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Pharmacology > opiods > Flashcards

opiods Flashcards

1
Q

what are opiods

A

substances, natural and synthetic, that bind to opioid receptors and produce an agonist effect

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2
Q

Opiods can be divided in terms of their chemical structure as follows

A

Phenanthrenes

Benzylisoquinolines

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3
Q

Opiod classification are?

A

Naturally occuring
semisynthetic
synthetic.

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4
Q

NAturally occuring opiod is

A

Morphine

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5
Q

Semisynthetic opiod(Analogs of Morphine) is

A

Heroin
Hydromorphone
Codeine

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6
Q

Name the Synthetic Opiods classes and their examples

A

1.Morphinan derivatives Levorphenol, butorphenol(these are used for Withdrawals)
2.Diphenyl derivatives
Methadone
3.Benzomorphans
Phenazocine, Pentazocine
4.Phenylpiperidines
Meperidine, Fentanyl, Alfentanil, Sufentanil, Remifentanil

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7
Q

OPiod classification and E.g–according to their agonist Agonist Activity

A

Agonist.

Partial agonist
Ie: buprenorphine: regardless of the dose the cannot produce full mu receptor effects like morphine.

Mixed agonist/antagonist
Ie: nalbuphine where agonist at one receptor, kappa and antagonist at mu reversing resp depression

Antagonist: ie: naloxone

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8
Q

OPiate receptors are stimulated by what kind of substances.

A

Endogenous substances

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9
Q

3 endogenous substances identifies in 1973 are

A

enkephalins
endorphins
dynorphins

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10
Q

What is the mechanis,m of action of synthetic opiods

A

Antinociceptive, inhibiting excitatory neurotransmitters ie. substance P
synthetic opioids mimic action of endogenous opioids by binding to opioid receptors

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11
Q

name the 3 types of opiod receptors

A

mu, kappa, and delta

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12
Q

Mu subtype are ? and where are they found in the body

A

MU 1,2,3

Primarily found in the Brain and SPinal Cord

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13
Q

ALl enogenous and Exogenous agonist act on Mu receptors T/F?

A

T

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14
Q

Mu-1 Receptor characteristics

A

*Bradycardia
*Analgesia
*Supraspinal (to a lesser degree spinal) analgesia
Hypothermia
*Miosis
*Urinary retention
*Spinal
*Euphoria
Low Abuse potential

*All endogenous and synthetic opioid agonists act on these receptors

Fentanyl can act here

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15
Q

Mu-2 receptor characteristics

A

Constipation (marked)
Hypoventilation
Physical dependence
Spinal analgesia

All endogenous and exogenous agonists act on these receptors
fentanyl can act here

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16
Q

Kappa Receptor characteristics

A 
Low Abuse potential
Miosis
Supraspinal 
spinal analgesia
Sedation
Dynophines only
Dysphoria
Diuresis

Only dynorphins act on these receptors

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17
Q

Delta receptor characteristics are ?

A 
Constipation (minimal)
Hypoventilation
Physical dependence
Supraspinal and spinal analgesia
Urinary retention
spinal
Enkaphalines

Only enkephalins act on these receptors

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18
Q

Memorize slide 15

A

Do IT NOW

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19
Q

Whats the mech of Action for opiod

A 
Net effect-
Increased potassium conductance
Calcium channel inactivation
Both 
Decrease in neurotransmitter release

Activation of receptors either

  1. directly decreases neurotransmission or
  2. inhibits the release of excitatory neurotransmitters ie Substance P
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20
Q

state opiods Pharmacokinetic characteristics and state how it affects mechanism of crossing,binding and
Onset .

A

Weak bases
Only unionized & unbound opioids can diffuse from blood to target tissue thus…
Higher % unionized the higher diffusible fraction and the faster the onset
Higher % unbound the faster the onset

Increase dose of opiods if acidotic pt.
Decrease dose if alkalotic pt.

