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Pharmacology Test #4 > Non-opioid Analgesics > Flashcards

Non-opioid Analgesics Flashcards

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1
Q

Amine autocoids

A

histamine, serotonin

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2
Q

Lipid derived autocoids

A

prostaglandins, leukotrienes

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3
Q

Peptide hormones

A

bradykinin, angiotensin

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4
Q

Autocoids

A

amine, lipid-derived, peptide hormones and cytokines

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5
Q

NSAIDs

A

Salicylates, arylpropionic acids, arylacetic acids, enolic acids

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6
Q

Salicylates

A

aspirin

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7
Q

Arylpropionic acids

A

Ibuprofen, naproxen

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8
Q

Arylacetic acids

A

Indomethacin, diclofenac, ketorolac, etodolac

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9
Q

Enolic acids

A

Piroxicam (Feldene) and meloxicam (mobic)

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10
Q

p-Aminophenols

A

acetaminophen

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11
Q

Therapeutic applications of NSAIDs

A

analgesic, antipyretic, anti-inflammatory

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12
Q

Three phases of inflammation

A

Acute (vasodilation, increased permeability)
Subacute (infiltration)
Chronic (proliferation)

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13
Q

Mediators that recruit inflammatory cells

A

Arachidonic acid metabolites, prostaglandins, thromboxanes, leukotrienes, and cytokines

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14
Q

What kind of inhibitors are NSAIDs?

A

COX inhibitors

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15
Q

Inhibition of COX-1 leads to

A

a reduction in thromboxanes, causing reduced platelet aggregation - thus NSAIDs also function as a blood thinner

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16
Q

COX1 enzymes, prostaglandins and prostacyclins serve what kind of role in the GI tract?

A

a protective role

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17
Q

COX-1 constitutively expressed in

A

platelets, stomach and kidney

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18
Q

PGE2 and PGI2 are protective in

A

stomach; inhibit acid secretion, promote mucus secretion

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19
Q

Inhibition of PGE2 and PGI2 can lead to

A

stomach ulcers

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20
Q

What do prostacyclins do?

A

vasodilation and reduce platelet aggregation

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21
Q

What do thromboxins do?

A

synthesis induces platelet aggregation, vasoconstriction, and inhibitor functions as a blood thinner

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22
Q

COX-2 constitutively expressed in

A

brain and spinal cord

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23
Q

When is COX-2 induced?

A

induced in the setting of inflammation and induced by cytokines and inflammatory mediators

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24
Q

MOA of aspirin

A

irreversibly inhibits COX1/2 by acetylation; modifies COX2 activity; duration of effect corresponds to time required for new protein synthesis

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25
Q

MOA of other NSAIDs (besides aspirin)

A

competitive (reversible) inhibitors of COX 1/2; some arylacetic acids also inhibit leukotriene synthesis, contributing to anti-inflammatory effects

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26
Q

Absorption of salicylates

A

rapidly absorbed from stomach and jejunum
aspirin mainly absorbed in jejunum
passive diffusion of free acid
delayed by presence of food

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27
Q

Distribution of salicylates

A

throughout most tissues and fluids, readily crosses placenta, competes with many drugs for protein binding sites

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28
Q

Metabolism and excretion of salicylates

A

Active secretion and passive reabsorption in renal tubule, increased excretion with increased urinary pH

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29
Q

Absorption of non-salicylate NSAIDs

A

well absorbed from GI tract

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30
Q

Metabolism of non-salicylate NSAIDs

A

Little first pass metabolism; multiple routes of metabolism; therapeutic effect poorly related to plasma levels

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31
Q

Excretion of non-salicylate NSAIDs

A

drugs and metabolites excreted primarily as conjugates; active secretion of parent drug in renal tubule

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32
Q

Aspirin’s main use is for

A

anti-coagulation

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33
Q

MOA of ibuprofen and naproxen

A

potent reversible COX inhibitors

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34
Q

Safest to use in CAD

A

Naproxen

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35
Q

Excellent alternative to ibuprofen and naproxen

A

acetic acid derivatives

36
Q

Acetic acid derivatives have an increased risk of what with prolonged use

A

increased risk of peptic ulcer and renal dysfunction with prolonged use

37
Q

Indomethacin (Indocin)

A

One of the most potent reversible inhibitors of PG biosynthesis; high incidence and severity of side effects long-term

38
Q

Indomethacin used for

A

acute gouty arthritis, ankylosing spondylitis and pericarditis

39
Q

Enolic acids used to treat

A

arthritis; great joint penetration; one of the least GI side effects

40
Q

At low doses, meloxicam is

A

COX-2 selective

41
Q

Acetaminophen is highly effective as an

A

analgesic and antipyretic; weak inflammatory activity

42
Q

Advantages to acetaminophen compared with NSAIDs

A

no GI toxicity; no effect on platelet aggregation; no correlation with Reye’s syndrome;

43
Q

Disadvantages to acetaminophen compared with NSAIDs

A

little clinically useful anti-inflammatory activity; acute overdose may lead to fatal hepatic necrosis

44
Q

Adverse affects of salicylates

A

gastrointestinal distress; treat with misoprostol

45
Q

Overdose of salicylates

A

manifests as metabolic derangement, more specifically metabolic acidosis and respiratory alkalosis; order ABG/BMP

