Oral surgery Flashcards

1
Q

What does the hypoglossus do?

A

Retract the tongue

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2
Q

What does the genioglossus do?

A

Protrude the gongue

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3
Q

What does the mylohyoid do?

A

Raises floor of the mouth

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4
Q

Where does the geniohyoid connect?

A

Genial tubercles to hyoid

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5
Q

What does the digastric do? connect to? innervated by?

A

Opens jaw
Digastric fossa to hyoid bone
Innervated by:
V - anterior belly
VII - posterior belly

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6
Q

Name the 4 extrinsic muscles of the tongue?

A
  • Styloglossus (XII) - styloid to tongue. Retracts + elevates the tongue.
  • Genioglossus (XII) - genial tubercles to tongue. Protrudes + depresses the tongue
  • Hypoglossus (XII) - Hyoid to tongue. Retracts + depresses the tongue.
  • Palatoglossus (X) - palate to tongue. Elevation of posterior tongue.
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7
Q

What are the intrinsic muscles of the tongue?
Names (4)
Function?
Innervation?

A

The intrinsic muscles originate and attach to other structures within the tongue.

There are four paired intrinsic muscles of the tongue and they are named by the direction in which they travel –
> superior longitudinal,
> inferior longitudinal,
> transverse
> vertical muscles of the tongue.

These muscles affect the shape and size of the tongue – for example, in tongue rolling – and have a role in facilitating speech, eating and swallowing.

The motor innervation to the intrinsic muscles of the tongue is via the hypoglossal nerve (CN XII).

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8
Q

What are the extrinsic muscles of the tongue and what are they innervated by?

A

The extrinsic muscles of the tongue originate from structures outside the tongue and insert onto it.

Genioglossus, Hyoglossus and Styloglossus are innervated by the hypoglossal nerve – with the exception of the Palatoglossus, which is innervated by the vagus nerve.

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9
Q

Genioglossus: attachments? function? innervation?

A

The genioglossus muscle is a large, thick muscle, which contributes significantly to the shape of the tongue.

Attachments: Arises from the mandibular symphysis. It inserts onto the body of the hyoid bone and the entire length of the tongue.

Function: Protrusion (‘sticking the tongue out’) and depression of the tongue.

Innervation: Hypoglossal nerve.

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10
Q

Hyoglossus: attachments? function? innervation?

A

The hyoglossus muscle is located in the floor of the oral cavity, immediately lateral to the geniohyoid.

Attachments: Arises from the hyoid bone and inserts onto the lateral aspect of the tongue.

Function: Depression and retraction of the tongue.

Innervation: Hypoglossal nerve.

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11
Q

Styloglossus: Attachments? Function? Innervation?

A

The styloglossus is a thin, paired muscle, located on either side of the oropharynx.

Attachments: Originates from the styloid process of the temporal bone and inserts onto the lateral aspect of the tongue.

Function: Retraction and elevation of the tongue.

Innervation: Hypoglossal nerve.

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12
Q

Palatoglossus: attachments? Function? Innervation?

A

The palatoglossus muscle is also associated with the soft palate – and is therefore innervated by the vagus nerve.

Attachments: Arises from the palatine aponeurosis and inserts broadly along the tongue.

Function: Elevation of the posterior tongue

Innervation: Vagus nerve.

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13
Q

Which nerves supply the 1) sensation and 2) taste the the anterior 2/3rd of the tongue?

A

1) In the anterior 2/3, general sensation is supplied by the trigeminal nerve (CNV). Specifically the lingual nerve, a branch of the mandibular nerve (CN V3).
* Lingual nerve (V3)

2) Taste in the anterior 2/3 is supplied from the facial nerve (CNVII). In the petrous part of the temporal bone, the facial nerve gives off three branches, one of which is chorda tympani. This travels through the middle ear, and continues on to the tongue.
* Chorda tympani (VII)

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14
Q

What nerve supplies sensation and taste the the posterior 1/3 or the tongue?

A

Both touch and taste are supplied by the glossopharyngeal nerve (CNIX).
* Glossopharyngeal nerve (IX)

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15
Q

Name the 4 intrinsic muscles of the tongue? What are they all innervated by?

A
  1. Superior longitudinal
  2. Inferior longitudinal
  3. Transverse
  4. Vertical

–> Hypoglossal nerve (XII)

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16
Q

What is the arterial and venous supply to the tongue?

A

The arterial supply to the tongue is mainly from the lingual artery (a branch of the external carotid artery). There are also contributions from the tonsillar branch of the facial artery.

Venous drainage is by the lingual vein – which empties into the internal jugular vein.

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17
Q

What is the lymphatic draining of the 1) anterior and 2) posterior part of the tongue?

A

The lymphatic drainage of the tongue is as follows:

Anterior two thirds – initially into the submental and submandibular nodes, which empty into the deep cervical lymph nodes

Posterior third – directly into the deep cervical lymph nodes

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18
Q

What is the foramen cecum?

A

The foramen cecum is a blind-ended pit located in the midline of the tongue at the junction of the anterior 2/3 and posterior 1/3.

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19
Q

What innervates the maxillary teeth?

A

Branches of the maxillary division of trigeminal.
- Anterior superior alveolar nerve (ASAN) supplies incisors to canines.
- Middle superior alveolar nerve (MSAN) supplies premolars and MB root of 1st molar
- Posterior superior alveolar nerve (PSAN) supplies molars.

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20
Q

What is the blood supply to the maxillary teeth?

A

Branches of maxillary artery:
- Anterior superior alveolar artery
- Middle superior alveolar artery
- Posterior superior alveolar artery.

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21
Q

What innervates the mandibular teeth?

A

Inferior alveolar nerve which is a branch of the mandibular division of trigeminal nerve. (V3)

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22
Q

What is the blood supply of the mandibular teeth?

A

Inferior alveolar artery (branch of the maxillary artery)

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23
Q

What bones make up the hard palate?

A

The hard palate forms the anterior aspect of the palate.

The underlying bony structure is composed of (i) palatine processes of the maxilla; and (ii) horizontal plates of the palatine bones.

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24
Q

What are the 3 foramina in the hard palate?

A
  1. Incisive canal – located in the anterior midline, transmits the nasopalatine nerve and descending palatine artery.
  2. Greater palatine foramen – located medial to the third molar tooth, transmits the greater palatine nerve and vessels
  3. Lesser palatine foramina – located in the pyramidal process of the palatine bone, transmits the lesser palatine nerve and lesser palatine artery.
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25
Q

What is the anatomy of the soft palate?

A
  • The soft palate is located posteriorly. It is mobile, and comprised of muscle fibres covered by a mucous membrane.
  • Anteriorly, it is continuous with the hard palate and with the palatine aponeurosis. The posterior border of the soft palate is free (i.e. not connected to any structure), and has a central process that hangs from the midline – the uvula.
  • The soft palate also forms the roof of the fauces; an area connecting the oral cavity and the pharynx. Two arches bind the palate to the tongue and pharynx; the palatoglossal arches anteriorly and the palatopharyngeal arches posteriorly. Between these two arches lie the palatine tonsils, which reside in the tonsillar fossae of the oropharynx.
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26
Q

What are the 5 muscles of the soft palate, their attachment, function and innervation?

A

There are five muscles which give the actions of the soft palate.

They are all innervated by the pharyngeal branch of the vagus nerve (CN X) – apart from Tensor veli palatini – which is innervated by the medial pterygoid nerve (a branch of CN V3).

  1. Tensor Veli Palatini
    > Attachments: Originates from the medial pterygoid plate of the sphenoid and inserts into the palatine aponeurosis.
    Function: Tenses the soft palate.
  2. Levator Veli Palatini
    > Attachments: Arises from the petrous temporal bone and the eustachian tube, before inserting into the palatine aponeurosis.
    > Function: Elevation of the soft palate.
  3. Palatoglossus
    > Attachments: Originates from the palatine aponeurosis, and travels anteriorly, laterally and inferiorly to insert into the side of the tongue.
    > Function: Pulls the soft palate towards the tongue.
  4. Palatopharyngeus
    Attachments: Arises from the palatine aponeurosis and the hard palate, and inserts into the upper border of the thyroid cartilage.
    > Function: Tenses soft palate and draws the pharynx anteriorly on swallowing.
  5. Musculus Uvulae
    > Attachments: Arises from the posterior nasal spine and the palatine aponeurosis, and inserts into the mucous membrane of the uvula.
    > Function: Shortens the uvula.
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27
Q

What is the arterial and venous supply of the palate?

A

The palate receives arterial supply primarily from the greater palatine arteries, which run anteriorly from the greater palatine foramen.

In addition, the anastomosis between the lesser palatine artery and ascending palatine artery provide collateral supply to the palate.

Venous drainage is into the pterygoid venous plexus.

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28
Q

How the the palate innervated?

A

Sensory innervation of the palate is derived from the maxillary branch of the trigeminal nerve (CN V). The greater palatine nerve innervates most of the glandular structures of the hard palate.

The nasopalatine nerve innervates the mucous membrane of the anterior hard palate and the lesser palatine nerves innervate the soft palate.

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29
Q

How does cleft lip occur?

A

Cleft lip – occurs when the medial nasal prominence and maxillary prominence fail to fuse.

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30
Q

How does cleft palate occur?

A

Cleft palate – can occur in isolation when the palatal shelves fail to fuse in the midline, or in combination with cleft lip.

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31
Q

What epithelium is attached to the superior and inferior aspect of the hard palate?

A

The hard palate is covered superiorly by respiratory mucosa (ciliated pseudostratified columnar epithelium) and inferiorly by oral mucosa (stratified squamous epithelium).

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32
Q

What is hyperalgesia and allodynia?

A

Hyperalgesia – increased sensitivity to pain

Allodynia – pain from a usually non-painful stimulus

These could both be symptoms of trigeminal neuralgia.

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33
Q

What is the journey of the maxillary division of trigeminal?

A

After arising from the trigeminal ganglion, the maxillary nerve passes through the lateral wall of the cavernous sinus, before leaving the skull through the foramen rotundum. It gives rise to numerous sensory branches:

Superior alveolar nerve (anterior, posterior and middle)
Middle meningeal nerve
Infraorbital nerve
Zygomatic nerve
Inferior palpebral nerve
Superior labial nerve
Pharyngeal nerve
Greater and lesser palatine nerves
Nasopalatine nerve

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34
Q

What do the ASAN, MSAN and PSAN exit and what do they innervate?

A

Anterior superior alveolar nerve
> Exits via the infraorbital foramen
> Innervates anterior maxillary antrum and incisor and canine teeth

  • Middle superior alveolar nerve
    > Exits via infraorbital foramen
    > Innervates medial and lateral maxillary antrum and premolars
  • Posterior superior alveolar nerve
    > Exits via the pterygomaxillary fissure
    > Innervates the posterior maxillary antrum and maxillary molars
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35
Q

What is the mandibular teeth supplied by? What is the journey of this nerve - what does its branches innervate?

A

Mandibular teeth are primary supplied by the inferior alveolar nerve, which is a branch of the mandibular nerve (V3). It carries both sensory and motor neurones, and exits via the foramen ovale.

  • The inferior alveolar nerve carries both sensory and motor axons to and from the respective trigeminal nuclei.
  • After branching from its parent nerve it gives rise to the mylohyoid nerve, a motor nerve to the mylohyoid and anterior digastric muscles.
  • The remaining sensory axons enter the mandibular canal, a narrow tunnel running through the mandible. Within this canal, the nerve provides branches to the mandibular teeth.
  • The nerve emerges through the mental foramen as the mental nerve. This provides sensory innervation to the lower lip and chin.

Inferior Dental Nerve (V3)
> Descends to the lateral pterygoid muscle, before
then entering the mandibular foramen
> Supplies lower molar and second premolar teeth

Mental nerve (V3)
> Exits via mental foramen
> Supplies chin, lower lip, facial gingiva and
mucosa from second premolar anteriorly

Incisive nerve (V3)
> Supplies teeth and PDL from first premolar anteriorly

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36
Q

What is local anaesthetic?

A

Any technique to render part of the body insensitive to pain without affecting consciousness.

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37
Q

What is the mode of action of local anaesthetic?

A
  • Peripheral nerve conduction works via depolarisation of nerve membranes.
  • Na moves into the neurone in nerve excitation.

–> LA works by blocking Na channels, preventing depolarisation of nerve membranes.

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38
Q

What are Amide local anaesthetics?
- components?
- broken down where?
- examples?

A
  • They contain an aromatic ring and lipophilic portion.
  • They are broken down in the liver.
  • Lidocaine
  • Prilocaine (contains felypressin - synthetic analogue of vasopressin)
  • Mepivacaine
  • Bupivacaine
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39
Q

Why do we not use prilocaine (which contains felypressin) in pregnant women?

A

Felypressin can induce labour in pregnant women, hence contraindicated in pregnancy.

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40
Q

What is an ester LA?
- components?
- broken down where?
- examples?

A
  • Containing a terminal amine and a hydrophilic portion?
  • Broken down in plasma and cholinesterase.
  • Articaine
  • Procaine
  • Amethocaine and benzocaine (topical anaesthetics)
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41
Q

Why is articaine not used in IDB?

A
  • Linked with permanent paraesthesia
  • As it is broken down in plasma, has a shorted half-life.
  • Used in higher concentrations which can cause paraesthesia
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42
Q

Why are prilocaine and articaine avoided in pregnancy?

A

Prilocaine contains felypressin which can induce labour.

Prilocaine and articaine may cause methaemoglobinemia (raised levels of methaemoglobin that can cause tissues to be deprived of adequate oxygen) which can lead to blue-baby syndrome if a pt is pregnant.

