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Pharmacology > Opioids > Flashcards

Opioids Flashcards

1
Q

2 opioid structures

A

phenanthrene

benzylisoquinolines

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2
Q

Opiate

A

term used to designate drugs derived from opium

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3
Q

Opioid

A

all substances;
natural & synthetic
that bind to opioid receptors and produce agonist effect

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4
Q

Opioid classification

A

Natural occurring
–Morphine

Semisynthetic analogs of morphine

  • –Heroine
  • –codeine
  • –Hydromorphone [[Dilaudid]]

Synthetic
–Exogenous [[4 groups]]

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5
Q

4 types of synthetic opioids

[[exogenous]]

A

Morphinan derivatives

Diphenyl derivative

Benzomorphans

**Phenylpiperdines

believed that synthetic opioids; [[exogenous]] mimic the activity of endogenous [[naturally occurring; enkephalins, endorphins and dynoprhins]] at the opioid receptors

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6
Q

Morphinan derivative

A

type of synthetic opioid [[exogenous]]

  1. Levorphenol
  2. Butorphenol

becoming popular to use for withdrawal

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7
Q

Diphenyl Derivative

A

type of synthetic opioid [[exogenous]]

  1. METHADONE

used for withdrawal; but can get addicted to methadone

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8
Q

Benzomorphans

A

type of synthetic opioid
[[exogenous]]

  1. Phenazocine
  2. Pentazocine
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9
Q

PHENYLPIPERDINES

A

type of synthetic opioid [[exogenous]]

OR DRUGS

  1. Meperidine [[demerol]]
  2. Fentanyl
  3. Alfentanil
  4. Sufentatil
  5. Remifentanyl
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10
Q

Opioid receptor activity classification

A

Agonist

Partial Agonist

Mixed agonist/ antagonist

Antagonist

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11
Q

Agonist

A

full mu receptor effects

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12
Q

partial agonist

A

Regardless of dose can not produce full mu receptor effects like morphine

Buprenorphine

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13
Q

mixed agonist/ antagonist

A

agonist at other opioid receptor [[kappa or delta]] but antagonist at mu receptor

ex. Nalbuphine ; reverses resp. depression
[[agonist at kappa; antagonist at mu]]

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14
Q

Antagonist

A

inhibits mu receptor activity

ex. Naloxone [[Narcan]]
reverses opioid

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15
Q

Opiate Receptors

A

mu [[mu1 and mu2]]

kappa

delta

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16
Q

3 endogenous agonists

[[naturally occurring]]

A

Enkephalins

endorphins

dynorphins

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17
Q

Opioid and pain modulating systems

A
  • ANTInociceptive; down regulates pain receptors

- Inhibits excitatory neurotransmitters [[Substance P]]

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18
Q

Mu 1

A

Supraspinal [[BRAIN]] Analgesia

Euphoria

Miosis [[pupil constriction]]

Bradycardia [[DIRECT action on vagus nerve]]

Urinary Retention

ALL endogenous and exogenous [[synthetic]] opioids work on Mu1

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19
Q

Mu 2

A

SPINAL analgesia

Physical Dependence

hypoventilation

Constipation

All endogenous [[natural]] and exogenous [[synthetic]] agonists act on Mu2

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20
Q

Mu receptors

A

Primarily in the CNS;
Brain and Spinal cord

some periphery

Mu1
Mu2

ALL endogenous [[naturally occurring]] and exogenous [[synthetic]] agonists act on Mu receptors

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21
Q

Bradycardia

A

Mu1 effect

DIRECT effect on Vagus nerve

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22
Q

Kappa receptors

A

ONLY Dynorphins work on KAPPA

Supraspinal[[Brain]] and spinal Analgesia

Dsyphoria [[Dynorphins, kappa]]

Sedation

Miosis [[constricted pupils]]

Diuresis

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23
Q

Delta

A

ONLY Enkephalins work on DELTA

Supraspinal [[Brain]] and spinal Analgesia

hypoventilation

physical Dependance

constipation and urinary retention

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24
Q

Opioids on G coupled opioid receptors

A

-Suppression/ inhibition of neurotransmitter [[substance P]]

-decreases adenylyl cyclase; cAMP
presynaptic
postsynaptic

G alpha i; decreases cAMP
[[increased conductance of K –> hyperpolarizes; decreases Ca into cell]]

