Therapeutics Flashcards

1
Q

What class of drug does penicillin come under?

A

beta-lactam

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2
Q

What is the mode of action of penicillin?

A

1) inhibits cross linking peptides
2) inactivates autolysin inhibitors - interferes with cell wall synthesis
3) targets rapidly dividing organisms

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3
Q

What is the spectrum of activity of penicillin?

A
  • narrow spectrum
  • most gram +ve cocci, gram +ve bacilli, some gram -ve cocci
  • anaerobic potential - fusobact spp, clostridium, anaerobic strep
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4
Q

What are the kill characteristics of penicillin?

A

Time dependent killing
- prefer dividing bacteria
- takes time for inhibition process and eventual microorganism rupture
- high blood levels

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5
Q

What are three common preparations of penicillin?

A

1) Penicillin G
2) Penicillin V
3) Procaine/benzathine penicillin

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6
Q

What is penicillin G?

A

Benzylpenicillin
- injectable form, gastric acid labile, low absorption so poor oral success

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7
Q

What is the half life of Penicillin G (benzylpenicillin)

A

30 mins

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8
Q

How is penicillin G administered?

A

injection

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9
Q

What is the peak serum time and peak serum level of penicillin G?

A

30-60mins
2microg/ml

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10
Q

What is the protein binding % of penicillin G?

A

45-68%

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11
Q

How does protein binding impact drug efficacy?

A

agents that are minimally protein bound penetrate tissue better than those that are highly bound, but they are excreted much faster

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12
Q

What is the oral absorption level of penicillin G?

A

20%

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13
Q

What is penicillin V?

A

phenoxymethylpenicillin
well absorbed, gastric acid stable, suitable for oral administration

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14
Q

How is penicillin V administered?

A

phenoxymethylpenicillin is an oral administration

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15
Q

What is the oral absorption level of penicillin V?

A

60-73%

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16
Q

What is the half life of Penicillin V?

A

30-45 mins

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17
Q

What is the peak serum time and level of penicillin V?

A

4microg/L and 30-60mins

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18
Q

What is the protein binding % of penicillin V?

A

75-89%

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19
Q

What is penicillin G used to treat?

A

reserved for severe infection (IV)

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20
Q

What is procaine/benzathine penicillin?

A

procaine benzylpenicillin
benzathine benzypenicillin

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21
Q

What bacteria are penicillins ineffective against?

A

beta-lactamase producing bacteria

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22
Q

How common is penicillin hypersensitivity and what are the symptoms?

A
  • common 8%
  • macropapular/urticarial rash
  • 20-49yrs, 75% anaphylactic fatalities
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23
Q

How many people with penicillin hypersensitivity have an immediate reaction to it?

A

96% in first 60 mins

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24
Q

what are the symptoms of an immediate penicillin hypersensitivity reaction?

A
  • mast cell degranulation and histamine release
  • nausea/vomiting, pruritus, erythema, urticaria, rash, wheeze, laryngeal oedema, angioedema, bronchospasm, hypotension, cardiovascular collapse
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25
Q

What is pruritus?

A

itchy skin

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26
Q

What are the features of a delayed reaction (rash) as a result of penicillin hypersensitivity?

A
  • vesicular, macropapular, bullous, urticarial, scarlatiniform
  • can be short-lived, does not always mean future use of penicillin is contra-indicated
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27
Q

What are some signs of delayed reactions to penicillin?

A

blood dyscrasia
- haemolytic anaemia, leukopenia, thrombocytopenia, aplastic anaemia

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28
Q

What are some risk factors regarding penicillin adminstration?

A
  • multiple drug allergies
  • atopic disease
  • asthma
  • allergic rhinitis
  • nasal polyps
    document and prevent
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29
Q

What is the likelihood of reaction upon re-exposure in people with a true penicillin allergy?

A

15-40% on re-exposure
4-6x greater likelihood than those with negative history

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30
Q

How long do the antibodies following hypersensitivity reaction to penicillin remain and what difference does repeated exposure make?

A
  • Serum IgE antibodies often retained 10-1000 days
  • re-exposure and risk of recurrent allergy higher in those with repeated exposure short-term or long IgE expression
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31
Q

What should be completed following an adverse drug reaction?

A

Yellow card

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32
Q

What are the three main mechanisms of penicillin evasion?

A

1) reduced drug binding to penicillin binding protein (PBP) (altering configuration)
2) hydrolysis of drug by beta lactamase enzymes (principle method of evasion)
3) development of tolerance by disabling autolysis mechanism (penicillin becomes bacteriostatic instead of bactericidal)

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33
Q

What five drugs interact with penicillin?

A

1) antagonism
2) NSAIDs/probenecid
3) warfarin
4) methotrexate
5) oral contraceptive pill

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34
Q

What drugs cause antagonism of penicillin and how?

A

administration of 2 drugs that results in neither working effectively. Penicillin is bactericidal and works on rapidly dividing bacteria, if you add bacteriostatic drugs (stop division), reduces effectiveness. Includes ABx like tetracycline, clindamycin and erythromycin

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35
Q

What interaction occurs when penicillin is given together with NSAIDs or probenecid?

A

NSAIDs and probenecid can increase half life by decreasing renal excretion of penicillin, causing increased plasma concentration

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36
Q

What interaction occurs when penicillin is given together with warfarin?

A

broad spectrum penicillins may affect INR

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37
Q

What interactions occur when methotrexate and penicillin are taken concurrently?

A

penicillin can decrease excretion of methotrexate, compete with eachother in tubules of kidney and ultimately lead to decreased tubular secretion of methotrexate and increased levels through retention, possible toxicity

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38
Q

What are the common unwanted effects of penicillin?

A
  • diarrhoea
  • nausea
  • skin rash
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39
Q

What are the uncommon unwanted effects of penicillin?

A
  • vomiting
  • urticaria and pruritus
  • arthralgia
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40
Q

What are some very rare unwanted effects of penicillin?

A
  • mucocutaenous candidosis
  • hypersensitivity reactions
  • toxicity severe renal failure
  • electrolyte accumulation
  • hepatotoxicity
  • diarrhoea/colitis
  • black hairy tongue
  • increased PT/INR/bleeding
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41
Q

What is a typical dose of penicillin?

A

250-500mg, 6 hourly for 3-5 days

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42
Q

What route of administration is most common for penicillin?

A

oral

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43
Q

Is there a loading dose used for penicillin?

A

yes

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44
Q

What is a loading dose?

A

loading dose is an initial higher dose of a drug that may be given at the beginning of a course of treatment before dropping down to a lower maintenance dose

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45
Q

Penicillin experiences antagonism with which drugs?

A

bacteriostatic ABx

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46
Q

What is the half life of penicillin?

A

30 mins

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47
Q

What is the mode of action of penicillin?

A

cell wall inhibitor

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48
Q

What drug classification is metronidazole in?

A

synthetic nitroimidazole antimicrobials

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49
Q

What needs to happen for metronidazole to be converted into its ultimate active form?

A

must be metabolised

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50
Q

What is the mode of action of metronidazole?

A
  • inhibition of DNA replication
  • fragment existing DNA (metabolites)
  • penetrates cells equally
  • enzymatic reduction (oxidoreductase)
  • mutation bacterial genome
  • bactericidal
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51
Q

What is the spectrum of activity of metronidazole?

A
  • obligate anaerobes
  • gram -ve anaerobes
  • bacteriodes (melaninogenicus)
  • clostridium (C.diff)
  • fusobacterium spp
  • prevotella
  • peptostreptococcus
    all anaerobic bacteria
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52
Q

What is the killing mechanism of metronidazole dependent on?

A

CONCENTRATION dependent
- no time requirement
- ensure concentration is sufficiently high for bacterial killing to be assured

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53
Q

What is the oral absorption % of metronidazole?

A

around 100%

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54
Q

What is the half life of metronidazole?

A

8 hours

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55
Q

What is the peak serum level and peak serum time of metronidazole?

A

4-6.5microg/mL
60-120 minutes

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56
Q

What is the protein binding % of metronidazole?

A

8-11%

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57
Q

Where does metronidazole penetrate?

A

wide volume distribution
penetrates saliva and CNS
foetal circulation (avoid in first trimester)

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58
Q

Where is metronidazole metabolised and eliminated?

A

metabolised liver - mutagenic potential, 5 active metabolites
eliminated kidney - can cause reddish/brown excretion colour

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59
Q

When should you avoid prescribing metronidazole in women?

A

women in first trimester
nursing mothers

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60
Q

What are the indications for use of metronidazole?

A

first choice
- anaerobes suspected
- acute necrotising forms of gingivitis
- pericoronitis (with systemic involvement)
- dental abscess
- beta-lactamase producing anaerobes
- alternative to penicillin (allergy)

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61
Q

What is the first choice of antibiotic?

A

metronidazole

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62
Q

Why is metronidazole considered safe?

A

high safety margin - no lethal dose

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63
Q

What drugs interact with metronidazole and what occurs?

A
  • alcohol = disulfiram-like reaction
  • phenytoin and phenobarbitol = reduce 1/2 life and essentially increase metbolism of metronidazole
  • cimetidine = decreases liver enzyme activity increasing 1/2 life, and decreasing plasma clearance
  • lithium
  • warfarin - potentiates anticoagulant effect
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64
Q

What are the main adverse side effects of metronidazole?

A
  • GI
  • nausea, vomiting, anorexia, diarrhoea, epigastric distress, abdominal cramping
  • constipation?
  • convulsive seizure
  • peripheral neuropathy (paraesthesia extremities)
  • dizziness, vertifo, incoordination, ataxia, irritability, depression, weakness, insomnia
  • prolonged or intensive
  • unpleasant taste, sharp/metallic, furred tongue, glossitis, stomatitis, candida
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65
Q

What are the rare but reversible side effects of metronidazole?

A
  • blood dyscrasia
  • temporary neutropenia
  • thrombocytopenia
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66
Q

What kind of resistance can occur with metronidazole?

A

limited resistance
- chromosomal/plasmid mediated - reducing active metabolites
- parasitic disease - developing countries
- helicobacter pylori

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67
Q

What is helicobacter pylori resistant to?

A

metronidazole

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68
Q

What causes the disulfiram-like reaction with metronidazole?

A

alcohol
- disulfirum blocks aldehyde dehydrogenase enzyme which blocks normal metabolism of alcohol
- acetylaldehyde cannot metabolise to acetate and therefore marked increase in acetaldehyde after alcohol consumption
- increased serum levels of acetaldehyde is what causes hangover
metronidazole and disulfirum similar structures and effect

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69
Q

What are the symptoms of a increased serum level of acetaldehyde?

A

“one massive hangover”
- vasodilation, hotness and flushing, increased HR, increased resp. rate, lowered BP, dry mouth/throat, bronchoconstriction, allergy reactions, nausea, headache

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70
Q

What is a typical dose of metronidazole?

A

200-400mg 8-12hourly for 3-5 days

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71
Q

What is a typical dose of metronidazole?

A

200-400mg 8-12hourly for 3-5 days

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72
Q

Metronidazole is administered via what route?

A

oral

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73
Q

Does metronidazole require a loading dose?

A

no

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74
Q

What are the two main interactions relating to metronidazole?

A

warfarin
alcohol

75
Q

What is the mode of action of metronidazole?

A

DNA inhibition

76
Q

What is the half life of metronidazole?

A

8 hours

77
Q

What drug classification does clindamycin come under?

A

lincomycin antibiotics

78
Q

What is the spectrum of activity of clindamycin?

A
  • G +ve/ G-ve bacteria - anaerobic/facultative/aerobic
  • penicillinase staph
  • bacteroides
  • prevotella
  • porphyromonas, veilonella
  • peptostrep, actinomyces
  • eubacteria and clostridium
79
Q

What is the mechanism of action of clindamycin?

A

inhibits protein synthesis
50S ribosomal subunit
bacteriostatic?
bactericidal at higher concentrations
same site/mechanism as macrolides; clarithromycin, erythromycin

80
Q

What % of clindamycin is absorbed orally?

A

90%

81
Q

What is the half life of clindamycin?

A

3 hours

82
Q

What is the peak serum level and peak serum time of clindamycin?

A

2.5microg/L
45-60mins

83
Q

Where is clindamycin distributed?

A

widely distributed/PMNs

84
Q

Where can clindamycin penetrate?

A

bone (not CSF)

85
Q

Where is clindamycin metabolised and excreted?

A

metabolised 90% in liver / conc. bile
excreted in urine

86
Q

Clindamycin can be potentially fatal in what instances?

A
  • recent ABx
  • middle aged/elderly
  • women
  • following surgery
  • GI disturbance
  • MX - vancomycin or metronidazole
87
Q

What does clindamycin interact with?

A
  • non-depolarisig neuromuscular blocking agents
  • absorption slowed by some anti-diarrhoeal drugs
  • antagonism with erythromycin
88
Q

What are the indications for use of clindamycin?

A
  • as for penicillin with oro-facial infections
  • penicillin allergy
  • refractory to penicillin/metronidazole
  • beta lactam resistance
89
Q

What does the BNF state regarding the use of clindamycin?

A
  • should not be used routinely
  • no more effective than penicillin
  • cross resistance with erythromycin - resistant bacteria
90
Q

What is a normal regimen of clindamycin?

A

150-300mg, 6 hourly for 3-5 days

91
Q

What route of administration is used for clindamycin?

A

oral

92
Q

Does clindamycin require a loading dose?

A

no

93
Q

When should you immediately cease use of clindamycin?

A

with diarrhoea

94
Q

What are the two main interactions of clindamycin?

A
  • neuromuscular blocking agents
  • erythromycin - antagonism
95
Q

What is a main unwanted effect of clindamycin?

A

antibiotic associated colitis

96
Q

What is the half life of clindamycin?

A

3 hours

97
Q

What is the mode of action of clindamycin?

A

protein synthesis inhibitor

98
Q

What drug class is paracetamol in?

A

analgesic and antipyretic drugs

99
Q

What is the proper name for paracetamol?

A

acetaminophen
or tylenol

100
Q

What is the mode of action of paracetamol?

A
  • central analgesic effect that is mediated through activation of descending serotonergic pathways.
  • limited inhibition of COX 1/2 and possibly 3 activity
101
Q

What is acetaminophen used as?

A
  • first line analgesic
  • acute and chronic
  • mild and moderate analgesic
  • antipyretic activity
102
Q

What does antipyretic mean?

A

prevent or reduce fever

103
Q

What are the effects of acetaminophen?

A
  • no effects on platelet aggregation
  • little effect respiratory
  • little effect cardiovascular
  • few ADRs (adverse drug reactions)
  • little to no gastric irritation
  • no relevant impact on uric acid secretion
104
Q

What are the indications for acetaminophen?

A
  • first line dental
  • inflammatory conditions
  • where NSAIDs are contraindicated (GI, asthma, Rey’s syndrome, congenital/acquired coagulopathies)
  • pre-emptive? less useful
105
Q

What are the pharmacokinetics of acetaminophen?

A
  • tablet, capsule, elixir or suppository, IV
106
Q

How is acetaminophen absorbed and where can it be distributed?

A

well absorbed GI
widely distributed (can freely cross placenta)

107
Q

How long is the half life of acetaminophen?

A

2-4 hours

108
Q

How long does it take to reach peak plasma time with acetaminophen?

A

60 mins

109
Q

What does half life mean?

A

the time it takes for the amount of a drug’s active substance in your body to reduce by half

110
Q

What is NAPQI and how is it eliminated?

A

toxic byproduct produced during metabolism of paracetamol (acetaminophen). It is normally produced only in small amounts, and then almost immediately detoxified in the liver.

111
Q

What are the two very rare skin reactions associated with acetaminophen?

A

Steven Johnson Syndrom
Toxic epidermal necrolysis

112
Q

What four factors cause need for careful prescribing of paracetamol?

A
  • liver disease
  • alcohol
  • malnutrition
  • dehydration
113
Q

What is the standard adult dose of paracetamol?

A

10-15mg/kg every 4-6hrs up to daily max of 4g
(8x500mg tablets)

114
Q

Patients taking enzyme (CYP450 2E1/1A2/3A4) inducing drugs are at risk of what?

A
  • may develop liver toxicity at lower plasma concentrations, NAPQI toxic byproduct
115
Q

What are examples of enzyme inducing drugs that can cause liver toxicity at lower acetaminophen plasma concentrations?

A

Scrappp
St John’s wort
Carbamazepine
Rifampicin
Alcohol
Phenobarbitol
Phenytoin
Primidone

116
Q

Acute liver damage can occur with what dose of paracetamol?

A

10-15g
as little as 8g depending on risk factors

117
Q

What dose of paracetamol can be fatal?

A

25g

118
Q

When does the maximal liver damage occur post ingestion of a paracetamol overdose?

A

3-4 days later

119
Q

What is the treatment of a paracetamol overdose?

A

activated charcoal
acetylcystein IV (oral methionine)

120
Q

How much paracetamol is metabolised in the liver and what happens to the rest?

A

95% metabolised in liver
<5% eliminated unchanged in urine

121
Q

Name 7 preparations of acetaminophen

A

1) panadol
2) lemsip
3) Beecham’s cold and flu
4) Calpol
5) Alvedon
6) Solpadol
7) Co-codamol

122
Q

What therapeutic activity does aspirin provide?

A
  • anti-pyrexic
  • anti-platelet/thrombotic
  • anti-inflammatory
  • analgesic - mild/moderate
123
Q

What drug classification does aspirin come under?

A

non-steroidal anti-inflammatory drug (NSAID)

124
Q

What is the proper name for aspirin?

A

acetylsalicylic acid

125
Q

What is the presentation and route of administration for acetylsalicylic acid?

A

aspirin
- white tablet
- dispersible form available too (dissolves to give solution)
- not dissolvable in mouth (can lead to sloughing and ulceration)

126
Q

What is the mode of action of NSAIDs?

A

COX (cyclo-oxygenase) isoenzyme inhibition (COX-1, COX-2, COX-3)
COX inhibition reduces eicosanoid (prostanoid) synthesis (reduced prostaglandin, prostacycline and thromboxane production)

127
Q

How does aspirin work?

A

irreversible inhibition of COX enxymes by acetylation

128
Q

The inhibition of COX enzymes due to NSAIDs reduce production of what three substances?

A

1) Prostaglandin (PGE2)
2) Prostacycline (PG12)
3) Thromboxane (TXA)

129
Q

What impact does the reduction in production of PGE2 and TXA in NSAID use have?

A
  • regulates BP
  • renal effects
  • inflammatory response
  • duration and intensity of pain
  • reduces fever
  • regulates gastric acid secretion
  • inhibits platelet aggregation and thrombosis
130
Q

Aspirin has more effective inhibition of which COX enzyme?

A

selective for COX-1>COX-2 (x100)

131
Q

What are the indications for use of aspirin?

A
  • acute pain
  • dental pain
  • rheumatic fever
  • rheumatoid arthritis
  • other inflammatory disease
  • fever
  • acute coronary syndrome/ischaemic stroke
  • anti-thrombotic
132
Q

What are the pharmacokinetics of aspirin?

A
  • rapidly absorbed GI, stomach, and SI
  • dose related efficacy
  • widely distributed
  • crosses placenta - can cause premature closure of ductus arteriosus, avoid in 3rd trimester
  • evident in breast milk
133
Q

How long is the half life of aspirin?

A

20-30mins

134
Q

What % of plasma binding is seen with aspirin?

A

80-90%

135
Q

What are the contraindications and side effects of aspirin?

A
  • GI - epigastric pain, nausea, dyspepsia, ulceration, bleeding
  • respiratory - AERD, bronchospasm
  • renal - 3x increase renal failure
  • CVS - K+, HBP, oedema
  • haematological - congential/acquired bleeding disease
  • gout (increases uric acid)
  • tinnitus at higher doses
  • skin reactions
  • glycaemic control - can cause hypo at high doses or hyper in massive doses
  • pregnancy
136
Q

How does aspirin cause ulcerogenesis?

A
  • prostaglandin inhibition
    decreases mucous production, increases acid production, mediates bicarbonate, influences cell permeability H+, mucous layer less hydrophobic
137
Q

What is a contraindication for use of aspirin regarding children?

A

Reye’s syndrome - avoid in children under 16, potentially fatal

138
Q

How much aspirin would cause and overdose and what happens?

A

10-30g
complex acid-base disturbance (carbon dioxide in muscle presents as hyperventilation, hyperthermia and dehydration, tinnitus, deafness, vasodilations and sweating)

139
Q

What are the principal interactions of aspirin?

A

4ANTS
Anticoagulants - warfarin
Antihypertensives - beta blockers, ACE inibitors, diuretics
Antidepressants - SSRIs
Anti-epileptics - valproate, phenytoin
NSAIDs
Thrombocytes (drugs that affect) - clopidogrel
Steroids - corticosteroids

140
Q

Name three types of antihypertensives

A

beta blockers
ACE inhibitors
diuretics

141
Q

You should avoid NSAIDs in which population groups?

A
  • pregnant women
  • asthmatics
  • anti-coagulated
  • methotrexate-taking
142
Q

What is the standard adult dose of aspirin?

A

300-900mg, 4-6 hourly, maximum of 4g daily
preferably with food

143
Q

What is the standard adult dose of ibuprofen?

A

400mg TDS (three times daily) max 2.4g per day

144
Q

What is the standard adult dose of diclofenac?

A

50mg TDS max 150mg/day

145
Q

What therapeutic activity does aspirin provide?

A

weak organic acid
anti-inflammatory, analgesic, anti-pyretic, anti-thrombotic

146
Q

What presentation/route of administration exists for aspirin?

A

solid tablet or dissolved solution

147
Q

What is the mode of action of aspirin?

A

acts to inhibit eicosanoids (PGE2, PGI, TXA) via COX pathway
irreversible effects (blunted platelets entire lifespan)

148
Q

What are the pharmacokinetics/dynamics of aspirin?

A
  • rapidly absorbed from stomach/primarily SI
  • 10% excreted unchanged, otherwise conjugated liver
149
Q

What are the side effects of aspirin?

A

unwanted effects relate bleeding tendencies due to irreversible inhibition of platelets
GI ulcerogenic properties

150
Q

What are the main contraindications for aspirin prescribing?

A
  • avoid in children secondary to Reye’s syndrome
  • avoid in pregnancy
151
Q

What is considered the most potent opiate?

A

morphine

152
Q

What drug classification are codeine and morphine?

A

opiates

153
Q

What is morphine?

A

opioid, analgesic

154
Q

What are opioids described as?

A

centrally acting analgesics

155
Q

What is morphine used to treat?

A

acute severe pain - continuous dull (rather than sharp intermittent)

156
Q

What effects can morphine cause?

A

drowsiness, sedation and euphoria
cough suppression (antitussive)
touch, pressure, vision and hearing unaffected

157
Q

What are the unwanted effects of morphine?

A
  • nausea and vomiting (initial)
  • urticaria and pruritus
  • respiratory depression
  • constipation (GI motility) - can delay absorption of other drugs
  • eye signs - pinpoint pupils
  • confusion in elderly
158
Q

What are the normal doses of morphine?

A

4 hourly
oral - 10-30mg
IV 2.5-15mg/70kg
SC 5-20mg/70kg
100mg in 24hours

159
Q

What are the contraindications and special considerations for administering morphine?

A
  • dependence
  • ulcerative colitis and antibiotic assoc colitis (AAC)
  • suspected head injury (vasodilation - can mask signs)
  • acute alcoholism
  • reduced respiratory
  • hepatic and renal insufficiency
  • hypersensitivity
160
Q

Overdose of morphine would cause death via what?

A

respiratory depression

161
Q

What is codeine?

A

opiate
naturally occurring opioid, not a controlled drug

162
Q

What is codeine used for and why is it not often used alone in dentistry?

A

mild to moderate pain
reportedly not useful as codeine alone

163
Q

What is cocodamol?

A

paracetamol and codeine

164
Q

What is codydramol?

A

paracetamol and dihydrocodeine

165
Q

What is stronger, dihydrocodeine or codeine?

A

dihydrocodeine

166
Q

Where is codeine metabolised and what does it produce?

A

liver - 10% morphine which is where the analgesic effect comes from

167
Q

What is the half life of codeine?

A

3 hours

168
Q

What is the potency of codeine compared to morphine?

A

8-10% of potency of morphine

169
Q

How long does codeine provide analgesia for?

A

2-4 hours

170
Q

What does the lack of CYP450 2D6 enzymes in 7% of the population result in?

A

incapable of the biotransformation in the liver of codeine to morphine so little analgesic effect

171
Q

What do ultrametabolizers experience when given codeine?

A

increased efficiency of turning codeine into morphine, nausea and vomiting

172
Q

What is dihydrocodeine metabolised to form and where?

A

dihydromorphine in the liver

173
Q

What analgesic effect is more reliable, dihydrocodeine or codeine?

A

dihydrocodeine

174
Q

What are the contraindications and side effects of codeine/dihydrocodeine?

A
  • nausea
    -hypotension
  • urticaria/pruritus
  • respiratory depression - low risk
  • constipation - with long term use
  • dependence/tolerance - low risk
175
Q

What is the standard dose of codeine/dihydrocodeine?

A

30-60mg, 4-6 hourly
max 240mg in 24hrs

176
Q

What are the indications and uses for codeine and dihydrocodeine?

A
  • mild to moderate pain
  • post operative pain
  • step 2 on WHO ladder
  • opiate adjunct
  • NSAIDs contraindicated
  • antitussive
  • antidiarrhoeal
177
Q

What are the principal interactions of codeine/dihydrocodeine?

A
  • alcohol - enhanced hypotension?
  • antihistamines - sedating
  • anxiolytics and hypnotics
  • antipsychotics - enhanced hypotension?
178
Q

What are the special considerations for prescribing codeine/dihydrocodeine?

A
  • beware in diarrhoea
  • constipation
  • dependency
  • 7% population cannot metabolise for analgesic effect
179
Q

What is co-proxamol?

A

paracetamol and dextropropoxyphene

180
Q

What is cocodaprin?

A

aspirin and codeine

181
Q

What is analgesic efficacy expressed as?

A

NNT (numbers needed to treat)

182
Q

What does NNT mean?

A

numbers needed to treat
number of pts who need to receive active drug for one to achieve at least 50% relief of pain compared with placebo over 4-6hr treatment period

183
Q

More effective drugs have what kind of value of NNT?

A

lower NNT, of just over 2

184
Q

What does an NNT of 2 mean?

A

for every 2 patients who receive the drug, one patient will get at least 50% relief as a result of the treatment