GNUR 294 EXAM IV Pharmacology of Coagulation Disorders:NEWEST-2022
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GNUR 294 (GNUR294)
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Loyola University Chicago
GNUR 294 EXAM IV Pharmacology of Coagulation Disorders:NEWEST-2022GNUR 294 EXAM IV Pharmacology of Coagulation Disorders:NEWEST-2022GNUR 294 EXAM IV Pharmacology of Coagulation Disorders:NEWEST-2022GNUR 294 EXAM IV Pharmacology of Coagulation Disorders:NEWEST-2022
gnur 294 exam iv pharmacology of coagulation disorders
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GNUR 294 EXAM IV
Pharmacology of Coagulation Disorders
Affects the clotting factors- anticoagulants
Prevent platelets aggregation, doesn’t change number of platelets- antiplatelet
Breaks down clot formation- thrombolytic drugs
Anticoagulants & Antiplatelets don’t break down clots
Drugs are geared towards one of these processes
A normal response
When you damage blood vessels, and there is injury the first thing to control hemodynamics
and homeostasis, the blood vessels spasm, and then builds a matrix that will seal the injured
vessels, and the clotting factors will come in and then from a thrombosis to clot, and stays
around to heal and then enzymes that will be secreted once healed to destroy and break
down clot
Anticoagulant/ Indirect Thrombin Inhibitor
o The most commonly used today
o Acute prevention of clot formation of enlargement by effecting those clotting factors
o Only given IV- prototype drug
o Some of the newer generations SQ
o Unfractionated – drugs molecules that differ in size from molecule to molecule.
Going to react differently from patient to patient. Needs to have labs drawn to see
that is it a therapeutic level for patient.
o Works fast and well, have to monitor blood work very frequently
o Because this considered a high risk medication there is an antagonist for heparin:
protamine sulfate. If you a patient that has gotten too much heparin
o Patient that is at risk for clotting-
o Think of Virchow’s triad- venous stasis, hypercoagulability, tissue injury
o Going to see venous stasis and tissue injury in hospitalized patients
o Also have patients who have are out of the hospital- people only on medications
(hormonal), someone on bed rest, flying in airplanes
o To prevent from a clot in occurring or to treat a patient of DVT forming will be
treated with heparin
o If it’s get dislodged, pulmonary embolism it will be preventing perfusion
o as it has been more developed some drugs that have evolved rom that
unfractionated strand to more a molecular weight. don’t really have to draw blood
o Draw aPPT- measured in seconds of time, the greater the number the longer it’s
going to take a lot someone’s blood
o 25-40 seconds: person not on heparin, we want to prolong that time. It will be 1 ½
to 2 times to clot from that patient’s baseline. Want it to prevent thrombin from
forming. aPPT: 60-80 seconds for a therapeutic level
o Physician will order heparin protocol, then have to recheck aPPT
o Thrombosis prevention in high risk- someone that predisposes them to more
clotting
o HIT- heparin induced thrombocytopenia, the antibodies are being formed towards
heparin but are affecting the platelets. The platelets will drop (patient will be at a
double risk for bleeding), due to a lot things are helping the cell walls, the patient
will be in a hypercoagulability state and increasing thrombosis size. No prevention.
Once they do have this they can never get heparin again
o HAS TO HAVE A CBC DONE EVERYDAY
o Patient factors that will have cause toxicity: metabolism problems, protein binding ,
medication error
o Severe hypertension- blood vessels might pop somewhere, cerebrovascular.
Heparin is sometimes used as a bridge for people who need anticoagulation long
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