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43
Q

What are the 2 forms of an LA molecule?

A
  1. Unionised lipophilic inactive form. (uncharged)
  2. Hydrophilic ionised active form (charged)
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44
Q

What are 3 reasons it is harder to anaesthetise infected areas?

A
  1. LA is a weak base (pH 7.8), requires a greater dose if injected into an acidic environment (abscess), less ionised active form.
  2. Vasodilation around the abscess, means that tissue perfusion is greater.
  3. Increased prostaglandins due to inflammatory response around the infected area, heightened response to pain.
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45
Q

What is the maximum safe dose of LA for Lidocaine?

A

1 cartridge of lidocaine per 10kg of patient

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46
Q

Lidocaine:
- max dose mg/kg
- max dose adrenaline mg/kg
- half life (mins)
- gold standard

A
  • 4.4mg/kg
  • 7mg/kg adr
  • 90 minutes
  • 2% Lidocaine with 1:80,000 adrenaline.
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47
Q

Articaine:
- max dose mg/kg
- max dose adrenaline mg/kg
- half life (mins)
- gold standard

A
  • 4.4mg/kg
  • 7mg/kg
  • 20 minutes
  • 4% articaine with 1:100,000 adr
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48
Q

Prilocaine:
- max dose mg/kg
- max dose adrenaline mg/kg
- half life (mins)
- gold standard

A
  • 5mg/kg
  • 8mg/kg
  • 90 minutes
  • 3% prilocaine with felypressin
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49
Q

What do infiltrations anaesthetise?

A
  • LA solution deposited around the terminal branches of nerves
  • Used to anaesthetise soft tissue and pulp where alveolar bone is thin
  • Used in maxilla and lower anterior teeth
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50
Q

Where is the IDN situated?

A

In the pterygomandibular space.
Lies posterior to pterygomandibular raphe and mesial to ramus of the mandible.
Muscular landmarks are the masseter laterally and superior constrictor muscle.
Medial pterygoid muscle lies mesially to pterygomandibular space.
Lingual nerve blocked by injection on retraction of IDB.

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51
Q

What does a long buccal block anaesthetise?

A

Distal and buccal mucosa to lower 6-8, aim for supra periosteal distal and buccal to last standing molar.

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52
Q

What are landmarks for an IDB?

A
  • Coronoid notch
  • Pterygomandibular raphe
  • 1cm above occlusal plane with a 35mm needle.
  • Aim from angle of contralateral premolars.
  • Make contact with bone, retract, aspirate, dispense majority. retract more, dispense for lingual block.
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53
Q

What does the IDB anaesthetise?

A
  • Dental pulps of all mandibular teeth to the midline.
  • Buccal gingivae anterior to the mental foramen.
  • Lingual gingivae.
  • Anterior 2/3rd of tongue
  • Floor of the mouth.
  • Lower lip
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54
Q

What are IDB complications?

A
  • Facial/Bell’s palsy –> by inserting the needly too far posteriorly, you may deposit LA into parotid bland, blocking the Facial nerve.
  • Trismus –> if needle inserted too mesially, inject into the medial pterygoid.
  • Damage to ID nerve
  • Intra-vascular injection - caused by not aspirating and not slow injection. Cause pale and incr heart rate.
  • Bruising/haematoma
  • Allergic reaction
  • Skin blanching
  • Needle breakage
  • Trauma, either idiopathically or via patient chewing lip due to loss of sensation
  • Palpitations due to idiopathic injection of intravascular adrenaline causing tachycardia.
  • Infection
  • Persistent anaesthesia/paraesthesia

(-if injected shallow, then sphenomandibular ligament may act as a barrier to inferior alveolar nerve)

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55
Q

What does a lingual infiltration anaesthetise?

A

The lingual gingivae/soft tissue.

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56
Q

What does a mental block anaesthetise?

A

Buccal gingivae and teeth of the lower anterior teeth. (1-5)

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57
Q

Name different nerves in the maxilla:

A
  1. Nasopalatine and greater palatine nerves.
  2. Superior alveolar nerve: split into anterior, middle and posterior branches.
  3. Pterygovenous plexus lies close to posterior superior alveolar nerve, must aspirate first.
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58
Q

What does a posterior superior alveolar block (PSA) anaesthetise?

A
  • PSA branch of maxillary division of trigeminal extending on the maxilla tuberosity.
  • Maxilla molars apart from the MB root of 6.
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59
Q

What does an infra-orbital block anaesthetise?

A
  • anaesthetises the middle superior and anterior superior alveolar nerves (Both V2)
  • inject above the U4 region
  • innervates buccal and pulpal features 1-5 and MB root of 6.
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60
Q

What nerves do palatal infiltrations anaesthetise?

A

Greater palatine injection anaesthetises palatal features 4-8.

Lesses palatine injection anaesthetises soft palate.

Naso-palatine injection, anaesthetisises 1-3.

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61
Q

Name some supplemental LA techniques:

A
  1. Intra-ligamentary
  2. Intra-pulpal
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62
Q

Why does LA failue?

A
  1. Operator dependent
    > poor technique
    > insufficient amount of LA used
    > choice of LA (articaine better infiltration perfusion)
  2. Patient dependent
    > anatomical (variation, accessory nerves)
    > pathological, if inflammation is present
    > psychological
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63
Q

what are some immediate complications of LA?

A
  1. Unilateral facial (Bell’s) palsy, due to injection to posterior into parotid gland, affecting VII facial nerve.
  2. Trauma, either idiopathic or via pt chewing lip due to loss of sensation
  3. Palpitations due to idiopathic injection of intravascular adrenaline causing tachycardia.
  4. Skin blanching
  5. Allergy
  6. Needle breaking
  7. Toxicity
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64
Q

What are delayed complications of LA?

A
  1. Haematoma/bruising
  2. Trismus
  3. Infection
  4. Persistent anaesthesia/paraesthesia
  5. Tissue necrosis
  6. Post-anaesthetic lesion (HSV, recurrent aphthae)
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65
Q

What LA routinely used in paediatric dentistry?

A

2% lidocaine + 1:80 000 adrenaline due to its low allergic characteristics.

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66
Q

Which is superior: 4% articaine more or 2% lidocaine for tx of posterior teeth?

A

4% articaine + 1:100,00 adrenaline is more superior to 2% lidocaine + 1:80,000 adrenaline for trx. of posterior teeth with irreversible pulpitis (Cochrane review St.Goerge G et al. 2018)

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67
Q

Why do we avoid articaine with caution for people with asthma or sulphites allergies?

A

Articaine can lead to bronchospasm in patients with asthma or sulphites allergies.

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68
Q

What is the onset of topical anaesthetics lidocaine and benzocaine?

A
  1. Lidocaine 5% (onset 2-5 mins)
  2. Benzocaine 20% (onset 30 secs)
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69
Q

What rate should LA be delivered at to minimise pain on administration?

A

1ml/min (cartridge volume = 2.2ml).
Pain on LA delivery is due to subcutaneous tissue expansion.

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70
Q

Why is Articaine more effective when administered in low pH environments (infected areas)?

A

Articaine has low pH which makes it more effective when administered in low pH environment such as abscesses as it can pass the cell membrane and get activated by blocking the Na-channels from inside the cell.

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71
Q

How many micrograms of lidocaine and adrenaline is there is a 2.2ml cartridge of Lidocaine 2% + 1:80 000 adr?

A

Lid.2%+ 1:80,000 Adr.- has total of 49.9micrograms of adrenaline and 46.9mg of lidocaine in a cartridge of 2.2ml.

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72
Q

What are indications for antibiotics prescription?

A
  1. Spreading infection: cellulitis, lymph node involvement, spreading swelling, trismus
  2. Systemic involvement: malaise, pyrexia
  3. Immunocompromised patients.
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73
Q

What patient factors do you need to think of before prescribing Abx?

A
  1. Allergy to antibiotics
  2. Renal function
  3. Pregnancy
  4. Oral contraceptive pill
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74
Q

What does the dose of the antibiotics depend on?

A

Age, weight, renal function, severity of the infection.

  • Use lowest dose possible for shortest possible time.
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75
Q

What does the duration of the antibiotic depend on?

A

Nature of the infection
Pt response to Abx

  • Too short results in resistance
  • Too long may produce unwanted side effects (antibiotic-associated colitis)
  • Use lowest dose possible for shortest possible time.
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76
Q

What Abx are bactericidal? (3)

A

Bactericidal = kill bacteria

  • Penicillin
  • Metronidazole
  • Cephalosporine
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77
Q

What ABx are bacteriostatic? (3)

A

Bacteriostatic = inhibit or slow growth of bacteria
1. Tetracycline
2. Erythromycin
3. Clindamycin

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78
Q

What is Amoxicillin?
- how does it work?
- spectrum?
- % allergy
- pregnant women?
- inactivated by what

A
  • Bactericidal, interferes with cell wall synthesis.
  • Broad spectrum
  • 1-10% have allergy to penicillin (rash or anaphylaxis)
  • Safe in pregnant patients
  • Inactivated by penicillinases (B lactamases), however Flucloxacillin isn’t).
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79
Q

What is Co-amoxiclav?
- What is it?
- active against penicillinases?
- indications?
- Side effects?
- Doses?

A
  • Amoxicillin + Clavulanic acid
  • Combination of 2 drugs means active against penicillinases (Beta-lactamases)
  • Indications - severe dental infections with spreading cellulitis
  • Side effects: stevens-johnson syndrome
  • 374mg or 625mg??
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80
Q

What is metronidazole?
- Effective against?
- Indications?
- contraindications
- side effects?
- typical dose?

A
  • Effective against anaerobic bacteria and protozoa.
  • Bactericidal, it inhibits synthesis by breaking down bacterial DNA
  • Indicated for ANUG, pericoronitis, oral infections (when Pen V contraindicated)
  • Reacts with alcohol + don’t use with warfarin
  • Side effect: oral candida overgrowth
  • 200mg tds
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81
Q

What is clindamycin?
How does it work?
Serious side effects?
routine?
Indications?
Typical dose?

A

Bacteriostatic, inhibits bacterial protein synthesis.
Serious side effects - pseudomembranous colitis
Not routine oral Abx
Indicated for bone (osteomyelitis) and skin (cellulitis) infections
150mg tds

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82
Q

What are tetracycline antibiotics?
How do they work?
Indications?
side effects?
Normal dose?

A
  • Bacteriostatic, inhibits protein synthesis.
  • Indicated for perio disease and sinusitis
  • Causes extensive staining (not indicated for children and pregnant women)
  • 250mg qds
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83
Q

What is erythromycin?
How does it work?
What does it interact with?
Risks?

A
  • Bacteriostatic, inhibits protein synthesis
  • Interacts with simvastatin, increases plasma concentration of simvastatin
  • Causes increased risk of myalgias, rhabdomyolysis and renal failure
  • Narrow spectrum, poor absorption, GI disturbances
  • Limited indications
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84
Q

How do NSAIDs work?

A

Non-selective inhibitors of COX1 and COX2?

They are analgesic, antipyretic and anti-inflammatory agents.

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85
Q

What are 4 examples of NSAIDS?

A
  1. Ibuprofen
  2. Aspirin
  3. Diclofenac
  4. Naproxen
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86
Q

What are 3 side effects of NSAIDs?

A
  1. Peptic ulceration
  2. Cardiac implications (arrhythmias, thromboses, MI)
  3. Increased bleeding tendency
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87
Q

What are contraindications for NSAIDS? (6)

A
  1. Pregnancy/breastfeeding
  2. Asthma
  3. Renal/liver disease
  4. Peptic ulcers
  5. Cardiac conditions (excluding ibuprofen)
  6. Allergy
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88
Q

Fainting:
- cause?
- symptoms?
- management?

A
  • Syncope or vasovagal attack due to anxiety or pain.
  • Symptoms include nausea, pallor, thread pulse, loss of consciousness, cyanosis and convulsions.
  • Lie down with feet in air, allow blood to return to brain. Ensure ABCDE and give oxygen.
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89
Q

Hypoglycaemia:
- cause?
- symptoms?
- management?

A
  • Poorly controlled insulin-dependent Diabetes Mellitus, fasting or infection.
  • Symptoms include; trembling, sweating, hunger, disorientation, slurring of worse, inability to concentrate, aggression, and LOC
  • Treat with glucose drink (10-20g) and complex carb.
  • If unconscious - glucagon 1mg I.M.
  • ABCDE and oxygen
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90
Q

Eplipsy:
- cause?
- symptoms?
- management?

A
  • Poorly controlled drug regime
  • Sx: LOC, convulsions, incontinence, cyanosis, confusion.
  • Treat by protecting pt from injury during convulsions.
  • If prolonged or repeated convulsion in short interval - buccal midazolam 10mg/ml
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91
Q

Adrenal insufficiency:
- cause?
- symptoms?
- management?

A
  • Caused by long term steroids and adrenal disease.
  • Sx: LOC, pallor, thread pulse, low BP.
  • Ensure ABCDE, oxygen, 100mg hydrocortisone given if need be
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92
Q

Anaphylaxis:
- cause?
- symptoms?
- management?

A
  • Caused by allergic reaction to penicillin or latex.
  • Sx: LOC, dyspnoea, flushing, itching, anxiety, pallor, cyanosis, weak pulse, low BP, oedema and cardiac arrest.
  • Treat with ABCDE, oxygen, adrenaline 0.5ml of 1:1000 adrenaline IM.
  • Call ambulance
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93
Q

Angina:
- cause?
- symptoms?
- management?

