Term
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Definition
Weak or partial agonists should not be used in conjunction with full agonists
Pregnancy
Impaired pulmonary function
Hepatic or renal function |
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Term
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Definition
Three main Symptoms
Respiratory Depression
Pinpoint pupils (miosis)
Can see dilation when patient becomes hypoxic
Coma |
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Term
| morphine, oxycodone, hydrocodone, codeine, hydromorphone |
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Definition
MOA - agonists at Mu opioid receptors (have some Kappa binding as well)
AE - codeine- N/V, constipation
morphine- itching |
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Term
| hydromorphone to morphine |
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Definition
| 1 mg hydromorphone = 7 mg morphine |
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Term
| fentanyl, meperidine (Demerol®) |
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Definition
MOA - agonists at Mu opioid receptors (have some Kappa binding as well)
AE - meperidine- toxic metabolite “normeperidine” that can accumulate; (especially in renal impairment) |
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Term
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Definition
Most potent Mu agonist. High lipophilicity (fat solubility)
IV form has Rapid Onset, short duration
100 times more potent than morphine
100 mcg fentanyl IV~ 10 mg morphine IV |
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Term
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Definition
Slow Onset- Used for CHRONIC pain, not acute
Take ~ 12 hours to start working
Commonly seen in cancer patients
NOT for opioid naïve patients
Caution in Geriatric patients, patches >25 mcg have a warning
Patches should only be increased in dose after every 3 days if not sufficient |
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Term
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Definition
Contraindicated:
in patients who are not opioid-tolerant
in the management of acute pain or in patients who require opioid analgesia for a short period of time
in the management of post-operative pain, including use after out-patient or day surgeries, (e.g., tonsillectomies)
in the management of mild pain
in the management of intermittent pain (e.g., use on an as needed basis [prn])
in situations of significant respiratory depression, especially in unmonitored settings where there is a lack of resuscitative equipment
in patients who have acute or severe bronchial asthma |
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Term
| opioid naive vs. opioid tolerant |
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Definition
| Patients who are considered opioid-tolerant are those who have been taking, for a week or longer, at least 60 mg of oral morphine daily, or at least 30 mg of oral oxycodone daily, or at least 8 mg of oral hydromorphone daily, or an equianalgesic dose of another opioid |
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Term
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Definition
Used to be popular, now mostly restricted to procedural use.
Toxic metabolite, “Normeperidine”, maximum use is 3 days! This metabolite can cause seizures and CNS stimulation
Not recommended in geriatric patients or renally impaired
Contraindicated with MAO-Is |
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Term
| methadone, propoxyphene was pulled off the market |
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Definition
MOA - agonists at Mu opioid receptors (have some Kappa binding as well), has NMDA antagonist properties
AE - QT prolongation |
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Term
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Definition
Mu agonst, NMDA antagonist. Has QT prolongation risk
Invented by the Germans in WWII
Seen used a lot for patients with addiction or for chronic pain
Controversial?- Russia banned the drug for addiction
Long-half life, once daily dosing
Propoxyphene: Pulled off the market |
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Term
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Definition
MOA - Weak Mu opioid agonist, also inhibits reuptake of serotonin and norepinephrine
AE - serotonin syndrome; Seizures (even at normal doses) |
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Term
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Definition
Weak Mu opioid agonist, also increases serotonin and norepinephrine levels
Can lower seizure threshold, caution in renal impairment
Watch for Serotonin Syndrome if given with other serotonin drugs (SSRI’s, etc.) |
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Term
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Definition
Nausea- approximately 25% of patients
Constipation- Most common AE in chronic therapy
Sedation/ decreased cognition- 20-60%
Respiratory Depression- The most serious AE
Pruritis- 10%
Others: Urinary retention |
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Term
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Definition
“All Mush No Push”
Opioids lock up GI Motility- Peristalsis
Will a stool softener work?
Will a stimulant work?
Prophylaxis- use before the patient gets constipated!!!!! |
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Term
| loperamide (Imodium®), diphenoxylate- atropine (Lomotil®) |
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Definition
opioids used to cause constipation
MOA - through opioid receptor binding, inhibits excessive GI motility and GI propulsion (peristalsis)
AE - "atropinism" like effects with Lomotil; Loperamide- Dysrhythmias |
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Term
| buprenorphine, nalbuphine |
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Definition
mixed agonists/antagonists (partial agonists)
Buprenorphine- partial Mu agonist, Kappa antagonist
Nalbuphine- Mu antagonist, Kappa agonist |
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Term
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Definition
kappa agonist
Ceiling dose for pain relief and respiratory depression
Antagonist at Mu, watch out if on chronic opioids
No Mu agonism, so little to no euphoria
-Kappa agonists can actually cause the opposite |
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Term
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Definition
partial Mu agonist
Caution in patients on chronic opioids
Binds very strongly to receptors- need high doses of naloxone in event of overdose |
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Term
| naloxone, methylnatrexone |
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Definition
opioid antagonists
MOA - high affinity for Mu receptor, competitive antagonist at Mu receptor (all 3 receptors)
AE - Reverses respiratory depression and analgesia (rebound pain!)
