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BDS 2 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What would happen if we didn’t use anaesthetic or analgesics?

A

Patients would gain dental phobia and would avoid the dentist.

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2
Q

What are ‘alternative’ techniques of pain/anxiety control?

A 
Psychotherapy
Accupuncture
Hypnosis
Pet therapy
Systematic desensitization
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3
Q

What is MDAS and why is a score of 19 significant

A

Modified dental anxiety score used to screen for IVS. 19 or above = phobia

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4
Q

If a patient is going to have IVS, what do they need to bring with them? What happens if they don’t?

A

An escort and to not be left with children, drive or operate heavy machinery for 24 hours. They cannot have the surgery if they do no have this.

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5
Q

What is the commonly used anaesthetic and what cartrages do we used?

A

Lidocaine/Lignocaine/Xylocaine 2%

1: 80,000 adrenaline
2. 2ml cartrages

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6
Q

Why should we be careful using LA for hemophiliacs?

A

ID blocks are done in the pterygoid plexus which has lots of blood vessels which can lead to excess bleeding with reduced clotting ability.

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7
Q

What are some contraindications LA

A

-If we are going into acute inflammation e.g. abscess (OK for regional block)
-Hemophiliacs or reduced clotting
-Allergies
-dontnneed it
-pregnant with felypressin
-
-

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8
Q

What can we use to ease the pain of an injection

A

Ethyl Chloride or topical lidocaine 5%

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9
Q

Where can we use infiltration’s for anesthetic?

A

Where there is porous bone and high vascular channels. In the maxillary teeth and possibly the posterior mandibular teeth.

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10
Q

What happens if we can not use infiltration’s?

A

we use a nerve block

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11
Q

What are the syringes we use in the dental hospital

A

Ultra safety plus - Singlue Use, self-aspirating

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12
Q

Why and When do we aspirate?

A

In every injection. to ensure we are not in the blood vessel and if we injected into the blood stream it would have systemic affects and adrenaline would cause heart palpitations

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13
Q

What types of aspiration do we have for LA?

A

Positive aspiration = actively pull back the plunger

Passive aspiration = release of pressure leads to aspiration

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14
Q

Describe the typical needle used for infiltrations and ID blocks

A 
ID block:
27 guage, 0.4mm diameter
34mm
double bevelled 
stainless steel
Infiltration:
30 guage, 0.3mm
19mm
double bevelled
stiainless
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15
Q

When do we use surface anaesthetic and what is it?

A

5% lidocain ointment

Not used routinely but used for childrens hospital

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16
Q

What speed do we use for injecting LA?

A

2ml/20 seconds for ID block in loose tissue

1ml/15 seconds for infiltration in tighter tissue

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17
Q

How do we know if anaesthetic has worked

A

wait a few minutes then question patient and test mucosa/drill dentine

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18
Q

What are the common anaesthetics?

A 
Lidocaine
Articaine 
Mepivocaine
Prilocaine
buvidocaine
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19
Q

When would we use articaine?

A

When we need a more potent anaesethetic (as it is 4%) such as anaesthetising adjacent teeth as the tooth in question is infected or mandibular infiltrations

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20
Q

Why do anaesethics have adrenaline?

A
  • To act as a vasoconstricter to prevent the anaesethic being taken away to increase the time of numbness
  • reduce bleeding
  • act against the vasodilation properties of anaesthetic agents
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21
Q

Why might a patient require lidocaine/articaine plain? What is it?

A

Plain = no adrenaline

This is used when the patient has heart problems like hypertension or arrythmia

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22
Q

What are the half lives of articaine or lidocaine

A 
Lidocaine = 90 minute half life
Articaine = 20 minute half life
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23
Q

What anesthetic should we not use with pregnant patients?

A

Prilocaine as it has felypressin as its vasoconstrictor which is very similar in structure to vasopressin which causes uterine contractions.
Mupivacane causes maternal cardiac problems

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24
Q

Which anaesthetic agent is short lasting? What is its onset, lasting time in pulp and soft tissue?

A

Mepivocaine 3% has an onset of 3-5 minutes with lasting time in the pulp of 20 - 40 mins and soft tissues 2-3 hours.

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25
Q

anaesethic can come with 1:50,000 and 1:100,000 epinephrine. What are the differences in effect?

A

No difference in onset, time or depth. Only difference is the higher concentration (1:50,000) leads to better haeostasis

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26
Q

What are the signs that La is working?

A

Blanching in the area, communication of ‘numb’ teeth and surroundings

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27
Q

What are the signs of toxicity/reactions to anesthetic?

A

confusion, auditory changes, tinnitus, dizziness, metallic taste

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28
Q

if a patient is allergic to anesthetic and we don’t spot the sings, what can happen?

A

-seizures, respiratory arrest, coma

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29
Q

What is the longest lasting LA? When is it used?

