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2.2 Haematology > Anticoagulants > Flashcards

Anticoagulants Flashcards

1
Q

Write about warfarin

A

Used in the treatment of VTE and PE
Used for the prophylaxis and treatment of thromboembolic complications associated with rheumatic heart disease, atrial fibrillation and or prosthetic heart valve replacement
Reduction in the risk of death, recurrent myocardial infarction and thromboembolic events such as stroke after MI
Used to maintain a level of anticoagulation to minimise the risk of thrombosis and haemorrhagic complication

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2
Q

How does warfarin work

A

Interferes with the biochemistry of vitamin K dependent factors in the liver and interferes with the production of functional factors

Two isomers: R and S, S has a greater anticoagulant effect

Taken orally and easily absorbed from the GIT

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3
Q

Who should avoid warfarin

A

Severe hypertension
Peptic ulcer
Bacterial endocarditis
Pregnant

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4
Q

Biochemically how does warfarin affect coagulation

A

Vitamin K is necessary for the synthesis of gamma carboxyl glutamate residues on FII, VII, IX and X in the liver

Gla residues serve as high affinity binding sites for Ca++

Vit K converts the glutamyl residues of the protein to gamma-carboxyglutamyl residues by the liver enzyme carboxylase

These residues comprise the Gla domain which along with Ca++ is important for the anchoring of the protein to negatively charged phospholipids on the platelet surface

Warfarin blocks the reaction by inhibiting the enzyme and preventing the reduction of vitamin K epoxide

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5
Q

How is warfarin monitored

A

Test = International normalised ratio (INR) which is calculated from the prothrombin time

Laboratory testing or point of care self testing

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6
Q

What are some complications of warfarin therapy
(5)

A

There is a narrow therapeutic range: bleeding or thrombosis can occur

Too much warfarin can cause bleeding

Can induce necrosis if protein C level is reduced

Formation of micro-thrombi in the skin, oxygen insufficiency and cell death

Outside range can increase mortality, risk of stroke and rate of hospitalisation

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7
Q

Why can warfarin cause reduced levels o f protein C

A

Warfarin reduces levels of all vitamin K dependent factors

But protein C has the shortest half life

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8
Q

How can warfarin be reversed

A

Discontinue warfarin if not urgrent

Administer vitamin K orally or through IV

Administer prothrombin complex concentrates

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9
Q

What are prothrombin complex concentrates

A

Contain FII, FVII, FIX, FX, PC, PS

Given when there is an urgent requirement to reverse warfarin effect e.g. bleed or surgery

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10
Q

Write about heparin

A

Used when there is need for rapid anticoagulant effect

Prevents VTE, treats DVT and PE, early treatment of unstable angina and MI, cardiac surgery or bypass, vascular surgery and coronary angioplasty

Selected patients with DIC

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11
Q

How does heparin work

A

Mediated through antithrombin (AT) in the coagulation cascade

Binding to antithrombin is through a unique pentasaccharide sequence randomly distributed in the heparin molecule

Inhibits platelet function

Antithrombin prevents the work of FXa and thrombin thus preventing formation of fibrin

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12
Q

Write about unfractionated heparin
(4)

A

Mucopolysaccharide with alternating units of sulphated glucosamine and glucaronic acid

The negative charge allows the binding to and inactivation of FIIa and FXa

Produced from porcine intestinal mucosa or bovine lung

Administered by IV infusion either as a bolus dose or by continuous infusion

metabolised in liver and excreted in urine

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13
Q

Write about the mechanism of action of unfractionated heparin

A

Binding to FXa causes a conformational change in FXa and its inactivation

Binding to FIIa: UFH binds to AT and FIIa requiring longer chain of heparin

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14
Q

Write about low molecular weight heparin

A

Prevention and treatment of VTE (DVT and PE), early treatment of unstable angina and MI

Produced from UFH by chemical process resulting in a heparin that has a lower molecular weight

Contain the unique pentasaccharide unit required for binding to antithrombin and FXa (has less effect on FIIa and others)

Improved bioavailability, T1/2 = 4 hrs

Preductable response

Reduced side effects regarding osteopeonia and HIT

Limited requirement for monitoring

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15
Q

How is heparin administered

A

Unfractionated = continuous IV

LMW heparin = subcutaneous route

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16
Q

What are the complications of heparin therapy

A

Osteonpenia
Bleeding
HIT (heparin induced thrombocytopenia)

