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Pharmacology > Analgesia Pharmacodymanics > Flashcards

Analgesia Pharmacodymanics Flashcards

1
Q

Opioid CVS effect:

A
  • CNS-Dose dependent BradyC (like atropine);
  • May cause Compensatory sympathetic response.
  • Less Sympathetic Outflow -> Dec BP
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2
Q

Opiod Central Resp effect:

A
  • RR: Decrease alot, may breath on command;
  • Increased resting pCO2;
  • Hypercarbia (alot, lasts past analgesia)/Hypoxia; Decreased Airway Reflexes (Central antitussive effect).
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3
Q

Opioid External Response:

A
  • chest wall rigidity,
  • vocal cord closure with high bolus doses (impairs ability to ventilate).
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4
Q

Opioid Neurolog effect (CMRO2, CBF, ICP):

A
  • CMRO2: Modest Dec;
  • CBF: Dec when administered with N2O;
  • ICP: Decreased. [ CBF and ICp can inc with hypercarbia),
  • no effect on SEP
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5
Q

Opioid GI effect:

A
  • Decreased Motility -> dec gastric emptying and peristalsis -> Inc Ileus;
  • Increase Chemotrigger Zone Trigger, Inc Vestibular Sensititivity;
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6
Q

Opioid GU effect:

A

Inc urinary Retention especially with spinals

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7
Q

Meperidine Benefit and AE:

A

Benefit: Can be used for postop shivering,

AE:

  • Direct myocardial depressant (may also become tachyc due to atropine like effect),
  • in CKD, Meperidine can lead to seizure (focal neuroexcitation after inc doses);
  • causes Histamine release -> Hypotension + tachycardia,
  • CBD pressure inc,
  • Serotonin Syndrome: Delirium + hyperthermia
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8
Q

Fentanyl: Benefit, AE

A

Benefit:

AE:

  • peak respiratory depression at 5-15 min (lag behind analgesics),
  • less emetic vs morphine;
  • Fast distribution and inc with large and repeated doses,
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9
Q

Alfentanil Benefit; AE:

A

Benefit: Rapid Peak effect useful for blunting response to single, brief stimulus;

AE: CYP3A4, inhibited by erythromycin, Navir, can inhibit clearance,
Use Ideal Body weight for High BMI

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10
Q

Morphine: Benefit; AE:

A

Benefit: Peak effected may be delayed 10-40 min

AE:

  • Adjust in CKD,
  • Histamine release,
  • ​slow crossing of blood brain barrier (10-40 min)
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11
Q

Hydromorphone Benefit, AE:

A

Benefit:

  • Less histamine release,
  • safer in renal impairment,
  • shorter time to peak effect

AE

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12
Q

Methadone MOA; AE:

A

MOA:Opiate agonist and NMDA R antagonist;

AE:

  • Respiratory depression, long half life but usaully need q6-8h dosing.
  • Can lead to QT prolongation (esp >200mg/d, try to use EKG prior to iniating/titrating).
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13
Q

Oxycodone AE, warning

A

AE

  • Cannot Crush/NGT use,
  • Rapid metabolizer may have high toxicity,
  • Highly abusive,
  • Poor metabolier (CYP2D6) may need higher dose
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14
Q

Codeine MOA, AE

A

MOA: Raises Pain Threshold without change to pain.

AE:

Ultrametabolizers esp in children can lead to OD from coedine (do not give to kids esp after tonsillecvtomy/adenoidectomy)

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15
Q

Butorphanol (MOA, Benefit, AE):

A

MOA:

  • partial agonist to mu receptor or compeititve antagon,
  • agonism of kappa and delta;

AE:

  • HTN, pulm-HTN,
  • Inc CO,
  • Mild GI and Billiary System, used on OB
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16
Q

Tramadol (MOA)

A

MOA:

  • Opiate agonist and TCA-Like Spinal inhib of pain (similar to SNRI)
  • M1 metabolite has 200x more afinity to mu opioid receptor
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17
Q

Tramadol (Benefit, AE)

A

Ben: Less Resp and GI effect.

AE:

  • in CKD, ETOH, CVA, TBI may lead to Seizures,
  • poor antagonist by naloxone
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18
Q

NSAID MOA:

A
  1. Inhibs Cyclooxygenase (COX)
  2. decrease inflammatory mediator (prostaglandins)
  3. dec pain, temp, inflam
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19
Q

NSAID COX1 AE:

A
  • GIB/Ulcers,
  • Decreased Renal perfusion (esp in hypovolemia,
  • Decrease Platlet Aggregation,
  • Dec Prostaglandin -> nsaids induced bronchospasm
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20
Q

NSAID COX2 AE:

A

Increase CVA and MI risk

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21
Q

NSAID Benefit limited?

