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BDS4 Revision > Oral medicine > Flashcards

Oral medicine Flashcards

1
Q

This is a photograph of a slide prepared from a biopsy taken from a 58-year-old man with smokers keratosis on the palate
The top arrow is pointing to a layer. What is this layer made of ?

A

Keratin is formed from the basal layer

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2
Q

This is a photograph of a slide prepared from a biopsy taken from a 58-year-old man with smokers keratosis on the palate

What type of epithelium can you see in this picture? (1)

A

Keratinised stratified squamous epithelium

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3
Q

This is a photograph of a slide prepared from a biopsy taken from a 58-year-old man with smokers keratosis on the palate
What is the brown pigment the lower arrow is pointing to?

A

Melanin

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4
Q

This is a photograph of a slide prepared from a biopsy taken from a 58-year-old man with a smokers keratosis palate

Describe the lesion clinically based on what you can identify in the slide. (2)

A

Thickened white area with some dark brown/grey areas on the palate - (reactive melanosis from smoking?)

This is painless.

There are other areas of the mouth with tobacco related staining.

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5
Q

This is a photograph of a slide prepared from a biopsy taken from a 58-year-old man with smokers keratosis on palate
Name two possible aetiological factors for the development of this lesion. (2)

A

Smoking (tobacco/ pipe)
Long term drinking of very hot beverages (trauma)
Chronic inflammation
Drugs - hydroxychloroquine

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6
Q

This is a photograph of a slide prepared from a biopsy taken from a 58-year-old man with a smokers keratosis lesion on the palate
Using the photograph of the biopsy how would you assess if the lesion was potentially malignant ()

A

Hyperkeratosis
Hyperchromatism
Atypia
Dyplasia
Pleomorphism
Infiltrate of macrophages

In the slide:
Visible change in nuceli staining due to more DNA material.
Increased layer of keratin
Areas of dysplasia
Abnormal variation in nucelus size. (Pleomorphism)

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7
Q

This is a photograph of a slide prepared from a biopsy taken from a 58-year-old man with a smoker’s keratosis lesion on the palate

What features in the clinical appearance would make you highly suspicious that the lesion was potentiallymalignant? (4)

A

Exophytic growth (3d)
Raised rolled margins,
Indurated (hard lesion)
Non-homogeneous (speckled/ Verrucous/ flat and raised lesion)

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8
Q

Mrs Patel is 45 and has soreness in her right cheek which is reddened on the buccal mucosa with a shorty Lacey edge immediately adjacent to tooth 47. This tooth is perfectly sound amalgam with abutments for rest seats and clasps on CoCr partial denture which has been worn for 5 years. Bleeding 6mm mesio-buccal pocket with associated grade 1 mobility. Periapical shows 47 has mesial bone loss but no periapical pathology.
What is your provisional diagnosis? (2) -

A

Traumatic keratosis from denture clasps

Lichenoid reaction to large amalgam restoration (Type IV hypersensitivity)

Localised periodontal disease to the 47 - worsened by RPD margins and clasps.

Raticular lichen planus?? incidental location

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9
Q

Mrs Patel is 45 and has soreness in her right cheek which is reddened on the buccal mucosa with a shorty Lacey edge immediately adjacent to tooth 47. This tooth is perfectly sound amalgam with abutments for rest seats and clasps on CoCr partial denture which has been worn for 5 years. Bleeding 6mm mesio-buccal pocket with associated grade 1 mobility. Periapical shows 47 has mesial bone loss but no periapical pathology.

What additional investigations could be undertaken and how would you arrange these?

A

Periodontal check - Assess risk factors, 6 point pocket chart and plaque and bleeding scores

Clinical photographs

Refer to Oral medicine for advice (Replacing amalgam with composite.)

May require incisional biopsy if the reaction doesn’t go away.

Referal to dermatology for patch testing for CoCr

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10
Q

Mrs Patel is 45 and has soreness in her right cheek which is reddened on the buccal mucosa with a shorty Lacey edge immediately adjacent to tooth 47. This tooth is perfectly sound amalgam with abutments for rest seats and clasps on CoCr partial denture which has been worn for 5 years. Bleeding 6mm mesio-buccal pocket with associated grade 1 mobility. Periapical shows 47 has mesial bone loss but no periapical pathology.