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17
Q

What increases your risk of heparin associated bleeding

A

Dose
Concomitant thrombolytic therapy or other drugs
Recent surgery
Trauma
Invasive procedures
Concomitant haemostatic defects

18
Q

What are the symptoms of HIT

A

Thrombosis
Skin necrosis
Anaphylaxis
Adrenal haemorrhage necrosis
Can be life-threatening

19
Q

How does heparin-induced thrombocytopenia occur

A

Caused by antibodies that bind to complexes of heparin and platelet factor 4, activating the platelets and promoting a prothrombotic state

HIT is more frequently encountered with unfractionated heparin than with low molecular weight heparin

20
Q

How is heparin monitored

A

No laboratory monitoring of UFH

UFH monitored by the APTT
- APTT ratio is reported for UFH with a therapeutic range assigned

21
Q

How is LMWH monitored

A

Monitored using a specific assay (anti Xa assay) due to the lack of sensitivity of the APTT

22
Q

What is the anti Xa assay

A

Based on the incubation of the test plasma containing heparin with a reagent containing excess AT and FXa

The residual FXa is mixed with a chromogenic substrate and the colour change is inversely proportional to the concentration heparin in the test plasma

23
Q

Compare heparin vs warfarin
(heparin)

A

Intravenous
Immediate onset of action
Short term use
Cheap
Needs careful monitoring

24
Q

Compare heparin and warfarin (warfarin)

A

Oral
Slow onset and offset
Long term use
Cheap
needs careful monitoring

25
Q

Give some examples of DOACs

A

Rivaroxaban and dabigatran

26
Q

When would DOACs be used

A

Reduce risk of stroke in non-valvular atrial fibrillation

prevention of VTE following hip or knee replacement

Treatment and ongoing prevent of VTE

27
Q

When would you not use DOACs

A

Renal impairment
Disorders of haemostasis
Clinically significant active bleeding
Prosthetic heart valve
Liver disease
Pregnant and breastfeeding women
Children under 18

28
Q

What is dabigatran

A

A direct thrombin inhibitor

29
Q

What is rivaroxaban

A

A factor Xa inhibitor

30
Q

How is dabigatran monitor

A

Not typically monitored in haematology lab

Ecarin clotting time
Dilute thrombin time

31
Q

How is rivaroxaban monitored

A

Not typically monitored in haematology lab

Anti-factor Xa

32
Q

Why are anticoagulants used to treat VTE

A

Prevention of thrombus growth within blood vessels

Prevention of recurrence of thrombosis

Prevention of thrombosis in high risk situations

33
Q

When would anticoagulants be used as a prophylaxis

A

Patients with high risk of thrombosis e.g. atrial fibrillation

Disrupted electrical activity to the atria

Irregular heartbeat with stasis of blood in the left atrium

Risk of stroke and VTE

34
Q

What is VTE (DVT/PE)
(6)

A

Venous thrombo embolism

High rate of morbidity and mortality if not treated

Third most common cause of death from cardiovascular disease after heart attack and stroke

A multi-causal disease with important gene-environment interactions

Case fatality between 1 and 5%

Incidence and fatality dependent on age

35
Q

Write about anticoagulants for arterial thrombosis

A

Little benefit because of the high platelet content of the clot

Artherosclerosis and the rupture of a plaque will cause arterial thrombisis

Treated with aspirin and other platelet antagonists not anticoagulants

36
Q

How is VTE diagnosed

A

The presence of a blood clot is investigated using both a clinical and laboratory assessment and the probability of having a clot is determined by the clinician

Clinical assessment is conducted using a clinical
assessment score called the Wells DVT (or PE) pre-test probability score

A numerical value is assigned based on the presence of particular signs or symptoms and an overall score is obtained to determine the probability of the person having a clot

The higher the score – the more likely that a DVT or PE is present

This allows the clinician to make decisions regarding further testing
and treatment

37
Q

What additional tests are done for VTE

A

D-dimer
Radiology

38
Q

How is D-dimer used for VTE diagnosis

A

The D-Dimer assay should have a high negative predictive value i.e. a negative result will exclude VTE (beware of positive results)

May be negative if small clot or if clot is >10 days old

39
Q

How is radiology used to diagnose VTE (DVT)

A

Venography, compression or ultrasonography is used for DVT

40
Q

How is radiology used to diagnose VTE (PE)

A

Pulmonary angiography
Ventilation-perfusion (V/Q) scan

2.2 Haematology (38 decks)

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