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SRNAPharmacology II > Opiods Agonist/Antagonists > Flashcards

Opiods Agonist/Antagonists Flashcards

1
Q

3 types of Opioids class

A

Opioid agonist Opioid antagonist Opioid agonist-antagonists

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2
Q

Opioids derived from

A

Opium, meaning juice

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3
Q

Narcotic is a greek word for

A

Stupor

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4
Q

Why is opiod unique?

A

Produces analgesia without loss of proprioception, touch or consciousness

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5
Q

Bind to receptor site to elicit a response definition

A

Agonist

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6
Q

ONLY this form have an AGONIST ACTIVITY

A

LEVOROTATORY

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7
Q

Blocks agonist from binding

A

Antagonist

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8
Q

Opiod agonist-antagonists

A

partially bind to mu receptors produces a limited response (partial Agonist) or no effect (competitive antagonist)

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9
Q

SEMI SYNTHETIC OPIOIDS are (CHOO)

A

Codeine Heroin Hydromorphone Oxycodone

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10
Q

Semisynthetic opiods are

A

modified morphine molecule

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11
Q

Synthetic opiods are FSAR MMT

A

Fentanyl, Sufentanyl, Alfentanyl, Remifentanyl Methadone, Meperidine, Tramadol

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12
Q

Mechanism of action : opiods in ______State bind stroly at _______opioid receptor site

A

ionized; anionic

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13
Q

Opioid agonists and neurotransmitters

A

inhibit neurotransmitters pre and post synaptic

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14
Q

IN CNS opioid action is

A

Brainstem and spinal cord

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15
Q

IN PNS opioids on

A

Primary afferent neurons

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16
Q

Opioids on primary afferent neurons are activated by 3 endogenous peptide opioid receptor ligands which are?

A

Enkephalins Endorphins Dynorphins

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17
Q

Opiods and endogenous ligands?

A

they mimic the endogenous ligands

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18
Q

Raphe magnus ligand

A

Enkephalin

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19
Q

Periventricular nuclei and periaqueductal grey

A

Morphine and dynorphin

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20
Q

What is the principal effect of opiod receptor activation?

A

Decrease neurotransmission

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21
Q

How do opiods prevent neurotransmitter release?

A

Due to presynaptic inhibition of Ca2+ channels which reduce the neurotransmitter release.

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22
Q

Opiods block the release of these neurotransmitters (ADNSS)

A

Ach, Dopamine, Norepinephrine, Substance P, Serotonin

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23
Q

Pre-synaptic opioid receptor is a

A

GPCR

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24
Q

What is the mechanism of presynaptic activity?

A

Leads to a decrease in cAMP decrease in Ca2+ ion influx and inhibits the release of excitatory neurotransmitters

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25
Q

Excitatory neurotransmitters blocked, (2)

A

Glutamate Susbtance P

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26
Q

Post synaptic opioid receptor action

A

Inhibit DEPOLARIZATION of neuron by inhibiting the production of adenylate cyclase , thereby inhibiting ion channel (Na and Ca) Inactviation of K+ channels lead to hyperpolarization of the cell

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27
Q

All opioid receptors are

A

G protein coupled receptors that INHIBIT ADENYLATE CYCLASE leading to decrease in cAMP

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28
Q

With opiod the resting MP becomes more ______ leading to _______of neuron to propagate a signal. There is ________ neuronal activity

A

negative, inability; decrease

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29
Q

The receptors mu, kappa and delta are all

A

GPCR with same mechanism of action, decrease cAMP

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30
Q

Mu and Morphine types of anesthesia

A

Supra spinal spinal

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31
Q

Mu 1 produces analgesia with ELMUH

A

Euphoria, low abuse potential, miosis, URINARY RETENTION, Hypotethermia

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32
Q

Mu 1 and Mu 2 agonist are EMS

A

Endorphins Morphine Synthetic opioids

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33
Q

Mu 2 responsible for CHAP marked

A

Constipation marked, hypoventilation, analgesia (spinal) and physical dependence

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34
Q

Kappa receptors responsible for (low SAD MD)

A

Low abuse potential, SEDATION, Analgesia (s+s) DYSPHORIA, MIOSIS, DIURESIS

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35
Q

Kappa agonist receptors - dynorphins inhibit

A

N-type Ca2+ channels leading to analgesia

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36
Q

Kappa agonists _____Respiratory depression

A

Less

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37
Q

Kappa agonists may cause

A

DIURESIS and DYSPHORIA

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38
Q

May be resistant to analgesic effect of Kappa

A

High intensity painful stimulation

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39
Q

On which receptor does OPIOD AGONIST- ANTAGONIST act principally?