Pharmaco - Methylnaltrexone only works on peripheral receptors; Naloxone has short half life |
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Term
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Definition
Used to treat an acute opioid overdose
Reverses the analgesia and respiratory depression
short half life
Competitively binds to opioid receptors
competitive antagonist |
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Term
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Definition
Used to treat opioid induced constipation
Specific only to GI tract |
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Term
| opioids and renal/haptic impairment |
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Definition
Renal Impairment
Morphine and Meperidine have active metabolites that can build up.
Tramadol build up- seizures
Hepatic Impairment
-All opioids to some extent are hepatically eliminated, caution is to be used |
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Term
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Definition
Hear a lot of patients say they are allergic
Throat swelling, difficulty breathing, hives
rash, increased HR, low BP
Upset stomach, itching, flushing, hallucinations
IgE mediated (Type I) |
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Term
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Definition
You will see anticonvulsants, antidepressants and lots more used for adjuvant therapies for pain
Think of what's going on!
Lidocaine patches-
Antidepressants- venlafaxine/duloxetine |
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Term
| Acetylsalicylic acid (ASA, aspirin) |
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Definition
MOA - Prevents synthesis and release of prostaglandins by interrupting the cyclooxygenase pathway (COX I and COX II)
ASA-irreversible
Indications - Rheumatoid Arthritis, osteoarthritis; Joint pain, swelling, inflammation (arthritis, tendinitis, bursitis, etc.); Fever; Mild – moderate pain; Primary/Secondary reduction for MI, TIA, stroke,; revascularization procedures; colorectal cancer
AE - BLEEDING ; Gastric distress, heartburn, nausea; Gastric bleeding / ulceration; Reye’s syndrome – associated with aspirin use in children |
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Term
| ibuprofen (Advil, Motrin), ketorolac (Toradol), indomethacin (Indocin) |
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Definition
MOA - Prevents synthesis and release of prostaglandins by interrupting the cyclooxygenase pathway (COX I and COX II)
NSAIDS- reversible
Indications - Joint pain, swelling, inflammation (arthritis, tendinitis, bursitis, etc.); Fever; Mild – moderate pain; Dysmenorrhea; Closing ductus arteriosus in pre-term infants (not aspirin)- indomethacin
AE - GI effects, BLEEDING, ULCERS; Ketorolac- max of 5 days usage!; THROMBOTIC EVENTS (MI,stroke); 71% indomethachin (200-300% smoking); renal impairment; Increased blood pressure; Not to be used in heart failure |
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Term
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Definition
How does ASA have cardio protective properties, while NSAIDS do not?
COX 1 inhibition- irreversible
Prevents synthesis of TXA2
Platelet half life is 7 days |
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Term
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Definition
Cox 2 inhibitor
MOA - Selective blockade of cyclooxygenase 2 enzyme; Reduces inflammatory prostaglandins while sparing those that protect the stomach; NSAIDS- reversible
AE - Boxed warnings: Cardiac Risk!; GI toxicity!
Pharmaco: Per Canadian labeling, doses >200 mg/day associated with cardiovascular events |
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Term
| acetaminophen (APAP, paracetamol, Tylenol® ) |
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Definition
MOA - Weak prostaglandin synthesis inhibition in the CENTRAL NERVOUS SYSTEM ONLY!; Also works on the heat regulating center of the brain (the hypothalamus)
AE - Extremely rare at therapeutic dosages; No gastric ulceration, renal impairment, bleeding
Liver toxicity / damage; High doses result in large levels of toxic metabolite and rapidly deplete glutathione
4000 mg/day LIMIT IN ADULTS!!! |
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Term
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Definition
NSAIDS- better tolerated than colchicine
-Indomethacin, naproxen, diclofenac
-No data showing any superiority of one vs the other
IV Glucocorticoids for acute attack
OR…. Colchicine, allopurinol, probenecid |
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Term
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Definition
MOA - Inhibits xanthine oxidase, thus decreasing uric acid production from DNA breakdown
Pharmaco/uses: Meant for chronic gout; Cancer therapy induced hyperuricemia |
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Term
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Definition
Anti-gout
MOA - Anti-inflammatory only for gout; Not fully understood. May decrease leukocyte infiltration/migration to joints where uric acid concentrations are high. Believed to disrupt microtubules
Pharmaco: Typically for acute
AE - narrow therapeutic index; GI symptoms- N/V/D; Myelosuppression; Fatalities in accumulation- multi-organ dysfunction and death |
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Term
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Definition
| MOA - Inhibits organic anion transporter in renal tubules, preventing uric acid reabsorption |
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