pharmacology Flashcards
What is Triad of General Anesthesia
unconsciousness
analgesia
muscle relaxation
4 stages of anaesthesia
Stage I - analgesia conscious, drowsy, amnesia Stage 2 - excitement Loss of consciousness but delirium, irregular cardiorespiration, apnea, spasticity, gagging Stage 3 - anaesthesia regular respiration, loss of reflex and muscle tone = operation Stage 4 - medullary paralysis depression of cardiorespiration, death
What sort of compounds are anaesthetic gasses/ vapours?
Halogenated ethers or hydrocarbons e.g. halothane (not used), isoflurane (still use)
Inhaled anaesthetics produce effet via what mechanism, describe the process?
Breathe vapour into lung, Blood gas exchange (rapid as big SA) into bloodstream.
What are the 3 characterstics of IV anaesthetics?
Rapidy onset, short acting, quickly metabolised/excreted
an example of IV anaesthetic?
Barbiturates (thiopentone)
What are the two most common methods of giving general anaesthetics?
Inhalation and injection
what are the 4 common anaesthetic procedures (using a combined approach)
note: serious surgery is done w combination of all these
- produce rapid unconsciousness w IV injection e.g. thiopentone
- maintain unconsciousness w inhalation agents e.g. N2O, halothan
- can be supplemented w IV analgesic agent e.g. IV fentanyl (not in its own right, but give pre-op to ensure initial analgesic phase is stable)
- produce muscle paralysis w nicotinic antag e.g. tubocurarine
name commonly used inhalation anaesthetics? there are 7 gasses
- N2O : rapid, low potency, in combo, obesteric, analgesic
- halothane : vet use, developing countries, hepatotoxicity
- enflurane: fast on and off, epileptogenic
- isoflurane: non-epileptogenic, cardiorespiratory depression
- desflurane: v fast on and off, day surgery
- sevoflurane: rapid, potent, hepatotoxic
- ethers e.g. cyclopropane, chloroform: s/e explosive
what are the 5 commonly used intraveous anaesthetics?
- thiopentone (barbiturate) : v fast onset (20s), highly soluble, NON-analgesic, resp depression
- etomidate : fast metabolism, low CR depression, involuntary muscle jerks
- propofol : v fast metab, day surgery
- ketamine : slow onset, dissociative, analgesic, hallucinogenic, bradycardia, hypertensive (NMDA anatg, horse tranquiliser)
- midazolam, other BZs : pre-op
what is anaesthetic potency relationship said in lipid Theory of Anaesthetic Action
the more lipophilic the compound, the higher the potency of the anaesthetic
describe how the lipid theory work?
- normal cell: na influx via VNaC
- anaesthetic use:
increased membrane fluidity
membrane expansion (deform)
protein expansion - A binds to lipid membrane, change conformation of proteins, VNac
- Unable to operate in normal way
- no na influx, no ap generation
what does the “luciferase inhibition correlates with anaesthetic potency” suggest the way A works?
- luciferase (luminance) can be isolated to produce pure soluble protein,
- anaesthetics interact with membrane proteins DIRECTLY eg. receptors and ligand gated ion channel
- on hydrophobic domain of the protein
- alter their function
what are A’s effects on inhibitory, excitatory receptors in brain, on NT?
- potentiate inhibitory rec response in brain, GABA
- inhibit excitatory rec response AMPA, NMDA
- overall, increase somatic inhibition in brain
- Potentiate and increase potency of NT,
what are the 2 ion channels A can act upon?
- NA channel blockage (inhibit AP)
- K channel opening
