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Pharmacology (Den 303) > Introduction to the pharmacology of analgesic agents > Flashcards

Introduction to the pharmacology of analgesic agents Flashcards

1
Q

Analgesia requirements

A

Appropriate treatment of dental pain
Knowledge of patients concurrent analgesic medications
for chronic pain
Recognition of adverse effects and avoidance of potential
interactions.

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2
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 (IASP definition)

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3
Q

Inadequate pain relief

A

Inadequate pain relief is a global concern for patients and
practitioners. Pain is not always cured and requires
continuous medical management, the same as any other
disease process

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4
Q

How many people in the UK suffer from persistent pain?

A

About 40%, or as many as 28 million people

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5
Q

Pain normal –>

injury pain path

A

protective –> acute or prolonged (interchangeable)
acute –> reflexes
prolonged –> inflammation and repair

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6
Q

Congenital insensitivity to pain

A

SCN9A gene mutation in humans:
-Nav1.7 voltage-gated sodium channel mutations in the asubunit
cause loss of function

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7
Q

Sources of pain

A

Injury

Disease

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8
Q

Sensory pathways

A

Transduction
Perception - somatosensory cortex
Transmission - thalamus, spinal cord, sensory fibres (touch, pain)
Perception/ learning - limbic (amygdala)

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9
Q

Pain modulation

A

Emotion and attention profoundly modulate nociception.
The amount of pain experienced does not necessarily relate to the severity of tissue damage
Anxiety increases pain transmission
Complex cultural and contextual influences

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10
Q

Chronic pain path

A

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

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11
Q

Therapeutic goal of prolonged or chronic pain

A

Return sensitivity to normal
thresholds, without loss of
protective function

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12
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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13
Q

Treatment of pain

A 
Reduce Tissue damage:
-non steroidal anti-inflammatory drugs (NSAIDS)
-steroids
-cooling
Nerve block: LAs
-spinal Cord: opioids
CNS:
-opioids
-psychological factors
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14
Q

WHO: cancer pain relief

A 
Believe patient
History of symptoms
Assessment of severity
Physical examination
Appropriate pain management
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15
Q

WHO Analgesic ladder

A

Step 1: mild to moderate pain
-non-opioids + adjuvant analgesics
Step 2: moderate to severe pain
-weak opioids + non-opioids + adjuvant analgesics
Step 3: secere pain
-strong opioids + on-opioids + adjuvant analgesics

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16
Q

Analgesic ladder assumptions

A

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

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17
Q

Placebo effect

A

Placebo is anything administered which is
pharmacologically and physiologically inert
Placebo not ineffective therapeutically. Can
have a measurable effect
Reassurance and confidence in one’s therapy may also have effect

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18
Q

WHO analgesic ladder: paracetamol

A

Mechanism of action unknown – Inhibitor of the
synthesis of prostaglandins.
Analgesic, antipyretic, not much anti-inflammatory
effect
Oral, soluble potions, intravenous, rectal
1g 4- 6 hourly adult dose 4g in 24h

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19
Q

WHO analgesic ladder: paracetamol - adverse effects

A

Uncommon
Hepatotoxicity if overdose. Early treatment with
N-acetyl-cysteine
Not absolutely contraindicated in liver disease

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20
Q

WHO Analgesic Ladder: NSAIDs

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 are effective at reducing acute
inflammation
Adverse effects due to extension of therapeutic effects

21
Q

WHO Analgesic Ladder: NSAIDs - GIT

A

Occult GI blood loss from minor breaches in mucosa (loss of PGE). Peptic ulceration.
General GI upset, indigestion

22
Q

WHO Analgesic Ladder: NSAIDs - Renal function

A

Reduction in intrarenal blood flow can cause renal failure

23
Q

WHO Analgesic Ladder: NSAIDs - platelets

A

COX inhibition, bleeding tendency

24
Q

WHO Analgesic Ladder: NSAIDs - CV

A

As a result of altered renal function,

fluid retention can precipitate heart failure

25
Q

WHO Analgesic Ladder: NSAIDs - respiratory

A

Some ‘aspirin sensitive’ asthmatics

26
Q

WHO Analgesic Ladder: NSAIDs - examples

A

Ibuprofen, Naproxen, Diclofenac
Newer COX2 Inhibitors: Parecoxib Celecoxib
COX 2: Less bleeding as GI tract and Platelets have
mainly COX1
Not less nephrotoxic