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25
Q

Fentanyl in your epidural

A

makes a denser block

2 mechs of action
LA; block transmission via VGNaC

opioid activity on Mu receptors but mostly Mu2 [[ spinal analgesia; M2]]

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26
Q

Explain the mechanism of action of Opioids

A

opioids work on G alpha i opioid receptors

G alpha i
decreased cAMP
increases K conductance
[[hyperpolarizes]]

increased K out of the cell
hyper polarizes the cell and inhibits VGCa and decreases Ca into the cell

*when you have pain Ca is sent into the cell and releases NT [[substance P]] signals pain

by increasing K conductance and hyperpolarizing the cell it decreasing Ca into cell and decrease the release of pain NT
decreasing nociceptive [[pain]] receptor activity

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27
Q

Activation of Receptors can be

A

Direct; directly decreases neurotransmission
[[decreases Ca into cell]]

inhibits the release of excitatory NT [[substance P]]

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28
Q

Opioids onset of action

A

higher % not protein bound
higher % unionized
^faster onset of action

all opioids are weak bases
B + B = nonionized!
B + A = ionized
[[pt is acidotic pH under 7.35; will need a larger dose; more ionized]]

only unionized and not protein bound can diffuse

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29
Q

Anomaly Opioid

A

Sufentanil

20% nonionized
93% protein bound

NOT Highly nonionized and highly protein bound
[[would think it would be a weaker; slow onset]]

BUT 1000x stronger than morphine

VERY diffuse-able [[partition coeff. 1727]]

*attributed to molecule size/ structure

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30
Q

Drugs in potency order

A

most potent to least

Sufentanil

Remifentanil

Fentanyl

Alfentanil

Dilaudid

Morphine

Demerol

more potent; smaller dose

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31
Q

Factors that alter pharmacokinetics of Opioids

A

Age
-neonates; give less [[decrease rate of elimination; bc immature CYP 450]]
-elderly; give less
[[weaker BBB]]

Weight
dose based on ideal body weight [[not actual]]

Renal Failure
decrease dose

Hepatic failure
decrease dose

^both kidney and liver failure will effect metabolism and elimination oof opioid
DECREASE DOSE

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32
Q

Spinal Analgesia

A

analgesia produces by receptor activation in the spinal cord and dorsal root ganglion

pain [[sensory; afferent; approaching; dorsal root ganglion to the dorsal horn of gray matter –> laminae II and III]]

pain signals synapses in the substantial gelatenosa [[laminae II & III]]

Direct stimulation of these receptors produces intense analgesia [[pain relief]]

how?
Gi; decrease cAMP; increase K conductance; decrease Ca into cell decrease/ inhibit release of substance P [[pain NT]]; decreases activity at nociceptive [[pain]] receptors

Mu2 and kappa and delta

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33
Q

Supraspinal [[BRAIN]] Analgesia

A

analgesia produced by receptor activation in the BRAIN [[periaquaductal/ periventricular gray matter]]

Mu1 and kappa and delta

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34
Q

Opioids in the Epidural space

A

more lipophilic drug will go right into venous system and you’ll have an immediate response; less lipophilic delayed response

less lipophilic drug more CEPHALAD movement; doesn’t diffuse right away so travels up

less lipophilic drug more cephalic movement

Morphine more cephalic movement than Fentanyl

35
Q

CNS effects of Opioids

A

Analgesia

Euphoria

Sedation; Drowsiness/ sleepy

respiratory depression

miosis

nausea [[direct via chemoreceptors; indirect via GI]]

decrease in CBF and ICP [[modest]]

**NO AMNESIA or ANESTHESIA
[[big doses in cardiac OR can get anesthesia but NO amnesia –> give Benzes or gases

36
Q

Cardiac effects of Opioids

A

ALL dose dependent

no impairment of CV function

-dose dependent Bradycarid

37
Q

Cardiac effects of Opioids

A

ALL dose dependent

no impairment of CV function

-dose dependent Bradycardia
decreases workload and increases supply; decreases demand
[[except DEMEROL; tachycardia]]

  • vasodilation
  • decrease CO and BP
38
Q

What opioid does not produce bradycardia

A

Meperidine [[DEMEROL]]

tachycardia

demerol structure similar to atropine; antimuscarininc effects

39
Q

What opioid does not produce bradycardia

A

Meperidine [[DEMEROL]]

tachycardia and
DIRECT myocardial depression

demerol structure similar to atropine; antimuscarininc effects

40
Q

What combination can cause CV depression

A

Morphine and Nitrous

**not with morphine alone

41
Q

Ventilatory effects of Opioids

A

dose dependent respiratory depression
[[give more; more depression]]

