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ANAESTHETICS Flashcards

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1
Q

what are the 3 functions of general anaesthetics?

A

unconsciousness
loss of reflexes
analgesia

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2
Q

what are the 2 forms of general anaesthetics?

A

parenteral and inhalation

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3
Q

what are some IV anaesthetics?

A

etomidate, midazolam, propofol, thiopental, ketamine, and opioid agonists.

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4
Q

what are the volatile anaesthetics?`

A

halothane, isoflurane, desflurane, and sevoflurane

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5
Q

what are parenteral anaetshetics used for?

A

induction of anaesthesia

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6
Q

outline the pharmacokinetics of parenteral anaesthetics?

A

they enter the blood stream and travel to highly lipophilic tissues such as brain and spinal cord wherre they can induce the anaesthetic state. they then enter back into the blood stream, get metabolised by the liver and excreted by the kidneys

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7
Q

what type of drug is thiopental?

A

a barbiturate and IV general anaesthetic agent

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8
Q

what are the side effects of thiopental?

A

cardiovascular depression which can lead to hypotension and respiratory depression
bronchoconstriction so unsuitable for asthmatics
ongoing drowsiness

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9
Q

why is thiopental used as a general anaesthetic agent in traumatic brain injury?

A

as it reduces ICP

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10
Q

what type of drug is midazolam?

A

a benzodiazepine

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11
Q

what are the side effects of midazolam?

A

cognitive dysfunctions like amnesia and postoperative respiratory depression

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12
Q

what can reverse the side efefcts of midazolam?

A

flumazenil - a GABA antagonist

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13
Q

why is propofol a good choice of anaesthetic agent for outpatient surgery?

A

as it have a short duration so recovry is faster

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14
Q

why is propofol preferred over thiopental?

A

it doesnt cause bronchoconstriction

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15
Q

what are the side efefcts of propofol?

A

vasodilation
cardiovascular depression which leads to hypotension
in rare cases it can inhibit mitochondrial fatty acid metabolism and cause propofol infusion syndrome - bradycardia, heart failure, metabolic acidosis, rhabdomyolysis, fatty liver

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16
Q

why is etomidate preferred for patients with coronary artery disease, cardiomyopathy, cerebral vascular disease or hypovolemia?

A

it causes less cardiovascular depression

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17
Q

whats the downside of etomidate?

A

adrenal suppression

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18
Q

what is ketamines moa?

A

blocking NMDA receptors

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19
Q

why is ketamine suitable for patients at risk of hypotension and asthamatics?

A

It stimulates the sympathetic nervous system:
as it increases bp and cardiac output
it also causes dilation of the bronchi

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20
Q

which drug causes dissociative anaesthesia?

what is this?

A

ketamine
where the patient is not completely unconcious so the patient can open eyes, breathe, swallow and move involuntarily but they dont remember the procedure or feel pain

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21
Q

whats a disadvantage of ketamine causing dissociative anaesthesia?

A

they can have hallucinations or delusions for a short while

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22
Q

what is the pharmacokinetics of inhaled anaesthetics?

A

given through a mask or tracheal tube, agent goes from alveoli of lungs into the blood and then to different parts of the body

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23
Q

what are examples of inhaled anaesthetics?

A

nitrous oxide and the halogenated inhalation anaetshetics e.g. halothane or desflurane,

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24
Q

what is nitrous oxides moa?

