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Heme/Lymph Exam > Anticoagulants & Analgesics > Flashcards

Anticoagulants & Analgesics Flashcards

1
Q

venous thromboembolism (VTE) - hereditary risk factors

A

*factor V Leiden mutation
*Protein C or S deficiency
*hyperhomocysteinemia
*prothrombin gene mutation
*decreased factor VIII levels
*dysfibroginemia
*antithrombin deficiency

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2
Q

venous thromboembolism (VTE) - acquired risk factors

A

*surgery
*trauma
*medical illness
*immobolization
*pregnancy
*contraception/HRT
*indwelling catheters
*malignancy
*air travel

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3
Q

venous thromboembolism (VTE) in malignancy

A

*key risk factor: HYPERCOAGULABILITY
-mucin production by adenocarcinomas
-tissue factor production

*risk is higher in certain tumor types: pancreatic cancer, lung cancer, breast cancer, CNS malignancies

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4
Q

4 classes of anticoagulants

A
  1. heparins
  2. vitamin K antagonists
  3. direct thrombin inhibitors
  4. factor Xa inhibitors
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5
Q

anticoagulant class: heparins - MOA

A

*activates antithrombin, which decreases action primarily of factors IIa (thrombin) and Xa
*has its predominant impact on the intrinsic (PTT) pathway of the coagulation cascade

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6
Q

indications for heparin

A

*immediate anticoagulation for:
-VTE prophylaxis/treatment [pulmonary embolism, DVT]
-acute coronary syndrome
-MI
-percutaneous coronary intervention

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7
Q

heparins - ADEs

A

*heparin-induced thrombocytopenia (HIT)
*bleeding

note - monitor PTT of pts on heparin

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8
Q

what lab test should you monitor in patients on heparin

A

PTT

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9
Q

heparin-induced thrombocytopenia (HIT) - pathophysiology

A

*complication of therapy with heparins
*development of IgG antibodies against heparin-bound platelete factor 4:
-antibody-heparin-PF4 complex binds and activates platelets, leading to removal by splenic macrophages and therefore LOW PLATELET COUNTS

*tx - discontinue heparin and start an alternative anticoagulant

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10
Q

heparin-induced thrombocytopenia (HIT) - diagnosis

A

*serotonin release assay = diagnostic gold standard
*4T score: thrombocytopenia, timing of platelet fall coincides with heparin use, thrombosis, oTher causes (injury, fall, etc)

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11
Q

heparin-induced thrombocytopenia (HIT) - management

A

*stop all heparin products
*initiate therapy with alternative anticoagulant (bivalirudin, argatroban, fondaparinux)
*note - reexposure to heparin should be avoided

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12
Q

low molecular weight heparin - examples

A

*enoxaparin
*dalteparin

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13
Q

low molecular weight heparin - MOA

A

*activate antithrombin → act mainly on decreasing factor Xa

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14
Q

enoxaparin

A

*example of a low molecular weight heparin
*indications:
-VTE prophylaxis/treatment
-acute coronary syndrome
*ADEs: heparin-induced thrombocytopenia, bleeding

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15
Q

dalteparin

A

*example of low molecular weight heparin
*indications:
-VTE prophylaxis/treatment
-myocardial infarction
*ADEs: heparin-induced thrombocytopenia, bleeding

note - not as commonly used in the US

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16
Q

what is the reversal agent for heparin

A

PROTAMINE SULFATE

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17
Q

protamine sulfate

A

*reversal agent of heparin

*MOA: positively charged peptide that binds negatively charged heparin

*indications: unfractionated and low molecular weight heparin overdosage/associated hemorrhage

*ADEs:
-hypersensitivity
-pulmonary hypertension
-dyspnea

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18
Q

vitamin K antagonists (warfarin) - MOA

A

*inhibits vitamin K epoxide reductase
*inhibits vitamin K-dependent clotting factors: factors II, VII, IX, and X
*also inhibits proteins C and S (which are anticoagulants)
*has its predominant impact on the extrinsic pathway of the coagulation cascade

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19
Q

warfarin - MOA

A

vitamin K antagonist (inhibits vitamin K epoxide reductase → decreased production of factors II, VII, IX, and X and proteins C and S)

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20
Q

warfarin - indications

A

*VTE treatment
*chronic anticoagulation

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21
Q

warfarin - onset of action

A

*vitamin K inhibition: takes about 5 days
*HYPERcoagulability for 0-48 hours after 1st dose; therefore, you have to “bridge them”

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22
Q

what lab test should you monitor in patients on warfarin

A

PT/INR

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23
Q

INR monitoring for patients on warfarin

A

*goal of therapy = INR
*INR monitoring:
-weekly during initiation/major dose adjustment
-monthly during maintenance

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24
Q

warfarin drug-drug interactions

A

*CYP2C9 inhibitors/inducers (fluconazole, amiodarone, rifampin)
*chemotherapy agents (capecitabine, aprepitant)
*oral contraceptives

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25
Q

warfarin food interactions

A

*green, leafy veggies (kale, turnip greens, iceberg lettuce)
*cereal
*lamb

essentially, you would need to eat these regularly and in consistent amounts; if not, there will be INR fluctuations

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26
Q

warfarin ADEs

A

*teratogenic effects
*skin/tissue necrosis (due to hypercoagulable state)
*vasculitis

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27
Q

reversal of warfarin

A

*Vitamin K (slow reversal)
*Kcentra (rapid reversal):
-4 factor prothrombin complex
-ADEs: headache, N/V, arthralgia, hypotension, stroke, DVT,PE

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28
Q

examples of direct thrombin inhibitors

A

*bivalirudin
*argatroban
*dabigatraban

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29
Q

bivalirudin - MOA

A

*directly inhibits thrombin (factor IIa)

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30
Q

bivalirudin - indications & ADEs

A

*indications: percutaneous coronary intervention; treatment of HIT
*ADEs: back pain, bleeding

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31
Q

argatroban - MOA

A

*directly inhibits thrombin (factor IIa)

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32
Q

argatroban - indications & ADEs

A

*indications: percutaneous coronary intervention, treatment of HIT
*ADEs: hypotension, bleedingg

*note - with co-administration with warfarin, argatroban can cause artificially high INR but it is purely lab artifact

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33
Q

dabigatran - MOA

A

*directly inhibits thrombin (factor IIa)

34
Q

dabigatran - indications & ADEs

A

*indications: primary or secondary VTE prevention
*ADEs: dyspepsia, bleeding, drug interactions

35
Q

dabigatran - reversal

A

*idarucizumab
*monoclonal antibody that binds dabigatran and its metabolites

36
Q

examples of factor Xa inhibitors

A

*apixaban
*edoxaban
*rivaroxaban
*fondaparinux
*betrixaban

note - naming convention: usually have an “x” in them or end with “-xaban”

37
Q

fondaparinux - MOA

A

*directly inhibits factor Xa

38
Q

rivaroxaban - MOA

A

*directly inhibits factor Xa

39
Q

apixaban - MOA

A

*directly inhibits factor Xa

40
Q

edoxaban - MOA

A

*directly inhibits factor Xa

41
Q

betrixaban - MOA

A

*directly inhibits factor Xa

42
Q

fondaparinux - indications & ADEs

A

*indications: VTE prophylaxis/treatment, acute coronary syndrome, treatment of HIT
*ADEs: fever, nausea, bleeding

43
Q

rivaroxaban - indications & ADEs

A

*indications: VTE prevention/treatment
*ADEs: bleeding, increased liver enzymes

44
Q

apixaban - indications & ADEs

A

*indications: prevention/treatment of VTEs
*ADEs: increased liver enzymes, bleeding

45
Q

what is the reversal agent of factor Xa inhibitors

A

andexanet alfa

46
Q

andexanet alfa

A

*factor Xa inhibitor reversal agent
*MOA: recombinant inactive form of factor Xa that acts as a decoy to bind anticoagulant
*ADEs: thromboembolic events, infusion site reaction

47
Q

pain classification: nociceptive pain

A

*musculoskeletal conditions
*inflammation
*direct tissue injury

48
Q

pain classification: neuropathic pain

A

*result of damage to nervous system
*acquired in most cases

49
Q

pathogenesis of acute cancer pain

A
  1. most related to iatrogenic sources (diagnostic tests/procedures or treatment of disease)
  2. can be related to the disease itself:
    -bone pain from pathologic fracture
    -visceral pain from acute obstruction
  3. adverse effects of treatment for cancer:
    -mucositis from chemotherapy or radiation
    -chemo induced neuropathy
50
Q

pathogenesis of chronic cancer pain

A
  1. tumor-related somatic pain:
    -bone pain from bone metastases
    -visceral pain from organ/soft tissue metastases
  2. tumor-related neuropathic pain:
    -leptomeningeal metastases
    -paraneoplastic syndromes (osteoarthropathy)
51
Q

challenges in treatment of cancer pain

A

*route of administration (mechanical and physiologic challenges)
*drug-seeking vs. true pain
*acute variance in pain
*adverse effect management

52
Q

WHO pain management algorithm ladder

A

*mild to moderate pain [scores 1-3]: treat with non-opioid analgesics (NSAIDs, acetaminophen)
*moderate to severe pain [scores 4-6 or 7]: mild opioids (e.g. codeine)
*severe pain [scores 7-10]: strong opioids (e.g. morphine)

53
Q

classes of analgesic agents

A
  1. non-opioid analgesics (acetaminophen, NSAIDs)
  2. opioid analgesics
  3. anticonvulsants
  4. antidepressants
54
Q

acetaminophen - MOA, drug class, indication

A

*MOA: prostaglandin blockade/inhibition
*drug class: non-opioid analgesics
*indication: mild to moderate pain [scores 1-3]

55
Q

acetaminophen - ADEs

A

*hepatotoxicity!
*masks a fever (important in oncology population)

56
Q

NSAIDs - examples

A
  1. salicylates (aspirin)
  2. propionic acids (ibuprofen, naproxen, ketoprofen)
  3. acetic acids (diclofenac, etodolac, sulindac, indomethacin, ketorolac)
  4. oxicams (meloxicam, piroxicam)
57
Q

NSAIDs - MOA, drug class, indications

A

*MOA: COX inhibitors
*drug class: non-opioid analgesics
*indications: mild to moderate pain [scores 1-3]

58
Q

NSAIDs - ADEs

A

*platelet inhibition
*gastrointestinal insult
*renal insult

59
Q

COX-2 inhibitor

A

*celecoxib is the only agent approved
*MOA: selective for COX-2 inhibition
*ADEs: peripheral edema, myocardial infarction, nephrotoxicity

60
Q

tramadol - MOA and drug class

A

*MOA: mu-receptor binding, serotonin/norepinephrine reuptake blockade
*drug class: mild opioid
*indication: moderate to severe pain [score 4-7/7]

61
Q

tramadol - ADEs

A

*nausea
*constipation
*headache

62
Q

opioid analgesics - MOA

A

*work on 3 different receptors: Mu, delta, and kappa (activates the Mu receptor predominantly)
*Mu receptors are concentrated in midbrain and dorsal horn

63
Q

opioid analgesics - class ADEs

A

*sedation (tolerance develops)
*nausea/vomiting (tolerance develops)
*constipation (tolerance does NOT develop; prevention is key)
*euphoria/dysphoria - related to rate of administration

64
Q

opioid-induced constipation

A

*result of Mu-receptor activation in the gut
*prophylaxis is a must (stimulant laxatives + stool softener)

65
Q

extended-release opioids: REMS

A

*all extended-release opioids require enrollment by the prescribed and the pharmacy in the REMS program
*purpose = heighten awareness of risks of inappropriate use
*require medication guide dispensing at each fill of a prescription by pharmacy

66
Q

mild opioids: indications & examples

A

*indication: first-line agents for patients with moderate to severe pain [score: 4-6/7]
*examples:
-codeine
-hydrocodone

67
Q

morphine: drug class & indications

A

*drug class: strong opioid
*indication: severe pain [score: 7-10]

68
Q

oxycodone: drug class & indications

A

*drug class: strong opioid
*indication: severe pain [score: 7-10]

69
Q

hydromorphone: drug class & indications

A

*drug class: strong opioid
*indication: severe pain [score: 7-10]

70
Q

oxymorphone: drug class & indications

A

*drug class: strong opioid
*indication: severe pain [score: 7-10]

71
Q

fentanyl: drug class & indications

A

*drug class: strong opioid
*indication: severe pain [score: 7-10]

72
Q

fentanyl dosage forms available

A

*IV/IM
*transmucosal
*transdermal
*buccal film
*sublingual liquid/spray
*buccal tablet
*oral lozenge
*intranasal solution
*sublingual tablet

73
Q

methadone: MOA & drug class & indications

A

*MOA: Mu activation/NMDA-receptor inhibition
*drug class: strong opioid
*indication: severe pain [score: 7-10], OPIATE DETOXIFICATION
*available forms: oral tablet, oral solution, injection

74
Q

buprenorphine: drug class, indication

A

*drug class: partial opioid agonist
*indication: chronic severe pain
*ADE: QTc prolongation

75
Q

naloxone - MOA, indication

A

*used for opioid REVERSAL
*MOA: competes and displaces opioids at all Mu receptor sites

76
Q

what drug is used for opioid reversal

77
Q

anticonvulsants - MOA, indications, ADEs

A

*MOA: bind to voltage-gated calcium channels and block GABA receptor
*used in treatment of NEUROPATHIC PAIN
*ADEs: dizziness, somnolence

78
Q

gabapentin: drug class, indications, MOA

A

*drug class: anticonvulsant
*indications: used effectively in post-herpetic neuralgias, but also used in new onset neuropathies
*MOA: bind to voltage-gated calcium channels and block GABA receptor

note - SLOW onset of improvement

79
Q

pregabalin: drug class, indications, MOA

A

*drug class: anticonvulsant
*indications: used effectively in post-herpetic neuralgias, but also used in new onset neuropathies
*MOA: bind to voltage-gated calcium channels and block GABA receptor

note - works faster than gabapentin

80
Q

antidepressant pain MOA

A

*serotonin-norepinephrine reuptake inhibitors possess analgesic qualities
*full mechanism not understood, but effects on NEUROPATHIC pain are well established

81
Q

venlafaxine: drug class, indication, ADEs

A

*drug class: antidepressant
*indications: neuropathic pain
*ADEs: cardiac conduction abnormalities, hypertension
*note - SLOW onset of improvement

82
Q

duloxetine: drug class, indication, ADEs

A

*drug class: antidepressant
*indications: neuropathic pain - chronic low back pain, osteoarthritis, diabetic peripheral neuropathy
*ADEs: nausea, dry mouth, insomnia, constipation
*note - SLOW onset of improvement

Heme/Lymph Exam (38 decks)

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