General Anaesthetics Part 1 - Steve Fitzjohn

Anna mph
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Anna mph
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Degree Neuropharmacology Flashcards on General Anaesthetics Part 1 - Steve Fitzjohn, created by Anna mph on 12/15/2015.

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Question Answer
What is general anaesthesia? A state of unconsciousness where the patient is unable to feel OR respond to pain
Which reflex is lost with an overdose of general anaesthetics? What does this lead to ? Cardiovascular - leads to respiratory depression and then death
What are the four stage of general anaesthetic? 1)Analgesia 2) Excitement 3) Surgical anaesthesia 4)Medullary Paralysis
What happens at the ? stage: Analgesia No amnesia or loss of touch sensation. Loss of nociception Drowsiness
Excitment Generally increased motor function Struggling Rapid eye movements Delirium Amnesia
Surgical Anaesthesia Unconscious Regular respiration Decline in muscle tone Loss of relfexes
Medullary Paralysis Loss of spontaneous respiration Depression of cardiovascular reflexes
When was N20 discovered? Late 1700s Joseph Priestly
Name two other analgesic gases Ether Chloroform
When was cocaine first used as an anaesthetic? 1877
When was a tube first used in a trachea to control breathing etc? 1910
What can curare be used as? Muscle relaxant (1940s)
When was halothane introduced and what was it used for? Side effect? 1950s general anaesthetics liver
What are the two groups of general anaesthetics? Inhalations and Injectibles
What does MAC stand for? What does it mean? Minimal Alveolar Concentration Concentration required to abolish a sensory response to a surgical incision in 50% of patients
How does MAC correlate with the oil:gas coefficient of the anaesthetic? The better higher the oil:gas coefficient (the better the gas dissolves in oil) the better it is as an anaesthetic (In terms of low MAC)
What is the lipid theory of general anaesthetic? Anaesthetic dissolves in lipid membrane (as is fat soluble) leads to membrane fluidificiation. Membrane becomes more fluid and disrupts shape of proteins (eg sodium channel). Prevents function.
What are the three main problems with lipid theory? 1 1) Stereoisomers (Hexibarbitol). Solubility of isomers is the same but one can be more potent (S is two times more potent)
2. 2) Temperature changes fluidity of plasma membranes. However changes in temperature do not induce anaesthesia. 1 degree change in body temp is equal to change in membrane fluidity as caused by general anaesthesia (but not anaesthesia caused)
3. 3) Increasing chain length Alcohol chain length increases, leading to increased solubility (ethanol Cm=2 at Tridecanol Cm=13 Tetradecanol Cm=14) At first EC50 for anaesthesia decreases but by Cm =13 EC50 decreases and no anaesthetic action at Cm=14
What is the Modern Lipid Theory Distribution of lateral forces
What is the protein theory? Anaesthetics interact with specific protein to cause anaesthesia
What is one explanation for why the potency of anaesthetics increases with lipid soluble? Anaesthetics are binding to hydrophobic area of proteins (more lipid soluble anaesthetic can reach protein better)
What are the four things that need to be shown when testing the protein theory? 1) Anaesthetic has effect on specific protein at clinical concentrations 2) Anaesthetic interacts directly with target protein 3) Protein expressed in relevant areas of brain 4) Change in protein function is relevant to anaesthesia
Where do volatile anaesthetics (halothane, isoflurane) bind on the GABAa subunit. a subunit
Where does ethanol bind on the GABAa receptor bind? a subunit, near or same place as volatile anaesthetics
What type of potassium channel is an important target for GA? Give an example Two-pore potassium channels, Trek-1.
What effect does chloroform have on a two-pore potassium channel? What slope of the IV graph dependent on? Potentiates K+ current through channel. Slope depends on conc. of chloroform.
Which other drug has this effect on the two-pore potassium channel? Halothane
Which type of anaesthetics bind to the GABAa receptor and where? Volatile - a subunit (v close to aB interface) Intravenous - bind to B subunit
Which volatile gases have no effect on GABAa receptor? Xenon, cylcic proprane
Which type of anaesthetics affect the two-pore K+ channels? Volatile and gaseous anaesthetics only
Which anaesthetics (actual drugs) block NMDA receptors? What is the point of this? Xenon Nitrous Oxide Ketamine Reduces excitatory glutamate trasnmission
What are the other potential targets for general anaesthetics? Ca2+ VG channels Na+ VG channels Glycine, nicotinic and 5-HT ligand gated ion channels
What are the two main actions of injectable drugs? (Propofol, etomidate, barbituates and neurosteroids) ACTIVATE GABAa receptors and Glycine receptors
What do the volatile anaesthetics mainly potentiate? GlyR, GABAR, K2p
What is the main effect of ketamine? NMDA antagonist
What are the main effects of xenon and N20? Activation K2p
What do you want to do in terms of glutamatergic transmission and how do you target this? Inhibit excitatory transmission 1) Decrease neurotransmitter release (pre) 2) Decrease action of neurotransmitter (post) 3) Decrease excitability of post synaptic neuron
What do you want to do to GABAergic or Glycinergic transmission? INCREASE
Where do General Anaesthetics act? Brain and Spinal cord
Which inhibitory neurotransmitter is most important in the spinal cord? Glycine
Why is targeting the spinal cord so important? Prevent reflexes/give immobility
Why is targeting the brainstem, hypothalamus and thalamus (arousal areas) important? Leads to unconcsciouness
What does targeting the cerebral cortex do? Contributes to lack of awareness and gives amnesia.
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