**drop RR but increase TV
[[slower deeper breaths]]
hypoxia and hypercarbia
[[lower RR blowing off less C02]]

decrease chest wall compliance; muscle rigidity
[[think fent–> right chest]]

constricts pharyngeal and laryngeal muscles

42
Q

NONtherapeutic ventilatory effects

A

decrease RR
increase TV

decrease hypoxic ventilation drive [[normal person its ok, C02 level is drive to breath; can become a problem in COPD patient]]

ventilatory response curve is shifted the the R
[[takes more C02 two get brain to breath; when waking pt up let C02 level rise; will need much higher C02 level to start breathing r/t opioids]]

43
Q

Respiratory depression effects with different opioids

A

Peak of respiratory depression is slower with morphine than with Fentanyl

respiratory depression with morphine lasts longer than with fentanyl

Why? bc fentanyl is more lipophilic
respiratory depression right away

[[give morphine 30 min before bringing pat to pacu fentanyl you can give 5 min before bringing them to pacu]]

44
Q

Factors that increase magnitude and duration of opioid induced respiratory depression

A

larger opioid dose

synergistic effect
[[opioid given with other anesthetic]]

*speed of injection

continuous vs intermittent injection

decreased clearance
liver and kidney failure pt

alkalosis
B + B = more nonionized
more crosses BBB

age
lower does in babies; immature CYP 450
lower dose in elderly; weaker BBB

secondary peak in plasma level from reuptake of opioid in muscle, fat, lungs and intestine
[[fentanyl first pass pulmonary; sits in lungs and comes back for second peak]]

45
Q

Skeletal muscle effects of opioids

A

Skeletal muscle rigidity
^makes ventilation difficult and sometimes impossible
[[decrease chest wall compliance]]
*give some muscle relaxant

  • laryngeal muscle
  • inhibition of GABA
  • increase in dopamine
46
Q

Renal/ GI/ Liver effects of Opioids

A

increased peristaltic tone of ureters
[[Mu1, kappa and delta receptor activity cause s urinary retention; now they also have a sense of urgency]]

**blocked catecholamine release and cortisol
[[reduced stress response during surgery]]

spasm of sphincter of oddi [[spinchter between GI and gallbladder]]

constipation; decreased GI motility
[[Mu2, kappa and delta receptor activity]]

prolonged gastric emptying
[[indirect effect of Nausea]]
Nausea direct effect –> chemoreceptors

47
Q

How do you treat spasm of sphincter of oddi

A

GLUCAGON

-reverses the spasm

48
Q

Pruritis caused by opioids

A

‘fentanyl nose itch’
cause unknown

histamine release with demerol and morphine can cause the itch

occurs mostly on face and nose

49
Q

Opioids that release Histamine

A

Morphine

Demerol

50
Q

Neuraxial [[epidural]] effects of Opioids

A

opioids placed in epidural space can undergo uptake into

  • fat
  • systemic absorption
  • diffusion into CSF

*diffusion into CSF depends on lipid solubility [[just like all diffusion]]

more lipid soluble drug faster diffusion into CSF; quicker peak CSF concentration

more lipid soluble less cephalad movement bc diffuses into CSF so quickly

less lipid soluble more cephalad movement bc doesn’t diffuse into CSF as quickly

morphine more cephalad movement than fentanyl
[[more less lipid soluble than morphine]]

51
Q

Side effects of neuroaxial [[epidural]] opioid use

A

-purities
‘fentanyl nose itch’

-N/V
[[direct via chemoreceptors
indirect via prolonged gastic emptying GI]]

-urinary retention

-ventilatory depression
[[more rapid with lipophilic agents]]

52
Q

cephalad migration

A

more pronounced in less lipophilic drugs

53
Q

MORPHINE

A

natural occurring; endogenous

poorly lipid soluble; highly ionized and protein bound 
23% nonionized 
35% protein bound 
1 potency
E1/2 t 1.7 - 3.3 hours 
[[DOA 4 hours]]

Histamine Releaser
Active metabolite
Morphine-6-glucuronide

IM peak effect 45 min
IV effect 15-30 min

effects;
analgesia
euphoria
sedation
nausea
purities
dry mouth
ventilatory depression [[slower effect than fentanyl]]
Bradycardia [[direct effect of vagus and inhibition of SA node]]
metabolized by the liver
kidneys –> extra hepatic metabolism or morphine

