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PHARMACOLOGY FRCA > Analgesic agents > Flashcards

Analgesic agents Flashcards

1
Q

what is the max safe dose of different local anaesthetic agents?

A

bupivacaine - 2mg/kg (2.5mg/kg with adrenaline)
levobupivacaine - 2.5mg/kg
lidocaine - 3mg/kg (7mg/kg with adrenaline)
prilocaine - 6mg/kg
ropivacaine - 3-4mg/kg

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2
Q

what is the trade name for bupivacaine?

A

marcaine

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3
Q

what is the trade name for levobupivacaine?

A

chirocaine

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4
Q

how do you calculate amount of local if mls and % is given?

A

10mg x ml - dose if 1% given
then divide e.g. by 2 if 0.5%

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5
Q

what is the general structure of a local anaesthetic agent?

A

hydrophillic tertiary amine
lipophilic aromatic ring
joined by ester or amide link - determines group

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6
Q

which are more stable amides or esters?

A

amides - ester link is more unstable

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7
Q

which fibres are most/ least affected by local?

A

small > big
myelinated > unmyelinated

hence best = B myelinated e.g. sympathetic pre ganglionic
next A delta

Aa and Ag - too big

C - non myelinated, most resistant

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8
Q

how are local anaesthetics metabolised?

A

esters - plasma esterases (cocaine also liver metabolism)
amides - liver metabolism

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9
Q

LAST can result in cardiac arrhythmias. how does this respond to treatment?

A

refractory to traditional treatment.

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10
Q

what is the dosing for intralipid LAST regime

A

1.5ml/kg bolus
15ml/kg/ hr infusion
second bolus - 1.5ml/kg
second infusion- 30ml/kg/hr
3rd bolus can be given

max 12ml/kg

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11
Q

what step of the WHO ladder does tramadol belong to?

A

2nd step

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12
Q

what is the dose of paracetamol in neonates?

A

10mg/kg QDS
max oral 60mg/kg/day
max IV 30mg/kg/day

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13
Q

what is the dose of paracetamol in children or <50kg

A

15mg/kg
max oral 75mg/kg/day
max IV 60mg/kg/day

max 4g/day

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14
Q

how do 5HT3 inhibitors interact with paracetamol?

A

paracetamol exerts some of its effects through 5HT3 reuptake blocking
Granisetron and Tropisetron have been shown to block the analgesic action of paracetamol. This is not seen with Ondansetron

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15
Q

what are the indications for aspirin?

A

pain
inflammation
MI - primary and secondary prevention
DVT prophylaxis
pre-eclampsia
TIA / ischaemic strokes

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16
Q

what does aspirin do to ventilaiton?

A

uncouples oxidative phos
so need more O2
hence increases ventilation
only significant in overdose

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17
Q

what does aspirin do to blood sugar?

A

reduced BMs at low dose
increased BMs at high dose

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18
Q

which overdose is raising urinary pH useful in?

A

aspirin - ion trapping in urine

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19
Q

what factors increase risk of paracetamol toxicity in overdose?

A

age
malnutrition - less glutathione
liver disease
smoking

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20
Q

which COX enzyme when inhibited gives beneficial effects vs side effects?

A

COX 1 - found in all cells inc stomach and kidney - side effects

cox 2 - found in inflammatory cells - responsible for beneficial effects when inhibited

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21
Q

what is a major side effect of the COX 2 specific inhibitors

A

better side effect profile e.g. GI bleeds etc
HOWEVER - thrombotic cardiac events

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22
Q

which of the COX enzymes is inducible?

A

cox 2

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23
Q

are NSAIDS acids or bases?

A

weak acids

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24
Q

where are enzymes absorbed from GIT?

A

in stomach, low pH - unionised
in duodenum less unionised however larger S.A

overall duodenum contributes to most absorption

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25
Q

what is the first pass metabolism and protein binding like for NSAIDs?

A

limited 1st pass metabolism
highly protein bound

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26
Q

can NSAIDs be used in those undergoing neuroaxial anaesthesia?

A

yes - platelet inhibition not as significant enough to cause bleeding/ haematoma

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27
Q

can nsaids be used in pregnancy?

A

No - risk of closure of ductus arteriosus

28
Q

why do nsaids cause bronchospasm

A

inhibtion of COX means that arachidonic acid favours lipo-oxygenase enzyme which makes leukotrienes

29
Q

can NSAIDs be used safetly in paeds

A

not completely - risk of reyes

30
Q

what are the DDIs of NSAIDs?

