Non-Narcotic Analgesics

Question 1

Role of prostaglandins in pain

Answer 1

• noxious stimuli causes release of prostaglandins
• PG increase sensitivity of nociceptors
• Transmission of ascending pain signal

Question 2

NSAIDs mechanism

Answer 2

• all work by inhibits cyclooxygenase (COX) enzymes

Question 3

Good effects of COX inhibitors

Answer 3

Antipyretic
Analgesic
Anti-inflammatory

Question 4

Bad effects of COX inhibitors

Answer 4

Decrease in GI mucous which may lead to GI ulceration

Question 5

Antipyretic use

Answer 5

Fever occurs due to actions of bacteria/viruses in the hypothalamus

• stimulante increase in COX-2, resulting in more PGE2
• PGE2 s a potent pyrogen, increase the set point in hypothalamus
• fever has a role in fighting infection

Question 6

Anti-inflammatory/analgesia use

Answer 6

• PGs cause vasodilation, increases blood to injured tissue which leads to enhancement of leukocyte infiltration
• mediated by PGE2 and PGI2

Question 7

NSAID Pharmacokinetics

Answer 7

• most well absorbed orally
• most undergo hepatic metabolism, renal excretion
• elimination half-lives vary widely between drugs (ibuprofen half live = 2 hours)

Question 8

NSAIDs AE’s

Answer 8

• Renal dysfunction
• Edema
• Gastrointestinal

Question 9

NSAID Renal Dysfunction

Answer 9

• Prostaglandins dilate blood vessels in the kidney
• using NSAIDs reduces PGs which causes constriction of the afferent arteriole, which reduces blood flow to the glomerulus, reducing GFR

Question 10

NSAIDs have high risk in patients with

Answer 10

• using vasoconstrictors
• low blood volume
• poor renal function
• elderly

Question 11

NSAIDs and Edema

Answer 11

• Increases Na+/fluid reabsorption

- Problem in patients with: Hypertension, heart failure

Question 12

NSAIDs and Gastrointestinal AE

Answer 12

• range from dyspepsia to serious ulcer

- Causes: decrease in protective mucous, direct, irritant effect

Question 13

How to reduce gastrointestinal side effects

Answer 13

• take with food
• take with misoprostol
• take with a proton pump inhibitor
• Use a COX-2 selective inhibitor

Question 14

Selective COX-2 Inhibitor

Answer 14

Rofecoxib only binds to COX-2 receptors

Problems arose with cardiovascular events and skin reactions

Question 15

Aspirin

Answer 15

• effective analgesic/anti-inflammatory
• hard on the stomach
• Acetylsalicylic Acid

Question 16

Effects of ASA

Answer 16

• Antiplatelet effects occur at low doses (80mg)
• ASA acetylation COX-1 in platelets, irreversibly inhibiting its actions
• used less as an antipyretic
• Contraindicated in children, particularly for treatment of fever
  Reye’s syndrome, ASA increases risk

Question 17

Analgesic/anti-inflammatory effects of ASA

Answer 17

Higher doses:

• Analgesia: 600-900mg
• Anti-inflammatory: 3000-6000mg

Question 18

ASA toxicity (early signs)

Answer 18

• Tinnitis
• Nausea, vomiting
• Hyperventilation
• Lethargy

Question 19

ASA overdose

Answer 19

• restless
• hallucinations
• seizures
• coma
• respiratory and metabolic acidosis
• respiratory failure

Question 20

ASA overdose management

Answer 20

Alkalinize urine to enhance solubility

Question 21

ASA and Asthma mechanism

Answer 21

Possibly due to activation of the lipoxygenase pathway

Can also occur with other NSAIDs

Question 22

Acetaminophen

Answer 22

• shares many features of NSAID, inhibits COX enzyme but lacks anti-inflammatory effects, and lacks many key AE’s of NSAIDs

Question 23

Acetaminophen uses

Answer 23

Analgesic and antipyretic

Question 24

Acetaminophen side effects

Answer 24

• generally well tolerated
• compared to NSAIDs, lower risk of GI adverse effects, cardiovascular/renal adverse effects
• high doses damages liver