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X CNT 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

define pharmacokinetics

A

what the body does to the drug (process of absorption and distribution)

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2
Q

what happens when a drug is administered?

A

absorbed into the blood stream to systemic circulation where it is distributed to tissues

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3
Q

define pharmacodynamics

A

the effects of the drug on the body

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4
Q

what happens when the drug reaches it’s site of effect?

A

there is pharmacological effect leading to the clinical response

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5
Q

what two effects are seen in the clinical response to a drug?

A

toxicity

therapeutic effect

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6
Q

what does toxicity describe in relation to clinical response to a drug?

A

the side effects

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7
Q

when may an animal be given a drug even when there are contraindications?

A

if the quality of life is sufficiently affected then a cost benefit analysis will indicate that it is worthwhile giving the drug

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8
Q

what are the 2 key ways in which drugs work?

A

non-cellular mechanisms

cellular mechanisms

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9
Q

what are the 4 main non-cellular ways in which drugs work?

A

physical effects
chemical reactions
physicochemical mechanisms
modification of body fluid composition

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10
Q

why do fluids work through non-cellular mechanisms instead of cellular mechanisms?

A

because the effects that they have on cells isn’t direct, it is instead mediated by osmosis that is caused by changes if fluid composition

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11
Q

give an example of a drug with physical effects

A

eye lubricant

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12
Q

give an example of a drug which works to modify body fluid composition

A

hypertonic saline

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13
Q

what are the 4 main cellular mechanisms in which drugs work?

A

physicochemical/biophysical mechanisms
cell membrane structure and function modification
enzyme inhibition
receptor mediated effects

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14
Q

give an example of drugs which affect cell membrane structure and function

A

insulin

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15
Q

give an example of drugs that work through enzyme inhibition

A

NSAIDs

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16
Q

give an example of drugs that work through receptro mediated effects

A

opioids

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17
Q

what are the targets for drug action?

A 
receptors
enzymes
transporters
ion channels
nucleic acid
miscellaneous
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18
Q

how may receptors aid drug action?

A

transduce signal from drug to produce conformational change and influence flow of ions

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19
Q

how can enzymes be affected by drug action?

A

may be activated or inhibited

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20
Q

how are ion channels affected by drug action?

A

open or close

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21
Q

how are transporters influenced by drug action?

A

carry a molecule across the membrane

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22
Q

give an example of receptors which are targeted by drugs

A

mu opioid receptor

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23
Q

give an example of enzymes which are targeted by drugs

A

COX 1 and 2

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24
Q

give an example of a drug that may be moved by transporters

A

insulin

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25
Q

give an example of a drug that affects ion channels

A

local anaesthetics

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26
Q

define ligand

A

a substance that forms a complex with a receptor (biomolecule) to serve a biological purpose (e.g. analgesia in the case of opioids)

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27
Q

what is the role of a receptor?

A

interacts with extracellular physiological signals and converts them to intracellular effects

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28
Q

describe the 3 step process involved in a receptor converting extracellular signalling to intracellular effects

A

receives a signal
transduces signal to
effector mechanism

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29
Q

what are the 2 ways receptors will be targeted by drugs?

A

agonist or inverse agonist

antagonist

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30
Q

what are the main effects of agonists/inverse agonists on receptors?

A

direct through ion channel opening or closing

transduction mechanisms leading to enzyme activation/inhibition, ion channel modulation and DNA transcription

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31
Q

what is an example of a receptor agonist/inverse agonist?

A

dexmedetomidine

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32
Q

what is the effect of antagonists on receptors?

A

prevents binding of other agonists/antagonists

produces no effect and blocks endogenous mediators

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33
Q

give an example of a receptor antagonist

A

atipam

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34
Q

what are the 2 effects of drugs on ion channels?

A

blockers

modulators

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35
Q

what is the effect of blockers on ion channels?

A

permeation blocked so no entry or exit

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36
Q

what is the effect of modulators on ion channels?

A

increased or decreased opening probability

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37
Q

where do modulators and blockers sit within ion channels?

A

blockers sit within the channel itself

modulators sit in the sub-unit

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38
Q

what are the 3 ways drugs can affect enzymes?

A

inhibition
false substrate
prodrug

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39
Q

how does a false substrate affect the enzyme?

A

is structurally similar to substrate but not the same so an abnormal metabolite is produced

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40
Q

how does prodrug worth with an enzyme?

