Antiplatelet, Anticoagulant and Antithrombotic Agents

Question 1

How are arterial thrombi usually formed?

Answer 1

Damage to endothelial tissue within the blood vessel

Question 2

How are venous thrombi usually formed?

Answer 2

Venous stasis which allows platelets and fibrin to build up causing a clot

Question 3

Do Anticoagulants break down existing clots?

Answer 3

No

Question 4

Do Anticoagulants prevent existing clots from becoming larger and prevent new clots from forming?

Answer 4

Yes

Question 5

List the categories of Anticoagulants

Answer 5

• Unfractionated Heparin and Low Molecular Weight Heparin
• Vitamin K Antagonists
• Antithrombin III Direct Inhibitors
• Direct Thrombin Inhibitor
• Direct Factor Xa Inhibitor

Question 6

How is the correct dosage and monitoring of therapeutic levels conducted.

Answer 6

Regular blood tests

Question 7

Why are regular blood tests performed on patients undergoing Anticoagulant therapy?

Answer 7

To determine dosage of medication, monitor therapeutic levels, platelet levels and side effects of medication (ie hyperkalaemia when using LMW Heparin’s)

Question 8

List some general pt education for pt’s taking Anticoagulant medication regarding when to seek medical advice due to side effects

Answer 8

Leg numbness/weakness, unexplained or prolonged bleeding, bleeding of gums when brushing, unusual nose bleeds, blood in urine or stool, coughing or vomiting blood.

Question 9

List general education for pt’s on Anticoagulant therapy

Answer 9

wear a medical alert bracelet, inform dentist or surgeon of anticoagulant use, seek doctor or pharmacist advice before taking analgesics (including OTC)

Question 10

How does UF and LMW heparin work?

Answer 10

Heparin works by binding to antithrombin III and accelerating its effect. This has the effect of neutralising active clotting factors (mainly activated factor II (thrombin) and factor X). By inactivating activated factor II (thrombin) fibrinogen can no longer be converted to fibrin therefore preventing a clot.

Question 11

What is the onset time of IV and SC UF heparin?

Answer 11

IV - instantly
SC - 20-60 minutes

Question 12

What is the half life of Heparin?

Answer 12

Generally between 1-6 hours, dependant on dose

Question 13

Nursing care for UF Heparin

Answer 13

• Shouldn’t be given IM
• Inject slowly, 1ml/min to avoid pain
• SC in anterior abdo or thigh

Question 14

What is the difference between UF heparin and LMW heparin?

Answer 14

UF has faster onset and withdrawal time
LMW lasts longer and is more predictable

Question 15

What is used to treat a Heparin overdose?

Answer 15

Protamine sulfate

Question 16

Examples of LMW heparins

Answer 16

enoxaparin, dalteparin and nadroparin

Question 17

Examples of heparin adverse effects

Answer 17

• Bleeding tendency (at high doses)
• Thrombocytopenia
• Hyperkalaemia
• Allergic reaction
• Osteoporosis (long term use)
• haematoma (at injection site)

Question 18

Example of Antithrombin III dependant inhibitor?

Answer 18

Fondaparinux

Question 19

How does a vitamin k antagonist work?

Answer 19

blocks vitamin k epoxide reductase therefore stopping gamma glutamyl carboxylase from being produced which prevents inactive clotting factors 2,7,9,10 from being activated to form a clot.

Question 20

How long is the onset of warfarin?

Answer 20

24-48 hours

Question 21

Some people have a genetic variation that results in a resistance to warfarin, true or false

Answer 21

true

Question 22

Uses of warfarin?