A

Bupivocaine for long surgeries

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30
Q

What percentage NaOCl can students and post-grads use? what is its main function

A

1% and 5.25% - antimicrobial agent and dissolve residual pulp tissue and organic matter

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31
Q

What percant EDTA do we use and what is its main function

A

17% for smear layer removal

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32
Q

why do we rarely use iodine for irrigation

A

common allergen

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33
Q

when is anaesthetic useful?

A

reduce pain during surgery
reduce pain after surgery
localise pain
reduction of haemorrhage during surgery

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34
Q

where should we avoid during giving a maxillary infiltration?

A

floor of nose anteriorly - causes pain

malar butress at 6’s

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35
Q

after how long do we assume failure of anaesthetic infiltration?

A

6-8 minutes

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36
Q

How would we anaesthetise the upper 6 with infiltration? why is this different

A

apply LA to the 7 and 6 as the malar buttress is thick with no vascular channels

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37
Q

what anaesthetic blocks can we provide? what teeth do they numb

A

superior posterior regional block - upper 8-6
infra-orbital regional block - upper 1-5 and mesiobuccal cudp of 6
Inferior alveolar nerve block - lower 1-8
Mental nerve block 1-5

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38
Q

when do we use intrapapillary/intrligamentary injections and how are they done

A

paediatrics as palatine injections are too painful
haemophiliacs to avoid superior posterior dental blocks
needle perpendicular to long axis of tooth and occlusal plane in buccal papilla 2mm
after palate blanches, inject palatine nerve

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39
Q

when would we use intraosseous injections?

A

if supplementary anaesthesia is needed, e.g. irreversible pulpitits

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40
Q

what is an intraosseous injection

A

anaesthetic injected directly into the cancellous bone

perpendicular to long axis of tooth

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41
Q

what is an analgesic

A

loss of pain

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42
Q

what is an anaesthetic

A

loss of sensation all together

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43
Q

what is the difference between general and local anaesthetic

A

GA looses consciousness and loss of sensation in whole body

LA is localised sensation relief

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44
Q

what two main chemical classifications of anaesthetics are there? which are used more and why

A

esters and amide intermediate chain

amides used more as esters are highly allergenic

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45
Q

what are the components of LA (5)

A 
anaesthetic agent
vasoconstrictor
vehicle solution to dissolve
reducing agent to keep stable
fungicide
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46
Q

what are the three major parts of the anaesthetic agent?

A

weak base with the structure:

  1. Aromatic (lipophilic dissolves in the lipid around the nerves to access the nerve itself) linked to an
  2. intermediate chain (links terminals - used to be esters but found as allergens so now amides are used.)
  3. with polar amino terminal (soluble in water so it can transfer in the interstitial fluids). Lidocaine has this general formula.
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47
Q

what are anaesthetic agents

A

weak organic bases that act on nerves to depress transmission of action potentials

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48
Q

why do anaesthetic agents have a non-polar organic and amid polar part?

A

Allows them to form an equilibrium of charged and non-charged particles
The LA is non-charged to travel over the epineurium, perineurium and endoneurium and then re-equilibrates its charged and non-charged ions and the charged ions bind the receptors and block Na channels
Lipophilic end alterns the membranes of the ion channels and blocks them.

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49
Q

are LA’s soluble in water? why? what do we do about this?

A

weakly soluble in water
because of non-polar aromatic part
dispensed in salts to make more soluble

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50
Q

name four amide and two ester LAs

A 
amide:
lidocaine
articaine
mupivocaine
prilocaine
bupivocaine

ester:
procaine
benzocaine

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51
Q

why is lidocaine more affective than procaine?

A

lidocaine has 25% non-ionised state so transfers across membrane
procaine has ~5% non-ionised state so less transfers across

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52
Q

why is anaesthetic less affective in infected areas?

A

infected areas are more acidic
acidic environments alter equilibrium of ionised and non-ionised anaesthetic
moves equilibrium to more ionised
less anaesthetic crosses the membrane
Increased vascularity means anaesthetic lasts in the area less time

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53
Q

what components of LA affect vasoconstriction

A

anaesthetic agent blocks sympathetic vasoconstriction causing vasodilation
adrenaline acts as a strong vasoconstrictor

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54
Q

which nerve fibres does anaesthetic act on (first?)

A

small pain nerve fibres first

sensory and motor fibres after time

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55
Q

what is the half life of articaine and lidocaine?

