Analgesia and Anaesthesia Flashcards
Pain in the orofacial region is transmitted mainly by trigeminal nerve. What is the exception to this?
Angle of the jaw supplied by upper cervical nerves
What algogenic substances (pain signals) can be inhibited by analgesics?
Substance P and Prostaglandins
What are the 2 main types of nociceptive axons?
a) A delta - fast and myelinated. Respond to high intensity mechanical stimuli
b) C polymodal - unmyelinated and slower. Mechanical thermal and chemical stimuli
What do the nociceptors in the a delta and c fibres send signals to?
Trigeminal ganglion and onto the brainstem
In the trigeminal nucleus caudalis, what are the following responsible for?
a) Mesencephalic nucleus
b) Principle nucleus
c) Spinal nucleus
a) Proprioception from PDL and muscle fibres in jaw close reflex
b) Proprioception for oral facial behaviour except jaw close reflex
c) Nociception (pain) from primary afferents of trigeminal nerve
Where do third order neurones synapse?
In the thalamus
What are the 2 mechanisms of pain modulation?
Descending impulses e.g. gate control
Sensitisation
In the process of sensitization, what is the definition of
a) Hyperalgesia
b) Allodenia
a) Increase in painful signal
b) A signal that isn’t usually painful now is
What is peripheral sensitisation?
- Nociceptors have increased responsiveness to lower thresholds and recruits sleeping nociceptors
- More persistent and intense = hyperalgesia
- Caused by chronic tissue damage so releases continual allogenic substances
What is central sensitisation?
- Second order neurones recieve prolonged stimulus so become sensitized - allodenia
- May occur as a result of nerve trauma, genetic and environmental factors
What does convergence present as?
What does divergence present as?
- Referred pain - brain can’t tell where pain is coming from
- Radiation of pain
What are the warning signs of persistent pain?
- Coming from multiple teeth
- No obvious pathology
- Numbness and tingling or burning sensation
- LA doesn’t provide pain reduction
- Pain has abnormal triggers
- Doesn’t disturb sleep
What do peripherally acting analgesics mainly target? E.g. parecetamol, NSAIDS, COX 2 inhibitors
Inflammatory cascade by inhibiting algogenic substances
For paracetamol
a) What are its properties?
b) What is the adult dose?
c) What pts should you avoid giving it to?
d) Where is it metabolised
a) Analgesic, anti-pyretic, weakly anti-inflammatory
b) 500mg-1g qds
c) Liver disease
d) Liver - NAPQI
What is the treatment for paracetamol overdose?
4hrs = activated charcoal
12hr = N-acetylcycteine
What is the MOA of NSAIDS e.g. ibuprofen, aspiring, diclofenac and mefenamic acid?
Non-selective block of COX enzyme
What are the properties of aspirin?
- Analgesic
- Anti-platelet
- Anti-inflammatory
- Anti-pyretic
- Rapid absorption GI
- 300mg can be used in suspected MI
What are the properties of ibruprofen?
- Low GI and CVS risk
- Analgesic
- Anti-pyretic
- Anti-inflammatory
- 1.2-2.4g total daily dose - for dentistry 400mg po tds
What are the adverse effects of NSAIDS?
- Gastric ulceration - avoid in liver disease pts
- Anti-platelet - don’t use in other coagulopathies as increased risk of bleed
- Can induce asthma attack, especially ibuprofen
- Non-selective Pg block leads to renal toxicity - avoid in kidney patients
- Reyes syndrome - no aspirin for under 16s
- Extensively protein bound so drug interactions
- CVS risk with Diclofenac and Indomethacin
What are COX2 inhibitors known by? Why are they different to aspirin?
- oxib e.g. Celecoxib
- Safe aspirin as selective block so decreased gastric side effects but increased Pg block so prothrombotic effect and increased risk of MI
What are centrally acting analgesias (opioids) antagonised by?
Naloxone
What receptor do opioids mainly work on and what effects does it cause?
- u
- Analgesia, respiratory depression, pupil constriction, euphoria, decreased GIT motility, dependence
What is the MOA of opioids?
- Descending inhibitory control of nociception through PAGM
- Peripheral afferent hyperpolarisation
What are the unwanted effects of opioid use?
- Respiratory depression
- Nausea
- Pupillary effects so dont use with head injuries
- Decreased urinary flow
- Dependence - tolerance - increased receptor number and sensitivity
What drug helps manage opioid addiction?
Methadone
What are the risks of Tramadol?
Seizure threshold and seretonin syndrome
What is the MOA of Benzodiazepines?
- Enhance effects of GABA which inhibits neurotransmission
- Mimics effects of glycine which is a inhibitory NT
What are the effects of Benzodiazepines?
- Muscle relaxation
- Sedative
- Anxiolytic
- Disinhibition
- Anticonvulant
- Anaethesia
- Amnesia
What is the drug of choice for sedation?