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21
Q

Slide 20 Memorise Pharmacokinetics of Opiod Agonist

A

Memorise

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22
Q

what are the Factors that can Alter Pharmacokinetics & dynamics of Opioids

A

Age
*Neonates show decrease rate of elimination d/t immature cyp P450

  • Elderly show greater brain sensitivity to the drug
  • Weight- dose based on lean body mass not actual weight in kg
  • Renal failure
  • Hepatic failure

Base on ideal body weight.

Reduce dose and extend time between doses for renal and liver failure

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23
Q

What is the difference in Mechanism of Action Between Spinal analgesic and Supraspinal analgesic

A

Spinal analgesic effects produced by receptor activation in spinal cord and dorsal root ganglian
Supraspinal analgesia produced by receptor activation in periaquaductal/periventricular gray matter in brain

Spinal in substantia gelatenosa: Direct stimulation of these receptors produces intense analgesia from inhibition of substance P release

Supraspinal in hypothalmus, amygdala. Believed that stimulation of these receptors reduce the transmission of nociceptive information from peripheral nerves into the spinal cord and up the neuraxis.

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24
Q

Perioperative cns Effects of Opiods

A 
Analgesia
Euphoria
Drowsiness/sleep
Respiratory depression
Miosis
Nausea- chemoreceptor trigger zone

Does not produce amnesia or anesthesia

Modest decrease in ICP

Decrease CBF

Advantages of opioids in neuro-anesthesia
Hemodynamic stability
Cerebrovascular stability

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25
Q

what are the Perioperative Cardiovascular Effects

of opiods

A

No impairment in CV function

Dose dependent bradycardia

Tachycardia with meperidine

Myocardial depression with meperidine

Decrease CO and BP
Vasodilation
Dose dependent brady from vagal stimulation

Decrease in CO and BP from vasodilation from histamine release with morphine and demerol. Venodilation decreases BP and CO with other opioids.

26
Q

what are the Perioperative Ventilatory effects of opiods

A

Dose dependent respiratory depression

Decrease compliance in chest wall

Constriction of pharyngeal and laryngeal muscles

Hypercarbia, hypoxia

27
Q

what are happens to resp rate and TV at low doses of opiods

A

Decrease RR with increased Vt (low doses)

28
Q

What happens to RR and TV at High opiod doses

A

Decrease RR and Vt (high doses)

29
Q

What happens to Ventilatory drive with opiods

A

Decrease hypoxic ventilatory drive

30
Q

What happens to resp response curve with opiods

A

Ventilatory response curve reduced and shifted to right

31
Q

Compare resp depression per onset and duration btwn Morphine and fentanyl

A

Peak onset of respiratory depression is slower for morphine than fentanyl

Respiratory depression produced by morphine lasts longer than fentanyl

32
Q

what are the factors that increase the magnitude/Duration of opiod-induced resp Depression

A

Increased dose

Intermittent bolus vs. cont. infusion

Speed of injection

Concurrent admin with other anesthetics

Synergistic effects

Decreased clearance

Age(Baby and elderly reduce dose pls)

Dont give drugs fast.

Alkalosis- increase unionized fraction increases brain penetration of drug

Secondary peaks in plasma levels from reuptake of opioid from muscle, fat, lung and intestine

33
Q

Opiod perioperative skeletal muscle effect

A 
Skeletal muscle rigidity-
Laryngeal muscles 
Inhibition of GABA
Increase in dopamine
Can make ventilation difficult or impossible
34
Q

Opiods PerioperativeRenal/GI/Liver Effects

A

Increase peristaltic and tone of ureters
Urgency

Blocked catecholamine release and cortisol

Spasm of sphincter of Oddi with increase in biliary pressure

Constipation-decrease GI motility

Prolonged gastric emptying

35
Q

What are causes and characteristics of Pruritic effects with opiod

A

Cause unknown
Histamine release most probable cause with some
Occurs primarily on face particularly nose
“fentanyl nose itch”

36
Q

Opiods Neuraxial effects and what determines diffusion into CSF

A

Opioids placed in epidural space may undergo uptake into
fat

systemic absorption
diffusion into CSF
Penetration into CSF depends upon lipid solubility
More lipid soluble, quicker peak CSF concentration