A
  • Caused by myocardial ischaemia, MI, due to pt being stressed or exercise induced.
  • Sx - crushing chest pain and retrosternal pain radiating down left arm.
  • Tx: GTN spray sublingually and oxygen.
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94
Q

How does GTN work?

A
  • venous dilation –> reduces venous return to hear –> decreases preload –> reduce inotropic effect –> reduced anginga
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95
Q

Myocardial infarction:
- cause?
- symptoms?
- management?

A
  • Occlusion of coronary artery causing tissue death.
  • Sx: LOC, severe crushing retro-sternal pain, vomiting, pallor, dyspnoea and weak pulse.
  • Tx: MONASH
  • morphine
  • oxygen
  • nitrate (GTN)
  • aspirin
  • seek help
  • heparin
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96
Q

Cardiac arrest:
- cause?
- symptoms?
- management?

A
  • Caused by MI and hypoxia, secondary to respiratory obstruction.
  • Sx: LOC, no central pulse.
  • Tx: Basic life support and Automated External Defibrillator (AED) until crash team arrives.
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97
Q

Asthma:
- cause?
- symptoms?
- management?

A
  • Attack triggered by anxiety, infection, exercise and sensitivity to allergen.
  • Sx: dyspnoea and wheezing on expiration
  • Tx: Salbutamol inhaler or nebuliser
  • Hydrocortisone and consider adrenaline if v severe.
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98
Q

Stroke or CVA:
- cause?
- symptoms?
- management?

A
  • Caused by cerebral haemorrhage, thrombosis and/or embolism.
  • Sx: LOC, headache, hemiplegia.
    FAST symptoms:
    > Face drooping
    > Arm weakness
    > Speech difficulty
    > Time to call for ambulance.
  • Tx with supine movement, airway, oxygen, BLS and monitor:
    –> don’t give aspirin as risk if haemorrhage (Brain bleed), make it worse.
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99
Q

Airway management:
- cause?
- symptoms?
- management?

A
  • Unconscious causes no pharyngeal reflexes, loss of muscle tone, not able to protect own airway.
  • Partial obstruction or complete obstruction, stridor or silence.
  • Clear upper airway (suction)
  • Triple airway manoeuvre, jaw thrust, head tilt, chin lift.
  • Heimlich manoeuvre if foreign body.
  • cricothyroidotomy.
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100
Q

What is BLS?

A
  • Compression of lower third sternum to depth of 5-6cm, with compression rate 100-120/minute and 30 compressions to 2 breaths.
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101
Q

How do you examine a pt with returning problems?

A

Visual:
- patient’s general appearance

E/O:
- temperature
- swelling
- facial asymmetry
- lymphadenopathy
- trismus, reduced opening of the jaw

I/O:
- site of surgery
- swelling
- bleeding
- suppuration
- halitosis

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102
Q

What is alveolar osteitis?

A

Dry socket!

Inflammation of the alveolar bone post extraction, due to loss of blood clot leaving exposed alveolar bone.

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103
Q

What are 4 symptoms of dry socket?

A
  1. Extremely painful (throbbing sensation)
  2. Associated with bad taste and odour
  3. Not relieved by analgesics
  4. Not associated with pyrexia, swelling or infection.
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104
Q

What are 5 factors that increase the risk of dry socket?

A
  1. Smoking
  2. Oral contraceptive pill
  3. Local infection (ANUG, pericoronitis)
  4. Excessive trauma during XLa.
  5. Immunocompromised patient: diabetes, immune suppression, radiotherapy and altered bone metabolism patients.
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105
Q

How do you manage dry socket?

A
  1. Irrigation of socket with saline solution.
    (Don’t use chlorhexidine as recorded death from allergic reaction)
  2. Smoking cessation
  3. Obtundent pack, Alveogyl, containing:
    > Eugenol: An analgesic + antiseptic
    > Iodoform: An antibacterial
    > Butamben: A mild anaesthetic
    > Penghawar djambi: Fibers from the tree fern, Cibotium barometz
    > Sodium lauryl sulphate: An ingredient in Alveogyl
    > Calcium carbonate: An ingredient in Alveogyl
  4. Analgesia to treat acute pain.
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106
Q

What is delayed bleeding after an extraction usually due to?

A

An infection

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107
Q

What is primary, reactionary and secondary bleeding after an extraction?

A
  1. Bleeding post XLA = primary
  2. Bleed <48 hours = reactionary, due to trauma to surgical site.
  3. Bleed due to infection or other causative factors = secondary
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108
Q

What is the management of post XLA bleeding?

A

Assess pt for vitals signs and airway clearance.

Consider treatment such as vitamin K and tranexamic acid if coagulation risk, as well as fluid transfusion.

  • consider pack and suture (surgicel), haemostatic acids, vasoconstrictors and suction.
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109
Q

What do you do for haemophilia patients if they come back bleeding?

A
  • Debride the socket (surgical area)
  • Remove clot remnants and try to identify the bleeding site.
  • Soft tissue management by placing compressive sutures (vicryl) and surgicel or fibrin blocks.
  • Bone wax if the bleed is from bone
  • Bleeding due to infection, either localised or systemic (pyrexia)
  • Consider prophylactic Abx???
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110
Q

What is surgicel used for and how does it work?

A
  • Use as a haemostatic agent (induces blood clot)
  • Made of an oxidised cellulose polymer
  • Used to control post-surgical bleeding due to intra-bony bleeds from inferior alveolar artery
  • Potential neurotoxic effects in mandibular canal.
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111
Q

What bacteria cause dental abscesses?

A

Polymicrobial anaerobic bacterial infections.
Usually three or more causative organisms can be isolated from a dental abscess, predominantly Gram-negative anaerobic bacilli.

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112
Q

when are the only times Abx are appropriate for oral infections?

A
  1. Systemic involvement — pyrexia, lymphadenopathy and malaise
  2. Immunocompromised
  3. Spreading infection — cellulitis and swelling
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113
Q

What is the first line analgesia for dental pain?

If pain is not tolerable, then was can be prescribed?

A

Ibuprofen and paracetamol are first-line analgesia.

Codeine phosphate or alternative NSAID, diclofenac, naproxen.

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114
Q

What analgesics can be used in pregnancy?

A

Paracetamol and short course of codeine.

No ibuprofen or other NSAID

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115
Q

What is the analgesic ladder?

A

1st line = paracetamol

2nd line = ibuprofen (NSAID); contraindicated in asthma, pregnancy, liver, kidney, Crohn’s disease.

3rd line = paracetamol + ibuprofen

4th line = co-codamol (combination of codeine and paracetamol)

5th line = tramadol (stronger dose of codeine); trx moderate to severe pain.

6th line = oramorph (strong painkiller for severe pain); pain from cancer or heart attacks.

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116
Q

What is the maximum dose of ibuprofen?

A

Max = 2400mg (2.4g) or 30mg/kg per day = 600mg x 4/day.

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117
Q

What is the maximum dose of paracetamol?

A

4000mg (4g) per day.
1g per dose, 4x/day.

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118
Q

What is best analgesic advise post op?

A

Ibuprofen and paracetamol, alternate between both every 4 hours.

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119
Q

Who is diclofenac contraindicated in?

A

People with IHD, CVD, PVD, and mild, moderate, or severe HF.

Available on prescription only. it is NSAID (not to be taken with other NSAIDs)

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120
Q

What drug interactions does warfarin have with NSAIDs and azole antifungals some antibiotics?

A
  • Increase bleeding risk
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121
Q

What can happen if statins are taken with azoles, erythromycin and clarithromycin??

A

myopathy

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122
Q

What medication can exacerbate asthma?

A

NSAIDs

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123
Q

What are cowhorn forceps designed to do?

A

Engage the furcation in mandibular first and second molars.

Can be used to section the mandibular molars into 2 single roots which can be removed separately.

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124
Q

What can eagle beaks be used for?

A

Maxillary first molars, engages buccal furcation and palatal single root.

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125
Q

What is the operator position for maxillary teeth?

A

Stand in front of the patient, chair should be elevated and tilted back. Stand at arm’s length away from pt.

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126
Q

What is the operator position for mandibular teeth?

A

Chair should be lowered so that pt’s shoulder is level with dentist’s elbow.
- LL = stand in front of pt
- LR = stand behind the pt

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127
Q

Describe holding the forceps and correct application:

A
  1. Initial movement must be apically along the PDL, with blades beneath the gingival margin
    — This reduces the chance of the crown breaking due to rotational axis being more apical
    — Wedges the blades down the root causing more displacement
    — Dilates the socket
  2. Second movement = apical force is maintained, with slow and deliberate movements
    — Conical rooted teeth movement is ROTATED
    — Multiple rooted teeth have a BUCCO-LINGUAL movement next
    — Mandibular anterior teeth should initially be moved labially
  3. Final movement
    — Posterior teeth are delivered buccally
    — Anterior teeth are delivered with rotations
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128
Q

What should you do once you extract a tooth?

A

The socket should be compressed firmly with finger and thumb (digital pressure) before applying pressure from the gauze.

This makes the socket a smaller wound and any fragments of buccal bone with attached mucoperiosteal are replaced.

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129
Q

What are post op instructions after an XLA?

A
  1. Avoid
    > hot or cold foods or drinks
    > exercise or effort
    > smoking, alcohol and mouthwashes for 24 hours.
    > LA lasts for 2-3 hours, can last longer.
    > playing with wound site or stitches with tongue or fingers.
  2. Salt water mouth rinses after 24 hours. Rinse after every meal for 1 week.
  3. OH - avoid area
  4. Bleeding - pink saliva normal. heavy bleeding use gauze
  5. Signs to look out for:
    - uncontrolled pain
    - uncontrolled bleeding
    - bad taste, smell, pus
    - spreading swelling
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130
Q

What is the function of the supporting hand during an extraction?

A
  • Gripping and supporting alveolus
  • Retracting soft tissues
  • Retrieve fractured restorations and fragments of tooth (preferable tooth tweezers) - protect airway
  • Support the lower jaw
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131
Q

If doing full mouth clearance, where do you start?

A

Lower posterior, unless one extremely painful tooth

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132
Q

How do you position your supporting hand during and extraction?

A

Lower R = Thumb in lingual sulcus, forefinger in buccal sulcus other 3 fingers under chin

Lower L = Curl up 4th and little finger. Middle finger in lingual sulcus, forefinger in buccal sulcus, thumb under chin

Upper R = Forefinger in palate, thumb in buccal sulcus curl up remaining 3 fingers

Upper L = Thumb in palate, forefinger in buccal sulcus, curl up remaining 3 fingers

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133
Q

What is the function of elevators?

A

Used to loosen or deliver teeth by severing the PDL.

Alveolar bone used as the fulcrum and not the adjacent tooth.

Firmly help in palm of the hand by the index finger supporting the blade by fingertip close to blade.

Very useful for conically rooted teeth.

by inserting the instrument onto the root surface so that the concave blade engages the root, and when the handle is rotated the lower cutting edge lifts the root.

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134
Q

What is the function of a luxator?

A
  • Thinner and sharper than elevators.
  • Fit in tight apical spaces, more efficient at cutting PDL
  • use in circular cutting motion whilst applying apical pressure
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135
Q

What are warwick-james elevators used for?

A

Removal or upper 8s.
Curved blade inserts into the concavity, with the handle then rotating and the blade turning against the root mass.

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136
Q

What are cryer’s elevators used for?

A

Blades larger and more pointed, at right angles to the hand.
- Used to loosen tooth or root from boy socket prior to forceps placement.
- Used for :
> extraction of impacted 8s, applying concave surface against mesial aspect of the root.
> for elevating fractured roots
> applying pressure to buccal aspect of lower molars where furcation can be engaged

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137
Q

What are lacks tongue depressor used for?

A

Examination of OC and oropharynx

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138
Q

What is Austin retractor used for?

A

To deflect and retract the periosteum from bone after incision

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139
Q

What is Minnesota retractor used for?

A

To retract mucoperiosteal flap only rest on bone

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140
Q

What is kilner cheek retractor used for?

A

Retraction to aid vision for upper 8s

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141
Q

What is lasters retractor used for?

A

XLA U8s, locks behind the tuberosity.

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142
Q

What is bowdler henry retractor used for?

A

XLA 8s

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143
Q

What should be assess pre-operatively before extractions?

A

History
Clinical examination
Radiographs
Special tests
Diagnosis
Treatment plan

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144
Q

What are anaesthetic choices for extractions?

A
  1. LA
  2. Conscious sedation (inhalation or IV) supplemented with local anaesthetic
  3. General anaesthetic
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145
Q

What are the principles of flap design?

A

Flap design needs to be sufficient for surgical procedure, to ensure adequate access and minimum damage to tissue.

  • Incision avoids vital structures.
  • Ensure flap has adequate blood supply.
  • Incise mucoperiosteal flap ensuring that you don’t separate the mucosa and periosteum. Full thickness flap.
  • Incise perpendicular to epithelial surface.
  • Include interdental papillae on the flap
  • At closure of mucoperiosteal flap, should rest on sound bone.
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146
Q

What do relieving incisions do?

A

They relieve the tension on the flap for adequate access.

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147
Q

Why do you need irrigation when using a bur on bone?

A

To avoid surgical emphysema.

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148
Q

What bur do you use for bone removal?

A

Flat fissure 4 bur

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149
Q

What scalpel is used for raising a flap?

A

Scalpel (15) used for cutting soft tissue with minimum trauma

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150
Q

What are tooth forceps use for?

A

Tooth forceps grasp tissue by puncturing rather than crushing.

Non-teeth forceps grasp by compression of opposing serrated edges.

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151
Q

How do tissue forceps work?

A

Scissor action incorporating a ratchet lock.
Useful for slippery tissue or when direction or traction must be varied.