A

articaine 20 mintues

lidocaine 90 minutes

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56
Q

how are esters and amides metabolised? what problems should we be aware of

A

esters metabolised by esterase’s in blood –> urine.
1 in 2800 lack enzymes for this and cannot have esters
amides metabolised in liver –> oxidised –> urine
liver disease patients will have slower metabolism

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57
Q

what are some characteristics of ideal anaesthetic

A 
anaesthetise nerves without damage
non-toxic
easy to administer
short half life
no allergern
non-addictive (cocaine)
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58
Q

what is the long lasting amide anaesthetic

A

bupivocaine

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59
Q

in america noradrenaline is used as a vasoconstrictor, why is this not used in the UK

A

increased BP much more than adrenaline so can cause strokes

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60
Q

what affects does fellypressin have

A

mimics vasopressin and initiates uterine contractions if pregnant sending pregnant women into labour
coronary vasoconstriction so avoid with heart problems

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61
Q

how does adrenaline affect the body

A

acts on beta 1 receptors on the heart (beta 2 is lungs) increasing HR
acts on alpha 1 receptors causing vasoconstriction of blod vessels increasing BP

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62
Q

what is the toxic dose (of lidocaine and lidocaine plain)

A

maximum does safe to give to a patient
lidocaine : 7mg/kg
lidocaine plain: 4.4.mg/kg

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63
Q

what is the maximum does for a 70kg man of lidocaine without adrenaline?

A

lidocaine 2%
cartriage 2.2ml = 2.2g of solution
2.2g = 2200mg solution
2% of 2200 = 44mg lidocaine in 1 cartridge

weight = 70kg
maximum dose = 4.4mg/kg (7mg/kg with adrenaline)
70 x 4.4 = 308mg
308 / 44 = 7 cartridges

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64
Q

when do we use prilocaine over lidocaine and when do we avoid prilocaine

A
  • lidocaine has adrenaline acts on HR bad for patients with heart problems/arrythmia
  • prilocaine has felypressin as vasoconstrictor with less effect on heart
  • avoid felypressin if pregnant as mimics vasopressin causing urterine contractions
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65
Q

if anaesthetic cartriage is brown what has happened

A

solution has oxidised - do not use

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66
Q

what do reducing agents do in anaesthetic

A

prevent oxidation of solution turning it brown

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67
Q

if LA is cloudy what is wrong

A

presence of fungi
loss of fungicide
do not use

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68
Q

what do statins do

A

inhibit HMG-CoA reductase

involved in synthetic conversion of Acetyl-CoA into cholesterol

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69
Q

why are prilocaine 4% and articaine 4% not used as ID blcoks

A

too strong/potent and can have very long lasting effects on nerve action if they hit the nerve

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70
Q

where is a needle most likely to break

A

hub junction

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71
Q

what do we do in case of needle snap

A

try remove immediately with artery forceps
if not, refer to oral surgery immediately under GA
write in notes

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72
Q

where is the most likely place for haematoma to occur after injection and why

A

posterior superior alveolar block due to pterygoid plexus

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73
Q

what can an ID block haematoma lead to

A

trismus if in medial pterygoid- locked jaw
bruising
Swelling near airway
infection leading to severe trismus

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74
Q

what non-immediate problems can occur after anaesthetic and how can we avoid this

A

self trauma e.g. biting soft tissues, burns on mouth

give pt advise not to eat anything hot or cold for 2 hours

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75
Q

what allergens are involved in giving anaesthetic (3)

A

anaesthetic injection (esters are much more allergenic than amides)
preventives but used less now
latex can be found in cartraiges

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76
Q

what should we do if we suspect an allergy to LA

A

send for sensitivity test at the dermatology department
positive allergy = use a different LA
negative = do infiltration with emergency kit by adrenaline and antihistamine

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77
Q

what are the toxic level effects of LA agent

A

low doses excite the CNs - normal dose
high doses depress CNS and heart function
prilocaine reduces RBC oxygen carrying capacity

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78
Q

how do we prevent toxic dose being given (3)

A

calculate maximum dose based on weight
inject slowly and look for reactions
aspirate before injection

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79
Q

what affect do anti-parkinsons drugs have on anaesthetic

A

reduce adrenaline rate of metabolism so reduce maximum dose by 50%

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80
Q

what do we do if we are unsure if a drug interacts with adrenaline and what is generally the case

A

look in the BSP guidelines to see interactions with the drug

most cases, limit to 2 cartridges or use plain anaesthetic

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81
Q

what considerations should be taken with pregnant women and anaesthetic

A

should be avoiding dental procedures
Bupivacaine should be avoided as it causes more maternal cardiac problems and foetal hypoxia in animal models
Felypressin theoretically could lead to uterine contraction and a decrease in placental blood flow
Prilocaine crosses placental barrier more readily than lidocaine
Lidocaine and Adrenaline are the LA of choice

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82
Q

when should we use esters over amide

A

liver disease when taking beta blockers

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83
Q

if the mandible has been irradiated or had reduced vascularity for another reason, how does this affect our choice of anaesthetic

A

we should avoid further vasoconstriction to prevent necrosis so use plain lidocaine or plain anaesthetic
Maybe use stronger more potent articaine

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84
Q

if patient is at risk of endocarditis how does this effect anaesthetic

A

avoid intraligamentary injections to avoid bacteraemia

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85
Q

what are some circumstances where we throw away a cartraige

A

large head bubble - contaminated
out of date
cloudy - fungicide
brown -

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86
Q

how should we store LA

A

at room temperature 0-25 dgerees
do not freeze
bring to room temp before applying