Renal Failure don’t give morphine

54
Q

Morphine Active Metabolite

A

Morphine-6-glucuronide

** active metabolite stronger than morphine

55
Q

Morphine and Bradycardia

A

DIRECT effect of the vagus nerve and inhibition of SA node

56
Q

What patient should morphine be avoided in

A

RENAL FAILURE

57
Q

Meperidine [[Demerol]]

A

synthetic [[exogenous]]
-Phenylpiperdine

Only Opioid with DIRECT cardiac depressant effects

ACTVIE metabolite;
normeperidine
^lasts ups to 3 days [[can cause seizures]]
only 1/2 as potent as meperidine

structurally similar to atropine
[[exhibits anti-muscarinis effects]]

blocks VGNaC [[like Locals]]

potent alpha 2 receptors agonist
[[calms patient; sedation]]

1/10th as potent as morphine 
7% nonionized
70% Protein bound 
E1/2t 3-5 hours 
[[DOA 2-4]]

produces the same amount of euphoria, sedation and analgesia as morphine; but 1/10th as potent

used to treat post shivering
[[kappa and alpha 2 receptor activity]]

58
Q

Meperidine is the only opioid with

A

DIRECT cardiac depressant activity

59
Q

Active metabolite of meperidine

A

normeperidine

lasts up to 3 days but only half as potent as meperidine

long duration of active metabolite can cause seizures

60
Q

What another use for meperidine

A

treats post op shivering

[[activity on kappa and alpha2]]

61
Q

What patient do you avoid meperidine in

A

Seizure patient

active metabolite hangs around a long time [[risk for seizures]]

62
Q

Hydromorphone [[Dilaudid]]

A

Semisynthetic; analog [[derived]] from morphine

5 potency
[[5 x as potent as morphine]]

DOA [[4 hours]]
need q 4 hour dosing

rapid elimination and redistribution

more sedation
less euphoria
^compared to morphine

63
Q

Fentanyl

A

synthetic [[exogenous]]
-Phenylpiperdine

more lipid soluble than morphine
*faster onset 
100 potency 
[[100 x more potent than morphine]]
8.5% nonionized
84% protein bound

shorter DOA than morphine
[[but DOA can be longer with multiple doses or infusion]]

Very CV stable [[hemodynamic stability]]
**good for helping with HR and BP changes with intubation

75% of initial dose undergoes first pass pulmonary uptake into the lungs

rapid redistribution to inactive tissue;
fat
muscles
lungs

multiple IV doses OR continuous IV infusion can SATURATE inactive tissue
**shut off infusion 45 min- 1 hour before case ends

plasma concentration DOES NOT decrease rapidly
DOA is prolonged
[[2nd peak plasma concentration]]

64
Q

Fentanyl is unique by

A

75 % of initial dose undergoes first pass pulmonary uptake

plasma concentration does NOT decrease rapidly and DOA is prolonged
^2nd peak plasma concentration

large Vd because more lipid soluble

65
Q

Whats causes 2nd peal plasma concentration of Fentanyl

A

75% of initial dose goes to the lungs [[inactive tissue]]

then mobilized from lung

can saturate your reserve [[accumulate in the lungs]] with multiple doses or continuous infusion

DOA can be prolonged from this second peak
**turn infusion off 45 min -1 hour before the case

66
Q

Clinical uses of Fentanyl

A

PAIN
analgesia adjunct for surgery

Blunts stimulation of incision; intubation
[[prevent the SNS response]]

very CV stable
[[large dose can be sole anesthetic]]

wide range of doses
1 - 20mcg/kg
cardiac can be 50 mcg/kg

*fentanyl lollipop for pediatrics
5-20 mcg/kg
*45 min prior to induction

67
Q

Sufentanil

A

Syntheic [[exogenous]]
-Phenylpiperdine
–Fentanyl Analog
[[also undergoes first pass pulmonary effect]]
–CV stable [[like fentanyl]]
[[helps decrease SNS stem with intubation/ incision]]

