Y5 Drug Profiles > BASIC - PAIN & PALLIATIVE CARE > Flashcards

BASIC - PAIN & PALLIATIVE CARE Flashcards

(98 cards)

Study These Flashcards
1
Q

Name of strong opioids?

A

Morphine, diamorphine, Oxycodone

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

4 indications for strong opioids?

A
  • Acute pain relief – ACS, post-operative
  • Chronic pain relief – Step 3 of ladder
  • Relieve breathlessness in palliative care
  • Acute pulmonary oedema (along with oxygen, furosemide, nitrates)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Mechanism of action for strong opioids?

How is oxycodone different?

A
  • Activation of opioid u (mu) receptors in CNS
  • Reduces neuronal excitability and pain transmission
  • In medulla – blunt response to hypoxia and hypercapnoea – reducing respiratory drive
  • Reduce SNS activity
  • Oxycodone is synthetic analogues of morphine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Adverse effects of strong opioids?

A 
o	Nausea and vomiting
o	Constipation
o	Pupillary constriction
o	Skin – itching, vasodilation, sweating
o	Respiratory depression
o	Neurological depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Can you develop tolerance and dependence in strong opioids?

A 
o	Tolerance does develop and may need to higher the dose over time
o	Dependence apparent with cessation
	Anxiety, pain, breathlessness
	Dilated pupils, skin cool and dry
o	Not a problem in therapeutic doses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Symptoms of toxicity in strong opioids?

A 
o	Persistent nausea and vomiting
o	Drowsiness
o	Confusion
o	Visual Hallucinations
o	Myoclonic jerks
o	Respiratory Depression 
o	Pinpoint pupils (not always useful if on long term)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When should dose reduction be done in strong opioids? What caution must you have?

A
  • Dose reduction in hepatic failure and renal impairment and in elderly
  • Do not give in respiratory failure except in palliative care
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Avoid strong opioids when? Why?

A
  • Avoid in biliary colic – may cause spasm in sphincter of Oddi (use pethidine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What other drugs should you avoid ideally with strong opioids?

A
  • Ideally avoid with other sedating drugs (antipsychotics, benzodiazepines, TCAs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Route of administration of strong opioids in acute and chronic setting?

A

o In acute setting – given IV

o Chronic pain – oral, IM, SC available

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

What is oral morphine available as?

A
  • Normal/Immediate release tablets and liquid – lasts 4 hours e.g. Oramorph
  • Modified/Slow release tablets, granules, capsules – lasts 12 hours e.g. morphine sulphate tablets (MSTs), Zomorph capsules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When would modified release morphine be used?

A

o Modified release morphine prescribed in regular treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is an appropriate dose of MR morphine? When would the dose be reduced?
How much % increase needed if not adequate?

A

 Dose usually MST 20mg bd appropriate as Step 3
• Elderly, frail or renal impairment patients (fentanyl used in renal excretion) may need lower doses
• Titrate dose up by 30-50% increments to relieve pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

For breakthrough pain, how much IR morphine given?

A

1/10-1/6 of the total daily regular dose in the PRN

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

What names would you use in prescription?

A

Brand name prescribing for strong oral opioids

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

What needs communicating to patient? (4)

A

o Explain that it is a highly effective painkiller and that ‘addiction’ is not an issue when it is used for pain control
o Warn patients that the dose may need to be increased over time as they become tolerant to its effects; this is normal and should not cause alarm
o Offer antiemetic (metoclopramide) and laxative (co-danthrusate or movicol)
o Do not operate heavy machinery or drive if feel drowsy or confused

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

When would you review strong opioid prescription?

A

o Review in 1-2 weeks to assess effectiveness

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

When given parenternally, what is the potency of MS and diamorphine?
What dose should be given of diamorphine then?

A

 Parenteral diamorphine 3 times more potent than oral morphine
 Parenteral MS is 2 times more potent
 Total 24-hour SC continuous infusion diamorphine dose should be 1/3 of total 24-hour oral morphine dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which strong opioids are given transdermally?

What do they look like?

A

o Fentanyl transdermal patches last 72 hours (can have buprenorphine patches)
 Suitable for severe chronic pain already stabilised on other opioids
 Buprenorphine looks like plaster and fentanyl is clear patch

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

When oxycodone used, what are the MR and IR names?

A

• Immediate release (oxynorm) and slow release (oxycontin)

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

Name of weak opioids?

A

Codeine, co-codamol, dihydrocodeine

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

Indications of weak opioids?