A

it acts as an NMDA receptor antagonist

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25
why id nitrous oxide used in dentistry and not medicine?
in order to achieve anaesthesia on its own the patient would need to inhale pure nitrous oxide which is unsafe as you wouldnt be breathing any oxygen so instead its used at lower concentrations for its analgesic effects
26
what does it mean by nitrous oxide has a 'second gas effect'?
when combined with other anaesthetics, it lowers the therapeutic dose required for other agents
27
why is it vital to monitor arterial oxygen saturation at all times when giving inhalation general anaesthetic agents?
as nitrous oxide and halogenated agents diminishes the normal response to hypoxia so we dont get signs like tachypnea
28
why is nitrous oxide contraindicated in people with pneumothorax and bowel obstruction?
as it can cause expansion of trapped gases in closed body cavities
29
what are the common halogenated inhalation anaetshetics?
halothane enflurane methoxyflurane desflurane
30
what are the side efefcts of halogenated inhalation anaesthetics?
vasodilation, cardiovascular depression and respiratory depression
31
who are halogenated anaesthetic agents contraindicated in?
those susceptible to malignant hyperthermia | those with increased ICP as it can increase it further
32
why is halothane no longer used in developed countries?
due to its severe, and sometimes fatal hepatotoxicity
33
why can halothane be used in asthmatics?
it dilates the airways
34
why is methoxyflurane not as widely used anymore?
it causes nephrotoxicity
35
why is desflurane not used as an induction agents?
it has a pungent, musty smell that can cause airway irritation leading to coughing
36
who is enflurane conraindicated in?
epilptic patients as it lowers the seizure threshold
37
what is malignant hyperthermia?
where the anesthetic agents cause increased release of calcium stored in muscle cells, causing them to contract without resting and generate heat.
38
what gene makes a person more susceptible to malignant hyperthermia?
RyR1 gene
39
what are symtoms of malignant hyperthermia?
muscle rigidity, rhabdomyolysis, hyperthermia, metabolic acidosis, tachycardia
40
what is rhabdomyolysis?
rapid breakdown of skeletal muscle and the products enter the urine
41
what are local anaetshetics used for?
to reversibly block pain sensation in a specific part of the body in order to perform small surgical seizures
42
whats the common suffix for local anaesthetics?
-caine
43
what are the 2 classes of local anaesthetics?
esters and amides
44
how do local anaesthetics work?
they inhibit conducton of action potentials across nerve fibres by blocking Na+ channels, and thus the perception of pain by the brain
45
how can local anaesthetic be administered?
topically infiltration - injection into tissue nerve block - medication is injected into the tissue near a major nerve
46
what does it mean by 'local anaesthetics are state dependant'?
they are more likely to affect neurons that are firing more rapidly as they bind more tightly to inactivated Na+ channels and prolong the inactivated state so we dont get an action potential and we dont register pain
47
which types of nerves do local anaeshetics have a larger effect on?
small and myelinated ones such as nerve fibres carrying pain sensation
48
at larger doses, what, other than pain, can local anaesthetics block?
conduction of temperature, tuch, pressure and then loss of motor function
49
what are some esters?
cocaine benzocaine procaine tetracaine
50
why are cocaine and benzocaine only for topical use?
because they have serious side effects
51
outline the moa of cocaine?
it blocks reuptake of catecholamines so they build up and this leads to vasoconstriction, tachycardia and arrhythmia
52
why does cocaine give a euphoric feeling?
it blocks reuptake of dopamine which regulates the reward pathway
53
what is methemoglobinemia? which local anaesthetic can cause this?
where the heme in RBCs get oxidised from Fe2+ to Fe3+ and they lose their ability to transport oxygen blood takes on an unhealthy chocolate colour and this can lead to cyanosis benzocaine
54
what local anaesthetic do we commonly use in spinal and corneal anaesthesia?
tetracaine
55
what are some amides?
lidocaine mepivacaine bupivacaine
56
what is the most frequently used amide local anaesthetic?
lidocaine
57
who is mepivacaine contraindicated for and why?
pregnant women as its toxic for newborns
58
what is the main indication for bupivacaine?
epidural anaesthesia during labour
59
what happens if bupivacaine is accidentally administered into a blood vessel?
its very cardiotoxic so would cause severe myocardial depression
60
what happens if local anaesthetics get into the blood stream?
they decrease the activity of inhibitory neurons first leading to restlessness, anxiety and seizures at larger doses they decrease the activity of all neurones which can lead to CNS depression and respiratory depression = can lead to death
61
what are neuromuscular blockers?
a class of medications that prevent ACh from binding to the nicotinic receptors at the neuromuscular junction which prevents the triggering of skeletal muscle contractions
62
what are the 2 types of neuromuscular blockers?
non-depolarizing and depolarizing
63
whats the difference between depolarizing and non-depolarizing neuromuscular blockers?
non-depolarizing bind to the same binding sites on the receptor as ACh but they dont trigger the opening of ion channels (competitive antagonist) depolarizing bind to the same nicotinic receptors as ACh and open the ion channels leading to depolarisation of the motor end plate (agonist)
64
whats the moa of non-depolarizing neuromuscular blockers?
they bind to nicotnic receptors so that ACh cannot bind and we therefore get decreased depolarization of the muscle fiber and weaker contraction
65
what are some examples of non-depolarizing neuromuscular blockers?
atracurium, vecuronium, rocuronium, pancuronium, tubocurarine
66
what are the indications for non-depolarizing neuromuscular blockers?
endotracheal intubation, surgical procedures and mechanical ventilation
67
what are some specific side effects of atracurium?
bronchoconstriction and vasodilation = causes hypotension, reflex tachycardia and flushing
68
why can atracurium be dangerous in patients in kidney failure?
as atracurium produces laudanosine which is a toxic metabolite that is neurotoxic - it can build up in the blood and triggr seizures
69
how can you reverse side effects of neuromuscular blockers? | how does this work?
by giving cholinesterase inhibitors e.g. neostigmine it raises concentrations of ACh in the synaptic cleft which will out-compete the neuromuscular blockers for the receptor sites
70
whats the moa of depolarizing neuromuscular blockers?
they mimic the actions of ACh, opening up the ion channels which leads to depolarization of the motor end plate- this continues until the nicotinic receptors become desensitized because these meds cant be broken down by acetylcholinesterase
71
what is the depolarizing neuromuscular blocker?
succinylcholine
72
whats the indication for succinylcholine?
as an adjunct to general anesthesia, to facilitate tracheal intubation, and to provide skeletal muscle relaxation during surgery or mechanical ventilation.
73
how long does succinylcholine's effects last?
less than 10 minutes because it rapidly leaks into the plasma where its broken down by pseudocholinesterase
74
how do you know if someone is actually asleep during anaesthesia?
look for movement, muscle tone, light reflexes, eyelid reflexes, lacrimation and eye position you can also measure the exhaled anaesthetic concentration to work out the concentration in circulation
75
whats the first stage of anaesthesia?
induction - period immediately after administration of the induction agent this is when patients lose conciousness
76
whats the second stage of anaesthesia?
excitement - the period following loss of coniosuness marked by excited and delirious activity including irregular respiratory and heart rate, uncontrolled movements, vomiting if not fasted, breath holding, pupillary dilation
77
whats the 3rd stage of anaesthesia?
the stage where surgery takes place we get skeletal muscle relaxation, respiratory depression, eye movements slow and stop, loss of laryngeal and corneal reflex, intercostal paralysis
78
what is the 4th stage of anaesthesia?
medullary paralysis This stage occurs if the respiratory centers in the medulla oblongata of the brain cease to function. Death can result if the patient cannot be revived quickly. This stage should never be reached. Careful control of the amounts of anesthetics administered prevent this occurrence.

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