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Primary Pharmacology > Analgesic Drugs > Flashcards

Analgesic Drugs Flashcards

1
Q

Opioid vs opiate

A

Opioid - acts at opioid receptor
Opiate - derived from opium poppy

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2
Q

Structural classification of opioids

A

Natural:
Morphine analogues - codeine, morphine

Semi-synthetic
Morphine analogues - diamorphine, dihydrocodeine
Thebaine derivatives - buprenorphine, oxycodone

Synthetic:
Anilinopiperidines - alfentanyl, fentanyl, remi, phenoperidine, sufentany,
Diphenylheptanes - dextropropoxhphene, methadone
Morphinans- levophanol, butorphanol
Phenylpiperdines - pethadine

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3
Q

Types of natural opioids

A

Phenanthrene (morphine, codiene, thebane - doesn’t do much itself but used for subsequent derivation of oxycodone, naloxone and buprenophine)

Benzylisoquinolines (papaverine, noscopine)

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4
Q

What are the opioid partial agonists and mixed agonist-antagonists?
Effect in patients

A

Partial - buprenorphine
Mixed - pentazocin, nalbuphine, nalorphine

Provide analgesia in opioid naive but withdrawal in dependant patients

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5
Q

Efficacy of buprenorphine

A

60-70%

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6
Q

What isomers of opioids exist? Clincial relevance

A

Opiates - all produced as steriospecific
Synthetic - all racemic

Most cases S are responsible for most clinical effects
Some eg tramadol require both

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7
Q

Rough structure of an opioid and binding

A

Five rings A-E with A and B in one plane and C and E perpendicular to them
A lies flush to receptor and E fits into a groove in it

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8
Q

Main groups of opioid receptor

A

MOP - mu
DOP - delta
KOP - kappa
NOP - Orphanin

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9
Q

Effect of MOP receptors

A

Open potassium channels causing hyperpolarisation and reduced firing

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10
Q

Location of MOP receptors

A

Primary afferent neurones
Peripheral sensory neurones
Periaquaductal grey matter
Nucleus raphe Magnus
Rostral ventral medulla
Thalamus
Cerebral cortex

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11
Q

Prototype and endogenous agonists at MOP

A

Prototype - morphine
Natural - leu-enkephalin, met-enkephalin, beta- endorphin

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12
Q

Action at DOP receptors

A

Potassium channel opening causing hyperpolarisation and decreased neuronal firing

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13
Q

Location of DOP receptors

A

Olfactory bulb
Cerebral cortex
Primary afferent neurones
Motor integration area
Nociception areas

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14
Q

Prototype and endogenous agonist at DOP

A

Prototype - ala-leu-enkephalin
Endogenous - leu-enkephalin, met-enkephalin, beta endorphin

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15
Q

Action at KOP receoptors

A

Directly close calcium channels reducing neurotransmitter release

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16
Q

KOP receptor location

A

Hypothalamus
Nocicption areas

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17
Q

Prototype and endogenous agonist at KOP

A

Prototype - ketocyclazocine
Endogenous - dynorphine, beta endorphins

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18
Q

Action of NOP receptors

A

Directly closing calcium channels reducing neurotransmitter release

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19
Q

Location of NOP receptors

A

Nucleus raphe Magnus
Primary afferent neurones

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20
Q

Endogenous ligand at NOP

A

Nociceptin
Orphanin

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21
Q

Structure of an opioid receptor

A

GPCR
7 transmembrane domains with extracellular n terminus and intracellular c terminus
2nd and 3rd loops responsible for binding.
Have inhibitory action on adenyl cyclase reducing cAMP formation

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22
Q

How do opioid receptors produce stimulatory responses

A

Inhibition of inhbition

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23
Q

Effect of stimulation of NOP
Clinical implication

A

Pro nociceptive effect (spinal and supraspinal) or antinociceptive in high concentrations
Thought to be responsible for setting pain thresholds and formation of tolerance.
NOP antagonists produce analgesia and reduce opiate tolerance

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24
Q

MOP and DOP have similar opiate effects all over
What differences do KOP receptors have in their action

A

Less resp depression
No effect on GI mobility
Dysphoria rather than euphoria
Less sedation or dependence
Cause diuresis

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25
Q

Best beneficial effects of opiates in anaesthesia

A

Analgesia - best for dull pain
Reduced fear and emotional response to pain
Induce sleep

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26
Q

CNS effects of opiates

A

Decreased level of consciousness
Sleep
Dose related decrease in MAC for volatiles
Increase cerebral vasoconstriction with vasodilor administration (eg volatiles)
Decreased spinal cord reflexes
Ataxia
Myoclonus (esp pethadine)
Miosis
Decreased thermoregulatory response and decreased BMR
Euphoria

