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xB12W7 > ANAESTHETICS > Flashcards

ANAESTHETICS Flashcards

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
Q

why id nitrous oxide used in dentistry and not medicine?

A

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

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26
Q

what does it mean by nitrous oxide has a ‘second gas effect’?

A

when combined with other anaesthetics, it lowers the therapeutic dose required for other agents

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27
Q

why is it vital to monitor arterial oxygen saturation at all times when giving inhalation general anaesthetic agents?

A

as nitrous oxide and halogenated agents diminishes the normal response to hypoxia so we dont get signs like tachypnea

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28
Q

why is nitrous oxide contraindicated in people with pneumothorax and bowel obstruction?

A

as it can cause expansion of trapped gases in closed body cavities

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29
Q

what are the common halogenated inhalation anaetshetics?

A

halothane
enflurane
methoxyflurane
desflurane

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30
Q

what are the side efefcts of halogenated inhalation anaesthetics?

A

vasodilation, cardiovascular depression and respiratory depression

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31
Q

who are halogenated anaesthetic agents contraindicated in?

A

those susceptible to malignant hyperthermia

those with increased ICP as it can increase it further

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32
Q

why is halothane no longer used in developed countries?

A

due to its severe, and sometimes fatal hepatotoxicity

33
Q

why can halothane be used in asthmatics?

A

it dilates the airways

34
Q

why is methoxyflurane not as widely used anymore?

A

it causes nephrotoxicity

35
Q

why is desflurane not used as an induction agents?

A

it has a pungent, musty smell that can cause airway irritation leading to coughing

36
Q

who is enflurane conraindicated in?

A

epilptic patients as it lowers the seizure threshold

37
Q

what is malignant hyperthermia?

A

where the anesthetic agents cause increased release of calcium stored in muscle cells, causing them to contract without resting and generate heat.

38
Q

what gene makes a person more susceptible to malignant hyperthermia?

A

RyR1 gene

39
Q

what are symtoms of malignant hyperthermia?

A

muscle rigidity, rhabdomyolysis, hyperthermia, metabolic acidosis, tachycardia

40
Q

what is rhabdomyolysis?

A

rapid breakdown of skeletal muscle and the products enter the urine

41
Q

what are local anaetshetics used for?

A

to reversibly block pain sensation in a specific part of the body in order to perform small surgical seizures

42
Q

whats the common suffix for local anaesthetics?

A

-caine

43
Q

what are the 2 classes of local anaesthetics?

A

esters and amides

44
Q

how do local anaesthetics work?

A

they inhibit conducton of action potentials across nerve fibres by blocking Na+ channels, and thus the perception of pain by the brain

45
Q

how can local anaesthetic be administered?

A

topically
infiltration - injection into tissue
nerve block - medication is injected into the tissue near a major nerve

46
Q

what does it mean by ‘local anaesthetics are state dependant’?

A

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
Q

which types of nerves do local anaeshetics have a larger effect on?

A

small and myelinated ones such as nerve fibres carrying pain sensation

48
Q

at larger doses, what, other than pain, can local anaesthetics block?

A

conduction of temperature, tuch, pressure and then loss of motor function

49
Q

what are some esters?

A

cocaine
benzocaine
procaine
tetracaine

50
Q

why are cocaine and benzocaine only for topical use?

A

because they have serious side effects

51
Q

outline the moa of cocaine?

A

it blocks reuptake of catecholamines so they build up and this leads to vasoconstriction, tachycardia and arrhythmia

52
Q

why does cocaine give a euphoric feeling?

A

it blocks reuptake of dopamine which regulates the reward pathway

53
Q

what is methemoglobinemia? which local anaesthetic can cause this?

A

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
Q

what local anaesthetic do we commonly use in spinal and corneal anaesthesia?

A

tetracaine

55
Q

what are some amides?

A

lidocaine
mepivacaine
bupivacaine

56
Q

what is the most frequently used amide local anaesthetic?

A

lidocaine

57
Q

who is mepivacaine contraindicated for and why?

A

pregnant women as its toxic for newborns

58
Q

what is the main indication for bupivacaine?

A

epidural anaesthesia during labour

59
Q

what happens if bupivacaine is accidentally administered into a blood vessel?

A

its very cardiotoxic so would cause severe myocardial depression

60
Q

what happens if local anaesthetics get into the blood stream?

A

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
Q

what are neuromuscular blockers?

A

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
Q

what are the 2 types of neuromuscular blockers?

A

non-depolarizing and depolarizing

63
Q

whats the difference between depolarizing and non-depolarizing neuromuscular blockers?

A

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
Q

whats the moa of non-depolarizing neuromuscular blockers?

A

they bind to nicotnic receptors so that ACh cannot bind and we therefore get decreased depolarization of the muscle fiber and weaker contraction

65
Q

what are some examples of non-depolarizing neuromuscular blockers?

A

atracurium, vecuronium, rocuronium, pancuronium, tubocurarine

66
Q

what are the indications for non-depolarizing neuromuscular blockers?

A

endotracheal intubation, surgical procedures and mechanical ventilation

67
Q

what are some specific side effects of atracurium?

A

bronchoconstriction and vasodilation = causes hypotension, reflex tachycardia and flushing

68
Q

why can atracurium be dangerous in patients in kidney failure?

A

as atracurium produces laudanosine which is a toxic metabolite that is neurotoxic - it can build up in the blood and triggr seizures

69
Q

how can you reverse side effects of neuromuscular blockers?

how does this work?

A

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
Q

whats the moa of depolarizing neuromuscular blockers?

A

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
Q

what is the depolarizing neuromuscular blocker?

A

succinylcholine

72
Q

whats the indication for succinylcholine?

A

as an adjunct to general anesthesia, to facilitate tracheal intubation, and to provide skeletal muscle relaxation during surgery or mechanical ventilation.

73
Q

how long does succinylcholine’s effects last?

A

less than 10 minutes because it rapidly leaks into the plasma where its broken down by pseudocholinesterase

74
Q

how do you know if someone is actually asleep during anaesthesia?

A

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
Q

whats the first stage of anaesthesia?

A

induction - period immediately after administration of the induction agent
this is when patients lose conciousness

76
Q

whats the second stage of anaesthesia?

A

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
Q

whats the 3rd stage of anaesthesia?

A

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
Q

what is the 4th stage of anaesthesia?

A

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.

xB12W7 (6 decks)

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