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Prescibing analgesics
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Prescibing analgesics

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  • 1. Prescribing Analgesics www.freelivedoctor.com
  • 2.
    • Non-opioid analgesics
    • Opioid analgesics
    • Drugs for neuropathic and functional pain
    • Antimigraine drugs
    Analgesics www.freelivedoctor.com
  • 3.
    • Acetaminophen (paracetamol)
    • NSAIDs – non selective
            • - Selective Cox 2 inhibitors
    Nonopioid analgesics www.freelivedoctor.com
  • 4. PARACETAMOL ( acetaminophen)
    • equivalent analgesic efficacy to aspirin
    • no useful anti-inflammatory action
    • used for mild to moderate pain, but aspirin is preferred if due to inflammatory process
    www.freelivedoctor.com
  • 5. PARACETAMOL ( acetaminophen)
    • Metabolism
    • is conjugated in the liver as the inactive glucuronide and sulphate
    • a number of minor oxidation products inc.
    • N-acetylbenzoquinoneimine (NABQI) are also formed
    • NABQI is highly chemically reactive and is usually inactivated by conjugation with SH (thiol) groups of glutathione
    • Supply of glutathione is limited and exhausted in overdose
    • NABQI then reacts with cellular macromolecules and causes cell death
    www.freelivedoctor.com
  • 6. PARACETAMOL ( acetaminophen)
    • Adverse effects
    • rare in therapeutic usage
    • occasional skin rash and allergy
    • Overdose can result in fulminant hepatic necrosis and liver failure
    www.freelivedoctor.com
  • 7. PARACETAMOL ( acetaminophen)
    • Paracetamol overdose
    • Ingestion of >10g of paracetamol may be fatal
    • may be lower in chronic alcoholics or subjects with underlying liver disease.
    • Clinical features
    • In severe poisoning
    • up to 24 hours - none or nausea and vomiting
    • > 24 hours - nausea and vomiting, right upper quadrant pain, jaundice, encephalopathy
    www.freelivedoctor.com
  • 8. PARACETAMOL ( acetaminophen)
    • Management
    • Blood for paracetamol at 4 hours post ingestion
    • Check treatment curve for N-acetylcysteine infusion ( if in doubt of severe poisoning, don’t delay)
    • Check prothrombin time and plasma creatinine , pH
    • acute renal (due to acute tubular necrosis) and hepatic failure and occur at 36-72 hours after ingestion
    • Indications for referral to liver unit are
    • - rapid development of Grade 2 encephalopathy
    • - PTT >45 secs at 48 hours or >50 secs at 72 hours
    • - rising plasma creatinine
    • - Arterial pH <7.3 more than 24 hours after ingestion
    www.freelivedoctor.com
  • 9. NSAIDs
    • Mechanism of action
    • inhibits cyclo-oxygenase (prostaglandin synthase) that is responsible for conversion of arachidonic acid to cyclic endoperoxides
    • 2 isoforms of enzyme
    • - COX-1 constitutive, present in platelets,
    • stomach and kidney
    • - COX-2 inducible by cytokines & endotoxins at sites of inflammation e.g., joints
    www.freelivedoctor.com
  • 10. NSAIDs
    • Main actions
    • 1.) Analgesic -effective against mild to moderate pain, do not cause dependence
    • 2.) Anti-inflammatory
    • 3.) Anti-pyretic
    • 4.)Anti-platelet- prevent thromboxane production, derived from prostaglandins and cause platelet aggregation
    • Others
    • 5.) Useful in treatment of dysmenorrhea, associated with increased prostaglandin synthesis and increased uterine contractility
    • 6.) Used to close the patent ductus arteriosus
    www.freelivedoctor.com
  • 11. NSAIDs
    • Adverse effects
    • 1.) Gastric or intestinal mucosal damage
    • - mucosal prostaglandins inhibit acid secretion, promote mucus
    • secretion, prevent back diffusion of acid into the gastric submucosa
    • - Inhibition thus results in erosions, ulceration, bleeding, perforation
