Lec 9- Analgesia II Flashcards
1
Q
Definition of pain
A
- An unplesant sensory and emotional experience, associated with actual or potential tissue damage, or described in terms of such damage
- BUT pain is very individual, so can be described as “What that patient says it is”
2
Q
Classification of pain
A
- Acute pain- usually has a diagnosable cause and an inherently protective function
-
Chronic pain- doesn’t have a protective function. Longstanding (> 3 months); often an adaptation of autonomic nervous system leading to physical and psychological effects
- Nociceptive- physical cause (a tumour, cut)
- Neuropathic- Nerve damage, difficult to treat
3
Q
Describing pain (SOCRATES)
A
- Site
- Onset
- Character
- Radiation- is it in one place
- Associated symptoms- visual, hearing, tingling, nausea
- Timing (duration, course, pattern)
- Exacerbating and relieving factors
- Severity
4
Q
Pain intensity scales
A
5
Q
WHO analgesic ladder
A
6
Q
Prescribing analgesia
A
- Oral administration whenever possible- patches are available but v.expensive
- Should be given at regular intervals
- Prescribe according to pain intensity as evaluated by a scale of intensity of pain
- Dosing of pain medication should be adapted to the individual
- 40% GP visits are about pain- possibly up to 70%
7
Q
Step 1- Non-Opioid- Paracetamol
A
- Thought to act through inhibition of CNS prostaglandins
- Analgesic; no anti-inflammatory activity
- Adult dose: 1 gram q.d.s (unless malnourished/ liver probs)
- Often under-utalised
- Hepatotoxicity in overdose, but safer than NSAIDs and opioids for chronic use at advised dose
- Often appropriate as first line, including for OA
- Oral (P medicine up to quantity of 32 x 500mg) IV, rectal
- Can take in combination with all other analgesics
8
Q
Step 1- Non-opioid- NSAIDs
A
- Inhibition of enzyme cyclo-oxygenase => Inhibition of prostaglandins (selectivity of COX varies)
- Analgesic and Anti-inflammatory
- The full anti-inflammatory effect may take up to 3 weeks
- About 60% of patients will respond to anyone NSAID
- Over-used in the UK, esp in the elderly
- Side effects: GI- all systemic NSAIDs cause this, renal- AKI, cardiac- cause sodium and potassium retention
- Ever increasing evidence of increased risk of thrombotic events, i.e. MI and stroke
- Use for the shortest time at the lowest effective dose
9
Q
Opioid Analgesics
A
- Receptor types- Mu, Kappa, Delta
- Different opioid analgesics have different affinities for the receptors => different potencies and side effect profiles
- Pharmacogenetics possible cause of inter-individual response
- Agonists, partial agonist and mixed agonist/antagonists
- Use in combination with non-opioid and adjuvants
- Useful for actue and chronic pain
- Until recently, considered ineffective for neuropathic pain
10
Q
Opioid analgesics- problems
A
- Respiratory depression- Reverse with naloxone (Mu ++, delta +)
- Pupillary constriction- (Mu++, Kappa +)
- Cough suppressant
- Sedation- Mu
- Nausea and vomiting (Mu in CTZ)
- Constipation- Mu, Kappa, Delta
- Regular stimulant and softening laxatives
- Severe- methylnaltrexone bromide (s/c)
- Euphoria/Dysphoria (Mu, Kappa)
- Tolerance
- Addiction/ physical dependence
11
Q
Step 2- Weak Opioids
A
- Use in combination with non-opioid
- Many combination products on UK market
- Codeine (Mu receptor)
- Pro-drug of morphine; 10% demethylated to form
- Morphine; 8% of Caucasians are CYP2D6 poor metabolisers, so reduced analgesic effect
- Also, consider CYP2D6 ultra-rapid metabolisers e.g. 29% of African/Ethiopian- increased risk of ADRs (also children)
- Constipation; cough suppressant
- Dihydrocodeine (u Receptor)- Potency also 1/10th that of morphine
12
Q
Weak Opioid- tramadol
A
- Action partially opioid and partially pre-synaptic re-uptake blockade of NA and 5-HT
- Potency 1/10th of morphine
- Little effect in patients lacking iso-enzyme CYP2D6
- Interactions with drugs affecting CYP3A4 and CYP2D6
- Use with caution in patients with low seizure threshold
13
Q
Weak opioid- Tapentadol
A
- Agonist at u receptor AND inhibits re-uptake of NA
- No active metabolites
- Dose does not need to be decreased in hepatic or renal impairment
- BUT fiarly new to market, so little clinical experience with this drug
14
Q
Step 3- Strong Opioids- Morphine
A
- Oral opioid of choice in the UK
- Acts at u receptor (partial agonist)
- Comparator for potency (1.0)
- Metabolised to morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G)
- M6G is an active metabolite
- Both metabolites renally excreted
- The range of preparations (brand prescribe MR preps- differences between brand)
- Start with immediate release preparation; move onto MR preps with immediate release breakthrough pain
15
Q
Strong opioids- Diamorphine
A
- Potency 2.5
- Pro-drug of morphine
- Greater water solubility as the salt so parenteral alternative to morphine if need high doses
- Highly lipid soluble, so crosses BBB more rapidly than morphine => more rapid onset, but also offset => increased addiction potential
