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nurs 366: pathopharm ii > HEMATOLOGY - anticoagulant, antiplatelet & thrombolytic drugs > Flashcards

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
Q

what is the mechanism of action of WARFARIN?

A

delayed onset
- inhibits synthesis of vitamin K dependent clotting factors – prothrombin & factor X

26
Q

what are the therapeutic uses of WARFARIN (vit K antag)

A

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
Q

what are the side effects of WARFARIN (vit k antag)?

A
  • bleeding
  • if pregnant: fetal hemorrhage & teratogenesis
  • if breastfeeding: enters breastmilk – do NOT take
28
Q

what are the precautions with WARFARIN (vit k antag)?

A

when discontinued –> coagulation is still stopped for 2-5 days bc of long half life (1.5-2 days)

29
Q

how do we administer WARFARIN?

A

oral

30
Q

how do we know WARFARIN’s effectiveness?

A

peak levels take several days to develop
- usually pt is on another anticoagulant (UH / LMW) until WARFARIN reaches a therapeutic level

31
Q

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?

A

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
Q

what are the three types of drug interactions for WARFARIN?

A
  • drugs increase WARFARIN effects
  • drugs promote bleeding
  • drugs that decrease anticoagulant effects
33
Q

which drugs can cause the three types of drug interactions with WARFARIN?

A
  • 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
Q

apparently foods can interact with WARFARIN (vit k antag), what kinds of foods interact with WARFARIN?

A

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
Q

what do we give if a pt overdoses on WARFARIN?

A

VIT K1 (PHYTONADIONE) – PO or IV
- fresh frozen plasma

36
Q

what are the two drug classes that are ANTIPLATELET drugs?

A
  • ASPIRIN
  • P2Y12 ADENOSINE DIPHOSPHATE RECEPTOR ANTAGONISTS
37
Q

what kind of inhibitor is ASPIRIN? what is ASPIRIN’s mechanism of action?

A
  • it is a a cyclooxygenase inhibitor
  • MAO: irreversibly inhibits cyclooxygenase –> blocks synthesis of TXA2 (thromboxane A2)
38
Q

what are the therapeutic uses of ASPIRIN?

A

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
Q

what are the adverse effects of ASPIRIN?

A
  • increases risk of Gi bleeding & hemorrhagic stroke
40
Q

what are the contraindications/precautions of ASPIRIN?

A
  • hypersensitivity to aspirin or NSAIDs
  • bleeding GI ulcers
  • bleeding disorders
41
Q

what drugs can interact with ASPIRIN?

A
  • NSAIDs
  • ACE inhibitors
42
Q

what is the medication administration of ASPIRIN? how long do its effects last? what are specific directions for this med?

A

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
Q

how do we know if ASPIRIN has been effective?

A

by preventing all the therapeutic uses under ASPIRIN

44
Q

what is the exemplary drug under P2Y12 ADENOSINE DIPHOSPHATE RECEPTOR ANTAGONISTS (antiplatelet)?

A

CLOPIDOGREL (Plavix)

45
Q

what is CLOPIDOGREL’s mechanism of action?

A

blocks P2Y12 ADP receptors on the platelets’ surface –> preventing ADP stimulated aggregation (antiplatelet)
- similar effects to Aspirin

46
Q

what are the therapeutic uses of CLOPIDOGREL?

A
  • prevents stenosis of coronary stent
  • secondary prevention of MI
  • ischemic stroke
  • vascular events
47
Q

what are the adverse effects of CLOPIDOGREL?

A

usually well tolerated
- bleeding
- abd pain
- dyspepsia (indigestion)
- diarrhea
- rash
- thrombotic thrombocytopenic purpura

48
Q

what are the interactions of CLOPIDOGREL?

A
  • use with caution with patients taking other drugs that PROMOTE bleeding (other anticoagulants + NSAIDs)
  • proton pump inhibitors –> reduce antiplatelet effects of CLOPIDOGREL
49
Q

how do we administer CLOPIDOGREL?

A

oral

50
Q

how do we know CLOPIDOGREL is effective?

A

preventing all the therapeutic uses

51
Q

what is so special about Thrombolytic (Fibrinolytic) drug?

A

its the only type of drug that DISSOLVES clots, thrombi that has already formed

52
Q

what is the exemplar drug of thrombolytic drugs?

A

ALTEPLASE (Activase & Cathflo Activase) – aka ATP
- others: TENECTEPLASE (TNKase) + RETEPLASE (Retavase)

53
Q

what is the mechanism of action of ALTEPLASE?

A

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
Q

what are the therapeutic uses of ALTEPLASE? when should you give this medication?

A

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
Q

what are the adverse affects of ALTEPLASE? what do nurses do before giving this drug?

A

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
Q

what is the medication administration of ALTEPLASE?

A

IV

57
Q

how do we know if ALTEPLASE is effective?

A

preventing the therapeutic uses

58
Q

what are ABSOLUTE contraindications of ALTEPLASE?

A
  • 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
Q

what are relative contraindications/cautions of ALTEPLASE?

A
  • 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

nurs 366: pathopharm ii (30 decks)

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