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27
Q

CVS effects of opiates

A

Preserve cvs stability more than other anaesthetic agents, very little impact in normovolaemic patients
Decrease central sympathetic outflow so can cause cvs depression in already compromised individuals
Morphine causes histamine release which can exacerbate this issue - can be reduced with use of histamine antagonist and volume loading

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28
Q

Effect of pethadine on heart

A

Tachycardia as homologous with atropine
Significant myocardial depression at high doses

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29
Q

How do opiates effect perioperative mortaility

A

Reduce stress hormone response associated with pain, laryngoscopy and airway manipulation reducing overall myocardial work, tissue catabolism and hyperglycaemia improving outcomes

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30
Q

Effect of opiates on respiratory function

A

Decreased rate, Tv,
Pauses, irregular breathing, apnoa
Decreases co2 sensitivity
Decreases airway reflexes
Decreases mucociliary function
Anticough action

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31
Q

GI effects of opiates

A

Decreas peristalsis,
Decreased secretions
Decreased gastric emptying
Increased pyloric, ileocaecal and anal tone
Increased nausea and vomiting

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32
Q

GI effects of opiates

A

Antidiueisis due to decreased renal blood flow and decreased GFR
Decreased vasopressin release in response to osmotic stimuli
Increased bladder tone

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33
Q

How common is anaphylaxis to opiatesi

A

Exceedingly rare!

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34
Q

How does resp depression differ between opiates

A

Same at equianalgesic dose

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35
Q

Who is most at risk of resp depression from opiates

A

Neonates and elderly

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36
Q

What could you do in an opiate apnoea patient who is conscious

A

Ask them to breath!
Voluntary resp control remains intact

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37
Q

Incidence of nausea with opiates
What increases this
What can be done about it

A

10-60%
Increased in pain free ambulatory patients
Changing opiates may help, as may switching to an oral preparation

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38
Q

What is a major gi side effect of opiates

A

Constipation that may lead to toxic mega colon in crowns patients

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39
Q

How fast does tolerance develop to gi effects of opiates

A

Nausea - quickly
Constipation - slowly

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40
Q

What is special about loperamide

A

Synthetic opiate that doesn’t cross bbb

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41
Q

Effect of opiates on urination

A

Both urinary retention and urinary urgency

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42
Q

Where is opioid purititus most commonly located
What is the mechanism

A

Face and nose
Unknown, independent of histamine

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43
Q

What is the severe end of outcomes from opiate muscle rigidity? Management

Which agents is it most common with

A

Difficulty in ventilating
Coadministration of induction agents and benzos
Muscle relaxants
Naloxone

Commonest with phenylpiperidines such as pethadine

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44
Q

Which opiates most markedly reduces shivering
Uses

A

Pethadine
Tramadol to a lesser extent

Maintaining hypothermia, managing shivering from epidurals, blood transfusions, postop.

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45
Q

Non opiate effects of pethadine

A

Local anaesthetic
Quinidine like antiarrhythmic effect

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46
Q

Effects of pethadine overdose

A

Cardiovascular collapse
Mydriasis
Hyperreflexia
Convulsions
Respiratory depression

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47
Q

What metabolite of morphine can causes long term issues? What issues?

A

Morphine 3 glucuronide
Neuroexictation, opioid antagonism causing hyperalgesia

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48
Q

Effect of norpethidine accumulation

A

Mood changes
Anxiety
Can have fatal effects

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49
Q

How protein bound are common opiates?

A

Alfentanil 92%
Fentanyl 85%
Remifentanil 70%
Naloxone 40%
Morphine 35%
Codeine 10%

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50
Q

Elimination half lives of common opioids

A

Remi 15mins
Naloxone 70mins
Alf and fent 100mins
Codeine and morphine 180mins
Tramadol 360mins

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51
Q

Vd of Alf, fent, codeine, morphine, Remi

A

L/kg
Alf 0.8
Fent 4
Codeien 5.4
Morphine 3.5
Remi 0.35

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52
Q

Timeframe of resp depression after intrathecal morphine

A

6-10hours

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53
Q

What side effects occur more often with intrathecal opiates

A

Nausea
Urinary retention
Puritis

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54
Q

What pharmacokinetic property of an opiate predicts it having a long effect intrathecally

A

Hydrophilic
Lipophilic bind rapidly to local sites then are absorbed intravascuarly

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55
Q

What features of opioids lead them to be absorbed into the csf from epdural administration

