders

A

Platelet/vWF vs Coagulopathy
- site of bleeding, petechiae, ecchymosis, haemarthrosis, bleeding after cut/scratches/ surgery

Characteristics of petechiae

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5
Q

Specific investigations of bleeding

A

Platelet
- CBC then vWF/platelet function test

Coagulopathy
- PT, APTT then mixing test and factor/inhibitor assay

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6
Q

Management options of bleeding disorders - MOA, indication, side effects

A

Platelet

  • platelet transfusion
  • DDAVP

Coagulopathy

  • plasma(FFP), cryoprecipitate, factor concentrates
  • rVIIa

Fibrinolysis
- tranexamic acid

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7
Q

Platelet disorders and causes

A

Quantitative

  • increased destruction
  • decreased production
  • increased sequestration in spleen

Qualitative

  • congenital
  • acquired e.g. drugs, uraemia, MDS
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8
Q

ITP

A

Diagnosis
Pathogenesis: increased destruction and decreased production
Treatment: platelet if <30, corticosteroids, IVIG (Splenectomy/ TPO-RA if unsuccessful)

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9
Q

Drug-induced ITP

A

Causes e.g. heparin, valproate, antibiotics
Pathogenesis
Onset
Treatment

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10
Q

Coagulopathies

A

Inherited

Acquired

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11
Q

vWD

A

Function of vWF
Inheritance
Clinical manifestations
Investigations

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12
Q

Haemophilia

A

Types
Inheritance
Severity and clinical manifestations
Treatment

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13
Q

Inhibitors of coagulation

A

Haemophilia (repeated factor concentrates)
Acquired haemophilia e.g. malig, infl, preg
Lupus anticoagulants

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14
Q

DIC

A

Common causes
Pathogenesis
Lab results
Treatment

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15
Q

Virchow’s triad and examples for each element

A

Endothelial injury
Circulatory stasis
Hypercoagulability

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16
Q

Congenital diseases causing hypercoagulability

A

Protein C/S deficiency
- inheritance, normal function, presentation

Factor V Leiden mutation (rare in Chinese)
- MOA

Antithrombin III deficiency
- inheritance, normal function, clinical presentation

Prothrombin mutation

17
Q

APS

A

Diagnosis

  • recurrent or spontaneous thrombosis
  • recurrent miscarriage
  • persistent elevation of anti–phospholipid Ab

Causes
- primary and secondary (AI, lymphoproliferative disease, post-viral, phenothiazines)

Treatment

18
Q

Manifestations of thrombosis

A

DVT and PE

- presentations and diagnostic methods

19
Q

Investigations of Thrombophilia

A

Indication in Hx

Investigations required

20
Q

Anticoagulant therapy treatment schemes

A

Standard treatment regime
- UFH/LMWH for 5 days —> bridge to warfarin for at least 3 months

Treatment schemes with NOAC

  • dabigatran - bridge from LMWH
  • rivaroxaban/apixaban - single drug
21
Q

Duration of treatment and indications

A

At least 3 months
- decide on stopping or indefinite extension thereafter — based on bleeding risk, age, compliance, any recurrent events, comorbidities, thrombophilia, D-diner after withdrawal

Indications

  • DVT/PE, stroke prevention in AF, prophylaxis in thrombophilia
  • high risk of stroke/PVD, ACS
22
Q

UFH/LMWH

A

MOA
Compare effects of inhibition on factors, and platelets
Specific uses of each
Administration route, dose
Monitoring
Complications (3) and management (of bleeding)

23
Q

Vitamin K antagonists

A 
MOA
Dosage and monitoring 
Target INR levels (2.5-3.5 or 2.0-3.0) for different patients 
Side effects 
Issues and interactions 
Management of warfarin overdose
24
Q

NOAC

A

Dabigatran vs Xa inhibitors
- target, bioavailability, dosing, renal excretion, protein binding, dialyzable

Efficacy and safety
Advantages vs warfarin
Limitations
Management of bleeding on NOAC (depends on severity)

ACP (27 decks)

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