Antiplates, Anticoagulants, and thrombolytics Flashcards
What is clotting?
Blood clotting, or coagulation, isan important process that prevents excessive bleeding when a blood vessel is injured. Platelets and proteins in your plasma work together to stop the bleeding by forming a clot over the injury.
Clotting must achieve two factores
1: formation of platelet plugs
2: coagulation
what are the clotting factors that are important for formation of clotts?
II prothrombin
VII (6) stable factors
IX (8) plasma thromboplastine
X (10) stuart power factors
All requires vitamin K for syntheses.
How it happen?
1: Injury
2: activatation of clotting cascade then platelet aggregation forms plug that stops bleeding.
3: coagulation which fibrin is a protein that reinforece plates plugs framework for thrombi; from fibrinogen)
4: in the meantime tissue VII activates X converts prothrombin to thrombin ( active form)
What is Anti-platelets?
What are the drugs?
They lower platelets aggression. Anti clogging of arteries preventing the platelets from forming the clothes. Prevent blood cells called platelets from clumping together to form clots.
Aspirin and clopidogrel
That prevent acute coronary syndrome (ACS), Transient ischemic attack ( TIA) this is temporary artery blockage in brain like stroke. Also PAD or peripheral arterial disease on legs.
Before getting Anti plates what should we assess?
And what are the sign and symptoms of aspirin ( salicylate )toxicity?
Check HGB levels, less than 7
Platelets ( normal 150-400 k) less than 150 notify providers
We should hold the drugs, question which prescription are they using and notify the providers.
Tinnitus, Hyperventilating
Notify the providers
What is Anti coagulation?
It is used to treat the prevent the blood clots in blood vessels and the hearts. Also called blood thinners. Slow down the body processing form making clots.
what is clotting removal?
Plasminogen to plasmin
fibrinolytics also called thrombolysism ( alteplase)
Thrombosis
Occures when blood clots block veins or artheries.
Venous embolus: Tail, frequency travels to pulmonary arteries.
Arteries: adhesion to vessels to wall after damage and repture of an atherosclerotic plaque.
consquence: DVT, pulmonary embolism, MI, angina, athersoclerois.
Anticoagulants MOA
drugs groups
Disrupt clotting cascade by suppressing production of fibrin. More effective aganist venous throbosis.
Groups:
Heparins
Vitamin K antagoinst
Direct thrombin inhibitors, direct facotor Xa or IIa inhabitors ( NOACs/ DOACs)
Heprin meds ( anticoagulants)
it is an anticoagulation. MOA : suppress coagulation by inactivating clotting factors ( thrombin and factor Xa) and helping anti thrombin.
types of heprin such as Unfractioned Heparin (IV) and low molecular weight heprain.
The low molecular weight heprain includes Heparin > 1.5 hr half life and Lovenox ( is a weight base) > 4.5-7 hrs half life
Unfraction Heprain :
= time sensitive, requirs dose adjustment based on aptt
=administer IV
=indiactons: rapid anticoagulation effects ( pe, and DVT) not good for pregancy and acute MI. etc..
Monitoring:
activativated partial thromboplastin time (aPTT)
usually takes 25-35 seonds
Goal is to increase 1.5 to 2.5 times
45 to 70 seconds onset
Heprin adverst effects
Heparin induced thrombocytopenia( low platelte) rapid loss of circulation plateltes. Moniter patients platlets count.
= monitors for sign of bleeding bleeding
decrease blood pressure, increase heart rate
Bruising/ petechiae/ hematomas
red or black stools, discolored urin
headache
if you suspect bleeding stop heparin immediatly.
bleeding is risk low due to short half life ( 1.5 hrs)
Antidote for heprain is Protamine Sulfate IV
Low molecular weight heparin
Always given SQ
Generic : Heparin, Enoxaparin (Lovernox)
Indications: DVT prophylaxis, treatment for established DVT, PE, prevention of ischemic complicationwith unstable angina/ STEMIs.
Cl: thrombocytopenia, uncontrolled bleeding , anemia.
Viatmin K antiagonist: Warfarin
Brand name Coumadin
MOA: Blockage of viatmain K so factors VII, IX, X canot be made
Indication (Use) : Long term prophylaxis( prevent it from happening) venois thrombosis, Pulmonary embolism (PE) prosthetic heart valves, and artrial fibrillation ( A. FIb) + disoragnize electric signals.
Takes several days to developed peak 3-5 days
coagulation remains inhibited for 2-5 days due to long half life.
Lab values: Internation normalized ratio (INR) standarlized value all labs use so there is not confusion.
INR (2-3) days and moniter frequently and then 2-4 weeks
Half life 1.5- 2 days
adverse effects; Bleeding
Antidote is vitamin K
patients education: diet ( greenleafy vegetables) lab works.
Direct thrombin inhabitor: Dabigitan ( pradaxa)
A new antcoagulant drug/ direct oral drugs
Pradaxa MOA: it is reversable of thrombin inhibitor,prevent conversion of fibrinogen into fibrin ( key enzymes in coagulation) and prevent activation of factor XIII.
drugs peak in 1 hr
indication: A.Fib, prevent stroke non valvular A. Fib.
AE: bleeding , Gi disturbance( take with foods)
Antidote: Idarucizumab (praxbind)
Direct factors of Xa inhibitors: Rivaroxaban (xarelto)
MOA: selective inhibitors of factors Xa thereby inhibiting production of thrombin
peak plasma level 2-4 hrs
indication: preventing of DVT, PE post THA/TKA, prevntion stroke in A. Fib, treatment of DVT, PE unrelated to orthopedic surgery.
AE: bleeding
Caution: Renal impairment
Other meds ….
Apixaban( Eliquis) MOA: inhabits of factor Xa.
indication: prevention of stroke and systemic embolism in nonvalvular A.fib.
caution: renal impairments
risky for pregnant woment
