Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

HHD 2 and Pharma > Opioid Analgesics > Flashcards

Opioid Analgesics Flashcards

1
Q

What are the 3 opioids given at each step of the WHO three-step analgesic ladder

A
  • Non-Opioids e.g e.g. Paracetamol or NSAIDs (Aspirin)
  • Weak- Opioids e.g. Codeine, Tramadol
  • Strong Opioids e.g. Morphine, Fentanyl
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the pain relief ladder associated with ?

A

Cancer pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is given with opioids to help manage pain

A

Given an Adjuvant which is not typically used for pain, but helps with the management e.g. antidepressants (Amitriptyline), anticonvulsants (Gabapentin, Carbamazepine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

History of Opioids:
- Where does the word opium stem from ?
- How many alkaloids does opium contain?

A

Greek for juice of the poppy

  • Contains 20 distinct alkaloids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
  • Who extracted morphine from poppy plant and in which year?
A

Friedrich Serturner in 1806

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

in which year did the proposal that opioids produce analgesia through receptor interaction occur ?

A

1950s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When was synthetic morphine developed and why

A

1921 - synthetic morphine (hydromorphine) developed – more potent less neurotoxic effects - Narcotics (opiates, opioids and derivatives)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Who and when was it discovered that endogenous opiates active opioid receptors

A

1975 and by Hughes & Kosterlitz they proposed and discovered that endogenous opiates activate opioid receptors (enkephalins (brain), endorphins, dynorphins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define Opioids and Opiates and highlight the differences between them

A

Opioid: any substance (endogenous or synthetic) that produces morphine-like effects, blocked by antagonists (naloxone)

Opiate: compounds such as morphine and codeine (only endogenous) that are found in the opium poppy

  • Opiates are only endogenous but opioids can be synthetic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Define an Analgesic drug
Define a Narcotic analgesic

A

Analgesic: a drug or agent which relieves and prevents pain without causing loss of consciousness

Narcotic analgesics: old term for opioids (induce sleep), hijacked as a generic term for drugs of abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Rank the analgesic effect of morphine, codeine and diamorphine (heroin)

A
  1. Diamorphine /diacetylmorphine
  2. Morphine
  3. Codeine
  • The potency increases with the increase of the diacetyl groups
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Therapeutic uses of Opioids:
What are the 4 main therapeutic categories/effects of opioids?
Provide details for each therapeutic category /effect

A
  1. Analgesia (Pain) – acute and chronic
    Limbic System: Euphoria effect
    Cortex/Midbrain: Antinociceptive
    Alters perception to pain
  2. Dyspnoea (Breathlessness)
    Medulla: reduced sensitivity to hypoxia
    Treat shortness of breath associated with Acute pulmonary oedema and myocardial infarctions
  3. Depression of Cough Reflex
    Brainstem cough centre at the receptor level - Antitussive effect (stops coughing )
  4. Diarrhoea Stomach/Intestines: increase tone, reduce motility and delay the transit time so we can get –>
    Associated with increased water and electrolyte reabsorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Unwanted effects of Opioids:
What are the 5 unwanted effects of opioids?
Provide details for each effect

A

Overstimulation can cause the following:
1. Respiratory Depression
Brainstem: reduced sensitivity of respiratory centre to arterial carbon dioxide

  1. Constipation:
    GI tract myenteric plexus: reduce gastric emptying, increase tone, reduce motility
  2. Nausea & Vomiting
    Medulla Chemoreceptor Trigger Zone
  3. Pruritus (Itching)
    Mast cell: histamine release leading to Urticaria (hives)
  4. Bronchoconstriction
    due to Mast cells releasing histamine
    Contraindication: asthmatic patients
  5. Pupil constriction
    Oculomotor Nucleus: stimulation
    Observed in opioid-dependent drug users
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Descending pain control system:
Where along the nociceptive pathway do opioids have an effect

A

Opioids have an effect at the dorsal horn of the spine -> where excitation of transmission neurons occurs -> b4 transmission continues to travel to the brain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do opioids have an effect along the nociceptive pathway?