Answer 22

• Prevention and management of DVT and PE
• Prevention and management of thromboembolism in AF, MI or prosthetic heart valves

Question 23

Warfarin adverse reactions

Answer 23

haemorrhage, nausea, vomiting, diarrhoea, taste alterations, abdo pain, pruitus, rash, uriciaria, fatigue, lethargy, headaches, dizziness, alopecia, elevated liver enzyme, hepatitis

Question 24

Nursing points for Warfarin (5 or more is good)

Answer 24

-Coumadin and Marevan are not to be interchanged
- large loading doses are not recommended
- bleeding can occur even within therapeutic range ( it may unmask a lesion)
- question inherited or acquired warfarin resistance if large daily dose is required to reach INR goal
- Avoid IM and monitor SC site for haematoma
- Observe for overdose, one early sign is bleeding from the gums
- Be aware that heparins are also commonly used with warfarin
- Base line INR is measured before starting warfarin and daily for first 5 days
- Warfarin should be stopped 5 days prior to procedure with moderate to high bleeding risk, A patient with high VTE risk can continue to use heparin
- Overdose is treated with Vitamin K 5-10mg over 30 seconds with fresh frozen plasma

Question 25

Patient teaching for warfarin

Answer 25

- Explain importance of carrying anticoagulant booklet, as it inlcuides lab results and daily dose - Advise Pt on importance of attending DR appointments for blood tests re dose - Advise Pt that tablet needs to be swallowed whole, at the same time every night - Do not take a "make up" dose if one dose is missed and consult DR or pharmacist - Pt should not stop warfarin abruptly and should not start/stop other medication (including OTC) without medical advice - Pt should maintain healthy diet but be advised to not eat too much vitamin K rich food ie leafy greens - Pt to seek medical advice if they start experiencing; bleeding gums, unusual or prolonged bleeding, unusual nosebleeds, vomiting or coughing blood, blood in urine or stool, blackness in extremities, toes that become dark purple or mottled or painful (3-10 weeks after starting therapy)

Question 26

How does an Antithrombin III dependant inhibitor work?

Answer 26

It binds directly to antithrombin III and selectively inhibits factor Xa

Question 27

When is Fondaparinux commonly used?

Answer 27

after hip, knee or abdo surgery

Question 28

What route is fondaparinux administered

Answer 28

subcut

Question 29

When should patients platelets be monitored when using fondaparinux?

Answer 29

Pre and Post therapy

Question 30

Examples of direct thrombin inhibitors

Answer 30

dabigatran and BIVALIRUDIN

Question 31

How do direct thrombin inhibitors work?

Answer 31

binds directly to free floating and clot-bound thrombin by binding to the thrombin's active site. Does not need a cofactor such as antithrombin

Question 32

What are direct thrombin inhibitors used for?

Answer 32

Used as prophylaxis of VTE after major orthopaedic surgery, stroke and systemic embolism in people with non valvular AF + additional risk factor

Question 33

General Nursing considerations for Dabigatran

Answer 33

- Not recommended with other anticoagulants or antiplatelets - Increased risk of bleeding if given with SSRI, SNRI, NSAID's with half life > 12 hours - Not recommended in Pt under 18 years old - Rapid reversal using idarucizumab

Question 34

Example of Direct factor Xa inhibitors

Answer 34

Apixaban, Rivaroxaban and Edoxaban

Question 35

How do direct factor Xa inhibitors work

Answer 35

Inhibits factor Xa from acting on prothrombin

Question 36

What are some contraindications for factor Xa inhibitors?

Answer 36

HIV protease inhibitors, azole antifungals, Heparins and oral anticoagulants fondarinux (except when switching anticoagulant medications)

Question 37

General nursing points for Direct factor Xa inhibitors

Answer 37

- Antiplatelets (except aspirin) should be stopped before surgery - Should be stopped 48 hours pre op if there is med-high risk of bleeding or 24 hours if low risk - Monitor for spinal haematoma - Not recommended as alternate to heparin therapy as initial management for PE in haemodynamically unstable Pt, if the Pt my receive fibrinolytic therapy or pulmonary embolectomy

Question 38

How does platelet aggregation occur?

Answer 38

platelets adhere to exposed collagen fibres via the glycoprotein Ia/IIa receptors and von Willebrand factor. Once the platelets have adhered to the collagen, they release ADP, Thromboxane A2 and thrombin. They then bind to platelet receptors and stimulate aggregation. This binding activates glycoprotein 2B/3A. This results in fibrinogen and von willebrand factor binding to the platelet, resulting in platelets being able to bind together ie platelet aggregation