Acute Pain Tx

Question 1

Acute Pain Goals of Tx

Answer 1

Primary goal depends on type of pain present and should be tailored to individual patient and circumstance

Acute pain: achieve level of pain relief that allows patient to attain certain functional goals (usually = get back to normal function) → cure

Realistic pain reduction = may be possible to fully eliminate pain, unlike in chronic pain
Prevent or minimize ADEs
Improve quality of life

Question 2

Non Pharm Tx

Answer 2

Question 3

ACet MOA

Answer 3

Believed to inhibit prostaglandins in the CNS and work peripherally to block pain impulse generations

Minimal effect on peripheral prostaglandin synthesis (no anti-inflammatory activity)

Question 4

Acet Place in Tx

Answer 4

Reduction of fever (1st line)
Mild-moderate acute pain
Pediatric moderate pain
Dementia (more aggressive, self it changes anything for them)

Question 5

ADE Acet

Answer 5

Liver toxicity
Overdose
May increase systolic BP (~3-4mmHg)
Rare neutropenia andthrombocytopenia

Question 6

C.I. Acet

Answer 6

Acetaminophen-induced liver disease
Hypersensitivity to acetaminophen, or any component of the formulation

Question 7

Cautions Acet

Answer 7

Acetaminophen is one of the most frequent causes of accidental poisoning in infants and toddlers

Hepatotoxicity has occurred in patients receiving high or excessive doses with therapeutic intent

Some patients may be more susceptible to acetaminophen hepatotoxicity (e.g., chronic alcohol use, those with liver disease, or those who are malnourished or taking other hepatotoxic drugs)

Question 8

Acet Dosing (IR reg strength, IR xtra, extended release), CHildren

Answer 8

Question 9

NSAIDS MOA

Answer 9

Non-Selective:
Inhibit cyclooxygenase-1 and 2 (COX-1 and 2) enzymes, which results in ↓ formation of prostaglandin precursors
Antipyretic, analgesic, and anti-inflammatory properties

COX-2 Inhibitors (Coxibs):
Inhibit prostaglandin synthesis by ↓ the activity of the enzyme, COX-2, which results in ↓ formation of prostaglandin precursors
Antipyretic, analgesic, and anti-inflammatory properties.
Do not inhibit COX-1 at therapeutic concentrations

Question 10

NSAIDs Place in Therapy

Answer 10

Mild to moderate pain (osteoarthritis, acute & chronic low back pain)
Dysmenorrhea-induced pain
Fever (only ibuprofen and naproxen)

Question 11

NSAIDS C.I.

Answer 11

CKD (CrCl < 40mL/min)
Hyperkalemia
Cirrhosis/ Liver impairment
GI Ulcer (duodenal/ peptic) + IBD
Uncontrolled Heart Failure
MI
Thrombocytopenia
Transplant

Question 12

ADE NSAIDS.Cox 2 efficay?

Answer 12

Dyspepsia
Edema
GI Bleed
N/V
Phototoxic Reaction
CNS : Dizziness, drowsiness, headache, tinnitus, confusion (especially in the elderly & with indomethacin). CNS effects may be dose related.
Minor or serious skin rashes, pruritus
COX-2 selective – similar efficacy & renal/CV toxicity to other NSAIDS, but less GI risk

Question 13

NSAIDs Caution

Answer 13

Asthma
CVD, HTN
Risk of bleeding increases perioperatively; discontinue pre-surg

Question 14

ASA MOA

Answer 14

Irreversibly inhibits COX-1 and COX-2 enzymes via acetylation which decreases formation of prostaglandin precursors
Antipyretic, analgesic, and anti-inflammatory properties (see dosing)

Question 15

ASA Place in Tx

Answer 15

Place in Therapy
Mild-moderate pain (short term use)
Reduction of fever

Question 16

Dosing ASA

Answer 16

< 300mg/d: reduce platelet aggregation
300-2400mg/d: antipyretic and analgesic (325-650mg po q4h prn)
2400-4000mg/d: anti-inflammatory
Max: 4g/day

Question 17

C.I. ASA

Answer 17

Hypersensitivity to NSAIDs, anaphylaxis
CKD (CrCl < 40mL/min)
GI Ulcer

Question 18

ADR ASA

Answer 18

Same as NSAIDS

Question 19

Cautoions ASA

Answer 19

Concurrent antiplatelet and/or anticoagulant therapy
Risk of Reye syndrome in children
Toxic in overdose (tinnitus, vertigo, hyperventilation, respiratory alkalosis, hyperthermia, coma, death)

Question 20

Pathway NSAID’s and Protection

Answer 20

Question 21

NSAID’s Dosing

Answer 21