What are mrs Patel’s options for management of these problems

A

Periodontal treatment (S3 guidelines) and review

Traumatic lesion- adjust the CoCr clasps/make a new denture and change location of clasps

then-
Oral med referal will decide if Lichen planus & identification of cause for correction- may be idiopathic.
Identifed through :
Blood test- Haematinics (deficiency)/ Autoantibody screening (For lupus erythematosis)/
Biopsy- To distinguish between lichen planus (unknown cause) and a lichenoid reaction (known cause)
MH- could be graft/host disease

From results:
Lichenoid reaction - only consider the removal of the amalgam in direct contact
- if asymptomatic a choice is to leave it however discuss the risks and benefits of removal: risk - removal of more tooth tissue & benefit = could be potentially malignant if we leave
- replace amalgam with composite
- if no resolution refer to oral med and potential biopsy

Lichen planus -Correct deficiency/ consider changing medications/ Symptom management (Chlorohexidine or benzdamine mouthwash. SLS free toothpaste

Biopsy result may mean referal for oral cancer.

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11
Q

Name 4 histological features of lichenoid reactions

A

Parakeratosis- keratinisation characterised by retention of the nuceli in the stratum corneum,
Chronic inflammatory cell infiltrate -lymphocytic band hugging the cell membrane
Basal cell Damage,
Patchy acantosis (Thickening)
Apoptosis, Sawtooth rete pegs

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12
Q

Your patient attends your practice & this is the clinical presentation.
Diagnose the patient.

A

Angular cheilitis

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13
Q

Name 2 microorganisms involved in this condition. (2)

A

Staphylococcus aureus
candida albicans

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14
Q

What type of sample should be taken in this case?

A

A swab of the commissures of the mouth

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15
Q

Name 1 immune deficiency disease and 1 gastrointestinal bleeding disease that can increase risk of Candida infections and why they are more susceptible? (2)

A

HIV: impaired immune function

Crohns disease: impaired nutrient absorption (Nutritional deficiencies= greater likelihood of infection)- You can also get oral symptoms of chron’s disease

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16
Q

Name one intra-oral disease and on extra oral disease that would be associated with this clinical presentation (1)

A

Intra-oral = Oral candidasis
Extra-oral= Oral facial granulomatosis (swollen lips= ideal location for candida )

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17
Q

Why is miconazole prescribed to patient when microbiological sampling is not available? (1)

A

Miconazole 2%
Effective against both candida and gram positive cocci such as staphyloccocus aureus. Therefore appropriate to use in all patients prior to sampling results
But shouldn’t be used in warfarin or statins patients.

(Two main candida yeast are candida albicans and candida glabrata- glabrata is resistant to fluconazole so we don’t use this unless we know the type of candida)

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18
Q

What two instructions should be given to this patient who wears a denture. (2)

A

Not to wear denture over night, take out before bed
o Denture hygiene instruction:
- Clean dentures after eating, before bed and in the morning with brush and soapy warm water
-Clean with denture cleaning solutions according to manufacturer guidelines
-Clean mouth with brush and toothpaste on soft tissues or CHX mouthwash

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19
Q

A patient attends with inflamed gingiva extending beyond the mucogingival margin.
Give a diagnosis (1 mark)

A

Desquamative gingivitis

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20
Q

A patient arrives at the oral med clinic complaining of pain and on examination the consultant diagnoses desquamative gingivitis. Describe desquamative gingivitis?

A

Inflamed gingivae with erythematous shedding and ulceration which involves the full width of the gingivae. (extends beyond the mucogingival margin)

This can present clinically for several disorders (Lichen planus/ Gingival pemphigoid/ plasma cell gingivitis- we need histology to differentiate)

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21
Q

A patient arrives at the oral med clinic complaining of pain and on examination the consultant diagnoses desquamative gingivitis.
Give 3 oral mucosal conditions associated with in this? (3 marks)

A

Pemphigus, Pemphigoid, Lichen planus, plasma cell gingivits

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22
Q

A patient arrives at the oral med clinic complaining of pain and on examination the consultant diagnoses desquamative gingivitis.
Give 2 local factors that may contribute to this (2 marks)

A

Plaque build up
Smoking
poor overhanging restorations
Partial dentures
SLS toothpaste

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23
Q

A patient arrives at the oral med clinic complaining of pain and on examination the consultant diagnoses desquamative gingivitis.
Describe how you would manage this?(5)

A
  1. Confirm diagnosis and any underlying conditions using:
    Blood tests
    Biopsy = Immunofluresence assay (Checking for pemphigus/ pemphigoid)
  2. advise use of SLS free toothpaste.
  3. OHI to Improve oral hygiene (Plaque aggrevates the lesions)
  4. Topical steroid use:
    Betamethasone mouthwash/ Beclomethasone metered dose.
    Topical Steroid gel Sinylar placed in a gingival veneer to remain in contact with the gums.
    Topical lacrolimus (ointment or mouthwash)
  5. Systemic immunosuppressant.
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24
Q

A patient arrives at the oral med clinic complaining of pain and on examination the consultant diagnoses desquamative gingivitis.
Name another gingival disease that is typically painful on presentation. (2)

A

Erythema multiforme- Mucosa ulceration & painful for patients to eat or drink

ANUG- Painful but doesn’t extend beyond the mucogingival margin.

