Antiplatelets and Anticoagulants Flashcards
in event of ruptured plaque in the arterial walls enumerate homeostatic action of the body in blood clotting
- vasoconstriction - reduce blood loss by activating platelets, stimulates endothelial cells to release chemical mediators, and pain reflex
- platelet plug formation - platelet aggregation formation by temporarily seals the broken blood vessel by:
- exposing collagen fibres (damaged endothelium)
- platelets sticks to collagen fibres
- plasma protein (von Willebrand’s factor) act as a glue to bind collagen fibres and platelets
- platelets are activated by releasing chemicals such as ADPs (recruiting more platelets in the area), serotonin and thromboxane A2 to enhance vascular spasm (vasoconstriction) and platelet aggregation
explain intrinsic and extrinsic pathways of blood clotting
intrinsic - when vessel endothelium ruptures exposing collagen fibres and platelet aggregation process occurs
extrinsic - trauma to tissue cells causing blood loss therefore platelet aggregation process starts
both pathways activates:
1. Factor X
2. Prothrombin
3. Thrombin (from prothrombin activator)
4. Fibrinogen
5. Fibrin (strands glue the platelets together and form a web like fibrin mesh)
difference of arterial and venous thrombosis
arterial - mainly caused by ruptured accumulated plaque in the arterial walls causing thrombus
venous - mainly caused by DVT when arterial walls are damaged causing the formation of thrombus
both blocking blood flow to vital organs
drugs used to prevent platelet aggregation and inhibit thrombus formation in the arteries. Therefore treating CADs
Antiplatelets
antiplatelet meds
aspirin
clopidogrel
ticagrelor
pharmacodynamics of aspirin
inhibit prostaglandin production by preventing COX
Low dose: inhibit COX 1 - platelet aggregation effect
High dose: inhibit COX 2 - antipyretic and analgesic benefits
adverse effects of aspirin
GI upset
increased bleeding risk - (haemophilia or bleeding disorder)
dizziness, vertigo, deafness - older pts
bronchospasm - asthma pts
clopidogrel and ticagrelor pharmacodynamics
inhibits ADP activation to prevent fibrinogen-platelet binding further reducing platelet activation and aggregation
nursing considerations for antiplatelets
can cause thrombocytopaenia (low blood platelet counts) and excessice haemolysis
educate pt about excessive bruising and bleeding
DO NOT GIVE AT LEAST 5 DAYS prior to invasive surgery
Anticoagulants MOA
prevent recurrence or repeated venous thromboembolism
stroke prevention in AF
management of STEMI and nonSTEMI
Parenteral and oral anticoagulants
parenteral: heparin, enoxaparin
oral: warfarin, dabigatran
2 types of heparin
unfractioned heparin and low molecular weight heparin (enoxaparin)
pharamacodynamics of unfractioned heparin
activates antithrombin II which inactivates factor Xa and IIa
kinetics: rapidly anticoagulates with short onset of action
indications of unfractioned heparin
pulmonary embolism and DVT
unfractioned heparin contraindication
pregnancy (heparin doesn’t cross placenta, can increase perinatal mortality for women and risk of maternal osteoporosis
CAUTIO FOR BLEEDING
adverse effects of unfractioned heparin
excessive bleeding
thrombocytopenia
allergies
hyperkalaemia (inhibits aldosterone stimulation)
pharmacodynamics of enoxaparin or low molecular weight heparin
binds and activates antithrombin III which inactivates factor Xa ONLY
kinetics: longer onset duration compared to standard heparin (less monitoring reqd)
adverse effects
similar to heparin but less common
considered safer to pregnancy compared to heparin
warfarin (oral anticoagulant) pharmacodynamics
inhibits epoxide reducatase (enzyme reduces inactive Vit K) therefore reduces active Vit K in the liver.
since Vit K synthesise clotting factors II, VII, IX and X
precautions for warfarin
CAUTION with other anticoagulants or antiplatelets - ASPIRIN AND NSAIDs can prolong bleeding time
USE paracetamol instead as analgesic
monitor:
hematuria (urine in blood)
nosebleeds
gingival bleeding
bruising
warfarin interactions
most antibiotics such as erythromycin and metronidazole (influence GIT bacterial production of Vit K and inhibits warfarin metabolism)
Tramadol - inhibits warfarin metabolism
nursing considerations for warfarin
educate timing and rationale for blood tests
monitor excessive bruising, bleeding in BMs, vomit, urine and nose
asses internal bleeding : low BPs, abdominal pain (painful, stiff and swollen)
educate drug interactions
Direct oral coagulants
dabigatran and rivaroxaban
dabigatran pharamacodynamics
direct inhibitor of factor IIa
prevents systemic embolism in AF
dabigatran contraindications
enoxaparin
concurrent use of aspirin, NSAIDs and SSRIs (increase bleeding times)
rivaroxaban pharmacodynamics
inhibits factor Xa
prevents systemic embolism in AF and venous thromboembolism (from hip or knee surgery)
rivaroxaban contraindications
aspirin, NSAIDs, grapefruit and garlic
Thrombolytic or fibrinolytic drugs MOA and types
act as thrombolytics (break and dissolve blood clots blocking blood flow) by activating plasminogen to form plasmin degrading fibrin breaking up thrombi
non-fibrin specific - streptokinase
fibrin specific - tenecteplase and alteplase
thrombolytics treats
acute MI
tenectoplase (fibrin specific fibrinolytic) pharmacodynamics
activates plasminogen to convert into plasmin degrading the fibrin matrix (fibrin blood clots) or stimulates fibrinolysis (breakdown of fibrin blood clots)
contraindication of tenecteplase
recent hemorrhage, trauma or surgery
coagulation defects
should not be mixed with other anticoagulants