A

KAPPA receptors

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40
Q

Delta receptors responsible for (PACUVA) minimal

A

Physical dependence, analgesia S+S, constipation minimal, urinary retention, ventilatory depression, antidepressant

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41
Q

Receptor to have ONLY SPINAL anesthesia efect

A

Mu 2

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42
Q

Receptor associated with marked constipation

A

Mu 2

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43
Q

Receptors associated with urinary retention

A

Mu 1 and delta

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44
Q

Receptor associated with low abuse potential

A

Mu 1 and kappa

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45
Q

Receptor associated with SEDATION

A

Kappa

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46
Q

Receptor associated with DIURESIS and DYSPHORIA

A

Kappa

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47
Q

Receptor associated with EUPHORIA

A

Mu 1

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48
Q

Opioids receptors are in the

A

Brain and spinal cord

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49
Q

Where in the brain are opiods receptors (PACH)

A

Periaqueductal gray matter of brainstem, amygdala, corpus striatum, and hypothalamus

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50
Q

Where in the spinal cord are opiods receptors

A

SUBSTANTIA GELATINOSA dorsal horn

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51
Q

Principal receptor in spinal cord

A

Mu

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52
Q

Endorphins inhibit release of

A

Neurotransmitters

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53
Q

Opiods given Neuraxial are not associated with

A

SNS denervation, Skeletal muscle weakness, loss of proprioception

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54
Q

Epidural dose vs subarachnoid which is stronger

A

Epidural 5-10 times subarachnoid dose

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55
Q

Epidural separated by

A

Dura and arachnoid

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56
Q

Path of opiods in epidural space

A

Undergoes uptake in epidural fat –> systemic absorption –> diffusion across the dura into CSF

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57
Q

What penetrates dura faster? (solubility / molecular weight)

A

HIghly lipid soluble, low molecular weight.

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58
Q

CSF concentration of sufentanyl peaks in

A

6 min

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59
Q

CSF concentration of Fentanyl peaks in

A

20 min

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60
Q

CSF concentration of MORPHINE peaks in

A

1-4 hours

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61
Q

Spinal cord ends at

A

L1

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62
Q

What is the most common location for epidural

A

LUMBAR spine, (largest region)

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63
Q

Epidural administration of morphine, sufentanyl and fentanyl mimics

A

IM injection

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64
Q

When Epinephrine administered with opioid it

A

Decreases systemic absorption

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65
Q

Subarachnoid (Intrathecal) LIPID soluble opiods? meaning Absorption in CSF is

A

Fentanyl , rapid absorption in CSF

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66
Q

Subarachnoid (Intrathecal) WATER Soluble opiods meaning Absorption in CSF is _________, meaning may cause _____

A

MORPHINE , no absorption, float in CSF, may cause delayed apnea

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67
Q

When subarachnoid morphine and EPINEPHRINE

A

Increase block density Decrease intravascular absorption Prolong duration of action of lipid soluble anesthetics no effect on protein bound LA.

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68
Q

Side effects of Neuraxial (PNUDS CVS NeWa)

A

Pruritus, N/V, Urinary retention, depression of ventilation, sedation, CNS excitation, viral reactivation, sexual ocular, GI thermoregulation, water retention, neonatal morbidity.

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69
Q

The side effects seen with neuraxial opiods administration is caused by

A

opiods in CSF and in systemic circulation

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70
Q

Side effect of neuraxial opiods that are dose dependent PNUR

A

Pruritus, N/V, Urinary retention, Respiratory depression

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71
Q

The most common out of the side effect of neuraxial opiods? characterized by

A

PRURITUS Localized FUN (localized in face, upper thorax, neck)

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72
Q

What can neuraxial opiod related pruritus treated wtih

A

BUPRENEX, treat without reversing analgesia

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73
Q

Urinary retention with neuraxial more common with

A

Young males

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74
Q

What is the mechanism of urinary retention with neuraxial opioid?

A

Interaction of the opiod with sacral spinal cord PNS sacral inhibition, detrusor muscle relax, increase bladder capacity,—> ↑ retention

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75
Q

Morphine can cause marked detrusor relaxation in ______ can last ____

A

15 min 16 hours

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76
Q

Most serious side effect of opioid

A

Respiratory depression

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77
Q

No respiratory depression after

A

24 hours

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78
Q

What is the respiratory depression caused by ?