A

Limited by maxing out pain reliefs but ae continues

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22
Q

Max Dose of Ibuprofen, Naproxen, Diclofenac

A
  • Ibuprofen 3200;
  • Naproxen 1250 mg;
  • Diclofenac 200mg
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23
Q

Tylenol Onset, Elim

A
  • 5-10 min,
  • rectal absoprtion is rapid but sporadic
  • cleared only by liver
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24
Q

Tylenol Benefit

A
  • Can be used in preggers,
  • does not affect inflammation, only temp and pain,
  • No GI-tract problems,
  • No platelet problems
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25
Q

Tylenol AE

A
  1. Can OD (both single or cummulative);
  2. Hepatic Necrosis due to depletion of antioxidant glutathione
  3. N acetyl-p-benzoquinone;

Tx with NAC within 8 hours. Rectal tylenol is slow and erratic

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26
Q

Toradol Benefit/AE:

A

Ben:

  • IV provide more analgesic vs inflam
  • no resp dep;
  • no cbd spasm,
  • roughly ~10 mg morphine .

AE

  • prolong bleeding,
  • platelet dsfxn only in spinal anesthesia not ga. can trigger renal dsyfxn
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27
Q

ASA Benefit/ AE:

A

Ben:

AE:

  • stop 10 days prior surgery stop/caution in gib,
  • hemorrhage,
  • low plt,
  • Caution in hemophilia, uremia or vWF, asthma
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28
Q

Celecoxib Benefit/AE:

A

AE:

  • relies on hepatic metabolism (reduce if liver dysfxn)
  • associated with ACS,
  • LFT inc,
  • htn,
  • edema,
  • ckd,
  • sulfa/asa allergy
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29
Q

MOA of NSAIDS

A

Blocks conversion of arachidonic acid to Prostagladins

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30
Q

Gabapentin moa, indicates, ae

A

MOA:binds voltage gates ca chan,
Indic: neuropathic pain, fibromyalgia, spinal stenosis,
AE: dizzy, sedate, weight inc, n/v

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31
Q

Pregabalin Moa, indicate, ar

A

MOA: binds to ca voltage gates,

Indicate: neuropathic, fibromyalgia,

AE: dizzy, sedate, edema ha

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32
Q

Topiramate moa, indicate, ae

A

MOA:na, ca chan enhance gaba.
Indic:Neuropathic chronic lumbar,
AE: sedation, weight loss

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33
Q

cyclobenzaprine indicate, ae

A

Indic: Spastic pain/Muscle Spasm;

AE: Dry mouth, drowsiness, headache, confusion

34
Q

Carisoprodol, MOA, Indicate, AE

A

MOA: Interneural inhibition,

Indic: Acute MSK pain,

AE: Dry mouth, drowsiness, headache, ams

35
Q

Baclofen, MOA, indicate, AE

A

MOA: Binds Gaba-B, inhibits Neuro transmitter release;

Indic: Spine origin spasticity, UMN dz, acute back pain, CN5 Neuralgia;

AE: Drowsiness, dizziness, nausea, ams

36
Q

Amitripyline MOA, Indicate, AE

A

MOA: TCA SNRI; AntiHis, AntiCholin,Anti 5HT

Indicate: Tension Headache, TMD, Facial-Myofascial pain;
AE: Ache: Dry mouth, constipation, Weight gain, drug interactions

37
Q

Duloxetine MOA, Indicate, AE

A

MOA: SNRI;
Indicate Neuropathic pain, fibromylagia.
AE: Nausea, drowsy, dry mouth constipation

38
Q

Tizanidine MOA, Indicate, AE

A

MOA: A2, Presynaptic inhibition of motor neurons;
Indicate: spasticity, paravertebral spasms;
Ae: dry mouth, somnolence, asthenia, dizziness

39
Q

Meperidine AE

A

Long 1/2 Life of Active Metabolite (normepeidine) esp Renal Pt is a proconvulsant

40
Q

Meperidine MOA

A

Affecting K receptor taht leads to Anti-shivering

41
Q

Meperidine Use

A

shivering from multiple causes including GA, Epidural, fever, transfusionRXN , and amphotericin B.