37
Q

What is the mechanism of Cephaladad migration

A

Drugs that do not penetrate csf or get into circulation are not lipid soluble.They travel Cephalad into the brain.
Cephalad movement of opioid in the CSF depends on lipid solubility
Highly lipid soluble will be limited in migration by uptake into the spinal cord ie. fentanyl
Whereas less soluble opioid will remain in CSF for transfer to cephalic location ie. morphine

Fentanyl penetrates csf and gets into circulation
Mso4 does not get absorbed at much..
Cephalad migration more pronounced with less lipollic drugs like morphine

38
Q

What does vascular absorption into epidural space depend on per opiods

A

Vascular absorption of opioid from epidural space depends on lipid solubility
More lipid soluble, quicker peak concentrations of opioid will be in blood
…in fact…effects may be due to systemic absorption rather than CSF

39
Q

What are the side effects of Neuraxial opiods

A 
Pruritis-most common
Nausea/vomiting
Urinary retention
Ventilatory depression
More rapid with lipophilic agents
Delayed with less lipophilic (6-12hrs)
40
Q

Morphine characteristics and effects

A

Causes bradycardia via direct stimulation of vagus nerve

Inhibition of SA node as well

Metabolized by liver

Active metabolite: morphine-6-glucuronide (M6G) > potency than MSO4

Kidneys play a key role in the extrahepatic metabolism of morphine

Renal failure will have effects due to M6G

41
Q

Meperidine characteristics and effects

A

Structurally similar to atropine, exhibits muscarinic effects

Also similar to local anesthetics-blocks Na Channels

Potent at alpha-2 receptors agonist effects

DOA 2-4 hours
Produces same amount of euphoria, sedation and analgesia as morphine

Normeperidine: active metabolite lasting 3 days, ½ as potent-CNS stim-szs reported

Used to treat postop shivering-kappa and alpha-2 receptors activity

1/10th as potent as morphine

Direct cardiac depressant
Alpha 2 agonist
Normeperidine last long time
Seizures

42
Q

Hydromorphone characteristics and effects

A 
5 X more potent than MSO4
Derivative of MSO4
Rapid elimination and redistribution
Q 4 h dosing needed
More sedation but less euphoria than MSO4
43
Q

Fentanyl characteristics and effects

A

More lipid soluble than morphine with shorter DOA - 75% of initial dose undergoing first pass pulmonary uptake.

Rapid redistribution to inactive tissue sites as fat, skeletal m. and lungs.

Multiple IV doses or cont. infusion produces progressive saturation of inactive tissue.

Plasma concentration does not decrease rapidly and DOA is prolonged-(secondary to peak in plasma levels.

Fentanyl produces secondary peak in plasma levels. This is due to immobilization of sequestered drug form inactive tissue sites. Accumulates with multiple doses.

Clinically impression that fentayl shorter DOA than MSO4 but can have longer DOA if infusion or multiple doses.
Has large volume of distribution secondary to more lipid soluble than MSO4 and plasma conc. maintained by slow reuptake from inactive tissue sites

44
Q

Fentanyl Use and clinical significance

A

Used as analgesic adjunct for surgery.
As adjuvant to blunt stimulation of incision, laryngoscopy.
As sole anesthetic in large doses due to hemodynamic stability.
100 times more potent than morphine.
Wide range of doses given 1-20 mcg/kg
Lozenges (fent lollipop) 5-20mcg/kg 45 minutes prior to induction

Transdermal patch 75-100mcg/hour peak 18-24 hours left on for 72 hours

45
Q

Sufentanyl characteristics and effects

A

Analogue of fentanyl
Twice as lipid soluble as fentanyl
Highly protein bound

Undergoes first pass pulmonary uptake

Rapidly metabolized in liver

Weakly active metabolite desmethylsufentanil

10 times more potent than fentanyl.

1,000 times more potent than morphine

46
Q

What are the Sufentanil Clinical Significance

A

Used as adjunct for surgery and induction.
Compared to morphine and fentanyl produces quicker induction earlier emergence and earlier extubation.
Used as infusion for outpatient surgery.

