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Clinical pharmacology and therapeutics > S9: opioids & respiratory pharmacology > Flashcards

S9: opioids & respiratory pharmacology Flashcards

1
Q

Compare nociception and pain

A

Nociception – non conscious neural traffic due to trauma or potential trauma to tissue
Pain – complex, unpleasant awareness of sensation modified by experience, expectation, immediate context and culture

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2
Q

Describe the pain pathway

A 
Nociceptors stimulated
Release of substance P and glutamate
Afferent nerve stimulated
Fibres decussate 
Action potential ascends 
Synapse in thalamus
Project to post central gyrus
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3
Q

List the different ways pain is modulated

A

Have modulators in peripheral system and in central system
Peripherally: substantia gelatinosa
Centrally: peri-aqueductal grey

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4
Q

Outline how pain is modulated peripherally

A

Tissue damage stimulates A delta & C afferent nerves, which enter the dorsal horn (substantia gelatinosa (SG) is found here) and project to the thalamus, causing pain and sensation
Laminae 1+5 are where pain fibres transmit
Tissue damage also sends inhibitory signals to the SG
Rubbing the painful area -> sends A beta fibres which stimulate the SG -> send inhibitory signals to laminae in dorsal horn, which reduces pain going to thalamus

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5
Q

Outline how pain is modulated centrally

A

Tissue damage stimulates A delta & C afferent nerves, which enter the dorsal horn and project to the thalamus, causing pain and sensation
Thalamus stimulates cortex & periaqueductal grey matter
Periaqueductal grey matter sends inhibitory signals to the dorsal horn via endogenous opioids -> reduces pain being sent to the thalamus

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6
Q

Describe endogenous opioids

A 
Enkephalins, endorphins and dynorphins 
Opioid receptors = G protein receptors 
Three receptor subtypes:
1) MOP/u
2) DOP/delta
3) KOP/K
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7
Q

Describe the MOP receptor

A

Most important clinically & causes most side-effects
Found predominantly in the brainstem and thalamus
GPCR

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8
Q

Describe the phosphorylation and uncoupling mechanism of opioid tolerance

A

Opioid binds to GPCR -> decreased cAMP -> decreased pain
ALSO: intracellular phosphorylation occurs, which changes the u receptors -> arrestin can bind and displace the G protein OR opioid may not have the same effect -> don’t get the same decrease in pain

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9
Q

Describe cAMP production mechanism of opioid tolerance

A

When opioid is removed: massive increase in cAMP
Causes neuronal excitability
Causes withdrawal symptoms – cramping, sweating, vomiting, diarrhoea -> common cause of death in addicts

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10
Q

Describe opioids

A

Exploit natural opioid receptors, either agonise or antagonise
Main therapeutic effects via u-receptors
Aim to modulate pain
Also indicated in: cough, diarrhoea & palliation

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11
Q

List examples of opioids

A

Strong agonists – morphine, fentanyl
Moderate agonists – codeine
Mixed agonist-antagonist/partial agonist – buprenorphine
Antagonists – naloxone

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12
Q

Describe the WHO analgesic ladder

A 
Used for chronic pain management
Simple analgesia – paracetamol, NSAIDs
Weak opioid – codeine 
Strong opioid – morphine, fentanyl 
(NB: for neuropathic pain use different drugs – anticonvulsants, tricyclics etc)
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13
Q

Describe morphine

A

Strong affinity to u receptors
Complete activation of u
Actions: analgesia, euphoria
Side effects: respiratory depression, emesis, GI tract, CVS, miosis & histamine release – caution in asthmatics

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14
Q

Describe fentanyl

A

100x potency compared to morphine, higher affinity for u receptor
Less histamine release, sedation & constipation
Actions: analgesia, anaesthetic
Side effects: respiratory depression, constipation & vomiting

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15
Q

Describe codeine

A

Approx. 1/10 potency of morphine
Actions: mild-moderate analgesia, cough depressant
Side effects: constipation, respiratory depression (worse in children)
NB: active metabolite of codeine requires CYP2D6 oxidation activity -> deficiency in this CYP enzyme means less active metabolite being produced & less analgesia

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16
Q

Describe buprenorphine

A

Very high affinity for u receptor, long duration of action
Actions: moderate to severe pain, opioid addiction treatment
Side effects: respiratory depression, low BP, nausea & dizziness

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17
Q

Describe naloxone

A

Competitive antagonism of opioid

Side effect: short half life, slow infusion

18
Q

Describe opioid overdose

A

Growing problem, large number of iatrogenic addicts
Respiratory depression most common cause of death
Naloxone infusion as treatment

19
Q

List contraindications of opioids

A 
Hepatic failure
Acute respiratory distress
Comatose 
Head injuries 
Raised ICP
20
Q

Describe asthma

A

Chronic inflammatory airway disease
Intermittent airway obstruction and hyper-reactivity
Small airways
Reversible both spontaneously & with drugs

21
Q

Describe control of asthma, what should be considered before stepping up/down treatment?