42
Q

Opioid Receptors Types

A

Mu, Kappa, Delta

43
Q

Mu Receptor effects

A

µ1: analagesia + Dependence. µ2: Resp Depression, Miosis, Euphoria, Dec GI Motil, Physical Dependence, µ1: analagesia + Dependence. µ3: Unknown

44
Q

Kappa Receptor Effect

A

Analagesia, Dysphoria, Sediation, Misosi, anti ADH

45
Q

Delta Receptor Effects

A

Analalgesia; Dependence, Antidepressant

46
Q

Methadone MOA and effects

A

Mu agonist, antagonism of NMDA and SSRI (leading to chronic neuropathic pain control with psych helping also). May lead to upregulation of NMDA receptors + NO release -> Hyperalgesia. Can still cause respiratory depression; QTc prolong [needs ekg monitoring]

47
Q

Naloxone AE

A

P-Edema, hyperalgesia

48
Q

NSAID MOA and limitation

A

Inhibit COX affecting synthesis of prostaglandin. [PGE2: sensitization nociceptors +hyperalgesia]; Has Ceiling effect.

49
Q

NSAID Benefit

A

Less opioid usage that leads to less N/V and sedation

50
Q

NSAID AE and rf of these

A

Plt Dysfxn, GI ulcer, Nephrotoxicity [esp with hypovolemia, CHF, CKD]

51
Q

COX2 inhibitor AE

A

Fluid retention and HTN

52
Q

COX 1 vs COX 2

A

1: Consitutive enzyme that produce prostaglandin for house keeping (gastric protection + hemostasis); 2: Inducible form of enzyme that produces prostaglandin that mediate pain, inflam, fever and carcinogenesis

53
Q

PGE2 effect

A

Sensitizing nocioreceptor to His + bradykinin; Enhance pain ntrainsmission at dorsal horn via inc release of substance P and glutamate from first order pain neurons. along with inhibiting neurotrans from descending pain modulating pathways

54
Q

Opioids with ceiling effect

A

Mixed agon/antagon such as nalbuphine

55
Q

Buprenoprhine Duration, MOA and effects

A

10 hours duration; Partial Mu agonism -> Ceiling Effect of Rep Depression [max resp depression 50% + Reduce w/d.

56
Q

Buprenoprine combined with what and why

A

Naloxone; which does not affect theraputic dose of buprenorphine to avoid abuse.

57
Q

Tx of acute opioid w/d

A

Clonidine (sx only : N/v sweating, diaphoresis, restlessness)

58
Q

Naltrexone OA and use

A

Opioid Antagonist that is used towards the end of opioid period diminished.

59
Q

Morphine 3 glucuronide Metabolite Effect

A

Majority of Metabolite from Liver 60%, Hyperalgesia; agitation, myoclonus, delirium

60
Q

Morphine 6 glucuronide

A

Drowsiness, n/v, coma, respiratory depression

61
Q

Codeine In peds

A

Neonates have Decreased CYP2D6 x 2 wks (which converts to active form, morphine) -> Less sensitivity to codeine vs kids

62
Q

Morphine in Peds

A

Neonates are more sensitive to morphine -> Decrease in ventilatory response at lower CO2 vs adults

63
Q

Metabolism of Morphine Which enzyme

A

UGT2B7 (UDP-Glucuronosyltransferase-2B7)

64
Q

Metabolism of Fentanyl and tramadol and effects on peds

A

to Norfentanyl and Nortramadol; CYP3A4 (also affects Methadone). premmies+Neonates Less of this enzyme -> more suscpetible

65
Q

Methadone Cardiac AE and CoRF

A

QT Prolongation esp with CYP3A4 inhbiitors.

66
Q

Best analgesic effectiveness of continuous epidural infusion; PC epidural analgesia; PCA and PRN

A

CEI>PCEA>PCA>PRN

67
Q

Why Epidural > Opioids

A

Less Mortality; PNA, Ileus, Less time before ambulation

68
Q

Fentanyl premedication effect

A

Sensitize pt to pain postop

69
Q

effect of ssri on opioids metabolism

A

inhibit cyp2d6, leading to slower onset for any codone derivative to morphine

70
Q

Opioid Effect CVS

A

Decreases sympathetic tone/inc muscarinic -> dec MAP, dec VR

71
Q

Opioids and LFT

A

Hypoalbuminemia increases free opioids in the blood, decreasing total requrirement

72
Q

Fastest Onset Opioid and why

A

Alfentanil (acceleration; 1.1min) due to low pka (6.5) -> low lipid solubility; 4s: 4x faster onset; 1/4 duration, 1/4 potency

73
Q

Strongest Opioid

A

Sufenanil (super)

74
Q

Opioid Onset of action Key Factor

A

Unionized Fraction/ Low Lipid solubility

75
Q

Opioid Duration Factor

A

Low solubility means longer

76
Q

CYP of Opioids (i1)

A
77
Q

Opioid Metabolism (i1)

A
78
Q

Opioid Table i1

A
79
Q

Schedule Drugs List

A
80
Q
A

Pharmacology (21 decks)

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