Palliative care Flashcards

1
Q

palliative care definition

A

an approach that increases the Qol of patients and their families
for those that are facing problems associated with life-threatening illness
is symptomatic rather than curative
through the identification of pain and other problems; physical, psychological and spiritual

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2
Q

how often does the GP have to visit at end of life

A

every 2 weeks or else will go to coroner

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3
Q

how long have I got?

A

doctors tend towards over optimism

this denies the opportunity to advace care plan, make other informed choices, risks futile infvestigations

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4
Q

gold standards framework - prognostic indicator guidance

A

three triggers for palliative care are used

  1. the surprise question - would you be suprised if the patient died in the next 6-12 months
  2. general indicators of decline - are there no further active treatment options
  3. specific clinical indicators - e.g. needing ventilator support
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5
Q

types of pain fibres

A

c fibres - unmyelinated
transmit dull, poorly localised, ill-defined sensation

a delta fibres - myelinated
transmit fast, sharp, well localised sensation - synapse with 2nd order neurons in the dorsal horn - gate control theory of pain

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6
Q

total pain

A

a concept that recognises pain as being physical, psychological, social and spiritual (PPSS)

describes how pain is not just a physical sensation but might be a consequence of lonliness, spiritual distress, inappropriate diet, influenced by financial problems…

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7
Q

WHO pain ladder

A
  1. NSAIDs and paracetamol
  2. weak opiods - DTC (do think codeine; dihydrocodeine, tramadol, codeine)
  3. strong opioids - FMOD (four more opioids down) - fentanyl, morphine, oxycodone, diamorphine)
  4. nerve block, epidurals, PCA pump, neurolytic block therapy, spinal stimulators)
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8
Q

counselling on morphine side effect

A

common initially - N+V
common ongoing - contipation
occasional - dry mouth, sweating, pruritus, hallucination

rare - with toxicity can cause respiratory depression

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9
Q

how can SE of morphine be minimised

A

by switching to an alternative:
- oxycodone - reduced hallucinations + nausea but INCREASED constipation
- fentanyl - (patch = continuous levels - don’t apply heat to patch (will work faster), don’t cut then and put on different parts, store them flat so is all even across patch)
is less constipating than morphine

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10
Q

dose conversion of morphine - what is 10mg of morphine equivalent to

A

100mg codeine

100mg dihydrocodeine

100mg tramadol

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11
Q

types of morphine

A
Immediate release:
- Oramorph liquid
- Sevredol tablets
Rapid onset 20 - 30 minutes (time to peak plasma concentration 15-60 minutes)
Starts to wear off at 4 hours 

Slow release:
MST (= morphine slow release tablet)
Zomorph
Given every 12 hours

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12
Q

Patient is on 20mg morphine BD + takes 5mg four times in 24 hours as PRN
how to titrate dose so that pain is controlled if it isn’t

A

is on 60mg total

so make new BACKGROUND dose 60mg

so give 30mg BD

for the breakthrough calculate 1/6th-1/10th of NEW daily dose so 60/10 = 6, 60/6 = 10
6-10mg PRN

SO 30mg BD + 6-10 PRN (4 times)

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13
Q

adjuvants to the WHO pain ladder

A
  • Anti-depressants – e.g. in neuropathic/nerve pain
  • Anti-convulsants – gabapentin, pregabalin, carbamazepine for nerve pain
  • Benzodiazepines – e.g. for nerve pain
  • Smooth muscle relaxants
  • Steroids
  • Bisphosphonates
  • Corticosteroids
  • Nerve block
  • TENS – gate control theory of pain
  • (Radiotherapy)
  • (Surgery, Chemotherapy)
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14
Q

analgesia in cancer pain

A
  • By mouth - don’t want to be sticking needles in them – mouth is the preferred method
  • By the clock – regular and PRN use
  • By the ladder - WHO pain ladder
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15
Q

somatic pain definition and management

A

aching, often constant. may be dull or sharp.
well localised pain

e.g. bone mets, arthritis, fracture

often treated with NSAIDs
degree of pain relief with opiods

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16
Q

visceral pain definition and management

A

constant or crampy
poorly localised
referred

often responds well to opioids
also consider steroids e.g. dexamethasone for tumour oedema

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17
Q

neuropathic pain

A

• caused by a lesion or disease of the somatosensory system, including peripheral fibres (Aβ, Aδ and C fibres) and central neurones

e.g. diabetic neuropthay (causing dyseathetic pain - abnormal), trigeminal neuralgia, nerve root compression

partially responsive to NSAIDs and opioids
other options include anti-depressants, anti-convulsatns, steroids, nerve block

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18
Q

incident pain

A
  • E.g. pain precipitated by movement
  • is a major problem for most patients with cancer pain – the problem is that doses of opioids high enough to control episodic incident pain are too high when that pain is absent, leading to adverse effects
  • and usual analgesics don’t work quickly enough to help
  • Traditional treatment has been oral liquid morphine (10mg/5ml )
  • Transmucosal opioids may be faster acting e.g. Fentanyl lozenge
  • Newer alternatives include sublingual and buccal Fentanyl tablets / nasal sprays
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19
Q

how is breakthrough pain dose calculated

A

as a 1/6th of total (24hr) morphinne requirements

e.g. for patients on 15mg BD MST - give 5mg oromorph for breatkrhough

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20
Q

maximum PRN dose of morphine

A

max 6 x a day

e.g. 2-4 hours PRN

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21
Q

side effects of opioids

A

most common = Constipation, nausea and sedation/drowsiness

others

  • Respiratory depression
  • Myoclonic jerks
  • Miosis
  • Dry mouth
  • Confusion
  • Visual hallucinations (Stop/reduce// switch - Haloperidol?)
  • Itching
  • Euphoria
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22
Q

how to manage the constipation, nausea and sedation SEs with opioids

A

Coprescribe laxative permanently e.g. polyethylene glycol and anti-emetic PRN first 5-7days

for sedation - assess – may pass / reduce but advise re e.g. driving

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23
Q

physical and pyschological dependence

A

physical = withdrawal syndorme occurs when an opioid is aburptly discontinued - this can happen in cancer patients

psychological = continued craving for an opioid which manifests as compulsive drug seeking behaviour - generally not seen in cancer care

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24
Q

rough percentage that you would increase background dose by for opioids

A

30-50%

25
Q

bone mets pain relief

A
not always responsive to morphine
NSAIDs
radiotherapy/surgery
bisphosphonates
steroids
26
Q

60mg morphine - patch equivelent

A

fentanyl 25mcg (microgram)

takes 12-72 hours to reach full strength on first application

27
Q

pros vs cons of syringe drivers - not just for a last resort

A

24 hour comfort, constant drug levels, once a day, independence and mobility, portable, combines several drugs, relatively non-invasive

disadvantages - staff training, infusion site problems, compatbility (some drugs aren’t compatable e.g. cyclizine and diamorphine cyrastalaize so stop the syringe driver working

28
Q

4 sources of input into the vomiting centre

A

chemoreceptor trigger zone
cerebral cortex
vestibular cortex
gut

29
Q

types of receptors in the chemoreceptor trigger zone

A

5HT - serotonin

D2 - dopamine

30
Q

symptoms of gastric stasis

A
epigastric fullness
early satiety
projectile or large volume vomiting
hiccups
regurgitation
nausea quickly relieved by vomiting
31
Q

treatment of gastric stasis

A

reduce volume of oral intake - little and often
reduce gastric secretions - H2 antagonists (rainitidine)

pro-kinetic agnets - dopamine D2 antagonists (metoclompramide or domperidone)

32
Q

domperidone vs metoclopramide

A

domperidone does not cross the BBB - words peripherally only so good for Parkinson’s disease

(domperidone does not act at d1 receptors like metoclopramide does)

33
Q

mecahnism of metoclopramide

A

dopamine D2 receptor antagonist and 5HT4 agonist

at CTZ and gut

34
Q

side effects of metoclopramide

A

risk of extrapyramidal SE as it crosses the BBB

abdominal cramps

Caution in young patients <20 years as risk of oculogyric crisis (dystonic reaction to certain drugs – prolonged involuntary upward deviation of the eyes)

35
Q

ondansetron mechanism of action

A

5HT3 receptor antagonist

acts at CTZ and gut

36
Q

uses of ondansetron

A

commonly used post surgery, chemo and radiotherapy

37
Q

side effects of ondansetron

A

constipation

QTc prolongation

38
Q

cyclizine mechanism of action

A

antimuscurinic and antihistamine activity

at CTZ and vestibular system

39
Q

cyclizine uses

A

good for motion sickness and vomiting secondary to raised ICP

good 1st line anti emetic in hospital

AVOID in HF

40
Q

side effects of cyclizine

A

due to antimuscurinic effects - dry mouth, constipation, sedation

41
Q

metoclopramide and cyclizine

A

Avoid prescribing together
Metoclopramide acts as a prokinetic through dopamine antagonism
Cyclizine slows gastric transit due to antimuscarinic effects therefore blocking the effect of metoclopramide

42
Q

where is the site of action of chemical and metabolic N+V

A

CTZ

via D2 and 5HT3 receptors

43
Q

treatment of nausea in chemical and metabolic causes (e.g. end stage renal failure)

A

D2 antagonists: haloperidol or levomepromazine

5HT3 antagonist - ondansetron

44
Q

SE of haloperidol

A

D2 receptor antagnoist at the CTZ

extrapyramidal SE
QTc prolongation
sedation

45
Q

levomepromazine mechanism

A
  • Broad spectrum antiemetic targets multiple receptor sites
  • Used as an antipsychotic but effective for nausea at low doses
  • Used commonly in palliative care e.g. bowel obstruction or if anti emetic and sedation needed
46
Q

levomepromazine SE

A

sedation

postural hypotension

47
Q

symptoms of raised ICP

A
  • Symptoms worse in the morning?
  • Headache – often described as pulsatile, may awaken the patient and usually last for hours
  • Nausea
  • Vomiting
48
Q

treating N+V due to raised ICP

A

anti-histaminie and anti-cholinergic agents

e.g. cyclizine

49
Q

treating motion sickness

A

anti-hitamine and anti-cholinergic agents

e.g. cyclizine

50
Q

metoclopramide and ondansetron

A

should not combine these IV due to risk of cardiac arrythmias

51
Q

bristol stool chart - types for constipation

A

type 1 and 2

52
Q

examples of stimulant laxatives

A

senna
bisacodyl

contradindicated in complete obstruction

they cause peristalsis by stimulating colonic nerves

53
Q

example of bulk forming laxative

A

isphaghula

54
Q

exampls of stool softener

A

docusate sodium

55
Q

examples of osmotic laxatives

A

lactuloase

movicol/macrogol

56
Q

causes of malignant bowel obstruction

A

o Extrinsic compression - Tumour, omental mets, malignant adhesions, radiation fibrosis
o Intraluminal occlusion e.g. annular tumour
o Motility disorder - Tumour infiltration of the mesentery

57
Q

management of malignant bowel obstruction if not suitable for surgery

A

pain/colic management with opiates of hyoscine butylbromide (aka buscopan - helps with abdominal spasms as is an antisecretory and is also used to stop respiratory secretions at end of life)
N+V - syringe driver with e.g. levomepromazine
dry mouth - ice chips and pineapple juice

58
Q

an alternative medication to hyoscine butylbromide (buscopan) for an antisecretory

A

octreotide

but is more expensive

both have SE of dry mouth