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152
Q

What are artery forceps used for?

A
  • Scissor action incorporating a ratchet lock.
  • Grasp vessel with tip projecting beyond the vessel to facilitate tying a ligature.
  • Compress vessel to facilitate haemostasis.
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153
Q

How are needle holders designed?

A

Designed to rotate in long axis as a pronation-supination action to drive curved needle through tissues.

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154
Q

What are the different types of needles and their uses?

A
  • Cutting needles used for resistant fibrous tissues.
  • Round bodied needles used for fragile tissue to produce minimal damage.
  • Traumatic is eyeless
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155
Q

Rules of suturing:

A
  • Suture from free to fixed tissue
  • Ideally suture forehanded (toward yourself)
  • Evert skin edges
  • Needle should enter the tissues perpendicular to surface
  • Follow curve of needle by pronation, supination to avoid ‘pulling through’.
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156
Q

What are different types of sutures:

A
  • Simple interrupted
  • Continuous
  • Vertical mattress - double stitch with return stitch in line with the first but taking a smaller bite.
  • Horizontal mattress - double stitch with return stitch parallel to the first.
  • Sub-cuticular continuous - avoids puncture wounds on surface (skin closure)
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157
Q

What are the different types of suture material?

A

Resorbable:
- PDS (polydioxanone suture) provides wound support for longer period of up to 50 days)
- Polyglactin
- 3/0 Vicryl
- Polysorb used for oral mucosa with 5/0
- Catgut - natural resorbable

Non-resorbable: nylon, prolene, silk.

158
Q

What are the benefits + disadvantages: of monofilament?

A
  • minimum tissue reaction
  • not braided so microorganisms can’t hide and cause infection
  • harder to handle as tend to spring apart.
159
Q

What are skin grafts?

A

Tissue that is totally freed from its donor site and placed at a recipient site to restore a defect.

Derives nourishment from tissue bed or recipient site.

Recipient site must be free of infection and bleeding controlled to avoid haematoma.

Split skin graft only include the superficial layer of the skin and some germinal cells.

Full thickness graft includes all layers of the skin (better cosmetics)

Mesh graft to allow exudate to escape and not build up

160
Q

What is a surgical free flap?

A

Named blood vessels detached and inserted at a distant site by microvascular anastomosis to local blood vessels

161
Q

What is an aspiration biopsy?

A

Aspirate or fluid collected from a lesion (MC, cytology and biochemistry)

162
Q

What is needle biopsy?

A

True cut biopsy, small core of tissue removed (histology)

163
Q

What is FNAC?

A

Fine needle aspiration cytology

164
Q

What is an excision biopsy?

A

Whole lesion is excised, need a wide clear margin for malignancies >1mm

165
Q

What is an incision biopsy?

A

Portion of the lesion is removed, including JE and normal tissue as well

166
Q

What is neuropraxia?

A

Temporary physiological nerve block

167
Q

What is axonotmesis?

A

Axon divided but endoneurium remains intact, mesial part eventually reconnect with the end organ

168
Q

What is neurotmesis?

A

Nerve divided, recovery unpredictable, may use an interposition nerve graft

169
Q

How can you avoid dental infections after an XLA?

A
  • Pre-op preparation
  • Aseptic technique
  • Minimal trauma
  • Surgical debridement and saline irrigation
  • Drainage of purulent discharge
  • Adequate wound closure and haemostasis (pack and suture)
  • Antibiotic
  • Oral hygiene and post-operative care (analgesia and wound care)
170
Q

What are indications for extractions of teeth?

A
  • Caries
  • Abnormal wear
  • Prophylaxis
  • Trauma
  • Idiopathic resorption
  • Non-functional teeth (teeth not in occlusion)
  • Periodontal disease
  • Supernumerary
  • Supplemental
  • Systemic disease
171
Q

What are pre-operative complications?

A
  • Inadequate pre-operative clinical and radiographic assessment.
  • Wrong tooth extracted (NEVER EVENT), Who checklist and notes correct.
    > Orthodontic XLA: charting may be incorrect.
    > Caries may be overlooked, with carious teeth changing Tx plan.
    > Permanent successors can be missing, therefore keep primary teeth
    > Orthodontic treatment plan may change.
172
Q

What are peri-operative complications?

A
  1. Bone fracture
  2. Root fractures
  3. Nerve injury
  4. Blood vessel injury
  5. Soft tissue injury
  6. Adjacent teeth injury:
  7. Inhaled and swallowed tooth
  8. Instrument fracture
  9. Damage to underlying dental follicle
  10. Displacement of teeth
  11. Cysts:
    > due to operator unaware of pathology.
    > can happen if carious teeth or root XLA without pre-op x-ray
    > cysts requires proper radiographic techniques
173
Q

What types of bone fracture can happen during an extraction?

A
  • Tuberosity fracture in lone standing upper molars
  • Mandible fracture due to excessive trauma
  • Displaced bony fragments into socket
  • Labial plate of upper canines can be damaged, can often see buccal mucosa moving (elevator and separate periosteum)
174
Q

How can a root fracture during XLA and what do you do?

A
  • Most common surgical complication
  • Only leave in situ if a vital tooth with no infection and small apices.
  • Non-vital = remove
  • Orthodontic and prosthetic tx may be delayed by leaving root in situ
175
Q

When may nerves be injured during extraction?

A
  • lower 8s - IDN and lingual (lip, chin and tongue numbness and altered sensation/tingling)
176
Q

How do you avoid blood vessel injury during XLA?
What do you do?

A
  • plan surgical flaps properly, protect with retractors
  • ION injury be repaired, injury due to blind instrumentation
  • soft tissue = identify and ligate, potential diathermy
  • bone:
    > compress bone with instrument
    > bone wax and pressure packs
177
Q

What soft tissue injuries can occur during and extraction?

A
  • burns
  • crush, forceps handle on opposing lip and or forceps breaking outside gingiva
  • slip with instrument due to poor finger rest
  • rotating burs causing laceration
178
Q

Which adjacent teeth are commonly the ones to be injured during XLA?

A
  • displacing lower 7s elevating lower 8s.
  • upper 1s elevating impacting 3s
  • developing premolar teeth beneath deciduous teeth
  • damage and fracture to adjacent teeth and restorations
179
Q

How can you damage an underlying dental follicle during XLA?

A
  • can be easily avulsed or damaged by elevating retained roots or deciduous molars. Also by surgical exploration for supernumerary teeth.
180
Q

Where can teeth be displaced during an XLA?

A
  • Maxillary antrum can become OAC
    > upper premolars and molars can be displaced into the maxillary antrum
    > removal via the caldwell-luc surgical procedure or via socket
    > prevention by careful use of luxator, avoid excessive upwards force
  • Soft tissue
    > lower 8s - lingual pouch, emergency as can move further into neck
    > upper 8s = pterygomaxillary space, risk of pterygoid venous plexus haemorrhage during incision to retrieve the displaced tooth
181
Q

What can make an extraction more difficult?

A
  • Patient factors: age, build, race and mental capacity.
  • Divergent roots - root morphology.
  • Sclerotic bone
  • Ankylosis
182
Q

What are post-operative complications of extractions?

A
  • Retained swabs: WHO checklist
  • Pain: analgesics
  • Infection: no smoking, mouthwashes and saltwater bathe, good OH
  • Dry socket
  • Self-inflicted trauma when anaesthetised
  • Swelling: anti-inflammatories (ibuprofen)
  • Bleeding
  • Bruising
  • Paraesthesia/altered sensation perisistent
183
Q

What are minimum surgical instruments?

A
  • Scalpel No15 blade
  • Austin and Kilner Retractors
  • Howarth’s periosteal elevator
  • Handpiece and burs
  • Elevators (couplands, Warwick-james and cryers)
  • Suture, needle holders and forceps.
184
Q

What are the principles of soft tissue flaps?

A
  • Increase vision
  • gain adequate surgical access
  • remove appropriate amount of bone
  • avoid important anatomical structures
  • appropriate design to encourage good wound healing.
185
Q

What are flap design principles?

A
  • Broad base to gain good blood supply.
  • Large enough for adequate access
  • Full thickness to include the periosteum
  • Margins of flap lie on sound bone when close
  • Avoid vital structures
  • Include interdental papillae
186
Q

What is a simple envelope flap?

A

Around the gingival margins with a scalpel
- No relieving incisions
- Extends mesially and distally as required for access
- Easy to suture closed

187
Q

What is a two-sided flap?

A
  • With a relieving incision, ensure anatomical structure maintained and not damaged.

Relieving incison:
- Good access can be extended distally as required.
- Usually move 1 tooth unit forwards
- Ensure flap margins are on bone and prevent flap margin collapsing palatally
- Include papilla and periosteum
- Large blood supply
- Combines with envelope technique.

188
Q

What is a three-sided flap?

A

Has mesial and distal relieving incision.
- can be used for things like buccal advancement flap for example.

189
Q

How do you place a relieving incision?

A
  • Move a tooth unit beyond tooth to be extracted.
  • Ensure flap margins are on bone
  • Include locating papilla
  • Prevent flap margin collapsing palatally
  • Avoid anatomical structures such as mental nerve
190
Q

How can you remove roots without a flap?

A
  • use the anatomy of multi-rooted tooth.
  • can be divided through the socket with a bur
  • individual roots separated, remove as separate entities
    > minimise bone removal required.
    > easy delivery of roots
  • Good for teeth with diverging roots (conflicting pathways of withdrawal)
  • Flat fissure 4 bur usually used
191
Q

What should you think about when removing bone?

A

Consider area of bone removal, alveolar bone preservation provides prosthetic advantage.

192
Q

How can you close a flap?

A

Resorbable or silk sutures
Cutting (normal or reverse) or non-cutting needle choice

193
Q

What are indications for XLA of 8s?

A

Follow current guidelines!!!

  • Localised infection and multiple incidence of pericoronitis
  • Unrestorable caries of third or second molar
  • Trauma (common to operculum of lower from upper 8s)
  • Tumour or cyst
  • Orthodontics and prosthetics
  • Dental pathology
  • Prophylaxis?
194
Q

What information from a DPT can help assess the difficulty of Extn of an 8?

A
  • Type of impaction (mesial/distal/horizontal)
  • Depth of LL8 compared the LL7
  • Proximity of roots to ID canal
  • Number, shape and form of roots
  • condition of LL7 and LL8 (caries, restorations etc)
  • Associated pathology
  • Quality/density of bone
  • Bone loss distal to 8
  • Working space between distal of 8 and ascending ramus.
  • Angulation of tooth
  • Ankylosis?
195
Q

How do you plan for a surgical extraction? (5)

A
  1. path of withdrawal
  2. point of application
  3. obstacles
  4. bone removal necessity
  5. flap design if required
196
Q

What classifications are used to describe unerupted wisdom teeth in various positions radiographically?

A
  1. Winters lines
  2. Pell and Gregory classification system
197
Q

What are the different types of impaction for wisdom teeth?

A

Vertical impaction
Mesio-angular impaction
Horizontal impaction
Distoangular impaction

198
Q

What is a coronectomy?

A

when a crown is deliberately removed from a vital tooth and the roots left.

Sometimes used in lower 8s, when there is close association with IDN.

199
Q

What are the complications with removal of 8s?

A
  • Elevated risk of tuberosity fracture for upper 8s.
    >. increased risk when using elevators, use forceps instead.
    > if buccally placed, then able to elevate otherwise do not use.
    > this is because the lingual gone around an 8 is very thin, easy to #
  • ION or lingual nerve injury
    > presents via numbness, tingling, pain, difficult to manage
  • Lingual paraesthesia
  • Lip paraesthesia
  • Fractured mandible
  • Damage to LL7
  • Soft tissue injuries
  • Pain, bleeding, bruising, swelling, infection
  • Trismus
200
Q

What is pericoronitis?

A
  • Infection under the operculum (gingival tissue) covering a partially erupted tooth, pain associated.
  • Well localised pain around a PE tooth.
  • Swelling of the operculum
  • Discomfort when swallowing
  • Trismus
  • Purulent discharge.
  • Might have traumatic occlusion
201
Q

How do you manage pericoronitis?

A
  • Determine if airway is compromised, if yes, then refer to emergency care.
  • Optimal analgesia, no ABx unless systemic or spreading infection or immunocompromised.
  • Scaling or debridement under LA to remove food debris packed under operculum
  • Irrigate with saline
  • XLA if repeated episodes of periocoronitis
  • XLA of opposing upper 8 if tooth causing traumatic occlusion and non-functional
202
Q

What is MRONJ?
Definition?

A
  • Medication related osteonecrosis of the jaw.

Exposed bone, or bone that can be probed through an intraoral or extra oral fistula, in the maxillofacial region that has persisted for more then 8 weeks in patients with a history of treatment with anti-resorptive or anti-angiogenic drugs, and where there has been no history of radiation therapy to the jaw or no obvious metastatic disease to the jaws.

203
Q

How do anti-resorptive drugs work?

A

They inhibit osteoclast differentiation and function, leading to decreased bone resorption and remodelling.

204
Q

What are the 2 main types of anti-resorptive drugs that are associated with MRONJ? What are they used for medically?

A
  1. Bisphosphonates
  2. Denosumab.

They are used in the management of osteoporosis and other non-malignant and malignant condition. They have a significantly positive effect on the quality of life of patients by reducing or delaying onset or tx complications, such as bone fractures and bone pain.

205
Q

How do bisphosphonates work?

A

They reduce bone resorption by inhibiting enzymes essential to the formation, recruitment and function of osteoclasts.

The drugs have a high affinity for hydroxyapatite and persist in the skeletal tissues for a significant period of time, with alendronate having a half-life in bone of around 10 years.

