Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
JGR-Non Opioids
| Question | Answer |
|---|---|
| What are the two most important neurotransmitters associated with pain? | Glutamate Substance P |
| What are the sensitizers that initiate action potentials that transmit pain impulses? | bradykinins Potassium Prostaglandins Histamine Leukotrienes Serotonin Substance P |
| What are the three pain modulation processes? | Gate control Endogenous Opiate System Descending pathway |
| What are the three receptors of the Endogenous Opiate System? | Mu Delta Kappa |
| Which is the most important receptor for analgesia? | Mu |
| What are the neurotransmitters of the Endogenous Opiate System that are released in response to severe/persistant pain? | Endorphines (enkephalins, dynorphin) |
| Where are the neurotransmitters of the Endogenous Opiate System release from? | Interneurons of the dorsal horn of the spinal cord |
| What is the result when opiates bind to G proteins associated with Mu receptors? | Inhibition of pre-synaptic release of glutamate Increased potassium conductance across the post-synaptic membrane |
| What is descending pathway modulation of pain? | Signals from the brain inhibits synaptic pain transmission at the dorsal horn through the actions of endogenous opioids, serotonin, norepinephrine, and GABA |
| What is the NMDA receptor? | Receptors involved in wind-up, normally blocked by Mg that remain open by binding to glutamate transmitting pain signals to the brain |
| What is wind up? | Excessive excitability and amplification of pain signals leading to increase in substance P and glutamate causes the activation of the NMDA receptors |
| What causes wind up? | repeated nerve depolarization release of glutamate holding open NMDA receptors allowing influx of Ca+ |
| What is the result of wind up? | increased pain in response to painful stimuli (hyperalgesia), pain in response to normally non-painful stimuli (allodynia), and spontaneous pain |
| What is the 5th vital sign? | Pain Assessment |
| What are the things you evaluate when assessing pain? | P-palliative/provocative factors Q-quality R-radiation S-severity/intensity T-temporal factors U-you |
| What are the main categories of pain medications? | Nonopioids Opioids Mixed Agonist-Antagonists Central Analgesic |
| What are the categories of non-opioids? | NSAIDS Salicylates Acetaminophen (APAP) |
| What are the categories of non-opioid NSAIDs? | Acetic Acids Propionic Acids Oxicams Fenamates Alkanones Salicylates Cox II selective Acetaminophen |
| What are the categories of opiods? | Phenanthrenes (Morphine-like) Phenylpiperidines (Meperidine-like) Diphenylheptanes (Methadone-like) |
| List the acetic acid NSAIDS | diclofenac (Voltaren®) etodolac (Lodine®) indomethacin (Indocin®) ketorolac (Toradol®) sulindac (Clinoril®) tolmetin (Tolectin®) |
| List the propionic acid NSAIDS | ibuprofen (Motrin®) fenoprofen (Nalfon®) flurbiprofen (Ansaid®) ketoprofen (Orudis®) naproxen (Naprosyn®) oxaprozin (Daypro®) |
| List the oxicams | meloxicam (Mobic®) piroxicam (Feldene®) |
| List the Fenamates | meclofenamate (Meclomen®) mefenamic acid (Ponstel®) |
| List the Alkanones | nabumetone (Relafen®) |
| List the Salicylates | aspirin diflunisal (Dolobid®) salsalate (Disalcid®) Choline Salicylate Choline Magnesium Trisalicylate Sodium Thiosalicylate |
| List the COX II selective: | celecoxib (Celebrex®) |
| What are the uses of non-opioid NSAIDS? | Analgesia for mild (1-3) to moderate pain (4-6) Effective for Inflammatory pain Anti-inflammatory Antipyretic Antiplatelet |
| What is the MOA for non-opioid NSAIDS? | reversible inhibition of COX 1 & 2 enzymes resulting in decreased prostaglandin formation |
| What substances mediate inflammation? | histamine, bradykinin, prostaglandins* among others |
| What is the function of Prostaglandins? | Regulate gastric and renal blood flow among other “house keeping” tasks in the body Mediate inflammation |