    • 2.) Disturbances of fluid and electrolyte balance
    • - inhibition of renal prostaglandin production results in sodium retention and oedema, possible hyponatraemia, hyperkalaemia, antagonism of anti-hypertensive agents
    • 3.) Analgesic nephropathy
    • - due to long term ingestion of mixtures of agents
    • - chronic interstitial nephritis, renal papillary necrosis, acute renal
    • failure
    www.freelivedoctor.com
  • 12. NSAIDs
    • Non selective Vs selective COX2 inhibitors
    • ↑ risk of cardiovascular adverse events with COX 2 inhibitors
    • Rofecoxib was withdrawn from the market
    • Higher BP, incidence of myocardial infarction, stroke
    • Mechanism _ ? Unopposed effect of cox 1 action
    • - ? Block protective effect of COX2 on
    • ishaemic myocardium or atherogenesis
    www.freelivedoctor.com
  • 13. NSAIDs
    • Classifications
    • Mild to moderate anti-inflammatory action
    • - propionic acid derivatives ibuprofen, naproxen
    • - fenamic acids mefanamic acid
    • Marked anti-inflammatory action
    • - salicylic acids aspirin
    • - pyrazolone derivatives azapropazone, phenylbutazone
    • - acetic acid derivatives diclofenac, indomethacin
    • - oxicam derivatives piroxicam
    • Selective COX2 inhibitors celecoxib, rofecoxib
    www.freelivedoctor.com
  • 14. Aspirin (acetyl salicylate)
    • Actions
    • Analgesic - central and peripheral action
    • Antipyretic - act in hypothalamus to lower the set point of temperature control elevated by fever,
    • also causes sweating
    • anti-inflammatory - inhibition of peripheral prostaglandin synthesis
    • respiratory stimulation - direct action on respiratory centre, indirectly by ↑ CO2 production
    www.freelivedoctor.com
  • 15. Aspirin (acetyl salicylate)
    • Metabolic effects
    • i.) ↑ peripheral O 2 consumption (uncoupled oxidative phosphorylation) hence ↑CO2 production with ↑ respiration, and direct analeptic action - respiratory alkalosis
    • ii) renal loss of bicarbonate with sodium, potassium and water
    • iii) dehydration
    • iv) metabolic acidosis - effects on Krebs cycle, ↑ ketone body, salicylic acid in blood, renal insufficiency due to vascular collapse, dehydration
    • v) hypoglycaemia or even hyperglycaemia can occur
    www.freelivedoctor.com
  • 16. Aspirin (acetyl salicylate)
    • Uricosuric effects
    • reduces renal tubular reabsorption of urate but treatment of gout requires 5-8g/d, < 2g/d may cause retention of urate.
    • antagonises the uricosuric action of other drugs
    • Reduced platelet adhesion- irreversible inhibition of COX by acetylation, prolongs bleeding time, useful in arterial disease
    • Note: low doses are adequate for this purpose since the platelet has no biosynthetic capacity and can not regenerate the enzyme
    • Hypothrombinaemia : occurs with large doses ie >5g/day
    www.freelivedoctor.com
  • 17. Aspirin (acetyl salicylate)
    • OVERDOSAGE
    • Ingestion of > 10 g can cause moderate/severe poisoning in an adult
    • Clinical features - ‘salicylism’
    • tremor, tinnitus, hyperventilation, nausea, vomiting, sweating
    • Management- mainly supportive
    www.freelivedoctor.com
  • 18. OPIATE ANALGESICS
    • Classification
    • Low efficacy Codeine
    • Dihydrocodeine
    • Dextropropoxyphene (coproxamol- withdrawn from market)
    • Medium efficacy Bupranorphine
    • meptazinol
    • High efficacy Morphine
    • Diamorphine
    • pethidine
    www.freelivedoctor.com
  • 19. OPIATE ANALGESICS
    • Routes of administration
    • Oral
    • Parenteral
    • Suppositories
    • Transdermal- Patch
    • s/c Syringe driver
    www.freelivedoctor.com
  • 20. OPIATE ANALGESICS
    • Mechanism of action
    • Bind to CNS opioid receptors whose natural ligands are endorphins and encephalins.
