2023-11-23T00:09:42+03:00[Europe/Moscow] en true <p>eliminate cause of injury &amp; clear debris </p>, <p>PGE2; Prostacyclin </p>, <p>increase: local BF, endothelial activation/vascular permeability, leukocyte infiltration </p>, <p>when source of pain is not cleared; inflammation will persist and cause pain</p>, <p>central PGE2 increases the excitability of spinal dorsal horn neurons-resulting in hyperalgesia/allodynia; COX1/COX2 are expressed in spinal cord and PG release upon peripheral pain stimuli </p>, <p>nociceptors detect stimuli and send it to CNS; inflammatory mediators are released by damaged cells to increase sensitivity &amp; potentiate pain/peripheral sensitization </p>, <p>PGE2; thermosensitive </p>, <p>arachidonic acid; cyclooxygenase (COX)</p>, <p>b</p>, <p>a</p>, <p>a</p>, <p>kidneys, gastric mucosa, platelet</p>, <p>reduce PG synthesis by inhibiting COX enzymes </p>, <p>anti-inflammatory, analgesic, antipyretic </p>, <p>inhibit chemotaxis, decrease sensitivity of vessels to inflammatory mediators </p>, <p>reverse peripheral sensitization &amp; central actions in CNS</p>, <p>suppress the production of PGE2 to decrease hypothalamus signaling; reducing fever</p>, <p>Age </p>, <p>GI; CV</p>, <p>NSAIDs counter the effects of PG; resulting in retention of salt &amp; water </p>, <p>PG maintain patency of afferent arterioles; inhibition reduces BF to glomerulus which can result in AKI</p>, <p>pro-thrombotic events, hypertension, decreased renal clearance</p>, <p>decreases; PGI2</p>, <p>PGI2</p>, <p>premature closure of ductus arteriosus; HF in baby; avoid in 3rd trimester, prolonged gestation </p>, <p>low</p>, <p>they remain in the synovial fluid </p>, <p>low-moderate pain, inflammation, fever, cardioprotection</p>, <p>oxaprozin, piroxicam, meloxicam</p>, <p>piroxicam, meloxicam</p> flashcards
NSAIDs (Overview)

NSAIDs (Overview)

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  • eliminate cause of injury & clear debris

    What is the purpose of inflammation?

  • PGE2; Prostacyclin

    What are the mediators of inflammation? (2)

  • increase: local BF, endothelial activation/vascular permeability, leukocyte infiltration

    What are the effects of PGE2 & Prostacyclin? (3)

  • when source of pain is not cleared; inflammation will persist and cause pain

    How does inflammation result in pain?

  • central PGE2 increases the excitability of spinal dorsal horn neurons-resulting in hyperalgesia/allodynia; COX1/COX2 are expressed in spinal cord and PG release upon peripheral pain stimuli

    How is pain triggered in the CNS? (2)

  • nociceptors detect stimuli and send it to CNS; inflammatory mediators are released by damaged cells to increase sensitivity & potentiate pain/peripheral sensitization

    How is pain triggered at the site of injury?

  • PGE2; thermosensitive

    __________ can act on EP3 receptors on _________ neurons triggering the

    hypothalamus to elevate body temperature.

  • arachidonic acid; cyclooxygenase (COX)

    Prostaglandins are produced from _______ and this is catalyzed by _______.

  • b

    Which is induced by inflammation?

    a) COX-1

    b) COX-2

  • a

    Which is constantly expressed in noninflammatory cells?

    a) COX-1

    b) COX-2

  • a

    Which is essential for TXA2 formation in platelets?

    a) COX-1

    b) COX-2

  • kidneys, gastric mucosa, platelet

    Which organs/cells does COX-1 maintain homeostasis of? (3)

  • reduce PG synthesis by inhibiting COX enzymes

    NSAIDs MOA?

  • anti-inflammatory, analgesic, antipyretic

    What are the effects of NSAIDs? (3)

  • inhibit chemotaxis, decrease sensitivity of vessels to inflammatory mediators

    What are the anti-inflammatory effects of NSAIDs? (2)

  • reverse peripheral sensitization & central actions in CNS

    What are the analgesic effects of NSAIDs?

  • suppress the production of PGE2 to decrease hypothalamus signaling; reducing fever

    What are the antipyretic effects of NSAIDs?

  • Age

    __________ correlates with an increased probability of developing serious

    AE to NSAIDs.

  • GI; CV

    Nonselective COX inhibitors have an increased risk for _______ events

    while Selective COX inhibitors have an increased risk for ________ events.

  • NSAIDs counter the effects of PG; resulting in retention of salt & water

    How do NSAIDs cause Hypertension?

  • PG maintain patency of afferent arterioles; inhibition reduces BF to glomerulus which can result in AKI

    How do NSAIDs decrease renal clearance?

  • pro-thrombotic events, hypertension, decreased renal clearance

    What are the CV/Renal AE's of COX inhibition? (3)

  • decreases; PGI2

    COX-2 inhibition _______ vascular ________.

  • PGI2

    - a potent endogenous anti-platelet

  • premature closure of ductus arteriosus; HF in baby; avoid in 3rd trimester, prolonged gestation

    What are the effects of NSAIDs in pregnancy? (2)

  • low

    NSAIDs will accumulate in areas of the body with _____ pH.

  • they remain in the synovial fluid

    What makes NSAIDs good for treating RA?

  • low-moderate pain, inflammation, fever, cardioprotection

    What are the CAs of NSAIDs? (4)

  • oxaprozin, piroxicam, meloxicam

    What are the longest-acting NSAIDs? (3)

  • piroxicam, meloxicam

    Which NSAIDs are used for RA & OA? (2)