**most potent

1000 x more potent than morphine
and
10 x more potent than fentanyl

2x more lipid soluble than Fentanyl

20% nonionized
Highly protein bound 93%

ACTIVE metabolite;
Desmethylsufentanil

rapidly metabolized by the liver
E1/2t 2 - 5 hours

68
Q

Active metabolite of Sufentanil

A

desmethylsufentanil

**weak

69
Q

Clinical uses for Sufentanil

A

adjunct for surgery and induction

used as infusion for OUTpatient surgery
*turn off 30 min before; as opposed to 45- 60 with fentanyl
[[QUICK on QUICK off]]

compared to morphine and fentanyl;
produces quicker induction
earlier emergence
earlier extubation

70
Q

Alfentanil

A

synthetic [[exogenous]]
–Phenylpiperdine
–Fentanyl Analog
[[blunt SNS stim]]

10 - 20 x more potent than morphine
1/5th as potent as fentanyl

RAPID onset [[1.4 min]]
89-90% in nonionized state
fent [[6.8 min]]
sufentanil [[6.2 min]]

Highly protein bound 92%
*even though more protein bound than fentanyl; greater diffusion than fentanyl

71
Q

Onset of action

Fentanyl

A

6.8 min

72
Q

onset of action

Sufentanil

A

6.2 min

73
Q

Onset of action

Alfentanil

A

1.4 min

74
Q

Clinical uses of Alfentanil

A

RAPID onset [[1.4 min]]
90% nonionized

useful for blunting hemodynamic responser to noxious stim [[intubation; incision]]

used for infusion in OUTpatient surgery

75
Q

Remifentanil

A

synthetic [[exogenous]]

  • -Phenylpiperdine
    • -chemically similar to fentanyl
      • *unique r/t ester linkage

100 x more potent than morphine
[[slightly more potent than fentanyl]]

-metabolized by tissue/ plasma esterase

  • rapid onset
  • short DOA [[plasma esterase]]

Small Vd

minimal accumulation in tissues even with infusion

76
Q

Clinical uses of Remifentanil

A

blunt noxious stim
[[just like fentanyl and other analogs]]

infusion for intermediate/ long surgeries; where rapid recovery is desired

  • neurosurgery [[scoliosis]]
  • outpatient surgery
  • great for extracting eggs
    [[very painful procedure but once procedure is over pain is gone and patient goes home]]
77
Q

Why is Remifentanil good for neurosurgery

A

able to quickly wake patient up halfway through case to check motor movement/ reflex

78
Q

Agonit/ Antagonist

A

ANTAGONIST at Mu

Agonist at Kappa

NO ventilatory depression !!
less physical dependance

Analgesia with little ventilatory depression

side effects similar to opioid agonist

can have some dysphoria from kappa receptor

[[Kappa receptor effects]]
analgesia [[supraspinal and spinal]]
dysphoria
sedation
mitosis
diuresis

ex. Nalbuphine [[Nubain]]
Butorphenol [[Stadol]]

79
Q

Nalbuphine [[Nubain]]

A

Agonist/ Antagonist

analgesia = to morphine

works on Kappa
[[and sigma]]

antagonizes opioid induced respiratory depression

**analgesia with no ventilatory depression

no adverse CV problems

**reverses spasm of sphincter of Oddi [[antagonizing]]

80
Q

Butorphenol [[Stadol]]

A

Agonist/ Antagonist

agonist on Kappa

weak antagonist or partial agonist of Mu [[dose dependent]]

5 x more potent than morphine for analgesia

**nasal spray for migraines

81
Q

Naloxone [[Narcan]]

A

Antagonist

Pure opioid antagonist

Blocks receptor site;
reverses analgesia and respiratory depression

Competitive antagonist for Mu, Kappa and Delta
[[can be overcome with higher opioid doses]]

DOA less than opioids
[[use trip bc shorter acting than the opioid your reversing]]

Titratable
[[dilute give slowly and tribute drip to effect]]

onset 1-2 min

reversal is dose dependent

Reversal is NOT benign

82
Q

Reversal effects with Narcan

A

tachycardia

HPTN

ventricular dysrhymias

severe pain

pulmonary edema in patient with CV disease
[[pulmonary HPTN, hydrostatic pulmonary edema]]

pulmonary edema in healthy patient
[[catecholamine release, increased SNS activity; that you blunted with opioid, increased preload]]

83
Q

Catecholamines

A

epinephrine

norepinephrine

84
Q

Which opioids produce active metabolites

A

moprhine
[[morphine-6-glucuronide]]

meperidine
[[normeperidine]]

sufentanil
[[desmethylsufentanil]]

Pharmacology (7 decks)

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