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87
Q

if storing adrenaline LA how does this affect our storage of LA

A

do not store in day light

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88
Q

what is Amlodipine, what problem does it cause and how can we fix it

A

calcium ion channel blocker for high blood pressure
causes gingival enlargement NOT gingival hyperplasia
only resolution is to change medication, surgery only leads to recurrence

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89
Q

someone has a paracetamol overdose. What will happen to their PT or APTT

A

paracetamol overdose leads to liver failure
liver produces factors in intrinsic and extrinsic pathways
increases PT and APTT

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90
Q

what coagulation factors does warfarin act on and why

A

factors II, VII, IX and X (common and extrinsic)
all of the vitamin K dependant factors
warfarin inhibits Vitamin K Epoxide reductase which reduces vitamin K epoxide back to vitamin K

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91
Q

what does warfarin do

A

inhibits vitamin K epoxide reductase which stops replenishment of vitamin K
vitamin K needed for activation of clotting factors II, VII, IX and X of intrinsic and common coagulation pathways
prevents this, thins blood

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92
Q

if someone is on warfarin and we need to thicken their blood in an emergency, what do we do and why

A

give them vitamin 2-10mg
reduces the need for vitamin K epoxide reductase
replenishes vitamin K to activate factors II, VII, IX and X of extrinsic and common pathways

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93
Q

what does aspirin do

A

completely inactivates COX 1 2 3
COX 1 2 3 are responsible for causing the release of thromboxane and prostaglandins
thromboxane causes platelet aggregation
prostaglandins act on pain receptors
aspirin therefor reduces pain and blood clotting

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94
Q

how long are the lasts of aspirin and why

A

7 days

lifespan of platelets as this is irreversible action on their COX complex

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95
Q

what are NOACs

A

oral anti-coagulants
act on final common coagulation pathway
thin blood

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96
Q

what is DDAVP, when is it given and what is its function

A

desmopressin, synthetic vasopressin, synthetic ADH
released endothelial stores of factor VIII
increases blood clotting via intrinsic pathway

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97
Q

if a patient is on NOACs (edoxoban) how does this affect how we do extractions

A

if more than three to be taken out, remove from medication

avoid morning dose then take dose 4h after extraction

98
Q

what can painkillers act as

A

anti-inflammatory
analgesic
anaesthetic
CNS depressers

99
Q

why could we use anaesthetic at bleeding extraction sites

A

to stop bleeding

adrenaline is a vasoconstrictor

100
Q

what is the arachnoid pathway

A

Phospohlipid–>arachidonic acid –> prostaglandins + thromboxane + leukotrienes
pathway to produce inflammatory mediators such as leukotrienes (release of cytokines) , thromboxane (platlete function) and prostoglandins (pain)

101
Q

how do analgesics like ibuprofen and aspirin act against pain and what are the side effects

A

inhibit COX-1 and COX-2 which catalyse the conversion of arachidic acid to prostaglandins which act on pain receptors to cause pain
also anti-inflammatory
gastric ulcers main side effect

102
Q

what are 5 effects of COX inhibitors

A 
reduced inflammation
reduced pain
decreased temperature
thinner blood
increased stomach acidity
103
Q

what medication must we take with most NSAIDs and why

A

secondary drug to protect the GI tract from acid as NSAIDs act on COX complex which catalyses conversion of arachidic acid to prostaglandins. Prostaglandins reduce gastric acidity.

104
Q

what are arthritis patients likely to be on and why

A

NSAIDs for joint pain releif

105
Q

what are 3 common NSAIDs

A

ibuprofen
aspirin
diclofenac

106
Q

what is diclofenac

A

NSAID

107
Q

what is NNT and what is a NNT = 1 and NNT =2

A

number needed to treat (for medications)
NNT 1 = everyone gets pain reduction by 50%
NNT = half of population get pain reduction by 50%

108
Q

what is BNF and how does it help

A

British national formulae
we can use it to look at interactions between drugs
dosage, how often and age restrictions of drugs

109
Q

why can pregnant women not have most drugs, especially codeine. what pain killer can they have

A

most drugs especially codeine cross placental barrier into babies blood, paracetamol doesn’t so is deemed safe.
if we dont follow this it can lead to congenital deformations (1st trimester) or growth problems (2n trimester)

110
Q

if a patient has liver/kidney disease what should we do if prescribing

A

avoid prescribing any drugs due to poor metabolism of drugs

consult GMP and pharmacist

111
Q

what affects do NSAIDs have in pregnancy

A

haemorrage, closure of ductus arteriosus, pulmonary hypertension of newborn, delayed labour, increased duration of labour and increased blood loss in labour.