Bisphosphonates are used to reduce the symptoms and complications of metastatic bone disease (particularly with breast cancer, prostate cancer and multiple myeloma). These drugs are usually delivered as regular high dose intravenous infusions in this patient group.

Bisphosphonates are also indicated in tx of osteoporosis and other less common disorders such as Paget’s disease, osteogenesis imperfecta and fibrous dysplasia. They are additionally used as prophylaxis to counteract the osteoporotic effects of glucocorticoids and to prevent bone related/skeletal complications in pts with primary hyperparathyroidism and cystic fibrosis. Patients in these groups can take the drugs orally (usually once a week) or the drugs can be given as quarterly or yearly infusions.

206
Q

Who are IV bisphosphates usually given to and why?

A
  • Bisphosphonates are used to reduce the symptoms and complications of metastatic bone disease (particularly that associated with breast cancer, prostate cancer and multiple myeloma). These drugs are usually delivered as regular high dose intravenous infusions in this patient group.
207
Q

In what patient groups can oral bisphosphonates be given to?

A
  • Osteoporosis
  • Paget’s disease
  • Osteogenesis imperfecta
  • Fibrous dysplasia
  • Prophylaxis to counteract the osteoporotic effects of glucocorticoids
  • Prevent bone-related/skeletal complications in pts with primary hyperparathyroidism and cystic fibrosis.
208
Q

What is denosumab and how does it work?

A

> Denosumab is a fully human monoclonal antibody which inhibits osteoclast function and associated bone resorption by binding to the receptor activator factor KB ligand (RANKL).

> It is indicated for the prophylaxis and tx of osteoporosis and to reduce skeletal-related events relating to metastasis.

> it is administered subcutaneously every 6 months in osteoporosis pts, with a higher dose given monthly in pts with metastatic disease.

Denosumab does not bind to bone and its effects on bone turnover diminish within nine months of treatment completion

209
Q

How do anti-angiogenic drugs work?

A

They target the processes by which new blood vessels are formed and are used in cancer treatment to restrict tumour vascularisation.

210
Q

Can anti-angiogenic drugs be used in combination with bisphosphonates?

A

Anti-angiogenic drugs can be used in combination with bisphosphonates in the management of cancer and there is some evidence that this results in greater MRONJ risk. This may also be true where anti-angiogenic drugs are used in patients with a previous history of bisphosphonate use.

211
Q

Can MRONJ affect implants already implanted?

A

Pts with dental implants placed prior to commencement with anti-resorptive or anti-angiogenic drugs have a small risk of spontaneous MRONJ at those sites.

Minimise risk with excellent OH at implant sites.

212
Q

Can osteoporosis pts have implants?

A

Osteoporosis pts considering dental implants during or after tx with anti-resorptive rugs are at risk of compromised bone healing and MRONJ following the procedure and have an additional small risk of long-term implant failure.

213
Q

Do drug holidays help to avoid MRONJ?

A

No evidence as drugs may persist in skeletal tissue for ears.

However, an acceptable Mx option for pt with osteoporosis who are being treated with six monthly subcutaneous injections of denosumab is to delay any non-urgent invasive dental tx in an asymptomatic tooth until month prior to pts next scheduled drug administration.
Resumption of denosumab tx following invasive dental procedure should be delayed until soft tissues/extraction socket have healed.

Liaise with medical practitioners.

214
Q

Which patients are placed in the low MRONJ risk category? (2)

A
  1. Pts treated for osteoporosis or other non-malignant disease of bone (e.g. patets) with oral or IV bisphosphonates for less than 5 years who are not taking concurrent systemic glucocorticoids.
  2. Pts being treated for osteoporosis or other non-malignant diseases of bone with denosumab who are not being treated with systemic glucocorticoids.
215
Q

Which pts are in high MRONJ risk category?

A
  1. Pts with a previous diagnosis of MRONJ
  2. Pts being treated with anti-resorptive or anti-angiogenic drugs (or both) as part of the management of cancer.
  3. Pts treated for osteoporosis or other non-malignant diseases of bone (e.g. paget’s disease) with oral bisphosphonates or quarterly or yearly infusions of IV bisphosphonates for more than 5 years.
  4. Pts treated for osteoporosis or other non-malignant diseases of bone with bisphosphonates or denosumab for any length of time who are being concurrently treated with systemic glucocorticoids.
216
Q

How do you classify people into MRONJ risk who have stopped bisphosphonate tx or denosumab tx?

A

Pts who have taken bisphosphonate drugs at any time in the past and those who have taken denosumab in the last nine months are allocated to a risk group as if they are still taking the drug.

217
Q

The reported MRONJ incidence varies widely across studies depending on factors including:

A
  • Condition being treated
  • Drug type/combinations
  • Duration of treatment
  • Dental treatment and other risk factors
218
Q

What are the current estimates of MRONJ incidence?

A
  1. <5% for cancer patients (taking antiresorptive drugs (bisphosphonates or denosumab).
  2. <0.05% for pts with osteoporosis

Variation btw studies makes it difficult to determine accurate estimates.

219
Q

Name examples of bisphosphonates:

A

Alendronic acid
Risedronate sodium
Zolendronic acid
Ibandronic acid
Pamidronate sodium
Sodium clodronate

220
Q

Name a RANKL inhibitor

A

Denosumab

221
Q

NAme 3 anti-antiogenic drugs:

A
  1. Bevacizumab
  2. Sunitinib
  3. Afibercept
222
Q

What are other drugs with possible association with MRONJ:

A
  • protein kinase inhibitors: axitinib, cabozantinib, dasatinib, everolimus, imatinib, osimertinib, pazopanib, regorafenib, sorafenib, temsirolimus;
  • monoclonal antibodies*: adalimumab, infliximab, ipilimumab, nivolumab, ranibizumab, rituximab, romosozumab, tocilizumab;
  • antimetabolites: azacitidine, methotrexate;
  • tumour necrosis factor alpha inhibitor: etanercept.
223
Q

What should happen before commencement of anti-resorptive or anti-angiogenic drug therapy, or as soon as possible thereafter?

A

Aim to get the patient as dentally fit as feasible, prioritising preventive care.

  • Higher risk cancer patients should preferable undergo a thorough dental assessment, with remedial dental tx where required, prior to commencement of drug therapy.
224
Q

What are symptoms of MRONJ?

A

Exposed bone
Loose teeth
Non-healing sores or lesions
Pus or discharge
Tingling, numbness or altered sensations
Pain
Swelling

225
Q

Should you prescribe Abs or antiseptic prophylaxis following XLAs to reduce MRONJ risk?

A

NO!

Do not prescribe antibiotic or antiseptic prophylaxis following extractions or other bone-impacting treatments specifically to reduce the risk of MRONJ.

226
Q

Should you carry out extractions in low risk MRONJ pts?

A

Perform straightforward extractions and procedures that may impact on bone in primary care.

Do not prescribe antibiotic or antiseptic prophylaxis unless required for another clinical reason.

227
Q

Should you do extractions in higher risk of MRONJ pts?

A
  • Explore all possible alternatives to extraction where teeth could potentially be retained e.g. retaining roots in absence of infection.
  • If extraction remains the most appropriate tx, proceed as for lower risk pts.
228
Q

When should you review a pts for MRONJ?

A

8 weeks.

Review healing. If the extraction socket is not healed at 8 weeks and you suspect that the patient has MRONJ, refer to an oral surgery/special care dentistry specialist as per local protocols.

229
Q

What are the benefits of anti-resorptive and/or anti-angiogenic drugs and why is it important that they continue to take these drugs?

A
  • Anti-resorptive drugs significantly reduce the risk of fractures, and subsequent chronic pain,, in pts being treated for osteoporosis.
  • Anti-angiogenic drugs restrict the growth of a tumour blood vessels and are an important part of some cancer treatments. Anti-resorptive drugs reduce bone pain and the risk of fractures in pts being treated for cancer.
  • Drug holidays to avoid the risk of MRONJ associated with dental care are not recommended because the benefits of taking the drugs to manage the pt’s medical condition are likely to outweight the small risk of developing MRONJ, and, in case of the bisphosphate or denosumab, stopping the drug does not eliminate the risk of developing MRONJ.
230
Q

What is the clotting process?

A
  1. Blood clotting is triggered naturally in response to damage to blood vessels from injury or invasive procedures.
  2. Platelets within the blood become activated locally, resulting in an increased tendency to adhere to each other and to damaged blood vessel endothelium (primary haemostasis)
  3. At the same time a cascade of reactions is initiated converting inactive coagulation factors to their active form, ultimately leading the toe production of protein fibres.
  4. Fibrin stabilises the platelet plug by crosslinking the platelets to each other and to the damaged blood vessel wall to prevent further blood loss (secondary haemostasis).
231
Q

What is the action of antiplatelet drugs?

A

They interfere with platelet aggregation by reversibly or irreversibly inhibiting various steps in the platelet activation required for primary haemostasis.

232
Q

What is the action of anticoagulation drugs?

A

They inhibit the production or activity of factors that are required for the coagulation cascade and in this way impair secondary haemostasis by inhibiting fibrin production.

233
Q

Why are anticoagulants and antiplatelets prescribed?

A

Certain medical conditions can predispose individuals to risk of thrombosis, where a blood clot (thrombus) block a blood vessel, at either the site of formation of after travelling to another critical site (thromboembolism), with potentially catastrophic consequences such as heart attack, pulmonary embolism or stroke.

Anticoags and antiplatelet drugs are prescribed to reduce the risk of such an event in:
> pts with vascular, thromboembolic or cardiac conditions.
> In pts with a history or stroke
> Following surgical procedures such as heart valve replacements, cardiac stents and joint replacements.

234
Q

NAme 4 DOACs:

A

Apixaban
Dabigatran
Rivaroxaban
Edoxaban

235
Q

Name 3 vitamin K antagnosits:

A

Warfarin
Phenindione
Acenocoumarol

236
Q

Name 3 injectable anticoagulants:

A

Dalteparin
Enoxaparin
Tinzaparin

237
Q

What 5 antiplatelet drugs.

A
  1. Aspirin
  2. Clopidogrel
  3. Dipyridamole
  4. Prasugrel
  5. Ticagrelor
238
Q

Stroke or TIA: anticoagulant/antiplatelet therapy?

A

Single or dual antiplatelets (often clopidogrel)

Lifelong

NB. Occasionally warfarin

239
Q

Stroke prevention in pt with AF: anticoagulant/antiplatelet therapy?

A

DOAC

Lifelong

Occasionally warfarin, rarely single or dual antiplatelets

240
Q

Thromboembolic disease e.g. DVT or PE: anticoagulant/antiplatelet therapy?

A

DOAC, warfarin or injectable anticoagulant

Tx usually 6 weeks to 6 months.
Prophylaxis can be lifelong.

NB: can be lifelong if there is recurrence or an ongoing untreatable risk factors (e.g. malignancy)

241
Q

Recent significant surgery: anticoagulant/antiplatelet therapy?

A

Injectable anticoagulant, or DOAC with or without aspirin

Usually 2-6 weeks

242
Q

Any heart surgery, but especially prosthetic replacement heart valve: anticoagulant/antiplatelet therapy?

A

Warfarin (or other VKA) or single antiplatelet

Long term

NB: occasionally a DOAC.

243
Q

Coronary heart disease (stable/unstable angina, Heart attack - STEM/STEMI): anticoagulant/antiplatelet therapy?

A

Usually single antiplatelet.

Dual antiplatelet for 6-12 months following angioplasty or stent insertion or MI

DOAc with single or dual antiplatelet if recent MI or AF.

Dual therapy for up to 12 months, single therapy with aspirin or clopidogrel therafter.

244
Q

Coronary stent: anticoagulant/antiplatelet therapy?

A

Single or dual antiplatelets

Dual therapy for up to 12 months, monotherapy lifelong

245
Q

Kidney failure requiring dialysis: anticoagulant/antiplatelet therapy?

A

Heparin or injectable anticoagulant

On day of dialysis

246
Q

Pregnancy with associated risk factors for venous thromboembolism (VTE): anticoagulant/antiplatelet therapy?

A

Aspirin (or injectable anticoag in some high-risk cases)

Until delivery (or 6 weeks after for LMWH).

NB: risks include obesity

247
Q

Treatment of DVT in pregnancy: anticoagulant/antiplatelet therapy?

A

Injectable anticoagulant

Until at least 6 weeks after delivery (or until at least 3 months of treatment in total)

248
Q

Peripheral Vascular Disease (PVD)/Peripheral Arterial Disease: anticoagulant/antiplatelet therapy?

A

Single or dual antiplatelets, DOAC with aspirin

Lifelong

249
Q

What medical conditions are associated with increased bleeding risk? (8)

A
  1. Chronic renal failure
  2. Liver disease (e.g. caused by alcohol dependence, chronic viral hepatitis, autoimmune hepatitis, primary biliary cholongitis)
  3. Haematological malignancy or myelodysplastic disorder
  4. Recent or current chemotherapy or radiotherapy
  5. Advanced heart failure
  6. Inherited coagulation disorders including all types of haemophilia and von Willebrand’s disease
  7. Acquired or inherited platelet disorders including immune thrombocytopenia (ITP)
  8. Connective tissue disorders including Ehlers Danlos Syndrome (EDS)
250
Q

How does chronic renal failure increase bleeding risk?

A

Associated with platelet dysfunction.

251
Q

How does liver disease increase bleeding risk?

A
  1. Reduced production of coagulation factors.
  2. Reduction in platelet number and function due to splenomegaly.
  3. Alcohol excess can also result in direct bone marrow toxicity and reduced platelet number.
252
Q

How can haematological malignancy or myelodysplastic disorder increase bleeding risk?