A

makes use of the enzyme function to convert prodrug to active drug. An active drug is produced by the reaction

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41
Q

how do transporters work to produce drug effects?

A

normal transport to allow drug to enter cell
inhibition of transporter to block transport
false substrate leading to accumulation of abnormal compounds

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42
Q

what are the 4 main types of receptors?

A

ligand gated ion channels
G-protein coupled receptors
kinase linked receptors
nuclear receptors

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43
Q

what are the fastest acting receptors?

A

ligand gated (milliseconds)

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44
Q

what are the slowest acting receptors?

A

nuclear receptors (hours)

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45
Q

how do ligand gated ion channels work?

A

lead to hyperpolarisation or depolarisation and therefore cellular effects

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46
Q

how do G-protein coupled receptors work?

A

change in cell excitability leads to activation of second messengers which cause protein phosphorylation. This leads to cellular effects

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47
Q

how do kinase linked receptors work?

A

receptor phosphorylates protein leading to gene transcription, protein synthesis and then cellular effects

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48
Q

how do nuclear receptors work?

A

receptors in the nucleus cause gene transcription this then leads to protein synthesis and cellular effects.

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49
Q

give an example of a ligand gated ion channel

A

nicotinic ACh receptor

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50
Q

give an example of a G-protein coupled receptor

A

muscarinic ACh receptor

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51
Q

give an example of a kinase linked receptor

A

cytokine receptor (linked to inflammation)

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52
Q

give an example of nuclear receptors

A

oestrogen receptors

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53
Q

define affinity

A

how well/avidly a drug binds to it’s receptor

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54
Q

define intrinsic activity/ efficacy

A

magnitude of a drugs effect once bound (0-1)

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55
Q

what is a full agonist able to do once bound to the receptor?

A

generate a maximal response

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56
Q

describe the affinity and intrinsic activity of full agonists

A

high affinity and high intrinsic activity

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57
Q

give an example of a full agonist drug

A

morphine is a full agonist at the mu opioid receptor

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58
Q

what type of receptor is a mu opioid receptor?

A

G-protein coupled receptor

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59
Q

what is a partial agonist drug?

A

one that has intrinsic activity of less than 1

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60
Q

what does receptor occupancy of a partial agonist drug lead to?

A

a sub maximal effect even if receptors are fully bound

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61
Q

give an example of a partial agonist drug

A

buprenorphine binds to the mu opioid receptor but does not produce a maximal effect even if the dose is increased

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62
Q

what is an inverse agonist?

A

drug binds and exerts an opposite effect to the endogenous agonist

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63
Q

give an example of an inverse agonist

A

antihistemines

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64
Q

define antagonist

A

exhibits affinity but no intrinsic activity

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65
Q

give an example of an antagonist

A

atipam antagonises a-2 adrenoreceptor against dexmedetomidine

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66
Q

define potency

A

the dose of a drug required to produce a response (more potent = less drug required for response)

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67
Q

what is therapeutic index a measure of?

A

maximum non-toxic dose divided by minimum effective does

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68
Q

what is the issue with using therapeutic index?

A

based on data that may not be clinically relevant
effective dose can be extremely variable depending on what is being treated
doesn’t account for idiosyncratic reactions

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69
Q

what does ADME stand for?

A

absorption
distribution
metabolism
excretion

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70
Q

what is ADME involved with?

A

what the body does to the drug

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71
Q

why is it important that drugs can cross cell membranes?

A

to enable them to reach their site of action so they may have an effect

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72
Q

what are the 5 main ways that drugs cross cell membranes?

A 
aqueous diffusion
passive lipid diffusion
facilitated diffusion
pinocytosis
active transport
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73
Q

what is the law which governs the rate of transfer of drug across biological membranes?

A

Fick’s law of diffusion

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74
Q

what are the 5 elements of Fick’s law of diffusion?

A 
diffusion coefficient
surface area of tissue
membrane thickness
partition coefficient
concentration gradient
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75
Q

what is the partition coefficient?

A

how drugs distribute themselves in water vs in oil

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76
Q

what sort of molecules are drug molecules usually?

A

small weak acids or weak bases

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77
Q

what is the level of ionisation of a drug determined by?

A

pKa of drug and pH of the surrounding tissue

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78
Q

how do non-ionised drugs cross biological membranes?

A

passive diffusion

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79
Q

how do ionised drug molecules cross biological membranes?

