ppt on anticoagulants

1. ANTICOAGULANTS
BY:
Danial hassan

2. Hemostasis
• Hemostasis is the prevention or stoppage of
blood loss from an injured blood vessel
• Process involves: formation of a platelet
plug, activation of clotting factors and
growth of fibrin meshwork into the blood clot
making it more stable.

3. Blood Platelets
•Platelets are formed from the cytoplasm of
bone marrow and are the smallest of the
blood cells.
Normal platelet count lies between 150-450 x
109/L

4. Primary Hemostasis
Enzymes and Receptors involved in Primary
Hemostasis:
1- Thromboxane A2– Increases platelet
activation and aggregation
2- Adenosine Diphosphate (ADP)– Induce
platelet aggregation
3- glycoprotein II B/ III A receptors on platelet
surface: for attaching with the blood vessel’s
endothelial wall (aggregation)

5. Glycoprotein IIb/IIIa Receptors for
Platelet Aggregation
ADP
Collagen
Thrombin
Epinephrine
Tx A2
Serotonin
GP IIb/IIIa
receptor
activation
IIb/IIIa
Shear forces

6. SECONDARY HEMOSTASIS
Clotting factors activation
• Factor X converts prothombin into thrombin
• Thrombin converts fibrinogen into fibrin
• Fibrin threads stabilize the blood clot already
formed.

8. TERTIARY HEMOSTASIS
• Tissue plasminogen activator released from
endothelium---- converts plasminogen in the
clot to plasmin---- fibrinolysis---- fibrin
dissolution to limit the clot (removing extra
part)

9. Definition of Anticoagulation
• Therapeutic interference with the clotting
mechanism of the blood (blood-thinning)
to prevent or treat thrombosis.

10. Indications of Anticoagulant Therapy
• Treatment and Prevention of Deep Venous
Thrombosis (DVT), especially in CBR
patients– most high risk for DVT
• Pulmonary Emboli
• Prevention of stroke in patients with atrial
fibrillation, artificial heart valves, cardiac
thrombus.
• Ischemic heart disease
• During procedures such as cardiac
catheterisation (angioplasty).

11. No ST elevation ST elevation
Acute coronary syndrome
Antiplatelet Rx
Antithrombin Rx
Complete
obstruction
Partial
flow
UA/NSTEMI STEMI

12. Drugs Affecting Primary
Hemostasis

13. Antiplatelet Drugs
• Antiplatelet drugs act by inhibiting platelet
activation, adhesion and aggregation.
• Include drugs that inhibit thromboxane A2,
ADP, glycoprotein IIb/IIIa receptors
• Platelet count is essential to be checked with
all anti platelet drugs.

14. Thromboxane A2 Inhibitors
• Work by inhibiting synthesis of
prostaglandins, thereby inhibiting
cyclooxygenase, the enzyme in
platelets that synthesizes thromboxane
A2 (which causes platelet aggregation).
• Aspirin is an example. It affects the
platelets for the life of the platelet i.e. 7-
10 days.
• Must be stopped atleast 7 days before
surgeries after consultation with the
physician.

15. Platelet Activation:
Effect of ASA
ADP
Collagen
Thrombin
Epinephrine
Tx A2
Serotonin
 Ca++
PGG2-PGH2
AA release
Tx A2
COX
Tx Syn
Tx A2
RBCs
Endothelial cells
ASA

16. Adenosine Diphosphate Receptor
Antagonists
• Example: Clopidogrel (Plavix), Ticlopidine
• Inhibit platelet aggregation by preventing
ADP-induced binding of platelets. This
reaction inhibits platelet aggregation and
persist for the lifespan of the platelet (7-10
days)
• Must be stopped atleast 7 days before
surgeries after consultation with the
physician.

17. COX (cyclo-oxygenase)
ADP (adenosine diphosphate)
TxA2 (thromboxane A2)
CLOPIDOGREL
ASA COX
ADP
ADP
C
GPllb/llla Collagen thrombin
TXA2
Activation
TXA2
ASA
Mode of Action of Clopidogrel1
1. Schafer AI. Am J Med 1996; 101: 199–209.

18. Glycoprotein IIb/IIIa Receptor Inhibitors
• Aggrastat and Reopro (Abciximab) are the
drugs that prevent the binding of GP IIb/IIIa
receptors on platelets with the vessel wall.
This action inhibits platelet aggregation.
• Indication: Used during and after
percutaneous transluminal coronary
angioplasty (PTCA) i.e. removal of
atherosclerotic plaque, to prevent
rethrombosis

19. Glycoprotein IIb/IIIa Receptor Inhibitors
cont.
• Contraindications: include active bleeding,
thrombocytopenia, history of hemorrhagic
stroke, surgery or trauma within past 6
weeks, uncontrolled hypertension or
hypersensitivity.