A
  • Step 2 on WHO analgesic ladder when simple analgesia (paracetamol) is insufficient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Metabolism of weak opioids? Mechanism of weak opioids? Why is codeine sometimes not effective?
Tramadol is what?

A
  • Metabolised in liver to produce small amounts of morphine (from codeine) or dihydromorphine (dihydrocodeine)
  • Agonists of opioid u (mu) receptors
  • 10% of Caucasians has less active form of key metabolising enzyme (CYP450 2D6) so may be ineffective
  • Tramadol is synthetic analogue of codeine, also a 5-HT and NA reuptake inhibitor – not a great drug
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Side effects of weak opioids?

A
  • Nausea
  • Constipation
  • Dizziness
  • Drowsiness
  • Neurological and respiratory depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Interactions of weak opioids? When should tramadol not be used?
- Ideally do not combine opioids and other sedating drugs (antipsychotics, benzodiazepines, TCAs) - Tramadol should not be used with drugs that lower seizure threshold (SSRIs, TCAs)
26
Contraindications of weak opioids?
- NEVER GIVE CODEINE OR DIHYDROCODEINE IV – histamine anaphylaxis - Acute respiratory depression, comatose patients
27
When are weak opioids used in caution and dose reduction necessary?
- Both renal and hepatic impairment – dose reduction | - Tramadol lowers seizure threshold – caution in epilepsy
28
Prescription of weak opioids? Typical codeine starting dose? | Any other considerations?
- Can be prescribed orally, IM - Starting dose – codeine 30mg orally 4-hourly - Consider prescribing laxative (Senna) for regular administration - Should be withdrawn gradually to avoid symptoms
29
Communication to patient about weak opioids?
- Advise patients to avoid driving or operating heavy machinery if they become drowsy or confused while taking the new painkiller - Mention that painkillers should always be stored out of reach of children
30
Review of weak opioids?
- Review after 1-2 weeks and assess need to move up and down ladder
31
What strengths does co-codamol come in? Typical starting dose of Step 2 on WHO ladder?
- Co-codamol comes in 3 strengths: o 8mg codeine and 500mg paracetamol o 15mg codeine and 500mg paracetamol o 30mg codeine and 500mg paracetamol - Prescribe codeine 30mg when progressing from ‘Step 1’ - Paracetamol can be given with opioids too
32
Indications of paracetamol?
- 1st line analgesic for acute and chronic pain | - Antipyretic
33
Mechanism of paracetamol?
- Weak cyclooxygenase (COX) inhibitor, involved in prostaglandin metabolism - Increase pain threshold and reduce (PGE2) concentrations in thermoregulatory region, controlling fever - Specifically, COX-2 isoform (inflammation) rather than COX-1 isoform (protecting gastric mucosa, regulating renal blood flow and clotting)
34
Adverse effects of paracetamol?
Few
35
Normal metabolism of paracetamol? What happens in overdose of paracetamol? Treated with?
- Overdose – liver failure o Metabolised by CYP450 enzymes to toxic N-acetyl-p-benzoquinone imine (NAPQI) which is conjugated with glutathione before elimination o NAPQI accumulation causes hepatocellular necrosis o Treated with acetylcysteine (depending on plasma paracetamol level, <12 hours and not vomiting) and activated charcoal (if <4 hours)
36
Dose reduction in paracetamol?
- Dose reduced in liver toxicity
37
Cautions about use of paracetamol?
o Chronic excessive alcohol use o Malnutrition o Low body weight o Hepatic impairment
38
Which drugs increase rate of NAPQI production in overdose?
- CYP450 inducers
39
Prescription of paracetamol?
- Oral paracetamol can be purchased in retail outlets - Regular administration or PRN - Available as tablets, caplets, capsules, soluble tablets or oral suspensions - IV is possible
40
Communication to patient about paracetamol? | When should effects be felt?
- Effects should be felt around half an hour after taking it - Warn them not to exceed the recommended maximum daily dose because of the potential risk of liver poisoning - Advise them that many medicines purchased from the chemist (e.g. cold and flu preparations) contain paracetamol - Warn them to check the label
41
Typical paracetamol dose?
0.5-1g every 4-6 hours, maximum 4g per day
42
Name of NSAIDs
Ibuprofen, diclofenac, etoricoxib
43
Indications of NSAIDs?
- PRN for mild-to-moderate pain | - Regular treatment of pain related inflammation
