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67 Cards in this Set
- Front
- Back
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APAP is an
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analgesic and antipyretic agent
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APAP's antipyretic action is by
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acting directly upon the heat regulating center in the hypothalamus: lowers the set point back to normal : dissipation of heat through vasodilation and sweating
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APAP's analgesic mechanism
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unknown
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Does APAP inhibit peripheral prostaglandin synthesis?
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No
but nsaids does |
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Does APAP have antiinflammatory or platelet inhibiting effects
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No
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APAP is used in what kind of pain
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mild to moderate
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max daily dose of APAP
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4 gms
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APAP should not be used in
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Liver Dz
caution in alcoholics and elderly |
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Healthy liver detoxify compound with
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Hepatic glutathione
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T or F APAP is #1 drug seen in overdose cases
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T
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Adverse effects of APAP
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Rare
Hypersensitivity reactions Neutropenia Pancytopenia |
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MOA of NSAIDs
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blocks production of the enzyme cyclooxygenase > inhibit the production of prostaglandins
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What are the two types of cyclooxygenases
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Cox 1 - found in blood vessels, kidneys and stomach - protect gastric mucosa
Cox 2 - found in brain and kidneys - necessary to cause inflammation |
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Action of prostaglandins
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involved in fever and pain and inflammation
Protect gastric mucosa, inhibit gastric acid secretion and cause vasodilation |
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NSAIDs ---------- inactivate cyclooxygenase
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Reversibly
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Aspirin causes ----------- inactivation
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irreversible
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Is there continuous platelet inhibition with nsaids?
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No
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Can nsaids be used for arterial thrombus prevention
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No
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Ibuprofen taken concurrently with aspirin can interfere with aspirin's antiplatelet activity T or F
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T
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What drug can interfere with aspirin binding to cyclooxygenase
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Ibuprofen
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Timing of Ibuprofen
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Interaction occurs when ibuprofen is taken within 30 mins after immediate release aspirin dosing or when ibuprofen taken eight hours or less prior to aspirin dosing
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Is timing only for ibuprofen
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No, for other nsaids too
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Name Cox 2 specific inhibitors -
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Celecoxib (celebrex)
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Benefits of celebrex
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Reduced incidence of GI events
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Cox 2 avoided in
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Pts with sulfa allergy
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SEs of Cox 2
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Higher incidence of thrombotic events including MI than traditional nsaids
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Adverse events of Cox 2
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GI complaints
Mild - Dyspepsia, nausea Severe - bleeding, ulceration, perforation of stomach or intestines Very low risk in pts <50 and high risk in >70 Reduced renal blood flow - decreased urine output, increased BUN and Cr, fluid retention Use cautiously in HF - fluid retention and peripheral edema |
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Acetic acid derivatives
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Diclofenac (voltaren)
Indomethacin Ketorolac (toradol) |
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Enolic acid derivatives
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Meloxicam
Piroxicam |
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Propionic acid derivatives
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Ibuprofen (Motrin, advil)
Naproxen (naprosyn, aleve) |
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Cox 2 inhibitors
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Celecoxib (celebrex)
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Indomethacin
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Very high adverse risk event, also used in the tx of gout
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Etodolac and nabumetone
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relatively low risk of GI effects
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Sulindac
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lower risk of renal adverse events
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Ketorolac
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used for acute to severe pain only, only nsaids available as injection
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Piroxicam
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high incidence of GI and renal adverse events
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Meloxicam
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very low risk of GI events
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Endogenous opioid peptides include
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enkephalins, endorphins and dynorphins
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Natural opioids are derived from
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seeds of poppy plant
Eg - Morphine, codeine, heroin |
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Synthetic opioid analgesics
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Hydrocodone
Hydromorphone Oxycodone Meperidine Fentanyl Methadone Propoxyphene |
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MoA of opioids
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Stimulation of opioid receptors in brain, spinal cord and GI tract
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Major classes of receptors
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Mu (1 and 2), kappa and delta
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Stimulation of Mu1 receptors cause
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inhibiition of transmission of pain signals from peripheral nerve endings in the brain
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Mu1 receptors primarity located in the
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dorsal horn of spinal cord
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Advese effects of opioids
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1. Sedation- stimulation of kappa receptors
2. Respiratory depression from stimulation of mu2 receptors 3. Constipation - delayed food digestion, decreased peristalsis, and delayed passage of stool 4. cause vasodilation - hypotension and flushing 5. Histamine release from mast cells - itching, flushing |
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MoA of opioids
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Stimulation of opioid receptors in brain, spinal cord and GI tract
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Major classes of receptors
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Mu (1 and 2), kappa and delta
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Stimulation of Mu1 receptors cause
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inhibiition of transmission of pain signals from peripheral nerve endings in the brain
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Mu1 receptors primarity located in the
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dorsal horn of spinal cord
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Advese effects of opioids
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1. Sedation- stimulation of kappa receptors
2. Respiratory depression from stimulation of mu2 receptors 3. Constipation - delayed food digestion, decreased peristalsis, and delayed passage of stool 4. cause vasodilation - hypotension and flushing 5. Histamine release from mast cells - itching, flushing 6. Nausea and vomitting 7. urinary retention, miosis (pupil constriction), euphoria |
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Histamine release seen more with following opioids
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Morphine
Meperidine Antihistamine often given with opioids |
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3 main problems of opioids
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Tolerance
Dependance Addiction |
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Brand name for Meperidine
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Demerol
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The major metabolite of meperidine
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normeperidine
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Normeperidine is -------- cleared
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renally
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Normeperidine build up causes
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irritability and seizures, even with normal renal fn
very dangerous for elderly pts |
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Potency of fentanyl
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very potent and very short acting
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Fentanyl IV form used frequently in
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preoperative sedation and post op analgesia
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Fentanyl is used as a transdermal patch T or F
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T, patch should be flushed down the toilet
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Methadone is primarily used in
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Detoxification, treatment, and maintenance of narcotic addicts
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Methadone used to manage
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severe pain
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Long acting opiate
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36-48 hrs
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Propoxyphene with acetaminophen
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Darvocet
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Mixed opioid agonist- antagonists
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Pentazocine (Talwin), buprenorphine (Buprenex), Tramadol (Ultram)
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Pentazocine rarely used due to
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adverse effect profile
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T or F Tramadol is a controlled substance
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F
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Tramadol can inhibit
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reuptake of serotonin
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