47
Q

what are the characteristics and effcts of Alfentanil

A

Analogue of fentanyl.

90% exists in unionized state= very rapid CNS onset (1.4 minutes compared to fentanyl, 6.8 and sufentanil, 6.2 minutes).

Highly protein bound

Despite more intense protein binding, alfentanil’s diffusible fraction is higher than that of fentanyl.

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

48
Q

what are the Alfentanil Clinical Significance

A

Rapid onset is useful for blunting hemodynamic response to noxious stimuli.
Rapid effect due to 90% of drug in non-ionized form.
Used as infusion for outpatient surgery.

49
Q

what are the characteristics and effects of Remifentanil

A

Chemically r/t fentanyl but unique d/t ester linkage.

Metabolized by tissue/plasma esterases (not pseudocholinesterases).

Rapid onset and duration.

Very small Vd, minimal accumulation in tissues, even with infusion.

Potency similar to fentanyl, 100 times more potent than morphine.

Used for Egg retrieval

50
Q

Remifentanil Clinical significance

A

Used to blunt noxious stimulus.

Infusions for interm/long surgeries where rapid recovery is desired.

Such as-neurosurgery, O/P surgery

51
Q

What are the MU antagonist and Partial agonist effects

Where else can they have a partial agonist effect

A

Mu antagonist/partial agonist, and partial agonist at kappa.
Analgesia with limited ventilatory depression and low probability of dependence.
Side effects sim. to opioid agonists.
May cause dysphoria-kappa receptors stimulation.

pentazocine, butorpheno, nalbuphine,
dezocine

52
Q

what are the charateristics and effects of Nubain

A 
Analgesic response equal to morphine.
Works at kappa and sigma receptors.
Antagonizes opioid induced respiratory depression while maintaining analgesia. 
No adverse CV problems.
Reverses spasm of sphincter of Oddi.
53
Q

Butorphenol (stadol)

characteristics and effects

A

Acts as agonist at kappa and weak antagonist or partial agonist at mu.

5 times more potent than morphine for analgesia.

Nasal spray for migraines

54
Q

NAloxone Characteristics and effects

A

Pure opioid antagonist

Blocks receptor sites and reverses respiratory depression and analgesia

Competitive antagonist at mu, kappa, and delta

Duration of action less than most opioids

Titratable
must give slowly

Onset 1-2 minutes, reversal is does dependent.

55
Q

What are the effcts of opiod reversal using Naloxone

A

Not benign.

Reversal of opioid effect you get tachy, HTN, ventricular dysrhythmais, severe pain also pulm edema.

Pulmonary edema in patients with CV disease.

Can induce pulmonary edema in healthy patients due to catecholamine release.

Reversal may cause hydrostatic pulm edema
Increase in sympathetic effects

56
Q

Drug doses Slide 56

A

Pls review

SRFA and SFRA

57
Q

How does Opioid receptor activation work to decrease pain

A

The principal effect of opioid receptor activation is a decrease in neurotransmission.8 This decrease in neurotransmission occurs largely by presynaptic inhibition of neurotransmitter release (acetylcholine, dopamine, norepinephrine, substance P), although postsynaptic inhibition of evoked activity may also occur

increased potassium conductance (leading to hyperpolarization), calcium channel inactivation, or both, which produce an immediate decrease in neurotransmitter
release

58
Q

What is the principal manifestation of opioid overdose

A

depression of ventilation manifesting as a slow breathing frequency, which may progress to apnea

59
Q

Whats is the triad of opioid overdose

A

Miosis, hypoventilation, and coma should suggest overdose with an opioid.

60
Q

Tolerance develops to analgesic, euphoric, sedative, depression of ventilation, and emetic effects of opioids but not to their effects on what?

A

Miosis and bowel Motility

61
Q

What are the symptoms of withdrawal per opiods

A

yawning, diaphoresis, lacrimation, or coryza. Insomnia and restlessness are prominent. Abdominal cramps, nausea, vomiting, and diarrhea reach their peak in 72 hours and then decline over the next 7 to 10 days.

Pharmacology (9 decks)

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