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pharmacology 10
| Term | Definition |
|---|---|
| Nociceptive origin | pain that arises from activation of nociceptors (pain receptors) in response to tissue injury or inflammation. Inflammation Arthritis Low back pain Headache Burns Trauma |
| Neuropathic origin | pain that arises from damage or dysfunction of nerves themselves Diabetic neuropathy Phantom limb Shingles Trigeminal neuralgia |
| Nociceptors | thin nerve fibers located in the skin, muscle, and other body tissues that carry pain signals. ⬤ The transmission of the pain message begins with activation of nociceptors in peripheral tissues |
| Cytokines | produce pain-causing inflammation. |
| Phospholipase A2 | stimulates arachidonic acid release |
| Cyclooxygenase | increases prostaglandin synthesis, an important mediator of pain. |
| Serotonin | stimulates nociceptors and causes pain. |
| Glutamate | enhances response to painful stimuli. |
| Substance P | produces pain sensations and controls pain perception. |
| Neurokinin A | is a neuropeptide: pain perception and transmission pain sensations |
| GABA | is inhibitory on nociceptors, reducing pain sensations. |
| Endorphins, enkaphalin, and dynorphin | bind to opioid receptors in the brain and spinal cord and block or dull pain sensations by inhibiting release of substance P and glutamate. |
| Mu (μ) receptor | produces analgesia, euphoria, respiratory depression, pupil constriction, decreased gastrointestinal motility, and physical dependence |
| Kappa (κ) receptor | binding produces analgesia, sedation, pupil constriction, dysphoria, and hallucinations. |
| Delta (δ) receptor | stimulation produces analgesia and decreases contractions of smooth muscle |
| Opioid agonist therapy | treatment for opioid use disorder involving opioid drugs involves taking an opioid agonist such as methadone (Methadose) or a mixed agonist, such as buprenorphine (Suboxone) |
| Opioid antagonists | (like naloxone and naltrexone) are medications that reverse opioid effects, especially respiratory depression, and are also used in the management of opioid and alcohol dependence. |
| Mixed agonists | opioid drugs that act as agonists in opioid‑naïve patients but as antagonists in patients already on opioids. They provide pain relief with less respiratory depression and lower addictive potential than traditional opioids. |
| Duration of action for controlled-release opioid analgesics | 72 hours (e.g., fentanyl patches) |
| Duration of action for immediate-acting opioids | 2 and 6 hrs |
| Nonopioid Analgesics | Nonsteroidal antiinflammatory drugs (NSAIDs) and aspirin (ASA) are widely used in the treatment of pain with or without inflammation. NSAIDS and ASA have analgesic, antiinflammatory, and antipyretic properties. |
| antipyretic | capable of reducing fever. |
| Nonopioid Analgesics MOA | NSAIDs decrease prostaglandin synthesis by inhibiting the action of cyclooxygenase (COX). ⬤ They inhibit COX-1 and COX-2. |
| COX-1 | found throughout the body and is important for control of blood flowing through the vasculature and regulation of platelet aggregation |
| COX-2 | formed in selected cells as part of the immune response and is involved in the biosynthesis of prostaglandins at the site of injury. |
| Salicylism | a condition that develops when salicylate levels in the body become too high. It is listed in the text as a serious adverse reaction of NSAIDs/aspirin. |
| Hepatoxicity | toxicitiy of the liver / adverse reaction to ketorolac |
| Agranulocytosis | body’s granulocytes (a type of white blood cell, including neutrophils, eosinophils, and basophils) are drastically reduced. - adverse reaction to indomethacin, flurbiprofen |
| Nerve injuries can cause a loss of | GABA inhibitory pathways. |
| Drugs used in the treatment of neuropathic pain | Antidepressants (amitriptyline) Antiseizure drugs (gabapentin, lamotrigine) Local anesthetics (lidocaine, mexiletine) Topicals (capsaicin) |
| Tricyclic Antidepressants | The first choice for the treatment of neuropathic pain They inhibit the reuptake of neurotransmitters at receptor sites in the spinal cord that are responsible for modulating pain sensation. . |
| Antiseizure Drugs Used to Treat Neuropathic Pain | Gabapentin, pregabalin, and carbamazepine |
| topiramate | Antiseizure Drugs Used to treat Neuropathic Pain works both by enhancing GABA’s inhibitory effects and by blocking voltage‑dependent sodium channels, |
| Lidocaine and mexiletine | block sodium channels. Local Anesthetics Used to Treat Neuropathic Pain |
| Lidocaine | patches are indicated for the treatment of nerve pain caused by herpes infection (shingles). |
| Capsaicin | is derived from chili peppers. is applied topically and it depletes substance P from nerve indicated for the treatment of diabetic neuropathy and shingles |
| Tension headache | produces bilateral pain, affecting both sides of the head, is mild to moderate in intensity, and is described as having a pressing or tightening quality. |
| cluster headache | a frequently reoccurring headache |
| Migraine | occurs as a result of biochemical and hormonal changes involving serotonergic and adrenergic pain modulating systems.\ may be preceded by an aura. |
| how migraine headaches develop | triggers release vasoactive neuropeptides, serotonin, prostaglandins and neurochemicals → blood vessel dilation, inflammation, nociceptor stimulation → throbbing headache pain. |
| Drug Treatment for Migraine Headache | Analgesics ⬤ Serotonin (5-hydroxytryptamine [5-HT]) agonists ⬤ Ergot alkaloids ⬤ Antidepressants (norepinephrine [NE] and serotonin reuptake inhibitors and MAOIs]) ⬤ Beta blockers ⬤ Antiseizure drugs |
| Triptans | most widely prescribed drugs for the treatment of migraine headaches. are administered at the first sign of migraine (aura) Selective serotonin (5-HT) receptor agonists receptors, which stimulate vasoconstriction. best taken Subcutaneous |
| T½ triptans | last 2 to 25 hours (e.g., frovatriptan, naratriptan) more effective in preventing HA recurrence |
| Warnings for Triptans | ⬤ Do not exceed recommended dosage. ⬤ If no improvement after first dose, do not take a second dose. ⬤ Do not exceed 2 doses per 24 hours. |
| Migraine preventive therapy | offered to persons that use medication more than twice per week, or when acute acting agents are contraindicated or have failed to relieve the headache. ⬤ Propranolol ⬤ TCAs ⬤ Divalproex ⬤ Botox |
| Nontriptan drugs used to treat migrains | Dihydroergotamine Ergotamine (act as serotonin agonists causing vasoconstriction) Opioids |
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