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25
Q

This image shows a special tests used by the lab
What are these two methods of analysis (2)

A

Direct immunofluorescence & histopathology

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26
Q

This image shows a special tests used by the lab
What would the pathologist report of immunofluoresence & the histopathology (3) and give a diagnosis (2)

A

Histopathology- Suprabasal split with Tzank cells.
Immunofluresence- Basket weave staining around the epithelial cells.
Pemphigus vulgaris

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27
Q

A picture is shown of direct immunofluorescence performed by the lab due to suspected pemphigus vulgaris.
What is Pemphigus vulgaris?

A

An immune mediated antibody directed intra-epithelial blistering condition

Mucosal erosion and mucosal surface loss producing blisters that burst and spread.
These ulcers are first seen on the oral mucosa and then on the skin.
The loss of epithelial covering leads to fluid loss and an infection risk. (this can be fatal)

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28
Q

A picture is shown of direct immunofluorescence performed by the lab due to suspected pemphigus vulgaris.
Why would pemphigus vulgaris occur?

A

Autoimmune: type 2 hypersensitivity reaction causing
1.antibodies to form against the desmosomes
2.producing intraepithelial bullae-
3. fluid between the cells
4. cells separating & Thinning
5. loss of epithelium.

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29
Q

Name one condition that would represent the lesion in the same way clinically as pemphigus vulgaris, but would be different histopathologically? (1)

A

Mucous membrane pemphigoid

Bullous pemphigoid (as pemphigus vulgaris can present as a blister before it bursts- this presents histopathologically as a subepithelial split.
Drug induced Pemphigus

Erythema multiforme (ulceration of the oral mucosa due to a type 3 hypersensitivity reaction)-

** FIND OUT **

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30
Q

A patient attends with a squamous cell carcinoma on the lateral border of the tongue which is 5cm in width. There are bilateral ipsilateral lymph nodes palpated <2cm in size. The presurgical examination shows that the cancer has not spread to any other structures.
- List 2 risk factors for oral squamous cell carcinomas

A

Alcohol
Smoking,
Betel quid (paan)
HPV

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31
Q

This patient has a squamous cell carcinoma at the lateral border of the tongue. It is 5cm in width. There are
bilateral ipsilateral lymph nodes palpated but <2cm. The presurgical examination shows that the cancer is not
spread to any other structures.
Stage tumour with the TNM system. (1)

A

T(tumour size)=3 as tumour >4cm
N(lymph node involvement-2 bilateral lymph node involvement but no more than 6cm.
M (metastasis)-0

T3 N2c M0

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32
Q

A patient attends with a squamous cell carcinoma on the lateral border of the tongue which is 5cm in width. There are bilateral ipsilateral lymph nodes palpated <2cm in size. The presurgical examination shows that the cancer has not spread to any other structures.
How would you grade the dysplasia histopathologically? (3)

A

Basal Hyperplasia
Increased basal cell numbers.
Architecture- regular stratifiication
Cytology-no cellular atypia.
Mild Dysplasia (removal of cause can help it regress)
Increased basal cell numbers
Architecture- changes in the lower third
Cytology- Mild atypia/ Pleomorphism/Hyperchromatism
moderate dysplasia
Architecture- change extends into the middle third. Rounder rete ridges
Cytology- moderate atypia/ pleomorphism/ hypercrhomatism
Severe dysplasia
Architecture- changes extend to the upper third (loss of stratification)
Cytology- severe atypia and numerous mitoses not at the bottom
Carcinoma in situ
Malignant but not invasive.
Abnromal architecture- all viable layers involved.
Cytology- pronounced cytological atypia with mitotic abnormalities.

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33
Q

This patient has a squamous cell carcinoma at the lateral border of the tongue. It is 5cm in width. There are
bilateral ipsilateral lymph nodes palpated but <2cm. The presurgical examination shows that the cancer is not
spread to any other structures.

