Opioids and Anti-Emetics

Card Set Information

Author:
stownsend
ID:
304532
Filename:
Opioids and Anti-Emetics
Updated:
2015-06-28 17:48:51
Tags:
BC CRNA Pharm
Folders:

Description:
Exam 2
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user stownsend on FreezingBlue Flashcards. What would you like to do?


  1. Definition of opioid
    all exogenous substances both natural and synthetic binding to opioid receptors producing morphine-like effects
  2. effect of opioids
    produce analgesia without loss of touch, proprioception or consciousness (Except in large doses)
  3. opioid agonist drugs
    morphine, fentanyl, sufentanil, alfentanil, merperidine, remifentanil, hydromorphine
  4. opioid agonist-antagonist drugs
    butorphanol and nalbuphine
  5. opioid antagonists
    naloxone, naltrexone, nalmefene
  6. Phenanthrene class
    morphine (T-shaped)
  7. Phenylpiperidines
    fentanyl family, meperidine
  8. semisynthetic opioids
    result from substitution of the morphine molecule (i.e codeine)
  9. synthetic opioids
    completely synthesized, not just morphine modified (ie. fentanyl family)
  10. opioid receptors
    • mu, kappa, delta,
    • sigma?
  11. opioid receptor location
    CNS (brainstem and spinal cord), periphery
  12. how opioids give analgesic effects
    directly inhibit the ascending transmission of noxious stimuli from the spinal cord to the dorsal horn. inhibit substance P release from primary sensory neurons and mitigate the transfer of painful sensations to the brain.
  13. endogenous ligands
    enkephalins, endorphins, dynorphins
  14. Opioid receptor mechanism of action
    • part of the G protein coupled receptors (like GABA)
    • close voltage gated Ca channels on pre-synaptic nerve terminals to reduce the NT (glutamate, substance P)
    • AND
    • hyperpolarize to inhibit post-synpatic neurons by opening potassium channels¬†

    inhibition via adenyl cyclase decreasing conductance of voltage gated Ca channels or opening outward flowing potassium channels
  15. Receptor activation causes...
    • decrease neurotransmission d/t presynaptic inhibition of NTs including Ach, dopamine, norepi, substance P
    • postsynaptic inhibition of evoked activity
    • increased K conductance leading to hyperpolarization, Ca channel inactivation or both which causes immediate drop in NT release
  16. Mu 1 receptors effect
    • analgesia, euphoria
    • low abuse potential, bradycardia, hypothermia, urinary retention and endorphins
  17. Mu 2 receptor effects
    analgesia, depression of ventilation, physical dependence, constipation, endorphins
  18. Kappa receptor effects
    analgesia, dysphoria, sedation, low abuse potential, miosis, diuresis, dynorphins
  19. Delta receptor effects
    analgesia, depression of ventilation, physical dependence, constipation (minimal), urinary retention, enkephalins
  20. pKa and base/acid opioids
    • basic drugs
    • pKa of all but alfentanil (7.1) and remifentanil (6.5) are above physiologic pH (around 8)¬†
    • therefore pH<pKa and ionized form predominates..moves to BH+
  21. lipid solubility for fentanyl and sufentanil
    ++++ very high (but sufentanil partition coefficient is 1700 and fentanil is 800)
  22. why does alfentanil have a more rapid onset and short duration than fentanyl even though it is less lipid soluble?
    has a high non-ionized fraction an physiologic pH and a small Vd
  23. lipid soluble opioids and lungs and what uptake depends on
    • high amount retained by lungs (first pass uptake)
    • depends on- prior accumulation of another drug, history of tobacco use increases uptake, inhalation anesthesia decreases uptake
  24. plasma concentration vs effect site- the slowest and fastest drugs
    • theres a more rapid uptake of alfentanil than fentanyl due to difference in ionization
    • plasma and effect site concentration- alfentanil (1.4 minutes), then fentanyl (3.6 minutes) and sufentanil is the longest (5-6 minutes)
  25. why is there a short elimination half time with alfentanil?
    small Vd and low lipid solubility
  26. morphine metabolism
    • conjugated with glucoronic acid to active metabolites
    • -morphine 6 glucoronide (more potent and longer acting than morphine itself)
    • -morphine 3 glucoronide
  27. Meperidine metabolism
    de-methylated to normeperidine (active metabolite) associated with seizure activity
  28. fentanyl, sufentanil and alfentanil biotransformation
    inactive metabolites
  29. remifentanil metabolism
    ester hydrolysis (very short half life and duration of action d/t elimination)
  30. Opioid effects on CV
    • generally stable
    • morphine and meperidine can cause histamine release which decreases BP and SVR
    • fentanyl family is associated with vagus mediated bradycardia
  31. Respiratory effects -opioids
    • decrease response to CO2
    • decrease hypoxic drive
    • blunt bronchoconstriction caused by manipulation airway during bronchoscopy
    • chest wall rigidity
  32. CNS effects of opioids
    • decrease CBF, ICP, O2 consumption (but less than barbs and benzos)
    • stimulate chemoreceptor trigger zone (PONV)
    • physical dependence
    • do not cause reliable amnesia alone
  33. GI effects of opioids
    • decrease gastric emptying time, decrease peristalsis, biliary spasms
    • can mimic common duct stone
  34. Endocrine effects of opioids
    • block stress hormone release more than volatiles (esp. fentanyl family)
    • -catecholamines, cortisol, ADH
  35. opioids and bile duct pressure
    demerol, morphine and fentanyl can cause increase common duct pressure and delayed gastric emptying
  36. Morphine  kinetic key points

What would you like to do?

Home > Flashcards > Print Preview