A

Cephalad migration of opioid in CSF and interaction with receptors in ventral medulla

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79
Q

Increase risk of respiratory depression

A

-Concomittant use of opiod of sedative use -High opiod use, low lipid solubility of opiod - Lack of opiod tolerance, advanced age - Increased intrathoracic pressure

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80
Q

Diagnosis of respiratory depression

A

↓ MV, ↓RR, ↓SPO2, somnolence →apnea, CP arrest

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81
Q

Sedation effect is dose related more common with

A

SUFENTANYL

82
Q

What is the sedation effect of sufentanyl caused by?

A

Due to interaction with non-opioid receptors in brainstem and Basal ganglia →Blocks glycine or GABA inhibition

83
Q

Viral reaction and opioid in OB patients

A

Theres been a link found between OB patients with REACTIVATION of herpes virus with EPIDURAL MORPHINE

84
Q

For Epidural,use only

A

preservative free

85
Q

Morphine : dull vs sharp pain

A

Better for dull

86
Q

In absence of pain, morphine causes

A

DYSPHORIA rather than Euphoria

87
Q

Morphine peak IV

A

15-30 mins rapid onset

88
Q

Morphine Peak IM

A

45-90 mins

89
Q

Hyperventilation will make blood more _______ and Increased _______fraction, increase passage to CNS

A

Alkaline, nonionized

90
Q

Hypoventilation (respiratory acidosis) will ______nonionized portion may lead to higher CNS concentration due to _______CBF and _______CO2 levels

A

increase; increase; increase

91
Q

Morphine rapidly accumulated in

A

liver, kidneys, skeletal muscles

92
Q

Metabolism of morphine : What is the principal pathway

A

Conjugation with GLUCURONIC ACID in hepatic, and extra hepatic (kidneys)

93
Q

Metabolism of morphine: Principal metabolite

A

Morphine-3- Glucuronide 75-80% inactive

94
Q

Metabolism of morphine: metabolite more potent than morphine

A

Morphine -6- Glucuronide 5-10%

95
Q

Morphine vs M6G

A

More potent, longer duration

96
Q

MAOIs and morphine

A

MOAI inhibit formation of glucuronide metabolites →exaggerated effects (can’t metabolize)

97
Q

Morphine metabolites excreted via

A

Urine

98
Q

_____Significant contribution to total metabolism

A

Renal metabolism

99
Q

Renal impairment and morphine

A

Accumulation of metabolites and UNEXPECTED resp depression.

100
Q

With morphine, decrease in plasma concentration after initial distribution is due to

A

METABOLISM

101
Q

Greater analgesis potency of morphine in

A

women

102
Q

Higher post op consumption in

A

Men

103
Q

Morphine high dose? will it have major effect on supine normovolemic patient?

A

1mg/kg; UNLIKELY to cause myocardial depression

104
Q

Change to supine to standing may cause ____and _______why?

A

Hypotension + syncope impairment of compensatory sympathetic NS response ↓vasomotor tone leading to ↓preload, CO and BP

105
Q

How to reduce morphine induced bradycardia

A

caused by histamine release give 5mg/min, supine, well hydrated patient

106
Q

Bradycardia associated with morphine mechanism

A

↑ activity of vagal nerve ↑stimulation of vagal nuclei Decrease SA node to AV conduction

107
Q

Produce histamine release substantially

A

1mg/kg over 10 min

108
Q

Which dose of opiods not causing histamine release?

A

Fentanyl 50mcg/kg over 10min

109
Q

What prevents the histamine release

A

Pretreatment w/ H1 and h2 blockers, does not prevent release but prevent changes in SVR and BP

110
Q

Opiods and nitrous may cause

A

CV depression

111
Q

All opiods cause dose dependent + depression of ventilation why?

A

Due to agonist effect @ MU2, ↓ brainstem ventilatory center characterized by ↓ responsiveness to CO2

112
Q

Codeine effect on cough

A

↓cough by effect on MEDULLARY COUGH center

113
Q

Morphine action on airway

A

↑ airway resistance ↑ Bronchial smooth muscle contraction ↑ histamine release

114
Q

With HYPOVENTILATION , morphine ____CBF and ICP

A

INCREASE

115
Q

With HYPERVENTILATION , morphine ____CBF and ICP

A

DECREASE

116
Q

Rapid administration of morphine may lead to _______

A

Skeletal muscle rigidity

117
Q

Risk from Greatest to least as far as skeletal or abdominal and thoracic rigidity

