Pain and analgesia Flashcards
Pain definition
Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
Pain effects
Physiological - systemic
-HR/ BP/ feel unwell
Physiological - emotional
-fear/ anxiety/ upset
If pain is untreated
Significant systemic effects
-please remember this and advise upon analgesic use
Management: type of pain
Acute or chronic
Site of pain
Cause of pain
Cause of pain
Inflammatory e.g. post operative pain / RA
Neuropathic e.g. Trigeminal neuralgia
Vascular e.g. temporal arteritis
Analgesia for pulpitis
Where: tooth
Physical cause of pain: inflammation
Acute or chronic: acute
Management: remove cause
Analgesia for periapical abscess
Where: perio tissues
Physical cause of pain: inflammation
Acute or chronic: acute
Management: remove cause
Analgesia for trigeminal neuralgia
Where: nerve
Physical cause of pain: neuropathic?
Acute or chronic: acute?
Management?
Analgesia for Burning Mouth Syndrome
Where: oral mucosa
Analgesia for TMJ
Where: joint/ muscles
Acute or chronic: both
Pain can be reduced at any point - peripheral
Remove cause: tooth, pulp etc.
Anti-inflammatories
LA
Pain can be reduced at any point - central
Distraction, relaxation, cognitive restructuring, CBT
Anti convulsants, depressants, NSAIDS
GA
Pain management: methods
Remove the cause Medication Regional anaesthesia: epidural infusion of LA +/- opioid Nerve blocks with LA +/- opioid Physical methods Psychological
Remove the cause
Surgery
Splinting
Medication
NSAIDS +/-
Paracetamol +/- opioids
Opioids (morphine)
Physical methods
Physiotherapy
Manipulation
TENS
Acupuncture
Psychological methods
Relaxation
Hyponosis
Psychoprophylaxis/ CBT
The prostaglandin pathway
For inflammatory pain
Stimulus –> phospholipase A2 which turns phospholipids into arachidonic acid (steroids and block this pathway)
arachidonic acid –> lipoxygenases –> 12-HETE, 15 HETE, LTA4 –> LTB4, LTC4, LTD4, LTE4
Arachidonic acid –cyclooxygenase (COX-1 and COX-2)–> PGH2 –> PGD2, PGR2, PGF28, PG2, PXA2
Arachidonic Acid pathway
Produces inflammatory mediators
Arachidonic acid –> prostaglandins via Cox I and Cox II –> inflammation, pain and swelling
Aspirin and ibuprofin act of Cox 1
Cox II inhibitors act on Cox II
Arachidonic acid –> cytokines –> inflammation, bronchoconstriction, airway obstruction, cell infiltration
5-LO inhibitors, Cys LT inhibitors, TNF antagonists
Action of NSAIDS
Act on COX-1 and COX-2
< ability of stomach to protect itself from acid contents, and result is greater propensity to erosion and ulceration (systemic not local)
E1, E2, F1 alpha, F2 alpha
> vascular permeability
Cause inflammation - wheal and flare
Contract smooth muscle - uterus/ gut/ bronchi
hyperalgesia in sensory afferent nerve fibres
< gastric acidity
D2
> hyperalgesia in sensory afferent nerve fibres
Inhibit platelet adhesion
Thromboxane
> vascular permeability
Aggregate platelets
Prostacycline
< vascular tone
< platelet adhesion
Cyclo-oxygenases
Catalyse conversion of arachidonic acid to biologically active prostaglandins by cyclooxygenase and peroxidase activity
Active prostaglandins physiological functions
Protection of GI tract Renal homeostasis Uterine function Embryo implantation and labour Regulation of sleep-wake cycle and body T
Cyclo-oxygenase-1
Found: most tissues particularly in platelets, stomach and kidney
Responsible for production of prostaglandins
Cox-1 levels >2-4x by inflammatory stimuli
Constitutive, suggesting it synthesises prostaglandins responsible for physiological housekeeping functions including GI protection
Prostaglandins
important for responses to circulating hormones and maintenance of gastric mucosal integrity and platelet function