112
Q

can NSAIDs be taken whilst breast feeding

A

deemed safe as amounts in breast milk are very minimal

aspirin can cause blood clotting problems if with low vitamin K so avoid this

113
Q

what doses do we give children - general conversion of adult dose

A

1st month up to a year = ⅛ adult dose
1-5 years = ¼ adult dose
6-12 years = ½ adult dose

114
Q

what dosages go with paracetamol

A

500mg-1g 4 x 6hours max 4g in 24 hours

115
Q

what does paracetamol act as

A

analgesic
antipyretic
not anti-inflammatory

116
Q

what dosages for ibuprofen and how does it act and what is its maximum daily amount

A

NSAID - analgesic and antipyertic

200mg-400mg TDS. No more than 2.4g in any 24 hours

117
Q

who shouldn’t take ibuprofen

A

asthmatics, kidenys and pregnancy

118
Q

what is diclofenac, where do we get it, what dosage do we give and who cannot have it

A

analgesic/anti-infammatory/NSAID/antipyretic
not OTC must get prescription
bad interactions with asthmatics and high allergern
75-150mg TDS

119
Q

why do NSAIDs cause problems with asthmatics

A

NSAIDs reduce prostaglandin production
prostaglandins control smooth muscle action
asthma is swollen bronchiole tubes and changing prostaglandin levels can alter bronchioles
Ibuprofen, aspirin and diclofenac

120
Q

what age is aspirin allowed for use and why

A

above the age of 16

below this age- risk of reyes syndrome

121
Q

what drug can cause Reyes syndrome

A

aspirin under age of 16

122
Q

when should we not recommend NSAIDs (6)

A 
history of stomach ulcers/bleeds
pregnancy
allergy to NSAIDs
asthma
on warfarin
if already on an NSAID
123
Q

when are opioids used for pain relief and are they used in dentistry

A

severe moderate pain - act on CNS
if NSAIDs are contra-indicated/on NSAIDs already
not used in dentistry

124
Q

how much is the NHS prescription fee and if a drug we are recommending is available OTC what should we do

A

£8.20

tell them to buy it OTC

125
Q

what painkillers should we (not) recommend

A

not aspirin if bleeding as this thins blood (extraction)

ibuprofen good but not asthmatics

126
Q

what is paracetamol and how does it work and compare to NSAIDS

A 
not an NSAID
antipyretic
analgesic 
not anti-inflammatory
blocks prostaglandin production
-doesnt antiinflammatory, very weakly blocks COX enzymes, doesn't cross placental border
127
Q

when is paracetamol recommended

A

if allergic or contra-indicated NSAIDS
not if liver failure/alcoholic
Pregnancy- doesn’t affect baby
tootheache or headache or fever

128
Q

table of analgesics

A

x NSAID analgesic anti-inflammatory anti-pyretic
paracetamol tick tick
aspirin tick tick tick tick
ibuprofen tick tick tick tick
diclofenac tick tick tick tick
codeine tick tick

129
Q

how is the BNF laid out

A 
by medication class e.g. epilepsy, heart failure etc.
in back we find index 
further back interactions of different drugs
130
Q

what can we prescribe in private, NHS and hospital dentistry

A

private - anything
NHS - anything in the DPF dental practitioner formulae (dental preperations)
hostpital - anything

131
Q

when would a dentistry prescribe codeine

A

after trying ibuprofen and paracetamol

132
Q

how are medicines classified

A

OTC over the counter or GSL general sales list
pharmacy only e.g. cocodamol 8/500
prescription only e.g. cocodamol 30/500 or amoxicillin
by their schedule

133
Q

what are the drug schedules

A

Schedule 1 – No medicinal use e.g. ecstasy, LSD
Schedule 2 – Subject to full controlled requirements, but have medicinal use e.g. cocaine (vasoconstrictor) e.g. heroin (diamorphine – given for MI)
Schedule 3 – subject to written requirements, but not safe, custody requirements or keep registers – just invoices for 2 yrs e.g. midazolam, temazepam
Schedule 4 – Benzodiazepines other than midaz/temaz and also Z-drugs - no CD requirements
Schedule 5 – Due to strength, are exempt from CD requirements – e.g. Oramorph

134
Q

what is midazolam and what schedule drug is it

A

schedule 3 due to strength

used for sedation purposes

135
Q

what is cocodamol, when is it used and what are the side effects. dosage

A

mixture of paracetamol and codeine opioid
constipation
500mg/8mg short course

136
Q

what dose of cocodamol can we use

A

1-2 tablets TDS (max 8/day) either
Co Codamol 8//500 - only OTC preparation
Co Codamol 15/500
Co Codamol 30/500

137
Q

what three strengths of co-codamol do we have and which are available OTC

A

Co Codamol 8//500 - only OTC preparation
Co Codamol 15/500
Co Codamol 30/500

138
Q

compare aspirin to paracetamol

A

aspirin irreversible inhibits COX1 and COX2 whereas paracetamol weakly inhibits COX2
aspirin causes gastric ulcers over time whereas paracetamol doesnt
aspirin is an NSAID but paracetamol is not
Both antiinflammatories and antipyretic

139
Q

what are the benefits of paracetamol over NSAIDs

A

can be used if NSAID contraindicated

do not affect GI tract so does not cause gastric ulcers

140
Q

what must be on an NHS prescription

A

pt details : name, DOB, adress
drug details : type, route e.g. oral, dose, how many times a day, how long
sign and print name of consultant with date
stamp with printed name of practice