A

Impaired coagulation or platelet function (even in remission)

253
Q

How does recent or current chemotherapy or radiotherapy increase bleeding risk?

A

Pancytopenia including reduced platelet numbers.

254
Q

How does advanced heart failure increase bleeding risk?

A

Results in liver failure.

(1. reduced production of coagulation factors. 2. reduction in platelet number and function due to splenomegaly. 3. alcohol can cause direct bone marrow toxicity and reduced platelet numbers)

255
Q

How can inherited coagulation disorders e.g. haemophilia or von/Willebrand’s disease) increase bleeding risk?

A

Defective or reduced levels of coagulation factors.

256
Q

How can acquired or inherited platelet disorders including immune thrombocytopenia (ITP) increase bleeding risk?

A

Reduce platelet numbers or abnormal platelet function

257
Q

How can connective tissue disorders including Ehlers Danlos Syndrome increase bleeding risk?

A

Vascular fragility (particularly in the vascular subtype) and platelet function abnormalities in some patient.

258
Q

What timeframes of chemo and radiotherapy increase bleeding risk?

A

Having received chemotherapy less than 3 months ago, or total body irradiation less than 6 months ago.

259
Q

What drugs groups can exacerbate bleeding risk?

A
  1. Anticoagulants or antiplatelet drugs
  2. Cytotoxic drugs or drugs associated with bone marrow suppression
    > e.g. leflunamide, hydroxychloroquine, sulfasalazine, penicillamine, gold, methotrexate, azathioprine, mycophenolate mofetil.
  3. Biological immunosuppression therapies
    > infliximab, adalimumab, etanercept tocilizumab, certolizumab, abatacept, anakinra
  4. Non-steroidal anti-inflammatory drugs (NSAIDs)
    > aspirin, ibuprofen, diclofenac and naproxen
  5. Drugs affecting the nervous system
    -> Selective serotonin reuptake inhibitors (SSRIs)
    -> Serotonin and noradrenaline reuptake inhibitors (SNRIs)
    -> Carbamazepine
260
Q

How cytotoxic drugs or drugs associated with bone marrow suppression effect bleeding risk?

A

These can reduce platelet numbers and/or impair liver function affecting production of coagulation factors.

261
Q

How can biologic immunosuppression therapies exacerbate bleeding risk?

A

These can cause thrombocytopenia and/or impair liver function.

262
Q

How can NSAIDs effect bleeding risk?

A

Impair platelet function to various extents.

263
Q

How can drugs affecting the nervous system exacerbate bleeding risk?

A

SSRIs and SNRIs have the potential to impair platelet aggregation and, although unlikely to be clinically significant in isolation, may in combination with other antiplatelet drugs, increase the bleeding time.

Carbamazepine can affect both liver function and bone marrow production of platelets. Patients most at risk are those recently started on this medication or following dose adjustments.

264
Q

How does warfarin work?

A

Vitamin K antagonist.

It inhibits vitamin k-dependent modification of prothrombin and other coagulation factors, which is required for their normal function.

265
Q

What are the limitations of warfarin?

A

A narrow therapeutic range

Sensitivity to diet and drug interactions

The requirement for frequent monitoring and dose adjustment

266
Q

How do DOACs work (the different types)?

A
  1. Dabigatran (direct inhibitor of coagulation factor thrombin).
  2. Apixaban (factor Xa inhibitor)
  3. Rivaroxaban (factors Xa inhibitor)
  4. Edoxaban (factors Xa inhibitor)

These drugs produce a more predictable level of anticoagulation than warfarin and do not require the same degree of monitoring, are easier to manage and are potentially more effective and safer.

267
Q

What are the reversal agents for DOACs?

A

Idarucizumab for dabigatran
Andexanet alfa for apixaban and rivaroxaban

268
Q

how are injectable anticoagulants administered?

A

Heparin, Low molecular weight heparin (LMWH), dalteparin, enoxaparin and tinzaparin, are administered intravenously or by subcutaneous infection.

269
Q

What is general advise for all pts taking anticoagulants and antiplatelet drugs requiring dental tx likely to cause bleeding?

A
  • Plan tx for early in day and week to allow for management of prolonged bleeding or rebleeding episodes, should they occur.
  • Provide pre-tx instructions (e.g. INR testing or modifications of meds schedule)
  • Treat as atraumatically as possible, use appropriate local haemostatic measures and only discharge the pt once haemostasis has been achieved.
  • Advise pt to take paracetamol, unless contraindicated, for pain relief rather than NSAIDs such as ibuprofen, aspirin, diclofenac, or naproxen.
  • If travel time to emergency care is a concern, place particular emphasis on use of measure to avoid complications
  • Provide pt with written post-tx advise and emergency contact details.
  • if pts is on time-limited courses, delay, non-urgent, invasive dental procedures where possible until meds have been discontinued.
  • if pt has another relevant medical condition(s) or is taking other meds that may increase bleeding risk, consult with pts prescribing clinician.
270
Q

What 4 things can be done for all bleeding risk pts?

A
  1. Treat early in the day + week –> to allow time for management of prolonged bleeding or rebleeding episodes, should they occur.
  2. Limit initial treatment area and assess bleeding before continuing.
  3. Consider staging extensive or complex procedures
  4. Strongly consider packing and suturing.
271
Q

In which pts would you not interrupt anticoagulant or antiplatelet therapy, except under direct written instructions from the pt’s cardiologist?

A
  1. pts with prosthetic metal heart valves, or coronary stents.
  2. Pts who have had a pulmonary embolism or deep vein thrombosis in the last three months..
  3. Pts on anticoagulant therapy for carioversion
272
Q

Which dental procedures are unlikely to cause bleeding?

A
  1. LA by infil, intralig or mental nerve block.
  2. LA by IANB, or other regional nerve blocks
  3. BPE
  4. Supra scale
  5. Direct or indirect restorations with supragingival margins
  6. Endodontics
  7. Impressions
  8. Fitting and adjustment of orthodontic appliances
273
Q

What dental procedures that are likely to cause bleeding have lower risk of post-operative bleeding complications:

A
  • Simple extractions (1-3 teeth with restricted wound size)
  • Incision and drainage of intra-oral swellings
  • 6PPC
  • Root surface debridement (RSD)
  • Direct or indirect restorations with subgingival margins
274
Q

What dental procedures that are likely to cause bleeding have higher risk of post-operative bleeding complications:

A

Complex extractions, adjacent extractions that will cause a large wound or more than three extractions at once.

Flap raising procedures:
- elective surgical extractions
- periodontal surgery
- preprosthetic surgery
- periradicular surgery
- crown lengthening
- dental implant surgery

Gingival recontouring

Biopsies

275
Q

DOACs: What do you do for low bleeding risk dental procedures?

A

Treat without interrupting medication.

Treat early in the day; limit initial treatment area and assess bleeding before continuing; stage extensive of complex procedures; strongly consider suturing and packing.

276
Q

DOACs: What do you do for HIGH bleeding risk dental procedures?

A

Advise pt to miss or delay morning dose before treatment
- apixaban or dabigatran
> take 2x/day
–> miss morning dose
–> usual time in evening

  • rivaroxaban or edoxaban
    > once a day, morning or evening
    –> if take morning dose, delay morning dose and take 4 hours after haemostasis has been achieved.
    –> if take evening dose, take at usual time in evening.

Treat early in the day; limit initial treatment area and assess bleeding before continuing; stage extensive or complex procedures; strongly consider packing and suturing.

  • advise pts when to restart their meds.
277
Q

Which 2 DOACs do pts take 2 times a day? What are the implications for high bleeding risk procedures?

A
  1. Apixaban
  2. Dabigatran
  • miss morning dose and take evening dose at usual time.
278
Q

Which 2 DOACs do you take once a day? What are the implications for high bleeding risk procedures?

A
  1. Edoxaban
  2. Rivaroxaban
  • if take morning dose. Miss the morning dose and take 4 hours after haemostasis has been achieved.
  • if take evening dose, just take the evening dose at the usual time.
279
Q

What do you need to do for Vitamin K antagonists before an extraction?

A

Check the INR, ideally no more than 24 hours before procedure (up to 72 hours if the patient is stably anticoaglated)
((–> A stable pt does not require weekly monitoring and who has not had any IRN measures >4 in the last 2 months. ))

280
Q

What should you do if an INR reading is below 4 before an Extn?

A
  • Treat without interrupting medication
  • Treat early in the day; limit initial treatment area and check bleeding before continuing; consider staging complex or extensive procedures; strongly consider packing and suturing.
281
Q

What should you do if an INR is 4 or above before an extraction?

A

Delay invasive treatment or refer if urgent.

282
Q

What do you do for prophylactic (low) doses of injectable anticoagulants (dalteparin, enoxaparin or tinzaparin) for XLAs?

A

Treat without interrupting medications.

  • Treat early in the day; limit initial treatment area and check bleeding before continuing; consider staging complex or extensive procedures; strongly consider packing and suturing.
283
Q

What do you do for treatment (higher) doses or uncertainty about the dose of injectable anticoagulants (dalteparin, enoxaparin or tinzaparin) for XLAs?

A

Consult with prescribing clinician for more information.

284
Q

How do you treat a pt for XLA on aspirin alone? (antiplatelet drug)

A

Treat without interrupting medication.

Treat early in the day; limit initial treatment area and check bleeding before continuing; consider staging complex or extensive procedures; use local haemostatic measures: packing and suturing.

285
Q

How do you treat a pt taking clopidogrel, dipyridamole, prasugrel or ticagrelor single or dual therapy (in combination with aspirin) - antiplatelets

A

Treat without interrupting medication

Expect prolonged bleeding. limit initial treatment area and consider staging extensive or complex procedures; strongly consider suturing and packing.

286
Q

What should you do if a patient is taking an anticoagulant/antiplatelet combination?

A

Consult with the patient’s prescribing clinician in order to assess the likely impact of the particular drug combination and the patient’s medical condition on their bleeding risk.

287
Q

What haemostatic measures should a dental practitioner have available?

A
  1. Absorbant gauze
  2. Haemostatic packing material (e.g. oxidised cellulose, collagen spone)
  3. Suture kit (needle holder, tissue forceps, suture material, scissors)
288
Q

What is tranexamic acid and is it used?

A

While there is evidence that tranexamic acid reduces the bleeding risk from dental treatment in patients on antithrombotic therapies when compared to placebo, it may not have significant benefit when compared to other haemostatic measures.

It is not included in the list of dental preparations in the BNF, can’t be prescribed by NHS.

This guidance does not advise primary care practitioners to prescribe transexamic acid for dental procedures.

289
Q

What increases the anticoagulant effect of DOACs?

A

NSAIDs - ibuprofen, aspirin, diclofenac, naproxen

Macrolide antibiotics: Clarithromycin, erythromycin, azithromycin

290
Q

What decreases the anticoagulant affect of DOACs?

A

Carbamazepine

291
Q

What increases the anticoagulant effect of vitamin K antagonists (warfarin)?

A
  1. metronidazole
  2. any other abx, including:
    - penicillins (phenoxymethylpenicillin, amoxicillin, co-amoxiclav)
    - macrolides (clarithromycin, erythromycin, azithromycin)
    - clindamycin
    - tetracylines
  3. NSAIDs (aspirin, ibuprofen, diclofenac)
  4. Miconazole, fluconazole - azole antifungals
292
Q

What decreases the anticoagulant effect of vitamin K antagonists (warfarin)?

A

Carbamazepine

293
Q

What increases the antiplatelet effect of aspirin?

A

NSAIDs, ibuprofen, diclofenac.

(may increase bleeding risk although note that the antiplatelet affect of aspirin may be reduced by ibuprofen if used regularly)

294
Q

What increases the antiplatelet affect of clopidgrel?

A
  • NSAIDs: aspirin, ibuprofen, diclofenac
295
Q

What decreases the antiplatelet affect of clopidgrel?

A
  • Erythromycin
  • Fluconazole
  • Omeprazole
296
Q

What increases the antiplatelet affect of dipyridamole?

A

Aspirin

297
Q

What increases the antiplatelet effect of prasugrel?

A
  • NSAIDs: aspirin, ibuprofen, diclofenac
298
Q

What increases the antiplatelet effect of ticagrelor?

A

NSAIDs: aspirin, ibuprofen, diclofenac

Clarithromycin, azithromycin

299
Q

What decreases the antiplatelet effect of ticagrelor?

A

Carbamazepine

300
Q

What increases the anticoagulant effect of injectable anticoagulants?

A

NSAIDs: aspirin, ibuprofen, diclofenac

301
Q

What is the definition of a haemorrhage?

A

The escape of blood from any part of the vascular system, either external or internal

302
Q

What are clinical signs of blood loss?

A
  • Increased heart rate
  • Decreased blood pressure
  • Cold pale extremities
303
Q

How can you classify haemorrhage?

A

immediate (primary)

Reactionary (<48 hours)

Delayed (secondary), 7-10 days

Post-op, indicative of infection.

304
Q

What is the sequence normal haemostasis?

A

Vasoconstriction –> platelet aggregation –> fibrin formation

  1. Vasoconstriction
    a. limits the amount of blood
  2. Platelet aggregation
    a. recruit further platelets to form a plug (primary haemostasis)
  3. Clotting cascade
    a. works via activation of clotting factors made by the liver due to proteolysis
    b. both an extrinsic (exposed tissue factor) and intrinsic (platelets) pathway
    c. intrinsic pathway works by clotting factors produced in the liver (XIII, IX, XI)
    d. activation of prothrombin –> thrombin
    e. activation of fibrinogen –> fibrin which causes a stable clot.
305
Q

how do you manage a haemorrhage?