44
Mechanism of NSAIDs? | How is etoricoxib different?
- Inhibit synthesis of prostaglandins from arachidonic acid by inhibiting cyclooxygenase (COX - COX-1 stimulates prostaglandin synthesis essential to preserve gastric mucosa, maintain renal perfusion (by dilating afferent glomerular arterioles) and inhibit thrombus formation at the vascular endothelium - COX-2 expressed in response to inflammatory stimuli stimulates production of prostaglandins that cause inflammation and pain - Therapeutic benefits of NSAIDs are principally COX-2 inhibition and adverse effects by COX-1 inhibition - Selective COX-2 inhibitors (e.g. etoricoxib) developed to reduce the adverse effects
45
SE of NSAIDs?
- GI toxicity - Renal impairment - Increased risk of MI/CVA - Fluid retention
46
Interactions of NSAIDs in: GI ulceration GI bleed Renal impairment
``` - GI Ulceration o Aspirin, corticosteroid - GI bleeding o Anticoagulants, SSRIs, venlafaxine - Renal Impairments o ACEi, diuretics ```
47
Contraindications of NSAIDs
o Severe renal impairment o Heart Failure o Liver failure
48
Cautions of NSAIDs in prior history of?
o Peptic ulcer disease o GI bleeds o CVD
49
Prescription of NSAIDs?
- Available as tablets, suspensions, gels, suppositories, injectable - Acute pain treatment should be stopped when resolved - Taken with food to minimise GI upset
50
Communication to patients about NSAIDs? Any time you should stop NSAIDs? What other meds could be prescribed?
- Warn patients that the most common side effect is indigestion and advise them to stop treatment and seek medical advice if this occurs - For patients with acute pain, explain that long-term use, e.g. beyond 10 days, is not recommended due to the risk of side effects - Advise patients requiring long-term treatment (particularly if they have renal impairment) to stop NSAIDs if they become acutely unwell or dehydrated to reduce the risk of damage to the kidneys - Can use gastroprotection for patients at increased risk
51
Names of antimuscarinics? (antispasmodics)
Hyoscine butylbromide (Buscopan)
52
Indications of antimuscarinics?
- IBS - Colicky pain in cancer - Palliative care - Reduce copious respiratory secretions (death rattle)
53
Mechanism of antimuscarinics? | What are the effects?
- Competitive inhibitor of Ach - Blocks the parasympathetic ‘rest and digest’ effects so: o Increase HR and conduction o Reduces smooth muscle tone o Reduces peristaltic contraction o Relax pupillary constrictor and ciliary muscles preventing accommodation
54
SE of antimuscarinics?
- Tachycardia - Dry mouth - Constipation - Urinary retention - Blurred vision
55
Contraindications of antimuscarinics?
Avoid - GI obstruction - Urinary retention - Arrhythmias
56
Cautions in antimuscarinics?
Caution | - Angle-closure glaucoma
57
Interactions of antimuscarinics?
- Adverse effects enhanced with other antimuscarinics e.g. TCAs
58
How are antimuscarinics given?
- Usually given SC, either by injection or syringe driver
59
Typical hyoscine dose in palliative care?
SC 20mg every 4 hours PRN, can be adjusted up to 20mg every hour Syringe driver - 20-120mg/24 hours
60
Name of 5-HT antagonist antiemetics?
Ondansetron, granisetron
61
Indications of 5-HT antagonists?
- Nausea and vomiting – prophylaxis and treatment | - Particularly chemotherapy
62
Mechanism of 5-HT antagonists?
- 5-HT3 antagonists in the CTZ and gut | - Particularly good at stopping emetogenic substances in blood causing nausea
63
SE of 5-HT antagonists?
- Constipation, diarrhoea, headaches
64
Contraindications of 5-HT antagonists?
- Prolonged QT interval
65
Which drugs should be avoided and why?
Avoid in drugs that prolong QT interval: | - Antipsychotics, amiodarone, ciprofloxacin, macrolides, quinine, SSRIs
66
Prescription of 5-HT antagonists?
- Oral, rectal or IV administration - 8mg BDS for 5 days starting before chemotherapy - Dose to be taken an hour before symptoms anticipated if oral (IV immediately) - Expensive so only used for chemotherapy N&V
67
Names of phenothiazine antiemetics?
Levomepromazine, prochlorperazine
68
Indications of phenothiazine antiemetics?
- Nausea and vomiting treatment and prophylaxis | - First generation antipsychotic
69
Mechanisms of phenothiazine antiemetics?
- Blockage of D2 receptors in CTZ and gut, H1 and Ach in vomiting centre and vestibular system
70
SE of phenothiazine antiemetics?
- Drowsiness - Postural hypotension - Extrapyramidal syndromes – acute dystonic reaction and tardive dyskinesia - Prolong QT interval
71
Contraindications of phenothiazine antiemetics?
o Severe liver disease | o Prostatic hypertrophy
72
Which drugs should be avoided and why?
- Drugs that prolong QT interval | o Antipsychotics, amiodarone, ciprofloxacin, macrolides, quinine, SSRIs
73
When is this prescribed? What monitoring is needed?
``` Prescribing - Specialist advice usually needed Monitoring - Prolactin baseline and 6 months, then yearly - EPSE ```
74
Typical dose of levomepromzine?
Oral - 6mg OD at bed | Syringe Driver - 5-25mg/24 hours
75
Names of H receptor antagonists antiemetics?
Cyclizine, promethazine
76
Indications of H antagonists?
- Prophylaxis and treatment of nausea and vomiting o Palliative care – cerebral and cerebellar problems o Motion sickness and vertigo
77
Mechanism of H antagonists?
- Blockage of the Histamine-1 and acetylcholine receptors predominate in vomiting centre and communication with vestibular system
78
SE of H antagonists?
- Drowsiness (cyclizine least drowsy) - Anticholinergic – dry mouth, throat, blurred vision, constipation - IV - tachycardia
79
Contraindications of H antagonists?
- Hepatic encephalopathy | - Prostatic hypertrophy (develop urinary retention)
80
Interactions with H antagonists?
- Sedation – benzodiazepines, opioids | - Anticholinergics increased with ipratropium or tiotropium
81
Prescription of H antagonists? Typical dose? | What communication is needed?
- Given orally, IV, IM - Typical prescription 50mg 8-hourly PRN (syringe driver 150mg/24 hours) - Communication o May affect driving and skills tasks
82
Name of dopamine antagonists antiemetics?
Metoclopramide, domperidone
83
Indications of dopamine antagonist antiemetics?
- Prophylaxis and treatment of nausea and vomiting in reduced gut motility - Palliative care – Nausea and vomiting due to gastric stasis and irritation, hiccups
84
Mechanism of dopamine antagonist antiemetics?
- D2 receptor is main receptor in chemoreceptor trigger zone (CTZ) - Dopamine promotes relaxation of stomach and LOS and inhibits gastroduodenal coordination - Blocking D2 has prokinetic effect
85
SE of dopamine antagonist antiemetics? | Why does domperidone not have some of these effects?
- Diarrhoea - Metoclopramide o Extrapyramidal syndromes – acute dystonic reaction (facial and skeletal muscle spasms) o Galactorrhoea, gynaecomastic - Domperidone does not cross BBB
86
Contraindications of dopamine antagonist antiemetics?
- Children and young adults - Parkinson’s (Metoclopramide) - Gastrointestinal obstruction/perforation, 3-4 days after GI surgery
87
Caution in dopamine antagonist antiemetics?
- Reduce dose in renal and hepatic impairment
88
Interactions of dopamine antagonists antiemetics?
- Risk of EPSE increased with antipsychotics | - Do not combine with dopaminergic agents for Parkinson’s - antagonise
89
Prescription of dopamine antagonist antiemetics?
o Short term use – 5 days o Dose 10mg up to TDS o Metoclopramide available IV/IM and orally
90
What monitoring should be done in dopamine antagonists antiemetics?
o Monitor extrapyramidal symptoms if prolonged use
91
Name of neuropathic agents?
Gabapentin, pregabalin
92
Indications of gabapentin/pregabalin?
- Focal epilepsies (if carbamazepine and other antiepileptics not adequate) - Neuropathic pain (diabetic nephropathy, palliative/cancer neuropathic pain) - Migraine prophylaxis (Gabapentin) - GAD (pregabalin)
93
Mechanism of gabapentin/pregabalin?
- Gabapentin is closely related to GABA neurotransmitter - Binds to voltage-sensitive calcium (Ca2+) channels, preventing inflow of Ca and neurotransmitter release - Reduces neuronal excitability - Pregabalin is structural analogue of gabapentin
94
SE of gabapentin/pregabalin?
- Drowsiness - Dizziness - Ataxia - Usually improve over first few weeks
95
When is dose reduction needed in gabapentin/pregabalin?
- Dose reduced in renal impairment
96
Interactions of gabapentin/pregabalin?
- Sedative effects enhanced when combined with sedating drugs (benzos)
97
Prescription of gabapentin/pregabalin?
- Oral, start at low dose and increase over weeks | - Appropriate escalating-dose regimens are listed in the BNF
98
What to avoid when on gabapentin/pregabalin?
- Avoid driving or operating machinery until confident side effects have settled
Y5 Drug Profiles
flashcards
Decks in class (17)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions