analgesia Flashcards

1
Q

dental practitioners formulary analgesia

A
aspirin
ibuprofen
diclofenac
paracetamol
dihydrocodeine
carbamazepine
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2
Q

what does pain result from?

A

trauma and infection - breakdown of membrane phospholipids into arachidonic acid
breaks down into prostaglandins
sensitise the tissues to other inflammatory products which results in pain

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3
Q

writing a prescription

A

GP14 (scotland)
write name and address - not label as could be removed
line underneath if you only partially fill box so no-one can add to it
use child’s weight to calculate dose

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4
Q

aspirin advantage over paracetamol

A

superior anti-inflammatory properties

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5
Q

aspirin full name

A

acetylsalicylic acid

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6
Q

aspirin properties

A

analgesic
antipyretic
anti-inflammatory
metabolic

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7
Q

aspirin - mechanism of action

A

decrease prostaglandin production
inhibits COX1 (and COX2)
- reduces platelet aggregation and predisposes to damage of gastric mucosa

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8
Q

aspirin - analgesic

A

mainly peripherally acting

inhibition of prostaglandin synthesis in inflamed tissues (COX inhibition)

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9
Q

aspirin - antipyretic

A

prevents temp raising effects of IL-1 and the rise in brain prostaglandin levels
therefore reduces elevated temperature in fever
doesn’t reduce normal temp

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10
Q

aspirin - anti-inflammatory

A

prostaglandins are vasodilators therefore also affect capillary permeability
good anti-inflammatory

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11
Q

aspirin - metabolic effects

A

BMR increase
platelets - reduces aggregation
prothrombin - increases PT time
decreases blood sugar

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12
Q

aspirin adverse effects

A

GIT problems
hypersensitivity
overdose
mucosal burns

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13
Q

aspirin adverse effects - GIT problems

A

stomach mucosa
prostaglandins (PGE2 and PGI2)
- inhibit gastric acid secretion
- increase blood flow through gastric mucosa
- help production of mucin by cells in stomach lining (cytoprotective action)

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14
Q

aspirin adverse effects - hypersensitivity

A

acute bronchospasm/asthma type attacks
minor skin rashes
other allergies
ask asthmatics if they have taken it before

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15
Q

aspirin adverse effects - overdose

A
hyperventilation
tinnitus, deafness
vasodilation and sweating
metabolic acidosis - can be life threatening
coma (uncommon)
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16
Q

aspirin adverse effects - mucosal burns

A

direct effect of salicylic acid
aspirin applied locally to oral mucosa results in chemical burns
aspirin has no topical effects
ensure taken with water

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17
Q

aspirin complete contraindications

A

U16s, breastfeeding
- Reye’s syndrome (50% mortality)
previous/active peptic ulceration
haemophilia
hypersensitivity to aspirin or any other NSAIDs
- inc pts who attacks of asthma, angioedema, urticaria or rhinitis have been ppt by aspirin or any other NSAID

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18
Q

Reye’s syndrome

A

fatty degenerative process in liver (and to a lesser extent kidney)
profound swelling in brain
clinically
- nausea, vomiting, lethargy
- later seizures and coma
mortality related to brain damage due to encephalopathy

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19
Q

aspirin cautions

A
epigastric pain
anticoagulants
pregnancy
pts on steroids
hepatic/renal impairment
asthma - ask
taking other NSAIDs
elderly 
G6PD-deficiency
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20
Q

aspirin cautions - epigastric pain

A

history or GORD but no ulcer diagnosed

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21
Q

aspirin cautions - anticoagulants

A

enhances warfarin and other coumarin anticoagulants

  • displaces warfarin from binding sites on plasma proteins so increases free warfarin
  • majority of warfarin is bound (inactive) so if more released therefore active - increases bleeding tendency
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22
Q

aspirin cautions - pregnancy

A

esp 3rd trimester - may impair platelet fct

  • increased risk of haemorrhage
  • increased risk of jaundice in baby
  • can prolong/delay labour (don’t know why)
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23
Q

aspirin cautions - pts on steroids

A

around 25% on systemic long-term steroids will develop a peptic ulcer
if they have an undiagnosed ulcer aspirin may = perforation

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24
Q

aspirin cautions - hepatic/renal impairment

A

metabolism liver, excretion mainly kidney

care/reduce dose/avoid if severe

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25
Q

aspirin cautions - taking other NSAIDs

A

combinations increase risk of SEs

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26
Q

aspirin cautions - elderly

A

more susceptible to SEs - smaller circulating blood vol, on other meds, have co-morbidities

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27
Q

aspirin cautions - G6PD deficiency

A

possible risk of acute haemolytic anaemia/haemolysis

acceptable up to a dose of at least 1g daily in most

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28
Q

prescribing aspirin

A

300mg tablets
send 40 tablets
2 tablets x4 daily, preferably after food
not licensed for U16s

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29
Q

aspirin thrombotic prophylaxis

A

thrombotic cerebrovascular/CV disease

  • a single dose 150-300mg given as soon as possible after the ischaemic event
  • maintenance tx 75mg daily
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30
Q

aspirin nehrotoxicity

A
PGE1 and PGI2 are powerful vasodilators
synthesised renal medulla and glomeruli
involved in control of renal blood flow and excretion of salt and water
inhibition of synthesis may = 
 - sodium retention 
 - reduced renal blood flow
 - renal failure

NSAIDs may cause interstitial nephritis and hyperkalaemia
prolonged abuse over years associated with papillary necrosis and chronic renal failure

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31
Q

aspirin in pts with history or active PUD needing NSAIDs

A

prescribe a PPI in conjunction

  • lansoprazole 15mg x1 daily, 5 days
  • omeprazole 20mg x1 daily, 5 days
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32
Q

paracetamol full name

A

acetaminophen

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33
Q

is paracetamol an NSAID?

A

not really

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34
Q

paracetamol properties

A

analgesic
antipyretic

little/no anti-inflammatory action

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35
Q

does paracetamol interact with warfarin?

A

not significantly

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36
Q

can paracetamol be given to children?

A

yes

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37
Q

why is paracetamol called a “safe” analgesic?

A

doesn’t appear to have much effect on peripheral prostaglandins - little/no gastric mucosal irritation
no effects on bleeding time

but causes severe problems in overdose

38
Q

paracetamol mode of action

A

COX metabolises arachidonic acid into hydroperoxidases, which exert a positive feedback to stimulate COX activity
paracetamol blocks this therefore indirectly inhibiting COX - esp in brain
works centrally
reduction of prostaglandins in the pain pathways of the CNS e.g. thalamus - main site of action

exact mode of action still unclear

39
Q

paracetamol alternative central mechanisms

A

decrease 5HT production
interference with excitatory a.a. NMDA in spinal cord pathways

exact mode of action still unclear

40
Q

paracetamol cautions

A

hepatic impairment
renal impairment
alcohol dependence (CNS depressant)

41
Q

paracetamol side effects

A
rare
rashes
blood disorders
hypotension reported on infusion
liver damage (and less freq kidney damage) following overdose
42
Q

paracetamol interactions

A
anticoagulants
 - prolonged regular use possibly enhances the anticoagulant effect of the coumarins
cytotoxics
domperidone (anti-emetic)
lipid-regulating drugs
metoclopramide (for nausea and vomiting)
43
Q

paracetamol dosage

A

500mg tablets
1-2 tablets every 4-6hours
max dose 4g daily (8 tablets)
always warn pt with regard to max dose and emphasise that they should not exceed this

44
Q

what amount of paracetamol can cause overdose?

A

10-15g (20-30 tablets) or 150mg/kg of paracetamol taken within 24hrs may cause severe hepatocellular necrosis and less freq renal tubular necrosis

45
Q

features of paracetamol overdose

A

anorexia, nausea, vomiting
- only early features of poisoning
- usually settle within 24hrs
persistence of these features beyond 24hrs is often associated with abdominal pain: right subcostal pain and tenderness, usually indicates development of hepatic necrosis

liver damage maximal at 3-4 days - jaundice, renal failure, haemorrhage, hypoglycaemia, encephalopathy, cerebral oedema and death

anyone who has taken an overdose - urgently hospital

46
Q

what has the long-term use of ibuprofen recently been associated with an increased risk of?

A

cardiac events

47
Q

compare ibuprofen to aspirin

A

similar effect to aspirin

  • less effect on platelets
  • slightly less irritant to gastric mucosa
48
Q

NSAIDs that can be prescribed

A

aspirin
ibuprofen
diclofenac

49
Q

ibuprofen dosage

A

400mg tablets x4 daily
preferably after food
max dose 2.4g

50
Q

ibuprofen cautions

A
prev or active peptic ulceration
elderly
pregnancy and lactation
renal, cardiac and hepatic impairment
history of hypersensitivity to aspirin and other NSAIDs
asthma
pt taking other NSAIDs
pt on long-term systemic steroids
51
Q

ibuprofen overdose

A

nausea, vomiting, tinnitus
more serious toxicity v uncommon
activated charcoal followed by symptomatic measures indicated if >400mg/kg ingested in last hour

52
Q

ibuprofen SEs

A

GIT discomfort
- occ bleeding and ulceration
hypersensitivity reactions e.g. rashes, angioedema and bronchospasm
others e.g. headache, dizziness, fluid retention etc

53
Q

COX

A

predominantly responsible for catalysing the reaction that produces prostaglandins associated with:

  • platelet aggregation
  • protection of gastric mucosa
54
Q

COX-2

A

enzyme responsible for generation of most of inflammatory prostaglandins (sometimes COX-1 also involved)

55
Q

what does PGE2 by COX2 in large amounts result in?

A

increased vasodilation
increased vascular permeability
sensitises pain fibre nerve endings to bradykinin, 5HT and other mediators

56
Q

what do the actions of prostaglandins depend on?

A

the pathological situation
whether they are formed by COX1 or COX2
whether they are formed in excessive amounts

57
Q

when can PGE2 have a protective effect?

A

when generated in low physiological amounts by COX-1 in gastric tissues

58
Q

COX2 selectives

A

analgesic actions of NSAIDs appear to result from inhibition of COX-2
so have selective COX2 inhibitors and spare COX1 - less gastric effect
e.g. celecoxib/celebrex

59
Q

advantage of COX2 selectives

A

fewer GIT damaging actions

COX2 generated P may also contribute to gastric mucosal integrity and damage repair
- but can say selective COX-2 inhibitors associated with lower risk of serious upper GIT SEs

60
Q

what are all NSAIDs (inc selective) contraindicated in?

A

pts with active peptic ulceration

61
Q

what are non-selective NSAIDs contraindicated in?

A

pts with history of peptic ulceration

62
Q

BNF NSAID recommendations dental

A

don’t use >1 oral NSAID at a time (inc selective)
for dental and orofacial pain only use selective in those with history of peptic ulcer
highly selective COX2 inhibitors don’t have effect on platelet aggregation - may be better tolerated by pts with clotting disorders
several selectives withdrawn due to CV risk
celecoxib not on dental list

63
Q

where does opioid analgesia act?

A

spinal cord - esp the dorsal horn pathways associated with paleo-spinothalamic pathway
central regulation of pain
produce their effects via specific receptors which are closely associated with the neuronal pathways that transmit pain to the CNS

64
Q

opioid

A

naturally occurring and synthetic molecules that produce their effects by combining with opioid receptors

65
Q

BNF opioid analgesia

A

relatively ineffective in dental pain

SEs

66
Q

opioid analgesia problems

A
dependence - physical, psychological
tolerance - only to depressant effects - to achieve the same therapeutic effects the dose of the drug needs to progressively increase
effects on smooth muscle
 - constipation
 - urinary and bile retention
67
Q

opioid analgesia CNS effect

A
depresses
 - pain centre (alters awareness/perception of pain)
 - higher centres
 - respiratory centre
 - cough centre
 - vasomotor
stimulate
 - vomiting centre (why dihydrocodeine limited value in dental pain)
 - salivary centre
 - pupillary constriction
68
Q

opioid analgesia common SEs

A

nausea, vomiting, drowsiness

larger doses - respiratory depression and hypotension

69
Q

opioid analgesia cautions

A
hypotension
hypothyroidism
asthma
decreased respiratory reserve
prostatic hyperplasia
pregnancy/breastfeeding
may ppt coma in hepatic impairment (reduce dose or avoid)
renal impairment (reduce dose/avoid)
elderly and debilitated (reduce dose)
convulsive disorders
dependence
70
Q

opioid analgesia contraindications

A

acute respiratory depression
acute alcoholism (effects enhanced by alcohol)
raised ICP/head injury
- interferes with respiration
- affects pupillary responses vital for neurological assessment

71
Q

codeine potency

A

1/12 morphine

72
Q

advantages of codeine

A

OTC
low dependence
effective orally
effective cough suppressant

73
Q

codeine SE

A

constipation

74
Q

codeine common OTC dose

A

usually in combination with NSAIDs or paracetamol

e.g. cocodamol 8mg codeine 500mg paracetamol

75
Q

dihydrocodeine potency

A

similar to codeine

76
Q

dihydrocodeine methods of administration

A

SC/IM (controlled drug)

oral (not controlled)

77
Q

dihydrocodeine dose

A

30mg every 4-6hrs

78
Q

dihydrocodeine SEs

A

nausea/vomiting
constipation
drowsiness
larger doses - respiratory depression, hypotension, ureteric spasm, biliary spasm etc

79
Q

dihydrocodeine key interactions

A

MAOI antidepressants

dopaminergics (Parkinsons)

80
Q

dihydrocodeine cautions

A
hypotension
asthma
pregnancy/lactation
renal hepatic disease
elderly/children
81
Q

dihydrocodeine contraindications

A

never in raised ICP/suspected head injury

82
Q

dihydrocodeine dental use

A

mod/severe pain

but BNF states due to vomiting SE little value for dental pain

83
Q

opioid overdose

A

varying degrees of coma, respiratory depression and pinpoint pupils
specific antidote Naloxone indicated if coma/bradypnoea
Naloxone shorter duration of action than many opioids so need close monitoring +/- repeated injections/infusion according to respiratory rate and depth of coma

84
Q

carbamazepine

A

on dental list
Tegretol
anticonvulsant
trigeminal neuralgia

85
Q

other drugs used for trigeminal neuralgia

A

gabapentin

phenytoin

86
Q

clinical features of trigeminal neuralgia

A
severe spasms of pain 'electric shock' lasts seconds
usually unilateral
older
trigger spot identified
F>M
periods of remission
recurrences often greater severity
87
Q

carbamazepine dose for trigeminal neuralgia

A
start 100mg x1-2 daily (but some pts may require higher initial dose)
increase gradually according to response
usual dose 200mg x3-4 daily
put to 1.6g daily in some pts
follow up - need bloods checked
88
Q

carbamazepine side effects

A

dizziness
ataxia
drowsiness
blood disorders

89
Q

carbamazepine contraindications

A

AV conduction abnormalities - unless paced
history of bone marrow depression
porphyria

90
Q

carbamazepine cautions

A
hepatic/renal/cardiac disease
skin reactions
history of haematological reactions to other drugs
glaucoma
pregnancy/breastfeeding
avoid abrupt withdrawal