20. Glycoprotein IIb/IIIa Receptor
Inhibitors
ADP
Collagen
Thrombin
Epinephrine
Tx A2
Serotonin
GP IIb/IIIa
receptor
activation
IIb/IIIa
Shear forces IIb/IIIa
inhibitor

21. Antiplatelet Agents
Mechanism of Action
ADP
(Fibrinogen
Receptor)
ADP = adenosine diphosphate, TXA2 = thromboxane A2, COX =
cyclooxygenase. Schafer AI. Am J Med. 1996;101:199–209.
clopidogrel bisulfate
TXA2
ADP
dipyridamole
phosphodiesterase
ADP
Gp IIb/IIIa Activation
COX
ticlopidine HCl
aspirin
Collagen
Thrombin
TXA2
Gp IIb/IIIa
antagonists

22. Drugs Affecting Secondary
Hemostasis

23. HEPARINE
• Binds to naturally occurring antithrombin III---
enhances its ability to inhibit thrombin (IIA), thereby
inhibiting fibrinogen conversion into fibrin

24. Monitoring required with Heparin
• Activated Partial Thromboplastin Time (APTT)-
-- Normal range: 25-30 seconds
• Timing
– Baseline APTT (before starting Heparine therapy
– Then, APTT is checked 6 hours after starting
Heparin infusion, and then after every 6 hours till
the infusion is in progress; based on the values of
APTT, dosage of heparin infusion is adjusted as per
the protocol

25. Low Molecular Weight Heparin
• Example : Enoxaparine
• Enriched with short molecular chains
• No monitoring required via APTT and lesser incidence of
thrombocytopenia----- due to lesser effect on thrombin (II
A); it primarily affects factor Xa
• However, PT and INR is to be checked with Enoxaparine
• Higher bioavailability than heparin (90% versus 60%)
• Longer half life than heparin (6 hours versus 1 hour)
• Must be stopped 12 hours before angiography in order to
avoid bleeding

26. WARFARIN
• Antagonizes vit K produced by the liver

27. Vitamin K
Synthesis of
Functional
Coagulation
Factors
VII
IX
X
II
Vitamin K-Dependent Clotting
Factors

28. Warfarin
No Synthesis
of
Coagulation
Factors
Antagonism
of
Vitamin K
Warfarin Mechanism of Action
Vitamin K
VII
IX
X
II

29. Enhances
Antithrombin Activity
Warfarin

30. Nursing Care for Patients on
Warfarin
• For patients on Warfarin, their Prothrombin time (PT)
and International Normalized Ratio (INR) has to be
checked regularly and informed to the physician;
Warfarin dose is adjusted according to the PT and INR
results
• Instruct patient to avoid eating green leafy vegetables
(rich in vitamin K) as they reduce the effectiveness of
Warfarin

31. Drugs Affecting Tertiary
Hemostasis

32. FIBRINOLYTICS/ THROMBOLYTICS
• Enhances the natural process of conversion
of plasminogen into plasmin--- dissolve fibrin
threads---dissolve the already formed clots/
plaque
• Revascularize the myocardium or brain
tissue by dissolving clots in coronary or
cerebral arteries
• Indicated in STEMI (100% blocked coronary
artery) or Acute Ischemic stroke
• Contraindicated in hemorrhagic stroke
• Examples: Streptokinase, tPA (tissue
Plasminogen Activator)

33. Nursing Care and Teaching for
Patients on Anticoagulants
• Explain the patient that their bleeding tendency has
increased, and that they are at high risk for bleeding
• Instruct patient to observe for bleeding from all orifices nose,
moth, anus, and to observe blood in sputum, urine and
stool; also instruct to report any bleeding
• Instruct patient to prevent themselves from injuries and cuts
• Instruct patient to use sharps very cautiously such as
razors, knives, needles, scissors etc.

34. Nursing Care and Teaching for
Patients on Anticoagulants
• Instruct patient for no Intramuscular injections and no tooth
brush
• In case of injury, instruct patient to apply direct pressure over
the area for ten to fifteen minutes in order to stop bleeding.
• Instruct patient to monitor appropriate lab results (Platelet
count with antiplatelets, APTT with Heparin, PT and INR with
Enoxaparine and Warfarin.
• Anticoagulants are contraindicated in all conditions of
hemorrhage i.e. hemorrhagic stroke, major bleeding from
surgical sites etc.

35. •THANKYOU