How much morphine crosses the dura

A

Lipophilicity
Molecular size

5%

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56
Q

In what time fram would epidural sufentanil, fentanyl and morphine peak in the csf

A

Suf - 6mins
fent - 20mins
Morphine 240 mins

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57
Q

Rough effect of first pass metabolism on oral opiate bioavailability
Where does it occur

A

50%
Liver and intestinal wall

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58
Q

What can alter peak plasma concentration of im or sc opiates
By how much

A

Five fold

Body temp
Site of admin
Haemodynamic status

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59
Q

What plasma proteins do opiates bind to

A

Mainly alpha1 acid glycoprotein but also albumin
Fent and Alf. Also bind to beta globulins
Morphine is mainly bound to albumin

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60
Q

What group of drugs would displace opiates from protiens increasing free fraction

A

Basic amines

61
Q

Are opiates weak bases or acids

Main pKa range
Extreams

A

Bases
Most around 7.9 (morphine) to 8.4 (fent)
Extreams are Alf at 6.5 and tramadol at 9.4

62
Q

Significance of Alfs pKa

A

PKa 6.5 thus mainly unionised thus lipid soluble

63
Q

What occurs to opiates in an acidic CNS environment
Significance due to receptor interaction?

A

Ion trapping - unionised enters, becomes ionised then trapped,
Ionised form activates recpetor

64
Q

Elimination of opiates
What is the primary determinant for clearance

A

Phase one and two metabolism. In liver with renal excretion of hydrophilic metabolites
Hepatic blood flow

65
Q

Specific metabolism of morphine

A

Glucuronidation (mainly liver, some in kidney and gi tract):
60-80% bio transformation to M3G
10% to M6G

Rest sulphation (higher in neonates who struggle to glucuronidate)

90% excreteted in urine
Rest in bile sweat and breast milk

66
Q

Significance of M6G

A

2-4 times more potent than morphine with longer half life.
Can cross bbb and is then eliminated even slower!

67
Q

How is diamorphine activated, to what?
Are the metabolites hydrophilic or hydrophobic

A

Rapid deacetylation in the csf, liver and plasma to 6monoacetylmorphine and morphine
Hydrophilic

68
Q

How is codeine metabolised

A

In liver to codeine conjugates and norcodeine with some urinary excretion of free codeine
10% metabolised to morphine by cyp2d6 (missing in 8% of Western Europeans)

69
Q

Metabolism of pethadine

A

Hydrolysis to pethadinic acid and n-demethylation to norpethidine which is hydrolysed to norpethidinic acid
Causes enzyme induction increasing proportion converted to norpethidine with chronic use (or with other enzyme inducers)

70
Q

Why does fent have a large volume of distribution
Impact on metabolism

A

Very lipid soluble
Rapid and continued peripheral tissue uptake limiting initial hepatic metabolism
May cause subsequent peaks as released and concentrations can vary 13 fold with perfusion

71
Q

How is fentanyl metabolised

A

Hepatic to inactive metabolites which are excreted in the urine

72
Q

How is remifentanyl metabolised with characteristics

A

Widespread and rapid non saturatable metabolism by desterification to carboxylic acid metabolite by non specific esterases in blood and tissues

73
Q

Is the main metabolite of Remi active or inactive
How is it excreted

A

Active but not clinically significant
Excreted in urine but no worries even in renal failure as so weak

74
Q

What causes offset of Remi - metabolism, redistribution or excretion

A

Metabolism

75
Q

What is context sensitive half life

A

Half life in the context do duration of infusion
As infusion length increases more drug sequestered in fat so causes longer t1/2 as it returns to central compartment

76
Q

What is the effect of a long infusion of Remi on t1/2
What about fentanyl

A

Remi - none
Fentanyl - increases from 3-5 phos to 7-12hrs

77
Q

What weight should opiate dosing be based on?
When should obesity be a caution in opiates

A

Ideal body weight
Caution in long infusions except Remi as can cause very long context sensitive Half life

78
Q

Which opiates are effected by renal failure? What happens

A

Morphine - huge increase in elimination half life of glucuronidated metabolites from 4 to up to 120hrs.
Pethadine - norpethidine accumulation, with CNS side effects not mediated by opioid receptors and thus not reversible with narcan

79
Q

Effect of hepatic failure on opiates

A

Very little except in transplantation and fulment hepatic failure. Other organs eg kidneys and gi tract take bigger role.
Reduction in liver clearance will decrease first pass increasing bioavailability of oramorph
Some issues such as synergistic CNS depression from encephalopathy need to be considered.
Acidosis can cause ion trapping increasing effect

