Anticoagulants Flashcards

1
Q

Physiologic process of stopping bleeding due to blood vessel injury; injury can be internal or external

A

Hemostasis

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2
Q

Anticoagulants are drugs that activate ____-_______

Includes:

A

Activate anti-thrombin

Include:

  1. Heparin
  2. Low Molecular Weight Heparins (LMV) - Lovenox
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3
Q

Heparin (Part 1)

A

-MOA:
Suppresses coagulation by helping anti-thrombin inactivate clotting factors, mainly thrombin and factor Xa

-Absorption:
Must be given IV or subQ since it does not cross membranes and cannot be absorbed. Does not enter the placenta or breast milk.

Short half-life (about 1.5 hours except if hepatic or renal damage)

-Indications:
Use in situations requiring RAPID suppression of coagulation

Ex. PE, evolving stroke, DVT, DIC, open heart surgery, renal dialysis, after surgery

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4
Q

Heparin Adverse Reactions include:

A
  • Hemorrhage
  • Spinal/Epidural Hematoma
  • Heparin Induced Thrombocytopenia
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5
Q

Heparin Adverse Reactions (Hemorrhage)

A
  • Check aPTT (activated partial thromboplastin time) before giving
  • Pt value should be 1 1/2-2x control (control = 30-45 sec) so approx. 60-80 sec
  • Call HCP if dosage is held (usually never hold heparin unless pt is externally bleeding!)
  • Assess pt for low B/P, broken capillaries in the eyes, bruising, petechiae, hematomas, blood in stools/urine, bloody nose
  • aPTT will be measured q6-q8h if on continuous IV heparin
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6
Q

Heparin Adverse Reaction (Spinal/Epidural hematoma)

A

risk is especially high for those with an epidural catheter (for pain); use of other anticoagulants, use of antiplatelet drugs, Hx of spinal trauma.

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7
Q

Heparin Adverse Reaction (Heparin Induced Thrombocytopenia - HIT)

A

HIT is an immune mediated disorder with thrombocytopenia and a paradoxical INCREASE in thrombotic events.

The underlying cause is development of antibodies against heparin- platelet protein complexes which activate platelets and damage the vascular endothelium.

(monitor for low platelet cts); can cause death

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8
Q

Heparin antidote:

A

PROTAMINE SULFTATE

  • Given by slow IV injection (20mg/min or 50mg/in 10 min)
  • Protamine binds ionically with heparin to neutralize anticoagulation action, up to 2 hours
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9
Q

Heparin (Part 2)

A

-Contraindications: do not use in thrombocytopenia, uncontrollable bleeding, in hemophilia, pt with eye, brain, or spinal cord surgery

-Administration:
Given in UNITS. IV continuous, IV push intermittent doses, SQ, Hep lock/hep flush (100 units/ml for flush)

  • SubQ given in abdomen, 2 inches away from umbilicus. Keep pressure on site. Do not massage
  • Dosage: 5,000-10,000 Units/q6h or SC; 25,000 units per 500 ml IV
  • 2nd most common med error in nursing
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10
Q

Low Molecular Weight Heparin includes:

A

LOVENOX, fragmin, and tinzaparin

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11
Q

LMW Heparin:

A
  • Fixed dose, no blood monitoring, longer half-life than Heparin
  • Pt can be taught to inject at home unlike heparin
  • MOA: the molecules are short and do not have quite the same effect as unfractionated heparin. LMW do not inactivate thrombin as well as heparin can.
  • Given SubQ in abdomen based on body weight
  • Can cause HIT, overdosage treated with PROTAMINE SULFATE. Major side effect is bleeding (duh)
  • Can cause permanent paralysis when undergoing spinal puncture/anesthesia. Cost $63/day compared to $8/day for unfractionated heparin but no blood monitoring costs tends to level out the costs
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12
Q

Warfarin (Coumadin)

A

-MOA:
Suppresses coagulation by decreasing production of factors VII, IX, X and prothrombin, all of which need Vitamin K to be produced. Warfarin inhibits the enzyme (VKORC1) needed to convert Vitamin K to the active form. Warfarin does NOT inhibit Vitamin K action directly;

-Indications:
Long term prevention of thrombosis, Prevention of thrombosis in pts with prosthetic heart valves; prevention of clotting in Atrial fibrillation. Reduces the risk of TIA’s and recurrent MI’s .

-Monitoring:
Prothrombin Time (very sensitive to alterations in Vitamin K levels. Normal PT is about 12; desired level is 1 1/2-2X control.  (adjusted similarly to heparin except coumadin is oral ).  More commonly used now is INR (international normalized ratio) which corrects for thromboplastin variability.
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13
Q

Monitoring Coumadin

Normal INR is 1.1

A
  • INR 2-3 X normal except may be higher depending on guidelines from the Cardiovascular Society issuing physician treatment guidelines based on research. (Sliding scale as with heparin).
  • PT levels change quicker, INR takes a week or more to change when coumadin dosages are being changed.
  • PT is checked daily, while the dosages are being adjusted
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14
Q

Adverse Effects of Coumadin

A
  • Hemorrhage - any bodily secretion or orifice

- Pregnancy - can cause fetal bleeding, death and teratogenesis (use heparin instead)

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15
Q

Coumadin Drug-Drug interactions

A

-MANY

  • Drugs that increase effects of coumadin DISPLACE the drug from albumin:
  • (ex. aspirin, sulfonamides, acetaminophen, azole, etc)

-Drugs that decrease effects of coumadin - cephalosporins

99% bound to albumin

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16
Q

Coumadin Pt. Education

A
  • Wear medical alert bracelet
  • Monitor blood levels as ordered
  • Do not use if pregnant
  • Hold before surgery (1-2 weeks)
  • Dietary: Keep dietary intake of Vit. K constant - don’t have to stop the foods
  • VERY SLOW ONSET OF ACTION (one week) and many patients will be initially placed on heparin and Coumadin together and then heparin will be withdrawn when blood levels are within therapeutic range
17
Q

Antidote for Warfarin (Coumadin)

A

VITAMIN K

18
Q

Dabigastran etexilate (Pradaxa)

A

-A reversible, direct thrombin inhibitor

-Indications:
Atrial fibrillation, Prevention of stroke, prevention of systemic embolism with nonvalvular (not an artificial value) atrial fibrillation.

Dosage: 150 mg bid

19
Q

Dabigastran etexilate (Pradaxa) advantages over warfarin

A
  • Rapid onset
  • no need to monitor anti-coagulation effect
  • Few drug-food interactions
  • Lower risk of major bleeding
  • Same dose for all patients regardless of age or weight
20
Q

Dabigastran etexilate (Pradaxa) Part 2:

A

-Well absorbed in GI but food delays absorption but does not prevent absorption.

-A/E:
Bleeding (no specific antidote but recombinant Factor VIIa can be tried). Stop drug before elective surgery; dyspepsia (35% of pts), can take with omeprazole or cimetidine

-Drug interactions:
Not metabolized by hepatic P450 enzymes; combined use with ketoconazole, amiodarone, verapmil, quinidine could cause excessive bleeding due to increased blood levels;

21
Q

Rivaroxaban (Xarelto)

A

-Directly Inhibits Factor Xa (activated Factor X) and thereby inhibits production of thrombin.

  • Advantages compared to Coumadin (warfarin):
  • Rapid onset
  • Fixed dosage
  • Lower bleeding risk
  • Few drug interactions
  • No need for INR monitoring
  • Indications:
    1. Prevention of DVT and PE following total hip or knee replacement surgery
    2. Prevention of stroke in patients with A. fib
22
Q

Rivaroxaban (Xarelto) Part 2:

A

-Pharmokinetics:

  • Administered orally
  • Substantial protein binding
  • Partial metabolism by CYP3A4 (cytochrome P450)
  • Bleeding is high risk in those with renal or hepatic impairment

-A/E:
Bleeding and spinal/epidural hematomas with permanent paralysis possible.

  • Do not use in moderate or higher RENAL/HEPATIC impairment
  • Do not use in pregnancy
23
Q

Anti-platelet Aggregators include:

A
  • Aspirin (oral)
  • Clopidogrel (Plavix) (Oral)
  • Glycoprotein IIb/IIIa receptor blockers (IV Infusion) ICU only*
24
Q

Aspirin

A

-Anti-platelet aggregator

-MOA:
Prevents platelet aggregation (clot formation) by suppressing production of an enzyme necessary for platelets to produce Thromboxane A2 (a prostaglandin). Inhibits synthesis of Prostacyclin from the endothelium of the arterial cell wall but as long as dosage is kept low this is NOT a problem.

-Indications:
PRIMARY Prevention of MI; Prevention of recurrence of MI, reduces risk of death from strokes, TIA’s, reduces risk of sudden death in USA ; Prevents reocclusion during coronary stenting (PCI)

-Dosage:
Low dose is either 81 mg or 325 mg/day

  • A/E: GI Bleeding, hemorrhagic stroke, enteric coated ASA is advocated but does not always work
  • May add a proton pump inhibitor to reduce gastric acidity
25
Q

Clopidogrel (Plavix)

A
  • P2Y12 Adenosine Diphosphate Receptor Blockers (ADP)
  • Antiplatelet Aggregators similar in action to aspirin and frequently given in addition to aspirin after PCI procedures to prevent thrombotic events
  • Generally given for six months to 2 years after the acute coronary event or procedure.
  • Prevents occlusion of coronary stents
  • Adverse Effects- Bleeding, bruising, thrombocytopenia, anemia, renal dysfunction and fever. Most often the first two weeks of therapy.
26
Q

Ticagrelor (Brilinta)

A
  • P2Y12 Adenosine Diphosphate Receptor Blocker (ADP)
  • Inhibits the receptor site on the surface of the platelet, thus preventing aggregation of platelets
  • In contrast to clopidogrel and prasugrel which cause irreversible blockade, this drug causes REVERSIBLE blockade and effects wear off faster.

-Indications:
Prevents occlusion of coronary stents, used for about 18-24 months post procedure.***

27
Q

Ticagrelor (Brilinta) Part 2:

A

-Adverse effects:
hemorrhage, dyspnea, cough, dizziness, noncardiac chest pain, diarrhea, bradycardia, ventricular pauses
.
-Nursing Implications:
Teach patient that drug must be discontinued 5 days before surgery;

Aspirin is usually given in low dosages along with the drug but high doses >100 mg should not be used due to danger of actually reducing benefits of ticagrelor.

28
Q

Abciximab (Reopro)

A

-GP IIb/IIIa Antagonists

-MOA:
Binds to platelets near the GP IIb/IIIa receptors and then prevents the receptors from binding FIBRINOGEN

-Indications:
Given in conjunction with Heparin (IV infusion) and aspirin to promote revascularization in patients undergoing thrombolytic therapy, acute MI and/or PCI.

  • A/E: Major major bleeding, especially at site of PCI access (femoral artery)
  • Stop Reopro if major bleed occurs (effects last 24-48 hours)
  • VERY EXPENSIVE. IV ONLY. WEIGHT BASED
29
Q

Thrombolytic Drugs

-plase (altePLASE, retePLASE, tenectePLASE

A

“clot busters” (fibrinolytic drugs)

  • Alteplase: (tPA) tissue plasminogen activator
  • identical to human tPA and is made by recombinant DNA technology

-Indications:
Acute MI, ischemic stroke (not hemorrhagic stroke), and acute massive pulmonary embolism.

-A/E:
Acute hemorrhage and death due to massive dissolving of all clots in the body;

-Contraindications:
hemorrhagic stroke, postpartum, surgery within two weeks. No IMs or SC’s, keep pressure on IV puncture sites.

-VERY EXPENSIVE:
must be given two doses in ER on admission within 2-6 hours of event

30
Q

Arterial thrombi begin with formation of a platelet plug, reinforced with fibrin; best prevented by:

A

Antiplatelet drugs: Aspirin, clopidogrel, ticagrelor

31
Q

Venous thrombi begin with formation of fibrin, then enmeshing with RBCs and platelets. Further venous thrombi are best prevented with:

A

Heparin since its action begins within minutes of IV administration

Long-term prevention can be done through Coumadin or one of the newer anti-coagulants

32
Q

Existing clots can be dissolved through very dangerous drugs such as:

A

tPA (thrombolytics)