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CPTP > Analgesia and Palliative Care > Flashcards

Analgesia and Palliative Care Flashcards

1
Q

WHO analgesic ladder

A

Non opioids (NSAIDs and paracetamol)

Weak opioids - codeine and tramadol (+/-adjuvants)

Strong opioids - morphine, fentanyl, oxycodone (+/-adjuvants)

Adjuvants = TCAs, steroids, bisphosphantes, muscle relaxants

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2
Q

Prescribing pain relief

A

Oral administration where possible
Analgesia @ regular intervals
Dosing adapted to pt increase the dose if breakthrough pain!!

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3
Q

Paracetamol MOA

A

Not fully understood believed to be due to reducing prostaglandin synthesis from arachdonic acid. Peripherally blocks pain impulses to reduce signalling and inhibit hypothalamic heat regulation

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4
Q

Max dose of paracetamol

A

1g QDS

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5
Q

Paracetamol OD

A

Can lead to thrombocytopenia and more importantly acute liver failure

<150mg/kg = unlikely to causes significant damage
>250mg/kg = significant risk
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6
Q

NSAIDs MOA

A

Inhibit the COX enzymes which convert arachdonic acid to prostaglandins and thromboxanes. Reduce prostaglandin levels to analgesic, vasodilation and anti-pyretic effects

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7
Q

CI NSAIDs

A

Liver or renal impairement
PMHx of PUD or GI bleed
Asthmatic
IHD

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8
Q

SE of NSAIDs

A

GI bleed due to reduced prostaglandins leads to high acid levels and inadequate mucus protection. Especially COX-1 selective ibuprofen and naproxen (Increase with SSRIs)

AKI cause vasoconstriction of the afferent arteriole, this is due to the loss of the normal vasodilator effects of prostoglandins

Bronchospasm due to compensatory increase in leukotriene production which cause bronchoconstriction

Increased cardiac vascular risk with COX-1 selective drugs such as celecoxib and rofetecoxib

Inhibit bone healing

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9
Q

Codeine phosphate MOA

A

Metabolised to morphine by CYP2D6 enzymes. It acts a partial agonist on the u opiod receptor expressed throughout the CNS and PNS. This leads to closure of N-type voltage depends Ca2+ and opening of Ca2+ dependent inwards K+ channels.

This = membrane hyperpolarisation, prolonging action potentials and inhibiting nociceptive pathways in the CNS

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10
Q

SE codeine

A

Constipation and nausea
Risk of opiate toxicity esp in those with renal failure
Resp depression and hypotension

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11
Q

CI codeine

A

COPD, acute asthma, hypotension, shock, hepatic and renal impairment

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12
Q

Tramadol

A

Similar MOA to codeine but acts on muscarinic and serotonin receptors. Lower incidence of constipation, increased risk of serotonin syndrome if combined with SSRI’s and SNRI’s

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13
Q

Strong opiods

A

Morphine - PO,IV, SC, PCA, - oromorph PO, MST
Fentanyl - patch
Diamorphine IV/SC
Oxycodone - SC, IV, PO

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14
Q

MOA morphine

A

Full agonist at the u opiod receptor. leads to closure of the N type voltage dependent Ca2+ channels opening of Ca2+ dependent inward K+ channels leads to a pre synaptic inhibition of neurotransmitters due to membrane hyperpolarisation

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15
Q

SE morphine

A 
Constipation and nausea
Pruritus 
Urinary retention and euphoria 
Hypotension
Bronchospasm
Respiratory depression
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16
Q

Opiate OD

A

PC myoclonic jerks, bilateral pin point pupils, reduced respiratory rate, hallucinations and confusion. Increased risk if alcohol misuse aswell

IV naloxone stat!

