Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
30 Cards in this Set
- Front
- Back
General Anaesthetics cause...
|
descending depression of the CNS
decreased awareness and response to pain |
|
toxic effect of general anaesthetics
|
depress blood pressure and respiration
liver / kidney damage |
|
how awareness and response to pain is reduced by general anesthetics
|
loss of consciousness
suppression of skeletal muscle reflexes and tone |
|
ideal characteristics of a general anesthetic
|
quick induction (low blood solubility), high potency (high lipid solubility), reversibility, good analgesia, amnesia, no hangover, lower / harmless metabolism, non-flammability, muscle relaxation, low toxicity
|
|
why are combinations of several agents used as general aesthetics?
|
because not one agent has all the ideal characteristics
|
|
describe volatile/ gaseous anaesthetics
|
simple, unreactive compounds, with numerous, small molecules
|
|
Halothane
|
volatile / gaseous general anaesthetic
|
|
Nitrous Oxide
|
laughing gas, volatile anaesthetic
|
|
two types of general anaesthetic
|
volatile / gaseous
intravenous |
|
intravenous agents
|
through injection
very rapid with short duration repeat dose for longer analgesia induction processes, short procedures |
|
examples of IV agents
|
1) Thiopentane
2) ketamine (barbituates) |
|
thiopentane
|
low TI
depress heart and respiration; medullary collapse |
|
ketamine
|
horse tranquiliser
dissociative amnesia barbituate, IV agent |
|
mechanisms of anaesthetics
|
1) synaptic transmission
2) reticular formation 3) Thalamus 4) hippocampus 5) lipid solubility |
|
reticular formation causes...
|
analgesia, unconsciousness
|
|
thalamus causes...
|
analgesia
|
|
hippocampus causes...
|
amnesia, unconsciousness
|
|
lipid solubility
|
interacts with hydrophobic structures
volume expansion of membranes protein binding |
|
opening of chloride channels is encourages by?
|
receptors e.g. GABA
|
|
opening of chloride channels causes..
|
Cl- entry into neurone
hyper polarisation inhibition (no Action Potential) |
|
general anaesthetics do what to the opening of chloride channels?
|
enhance it
|
|
premedication drugs used in surgery
|
hyosine, morphine, lignocaine, tubocurarine, soxamethonium
|
|
muscle relaxants
|
tubocurarine
soxamethonium interfere with muscarinic and nicotinic receptors |
|
hyosine
|
muscarinic receptor antagonist
dries up saliva secretions and bronchal mucus |
|
morphine
|
opiate analgesic
prevents post op pain |
|
lignocaine
|
local anaesthetic
blocks conduction in sensory nerves |
|
muscarinic receptors affect:
|
smooth gut muscle
|
|
nicotinic receptors affect:
|
Ach, skeletal muscle
|
|
Tubocurarine
|
non depolarising
competes with Ach long lasting reversible with ChE inhibitor |
|
Soxamethonium
|
depolarising
cation channels stay open short acting not reversible with ChE inhibitor |