    www.freelivedoctor.com
  • 21. OPIATE ANALGESICS
    • Actions
    • CNS
    • Depression Stimulation
    • Analgesia vomiting
    • Respiratory depression miosis
    • Depression of cough reflex ↑ spinal reflexes
    • sleep (convulsions)
    • mood changes- Euphoria
    • Dependence – also affects other systems
    www.freelivedoctor.com
  • 22. OPIATE ANALGESICS
    • Smooth muscle stimulation
    • GI muscle spasm causing delayed transit and constipation
    • Biliary spasm
    • Bronchospasm
    • Cardiovascular
    • Dilation of resistance vessels (arterioles) and capacitance vessels (veins)
    www.freelivedoctor.com
  • 23. OPIATE ANALGESICS
    • Smooth muscle stimulation
    • GI muscle spasm causing delayed transit and constipation
    • Biliary spasm
    • Bronchospasm
    • Cardiovascular
    • Dilation of resistance vessels (arterioles) and capacitance vessels (veins)
    • Hazards of Clinical Use
    • Respiratory depression
    • Retention in hepatic and renal impairment
    • Dependence
    www.freelivedoctor.com
  • 24. OPIATE ANALGESICS
    • Dependence
    • Up to 8 h- Mild psychological withdrawal stress
    • 8-12 h - increasing nervousness, restlessness and anxiety
    • 12-24h - yawning, sweating, runny eyes and nose
    • 24 h - pupils dilate, waves of goose flesh
    • 36 h - twitching of muscles, leg & abdominal cramps
    • vomiting and diarrhoea and anorexia, insomnia
    • tachypnoea, ↑ BMR and mild pyrexia
    • 48-72 h - peak withdrawal symptoms
    • up to 10 d- symptoms gradually subside
    • Complete recovery requires 3-6 months
    • Note : Withdrawal syndrome can be in part alleviated by long acting opioid such as methadone
    • Reduction of rebound sympathetic activity with clonidine may be needed
    www.freelivedoctor.com
  • 25. OPIATE ANALGESICS
    • Opioid overdose
    • Death usually due to respiratory depression
    • Cardiovascular function usually well preserved unless severe anoxia
    • Treatment with iv naloxone
    • May need infusion - naloxone has shorter t 1/2 (1h), particularly for opioids with long t 1/2 – (methadone) and tight binding (bupranorphine)
    www.freelivedoctor.com
  • 26.
    • Mild pain
    • Non-opioid analgesics paracetamol
    • NSAIDs aspirin, ibuprofen
    • Moderate pain
    • 1. Low efficacy opioid dihydrocodeine
    • 2. low efficacy opioid + NSAID dihydrocodeine + ibuprofen
    • 3. Moderate efficacy opioid + NSAID meptazinol + ibuprofen
    • Severe pain
    • 1. High efficacy opioids morphine
    • 2. High efficacy opioids + NSAIDS morphine + ibuprofen
    • Overwhelming pain
    • 1. High efficacy opioid + anxiolytic morphine + diazepam
    • and/or major tranquilliser morphine + chlorpromazine
    Overall Management of Pain www.freelivedoctor.com
  • 27.
    • Keep it simple
    • Become familiar with a couple of agents from each class. If in doubt, check in BNF
    • Familiarise with used of control drug (opioid)
    • Identify and treat the underlying pathology wherever possible
    • Be careful with potential overdoses and dependency
    • Explanation and reassurance contribute greatly to analgesia
    Messages www.freelivedoctor.com