A

Rinse the mouth with warm water to remove excess blood.
Place a rolled-up piece of cotton or gauze swab with saline and apply pressure for 20 mins
Avoid alcohol, smoking or exercise for 24 hours of XLA to avoid disturbing blood clot.
If bleeding will not cease
> apply surgicel dressing (oxidised cellulose)
> suture the wound to achieve soft tissue closure and stabilise socket edges.

306
Q

What are developmental causes of haemorrhage?

A
  1. haemophilia, A, B or C
  2. von willebrand disease
  3. hereditary haemorrhagic telangiectasia
  4. haemangioma
307
Q

What are traumatic causes of haemorrhage?

A
  1. Crush wounds
  2. Penetration injuries
  3. Fractured bones that sever vessels.
308
Q

What can disrupt the clotting cascade?

A
  1. Warfarin, effects clotting factors, II, VII, XI and X
  2. Heparin, effects anti-thrombin activity.
  3. Liver disease, effecting vitamin K
  4. Inherited conditions affecting clotting cascade - haemophilia, Von Willebrand.
309
Q

What platelet problems can increase haemorrhage risk?

A

Thrombocytopenia
Aspirin (thrombocytopathy)

310
Q

What can cause vessel wall injury that increases haemorrhage risk?

A
  1. Scurvy due to lack of vitamin C
  2. hereditary, haemorrhagic telangiectasia
  3. haemangioma (Sturge Weber syndrome)
  4. Ehler Danlos syndrome affective connective tissue
  5. Anaphylactoid purpura.
311
Q

How does heparin work?

A

It inhibits activation of factor X, inhibiting prothrombin –> thrombin.

Used for DVT prophylaxis post-op as short acting.

312
Q

How do antiplatelets work?

A

Decrease platelet aggregation and inhibit thrombus formation in artery.

used in management of stroke, IHD and intracerebral haemorrhage.

313
Q

What does a full blood count measure?

A
  • Levels of platelets
  • Haemoglobin
  • Haematocrit
  • Baseline rpt at 24 hours
314
Q

How can you treat local haemorrhage?

A
  • Identify site of haemorrhage
  • Apply pressure and elevate area, act fast
  • Application of LA as adrenaline is vasoconstrictor
  • Pack with surgicel and apply gauze
  • Suture and ligate the vessels
  • Diathermy to area if possible.
315
Q

How can you treat systemic haemorrhages?

A
  • Monitor vital signs
  • Consider fluid replacement
  • Consider analgesia
  • Consider therapeutics: FFb, clotting factors, tranexamic acid, desmopressin and vit K)
  • Consider antibiotics
316
Q

What are the complications of haemorrhage?

A
  • Hypovolaemic shock
  • Fluid replacement: haemodilution, fluid overload, renal failure or dehydration if inadequate.
  • Blood transfusion
  • Retro maxillary haemorrhage can cause airway obstruction
  • Retrobulbar haemorrhage can cause blindness.
317
Q

Should you do IDN blocks in haemophilia patients?

A

No, it is contra indicated due to potential haematoma causing an obstructed airway, instead use infiltration and intraligarmentary techniques.

318
Q

What is the normal range for an adult platelet count?

A

150-400 x 10^9 / ltr

319
Q

What is infective endocarditis?

A

IE is a rare condition with significant morbidity and mortality. It may arise after bacteraemia in a person with a predisposing cardiac condition.

It is an infection of the lining of the heart, often involving the heart valves, caused mainly by bacteria which enter the blood from outside the body.

320
Q

What do the 2016 NICE guidelines say about Abx prophylaxis for IE risk pts?

A

Antibiotic prophylaxis is NOT recommended routinely for people undergoing dental procedures.

321
Q

What adults and children with structural cardiac defects are at risk of developing infective endocarditis?

A
  1. Acquired valvular heart disease with stenosis or regurgitation
  2. Hypertrophic cardiomyopathy
  3. Previous infective endocarditis
  4. Structure congenital heart disease, including surgically corrected or palliated structural conditional, but excluding isolated atrial septal defect, fully repaired ventricular septal defect or fully replaced patent ductus arteriosus, and closure devices that are judged to be endothelisalised.
  5. Valve replacement.
322
Q

Which categories include a sub-group of pts who will require special consideration in IE Abx prophylaxis?

A
  1. Previous infective endocarditis
  2. Structural congenital heart disease
  3. Valve replacement
323
Q

What patient advise should be given to pts with IE risk?

A
  1. benefits and risks of antibiotic prophylaxis, and an explanation of why antibiotic prophylaxis is no longer routinely recommended.
  2. The importance of maintaining good oral health
  3. Symptoms that may indicate infective endocarditis and when to seek expert advise
  4. The risks of undergoing invasive procedures, including non-medical procedures such as body piercing or tattooing.
324
Q

Is prophylaxis against infective endocarditis recommended?

A

Antibiotic prophylaxis against infective endocarditis is not recommended routinely:
> for people undergoing dental procedures.

Chlorhexidine mouthwash should not be offered as prophylaxis against infective endocarditis to people at risk of IE undergoing dental procedures.

325
Q

What should you if a pt at IE risk has an infection?

A
  • Any episodes of infection in people at risk of IE should be investigated and treated promptly to reduce the risk of endocarditis developing.
  • If a person at risk of IE is receiving antimicrobial therapy because they are undergoing a GI or genitourinary procedure at a site where there is a suspected infection, the person should receive antibiotics that covers organisms that causes infective endocarditis.
326
Q

What sub-group of IE risk pts require special consideration?

A
  • Prosthetic valve, including trascatheter valves, or where any prosthetic material was used for valve repair.
  • Previous infective endocarditis
  • Congenital heart disease (CHD):
    > any type of cyanotic CHD
    > any type of CHD repaired with a prosthetic material, whether placed surgically or by percutaneous techniques, up to 6 months after the procedure or lifeling if residual shunt or valvular regurgitation remains.
327
Q

What should you do for all patients at increased risk of IE?

A

Assess whether the patient should be considered for routine or non-routine management based on their specific cardiac condition.

  • pts who have a cardiac condition from the special consideration subgroup may require non-routine management. These special consideration pts should be assess in consultation with their cardiology consultant, cardiac surgeon or local cardiology centre.

–> routine management, where invasive dental treatment is provided without antibiotic prophylaxis, will be appropriate for the vast majority of pts at increased risk of IE.

328
Q

What is the definition of invasive dental procedures?

A

Invasive procedures are those that involve manipulation of dento-gingival junction, periapical regions or perforation of the oral mucosa (excluding local anaesthetic injections in non-infected soft tissues).

e.g. placement of matrix bands
- subgingival restorations, including fixed pros
- endo tx before apical stop has been establised
- PMCs
- Full periodontal exams
- RSD/sub PMPR
- Incision and drainage of abscess
- Dental extractions
- Surgery involving elevation of muco-periosteal flap or muco-gingival area
- Placement of dental implants including temporary anchroage devices, mini-impants
- Uncovering implant sub-structures.

329
Q

Is antibiotic prophylaxis recommended following exfoliation of primary teeth or trauma to the lips or oral mucosa?

A

NO

330
Q

How do you treat emergency pts that are IE risk?

A

Ensure that any episode of dental infection in pts at incr risk or IE are investigated and treated promptly to reduce the risk of IE developing.

  • where tx of dental emergency is beyond your competency, seek advise from an appropriate expert based on your clinical judgement and the individual circumstances.

If a pt with a cardiac condition who is not registered with the practice presents with a dental emergency, consider seeking advise on the appropriateness of antibiotic prophylaxis from your local cardiology centre.
- Where it has not been possible to obtain advice from pt’s cardiology consultant, cardiac surgeon or local cardiology centre, it may be necessary to make a shared decision on antibiotic prophylaxis, based on a discussion with the patient regarding their values and preferences.

331
Q

prescribing advice to give to pts with IE risk?

A
  • Treatment with beta-lactam antibiotics, such as amoxicillin, can result in hypersensitivity reactions.
    –> reports of anaphylactic reactions to amoxicillin prophylaxis are extremely rare.
    –> however, pts with a history of penicillin allergy are at increased risk of immediate hypersensitivity and amoxicillin prophylaxis should not be prescribed for this pts.
  • The use of broad spectrum Abx, such as amoxicillin or clindamycin, is associated with the rise in Clostridium difficile-associated disease observed in both primary and secondary cares.
332
Q

When should you prescribe the Abx for antibiotic prophylaxis in pts in IE risk that need Abx prophylaxis?

A

Provide the pt with a prescription for Abx prophylaxis at the appointment prior to the planned procedure unless you hold a supply of Abx in your practice.

  • Consult pt cardiologist, cardiac surgeon or local cardiology centre. They may suggest a regimen.
333
Q

What advise on adverse effects should be given to pts taking Abx prophylaxis for IE risk?

A

Give advice on possible adverse events such as hypersensitivity, anaphylaxis and antibiotic-related colitis. It may also be helpful to discuss the issues surrounding antibiotic resistance with the patient.

Ensure that patients prescribed an antibiotic are aware that they should seek urgent medical attention if they develop colitis (diarrhoea, which can be severe).

334
Q

When should antibiotics for IE Abx prophylaxis be taken?

A

Arrange for the Abx to be taken in practice 60 mins before the planned procedure is due to commence.

  • Advise pt to bring the abx with them to the dental practice on the day of the procedure and ensure that the patient remains in the practice in the interval between taking the antibiotic and the start of treatment.

-Alternatively, if the pt expresses a preference to take the Abx at home or at another location outside the practice, and has not previously had an adverse reaction to prophylaxis, it is acceptable to agree this.

335
Q

What Abx prophylaxis would you presribe a IE who has recieved a course of Abx for medical or dental infection in the preceding six weeks?

A

Select a drug from a different antibiotic class for the prophylaxis prescription.

If the following amoxicillin or clindamycin regimens are unsuitable, contact an expert, such as a consultant microbiologist or community pharmacist, for advise on an alternative drug regimen.

336
Q

A. If Abx prophylaxis is required, what is an appropriate oral regimen?

B. What if pt is allergic to penicillin?

C. What if pt is allergic to penicillin and unable to swallow capsules?

D. Pt who require intravenous prophylaxis?

E. Pt who require IV prophylaxis but allergic to penicillin?

A

A. Amoxicillin, 3g oral powder sachet.
- give 3g (1 sachet) 60 minutes before procedure.

B. Clindamycin capsules, 300mg.
- 600mg (2 capsules) 60 minutes before procedure.

C. Azithromycin oral suspension 200mg/5ml
- 500mg (12.5ml) 60 minutes before procedure.

D. Amoxicillin
- 1g i.v. just before procedure or at induction of anaesthetic

E. Clindamycin
- 300mg i.v. just before the procedure or at induction of anaesthesia.

337
Q

What is the risk of infective endocarditis?

A

It is a very rare but serious condition. The risk of infective endocarditis in the general population is less than 1 case per 10,000 people per year. However, their cardiac condition puts them at increased risk of developing infective endocarditis.

Invasive dental procedure, such as an extraction, may increase the chances of bacteria entering the blood stream.

Everyday activities, such as toothbrushing, flossing and chewing can also cause transient bacteraemia and stress importance of good OH to reduce the risk from oral bacteria.

338
Q

What are symptoms of infective endocarditis and what should a pt do if they experience them?

A

Contact their GMP ASAP if they notice any of the following symptoms, particularly if they occur together as a flu-like illness:

  • high temperature (fever) of 38 or above
  • sweats or chills, especially at night
  • breathlessness, especially during physical activity
  • weight loss
  • tiredness (fatigue)
  • muscle, joint or back pain (unrelated to recent physical activity)

> Emphasise that these symptoms are more likely to be caused by a less serious type of infection but should be investigated.
Ensure that the pt known to tell any medical professional they seek advise from about any recent invasive dental treatment they may have had.

339
Q

What are indication of surgical endodontics?

A
  • Presence of peri-radicular disease
  • Non-surgical RCT has failed
  • Re-RCT cannot be undertaken
  • Trauma
  • Perforations and fractured instruments
  • Developmental anomalies prevent non-surgical RCT.
340
Q

What are contraindications to surgical endodontics?

A
  • Patient specific factors
  • Anatomical factors, such as lack of access, associated nerves and structures
  • Periodontal disease
  • Operator skill
341
Q

What are the three most common flap designs for endo surgery?

A
  1. Semilunar flap: full thickness flap in alveolar mucosa at level of tooth apex.
    > Seldom used due to poor access and scarring
    > Haemostasis often an issue
    > No involvement of margin and interdental gingiva
  2. Leubke-Ochsenbein flap (sub marginal)
    > Scalloped horizontal incision in attached gingiva and two vertical relieving incisions.
    > Adequate attached gingiva present (3-5mm)
    > Best for epithelial wound closre
    > However unable to extend flap if needed and rarely indicated in the mandible.
    > Disruption of blood supply to marginal tissues
  3. Muco-periosteal flap: two vertical relieving incisions
    > Horizontal intrasulcular incision
    > Enhanced surgical access, visibility and wound healing
    > Minimal vascular supply causing more difficult wound closure than other techniques.
342
Q

When would you carry out a root apex resection?

A

Remove resorptive processes
Remove anatomical variation
Remore perforations
Gain access to diseased soft tissue
Evaluate and create apical seal

343
Q

How do you carry out a root apex resection?

A

Remove apical delta (3mm) to allow adequate visual access for canal and apical instrumentation.
- Angle of resection should be 90 degrees
- Bevels improve access but have disadvantages
- Acute angle may miss canals, better to have a flat resection.