A

Fentanyl > Remifentanyl > Morphine

118
Q

Opiods and the biliary tract

A

may cause spasm of biliary tract Increase intrabiliary pressure associated with epigastric distress and biliary colic

119
Q

Equal doses of opiods increase bile duct pressure percentage for each agent

A

Fentanyl 99% Meperidine 61% Morphine 53%

120
Q

What my reverse opiod induced biliary smooth muscle spasm

A

Glucagon 2mg IV

121
Q

Morphine and peristaltic

A

Decrease peristaltic contraction, increase tone of pyloric sphincter

122
Q

First mechanism of opiod induced N/V due to

A

Direct stimulation of chemoreceptor trigger zone in floor of fouth ventricle

123
Q

2nd mechanism of opioid induced NV due to

A

may act as partial dopamine agonist

124
Q

3rd MOA of opioid induced NV

A

Caused by increase GI secretions and delayed passage of interstinal contents.

125
Q

Why erythemia and urticaria at injection site

A

Histamine release

126
Q

Morphine cause neonatal resp depresion because

A

immature BBB, chronic opioid use by mom

127
Q

Giving narcan to mother can

A

lead to life threatening NEONATAL ABSTINENCE SYNDROME

128
Q

Morphine and drug interaction. Respiratory depression exaggerated by (TAMP)

A

TCAs Amphetamines MAOIs Phenothiazine

129
Q

Tolerance and physical dependence can happen with

A

All opiods

130
Q

How long does tolerance takes to develop

A

2-3 weeks

131
Q

Tolerance develops to _____, ______, _______, _______ (SEDA-em)but not to ______And _________

A

Sedation, euphoric, depression of ventilation, analgesia , and emetic NOT to MIOSIS and CONSTIPATION

132
Q

Initial withdrawal symptoms are DYL RIC

A

Diaphoresis, yawning, lacrimation, restlessness, insomnia, coryza

133
Q

When does the abd pain, NV peak

A

72 hours

134
Q

Prevention of withdrawal with ______MOA?

A

Clonidine - diminishes transmission in sympathetic pathway in the CNS and prevent withdrawal

135
Q

What is the principal manifestation of overdose

A

Respiratory depression

136
Q

Pupils are ____ and_____Unless there is severe hypoxemia _____

A

symmetric; miotic; mydriasis

137
Q

What is the triad of OPIOD overdose (MCH)

A

MIOSIS HYPOVENTILATION COMA

138
Q

Overdose treatment

A

Mechanical ventilation Narcan 0.4 - 2mg q 2-3 mins

139
Q

After ____Mg of narcan question diagnosis

A

10

140
Q

Continuous infusion of narcan dose

A

0.8mg/kg/hr (may cause withdrawal)

141
Q

What are analogues of Meperidine –> FSAR

A

Fentanyl, Sufentanyl, Alfentanyl, Remifentanyl

142
Q

Meperidine potency vs morphine

A

1/10 th

143
Q

Duration of meperidine

A

2-4 hours

144
Q

Meperidine metabolism

A

90% to NORMEPERINE via demethylation

145
Q

Route elimination for meperidine

A

urinary

146
Q

Renal failure and meperidine

A

accumulation of NORMEPERIDINE metabolites → increase risk for Seizures

147
Q

Normal kidney meperidine clearance? kidney issues?

A

15 hours >35 hours

148
Q

Meperidine half time

A

3-5h

149
Q

Meperidine protein binding is ___% which in elderly

A

60; decrease binding, increase plasma

150
Q

Principally use for analgesia during L&D

A

Meperidine

151
Q

What are responsible for the anti-shivering effect of Meperidine?

A

Stimulation of kappa 10% of drug activity also a potent alpha 2 agonist

152
Q

Also use for post op shivering

A

Clonidine

153
Q

Side effects of MEPERIDINE

A

Orthostatic hypotension (worse than morphine)

154
Q

Meperidine may also cause

A

Serotonin syndrome ( HTN, Diaphoresis, hyperthermia)

155
Q

Fentanyl potency compared to morphine

A

100 times more potent

156
Q

Onset and duration of fentanyl compared to morphine

A

Rapid onset and shorter duration of action due to its rapid redistribution to tissue

157
Q

Fentanyl upon administration : % undergoes

A

75% undergoes rapid 1st pass PULMONARY uptake limiting amount reaching systemic circulation