141
Q

what does this mean on a prescription: PO

A

per orum - oral

142
Q

what is the difference between an NHS or private prescription

A

private must include GDC code so pharmacy can track and confirm registration, NHS must have a stamp of the hospital

143
Q

what does this mean on a prescription: PV

A

vaginally

144
Q

what does this mean on a prescription: PR

A

rectum

145
Q

what does this mean on a prescription: IV

A

intravenous

146
Q

what does this mean on a prescription: IM

A

intramuscular

147
Q

what does this mean on a prescription: SC

A

sub cutaneous

148
Q

what does this mean on a prescription: top

A

topical

149
Q

what does this mean on a prescription: M/W

A

mouthwash

150
Q

what does this mean on a prescription: PRN

A

take when required, no pain = no take

151
Q

what does this mean on a prescription: stat

A

immediately

152
Q

what does this mean on a prescription: QDS

A

4 times daily

153
Q

what does this mean on a prescription: TDS

A

3 times daily

154
Q

what does this mean on a prescription: BD

A

twice a day

155
Q

what does this mean on a prescription: nocte

A

night

156
Q

what does this mean on a prescription: QHS

A

every night before bed

157
Q

if there are severe adverse reactions to a drug marked with a black traingle in the BNF, what do we do

A

immediately notify the MHRA - medical and healthcare products regulatory advisory
Report all serious patient incidents to the National Reporting and Learning System if such incidents are not automatically reported where you work
Inform the patient’s general practitioner, the pharmacy that supplied the medicine, the local controlled drugs accountable officer and the medicines manufacturer

158
Q

what is MHRA

A

medical and healthcare products regulatory advisory

advise if adverse reaction to a medicine

159
Q

what are some ester anaesthetics

A

procaine and mupivacaine

160
Q

what is the implication of giving a haemophiliac a ID block

A

haemorrhage and bleeding

swelling that can possibly block airway

161
Q

how long is the half life, pulpal anaesthesia and soft tissue anaesthesia of lidocaine

A

Half life 90 minutes
pulpal anaesthesia 45mins
soft tissue anaesthesia 2-3hours

162
Q

how long is the half life, pulpal anaesthesia and soft tissue anaesthesia of articaine

A

20 minute half life
pulpal anaesthesia 45mins
soft tissue anaesthesia 2-3hours

163
Q

why is aspiration especially important for articaine

A

intravenous injections of articaine can lead to convulsions (epileptic fits)

164
Q

what percentages do we use of lidocaine, lidocaine plain, procaine, procaine plain, articaine

A 
lidocaine 2%
lidocaine plain 4%
procaine 3%
procaine plain 4%
articaine 4%
165
Q

what are the maximum doses for articaine (and for articaine for children), lidocaine and lidocaine plain

A

articaine = 7mg/kg (for children 5mg/kg)
lidocaine plain = 4.4mg/kg
lidocaine = 7mg/kg

166
Q

how do we estimate a child’s weight

A

(age + 4) x 2

167
Q

what is the average weight of an adult

A

70kg

168
Q

what are some advantages and disadvantages of ultra-safety plus

A

single use - sterile (more waste, less sterilization)
needle sheath
auto-aspirator
no recapping neccessary

169
Q

how can we reduce anxiety for a child having a needle

A

show them the needle, explain that it is sleepy juice for the tooth
don’t let them see it going in
explain every step
distract them

170
Q

if a child is extremely anxious, what options do we have for operative procedures

A

systematic desensitisation

sedation

171
Q

what alterations to oral anaesthetic occur in children

A

always use topical anaesthetic 5% lidocaine ointment 2-5 minute onset
weaker, thinner more porous bone so infiltrations can be used for all teeth in young
mandibular foramen is lower and more distal so aim lower down for ID block

172
Q

when do we provide intrapapillary injections

A

in children for palatal anaesthetic as palatal injections are too painful

173
Q

explain how to numb the palatal aspect of a child’s upper teeth

A

topical anaesthetic 5% lidocaine ointment on buccal side and palatal side
intrapapillary injection:
- inject at into the papilla parallel to occlusal plane and perpendicular to long axis of tooth 1-2 mm and inject slowly
- repeat at adjacent papilla until palatal blanching meets
- papillary injection

174
Q

how do we change ID blocks for children

A

instead of coming from premolar region, come from first molar region as more distal
aim more down as mandibular foramen is lower

175
Q

when do we provide no ID block, altered child ID block and adult ID block

A

no ID block before age of 6
6-9 altered ID block
9+ use adult

176
Q

what is the rule of 10 for children’s pulpal anaesthesia and when do we change the number and why

A

Age + How many teeth away from the midline < 10 = just infiltration
Age + How many teeth away from midline >10 = ID block
rule of 12 for articaine as it is more potent and soluble

177
Q

if a seven year old needed pulpal anaesthesia with lidocaine on their lower right 4, what injection would we do and why? would it change if it was with articaine?

