24 Topical Local Anaesthetics Flashcards
Idea properties if a TLA
Rapid onset and recovery
Low allergy
Low toxicity
Effective anaesthetists
Mechanism of TLA
Block AP in nerve fibres by blocking transient increase in membrane conductance to sodium ions
What’s receptor theory mechanism of TLA
All TLA are weak bases and are ionised at physiological pH
This uncharged part is lipophilic and penetrates membranes easily
The charged part binds to a site on the voltage gated Na+ channel and blocks channel
What does onset time depend on for a TLA
Concentration of drug and diffusion time
Vasodilation as more dilate is quicker onset
Alkaline pH where a lower pH means there’s inflammation which increases anaesthetic effect
What does activity duration time of a TLA depends on
Vasoconstriction prolonging action
Lipid solubility and protein binding
Why do TLAs mainly only have pain blocking effects
Pain and temp receptors are unmyelinayed and have a longer conduction velocity
What are the types of TLA
Ester link
- amethocaine 0.5-1%
- oxybuprocaine HCL 0.4%
- proparacaine 0.5%
Amide link
- lignocaine 2%
Why do we have more than 1 TLA
Proparacaine, oxybuprocaine and amethocaine are esters of PABA (an allergen) and during metabolism this is released and is metabolised by plasma cholinesterases
MG px take anticholinesterase meds e.g neositigmine so can’t take it
Amide is metabolised in liver and lasts long so avoid in px with liver disease
Onset max time and recovery of TLAs
Onset 30sec
Max 1 min
Recovery 20min
Side effects of TLAS
Sting
Allergy
Corneal epithelial desquamation
Slows corneal wound healing
Reduces reflex tearing and TBUT (disrupts microvilli)
Why put TLA before another drug
TLA damages tight junctions between normal epithelium
Reduces barrier function so allows drug to pass easier
So more enters and more effective