A

selective transport mechanisms, facilitated diffusion or pinocytosis

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80
Q

what process in the body may affect drug absorption?

A

infection/inflammation can change tissue pH and make it more acidic

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81
Q

what is drug absorption mainly influenced by?

A

route of administration and drug formulation

peripheral shutdown if present

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82
Q

define bio-availability

A

the fraction of a dose reaching the systemic circulation after administration IM compared to the same does administered IV

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83
Q

what are the 8 key routes of drug administration?

A 
IV
IM
SC
oral
inhalational
epidural 
transmucosal (oral and rectal)
transepithelial (skin, cornea, nasal mucosa)
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84
Q

where does drug absorption primarily take place after oral administration?

A

small intestine

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85
Q

what types of drug molecules are usually poorly absorbed through oral administration?

A

low lipid soluble and strong acids and bases

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86
Q

what are the 4 main factors which affect GI absorption?

A

gastrointestinal motility
splanchnic blood flow
particle size and formulation
physicochemical factors

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87
Q

how can gastrointestinal motility affect GI absorption of drugs?

A

fast and slow can mean that not enough of the drug is absorbed

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88
Q

how may splanchnic blood flow be reduced and so reduce drug absorption?

A

dehydration and reduced BP

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89
Q

what is first pass metabolism of drugs?

A

enzymes in gastrointestinal wall and liver that metabolise drugs

90
Q

what is the fastest route of drug administration?

A

IV

91
Q

what is challenging about IV drugs?

A

access can be difficult

92
Q

what influences the rate of IV injection?

A

peak concentration (faster admin = higher peak concentration)

93
Q

define peak concentration of drugs

A

maximum serum concentration of a drug in a specific area

94
Q

what can be used to maintain plasma concentrations of IV drugs?

A

constant rate infusions (CRI) or target controlled infusions (TCI)

95
Q

describe the basic path of IV drugs once administered

A

right heart - lungs - systemic circulation

96
Q

why is IM injection variable?

A

local blood flow

diffusion through tissue

97
Q

why may IM injections produce an adverse response?

A

they are often painful but varies from drug to drug

98
Q

what must happen on administration of IM drugs before injection?

A

aspirate (draw back)

99
Q

how does absorption of SC injection compare to IM?

A

slower and more unpredictable

100
Q

what influences absorption of SC injections?

A

injection site, temperature of skin, dehydration and shock

101
Q

what drugs are given through inhalation?

A

drugs that can be vapourised or aerosolised

102
Q

what is a benefit of epidural, transmucosal or transepithelial administration of drugs?

A

direct to site of action so doses can be lower

103
Q

define apparent volume of distribution

A

amount of drug administered / plasma concentration

104
Q

what are the 5 key factors which determine drug distribution?

A 
protein binding
tissue binding
organ blood flow
membrane permeability
drug solubility
105
Q

what are the 2 proteins involved in plasma protein binding?

A

albumin

alpha-1 acid glycoprotein

106
Q

what does albumin bind to during plasma protein binding of drugs?

A

weak acids

107
Q

what does alpha-1 acid glycoprotein bind to during plasma protein binding of drugs?

A

weak bases

108
Q

what is the effect of plasma protein binding of drugs during distribution?

A

doesnt elicit a response. It takes up drug and removes it from circulation so preventing it from working on receptors

109
Q

what happens to the unbound/free fraction of the drug that is not plasma protein bound?

A

can interact with receptors/diffuse across membranes

110
Q

why may plasma protein binding vary from patient to patient?

A

those with low albumin will have a larger unbound/free fraction

111
Q

what are the 2 types of tissue binding of drugs?

A

specific and non-specific

112
Q

where are drugs initially distributed to?

A

organs with high blood flow

113
Q

what is an advantage of drugs being initially distributed to organs with high blood flow?

A

good for anaesthetics as they go to the brain first

114
Q

what is a disadvantage of drugs being initially distributed to organs with high blood flow?

A

anaesthetic drugs will negatively affect the heart quickly as this also has good blood flow

115
Q

how does membrane permeability affect drug distribution?

A

higher membrane permeability = faster effect

116
Q

what may happen to highly lipid soluble drugs?

A

accumulate in fat and then be released as the fat is metabolised. This can lead to the ‘hangover’ effect and keep the plasma concentration of a drug higher for longer leading to prolonged recovery

117
Q

what must be assumed about all drugs with regards to pregnant or lactating animals?

A

drugs will cross placenta and be secreted into milk

118
Q

define drug clearance

A

the volume of plasma from which a drug is completely removed per unit time

119
Q

define half life of a drug

A

the time taken for plasma drug concentration to fall to 50% of it’s initial value

120
Q

what is the equation used to calculate drug half-life?

A

K= clearance / volume of distribution

121
Q

what is the termination of drug effects caused by?

A

primarily biotransformation then excretion

122
Q

where does biotransformation usually occur?

A

in the liver

123
Q

where does excretion of drugs usually happen?

A

the kidneys

124
Q

what compounds does the kidney excrete most easily?

A

polar water soluble compounds

125
Q

why is biotransformation in the liver so crucial?

A

most drugs are lipophillic and highly plasma protein bound which the kidneys cannot excrete easily. Biotransformation converts them into easily excreted molecules

126
Q

what is the primary organ of metabolism?

A

the liver

127
Q

what are the 2 stages of hepatic metabolism?

A

I: conversion of drug to polar metabolite
II: conjugation with substrates

128
Q

what reactions are used in phase I of hepatic metabolism?

A

oxidative, hydrolytic or reductive

129
Q

what is required in phase II of hepatic metabolism?

A

energy

130
Q

what is the aim of phase II hepatic metabolism?

A

to make resultant polar compound more readily excreted

131
Q

what reaction does not occur in phase II hepatic metabolism of cats that can cause longer lasting effects of propofol?

A

glucuronidation

132
Q

what reaction does not occur in phase II hepatic metabolism of dogs?

A

acetylation

133
Q

what are the 4 effects of hepatic metabolism?

A

drugs may be activated
drugs may have active metabolites
drugs may have toxic metabolites
enzymes involved in metabolism may be inhibited or induced (long term drug use)

134
Q

what type of excretion of drugs is most common?

A

renal excretion

135
Q

what are the 3 other types of excretion of drugs from the body?

A

biliary
exhalation
GI tract

136
Q

what are the 2 types of renal excretion of drugs?

A

active

passive

137
Q

where does active renal excretion of drugs occur?

A

tubular secretion

138
Q

where does passive renal excretion of drugs occur?

A

glomerular filtration

139
Q

what may need to happen to drug doses in animals with renal compromise?

A

may need to be altered

140
Q

what happens during enterohepatic circulation of drugs?

A

drug is metabolised (often through glucuronidation)
billiary excretion
deglucuronidation by gut microflora
reabsorption from gut

141
Q

what can be explained by enterohepatic circulation of drugs?

A

longer lasting effects of drugs

142
Q

how long does enterohepatic circulation continue for?

A

until plasma concentration drops

143
Q

how may antimicrobial agents be classified?

A

according to the type of organism against which they are effective

144
Q

what do bacteriostatic antimicrobials do?

A

arrest bacterial multiplication so stop proliferation and allow individuals immune system to clear the infection

145
Q

what do bacteriocidal antimicrobials do?

A

act by primarily killing bacteria so useful for immunocompromised animals

146
Q

what is the outcome of concentration dependent antibiotics related to?

A

peak antibiotic concentration achieved at the site of infection relative to the MIC

147
Q

what is MIC?

A

minimum inhibitory concentration (HIGH DOSE)

148
Q

what is the outcome of time dependent antibiotics related to?

A

concentration of drug being kept above MIC for high proportion of time between each dose (SUSTAINED DOSE)

149
Q

what are the 3 mechanisms of action of antibiotics?

A

interference with cell wall leading to cell rupture due to osmotic pressures
interference with structure of the plasma membrane
interference with microbial DNA or its replication or repair

150
Q

what are the 6 principles of antimicrobial therapy?

A 
make a diagnosis
remove barriers to cure
decide whether chemotherapy is necessary
select the best drug
administer the drug in optimum dose and frequency and by the optimum route
test for cure
151
Q

how should be the best drug be selected?

A

specificity
pharmacokinetic factors
the patient

152
Q

what are pharmacokinetic factors?

A

right dose at the right time

153
Q

what could be involved in removing barriers to cure?

A

holistic approach e.g. debriding wound

154
Q

what affects the breakdown of local anaesthetics?

A

whether there are ester and amide linkages

155
Q

where are side effects of local anaesthetic seen?

A

CVS

CNS

156
Q

when are the 5 main occasions for local anaesthetics to be used?