A

Bind to receptors on the Descending pain pathway from the midbrain and brainstem and have an inhibitory effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where are the opioid receptors found? and give the specific names

A

These receptors can be found in the
The cortex of the brain: A: amygdala, IC: insular cortex and H: hypothalamus
Midbrain : PAG: periaqueductal grey
Medulla of the brain: RVM: rostroventral medulla
Spinal cord: DH: dorsal horn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 3 ways opioids cause analgesia?

A

BY :
- Activating the descending pathways
- Inhibiting transmission in the dorsal horn
- Inhibiting excitation of sensory nerve terminals in the periphery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the 2 opioid MoA?

A
  1. Pre-Synaptically :
    Opioids bind to the opioid receptors –>
    Inhibiting Ca2+ channels from opening - so there’s no influx of ca2+ so no neurotransmitters are released –>
    Reduction in NT release into the synaptic cleft
    BUT Excitation is possible through the inhibition of inhibitory neurones
  2. Post - Synaptically
    Opioids bind to the opioid receptors –>
    Open K+ channels
    Facilitate hyperpolarising as K+efflux across the plasma membrane
    Limiting neuronal excitability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What regulates the opioid euphoric feeling

A

the Limbic system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What regulates the opioid Antinociceptive (pain relief) effect ?

A

the Cortex/Midbrain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What regulates the opioid Antinociceptive (pain relief) effect?

A

the Cortex/Midbrain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the 5 route of opioid administration?

A
  1. Oral: and be sublingual
  2. Injection: intravenous, intramuscular, subcutaneous
  3. Transdermal patch: epidermal
  4. Intrathecal opioid infusion: administered via an implantable infusion pump in the spinal cord- (long-term chronic pain)
  5. Patient-controlled analgesia (PCA): a pump that allows you to take control of your pain relief
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are 2 common examples of Opiate analgesics?

A

Morphine and Codeine - found naturally in poppies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the Main Pharmacological effects of morphine?

A

Morphine (1806)
Main pharmacological effects: analgesia, euphoria, sedation, respiratory depression, suppression of cough, pupillary constriction, reduced GI motility (constipation), histamine release (itching, bronchoconstriction, hypotension)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the main Unwanted side effects of Morphine ?

What are the effects with an acute overdose of morphine

A

Most troublesome unwanted effect :
- nausea & vomiting
- reduced GI motility (constipation)
- respiratory depression,
- addiction

Acute overdose: coma and respiratory depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Codeine is a weaker opiate analgesic than morphine. How much weaker?

A

Codeine Has 20% analgesic potency of morphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Codeine is a weaker opiate analgesic compared to Morphine.
How much weaker ?
and why

A

Codeine has 20% analgesic potency of morphine
Due to a methyl group added

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the therapeutic uses of Codeine?

A

Therapeutic use:
mild-to-moderate pain (headache),
diarrhoea,
a cough suppressant (dose; antitussive< analgesic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is codeine usually combined with ? and what does it produce

A

Analgesic preparations: combine codeine (8 mg) with paracetamol (Co-codamol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the adverse effects of codeine ?

A

Adverse effect: constipation, no euphoria (rarely addictive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Codeine is a prodrug, where is it processed and what does it become

A

Prodrug is demethylated in the liver by CYP2D6 enzyme into morphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What percentage of the population is resistant to codeine and why?

A

10% population resistant to effects of codeine
Genetic polymorphism causing these pipo to have poor metabolisers in liver to process the prodrug into morphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Opioid analgesics arerelatively ………in dental pain.

A

Opioid analgesics arerelatively ineffectivein dental pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Which 3 drugs are adequate for most cases of dental pain (opioid is rarely required)

A

Paracetamol, NSAIDs (ibuprofen), or aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Why was Dihydrocodeine firsted developed?

A

Developed as an antitussive to reduce the spread of tuberculosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the potency of Dihydrocodeine relative to morphine

A

Defined as a weak semi-synthetic opioid analgesic:
20% analgesic potency of morphine. - similar to codeine (partial agonist)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

When is dihydrocodeine used?
What is the common dose ?

A

Used for moderate-to-severe pain
(30 mg dose, every 4-6 hours)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is dihydrocodeine commonly combined with and what does it form?

