Karteikarten
General Anaesthetics Part 1 - Steve Fitzjohn
Karten in diesem Stapel (45)
- 1What is general anaesthesia?A state of unconsciousness where the patient is unable to feel OR respond to pain
- 2Which reflex is lost with an overdose of general anaesthetics? What does this lead to ?Cardiovascular - leads to respiratory depression and then death
- 3What are the four stage of general anaesthetic?1)Analgesia
2) Excitement
3) Surgical anaesthesia
4)Medullary Paralysis - 4What happens at the ? stage: AnalgesiaNo amnesia or loss of touch sensation.
Loss of nociception
Drowsiness - 5ExcitmentGenerally increased motor function
Struggling
Rapid eye movements
Delirium
Amnesia - 6Surgical AnaesthesiaUnconscious
Regular respiration
Decline in muscle tone
Loss of relfexes - 7Medullary ParalysisLoss of spontaneous respiration
Depression of cardiovascular reflexes - 8When was N20 discovered?Late 1700s Joseph Priestly
- 9Name two other analgesic gasesEther
Chloroform - 10When was cocaine first used as an anaesthetic?1877
- 11When was a tube first used in a trachea to control breathing etc?1910
- 12What can curare be used as?Muscle relaxant (1940s)
- 13When was halothane introduced and what was it used for? Side effect?1950s
general anaesthetics
liver - 14What are the two groups of general anaesthetics?Inhalations and Injectibles
- 15What 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 - 16How 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)
- 17What 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.
- 18What are the three main problems with lipid theory? 11) Stereoisomers (Hexibarbitol). Solubility of isomers is the same but one can be more potent (S is two times more potent)
- 192.2) 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)
- 203.3) 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 - 21What is the Modern Lipid TheoryDistribution of lateral forces
- 22What is the protein theory?Anaesthetics interact with specific protein to cause anaesthesia
- 23What 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)
- 24What 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 - 25Where do volatile anaesthetics (halothane, isoflurane) bind on the GABAa subunit.a subunit
- 26Where does ethanol bind on the GABAa receptor bind?a subunit, near or same place as volatile anaesthetics
- 27What type of potassium channel is an important target for GA? Give an exampleTwo-pore potassium channels, Trek-1.
- 28What 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.
- 29Which other drug has this effect on the two-pore potassium channel?Halothane
- 30Which type of anaesthetics bind to the GABAa receptor and where?Volatile - a subunit (v close to aB interface)
Intravenous - bind to B subunit - 31Which volatile gases have no effect on GABAa receptor?Xenon, cylcic proprane
- 32Which type of anaesthetics affect the two-pore K+ channels?Volatile and gaseous anaesthetics only
- 33Which anaesthetics (actual drugs) block NMDA receptors? What is the point of this?Xenon
Nitrous Oxide
Ketamine
Reduces excitatory glutamate trasnmission - 34What are the other potential targets for general anaesthetics?Ca2+ VG channels
Na+ VG channels
Glycine, nicotinic and 5-HT ligand gated ion channels - 35What are the two main actions of injectable drugs? (Propofol, etomidate, barbituates and neurosteroids)ACTIVATE GABAa receptors and Glycine receptors
- 36What do the volatile anaesthetics mainly potentiate?GlyR, GABAR, K2p
- 37What is the main effect of ketamine?NMDA antagonist
- 38What are the main effects of xenon and N20?Activation K2p
- 39What 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 - 40What do you want to do to GABAergic or Glycinergic transmission?INCREASE
- 41Where do General Anaesthetics act?Brain and Spinal cord
- 42Which inhibitory neurotransmitter is most important in the spinal cord?Glycine
- 43Why is targeting the spinal cord so important?Prevent reflexes/give immobility
- 44Why is targeting the brainstem, hypothalamus and thalamus (arousal areas) important?Leads to unconcsciouness
- 45What does targeting the cerebral cortex do?Contributes to lack of awareness and gives amnesia.
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- Degree Neuropharmacology Karteikarten am General Anaesthetics Part 1 - Steve Fitzjohn, erstellt von Anna mph am 15/12/2015.
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