A

part of balanced anaesthesia (e.g. epidural under GA)
Anaesthesia in a standing/conscious patient
Post-operative pain relief
Desensitisation for procedures (e.g. EMLA)
Lameness investigation in horses

157
Q

what is the difference between epidural and spinal anaesthesia?

A

epidural - injected into the epidural space via a catheter

spinal - injected directly into CSF via a much smaller needle

158
Q

give an example of when local anaesthesia may be used

A

infraorbital block for dental surgery

159
Q

give an example of when topical local anaesthesia may be used

A

desensitisation of feline larynx prior to endotracheal intubation

160
Q

what is potency a measure of in pharmacology?

A

drug activity expressed in terms of the amount required to produce an effect of given intensity

161
Q

what increases as local anaesthetic potency increases?

A

toxicity

162
Q

what 4 factors affect the duration of local anaesthetic action?

A

ease of penetration into nerve cell and amount of drug reaching the sodium channel
strength of binding to the sodium channel
speed of removal
metabolism of the local anaesthetic

163
Q

what is ease of penetration into nerve cell and amount of drug reaching the sodium channel of local anaesthetics due to?

A

lipid solubility

164
Q

what is speed of removal of local anaesthetic dependent on?

A

tissue perfusion

165
Q

what may be added to local anaesthetics to reduce speed of removal?

A

vasoconstrictors (e.g. adrenaline)

166
Q

how are ester links in local anaesthetics hydrolysed?

A

plasma esterases

167
Q

does CSF contain esterases?

A

no - esters cannot be broken down there and must diffuse out into other tissues

168
Q

what are amide linkages broken down by?

A

cytochrome P450 enzymes

169
Q

what may prolong or limit metabolism of amide local anaesthetics?

A

hepatic disease

170
Q

what can increase the breakdown of amide local anaesthetics?

A

drugs such as barbiturates induce enzymes which will increase breakdown

171
Q

what can decrease the breakdown of amide local anaesthetics?

A

drugs that inhibit the P450 enzymes e.g. midazolam

172
Q

what are the 3 main formulations of Lidocaine?

A

sterile solutions for parenteral use
aerosol sprays for nasal/airway use
topical patches

173
Q

how water soluble are local anaesthetics?

A

poor

174
Q

how is the low water solubility of local anaesthetics over come?

A

making a salt solution

175
Q

what is the effect of making a salt solution to increase water solubility of local anaesthetics?

A

lowers pH of solution if a hydrochloride salt which can cause stinging on injection

176
Q

what is baricity?

A

weight of one substance compared with the weight of an equal volume of another substance

177
Q

what is the baricity comparator for spinal anaesthesia?

A

CSF

178
Q

why is baricity essential in spinal local anaesthetics?

A

because we don’t want anaesthetics to spread higher into epidural space, as it would effect respiration

179
Q

how are solutions made heavier to address issues baricity in local anaesthetics?

A

glucose is added

180
Q

what are the key effects of vasoconstrictors in local anaesthetics?

A

reduces risk of toxicity
reduces bleeding at the injection site
reduces speed of systemic absorption and so prolongs duration of action

181
Q

what happens when local anaesthetics are absorbed systemically?

A

they are available for systemic effects

182
Q

what must happen to a local anaesthetic drug for it to be systemically active?

A

must be unbound and unionized

183
Q

what types of local anaesthetics have a longer duration of action and lower risk of toxicity?

A

those which bind more easily to plasma proteins

184
Q

what is the effect of lower pH on local anaesthetic binding?

A

reduces affinity for protein binding and increases risk of toxicity

185
Q

what are the 2 levels of toxicity of local anaesthetics?

A

neurotoxicity

cardiovascular toxicity

186
Q

what must be considered when injecting local anaesthetic?

A

dose
injection site
care with smaller patients

187
Q

what effect does site of injection of local anaesthetic have?

A

determines the rate of uptake into the systemic circulation

188
Q

at what concentrations of local anaesthetic is CNS toxicity often seen?

A

lower than CVS

189
Q

what are the symptoms of generalised CNS depression that are proportional to the unbound drug?

A

minor behavioral changes
muscle twitching and tremors
tonic-clonic convulsions
CNS depression/respiratory depression and death

190
Q

how is CNS toxicity treated?