A

Analgesic preparations can be combined with paracetamol (Co-dydramol), Aspirin or NSAIDs

Advantage over codeine, metabolites unimportant: even poor metabolisers have good response to dihydrocodeine
Adverse effect: constipation, nausea and vomiting, pruritus (histamine release)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the advantages of using dihydrocodeine over codeine?

A

The advantage over codeine, metabolites are unimportant since it’s not metabolites in the liver CYP2D6: even poor metabolisers have a good response to dihydrocodeine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the adverse effects of dihydrocodeine

A

Adverse effect: constipation, nausea and vomiting, pruritus (histamine release)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Use of Opioids in compound analgesics:
Why do we combine compound analgesics with opioids?

  • What is the rationale
A

Compound analgesic preparations that contain a simple analgesic (such as aspirin or paracetamol) with an opioid component to –> reduce the scope for effective titration of the individual components in the management of the pain of varying intensity.

Rationale: co-administration of two drugs that produce analgesia by different mechanisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the 3 benefits of combining compound analgesics with opioids ?

A
  1. Additive effect so less of each drug is given to produce the same degree of analgesia
  2. Reduce the intensity of producing unwanted side effects by each drug
  3. Combining a non-opioid with an opioid analgesic can provide greater relief of pain than either analgesic given alone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

With dental and orofacial pain when do we get an analgesic effect with combination analgesic preparations?

A

In dental and orofacial pain:
this applies only when an adequate dose of each analgesic is used
most combination analgesic preparations do not provide greater relief of pain

44
Q

What are the 3 common compound analgesics and opioid combinations

A
  1. Codeine/Paracetamol =
    Co-codamol
  2. Dihydrocodeine/Paracetamol =
    Co-dydramol
  3. Codeine/Aspirin = Codis
45
Q

With dental and orofacial pain combination preparation analgesics have what type of effect? and what should be done instead

A

combination preparations have the disadvantage of increasing opioid-induced side effects

an adequate dose of the non-opioid component given alone is usually sufficient

46
Q

How did we confirm that opioids were having an effect on the body

A

when we discovered they were binding to μ (Mu) opioid receptors by using 3H-naloxone an antagonist - 1973 Pert and Snyder

47
Q

Which structural component of naloxone allows it to have an antagonistic activity

A

Bulky substitution on the nitrogen atom of morphine introduces antagonist activity

48
Q

Name 3 Naloxone characteristics which make it a great opioid antagonist.

A
  1. Short-acting (rapidly metabolised in the liver)
  2. affinity for all classic opioid receptors – first pure opioid antagonist
  3. Rapid reversal of the effects of morphine and other opioids
49
Q

Name 2 adverse characteristics of naloxone.

A
  1. Exacerbate clinical pain (e.g. following dental surgery)
  2. Little effect on pain threshold under normal conditions, BUT during heightened sensitivity to pain (hyperalgesia) under stress-induced or inflammation-induced analgesia (when endogenous opioids are produced) can increase pain because it prevents the opioids binding on the same receptors
50
Q

What are the 3 main clinical uses of opioids?

A

Main clinical uses:

  1. Treat respiratory depression caused by opioid overdose
  2. The reverse effect of opioid analgesia, used during labour, on the respiration of the newborn baby
  3. Oral naloxonecan reduce opioid-related constipation (Oxycodone)
51
Q

Name two additional opioid (μ-receptor) antagonists other than Naloxone

A

Naltrexone and Methylnaltrexone bromide (Alvimopan)

52
Q

What is the half-life of Naltrexone
and what its MOA

A

Long-acting (half-life ~10 hours)
Similar mechanism of action to Naloxone

53
Q

What are the 3 main clinical uses of Naltrexone

A

Main clinical uses

  1. Subcutaneous implant for ‘detoxified’ alcoholics/addicts – nullifies relapse
  2. Reduce alcohol consumption in alcoholics, since part of the ‘high’ of alcohol comes from the release of endogenous opioid peptides
  3. Treat pruritus (itching) in chronic liver disease (endogenous opioid peptide involvement
54
Q

Can Methylnaltrexone bromide cross the BBB?