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17
Q

Safe prescribing of opioids

A

Always prescribe with an antiemetic and laxitive
PRN breakthrough is 1/6th-1/10th of daily dose
Metabolised @ liver review dose regularly for efficacy and side effects
In renal failure/AKI opioids can accumulate so beware

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18
Q

Interactions of morphine

A

CNS depressants such as alcohol, sedatives and hypnotics increase the risk of resp depression

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19
Q

Acute severe pain

A

Burns, #NOF, amputation IV 2mg rapid acting and strong enough to make patient comfortable . Titrate dose up to symptom relief. Crucial to monitor resp rate and BP!

Give with metaclomprimide and a laxative

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20
Q

Post op analgesia

A

Combination of opiod and non opioids

IV via PCA. Allows pt to control their pain via a button set to deliver a pre set bolus. There is then a fixed lock out time until another can be delivered

Oral analgesia - paracetamol, NSAIDs and MST

Epidural increased side effect profile - pruritus, urinary retention and N/V. Small change of haematoma, infection etc

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21
Q

Pros and cons of PCA

A

+ve - No nurse input needed once set up, pt doesn’t have to wait, autonomy, excellent pain relief

-ve - calculations are needed which increases the risk of error and potentially OD, lack of concordance between machines makes set up challenging, drug security, confusion about use

Discontinue as pain subsides, trip hazard, its dislike being connected to things!

22
Q

Discharge and pain relief.

A

Regular analgesia oral route only
Information about frequency of dosing and max dose available
Advice when to take, whether to avoid alcohol etc
SE to watch for
Inform GP about length go course and arrange follow up

23
Q

Neuropathic pain PC

A

Sharp stabbing burning pain, linked to allodynia (pain from non painful stimuli), numbness and itching

May be seen in patients with MS, shingles, chemotherapy etc

24
Q

Tricycle antidepressants (Amitriptyline) MOA

A

Act to inhibit the reuptake of noradrenaline and serotonin giving increased availability in the synaptic cleft. This increased concentration and prolonged effect of neurotransmitters allows greater action potential transmission. Block the h1 and act receptors

25
Q

Indications for TCAs

A

Neuropathic pain, depression and panic disorder. can take 2 weeks to work

26
Q

SE TCAs

A

Antagonise H1 receptors = sedation
Muscarinic ach = urinary retention, dry mouth, pupil dilation, fever and tachycardia
a1 adenoreceptors = postural hypotension

Cardiac arrhythmia, prolongation of PR and QT interval, anxiety, severe confusion

27
Q

Interactions TCA

A

MAOIs - increased risk of hypertensive crisis and hyperpyrexia
Increased risk of OD and serotonin syndrome with SSRIs
Antagonise and reduced the seizure threshold of antiepileptics

28
Q

Gabapentin and pregabalin MOA

A

Act as GABA analogues, bind to a2 delta protein of voltage gated Ca2+ channels exhibiting a neuroinhibitory effect

Can be used for neuropathic pain and partial seizures that have 2ndary generalisation

29
Q

SE of gabapentin and pregabalin

A

GI upset - N/V, diarrhoea
Wt gain, myoclonic jerks
Visual disturbances - diplopia and blurred vision
Leucopenia
Pleural effusions
Cerebellar side effects - DANISH (often with rapid withdrawal or titration)

30
Q

Interactions of pregabalin or gabapentin

A

Increase the risk of CNS depression when given with opiates

Reduced bioavailability when taken with antacids

31
Q

Other adjuvants

A

Corticosteroids = used if MSCC, increasing ICP, soft issue infiltration and liver capsule pain

Bisphosphanates = bone pain and hypercalcemia

Antispasmodics = hyoscine butyl bromide for bowel colic and bladder spasms

Muscle relaxants = baclofen and benzodiazepams used for seizures also

32
Q

Lidocaine patches

A

Opiod sparing effect

33
Q

Opiate titration

A

Initially may be IR or MR.
Breakthrough dose = 1/6-1/10 of daily dose
To recalculate daily dose = total dose + PRN breakthrough
Don’t increase daily dose above 50%
Monitor regularly, docusate and metacloprimide

34
Q

Prescribing different morphine preparations

A

Modified release = 1/2 dose of instant release

SC morphine = 1/2 dose of oral

SC dimorphine = 1/3 dose of oral morphine or 3/2 dose of SC morphine

35
Q

Common causes of constipation at the end of life

A

Opiates
Hypercalcemia
Bowel obstruction
Dehydration

Don’t neglect other causes its not always the morphine!!

36
Q

Syringe driver

A

SC morphine given continously throughout the day to ensure maximum pain relief at the end of life. If starting syringe driver ensure it is commenced 4hrs before the next scheduled analgesic dose to prevent gap in pain relief.

37
Q

Different opiods

A

Alfentanil - 30x stronger than morphine used for pt in renal failure with eGFR <30 due to no accumulation of toxic metabolites

Diamorphine - 2x as strong as morphine used when morphine dose exceeds 360mg/2hrs as this is the largest volume the syringe driver can hold

Fentanyl - 100x as strong available in transdermal patches

38
Q

4 medications at the end of life

A

Pain and breathlessness
Agitation
N/V
Respiratory secretions

39
Q

Pain and breathlessness

A

eGFR >30 = 2.5mg morphine SC

eGFR <30 = 100 micrograms alfentanil SC

40
Q

Agitation

A

2.5mg midazolam SC. Short acting benzodiazapem to help with agitation, restlessness, anxiety and myoclonus. Enhances effect of GABA allowing neuronal inhibition

41
Q

Nausea and vomiting

A

eGFR > 30 Cyclizine 50mg 8hrs
- H1 receptor antagonist acts on the chemoreceptors in the medulla oblongata. Inhibits the chemoreceptor trigger zone
SE = drowsiness, headache, antiach effects, increased sedative effect with opiods, renal excreted

eGFR < 30 Haloperidol 1mg SC QDS
Atypical antipsychotic mixed antagonist for muscarinic, serotonin and histamine receptors

42
Q

Respiratory secretions

A

eGFR > 30 = hyoscine hydrobromide

eGFR < 30 = hyoscine butylbromide

43
Q

Prescribing in renal failure

A

Kidney is an important organ to regulate body fluids, remove metabolic waste, excrete drugs and maintain electrolyte balance

Crucially give smaller doses more frequently, be aware of nephrotoxic drugs, ensure the pt is hydrated, caution in drugs with a narrow therapeutic window

44
Q

Distribution in renal impairment

A

Due to reduced protein levels there is often increased free concentration of the drug leads to increased pharmacokinetic effects

45
Q

Drug absorption

A

Can be altered if gastric pH is increase or with the presence of oedema in the interstitial mucosa. This leads to a reduced bioavailability

46
Q

Metabolism

A

Most drugs are biotransformed to metabolites and then excreted. If the t1/2 for a drug to be metabolised is increased then it will take longer to be eliminated

47
Q

Excretion

A

Effect of renal disease is most obvious with the elimination of the drug.

Renal clearance = urinary excretion
plasma drug conc

48
Q

Creatinine clearance

A

1.23 (female) x 140-age x wt
serum creatinine

When this falls <15 large reduction in dose
30-60 reduce dose

49
Q

Corrected dose

A

Normal dose x pt creatinine clearance

normal cr clearance

50
Q

Pre-renal nephrotoxic drugs

A

NSAIDs = by inhibition of prostaglandin synthesis lead to a vasoconstriction of the afferent glomerular arteriole. This means the glomerulus is underperfused

ACEi/ARBs = reduce circulation levels of angiotensin this prevents vasoconstriction of the efferent arteriole and leads to reduced glomerular filtration pressure

51
Q

Intrinsic nephotroxic drugs

A

ATN = aminoglycosides, ciclosporin

TIN = pencillins, diuretics, NSAIDs, sulphonamides, rifampicin

52
Q

Post renal nephrotoxic drugs

A

TCAs may result in urinary retention

Methotrexate = crystaluria UTI

CPTP (11 decks)

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