27
Q

COX2 and CV disease

A

Absence of antiplatelet effects
Slightly pro thrombotic
> risk MI and Stroke
–> contraindicated

28
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

29
Q

Weak opioids - moderate - severe pain

A

Codeine/ Di-hydrocodeine

  • both are metabolised to morphine. Metabolism
    varies. Some people have minimal enzyme and hence less effective.
  • weak opioid effects
30
Q

Weak opioids - moderate - severe pain: CV

A

Reduced sympathetic outflow,
increased vagal tone. Bradycardia, hypotension,
excitation

31
Q

Weak opioids - moderate - severe pain: respiratory

A

Inhibit cough reflex, respiratory depression

32
Q

Weak opioids - moderate - severe pain: GIT

A

< gastric motility. Constipation, nausea

and vomiting.

33
Q

CNS opioid effects

A

Sedation, euphoria, (dysphoria), excitation
ANALGESIA
Spinal Cord: < pain fiber transmission kappa opioid receptors
Brainstem: < pain projection to higher
centers. Mu opioid receptors
Respiratory depression, reduced brainstem response to hypoxia and hypercarbia.

34
Q

Reversal of opioid effects

A

Naloxone 400 mcg i.v. dramatic reversal
of mu receptor opioid effects.
Far less effective on newer synthetic opioid like
substances as their effects in the CNS are less well
defined

35
Q

Opioid dependency

A

Chronic opioid use: reduced effect as CNS
becomes more tolerant. Dose increase.
Acute withdrawal: Hypertension, tachycardia,
tachypnoea, diarrhoea, sweating, anxiety, hallucinations.
Any chronic opioid medication will precipitate some
withdrawal reaction if stopped suddenly

36
Q

Newer oral opioids

A

Tramadol and Nefopam
As effective as codeine, less variability, much less
constipation hence very frequently prescribed.
“Oramorph”lower dose oral morphine.
Usual opioid effects: sedation, dizziness, nausea
Occasionally flushing / sweating with tramadol

37
Q

Tramadol adverse effects

A 
> number of fatalities from overdose causing respiratory depression.
Dependency develops with long term use which is
difficult to withdraw.
New legislation: Controlled drug (class 3). Limit to
maximum prescription. Must be signed for
38
Q

Weak opioid/ paracetamol combinations

A

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

39
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, increased
sensitivity
Aim for minimum duration of prescription

40
Q

WHO analgesic ladder - severe pain

A 
Morphine; oral, s.c., i.v.
Diamorphine s.c., i.v.
Fentanyl patch (transdemal)
Oral dose is approx 3x the i.v. dose for
the same efficacy
41
Q

Post op analgesia

A

If required i.v. in recovery 2mg increments every 3
minutes until comfortable (10 to 20mg) in a recovery
setting. Must be given by trained staff
Ward care: Morphine 10mg s.c. 3 hourly usually coprescribed
antiemetic; Ondansetron or cycizine

42
Q

Morphine px controlled post op analgesia

A

Syringe driver intermittent i.v. bolus delivery initiated by
patient (push button)
1mg minimum frequency every FIVE minutes
Multiple studies show: approximately 1/3 dose compared
to nurse administered s.c. morphine

43
Q

Routes of opioids administration

A 
Oral
i.v.
s.c. and i.m.
Rectal
Intrathecal
Epidural
Buccal
Trans dermal
44
Q

Severe pain: chronic pain

A 
Oral morphine syrup or tablets
Morphine s.c. infusion
Diamorphine s.c. infusion
Fentanyl transdermal patch lasts 5 days
Buprenorphine patch
45
Q

Gabapentin and pregabalin (type of co-analgesic)

A

Effective for chronic neurogenic pain
< central transmission and pain projection
Adverse effect: sedation, dizziness, nausea,
occasionally hypotension

46
Q

Antidepressant drugs (type of co-analgesic)

A

Amitryptiline
Duloxetine & Citalopram
Have useful adjuvant effects in neurogenic pain.
Also some antidepressant effects can be useful.
Adverse effects GI and CVS

47
Q

Co-analgesics

A

Other drugs, nerve blocks, surgery, radiotherapy, complementary therapies, addressing psychosocial issues

48
Q

Pain management

A

Assessment of severity in context of daily living
and functioning.
Acute pain; large variation in requirements
complex. The amount of analgesia required is
“enough to stop the pain”. That is the correct dose.
Synergism different drug actions, psychological
factors

Pharmacology (Den 303) (3 decks)

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