A

Does not cross BBB
Only effective in the periphery

55
Q

What is the main clinical use of methylnaltrexone bromide

A

Main clinical uses:
Block opioid-induced constipation

56
Q

Endogenous Opioids & Receptors:
Name the structural motif found in both endogenous opioids (Ones found in Morphine and ones found the body) — > allows the binding of the opioid to the receptor-binding sites

A

The receptor binding site on opioids resembles the ‘tyrosine residue’ motif in endogenous opioid peptides

57
Q

Name the 5 endogenous peptides and rank them in order of Mu-opioids receptor agonist activity/affinity

A
  1. Beta- Endorphin
  2. Leu-enkephalin
    3.Met-enkephalin
  3. Dynorphin
    5.Orphanin FQ/Nociceptin
58
Q

What was the classical Opioid recepto terminology

A

Opioid receptor classical terminology:
μ, δ, κ

59
Q

What is the new revised opioid receptor terminology?

A

Revised terminology:
MOPr (μ),
DOPr (δ),
KOPr (κ) and
NOPr (ORL1; recent)

60
Q

What type of receptors are 4 types of opioid receptors ?

A
  • All 4 are either Homomeric or heteromeric G protein-coupled receptors
  • All 4 receptors are coupled to the G protein Gi/Go - inhibitory effects
61
Q

Name all the endogenous opioids that act on these 4 opioid receptors.

A

All endogenous opioids include Endorphins, Enkephalin, Dynorphin and (Orphanin FQ or Nociceptin; recent)

62
Q

How many opioid peptides do we have

A

Twenty or more opioid peptides, only 4 receptors

63
Q

Name the one endogenous peptide that has an affinity/ agonist activity on the NOPr (ORL1) receptor

A

Orphanin FQ/nonciceptin

64
Q

Dynorphin has the most agonist activity on which receptor

A

KOPr

65
Q

Responses to morphine and thought to be mediated by which receptor ?

A

Responses to morphine and thought to be mediated by MOPr (μ)

66
Q

Opioids bind to which receptor type causes dysphoria and hallucinations

A

binding to KOPr

67
Q

Opioids need to bind to which receptor to get the catatonia effect

A

NOPr

68
Q

Heroin is more souble than which opioid

A

morphine
crosses the BB. ore easily and more addicitve

69
Q

What is Oxycodone?
What is its metabolism?

A

Strong μ-opioid receptor agonist (κ opioid-receptor agonist evidence uncertain)
Metabolism: liver by CYP3A4 (noroxycodone) & CYP2D6 (oxymorphone)

70
Q

What Drug interactions does Oxycodone have?
Why was it designed?

A

drug interactions: inhibitors & inducers of enzymes

Semi-synthetic (from thebaine, an opiate alkaloid) replacement for diamorphine (heroin; Bayer stopped production)

Designed as an improvement to diamorphine – thought to have similar potency, less addiction

71
Q

How is oxycodone formulated

A

slow release tablet, addicts grind up tablets (reformulated make it difficult to crush)

72
Q

Oxycodone is a major drug of abuse where was is it commonly abused ?

A

Most commonly abused opioid in USA and Canada

73
Q

What is Pethidine ?
What is used for ?
What its effect relative to morphine ?

A

Strong synthetic μ-opioid receptor agonist

Moderate to severe pain (less effective than morphine)

acute pain relief (quicker than morphine, more lipid soluble)

obstetric analgesia (labour pains)
peri-operative analgesia

diverticulitis (inflammation colon)

74
Q

What was Pethidine first developed as?

A

First developed as a anti-muscarinic to treat the pain associated with biliary spasms (gallstones) or renal colic (kidney stones) in 1939

75
Q

What are the negative effects of Pethidine ?

A

Produces tachycardia, dry mouth

  • Its sister drug USA ‘meperidine’ was a major opioid used in the 1970’s/80’s - thought to be less addictive than morphine BUT it is as addictive as morphine and has little to no anti-muscarinic effects ABSOLUTELY USELESS
76
Q

Where is pethidine metabolised

A
  • In the Liver
  • Metabolism: partly N-demethylated in the liver to norpethidine (hallucinogenic and convulsant effects
77
Q

What are the contradictions of pethidine

A

CNS excitation or depression (hypertension or hypotension) when pethidine given with MAOIs - Monoamine oxidase inhibitors
additive anti-muscarinic effect

78
Q

What is fentanyl?
Where was it dervived from ?
What are the 3 derivatives of fentanyl ?