Midazolam: 5mg in 5ml ph3.5
What drugs do benzodiazepines have a synergistic effect with?
Opiates
What are the side effects of benzodiazepines/ midazolam?
- Respiratory depression - decreases response to CO2
- Reduced BP
- Heart rate increases
- Synergistic with other CNS depressants e.g. opiates, alcohol, antihistamines
What drugs inhibit midazolam?
Erythromycin and cimetidine
What are the effects of nitric oxide?
- Depressive and euphoriant effects
- Myocardial depressant at high dose
- Mild depression of alveolar ventilation
- Analgesia
- Relaxation
- Paraesthesia
- Amnesia
What is the maximum N20?
100ppm over 8hrs
What are the side effects of chronic nitric oxide exposure?
- Pernicious like anaemia (impaired DNA synthesis and bone marrow depression)
- Peripheral neuropathy (paraesthesia)
- Liver disease
- Increased miscarriage and decreased fertility
What are the theories of the MOA of local anaesthesia?
- Membrane expansion
- Specific receptor - LA binds to h gate on sodium channel holding gate closed and the cell in refractory period
What 3 parts is an LA molecule made up of?
- Aromatic group (lipophilic)
- Intermediate chain (ester or amide link)
- Substituted amino terminal (hydrophilic)
Which of the LAs are
a) Amides
b) Esters (more allergies)
a) - Lidocaine
- Articaine
- Bupivacaine
- Prilocaine
- Mepivacaine
- Ropivacaine
- Levobupivacaine
b) - Benzocaine (topical)
- Procaine
- Amethocaine
Why is an LA with a higher proportion of uncharged molecules after injection most effective?
Enters the cell quicker (has to be uncharged to enter cells)
What does a a) low pH and b) low pka mean for number of uncharged molecules
a) Less uncharged molecules e.g. infected tissues
b) More uncharged molecules so quicker onset of action
What is partition coefficient of LA and which ahs a higher partition coefficient, lidocaine or procaine?
Measure of lipid solubility, so higher partition coefficient means more lipid soluble so enters cell quicker
Lidocaine
Lidocaine is 64% protein bound and bupivacaine is 96% protein bound. Which has a longer half life?
Lidocaine = 90 mins Bupivacaine = 160 mins
What is the only LA that is not a vasodilator?
Cocaine
What are the vascular effects of adrenaline?
- Alpha adrenoreceptors : skin and mucous membrane vasoconstriction
- Beta adrenoreceptors : skeletal muscle and liver vasodilation
What are the metabolic effects of adrenaline?
- Alpha : inhibiton of insulin release so increased blood glucose
- Beta : activates sodium potassium pumps
What are the cardiac and pulmonary effects of adrenaline?
- Cardiac: activation of beta, increases rate and force of contraction
- Pulmonary: activation of beta, bronchodilator
How does adrenaline affect wound healing?
- Decreased O2 tension in tissues
- Increased fibrinolysis - decreased stability of blood clots
What is the amount of adrenaline in an LA cartridge?
1:80000 so 2.2ml contains 27.5ug/ml
What are the effects of felypressin? How much is in a cartridge of LA?
- Coronary artery vasoconstriction
- Oxytoxix action on uterus (induce labour)
- 2.2ml contains 1.2ug
What does the rate of LA entering the bloodstream depend on?
- Vasodilatory ability
- Protein binding
- Presence of vasoconstrictor
- Route of administration
- Dose volume and concentration
What LA is partly metabolised in the lung?
Prilocaine
What is the metabolism of
a) Esters
b) Amides
a) In blood by pseudocholinesterase and some in liver. Non active metabolites
b) In liver. Metabolites possess LA and sedative properties
NB articaine also pseudocholinesterase
What is the amount of LA that causes CNS toxixity?
5mg/L
What is the rule of thumb for lidocaine dose per kg?
1/10 cartridge per kg or 1 cartridge per kg
Why can liver disease cause overdose with LA?
- Major site of metabolism and pseudocholinesterase produced in liver
- Reduce dose
In LA Toxicity what is the effects on
a) CNS
b) CVS
a) At low dose = excitatory. At high dose = inhibitory, depressant effect (confusion, drowsiness, shivering) and then unconsciousness and respiratory arrest
b) Depressant action of heart
What is different in the positioning of a patient for LA overdose and adrenaline overdose?
LA = Lie pt flat and maintain airway
Adrenaline = patient semi-supine to minimise increase in cerebral BP
What is the difference between afferent and efferent neurons?
Afferent = sensory nerve passing impulses from receptors to the CNS
Efferent = motor nerve conveying information from CNS to muscles/glands
What is the management of an opiod overdose?
ABC 100% high flow O2
Naloxone 0.2-0.4mg IV
Repeat every 3 mins up to 10mg
What is the dosing regimen of codeine?
30-60mg