A 
4 + 7 = 11 
rule of 10 for lidociane
11 > 10 therefore provide ID block
with articaine we use rule of 12
11<12 therefore infiltration
178
Q

what do we do if an ID block fails and why is this a last port of call

A

intraligamentary injection into the periodontium

higher risk of bacteraemia and can affect developing teeth

179
Q

what is anaesthetised during intraligamentary injection

A

immediate pulpal anaesthesia

not tongue, lip or gingiva

180
Q

how do we do an intraligamentary injection

A 
using peripress (stronger system)
50-60 degrees to occlusal plane
interproximal space
advance needle until bony resistance
0.4-0.6ml mesial and repeat distally
181
Q

what angle of injection do we use for intraligamentary injections

A

50-60 degrees to occlusal plane

182
Q

what is the ‘wand’ and when do we use it

A 
computer controlled anaesthetic delivery
for anxious children
less intimidating
slow delivery
good for palatal
183
Q

what drugs cause MRONJ

A

bisphosphonates
Monoclonal antibodies - e.g. Denosumab
Tyrosine Kinase inhibitors - e.g. Sunitinib are all small cell receptor antagonists

184
Q

what increases risk of MRONJ with bisphosphonates

A

steroids or IV

185
Q

what are bisphosphonates

A

drugs reduce bone turnover by altering osteoclasts to treat some cancers, osteoporosis and pagets disease

186
Q

what is the structure of bisphosphonates

A

a central carbon
2 phosphonate groups PO3
2 variable R groups

R groups can be N (nitrogen) containing or non-N containing

187
Q

what are the implications of the different R groups on bisphosphonates and how do they work

A

can be N or non-N containing R groups
N = Prevents formation of proteins needed to maintain osteoclast cytoskeleton (loss of ruffle border which is the surface used for breaking down bone) Most clinically important ones: alendronate, risedronate, pamidronate, etc.

non-N = Compete with ATP leading to osteoclast apoptosis - Too toxic to be used clinically usually as they kill off osteoclasts

188
Q

what are the 2 main circumstances we use bisphosphonates and what is there risk of developing MRONJ

A

metastatic breast cancer - IV medication high dose 10% risk of MRONJ
osteoporosis - low dose 1/100,000 , 1/1000 after extraction
risk increased with steroids

189
Q

how does MRONJ occur because of bisphosphonates (3)

A

bisphosphonates:

  • act as anti-angiogenesis so reduce blod flow to bone
  • can kill/reduce action of bone cells
  • toxic to overlying soft tissues so prevent healing over
190
Q

what is a drug holiday

A

how long a drug is stopped useage

191
Q

what drug holidays benefit MRONJ reduced risk

A

bisphosphonate 12m reduces risk

3m has some merit

192
Q

what must we consider when considering a drug holiday

A

do the pros of stopping the medication outweigh the risks involved with keeping the drug on

193
Q

for MRONJ high risk patients, what will antibiotics do?

A

not reduce incidence but reduce severity

194
Q

what dosage of ibuprofen can we advise

A

200-400mg TDS

195
Q

what dosage diclofenac can we advise

A

25-50mg TDS

196
Q

what dose aspirin can we advise

A

300-900mg 4DS - not for asthmatics, bloodthinner

197
Q

what must IRN be for single and multiple extractions

A

single: <4 in last 72 hours
multiple: <3.5 in last 72 hours

198
Q

what allergern is found in fluoride varnish that cannot be given to asthmatics and what is an alternative

A

colophony in duraphat - use flourimax

199
Q

what ppm of flouride is in flouride varnish

A

22,600 ppm F-

200
Q

what is xylitol

A

stops metabolism of strep. Mutans - major carious bacteria
found in sugar free chewing gum
natural sweetner

201
Q

what is Riva Star

A

Silver Diamine flouride rubbed on carious lesions to arrest and turn black

202
Q

what separates aspirin from other NSAIDs

A

it irreversibly blocks COX I and COX II
others only reversibly block
more potent and last longer

203
Q

what organ (system) are aspirin and ibuprofen likely to act on

A 
aspirin = GI tract stomach ulcers
ibuprofen = kidneys
204
Q

if a drug is anti-pyretic, where does it act

A

hypothalamus

temperature control

205
Q

what are corticosteroids

A

produced in the cortex of adrenal gland
steroids - 4 ring steroid skeleton
all end in ‘one’ and are analgesics and anti-inflammatory

206
Q

how do steroids work compared to NSAIDs

A

steroids inhibit phospholipase A2 which catalyses conversion of phospholipids to arachidonic acid (therefore preventing production of prostaglandins)
NSAIDs inhibit COX1/2 preventing catalysation of arachidonic acid to prostoglandins

207
Q

what are some side effects of corticosteroids

A 
immunosupressant
redistribution of body fat
acute adrenal insufficency
osteoperosis
gastric ulcers
hyperglaecaemia
208
Q

where are etser LAs and amide LAs metabolised

A

esters in blood plasma

amides in liver

209
Q

which LA is safest and least safe for children

A

lidocaine most safe

mupivocaine least safe

210
Q

why is articaine metabolised faster than other anaesthetics

A

articaine is mainly amide but has 1 ester chain

metabolised in the liver AND blood plasma

211
Q

why can mepivacaine be used without adrenaline successfully

A

mepivacaine causes least amount of vasodilation

212
Q

what are the functions of a vasoconstrictor inLA (4)

A

promote haemostasis
reduce toxicity
prolong numbness
counteract vasodilation

all because they slow blood flow

213
Q

What drugs are commonly causing gingival hyperplasia

A

Cyclosporine- immunosupressant, crohns
Phenytoin - anti-convulsant, epilepsy
Amlodipine - beta channel blocker, high BP

214
Q

give three things we avoid giving to patients with an aspirin allergy

A

aspirin analgesic
bongela = derivatives of salicylic acid
CaOH base = salicylate ester component

215
Q

give 2 reason polypharmacy might cause dental problems

A

sugar containing medications increase caries risk

xerostomia

216
Q

what is herparin

A

anticoagulant

217
Q

what affects do steroids have on haemostasis

A

make skin thinner causing bruising and bleeding

218
Q

how do we treat venous and arteriole thrombosis

A 
arterial = antiplatelet = aspirin, clopidogrel
venous = anticoagulant = herparin, LMWH, warfarin, edoxaban
219
Q

what are 2 antiplatelet drug

A

aspirin

clopidogrel

220
Q

what are some anticoagulants and how are they applied (3)

A

warfarin- PO
herparin - IV
low molecular weight heparin LMWH - SC

221
Q

what are DOACs

A

direct oral anti-coagulants e.g. edoxaban, rivaroxaban

222
Q

how does heparin work and how do we apply it and why

A

acts on anti-thrombin increasing activity
decreases fibrin so decreases platelet plug strength
give SC or IV as not absorbed in gut

223
Q

compare herparin and warfarin

A

heparin =

  • given IC or IV as not absorbed by gut
  • acts on anti-thrombin reducing coagulation cascade
  • acts on common pathway

warfarin =

  • vitamin K antagonist
  • prevents production of factors II, VII, IX and X
  • acts on coagulation cascade
  • given orally
  • acts on intrinsic, common and extrinsic pathwyas
224
Q

how long does it take warfarin to start and stop

A

3-4 days to start

4-5 days to stop

225
Q

what determines the patients warfarin dose

A

stability of patients INR

226
Q

what is the target INR for a pt with recent DVT or PE

A

2/3

227
Q

why are DOACs better than warfarin

A 
less affect
quicker time on and time off
predictable affect on coagulation
no regular blood monitoring 
no effects with food or alcohol
very few interactions with drugs
short half life 10-15 hours
228
Q

what is the half life of a DOAC

A

~10-15 hours

229
Q

what are the dis-advtanges of warfarin

A

slow time on and time off
heavy bleeding e.g. nose bleeds, worse menstrual bleeding, bruising
interactions with other drugs and alcohol
avoid vitamin K e.g. leafy greens
not predicatable how it will affect warfarin
regular blood monitoring needed

230
Q

how do most DOACs work

A

act on common coagulation pathway (most on factor X)

231
Q

disadvantages of DOACs (2)

A 
renally exerted (not with kidney disease)
no direct antidote for reversal
232
Q

when can we not use DOACs over warfarin

A

triple positive APLs - antiplatelet syndrome
heart valve replacement
increased incidence of stroke/MI with DOACs

233
Q

how do we treat iron deficiency

A

TREAT UNDERLYING CAUSE
200mg ferrous sulphate daily (not TDS like BSP says)
until Hb count back to normal and further 3 months o build up stores

234
Q

how much vitamin B12 do we give if they cannot absorb (malabsorption, loss of part of GI tract)

A

1mg IM every 2 days until Hb back to normal

1mg IM every 3 months lifelong

235
Q

do we provide folate or b12 first if deficient in both

A

b12

236
Q

how do we treat folate deficency

A

oral folate 5mg a day

for all causes

237
Q

which 3 anaesthetics do we avoid during pregnancy

A

prilocaine crosses placental blood barrier
procaine involves felypression –> uterine contractions
mepivacaine causes material cardiac problems

238
Q

What 3 senarios do we never interuppt anticoagulant/antiplatelet action

A

Patients with stents or metal heart valves
Patients who have had a Pulmanory embolism or DVT in past 3 months
Patients on therapy for cardioversion

239
Q

What is a rare side effect of prilocaine? What effects does it have

A

Methaemaglobinaemia

Causing shortness of breath, cyanosis (going blue) and headaches

240
Q

What is the best analgesic for neuralgic pain

A

Carbamazepine

BDS 2 (13 decks)

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