Pharmacology of non-opiate drugs for pain Flashcards by Brianna Lent

What is Aspirin’s chemical structure
A. Arylpropionic acids
B. Arylacetic acids
C. Salicylates
D. Enolic acids

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What is the structure of Ibuprofen and naproxen
A. Arylpropionic acids
B. Arylacetic acids
C. Salicylates
D. Enolic acids

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What is the chemical structure of Indomethacin,diclofenac, ketorolac and etodolac
A. Arylpropionic acids
B. Arylacetic acids
C. Salicylates
D. Enolic acids

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What is the chemical structure of Piroxicam and meloxicam
A. Arylpropionic acids
B. Arylacetic acids
C. Salicylates
D. Enolic acids

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What are the uses of NSAIDS

analgesic, anti-inflammatory, antipyretic, and prophylactic

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T of F: NSAIDs can not be used to reduce risk of Myocardial infarction-antiplatelet effect

False they can be used (aspirin)

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Rubor, tumor, calor, dolor ”

Redness, swelling, heat, pain all signs of inflammation

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what are the three phases of inflammatory response

Acute: Vasodilation => increased permeability
Subacute: Infiltration
Chronic: Proliferation

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List the eicosanoids recruited by inflammatory cells

Eicosanoids: Arachidonic acid metabolites
prostglandins
thromboxanes
leukotrienes
cytokines

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What are prostglandins responsible for
A. Swelling
B. Pain
C. redness, heat, and pain

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What are Leukotrienes responsible for
A. Swelling
B. Pain
C. redness, heat, and pain

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What are cytokines responsible for
A. Swelling
B. Pain
C. redness, heat, and pain

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T or F: NSAIDs are COX inhibitors in the arachadonic acid pathway

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T Or F Aspirin unlike other NSAIDs reversibly inhibits COX enzymes

False It irreversibly inhibits COX

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How does Aspirin irreversibly inhibit COX

Irreversibly inhibits cyclooxygenase1/2 by acetylation of COX (Ser529)
Modifies COX 2 activity -> produce lipoxins
Duration of effect corresponds to time required for new
protein synthesis

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what are some competitive reversible inhibitors of COX 1&2

indomethacin and diclofenac (they may also inhibit leukotrient synthesis contributing to anti-inflammatory effect

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What is Aspirin use prophylactically for

anticoagulation

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Clinical pearls of Aspirin

no tolerance development to analgesic effects
Risk of reyes syndrome in children

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How quickly is Aspirin/salicylates absorbed
A. Slowly absorbed
B. Intermediately absorbed
C. rapidly absorbed

C
passive diffusion of unionized acid at gastric pH delayed by presence of food

Where are Aspirin/salicylates distributed

Throughout most tissues & fluids
Competes with many drugs for protein binding sites

what is salicylate’s half life
A. 2-4 hrs
B. 20-30hrs
C. 6-20hrs
D. 5-10hrs

C.
Dose dependent conjugation

T or F: Increased excretion of aspirin and salicylates with increased urinary pH

what are the mild effects of salicylism/aspirin poisoning
A. vertigo
B.nausea
C. fever
D. tinnitus
E. metabolic acidosis
F. hearing impairment

A, D, F

what are the CNS effects of salicylism/aspirin poisoning
A. vertigo
B.respiratory alkalosis
C. fever
D. tinnitus
E. metabolic acidosis
F. hearing impairment

B respiratory alkalosis is caused by hyperventilation
E metabolic acidosis: lowering of blood pH

Treatment in acute medical emergency in aspirin poisoning

reduce salicylate load, increase urinary excretion (dextrose,sodium bicarb) trap in urine pka of salicylate is 3.0> inonized in urine cant go back treat by correcting metabolic imbalances

T or F: Arylpropionic acids are all potent reversible COX inhibitors

T (ibuprofen and naproxen)

what is the half-life of ibuprofen and naproxen

2hr for ibuprofen and 14 hours for naproxen

Diclofenac

an arylacetic acid derivative Increased risk of peptic ulcer and renal dysfunction with prolonged use Arthrotec (diclofenac/misoprostol) for chronic use. Misoprostol = PGE1 analog

Indomethacin (Indocin)

an arylacetic acid derivative One of most potent reversible inhibitors High incidence & severity of side effects long-term

Sulindac (Clinoril)

an arylacetic acid derivative Less toxic derivative of indomethacin

What are enolic acids used for

Used to treat arthritis Great joint penetration (One of the least GI side effects)

T or F: at low doses meloxicam is Cox-1 selective

False it is COX 2 selective

What is the half life of piroxicam A. 17 hrs B. 30 hrs C 46hrs D 57 hrs

List the adverse effect of NSAIDs

peripheral edema increased risk of bleeding inhibition of uterine motility Gi distress/ulcerations

what is acetaminophen

a highly effective analgesic and antipyretic

T or F: Acetaminophen does not have GI toxicity

T or F Acetaminophen overdose may lead to fatal hepatic necrosis

What are the adverse effects of acetaminophen

renal toxicity papillary necrosis, greater than aspirin, NSAIDS hepatic necrosis increase in toxic acetaminophen metabolites

SIDE EFFECT PROFILE OF SELECTIVE COX INHIBITORS

Reduce ulcers and GI bleeds Withdrawn due to high chance of blood clots strokes and heart attacks

NSAID contraindications

chronic kidney disease, peptic ulcer disease, history of GI bleed cardiovascular risk high doses can interfere with bone healing can also cause asthma exacerbations

Benzocaine

a local anesthesia and sodium channel blocker esters have higher allergy risk

List the anticonvulsants that are sodium channel blockers

Lamotrigine, carbamazepine, and oxcarbazepine

what tricyclic antidepressants that are NA channel blockers

Amitriptyline and nortriptyline

NA channel blockers with SNRI functionality

SNRIs increase norepinephrine levels Can act on alpha2A-adrenergic receptors in spinal cord Provide analgesia duloxetine and venlafaxine

SNRIs lacking Na channel functionality

milnacipran

Calcium Channel blockers as possible analgesics

Gabapentin (Neurontin), Pregabalin (Lyrica)  α2 δ – Cav1, 2 selective  Not metabolized, not protein bound  No drug-drug interactions  T1 / 2 =4-8hr