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Pharmacology Test #4 > Non-opioid Analgesics > Flashcards

Non-opioid Analgesics Flashcards

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
MOA of other NSAIDs (besides aspirin)
competitive (reversible) inhibitors of COX 1/2; some arylacetic acids also inhibit leukotriene synthesis, contributing to anti-inflammatory effects
26
Absorption of salicylates
rapidly absorbed from stomach and jejunum aspirin mainly absorbed in jejunum passive diffusion of free acid delayed by presence of food
27
Distribution of salicylates
throughout most tissues and fluids, readily crosses placenta, competes with many drugs for protein binding sites
28
Metabolism and excretion of salicylates
Active secretion and passive reabsorption in renal tubule, increased excretion with increased urinary pH
29
Absorption of non-salicylate NSAIDs
well absorbed from GI tract
30
Metabolism of non-salicylate NSAIDs
Little first pass metabolism; multiple routes of metabolism; therapeutic effect poorly related to plasma levels
31
Excretion of non-salicylate NSAIDs
drugs and metabolites excreted primarily as conjugates; active secretion of parent drug in renal tubule
32
Aspirin's main use is for
anti-coagulation
33
MOA of ibuprofen and naproxen
potent reversible COX inhibitors
34
Safest to use in CAD
Naproxen
35
Excellent alternative to ibuprofen and naproxen
acetic acid derivatives
36
Acetic acid derivatives have an increased risk of what with prolonged use
increased risk of peptic ulcer and renal dysfunction with prolonged use
37
Indomethacin (Indocin)
One of the most potent reversible inhibitors of PG biosynthesis; high incidence and severity of side effects long-term
38
Indomethacin used for
acute gouty arthritis, ankylosing spondylitis and pericarditis
39
Enolic acids used to treat
arthritis; great joint penetration; one of the least GI side effects
40
At low doses, meloxicam is
COX-2 selective
41
Acetaminophen is highly effective as an
analgesic and antipyretic; weak inflammatory activity
42
Advantages to acetaminophen compared with NSAIDs
no GI toxicity; no effect on platelet aggregation; no correlation with Reye's syndrome;
43
Disadvantages to acetaminophen compared with NSAIDs
little clinically useful anti-inflammatory activity; acute overdose may lead to fatal hepatic necrosis
44
Adverse affects of salicylates
gastrointestinal distress; treat with misoprostol
45
Overdose of salicylates
manifests as metabolic derangement, more specifically metabolic acidosis and respiratory alkalosis; order ABG/BMP
46
Mild effects of salicylism/aspirin poisoning
vertigo, tinnitus, and hearing impairment
47
CNS effects of salicylism/aspirin poisoning
nausea, vomiting, sweating fever, stimulation followed by depression, delirium, psychosis, stupor coma
48
Treatment of salicylism/aspirin poisoning
reduce salicylate load; charcoal, correct metabolic imbalance
49
Adverse effects of non-salicylate NSAIDs
GI intolerance/ulceration; renal function; transient inhibition of platelet aggregation; inhibition of uterine motility
50
At high doses or in the presence of alcohol, acetaminophen is metabolized into
NAPQI which is a toxic metabolite
51
NAPQI can be conjugated with
glutathione, depletion of which will further increase NAPQI levels
52
Adverse effects of acetaminophen
renal toxicity, papillary necrosis; dose-dependent potentially fatal hepatic necrosis
53
Non-selective COX1/2 inhibitors
aspirin, acetaminophen, non-salycilate NSAIDs
54
Selective COX2 inhibitors
Rofecoxib (Vioxx)
55
Why was Vioxx withdrawn
due to high chance of blood clots, strokes and heart attacks
56
NSAIDs should be avoided in
chronic kidney disease, peptic ulcer disease, history of GI blood
57
All NSAIDs when used in high doses can interfere with
bone healing
58
All NSAIDs carry what kind of risk
cardiovascular risk in patients with coronary heart disease in the short term, but this risk is highest in diclofenac and lowest in naproxen
59
Antiproliferative agents
methotrexate, cyclophosphamide, azathioprine suppress B and T cell proliferation and function leflunomide inhibits T cell proliferation and B cell autoantibody production
60
IL-1 blocking agents
Anakinra (Kineret) | recombinant human IL-1 receptor antagonist
61
TNF-alpha blocking agents
Etanercept (Enbrel), infliximab (Remicade), adalimumab (Humira)
62
TNF-alpha agents used to treat
rheumatoid arthritis, Crohn's, ulcerative colotis
63
All DMARDs can cause
fatal toxicities
64
Anti-gout drugs for acute gout
Colchicine and NSAIDs
65
MOA of colchicine
binds to tubulin, interferes with mitotic spindle function, causes depolymerization of microtubule
66
Anti-gout drugs for chronic gout
Allopurinol, Febuxostat, Probenecid
67
Allopurinol
inhibitor of xanthine oxidase
68
Febuxostat
new non-purine inhibitor of xanthine oxidase; more effective at reducing serum uric acid and tophus area than allopurinol
69
Probenecid
competes for renal tubular anion transporter; blocks active reabsorption of urate in proximal tubules; increases uric acid excretion
70
Ion channels that play an important role in the initiation and propagation of pain signals from the periphery
TRP, Nav and Cav channels - they can be targeted to provide analgesia
71
Blocking sodium channels prevents
hypopolarization/depolarization and thus blocks action potentials
72
Gain of function mutations of the sodium Nav1.7 channel causes
patients severe pain
73
Loss of function mutations of the sodium Nav1.7 channel causes
loss of pain sensation
74
Topical anesthetics
lidocaine, benzocaine, and oxybuprocaine (ophthalmology)
75
Sodium channel blockers
Lamotrigine (Lamictal), Amitryptilline (Elavil), and Carbamezipine (Tegretol)
76
Lamotrigine (Lamictal)
off label peripheral neuropathy, migraine | Stevens Johnson syndrome
77
Amitryptiline (Elavil)
post-herpetic neuralgia, polyneuropathy, fibromyalgia, visceral pain
78
Carbamezipine (Tegretol)
trigeminal neuralgia, bipolar disorder, seizures | teratogenic
79
Nortryptilic
metabolite of amitryptiline
80
Oxcarbazepine
fewer side effects than carbamezipine, excreted in breast milk
81
Sodium channel blockers with SNRI's functionality
Duloxetine (Cymbalta), Venlafaxine (Effexor)
82
Duloxetine (Cymbalta)
SNRI; diabetic pain, fibromyalgia, and peripheral neuropathy
83
Venlafaxine (Effexor)
off label diabetic neuropathic pain; SNRI;non-selective opiod effects
84
SNRIs lacking sodium channel functionality
Milnacipran (SNRI, fibromyalgia); Tapentadol (NRI and MOR agonist, diabetic neuropathic pain)
85
SSRIs for pain associated depression
fluoxetine, paroxetine, setraline, escitalopram, citalopram
86
Major function of calcium channel blockers
heart rate, blood pressure
87
Calcium channel blockers
gabapentin, pregabalin, ziconotide, levetiracetam

Pharmacology Test #4 (9 decks)

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