80
Q

Drug drug interactions of opiates

A

Synergistic CNS depression with other CNS depressants eg propofol and benzos
MOAIs can cause fatal sequalae especially tramadol and pethadine - can be excitatory or inhibitory reactions

81
Q

Which opiate is safest with moais

A

Morphine

82
Q

Highest receptor affinity of naloxone

A

Mop

83
Q

Duration of action of naloxone

A

30mins

84
Q

What symptoms can naloxone help with

A

Resp depression
Itching
Urinary retention

85
Q

Oral bioavailability of naloxone

A

2%

86
Q

What is naltrexone

A

Analog of naloxone with a longer t1/2 of 8hrs
Effective orally due to low first pass metabolism
Blocks opiate euphoria so used in dependency management

87
Q

HOw does tramadol act?

A

Weak agonist at all opioid receptors (with slight preferece to MOP)
Blocks NA and 5HT reuptake
Facilitates release of 5HT

88
Q

Potency of tramadol at opiate receptors vs morphine

A

Roughly 10%

89
Q

What are the isomers of tramadol
Significance

A

+ and - , comes as racemic mix
Have separate effects
+ for mop and 5Ht
- for na

90
Q

Oral bioavailability of tramadol
Protein binding

A

68%
20%

91
Q

Metabolism of tramadol

A

Hepatic
Demethylation and conjugation
Excretion of metabolites in urine
Metabolites very active so caution in renal failure

92
Q

Side effects of tramadol

A

Less resp depression than equianalgesic dose of morphine
Minimal cvs effects
Dizziness
Sedation
Nausea
Dry mouth
Sweating
Rashes
Physical dependence

93
Q

Pharmacokinetic properties of nsaids
Consequence

A

Rapid onset all routes
Highly protein bound
Small vol of distribution
Unbound fraction active

Effects potentiated by other protein bound drugs eg oral anticoagulants, hypoglycaemics, sulphonamides, anticonvulsants

94
Q

Difference between aspirin and nsaid actions on cox

A

Aspirin acetalates irreversibly
NSAIDs act by competative inhibition

95
Q

Main effect of nsaid cox inhibition

A

Decreased prostaglandin synthesis

96
Q

What activates arachadronic acid

A

Phospholipase

97
Q

Cox independent pathways from arachidonic acid

A

5 lipoxygenase to leukotrines
11,12,15 Lipoxygenase to hydroporoxhkosalenoic acid

98
Q

Products of cox metabolism of arachidonic acid

A

Prostaglandins
Thromboxane a2
Prostacyclin

99
Q

Functions of prostaglandins

A

Gastric protection
Maintainance of renal tubular function
Renal vasodilation
Bronchodilation
Vasodilation
Prevents platelet adhesion

100
Q

Base group of prostaglandins

A

Eicosanoid (20 carbon chain) from aa

101
Q

Where is cox 1 found
What does it do
Structure

A

ER of prostaglandin producing cells integrated into the lipid bilayer
Adds a 15 hydroperoxy group to aa forming pgg2 then reduces it to form pgh2 - has two active sites a cyclooxygenase site and a peroxidase site with a channel allowing aa access.

102
Q

What makes cox 2 different to cox 1

A

Overall slightly lighter with a similar structure to cox 1 but larger volume central channel and slightly different aa structure allowing binding of larger drugs.

103
Q

Where is cox 2 found? What stimulates its production? By how much?

A

Found in brain, kidneys, uterus, synovial cells, fibroblasts. Increases 10-80 fold when exposed to growth factor, cytokines, bacterial lipopolysaccarides

104
Q

NNT for ibuprofen post op
Morphine?
Codeine

A

2.4
Morphine 2.9
Codeine 16.7!

105
Q

How much do NSAIDs reduce opiate consumption

A

25-50%

106
Q

Opiate side effects

A

Bleeding
Gastric ulcers
Bronchospasm
Renal impairment

107
Q

What proportion of asthmatics have difficulties with NSAIDs

A

10-15%

108
Q

How common is nsaid induced renal impairment post op
What raises risk

A

Rare,
Age, other nephrotoxics, vasoconstrictor use

109
Q

Examples of cox 2 inhibitors

A

Celecoxib
Etorcoxib
Parecoxib
Meloxicam

110
Q

What is the general problem with cox2 inhibitors
Why

A

Increased prothrombotic issues esp cardiovascular
Inhibition of endothelial prostacyclin which causes platelet disaggregation

111
Q

NNT for parecoxib 40mg

A

2.2!

112
Q

Advantages of cox 2 inhibitors

A

Less (not none) peptic ulceration
No impaired platelet function (no COX 2 in plateletls)

113
Q

Effect of cox 2 on renal function

A

Similar to normal NSAIDs

114
Q

What is parecoxib converted into after administration

A

Valdecoxib

115
Q

What is the benefit of paracetamols lower protein binding vs NSAIDs

A

Less drug drug interactions

116
Q

How does paracetamol work

A

Inhibits prostaglandin synthesis in the CNS - minimal effect peripherally
No clear binding site ? Central cox 2 or 3 but just hypothesis not proven
? Prostaglandin syntheisis inhibition at transcriptional level
. Cannaboid receptor agonist

117
Q

NNT of paracetamol
What about combination with codeine

A

3.8
Combo 2.2 - much better than either alone

118
Q

Who is more at risk of paracetamol related liver damage
Why

A

Those on enzyme inducers
Degradation of paracetamol to toxic NAPQI is CYP450 dependant, other routes are enzyme in dependant conjugation.

119
Q

When is paracetamol toxicity damage at is maximum
What dose in 24o leads to significant damage

A

3-4 days after injestion
>150mg/kg

120
Q

Examples of alpha 2 agonists

A

Clonidine
Dexmedetomidine

121
Q

Side effects of alpha 2 agonists as an analgesic

A

Sedation
Hypotension
Bradycardia

122
Q

Most effective way of administering clonidine

A

Epidural

123
Q

Distribution half life of dexmedetomidine
Terminal half life
Vd

A

8 mins
3 hrs
170L

124
Q

Mechanisms of anticonvulsants in neuropathic pain

A

Frequency dependant na channel block
Calcium channel blockade
Potentiation of gaba

125
Q

NNT and NNH for carbamazepine

A

2.6
3.4

126
Q

Side effects of anticonvulsants as analgesics

A

Sedations
Rash
Anorexia
Dizziness
Ataxia
Steven Johnson syndrome
Hepatic impairment
Renal failure

127
Q

How does amitryptiline work as an analgesic

A

Inhibition of adrenaline reuptake enhancing decending inhibititory pain pathways

128
Q

Side effects of tcas

A

Dry mouth
Sedation
Postural hypotension
Glaucoma
Paralytic ilius
Arrhythmia

129
Q

What are the cannaboid receptors
Where are they found

A

GPCRs
CB1 brain and spinal cord
CB2 peripherally

130
Q

Examples of cannaboid receptor agonists

A

Delta9 tetrahydrocannabinol (natural active component) - highly lipophilic but low potency
Nabilone - less lipophilic more potent
Anandamide - endogenous ligand CB1

131
Q

Effects of delta 9 tetrahydrocannabinol

A

Antiemetic
Analgesia
Tachycardia
Hypotension
Weakness
Increased appetite
Euphoria then drowsiness
Psychological interference

132
Q

What is the dose of a lidocaine analgesic 8ish fusion

A

0.5-1.5mg/kg/hr

133
Q

NMDA receptor involvemtn in pain

A

Spinal central sensitisation pathways after damage

134
Q

Types of pain ketamine effective against

A

Both Nociceptive and neuropathic

135
Q

Time to peak effect of alfentanil?
Duration

A

90s
5-10mins

136
Q

Potency of alfentanil vs morphine

A

10-20times

137
Q

Contraindication to alfentanil, Remi and fentanyl

A

MOAI

138
Q

Potency of codeine vs morphine

A

20%

139
Q

Other potentially benfiecial effects of codeine beyond analgesia

A

Antidiarrhoeal
Antitussive

140
Q

Bioavailability of diclofenac

A

60%

141
Q

Doses of diclofenac by route

A

Oral 75-150mg/day in 2-3 divided doses
Rectal 100mg 18hourly (150mg/day)
IM 75mg Bd
iV 75mg 6hrly

142
Q

Metabolism of diclofenac

A

Hepatic hydroxylation then conjugation followed by renal excretion

143
Q

Potency of fentanyl vs morphine

A

60-80x

144
Q

Cardiovascular effect of fentanyl

A

Minimal hence use in cardiac anaesthesia.
In very high doses some Bradycardia and hypotension

145
Q

Paediatric dose of ibuprofen

A

20mg/kg in divided doses

146
Q

Epidural fent and morphine dose

A

Much the same as iV (50-100mcg and 5-10mg)

147
Q

Intrathecal morphine dose

A

0.2-1mg

148
Q

Standard concentration of remifentanil for tci

A

50mcg/ml

149
Q

How long is reconsitituted Remi stable for

A

24hrs at room temp

Primary Pharmacology (18 decks)

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