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Oncology, pharmacology, anaesthetics (IHD DEN303) > Analgesia > Flashcards

Analgesia Flashcards

1
Q

Pain definition

A

An unpleasant sensory and emotional experience which we primarily associate with tissue damage or describe in terms of tissue damage or both

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2
Q

Inadequate pain relief

A

Global concern for pts and practitioners

Pain not always cured and requires continuous medical management, the same as any other disease process

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3
Q

How many people in the UK suffer from persistent pain?

A

About 40%

Around 28 million people

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4
Q

Pain pathway - why we feel pain (injury)

A

Normal –> protective
–> acute –> reflexes
–>prolonged –> inflammation and repair
(acute can –> prolonged)

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5
Q

Congenital insensitivity to pain

A

SCN9A gene mutation in humans

-Nav1.7 voltage-gated sodium channel mutations in a-subunit cause loss of function

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6
Q

Sources of pain

A

Injury

Disease

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7
Q

Fracture types

A

Oblique: diagonal break across bone
Comminuted: break in three or more pieces and fragments are present at same fracture site
Spiral: break spirals around bone (common in twisting injury)
Compound: broken bone pierces skin, causing risk of infection

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8
Q

Sensory pathways

A

Transduction: conversion of a sensory stimulus from one form to another e.g. nerve endings in skin?
Transmission: thalamus, spinal cord, sensory fibres (touch, pain)
Somatosensory cortex: perception
Limbic (amygdala): perception/ learning

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9
Q

Pain modulation

A

Emotion and attention profoundly modulate nociception
Amount of pain experienced does not necessarily relate to severity of tissue damage
Anxiety > pain transmission
Complex cultural and contextual influences

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10
Q

Chronic

A

Abnormal –> non-protective –> chronic (pain as disease)

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11
Q

Therapeutic goal for chronic and prolonged pain

A

Return sensitivity to normal thresholds without loss of protective function

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12
Q

NSAIDS and opioids problematic

A

??

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13
Q

Dental pain

A

Infection - acute inflammation
Exposed nerve endings: neurogenic pain
Swelling in confined space: pressure effects
Fear and anxiety

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14
Q

Treatment of pain

A 
< tissue damage
-NSAIDS (non steroidal anti inflammatory drugs)
-steroids
-cooling
Nerve block: LA
Spinal cord: opioids
CNS: opioids, psychological factors
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15
Q

WHO cancer pain relief steps

A 
Believe the pt
History of symptoms
Assessment of severity
Physical examination
Appropriate pain management
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16
Q

WHO analgesic ladder

A

Step 1: mild to moderate pain
-non-opioids e.g. paracetamol +/- NSAID
Moderate
-weak opioids e.g. tramadol, dihydrocodeine +/- non-opioids e.g. paracetamol +/- NSAID
Step 3: severe pain
-strong opioids e.g. morphine, diamorphine, fentanyl patch +/- non-opioids e.g. paracetamol and/ or NSAID
Co-analgesics: other drugs, nerve blocks, surgery, radiotherapy, complementary therapies, addressing psychosocial issues

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17
Q

Analgesic ladder assumptions

A

Synergism
Overall philosophy assessing severity, starting at lowest level and increasing if necessary
Joint Royal Colleges Report (1988) quality of analgesia in hospital practice is inadequate

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18
Q

Placebo effect

A

Placebo is anything administered which is pharmacologically and physiologically inert
Not ineffective therapeutically
-can have measurable effect
Reassurance and confidence in one’s therapy may also have an effect

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19
Q

WHO analgesic ladder: paracetamol

  • mechanism
  • effect
  • route
  • dose
A

Mechanism of action unknown - inhibitor of the synthesis of prostaglandins
Analgesic, antipyretic, not much anti-inflammatory effect
Oral, soluble potions, IV, rectal
1g 4-6 hourly adult dose
-4g in 24hr

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20
Q

Paracetamol: adverse effects

A

Uncommon
Hepatotoxicity if overdose
-early treatment with N-acetyl-cysteine
-not absolutely contraindicated in liver disease

21
Q

WHO analgesic ladder: NSAIDs

  • examples
  • mechanism
  • effect
A

Aspirin, ibuprofen, naproxen, indomethacin
Irreversible inhibitor of cyclo oxygenase (COX1 and/ or COX2) enzyme
COX generates inflammatory mediators: prostaglandins and thromboxanes
COX widely distributed, different isotypes
COX inhibitors effective at < acute inflammation

22
Q

NSAIDs adverse effects

A

Due to extension of therapeutic effects
GI tract:
-occult GI blood loss from minor breaches in mucosa (loss of PGE)
-peptic ulceration
-general GI upset, indigestion
Renal function: < in intrarenal blood flow can cause renal failure
Platelets: COX inhibition, bleeding tendency
CV: as result of altered renal function, fluid retention ca precipitate heart failure
Respiratory: some ‘aspirin sensitive’ asthmatics

23
Q

COX2 inhibitiors

A

Newer
Parecoxib celecoxib
< bleeding as GI tract and platelets have mainly COX1
Not less nephrotoxic

24
Q

COX2 and CV disease

A

Absence of antiplatelet effects
Slightly pro thrombotic
> risk of MI and stroke
Contraindicated in CV disease

25
Q

NSAIDs and elective surgery

A

Need to stop at least 5 days before elective surgery
Bleeding at operation: platelet transfusion
Consider platelets if emergency surgery

26
Q

Weak opioids: moderate to severe pain

  • type
  • mechanism
  • effect
A 
Codeine or di-hydrocodeine
Both metabolised to morphine
-metabolism varies
-some people have minimal enzyme and hence less effective
Weak opioid effects
27
Q

Weak opioids: moderate to severe pain

-adverse effects

A 
CV: < sympathetic outflow, > vagal tone
-bradycardia
-hypotension
-excitation
Respiratory: inhibit cough reflex, respiratory depression
GI tract: < gastric motility
-constipation
-nausea
-vomiting
28
Q

CNS opioid effects

A

Sedation, euphoria,(dysphoria), excitation

29
Q

Analgesia in SC and brainstem

A

Spinal cord: < pain fibre transmission, kappa opioid receptors
Brainstem: < pain projection to higher centres, Mu opioid receptors

30
Q

CNS opioid adverse effects

A

Respiratory drepression, < brainstem responseto hypoxia and hypercarbia

31
Q

Reversal of opioid effects

A

Naloxone 400mg IV

  • dramatic reversal of Mu receptor opioid effects
  • far less effective on newer synthetic opioid-like substances as their effects in CNS are less well defined
32
Q

Opioid dependency

A

Chronic opioid use: < effect as CNS becomes more tolerant

-dose increase

33
Q

Opioid withdrawal

A 
Acute withdrawal -->
-hypertension
-tachycardia
-tachypnoea
-diarrhoea
-sweating
-anxiety
-hallucinations
Any chronic opioid medication will precipitate some withdrawal reaction if stopped suddenly
34
Q

Newer oral opioids

  • types
  • effectiveness
  • effects
A

Tramadol and Nefopam
As effective as codeine, much less constipation hence very frequently prescribed
‘Oramorph’ - lower dose oral morphine
Usual opioid effects: sedation, dizziness, nausea
Occasional flushing/ sweating with tramadol

35
Q

Tramadol adverse effects

A

> number of fatalities from OD causing respiratory depression
Dependency develops with long term use
-difficult to withdraw

36
Q

Tramadol legislation

A 
Controlled drug (class 3) 
Limit to maximum prescription
Must be signed for
37
Q

Weak opioids/ paracetamol combinations

A

Co-codamol, co proxamol, various
Now less popular than either nefopam or tramadol
Need to include paracetamol in total 24hr maximum of 4g
Check BNF if an unfamiliar oral analgesic

38
Q

Group cautions prescribing opioids

A

Dependent on hepatic metabolism and renal excretion of metabolites
-some active metabolites
Prolonged effect in liver or renal impairment
Respiratory disease, sleep apnoea, > sensitivity
Aim for minimum duration of prescription

39
Q

WHO analgesic ladder: severe pain

  • types
  • dose
A

Morphine; oral, SC, IV
Diamorphine: SC, IV
Fentanyl patch (transdermal)
Oral dose approx. 3x IV dose for same efficacy

40
Q

Post-op analgesia

A

If required IV in recovery 2mg increments every 3min until comfortable (10 - 20mg) in recovery setting
-must be given by trained staff
Ward care: morphine 10mg SC 2 hourly usually co-prescribed antiemetic; Ondansetron or cycizine

41
Q

Morphine pt controlled analgesia

A

Syringe driver intermittent IV bolus delivery initiated by pt (push button)
1mg minimum frequency every 5 mins
Multiple studies show approx. 1/3 dose compared to nurse administered SC morphine

42
Q

Routes of opioids administration

A 
Oral
IV
SC and IM
Rectal
Intrathecal (spinal canal --> CSF)
Epidural
Buccal
Trans dermal
43
Q

Severe pain: chronic pain

A 
Oral morphine syrup or tablets
Morphine SC infusion
Diamorphine SC infusion
Fentanyl transdermal patch lasts 5 days
Buprenorphine patch
44
Q

Gabapentin and pregablin

A

Effective for chronic neurogenic pain

< central transmission and pain projection

45
Q

Adverse effects of gabapentin

A

Sedation, dizziness, nausea, occasionally hypotension

46
Q

Antidepressant drugs

A

Amitryptiline
Duloxetine and Citalopram
Have useful adjuvant effects in neurogenic pain
-also some antidepressant effect can be useful

47
Q

Antidepressant drugs adverse effects

A

GI and CVS

48
Q

Psychological support

A

Pain management

49
Q

Pain management

A

Assessment of severity in context of daily living and functioning
Acute pain; large variation in requirements complex
-amount of analgesia (i.e. correct dose) required is ‘enough to stop pain’
Synergism of different drug actions, psychological factors

Oncology, pharmacology, anaesthetics (IHD DEN303) (6 decks)

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