A

Minimal symptoms during day and night
Minimal need for reliever medication
No exacerbations
No limitation of physical activity
Normal lung function
Aim for early control with stepping up OR down as required
Before stepping up or down: adherence, inhaler technique & eliminate/reduce trigger factors

22
Q

Describe inhaled corticosteroids

A

Regular preventer when reliever alone not sufficient
Pass through plasma membrane, activate cytoplasmic receptors, activated receptor then passes in to nucleus to modify transcription
Reduces mucosal inflammation, widens airways, reduces mucus
Reduces symptoms, exacerbations & prevents death

23
Q

What are the adverse effects, warnings, contraindications and important drug interactions of inhaled corticosteroids?

A

Adverse effects: can cause local immunosuppressive action -> candidiasis, hoarse voice
Warnings, contraindications: pneumonia risk possible in COPD at high doses
Important drug interactions: if taken correctly, very few significant ADRs

24
Q

List examples of inhaled corticosteroids

A

Beclomethasone
Budesonide
Fluticasone

25
Q

Describe the basic mechanism of how steroids work

A

Gene activation – increased activation of B2 receptors, anti-inflammatory mediators & also inhibit release of arachidonic acid
Gene repression – inflammatory mediators: interleukins, chemokines & cytokines

26
Q

Describe inhaled corticosteroids pharmacokinetics

A

Poor oral bioavailability
High affinity for glucocorticoid receptor
If steroid is absorbed p.o: almost complete first pass metabolism
But at high doses, all ICS have potential to produce systemic side effects

27
Q

Describe B2 agonists

A

SABA: symptom relief through reversal of bronchoconstriction, only to be used p.r.n.
LABA: add on therapy to ICS and p.r.n. SABA
Major action on airway smooth muscle & also mucus clearance by action of cilia
Prevention of bronchoconstriction prior to exercise

28
Q

List examples of B2 agonists

A

Fast, short acting: salbutamol, terbutaline
Fast, long acting: formoterol
Slow, long acting: salmeterol

29
Q

What are the adverse effects, warnings, contraindications and important drug interactions of B2 agonists?

A

Adverse effects: adrenergic – fight or flight effects, SVT
Warnings, contraindications: LABA should only be prescribed alongside ICS, alone can mask airway inflammation and near-fatal & fatal attacks; tachycardia may provoke angina
Important drug interactions: B-blockers may reduce effects of B2 agonists

30
Q

Describe leukotriene receptor antagonists

A

Montelukast
Alternative to LABA 2nd step in NICE guidelines
Leukotrienes released by mast cells/eosinophils – increased bronchoconstriction, increased mucus, increased oedema
Leukotriene receptor antagonist block CysLT1 at CYSLTR1

31
Q

What are the adverse effects, warnings, contraindications and important drug interactions of leukotriene receptor antagonists?

A

Adverse effects: headache, GI disturbance, dry mouth, hyperactivity
Warnings, contraindications: used as an add on in specific circumstances
Important drug interactions: no major drug interactions reported

32
Q

Describe tiotropium

A

Long acting muscarinic antagonist (acts at M3 receptors) – severe asthma & COPD
Block vagally mediated contraction of airway smooth muscle
Adverse effects: infrequent – anticholinergic effects (dry mouth, urinary retention, dry eyes)

33
Q

Describe theophylline

A

For chronic poorly controlled asthma
Adenosine receptor antagonist, decreases bronchoconstriction
Warnings, contraindications: narrow therapeutic index, arrhythmias
Important drug interactions: CYP450 inhibitors – increase concentrations of theophylline

34
Q

Describe self management plans for asthmatics

A

Written instructions on when and how to step up AND down treatment
Should be reviewed following treatment for exacerbation and on discharge from hospital following acute attack

35
Q

List the treatment for acute severe and life-threatening asthma

A

Oxygen
High dose B2 agonist
Oral steroids (prednisolone) should be prescribed minimum 5 days
Nebulised ipratropium bromide (short acting muscarinic antagonist)
Consider i.v. aminophylline is life threatening/near fatal & no success with above – caution if taking p.o. theophylline

36
Q

List the 5 tasks of management for COPD

A 
Confirm diagnosis
Smoking cessation
Breathlessness score
Vaccination 
Medication
37
Q

Describe the treatment of acute exacerbations of COPD

A

Nebulised salbutamol and/or ipratropium should be prescribed (if patient is hypercapnic/acidotic nebuliser should be driven by air & not oxygen)
Oral steroids – can be less effective than asthma due to reduced action on neutrophils
Antibiotics
Review of chronic treatment & action plan

38
Q

List inhaler options

A

Pressurised metered dose inhalers (pMDI)
-inhalation and actuation of device, slow breath in and hold, can be used with a spacer to improve delivery
Breath-actuated pMDI
-automatic actuation upon inspiration
Dry powder inhalers (DPI)
-micro-ionised drug plus carrier powder, own inspiratory flow – fast deep inhalation

39
Q

List features of acute severe asthma

A

Unable to complete sentences
Peak flow 33-50% best or predicted
Respiratory rate > 25
Heart rate > 110/min

40
Q

Describe why inhaled drug particles that are too small & too big are ineffective in asthma management

A

Too small = inhaled into alveoli and exhaled without being deposited in the lungs
Too big = deposited in the mouth and oropharynx

Clinical pharmacology and therapeutics (14 decks)

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