A

symptomatic treatment
Benzodiazapines to control seizures
O2 supplementation
intubation and control of ventilation if respiratory seen/needed

191
Q

what are the 2 main symptoms of CVS toxicity due to local anaesthetic?

A

hypotension

dysrhythmias

192
Q

how does CVS toxicity from local anaesthetic lead to hypotension?

A

depression of myocardial activity
direct relaxation of vascular smooth muscle
loss of vasomotor sympathetic tone

193
Q

how does CVS toxicity due to local anaesthetic cause dysrhythmias?

A

commonly seen with bupivacaine
lipophilicity means that there is rapid entry to open sodium channels during systole
drug remains bound to sodium channel during diastole
presents as re-entrant arrythmias

194
Q

how is CVS toxicity from local anaesthetic treated?

A

symptomatic treatment
manage bradycardias with an anticholinergic
fluid therapy with inotropic support if needed
intralipid IV could be used to mop up local anaesthetic

195
Q

how can local anaesthetic toxicity be prevented?

A

don’t exceed ‘safe’ maximum dose
if a greater volume is needed dilute the local anaesthetic with 0.9% NaCl
use appropriately sized syringes to draw up dose (accuracy)
use appropriately sized needles to minimise tissue trauma
aspirate before injection to confirm you are not in a blood vessel

196
Q

what volatile agents are licensed for use in dogs and cats?

A

isoflurane and sevoflurane

197
Q

what was suggested by CEPSAF to do with gas induction of anaesthesia?

A

gas induction was associated with increased risk of anaesthetic related death

198
Q

describe the characteristics of the ideal inhalational agent

A 
non-irritant to mucous membranes
minimal effects on CVS and respiratory function
rapid uptake and elimination
non-toxic
non-flammable and chemically stable
easily vaporised
good analgesia and muscle relaxation
199
Q

what does MAC stand for?

A

minimum alveolar concentration

200
Q

what is MAC?

A

concentration of VA required to prevent response to supramaximal noxious stimuli

201
Q

what can MAC be used to compare?

A

potency of agents

202
Q

what is the difficulty of using MAC as a reliable measure of potency?

A

measured in a lab and there are factors which affect it

203
Q

what factors can MAC be reduced by?

A 
other drugs (e.g. premed)
hypothermia
pregnancy
extremes of age (geriatric and neonatal)
hypothyroidism
204
Q

what factors can MAC be increased by?

A

hyperthermia
neonates
hyperthyroidism
administration of catecholamines and sympathomimetics

205
Q

define vapour

A

gaseous state of a substance that at ambient temperature and pressure is a liquid

206
Q

define gas

A

exists in gaseous form at room temperature at sea level

207
Q

define partial pressure

A

pressure that individual gas exerts in a mixture of gases

208
Q

define partition coefficient

A

ration of the concentration of a compound in two solvents at equilibrium

209
Q

how does concentration of VA in inspired air affect uptake of anaesthetic gases?

A

drugs move down their concentration gradient, higher concentration of inspired air VA will lead to faster uptake

210
Q

what is the mechanism of action of anaesthetic agents?

A

unclear - site of action is the brain

211
Q

how does alveolar ventilation affect uptake of anaesthetic gases?

A

good alveolar ventilation leads to enhanced uptake of agent

212
Q

how does alveolar ventilation affect recovery?

A

increased alveolar ventilation improves recovery as anaesthetic gas is blown off

213
Q

is panting effective in alveolar ventilation?

A

no - just moves animals dead space air so exchange is not occurring

214
Q

how does blood gas solubility affect distribution of anaesthetic gases?

A

lower blood gas solubility leads to faster onset and recovery from anaesthesia

215
Q

how does cardiac output affect distribution of anaesthetic gases?

A

lower cardiac output leads to faster onset

216
Q

how does blood tissue solubility affect distribution of anaesthetic gases?

A

impacts how well distributed agent is (increased solubility = better distribution)

217
Q

how can concentrations of anaesthetic gases be reduced so their side effects are reduced?

A

provision of effective analgesia so that less VA is required during surgery to keep patient comfortable

218
Q

what are the main side effects of inhalant anaesthetics?

A

dose dependent respiratory and cardiovascular depression

219
Q

what is the role of balanced anaesthesia?

A

reduction of side effects while benefiting from desired effects of drugs

220
Q

why is monitoring of anaesthetic so essential?

A

supportive therapy of any issues can be provided quickly (e.g. fluids or ventilation)

X CNT 1 (4 decks)

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