344
Q

What are the types of endodontic surgery?

A
  • root apex resection
  • incision for drainage of by-products of tissue breakdown
  • trephination to alleviate acute pain due to purulent material at apex
  • retrograde filling of canal
345
Q

How do you retrograde fill a canal?

A

> Clean and prepare apical 3mm
Hermetically seal apex
Material must be non-resorbable and biocompatible to allow cementoblasts to repair the tissue, must also be radiographically visible.
Mineral Trioxide Aggregate (MTA) used

346
Q

When someone is taking corticosteroids, what should you think of before dental procedure?

A

STEROID COVER

347
Q

What is the risk of the HPA system isn’t working?

A

Adrenal crisis - life threatening hypotension, severe drop in blood pressure.

Dental procedures have attributed to 4.6-9% of adrenal emergencies.

Patients at risk of adrenal crisis require consideration for steroid replacement within the dental setting to prevent this occurrence.

348
Q

What is at risk of an adrenal crisis?

A

Primary adrenal insufficiency - Addison’s disease

Secondary adrenal insufficiency - glucocorticoid/steroid therapy

349
Q

What are symptoms of Addison’s disease?

A

(Addisons is when the adrenal glands are damaged and they don’t produce enough cortisol)
a. Recurrent bacterial infections - chronic oral candidsosis
b. Mucosal hyperpigmentation
c. Hypotension
d. Skin hyperpigmentation
e. Weight loss - anorexia
f. Low blood pressure, dizziness, faints, fatigued, run down.

–> These pts will need steroid cover for dental tx.

350
Q

Which patients tent to use glucocorticoids?

A

Common in specialities such as:
- rheumatology (arthritis),
- gastroenterology (Crohns, UC)
- dermatology
- COPD
- asthma

i.e. anti-inflammatory and immunosuppressive properties.

351
Q

What dose of different glucocorticoids is the equivalent of 5mg of prednisolone?

A
  1. Cortisone - 25mg
  2. Hydrocortisone - 20mg
  3. Prednisone - 5mg
  4. Prednisolone - 5mg
  5. Triamcinolone - 4mg
  6. Methylprednisolone - 4mg
  7. Dexamethasone - 0.75mg
352
Q

What dose makes someone at risk for adrenal crisis?

A

Pts taking 5mg prednisolone or more, for one month or longer, may be at risk of adrenal insufficiency.

353
Q

What is the general rule for steroid cover?

A

Double normal oral dose for 24 hours -
> Day of, one our prior to surgery
> Day after treatment double normal dose. Then return to normal.

354
Q

What does www.addisonsdisease say as steroid cover for
a. major dental surgery e.g. extraction with LA or GA
b. dental surgery e.g. RCT with LA
c. minor dental procedure e.g. replace filling, scale and polish

A

a. Major dental surgery
- Pre op = 100mg hydrocortisone IM just before anaesthesia
- Post op = double dose oral medication for 24 hours. Then return to normal dose.

b. Dental surgery
- Pre op = double oral dose (up to 20mg hydrocortisone) one hour prior to surgery
- Post op = double dose oral med for 24 hours. Then return to normal dose.

c. Minor dental surgery
- Pre op = take an extra oral dose, 60 minutes ahead of the procedure
Post op = an extra dose when hypoadrenal symptoms occur afterwards. Then return to normal dose.

355
Q

What is ASA class 1?

A

A healthy patient

e.g. healthy, non smoker, no/minimal alcohol

356
Q

What is ASA class 2?

A

A patient with mild systemic disease

e.g. smoker, pregnancy, anxiety, well controlled diabetes, well controlled hypertension

357
Q

What is ASA class 3?

A

A patient with severe systemic disease

e.g. Poor controlled diabetes, poor controlled hypertension, history of MI, COPD, CVA, TIA

358
Q

What is ASA Class 4?

A

A patient with a severe systemic disease which is a constant threat to life

e.g. Recent History of MI/CVA (<3/12) Ongoing cardiac ischaemia, valve dysfunction.

359
Q

What is ASA class 5?

A

Moribund patient not expected to live more than 24 hours with or without an operation

e.g. Rupture aortic or thoracic aneurism, intra-cranial bleed with mass effect.

360
Q

LA:
What drugs does it interact with? (2)
Side effects?
Management?

A
  1. Beta blockers
    - hypertensive response
    - limit to 3-4 cartridges
  2. TCA anti-depressants
    - increased SNS response
    - limit to 3-4 cartridges
361
Q

NSAIDs:
What drugs does it interact with? (7)
Side effects?
Management?

A
  1. Warfarin
  2. Aspirin
  3. DOACs
    > Increase bleeding risk
    > Consult with doctor
  4. ACE- inhibitors
  5. Beta-blockers
  6. Diuretics
    > Decrease hypotensive effect of the drugs
    > Consult doctor
  7. SSRIs
    > Increased bleeding risk
    > Careful NSAID use
362
Q

Azole antifungals:
What drugs does it interact with? (2)
Side effects?
Management?

A
  1. Warfarin
  2. DOACs
    > Increased bleeding risk
    > Prescribe nystatin instead
363
Q

Macrolide antibiotics (mycin):
What drugs does it interact with? (4)
Side effects?
Management?

A
  1. Warfarin
  2. Clopidogrel
  3. Simvastatin
  4. Ca channel blockers
    > Increase bleeding risk
    > Avoid - use alternative Abx
364
Q

Tetracycline abx:
What drugs does it interact with? (1)
Side effects?
Management?

A
  1. Warfarin
    > Increase bleeding risk
    > avoid - use alternative
365
Q

Penicillin antibiotics:
What drugs does it interact with? (2)
Side effects?
Management?

A
  1. Warfarin
    > Increase bleeding risk
    > advise vigilance
  2. Contraceptive pill
    > decreased effect
    > advise other pills
366
Q

Metronidazole:
What drugs does it interact with? (3)
Side effects?
Management?

A
  1. Warfarin
  2. NSAIDS
    > Increased bleeding risk
    > Avoid use
  3. Phenytoin
    > Synergistic response
    > Monitor closely
367
Q

What is Le Fort 1?

A
  • Floating palate involves lateral bony margin of the nasal opening
  • Swelling of the upper lip and ecchymosis in buccal sulcus beneath zygomatic arch
  • Malocclusion and mobility of teeth may be present
  • Test by grasping maxillary teeth, characteristic grate felt
368
Q

What is Le Fort II?

A
  • Dish face deformity, gross oedema of soft tissue in mid face region.
  • Step deformity in infraorbital margin
  • Mobile mod face
  • Paraesthesia of cheek
369
Q

What is Le Fort III?

A
  • Separation of frontozygomatic suture
  • Depression of ocular levels (enophthalmos)
  • Tilted occlusal plane
370
Q

What are clinical features of mandibular fractures?

A
  • Lacerations, bleeding, swelling.
  • Malocclusion and step deformity of teeth.
  • Paraesthesia of mandible due to IDN damage
  • Sublingual haematoma
371
Q

What should be taken to assess for a mandibular fracture?

A

DPT and PA mandible

372
Q

What is a Guardsman fracture?

A

Bilateral condylar fractures and mental bone fracture

373
Q

What are Depressor muscles?

A

Digastric
Geniohyoid
Genioglossus
Mylohyoid

374
Q

What are elevator muscles (MoM)?

A

Masseter
Temporalis
Medial pterygoid
Lateral pterygoid

375
Q

What is a favourable vs unfavourable mandible fracture?

A
  • Favourable = # whereby the muscles pull resists the displacement of the fragments.
  • Unfavourable = # whereby the muscle pull distracts the fragments away from each other, causing a displacement.
376
Q

What are the 4 mandibular fracture principles?

A
  1. Reduction
    - open: surgically viewing the fracture line and repositioning to ensure no step deformity.
    - closed: judgement as to avoid damage to internal structures (VII if Condylar #)
  2. Fixation
    - Internal: surgery to access the fracture, fixed via arch bars, screws and plates
    - External: inter-arch wires, Leonards buttons
  3. Immobilisation
  4. Rehabilitation

(may have to Extn tooth if in the way of a mandibular fracture).

377
Q

What are the clinical features of a zygomatic fracture?

A

Flattened zygomatic prominence (assess looking down)
Swelling and bruising over cheek
Steep deformity
Periorbital ecchymosis and subconjunctival haemorrhage
Paraesthesia or infraorbital nerve

378
Q

What are Campbells lines?

A
  1. Supraorbital
  2. Infraorbital
  3. Maxillary sinus/Supramaxillary
  4. Mandible and occlusal plane

Trapnell line =
5. Lower border or mandible

379
Q

What are complications of a zygomatic fracture?

A
  1. Cosmetic deformity due to flat face.
  2. Impaired mandibular movement
  3. Diplopia due to damage to inferior rectus muscle
  4. Retrobulbar haemorrhage, due to ciliary artery damage, blocking blood vessels, supplying oxygen to the optic nerve = anterior ischaemic optic neuropathy.
380
Q

How do you assess the current status of the patient and the M3M?

A

History (medical, social and dental)
Clinical examination
Appropriate radiological investigations

381
Q

What factors need to be taken into account regarding M3M status?

A
  1. Patient age and medical status
  2. Risk of complications (e.g. risk of inferior alveolar nerve injury, risk of leaving M3M in situ)
  3. Patient access to appropriate treatment (e.g. Army personnel on long deployment, Long-term travel)
  4. Opposing third molar/contralateral third molar status, if patient. is undergoing a general anaesthetic.
382
Q

What should you do for an asymptomatic diseased/high risk of disease development M3M?
What quiescent pathology may this include?

A
  • The likelihood that disease will develop is assessed by the clinician into high or low risk. If the risk is high, surgical intervention should be considered.
  • IF there is any doubt and the tooth has a higher risk of surgical complications (close approximation to the inferior alveolar nerve) then active surveillance is recommended until symptoms develop or early disease progression has been proven.

Quiescent pathology may include undiagnosed second or third molar:
- Caries
- Periodontal disease
- Resorption (internal or external)
- Cysts of tumours

383
Q

When would you consider therapeutic extractions for a symptomatic diseased/high risk of disease development M3M?

A
  • Single severe acute or recurrent subacute pericoronitis
  • Unrestorable caries of the M3M or to assist restoration of the adjacent tooth.
  • Periodontal disease compromising the M£M and/or adjacent tooth
  • Resorption of the M3M and/or adjacent tooth
  • Fractured M3M
    M3M periapical abscess, irreversible pulpitis or acute spreading infection
  • Surrounding pathology (cysts or tumours) associated with the M3M

Tx to be considered:
- Therapeutic removal of M3M (or coronectomy)
- Removal of upper third molar

384
Q

What should you do in the absence of disease or if there is a low significant risk of disease development in M3M?

A

Clinical review is required, supplemented with radiographic assessment if indicated. An assessment of risk of disease needs to be made and review interval made accordingly.

385
Q

What factors do you do consider for prophylactic removal of M3M in asymptomatic non-diseased/low risk of disease development?
medical factors: 3)
surgical factors: 3)

A

Medical factors: patients undergoing planned medical treatment/therapy that may complicate the likely surgery of M3Ms include:
- Pharmaceutical therapy (bisphosphonates, antiangiogenics, chemotherapy)
- Radiotherapy of head and neck
- Immunosuppressant therapy

Surgical factors: The third molar lies within the perimeter of a surgical field.
> Mandibular fractures
> Orthognathic surgery
> Resection of disease (benign and malignant lesions).

–> Leave deeply impacted M3Ms with no associated disease.

386
Q

What other diagnoses cause pain in the M3M region? (6)

A
  1. Temporomandibular disorders.
  2. Parotid disease
  3. Skin lesions
  4. Migraines or other primary headaches
  5. Referred pain from angina, cervical spine.
  6. Oropharyngeal oncology
387
Q

What may cause impaction of M3M?

What may impaction be associated with?

A

Lack of space
Obstruction
Development in an abnormal position

May be associated with pathological changes including:
- pericoronitis
- an increased risk of caries and periodontal disease in adjacent teeth
- orthodontic problems in later life.

388
Q

What are the risks of removal of an impacted third molar?

A
  1. Temporary or permanent nerve damage
  2. Alveolar osteitis (Dry socket)
  3. Infection
  4. Haemorrhage
  5. Temporary local swelling, pain and restricted mouth opening.
389
Q

What are 6 questions you could ask someone to detect sepsis?

A
  1. Slurred speech
  2. Extreme muscle shakes
  3. Passing urine in 24 hours (kidneys failing) - in children 12 hours
  4. Severe breathlessness
  5. It feels like you’re going to die - sense of impending doom
  6. Skin rash - mottled or discoloration of any parts of body
390
Q

What are risk factors for sepsis? (5)

A
  1. Very young (under 1 year) and older people (over 75 years) or very frail people
  2. Recent trauma or surgery or invasive procedures (within the last 6 weeks).
  3. Impaired immunity due to illness (for example, diabetes) or drugs (for example, people receiving long-term steroids, chemotherapy or immunosuppressants).
  4. Indwelling lines, catheters, intravenous drug misusers, any breach of skin integrity (for example, any cuts, burns, blisters or skin infections).
  5. Additional risk factors for women who are pregnant or who have been pregnant, given birth, had a termination or miscarriage within the past 6 weeks:
    > gestational diabetes, diabetes or other comorbidities
    > needed invasive procedure such as caesarean section, forceps delivery, removal of retained prodcuts of conception
    > prolonged rupture of membranes
    > close contact with someone with Group A streptococcal infection
    > continued vaginal bleeding or an offensive vaginal discharge.