Pain and Analgesics Flashcards
What is nociceptive pain?
Cause by physical damage or response to inflammatory soup
Results in activation of free-nerve endings
Respond to mechanical, chemical, pressure and temperature changes
Physiological/acute pain - easily treatable
Responds to analgesics
What is neuropathic pain?
Pain resulting from damage/changes in the pain neurons themselves
Often chronic and difficult to treat
Shooting/burning pain
Paraesthesias: Pins and needles
Tingling, Numbness, Burning and Throbbing
If a patient has these symptoms, what type of pain do they have? Low-back pain Myofascial pain Arthritis Visceral pain: Pancreatitis Interstitial cystitis Endometriosis
Nociceptive pain
What is allodynia?
Allodynia refers to central pain sensitization (increased response of neurons) following normally non-painful, often repetitive, stimulation. Allodynia can lead to the triggering of a pain response from stimuli which do not normally provoke pain
If a patient has these symptoms, what type of pain do they have? Phantom limb Trigeminal neuralgia Post-stroke pain Post-herpetic pain Complex regional pain syndrome Malignant pain
Neuropathic pain
What can cause the worst ever headache?
Sub arachnoid haemorrhage
What is the inflammatory soup?
The ‘inflammatory soup’ produced contains substances that activate free-nerve endings. It can cause problems with some of the local anaesthetics; as it changes the pH affecting their ability to cross the membrane into the nerve.
What are rubefacients and capsaicins and how do they help with pain modulation in periphery?
They are creams, which trigger pain pathways and thus distract the brain by diluting the effects.
How is Nociceptive pain sensed?
Nociceptive pain sensed by free ending on C- (groan) and Aδ- (ouch) fibres
If you fall over and hurt yourself and then rub on your wound with you hand (mechanical stimulation), what will this do?
Mechanical stimulation activates inhibitory interneurons
Reduces pain transmission by inhibiting 2nd order cells
Describe the biopsychosocial model of pain perception
Incorporates all aspects of pain and associated behaviours:
Illness behaviour
Psychological distress
Attitudes and beliefs
Name the non-pharmacological options to treat pain.
Exercise, physiotherapy
Acupuncture
TENS (Transcutaneous electrical nerve stimulation)
Name the invasive procedural options to treat pain.
Nerve blocks/injections (Trigger points and Joints)
Ablation
Implants (Pumps and Neuromodulators)
Placebos have similar effects
Name the pharmacological options to treat pain.
Nociceptive Pain – NSAIDs and Opioids:
Ibuprofen
Co-codamol
Morphine
Neuropathic Pain* – Tricyclic antidepressants & antiepileptics:
Nortriptyline/Amitriptyline
Gabapentin ± Amitriptyline
Carbemazepine alone (never in combo)!
Describe the general NSAID mechanism of action.
NSAIDs Block production of prostaglandins by inhibiting COX (cyclo-oxygenase) enzymes
Cyclooxygenases breakdown arachidonic acid to give prostaglandins
What are the three forms of Cyclo-oxygenase and what are their functions?
COX 1 – Normal cell function (NSAID)
COX 2 – Inflammation (NSAID)
COX 3 – Fever? Does it exist? (Paracetamol)
Describe the MoA of NSAIDs at a neuronal level.
Decreased production of prostaglandins by NSAIDs results in less activation of the prostanoid receptor and thus no depolarisation of the voltage gated Na+ channels
Name some NSAIDs
Aspirin, Ibuprofen, Naproxen, Diclofenac, Indomethacin and COX-2 inhibitors: Celecoxib and Etoricoxib (lower GI effects)
What are the side effects of NSAIDs?
GI problems: heartburn, nausea, vomiting, diarrhoea, bleeding/ulceration
CV incidents: thrombosis (esp. Cox-2)
Headache
Tinnitus
What are side effects of NSAID intoxication?
Salicylism: Salicylate toxicity may occur with high dose acute or chronic ingestion of NSAIDs (1% mortalilty)
Name two opioids.
Morphine (gold standard) and Heroin (diamorphine).
Act on opioid receptors (OP1-4)
Name opioid agonists, partial agonists/mixed anatagonists and antagonists.
Agonists:
Strong - morphine, diamorphine,
Weak - codeine, dihydrocodeine
Partial agonists/mixed agonist-antagonist
buprenorphine (long half life)
Antagonists (stops highs of opioids)
naloxone, naltrexone
What are the 4 ways opioids decrease neuronal transmission by?
Decreasing opening of voltage-dependent Ca2+ channels
Increasing K+ outflow via KATP and KIR channels
Decreasing Ca2+ release from intracellular stores
Decreasing exocytosis of transmitter vesicles
(reduction of neuronal transmission via hyperpolarisation)
Name some symptoms of Opioid toxicity.
Respiratory depression
Conscious depression/mood alterations
Miosis
What is Tramadol?
Synthetic opioid (agonist)
Also has atypical antidepressant effects (SNRI)
Great pain killer
Some very interesting side-effects (visual hallucinations)