| What are Cyclooxygenase 1 & 2 ? | Enzymes required for synthesis of prostaglandins COX 1 is ubiquitous=> maintain homeostasis COX 2 is manufactured in activated macrophages in response to injury |
| How do NSAIDS relieve pain and inflammation? | By inhibiting COX I and II preventing formation of prostaglandins which sensitize pain receptors and trigger inflammation. |
| What are the main side effects caused by NSAIDS? | Cardiovascular Thrombotic events (MI and Stroke) GI: nausea, dyspepsia, diarrhea, ulcers, GI bleeding Renal insufficiency Fluid retention: HTN |
| How do NSAIDS cause GI problems? | Direct irritant effect, Enterohepatic cycling Systemic prevention of gastroprotection |
| How do NSAIDS cause CV problems? | By inhibiting COX I and II disrupting normal production of thromboxanes |
| What are the NSAID drug interactions? | Low dose Aspirin: increase GI bleeding ACE inhibitors: reduce anti-HTN effects Corticosteroids: increase GI ulceration Warfarin: increase drug levels & risk of bleeding Displace other highly protein bound drugs: warfarin sulfonylureas methotrexate |
| Do you give higher doses of NSAIDs for analgesia or inflammation? | Inflammation |
| What is the MOA of aspirin? | Irreversible cox I and II inhibitor |
| Name the nonacetylated salicylates | Salsalate Difusinal Salicylate salts (magnesium, choline, sodium salicylates) |
| Are nonacetylated salicylates better analgesics or anti-inflammatories? | Anti-inflammatories |
| Who would benefit from using nonacetylated salicylates? Why? | Asthmatics and those with bleeding disorders or renal dysfunction Because it has less effect on COX |
| Which is more potent, aspirin or diflunisal? | Diflunisal |
| Does Diflunisal reduce fever? | No |
| What NSAID is subject to enterohepatic cycling? What needs to be done with the dose? | Diflunisal Reduce the dose |
| What effect does salicylate toxicity have on the ears? | Tinnitus |
| What is the most commonly used NSAID in the US? | Ibuprofen |
| Which NSAID presents the lowest cardiovascular risk? Highest? | Naproxen Celecoxib |
| Which NSAID contains Sulfa group? | Celecoxib |
| What are the dosing restriction for Ketorolac? | Not to exceed 5 days due to severe GI side effects |
| Which NSAIDs generally have less GI side effects? | COX II preferential |
| Which NSAIDS are COX II preferential? | diclofenac (Voltaren®)* etodolac (Lodine®)* nabumetone (Relafen®)* meloxicam (Mobic®)* |
| Which NSAID is associated with unique neurological side effects and may affect TNF? | Flurbiprofen- cogwheel rigidity, ataxia, tremor and myoclonus |
| What is the only non-acid NSAID? | Nabumetone |
| Which NSAID has long half-life permitting once daily dosing? | Nabumetone |
| Which NSAID has no enterohepatic cycling? | Nabumetone |
| What is the MOA for acetaminophen? | inhibits the synthesis of prostaglandins in the CNS (COX inhibition) and blocks pain impulses in the periphery |
| What are the uses for acetaminophen? | Mild pain (1-3) Antipyretic |
| How much should you reduce the dose of acetaminophen in patients with renal impairment or liver disease? | 50-75% |
| What dose of acetaminophen is hepatotoxic? Potentially fatal? | 10-15g hepatotoxic 20-25g fatal |
| How is acetaminophen metabolized? | Most excreted in urine Some converted to NAPQI which reacts with glutathione and is rendered harmless Large amounts of NAPQI overwhelms available glutathione and becomes hepatotoxic |
| What is the treatment for acetaminophen toxicity? | NAC (charcoal) |
| How does NAC work? | It is metabolized to cysteine, a precursor to glutathione |
| what is the main use of non-acetylated salicylates? | anti-inflammation |
| what is the gate control pain modulation system? | counter-irritant blocks pain reception. (Heat on sore muscles) |
| what drug toxicity causes tinnitus? | salicylate toxicity |
Created by:
joannasan
Popular Pharmacology sets