Antiplatelets and Anticoagulants Flashcards

1
Q

in event of ruptured plaque in the arterial walls enumerate homeostatic action of the body in blood clotting

A
  1. vasoconstriction - reduce blood loss by activating platelets, stimulates endothelial cells to release chemical mediators, and pain reflex
  2. 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
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2
Q

explain intrinsic and extrinsic pathways of blood clotting

A

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)

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3
Q

difference of arterial and venous thrombosis

A

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

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4
Q

drugs used to prevent platelet aggregation and inhibit thrombus formation in the arteries. Therefore treating CADs

A

Antiplatelets

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5
Q

antiplatelet meds

A

aspirin
clopidogrel
ticagrelor

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6
Q

pharmacodynamics of aspirin

A

inhibit prostaglandin production by preventing COX
Low dose: inhibit COX 1 - platelet aggregation effect
High dose: inhibit COX 2 - antipyretic and analgesic benefits

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7
Q

adverse effects of aspirin

A

GI upset
increased bleeding risk - (haemophilia or bleeding disorder)
dizziness, vertigo, deafness - older pts
bronchospasm - asthma pts

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8
Q

clopidogrel and ticagrelor pharmacodynamics

A

inhibits ADP activation to prevent fibrinogen-platelet binding further reducing platelet activation and aggregation

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9
Q

nursing considerations for antiplatelets

A

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

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10
Q

Anticoagulants MOA

A

prevent recurrence or repeated venous thromboembolism
stroke prevention in AF
management of STEMI and nonSTEMI

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11
Q

Parenteral and oral anticoagulants

A

parenteral: heparin, enoxaparin
oral: warfarin, dabigatran

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12
Q

2 types of heparin

A

unfractioned heparin and low molecular weight heparin (enoxaparin)

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13
Q

pharamacodynamics of unfractioned heparin

A

activates antithrombin II which inactivates factor Xa and IIa

kinetics: rapidly anticoagulates with short onset of action

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14
Q

indications of unfractioned heparin

A

pulmonary embolism and DVT

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15
Q

unfractioned heparin contraindication

A

pregnancy (heparin doesn’t cross placenta, can increase perinatal mortality for women and risk of maternal osteoporosis
CAUTIO FOR BLEEDING

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16
Q

adverse effects of unfractioned heparin

A

excessive bleeding
thrombocytopenia
allergies
hyperkalaemia (inhibits aldosterone stimulation)

17
Q

pharmacodynamics of enoxaparin or low molecular weight heparin

A

binds and activates antithrombin III which inactivates factor Xa ONLY

kinetics: longer onset duration compared to standard heparin (less monitoring reqd)

18
Q

adverse effects

A

similar to heparin but less common

considered safer to pregnancy compared to heparin

19
Q

warfarin (oral anticoagulant) pharmacodynamics

A

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

20
Q

precautions for warfarin

A

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

21
Q

warfarin interactions

A

most antibiotics such as erythromycin and metronidazole (influence GIT bacterial production of Vit K and inhibits warfarin metabolism)

Tramadol - inhibits warfarin metabolism

22
Q

nursing considerations for warfarin

A

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

23
Q

Direct oral coagulants

A

dabigatran and rivaroxaban

24
Q

dabigatran pharamacodynamics

A

direct inhibitor of factor IIa
prevents systemic embolism in AF

25
Q

dabigatran contraindications

A

enoxaparin
concurrent use of aspirin, NSAIDs and SSRIs (increase bleeding times)

26
Q

rivaroxaban pharmacodynamics

A

inhibits factor Xa
prevents systemic embolism in AF and venous thromboembolism (from hip or knee surgery)

27
Q

rivaroxaban contraindications

A

aspirin, NSAIDs, grapefruit and garlic

28
Q

Thrombolytic or fibrinolytic drugs MOA and types

A

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

29
Q

thrombolytics treats

A

acute MI

30
Q

tenectoplase (fibrin specific fibrinolytic) pharmacodynamics

A

activates plasminogen to convert into plasmin degrading the fibrin matrix (fibrin blood clots) or stimulates fibrinolysis (breakdown of fibrin blood clots)

31
Q

contraindication of tenecteplase

A

recent hemorrhage, trauma or surgery
coagulation defects
should not be mixed with other anticoagulants