46
Q

Mild effects of salicylism/aspirin poisoning

A

vertigo, tinnitus, and hearing impairment

47
Q

CNS effects of salicylism/aspirin poisoning

A

nausea, vomiting, sweating fever, stimulation followed by depression, delirium, psychosis, stupor coma

48
Q

Treatment of salicylism/aspirin poisoning

A

reduce salicylate load; charcoal, correct metabolic imbalance

49
Q

Adverse effects of non-salicylate NSAIDs

A

GI intolerance/ulceration; renal function; transient inhibition of platelet aggregation; inhibition of uterine motility

50
Q

At high doses or in the presence of alcohol, acetaminophen is metabolized into

A

NAPQI which is a toxic metabolite

51
Q

NAPQI can be conjugated with

A

glutathione, depletion of which will further increase NAPQI levels

52
Q

Adverse effects of acetaminophen

A

renal toxicity, papillary necrosis; dose-dependent potentially fatal hepatic necrosis

53
Q

Non-selective COX1/2 inhibitors

A

aspirin, acetaminophen, non-salycilate NSAIDs

54
Q

Selective COX2 inhibitors

A

Rofecoxib (Vioxx)

55
Q

Why was Vioxx withdrawn

A

due to high chance of blood clots, strokes and heart attacks

56
Q

NSAIDs should be avoided in

A

chronic kidney disease, peptic ulcer disease, history of GI blood

57
Q

All NSAIDs when used in high doses can interfere with

A

bone healing

58
Q

All NSAIDs carry what kind of risk

A

cardiovascular risk in patients with coronary heart disease in the short term, but this risk is highest in diclofenac and lowest in naproxen

59
Q

Antiproliferative agents

A

methotrexate, cyclophosphamide, azathioprine
suppress B and T cell proliferation and function
leflunomide
inhibits T cell proliferation and B cell autoantibody production

60
Q

IL-1 blocking agents

A

Anakinra (Kineret)

recombinant human IL-1 receptor antagonist

61
Q

TNF-alpha blocking agents

A

Etanercept (Enbrel), infliximab (Remicade), adalimumab (Humira)

62
Q

TNF-alpha agents used to treat

A

rheumatoid arthritis, Crohn’s, ulcerative colotis

63
Q

All DMARDs can cause

A

fatal toxicities

64
Q

Anti-gout drugs for acute gout

A

Colchicine and NSAIDs

65
Q

MOA of colchicine

A

binds to tubulin, interferes with mitotic spindle function, causes depolymerization of microtubule

66
Q

Anti-gout drugs for chronic gout

A

Allopurinol, Febuxostat, Probenecid

67
Q

Allopurinol

A

inhibitor of xanthine oxidase

68
Q

Febuxostat

A

new non-purine inhibitor of xanthine oxidase; more effective at reducing serum uric acid and tophus area than allopurinol

69
Q

Probenecid

A

competes for renal tubular anion transporter; blocks active reabsorption of urate in proximal tubules; increases uric acid excretion

70
Q

Ion channels that play an important role in the initiation and propagation of pain signals from the periphery

A

TRP, Nav and Cav channels - they can be targeted to provide analgesia

71
Q

Blocking sodium channels prevents

A

hypopolarization/depolarization and thus blocks action potentials

72
Q

Gain of function mutations of the sodium Nav1.7 channel causes

A

patients severe pain

73
Q

Loss of function mutations of the sodium Nav1.7 channel causes

A

loss of pain sensation

74
Q

Topical anesthetics

A

lidocaine, benzocaine, and oxybuprocaine (ophthalmology)

75
Q

Sodium channel blockers

A

Lamotrigine (Lamictal), Amitryptilline (Elavil), and Carbamezipine (Tegretol)

76
Q

Lamotrigine (Lamictal)

A

off label peripheral neuropathy, migraine

Stevens Johnson syndrome

77
Q

Amitryptiline (Elavil)

A

post-herpetic neuralgia, polyneuropathy, fibromyalgia, visceral pain

78
Q

Carbamezipine (Tegretol)

A

trigeminal neuralgia, bipolar disorder, seizures

teratogenic

79
Q

Nortryptilic

A

metabolite of amitryptiline

80
Q

Oxcarbazepine

A

fewer side effects than carbamezipine, excreted in breast milk

81
Q

Sodium channel blockers with SNRI’s functionality

A

Duloxetine (Cymbalta), Venlafaxine (Effexor)

82
Q

Duloxetine (Cymbalta)

A

SNRI; diabetic pain, fibromyalgia, and peripheral neuropathy

83
Q

Venlafaxine (Effexor)

A

off label diabetic neuropathic pain; SNRI;non-selective opiod effects

84
Q

SNRIs lacking sodium channel functionality

A

Milnacipran (SNRI, fibromyalgia); Tapentadol (NRI and MOR agonist, diabetic neuropathic pain)

85
Q

SSRIs for pain associated depression

A

fluoxetine, paroxetine, setraline, escitalopram, citalopram

86
Q

Major function of calcium channel blockers

A

heart rate, blood pressure

87
Q

Calcium channel blockers

A

gabapentin, pregabalin, ziconotide, levetiracetam

Pharmacology Test #4 (9 decks)

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