A

Fentanyl (1960)
Strong synthetic μ-opioid receptor agonist
Derived from the structure of pethidine
Derivatives of Fentanyl: Alfentanil, Sufentanil, Remifentanil

79
Q

Fentanyl potency

A

Potency:
100x more potent than morphine
500x more lipid soluble than morphine;
rapid onset
shorter duration than morphine

80
Q

Name the 3 clinical uses of Fentanyl

A

Clinical uses:
enhancement of anaesthesia, severe chronic pain,
breakthrough pain

81
Q

How is fentanyl administered

A

Via transdermal patches

82
Q

What are the does available for the transdermal fentanyl patches

A

Transdermal Patch (Doses 12, 25, 50, 75, 100 µg/h)

83
Q

72-hour Fentanyl patches ~ equivalent X hour doses of oral morphine:

12µg/h Fentanyl = X mg/24h oral morphin

A

72-hour Fentanyl patches ~ equivalent 24-hour doses of oral morphine

12µg/h Fentanyl = 30 mg/24h oral morphin

84
Q

What are the 4 disadvantages of fentanyl

A

Disadvantages:
- slower onset of action: 8 – 12 hours
- rate of absorption affected: body temperature, skin type, fat, site placement
Fever- /external heat : increased side effects (respiratory depression)
- remove patch: breathing problems, confusion, drowsiness

85
Q

Loperamide (imodium):

  • What does it treat?
  • Why doesn’t it have an analgesic effect?
  • Which Mu-Opioid receptors does it act on?
  • What potency level does it have relative to morphine?
  • What therapeutic effect does it have?
A

Loperamide (1976: FDA approval)
μ-opioid receptor agonist:

Treats: acute diarrhoea, IBS

No analgesic activity: does not cross BBB (efflux by P-glycoprotein)

Acts on the μ-opioid receptors in the myenteric plexus of the large intestine:

decreases its activity (50x morphine),

Therapeutic effect: reduces smooth muscle tone, decreases GI motility, slows transit time so it enhances water/ion absorption

86
Q

Why is loperamide poorly absorbed into circulation?

What 2 adverse effects does loperamide have?

A

Poor absorption into circulation:
P-glycoprotein pump back into the intestinal lumen
Enterohepatic recycling

Adverse effects: constipation, abdominal cramping

87
Q

What is tolerance?
Which 3 methods can tolerance to a drug occur?

A

Tolerance: progressively decreased responsiveness to a drug upon repeated drug administration:

  • an increase in the dose is needed to produce the original pharmacological effect
  • loss of sensitivity to drug is developed quickly (a few days during repeated administration of drug)
  • involves desensitisation of the μ-opioid receptor
88
Q

What is Dependence?
What are the two types of dependence?
Give detail in regard to the symptoms

A

Dependence: state in which withdrawal of the drug causes adverse physiological effects (withdrawal syndrome)
whenever an opioid administered for more than a few days, comprises of two components:

Physical dependence: associated with the withdrawal syndrome and lasts for a few days (restlessness, irritability, runny nose, diarrhoea, abdominal cramping, nausea & vomiting, sweating, insomnia, shivering, piloerection, tachycardia, hypertension)

Psychological dependence: associated with craving and can last for months or years (rarely occurs in patients being given opioids as analgesics

89
Q

What is addiction?

A

Addiction: behavioural pattern of drug use, characterised by overwhelming need to use a drug (compulsive use), securing its supply, and a high tendency to relapse after withdrawal

drug self-administration without making a distinction between physical or psychological dependence

90
Q

Name the two opioids used for heroin withdrawal

A

Methadone and Buprenorphine

91
Q

What type of opioid is Methadone?
What percentage of bioavailability does it have?

A

Methadone: potent synthetic µ-opioid receptor agonist, well absorbed with good oral bioavailability (75%)

92
Q

what is the main use of methadone?
and why

A

main use: a substitute for opioids (heroin) in addicts due to its slow onset & offset
reduces the incidence of withdrawal symptoms from heroin, BUT methadone dependence can develop

93
Q

What type of opioid is Buprenorphine?