A

increase warfarin - plasma protein binding
increase lithium

31
Q

what precursor does B-endorphin come from?

A

B-endorphin and ACTH are both derived from the same precursor, pro-opiomelanocortin (POMC)

32
Q

what is the main receptor of enkephalins and dorphins?

A

enkelphalins = mu and delta
dynorphins = kappa

33
Q

what endogenous opioid is involved in appetite and circadian rhythm?

A

dynorphins

34
Q

what type of receptors are opioid receptors and what does activation lead to?

A

Gi
K+ channel activation and hyperpolarisation
closure of VG Ca channels

hence reduced conductance and NT release

35
Q

which receptors does naloxone antagonise?

A

mu, delta , kappa

36
Q

give examples of opiates

A

Morphine, Codeine and Thebaine are examples of opiates - natural

everything else and above = opioids

37
Q

how does pentazocine act at opioid receptors

A

Pentazocine is an example of an agonist/antagonist which antagonises the action of morphine at mu receptors

38
Q

what hormonal side effects do opiates have?

A

reduce ACTH, LH, FH , prolactin
increase ADH

39
Q

do all opioid side effects occur via opioid receptors?

A

Pruritis is by histamine release from mast cells

40
Q

what is the typical duration of a bolus of morphine?

A

2-3 hours

41
Q

what is the principle metabolite of morphine?

A

morphine 3 glucuronide
(M6G - is the other but also active)

42
Q

how much more potent is diamorphine than morphine?

A

x2

43
Q

which is the most rapidly acting opioid?

A

alfentanil

44
Q

how does potency of pethidine compare to morphine?

A

1/10th the potency of morphine

45
Q

what metabolises remifentanil?

A

non specific tissue esterases

46
Q

which of the opioids are Phenylpiperidines vs morphinans

A

morphinans - oxycodone, diamorphine and morphine

phenylpiperidines - fentanyl, pethidine, alfentanil

esters - remifentanil

47
Q

In equi-analgesic doses all opioids cause serious side-effects to a similar degree - true or false

A

TRUE

48
Q

are opioids sterioisomers?

A

yes - their enantiomers do not have activity at opioid receptor

49
Q

which opioid receptor is responsible for major side effects?

A

u

50
Q

how does tramadol action differ from traditional opioids?

A

u agonist
but also 5HT3 and NA reuptake inhibitor

51
Q

what is the general oral bioavailability of most opioids?

A

low

52
Q

what is the elimination half life of morphine? and fentanyl?

A

3 hours - morphine
3-4hrs - fentanyl

53
Q

do fentanyl and afentanil have active metabolites?

A

no

54
Q

what particular opioid side effect does tramadol avoid/ reduce?

A

respiratory depression

55
Q

what PCA should be used in renal failure?

A

fentanyl - less risk of build up of active metabolities

56
Q

what is codeine metabolised to?

A

mostly codeine 6 glucuronide - 80%
10% to morphine

57
Q

which has a higher oral bioavailability out of codeine, dihydrocodeine and morphine ?

A

codeine

58
Q

how does dihydrocodeine compare to morphine and codeine?

A

more potent than codeine
but still a weak opioid like codeine

Dihydrocodeine has a lower bioavailability than codeine, which is why they have similar doses, despite dihydrocodeine being more potent.

59
Q

what are the routes of administration of buprenorphine?

A

transdermal
sublinguial / buccal
IV

60
Q

how does buprenorphine interact with MOP and KOP?

A

MOP - partial agonist, high affinity but lower efficacy than full agonist
KOP - antagonist

61
Q

what are the side effects of naloxone?

A

Naloxone can cause sweating, nausea, restlessness, trembling, vomiting, flushing and headache.
can increase sympathetic tone

62
Q

what is the use of naltrexone?

A

opioid and alcohol dependence
not opioid OD

it is a competitve MOP antagonist

63
Q

how do you manage opioid dependance for surgery?

A

stop any antagonists e.g. naltrexone / buprenorphine
may need more opioids
continue after

64
Q

which has a shorter half life naloxone or morphine?

A

morphine
hence need multiple doses of naloxone or infusion
repeated up to max of 10mg

65
Q

which opioids are available as transdermal patc

A
66
Q
A

PHARMACOLOGY FRCA (12 decks)

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