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Olivia MD3 1st semester > Pain medication > Flashcards

Pain medication Flashcards

1
Q

what type of pain stimulus can’t we detect?

A

radiation e.g. sun damage

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2
Q

what type of pain nerve fibres are more likely to be found in somatic nervous system

A

A delta fibres

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3
Q

what type of pain fibres are more likely to be found in the visceral system?

A

c fibres (because slow transmission)

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4
Q

what are some ways you can classify pain?

A 
neuropathic
somatic
visceral
inflammatory
acute
chronic
referred
psychosomatic
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5
Q

under anaesthetic what parts of the pain nervous system are blocked?

A

cognitive tertiary pain centre asleep-hypnosis

muscle (primary pain centre) under paralysis

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6
Q

what happens to pain threshold and pain tolerance levels in the older patient? and what is the implication of this?

A

As age increases, pain threshold increases but pain tolerance decreases.

This can mean that pain in elderly patients can present late; so need to be more suspicious about the degree/severity of the tissue damage

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7
Q

what type of pain does NSAIDs manage the best?

A

peripheral inflammatory pain

also has a central component- by inhibiting COX in the brain

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8
Q

mechanism of paracetamol?

A

unknown actual mechanism

but appears to stop upregulation of pain receptors

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9
Q

what type of pain are opiates good for?

A

acute nociceptive pain

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10
Q

what is heroin

A

is a type of opiate

  • -> converts to morphine in the brain
  • -> double to potency of morphine
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11
Q

SE of opiates?

A

reduced respiratory drive (very rare with good titration of opioids)
N+V (in about 40% of patients)
constipation (most common SE)
itch (intrathecal or injectable opioids)
poor dental hygiene (less saliva/dry mouth, particularly for methadone)
cerebral dysfunction (usually signs of toxicity)

with prolonged use- reduced HPA axis and reduced bone mineral density

  • risk of tolerance
  • risk of opiate increased hyperanalgesia
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12
Q

why are opiate medications generally ineffective in chronic pain?

A

with chronic use of opiates, tolerance increases and opiate induced hyperanalgesia occurs

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13
Q

what type of opiate is good for chronic pain and addiction medicine and why?

A

bupremorphine, a partial agonist and blocker; also acts on kappa receptors; milder effect

methadone replacement therapy- longer half life

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14
Q

what happens when you withdraw from chronic opiate use?

A

diarrhoea, sweating
all over generalised pain
increased respiratory rate

–> generally the opposite effect

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15
Q

what do we need to give for patients who have been on post operation opiates?

A

need to give oxygen, especially as night (this is to prevent hypoxia)

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16
Q

what is ketamine?

A

NMDA receptor blocker; for acute and neuropathic pain

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17
Q

what is gabapentin (describe what type of drug it is)

A

calcium channel blocker (anti-convulsant originally)

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18
Q

what does psychology, CBT, mindfulness do to the pain system

A

increase descending inhibition of pain systems

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19
Q

what is a downside of fentanyl?

A

easy to gain tolerance; short acting

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20
Q

what is pethidine usually used for now?

A

labour (obstetrics)

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21
Q

what are the downsides of pethidine?

A

risk of seizures
addictiveness

not really used much now

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22
Q

describe tapentadol

A

inhibits noradrenaline reuptake pathways
weaker opioid effect- better for the bowel/GIT system
?less addictive than other opiates

good for chronic pain

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23
Q

what factors should you consider in managing a patient’s chronic pain?

A

who is the person? (e.g. education status/premorbid function/overlying mental illness/workers compensation etc)

what is the mechanism?
(inflammatory/neuropathic/nociceptive etc)

what is the impact?
(functioning/ consider other supportive therapy e.g. psychotherapy for example)

–> considering these questions will help to dictate mx

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24
Q

why is pain good for the body?

A

helps to detect potential for tissue damage, allowing higher CNS centres to make compensatory behavioural changes e.g. step off the pin on the floor; take hand away from flame on stove

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25
Q

what condition is carbamazepine is used first line for pain relief?

A

trigeminal neuralgia

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26
Q

where are miu receptors located in the CNS system in high numbers?

A
  1. periaquaductal gray area of midbrain

2. spinal cord

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27
Q

what is opioid induced hyperanalgesia?

A

Opioid-induced hyperalgesia is a state of nociceptive sensitization with a paradoxical response whereby a patient receiving opioids for the treatment of pain may actually become more sensitive to certain painful stimuli and in some cases, experience pain from ordinarily nonpainful stimuli (allodynia)

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28
Q

what do you need to consider before commencing a patient on opiate medication for their pain?

A
  • what type of pain is it? acute or chronic pain?
  • is there a risk of addiction?
  • is there a risk of psychiatric illness +/- suicidal intent?
  • are there any other available options for other types of analgesia
  • is non-opiate non-adjuvant therapy needed?
  • does this patient present risks to opiate side effects including respiratory depression etc?
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29
Q

a female patient has MSK type pain and is using panadol intermittently for this. She says the pain is getting worse and that she has had it for many months. She requests a stronger analgesic drug. What might you recommend?

A
  1. first try scheduling regular paracetamol rather than using it on a PRN basis
  2. encourage non-pharmacological approaches such as psychological support/aerobic exercise/weight loss
  3. arrange follow up and review
30
Q

benefits of transdermal opioid patches?

A

passes first pass metabolism hence reduced GIT effects
easy to apply
lasts for up to 72 hrs
good for chronic pain

31
Q

what is durogesic?

A

fentanyl

32
Q

what is norspan?

A

buprenorphine

33
Q

what are some disadvantages of using transdermal opioid patches?

A

localised skin reactions to the patch
patient may apply more than one and this may lead to opioid complications such as resp depression (like the sim patient last year)

34
Q

what is the best treatment of chronic pain?

A

multimodal approach to chronic pain
this includes drugs both opioid and non-opioid, psychotherapy, social support, compensatory mechanisms etc

there is a limited role of opioid medications in chronic pain

35
Q

what is the half life of oral morphine?

A

4 hrs so needs to be given 4hrly

36
Q

what is good about fentanyl?

A
  • no oral form

- not metabolised by kidneys–> hence can be used in reduced renal function/CKD

37
Q

describe the WHO pain ladder?

A
  1. Simple analgesia- NSAIDs/panadol
  2. Weaker opiates- codeine/tramadol/tapentadol
  3. Stronger opiates- morphine/fentanyl/hydromorphine/oxycodone/methadone/buprenorphine/pethidine
38
Q

what is the conversion ratio of hydromorphine to morphine?

A

5-7: 1

39
Q

what is the strongest opiate?

A

hydromorphine

40
Q

what is the most abused prescription opiate?

A

oxycodone

41
Q

how long does methadone last in the system?

A

depends on cytochrome p450 system in each individual

from 3hrs to 150hrs

42
Q

what are some benefits of methadone

A

prevent opiate withdrawal for many hrs/days–> so good for withdrawal/opiate replacement therapy

blocks NMDA receptor–> prevents acute pain–> chronic pain

useful in neuropathic pain (NA reuptake inhibitor)

43
Q

what is targin?

A

oxycontin/naloxone

44
Q

what is the ceiling dose of targin?

A

40/20mg bd

45
Q

what are some disadvantages of targin?

A

ceiling dose at 40/20mg bd –> naloxone outweighs analgesic effects at higher doses

in patients with liver issues–> naloxone toxicity can occur

usually the cancer patients have constipation due to other causes and so naloxone is not helpful anyway.

46
Q

What is MS contin?

A

slow release morphine

47
Q

what are the dangers of panadeine fort/codeine?

A

risks of paracetamol toxicity as it is so readily available

respiratory arrest of infant during breastfeeding due to codeine

really addictive

differently metabolised depending on individual cytochrome p450

48
Q

how does codeine work?

A

converts to morphine via cytochromeP450, 2D6

49
Q

what is the main sign that indicates opioid toxicity?

A

myoclonus

50
Q

what are some examples of adjuvant analgesics?

A 
anti-depressants (TCA)
clonidine (alpha 2 adrenergic receptor agonist)
ketamine
anti-convulsants (pregabalin/gabapentin)
antibiotics
oxygen
steroids! (euphoric effect)
51
Q

what are some SE of anti-convulsant analgesics

A

drowsiness
ataxia
weight gain
peripheral oedema

52
Q

SE of NSAIDs?

A

renal issues–> potential for triple whammy
fluid retention–> can exacerbate HT and CCF
gastric ulcers
interactions with other drugs-> increased bleeding risk

53
Q

how long does the analgesic effect from a fentanyl patch last for?

A

15-20mins

54
Q

how might we manage the pain caused by radiotherapy?

A

NSAIDs/steroids bc it is usually inflammatory type pain

55
Q

tell me about norspan, what is it, how often is the dosage and what are the dosages?

A

Norspan= buprenorphine
controlled release transdermal patch
dosed every 7 days
dosage increments are 5,10,20 micrograms/hr

56
Q

what is oxycontin and how often do we dose it?

A

oxycodone SR every 12 hrs

57
Q

what is the difference between mscontin and msmono tablets?

A

both are morphine sulfate but one is 12 hrly dosing and one is 24 hrly dosing

58
Q

what is oxynorm and what forms does it come in?

A

oxycodone immediate release- comes in injection/infusion/tablets/liquid

59
Q

what is sevredol?

A

immediate release morphine sulfate

60
Q

what are some SE of tramadol

A

Tramadol can cause dizziness, sweating, dry mouth, nausea and postural hypotension in some patients. It can induce seizures, even within the therapeutic dose range.

61
Q

why might tramadol and codeine not be effective in some patients?

A

some patients do not have the cytochrome p450 2D6 pathway required to metabolise these drugs to morphine analogues

62
Q

what is the potency of oxycodone to oral morphine?

A

3:1

63
Q

describe the mechanism of action of opioids in general?

A

Opioids act by causing presynaptic inhibition of neurotransmitter release from C-fibre terminals, postsynaptic inhibition of evoked activity in nociceptive pathways, or disinhibition of other circuits regulating nociceptive transmission.

Supraspinal opioids increase descending inhibition of spinal nociceptive transmission.

64
Q

what type of drug is clonidine?

A

alpha 2 adrenergic agonist

65
Q

how might we manage pain from bony metastases?

A

bisphosphonate therapy (though bisphosphonates actually have no effect on pain centres/pathways)

66
Q

what are some drugs that we can use for neuropathic pain?

A

TCA antidepressants like amitriptyline, nortriptyline

anticonvulsants like valproate, pregabalin, gabapentin, carbamazepine

methadone

ketamine

67
Q

what is a SE of ketamine?

A

hallucinations, dissociation

68
Q

why are modified release preparation of opiates generally preferred by doctors for malignant pain?

A

modified release preparations reduce peaks and troughs in blood opioid concentrations, thus reducing drowsiness and breakthrough pain

69
Q

if a patient has been taking 30mg of oral morphine (modified release) 12 hrly, and requires 3 x breakthrough 10mg oral morphine (immediate release), what change to this analgesia regime should we consider? How might we do this?

A

So if there is 3 break through episodes of pain in 1 day, then we need to consider changing the MR dose of morphine.

so the patient is taking 30 x 2= 60mg for 1 day of MR oral morphine, and 3 x 10mg of IR morphine. 60+30= 90mg.

so to manage their pain they need a total dose of 90mg of oral morphine over 24 hrs.

We want to give it 12 hrly, so 90/2= 45mg. MR morphine comes in 50mg so 50mg bd may be the new regime.

70
Q

tell me about breakthrough opiate pain management and what doctors need to consider e.g. some practice points?

A

breakthrough doses generally should be 1/12 to 1/6 of the total daily morphine dose.

Breakthrough opiates are generally immediate release, and should be taken as needed by the patient. Advise the patient not to withhold it if they require extra pain relief, and to continue their baseline daily MR opiate regime as normal.

Try to leave at least 30mins between each breakthrough dose.

If the patient requires 3 or more breakthrough doses in a day, you need to reconsider the analgesia regime. In general, you add the breakthrough doses to the regular total 24hr dose of morphine

Olivia MD3 1st semester (16 decks)

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