158
Q

Effect equillibration time of fentanyl

A

6.4 min

159
Q

Fentanyl metabolism

A

N-demethylaton –> Norfentanyl , detectable for 72 hours, NOT ACTIVE

160
Q

Elderly have increase half time due to

A

Decrease clearance, Decrease Hepatic blood, decrease albumin, decrease hepatic enzymes activity

161
Q

2 hours continuous infusion

A

FASR graph, saturation of inactive tissues with prolonged infusion

162
Q

Cardiopulmonary bypass

A

Decrease plasma concentration of opioids Decrease greater with fentanyl, less with alfentanyl and sufentanyl

163
Q

Fentanyl dose for analgesia

A

1-2mg/kg

164
Q

As adjunct to inhaled anesthetics to blunt tachy and HTN associated with laryngoscopyq

A

2-20mcg/kg

165
Q

High dose produce surgical anesthesia

A

50-150mcg/kg

166
Q

High dose of fentanyl produce

A

stable hemodynamic, no CV depressant , no histamine release

167
Q

No histamine release with

A

Fentanyl

168
Q

Fentanyl depresses

A

Carotid sinus baroreceptor reflex control of heart rate

169
Q

Morphine and fentanyl more bradycardia with

A

Fentanyl

170
Q

Increase in ICP with

A

Fentanyl and sufentanyl

171
Q

Sufentanyl potency

A

5-10 more potent than fentanyl

172
Q

Effect site equillibration of Sufentanyl

A

6.2 min

173
Q

Protein binding of Sufentanyl

A

92.5% low Vd, significant 1st pass metabolism

174
Q

Termination of action of sufentanyl via

A

Redistribution

175
Q

Dose of Sufentanyl

A

0.1 -0.4mcg/kg

176
Q

Compared to fentanyl, sufentanyl cause

A

longer analgesia, less ventilatory depression, Rapid induction , early emergence

177
Q

SE of Sufentanyl

A

Chest wall rigidity, N/V , bradycardia

178
Q

Alfentanyl potency

A

1/5 - 1/10 less potent

179
Q

Use of Alfentanyl

A

Laryngoscopy Retro bulbar block

180
Q

Alfentanyl ; Rapid effect equilibration time of _____Why?

A

1.4min ; cause of low pKa 90% in NI form

181
Q

Do not use in parkinson patients

A

Alfentanyl

182
Q

General dose of Alfentanyl

A

5-15mcg/kg q5-20 min

183
Q

Remifentanyl acts on which recepotr

A

Mu receptor

184
Q

Potency of remifentanyl

A

15-20 times more than alfentanyl similar potency to fentanyl

185
Q

Metabolism of REMIFENTANYL

A

Hydrolysis by non-specific plasma tissue esterases

186
Q

What is the only opiod metabolized by the liver? and also not affect by ?

A

REMIFENTANYL ; renal disease

187
Q

3 REASONS remifentanyl is good

A

rapid onset , short duration of action NON cum effect Rapid recovery after d/c

188
Q

How long does it take for remifentanyl to reach steady state ______ complete offset in ______ clearance rapid at ____L/min

A

10 mins; 6-8 min; 3

189
Q

Use for transient analgesia with retra bulbar block

A

1 mcg/kg over 60-90 sec

190
Q

Disadvantage of REMI

A

Short duration,POST OP PAIN SIGNIFICANT

191
Q

Codeine half life equivalent to asa Histamine release : y/n

A

3-3.5 hr 60 mg to 650 ASA 120mg IM = 10mg yes

192
Q

Dilaudid potency to morphine

A

8 times more potent, shorter duration (every else as morphine)

193
Q

Tramadol is a

A

Central acting, moderate on mu, weak on kappa and delta

194
Q

Tramadol compared to morphine MOA Dose Disadvanage:

A

5-10 times less potent than morphine Inhibit NE and serotonin neuronal uptake 3mg/kg Ceiling effect seizure

195
Q

OPIOD AGONIST - ANTAGONIST

A

Butorphanol- stadol Nalbuphine - NUBAIN

196
Q

Narcan

A

HIGHER affinity to opiod receptor, prevent agonists from binding

197
Q

Pruritus treated with

A

Narcan , nalbuphine

198
Q

Dose of NARCAN

A

1-4mcg/kg

199
Q

Narcan metabolized by

A

LIVER

200
Q

Vomiting occurs with narcan but

A

It occurs with awakening, meaning patient can protect their airway.

201
Q

GRAPH for Context (FASR)

A

SRNAPharmacology II (32 decks)

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