What kind of efficacy does it have?

What effect does it have when combined with heroin?

Which other opioid is it combined with to manage opioid dependence?

A

Buprenorphine: potent semisynthetic µ-opioid receptor partial agonist (~25x more potent than morphine)

  • low efficacy compared to full agonists, able to antagonist effects of agonists (heroin, morphine) at opioid receptors
  • when heroin is injected ‘on top’ of buprenorphine, less euphoria is achieved
  • marketed as sublingual preparation combined with naloxone for the management of opioid dependence
94
Q

Morphine ions can get trapped in the brain what does this cause?

A

Morphine ions trapped in the brain which can potentially lead to increased toxicity

95
Q

Morphine is a ____ base

A

WEAK base

96
Q

what happens to morphine in the brain

A

becomes at ion - charged because it gains an H+ when it crosses the BBB because the brain is more acidic . so it then cant recross the bbb so its trapped

97
Q

Morphine is extensively metabolised by the gut wall and liver into?

A
  • Morphine-3-glucuronide (M3G) – 70%
  • Morphine-6-glucuronide (M6G) – 10%
  • Sulphate conjugates
98
Q

What is the potency of the M6G relative to morphine

A

M6G is 10-20x more potent than morphine and is normally excreted in urine

99
Q

Why can morphine be toxic in pts with renal disease

A

morphine metabolites, M3G and M6G, accumulates in renal failure and accounts for increased sensitivity to morphine

100
Q

What is Neuropathic pain

A

Neuropathic pain is the severe, debilitating chronic pain that occurs in conditions such as neuropathy and trigeminal neuralgia (TGN; trigeminal nerve):

101
Q
  • What is neuropathic pain often thought to be?
  • Name the new opioid drugs that are effective for neuropathic pain

-Name the anti-epileptic drug that is thought to be effective for neuropathic pain

A

It was often thought neuropathic is opioid-resistant

Newer opioids including Tramadol and Tapentadol can be effective

Antiepileptic drug, Carbamazepine is effective in TGN

102
Q

Carbamazepine is used for which conditions?

  • MoA?
A

Carbamazepine (Tegretol; Novartis)

It has been used as an anticonvulsant and antiepileptic in the UK since 1965

blocks voltage-gated sodium channels (VGNC) used to treat TGN
certain VGNC subtypes are upregulated by nerve damage & contribute to the sensation of pain
a GABA receptor agonist (inhibitory neurotransmitter)

Start 100 mg 1-2 times a days, titrate up to achieve effective response (in some cases 1.6–2 g daily in divided doses may be needed)
Use to differentiate dental pain from TGN

103
Q

What dose is commonly given for carbamazepine

A

Start 100 mg 1-2 times a day, titrate up to achieve an effective response (in some cases 1.6–2 g daily in divided doses may be needed)

104
Q

What is Tramadol ?
What are the 3 MoA of tramadol?
What is tramadol prescribed for ?

A

Tramadol is a synthetic analogue of codeine,

Triple mode of action:
- weak agonist µ-opioid receptor (similar to codeine and pethidine)
- weak noradrenaline uptake inhibitor
- weak serotonin uptake inhibitor

Most prescribed weak opioid in UK - moderate to severe pain

105
Q

What are the side effects of tramadol?

tramadol contraindication ?

A

Side Effects:In equi-analgesic dose to morphine, tramadol produces less:
- respiratory depression
- cardiovascular depression
- constipation
BUT shares the most common side effects of opioids (e.g. vomiting, drowsiness)

Contraindication: in patients on MAOI or with a history of epilepsy.

106
Q

What is Tapentadol ?
MoA?
What is the potency of tapentadol relative to oxycodone?

A

Most recent opioid analgesic, with dual action:
- agonist µ-opioid receptor
- weak noradrenaline uptake inhibitor

Potency: equal to oxycodone, greater then tramadol

107
Q

What are the clinical uses of tapentadol ?

A

Clinical use:
moderate to severe pain for:
- Acute: following injury, surgery, etc.

  • Chronic: musculoskeletal pain
    Specifically indicated for controlling the pain of diabetic neuropathy

HHD 2 and Pharma (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions