HEMATOLOGY - anticoagulant, antiplatelet & thrombolytic drugs Flashcards

EXAM 2 content

1
Q

what is a thrombus?

A

stationary clot attached to the vessel wall or within the heart

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2
Q

what is an arterial thrombi? what kind of drugs do they respond well to?

A

they form under conditions of high blood flow
- composed of plate aggregates held by fibrin strands
- responds well to antiplatelet drugs

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3
Q

what is a venous thrombi? what kind of drugs do they respond well to?

A

forms under conditions of low blood flow
- composed of RBCs w/ large amounts of fibrin, few platelets
- responds well to anticoagulant drugs

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4
Q

if the body has a thrombus, what will the body naturally do to it?

A

if body has a thrombus it will reduce through plasmin (enzyme that degrades fibrin meshwork of clot) & breaks it down over time
OR

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5
Q

what happens if the body can’t break down the clot?

A
  • will obstruct blood flow to tissues or organs –> depriving them of essential nutrients
    OR
  • will become an embolus – when a thrombus detaches from the vessel wall & circulates in bloodstream –> life threatening depending on site of occlusion
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6
Q

what 3 classes of drugs do providers prescribe if a pt has increased coagulation, clotting, clumping? what does each class of drug most effective for? what do all 3 have an increase risk for?

A
  • anticoagulant drugs: disrupts coagulation cascade + suppresses production of fibrin (does NOT dissolve clots) – best for venous & atrial thrombosis
  • antiplatelets drugs: inhibits platelet aggregation (clumping) – best for preventing arterial thrombosis
  • thrombolytic drugs: promotes lysis of fibrin + dissolves thrombi & newly formed thrombi (only drug that dissolves clots)

all increase risk of bleeding

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7
Q

what drugs are under anticoagulants?

A
  • UNFRACTIONATED HEPARIN
  • LOW MOLECULAR WEIGHT (LMW) HEPARIN
  • FONDAPARINUX
  • VITAMIN K ANTAGONIST
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8
Q

what is the mechanism of action of heparin & its derivatives

A

activates antithrombin
- enhances antithrombin: protein that inactivates thrombin & factor Xa (major clotting factors) –> production of fibrin is reduced, clotting suppressed

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9
Q

what are the adverse effects of UNFRACTIONATED HEPARIN?

A

all bleeding related
- hemorrhage
- spinal/epidural hematoma
- heparin induced thrombocytopenia
- hypersensitivity

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10
Q

what are the warnings of UNFRACTIONATED HEPARIN?

A

use with caution in patients with bleeding risk

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11
Q

what are the contraindications of UNFRACTIONATED HEPARIN (UH)?

A
  • thrombocytopenia (<50,000)
  • uncontrolled bleeding
  • lumbar puncture, regional anesthesia
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12
Q

what are the different types of indications since dosing varies with UNFRACTIONATED HEPARIN? which types of tests requires or doesn’t require monitoring?

A
  • prevention: 5,000 units q 8-12 hours – aPTT monitoring is NOT required
  • treatment: continuous IV infusion – aPTT monitoring IS required
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13
Q

why is aPPT monitoring not required for prevention type of treatmemt?

A

bc the dose is small & heparin has a short half life

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14
Q

what do we use if a pt overdoses on heparin? how do we administrate it?

A

PROTAMINE SULFATE – antidote
- slow IV injection

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15
Q

what are the two tests used to monitor the effectiveness of UNFRACTIONATED HEPARIN (UH)?

A
  • activated partial thromboplastin time (aPTT, most common)
  • anti factor Xa heparin assay
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16
Q

what is the normal value of aPPT? therapeutic levels? how often do we measure?

A
  • normal value = 40 seconds
  • therapeutic levels = increases 1.5-2x more –> 60-80 secs
  • measure q4-6 hours during initial phase of therapy
  • effective dosage established = measure daily
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17
Q

what does anti factor xa heparin assay measure? what levels indicate UH is therapeutic? what is so good ab this test?

A
  • measures heparin & its activity
  • antithrombin binding to Xa is increased
  • therapeutic range = 0.3-0.7 IU/mL
  • great bc its more accurate than aPPT but more expensive
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18
Q

what is the exemplar drug for LMW heparin? how are they different from UH?

A

ENOXAPARIN (LOVENOX)
- other: Dalteparin (Fragmin)
- has molecules that are shorter than UH

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19
Q

what are the therapeutic uses of ENOXAPARIN (LMW)?

A
  • prevention of DVT after surgery (abd, hip + knee replacement)
  • treatment of established DVT, w/ or w/o PE
  • prevention of ischemic complications (unstable angina, non Q wave MI, STEMI)
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20
Q

what are the adverse effects of ENOXAPARIN (LMW)?

A
  • bleeding (always)
  • severe neurologic injury with pts undergoing: spinal puncture, spinal or epidural anesthesia
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21
Q

what are the contraindications/precautions of ENOXAPARIN (LMW)?

A
  • serious harm increased by concurrent use of ANTIPLATELET drug or ANTICOAGULANT
  • if overdose –> PROTAMINE SULFATE
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22
Q

how are we administering ENOXAPARIN (LMW)? how do we determine the dose?

A

SQ – daily or twice a day
- dose is based on: indication, weight & renal function –> can be used at home but expensive

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23
Q

how do we know if ENOXAPARIN (LMW) has been effective?

A

does not require routine coagulation monitoring –> more tolerable + decr cost of lab monitoring

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24
Q

what is the exemplar drug for vitamin K antagonist?

A

WARFARIN (Coumadin & Jantoven)

25
what is the mechanism of action of WARFARIN?
delayed onset - inhibits synthesis of vitamin K dependent clotting factors -- prothrombin & factor X
26
what are the therapeutic uses of WARFARIN (vit K antag)
long term prophylaxis of thrombosis - prevention of venous thrombosis & associated PE - prevention of thromboembolism in pts with prosthetic heart valves - prevention of thrombosis in pts with atrial fibrillation - reduces risks of recurrent transient ischemic attacks & recurrent MI
27
what are the side effects of WARFARIN (vit k antag)?
- bleeding - if pregnant: fetal hemorrhage & teratogenesis - if breastfeeding: enters breastmilk -- do NOT take
28
what are the precautions with WARFARIN (vit k antag)?
when discontinued --> coagulation is still stopped for 2-5 days bc of long half life (1.5-2 days)
29
how do we administer WARFARIN?
oral
30
how do we know WARFARIN's effectiveness?
peak levels take several days to develop - usually pt is on another anticoagulant (UH / LMW) until WARFARIN reaches a therapeutic level
31
what lab monitoring do we use for WARFARIN (vit k antagonist)? what is it determined by? what is the goal? therapeutic level? how long does it take to reach desired INR?
international normalized ratio (INR) - goal = treatment to increase INR - therapeutic level of 2-3 (2.5-3.5) - if below rec range is below --> WARFARIN needs to be increased & vice versa - if dose is changed: takes a week or more to reach desired INR
32
what are the three types of drug interactions for WARFARIN?
- drugs increase WARFARIN effects - drugs promote bleeding - drugs that decrease anticoagulant effects
33
which drugs can cause the three types of drug interactions with WARFARIN?
- heparin - aspirin & other antiplatelet drugs - acetaminophen: found can increase risk of bleeding these are not contraindication, just give caution with more frequent lab monitoring
34
apparently foods can interact with WARFARIN (vit k antag), what kinds of foods interact with WARFARIN?
foods containing vitamin K -- can reduce anticoagulant effects of WARFARIN - foods: mayo, canola oil, soybean oil & green leaf veggies - they do not need to be avoided BUT intake needs to be CONSTANT - if vit k intake increases = warfarin dose increase = pos. relationship
35
what do we give if a pt overdoses on WARFARIN?
VIT K1 (PHYTONADIONE) -- PO or IV - fresh frozen plasma
36
what are the two drug classes that are ANTIPLATELET drugs?
- ASPIRIN - P2Y12 ADENOSINE DIPHOSPHATE RECEPTOR ANTAGONISTS
37
what kind of inhibitor is ASPIRIN? what is ASPIRIN's mechanism of action?
- it is a a cyclooxygenase inhibitor - MAO: irreversibly inhibits cyclooxygenase --> blocks synthesis of TXA2 (thromboxane A2)
38
what are the therapeutic uses of ASPIRIN?
for arterial thrombosis - primary prevention of MI (first MI in men & women in 65+ yo) - ischemic stroke / TIAs - chronic stable angina/unstable angina/acute MI/ previous MI - coronary stenting
39
what are the adverse effects of ASPIRIN?
- increases risk of Gi bleeding & hemorrhagic stroke
40
what are the contraindications/precautions of ASPIRIN?
- hypersensitivity to aspirin or NSAIDs - bleeding GI ulcers - bleeding disorders
41
what drugs can interact with ASPIRIN?
- NSAIDs - ACE inhibitors
42
what is the medication administration of ASPIRIN? how long do its effects last? what are specific directions for this med?
81-325 mg Oral, once daily - effects lasts 7-10 days after LAST dose -- giving to pts going under invasive procedures directions: - do not crush enteric coated tables - avoid taking on an empty stomach --> can cause nausea
43
how do we know if ASPIRIN has been effective?
by preventing all the therapeutic uses under ASPIRIN
44
what is the exemplary drug under P2Y12 ADENOSINE DIPHOSPHATE RECEPTOR ANTAGONISTS (antiplatelet)?
CLOPIDOGREL (Plavix)
45
what is CLOPIDOGREL's mechanism of action?
blocks P2Y12 ADP receptors on the platelets' surface --> preventing ADP stimulated aggregation (antiplatelet) - similar effects to Aspirin
46
what are the therapeutic uses of CLOPIDOGREL?
- prevents stenosis of coronary stent - secondary prevention of MI - ischemic stroke - vascular events
47
what are the adverse effects of CLOPIDOGREL?
usually well tolerated - bleeding - abd pain - dyspepsia (indigestion) - diarrhea - rash - thrombotic thrombocytopenic purpura
48
what are the interactions of CLOPIDOGREL?
- use with caution with patients taking other drugs that PROMOTE bleeding (other anticoagulants + NSAIDs) - proton pump inhibitors --> reduce antiplatelet effects of CLOPIDOGREL
49
how do we administer CLOPIDOGREL?
oral
50
how do we know CLOPIDOGREL is effective?
preventing all the therapeutic uses
51
what is so special about Thrombolytic (Fibrinolytic) drug?
its the only type of drug that DISSOLVES clots, thrombi that has already formed
52
what is the exemplar drug of thrombolytic drugs?
ALTEPLASE (Activase & Cathflo Activase) -- aka ATP - others: TENECTEPLASE (TNKase) + RETEPLASE (Retavase)
53
what is the mechanism of action of ALTEPLASE?
it is identical to human tPA - binds with plasminogen --> forms active complex --> converts plasminogen into plasmin --> DIGESTS fibrin meshwork of clots - degrades fibrinogen & other clotting factors --> increase risk of hemorrhage
54
what are the therapeutic uses of ALTEPLASE? when should you give this medication?
give ALTEPLASE within 4-6 hours of symptom onset - acute MI - acute ischemic stroke - acute massive PE small doses can also be used to restore patency in clogged central venous CATHETERS
55
what are the adverse affects of ALTEPLASE? what do nurses do before giving this drug?
BLEEDING - intracranial hemorrhage nurses has a full checklist -- make sure there are no contraindications, increase risk of bleeding & has all the indications to take the drug
56
what is the medication administration of ALTEPLASE?
IV
57
how do we know if ALTEPLASE is effective?
preventing the therapeutic uses
58
what are ABSOLUTE contraindications of ALTEPLASE?
- any prior intracranial hemorrhage or known intracranial neoplasm - known structural cerebral vascular lesion - ischemia stroke in past 3 mo EXCEPT ischemic stroke in 4.5 hrs - active internal bleeding (not including menses) - suspected aortic dissection
59
what are relative contraindications/cautions of ALTEPLASE?
- severe, uncontrolled htn 180/110 - history of chronic, severe poorly controlled htn - hx of prior ischemic stroke, dementia, or intracerebral pathology - CURRENT use of anticoagulants in THERAPEUTIC doses (INR 2-3+) - bleeding diathesis - traumatic or prolonged CPR (10 mins +) or major surgery (< 3 weeks ago) - recent internal bleeding (within 2-4 wk) - noncompressible vascular punctures - pregnancy - active peptic ulcer