What interventions (medical or surgical) other than surgery could the patient have? (3)

A

None - paliative
Radiotherapy,
Chemotherapy,
combination of both

Immunotherapy

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34
Q

This patient has a squamous cell carcinoma at the lateral border of the tongue. It is 5cm in width. There are
bilateral ipsilateral lymph nodes palpated but <2cm. The presurgical examination shows that the cancer is not
spread to any other structures.
After removing the oral squamous cell carcinoma from the tongue, how would you restore the function of the tongue?

A

Using a Soft tissue graft to rebuild the tongue e.g
- radial forearm
- rectus abdominus

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35
Q

What is an erosion?

A

Partial thickness loss of the epithelium
can only be diagnosed histologically.

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36
Q

What is an ulcer?

A

Full thickness loss of the epithelium where you can see the underlying connective tissue and fibrin may be deposited on the surface.
This acn only be diagnosed histologically.

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37
Q

How would you differ between recurrent major and minor apthous ulceration?

A

Minor apthous ulcer
<10mm (1cm) diameter
Shape: Red halo (erythematous) and a yellow fibrinous base.
Location- only affects non-keratinised mucosa.
Duration- Heals within 1-2 weeks
Outcome (heals without scarring)

Major apthous ulcer
size= >1cm in diameter
Shape: oval or irregular perilesional erythematous halo with fibrinous exudate covering the tissue.
Location- can affect keratinised/ non keratinised.
Duration- can last for months
Outcome- May scar when healing.

Herpetiform
Multiple small ulcers (around 2mm in size)
Shape- can coalesce into larger areas of ulceration
Location- only on non-keratinised mucosa
Duration- lasts 2 weeks
Outcome- heals without scarring/.

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38
Q

What are the potential problems of recurrent aphthous stomatitis? (4)

A
  • Infections
  • Dehydration and malnutrition
  • Problems wearing dentures
  • Can affect speech and mastication
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39
Q

What can cause recurrent apthous stomatitis? (7)

A
  • Genetic predisposition
  • Systemic disease
  • Stress
  • Mechanical injuries
  • Hormone fluctuations
  • Microelement deficiencies (iron, B12, folic acid) – cause or a symptom
  • Viral and bacterial infections

Host factors:
-Genetic – HLA Type A2 and B1w
-Nutritional/deficiencies – iron, folate, B12
-Systemic disease – menorrhagia, chronic GI blood loss, dietary malabsorption (Crohn’s, coeliac, pernicious anaemia), UC, OFG
- Endocrine – females > males
-Immunity – CD8>CD4 at ulcer stage
- Environmental factors: § Trauma
-Allergies – SLS toothpaste/ dietary problems
Other – smoking, infection, stress

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40
Q

How can we treat recurrent apthous stomatitis?

A

Correction of blood deficiencies
Ferritin (Iron) Folic acid. Vit B12.
Refer for investigation if coeliac positive
Endoscopy and jejunal biopsy
Avoid dietary triggers (SLS toothpaste/ identified from testing)

Drugs-
Non steroidal topical therapy (for inconvenient lesions)
-Chlorohexidine mouthwash
-Benzdamine mouthwash or spray
Steroid based treatment
Hydrocortisone mucoadhesive pellet
Betamethasone mouthwash (1mg in 10ml water twice daily)
Beclomethasone metered dose inhaler (50microg)

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41
Q

A patient enters your surgery and you suspect after your initial examination that they may have trigeminal neuralgia.
Describe the nature of the pain from trigeminal neuralgia (2 marks)

A

An intense stabbing pain which extends along the course of branch affected - maxillary or mandibular usually

Unilateral

Lasts 5-10 seconds

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42
Q

A patient enters your surgery and you suspect after your initial examination that they may have trigeminal
neuralgia.
Name the 2 most frequent causes of trigeminal neuralgia are?

A

Idiopathic
Vascular compression of the trigeminal nerve.

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43
Q

A patient enters your surgery and you suspect after your initial examination that they may have trigeminal
neuralgia.

Name 2 clinical investigations you could do into these. (3)

A

OPT to rule out dental cause
Trigeminal nerve reflex testing
MRI

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44
Q

A patient enters your surgery and you suspect after your initial examination that they may have trigeminal
neuralgia.
What 2 neurological disorders can give rise to this condition?

A

MS

A tumour compressing on the trigeminal nerve - Space occupying intracranial tumours/lesion

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45
Q

A patient enters your surgery and you suspect after your initial examination that they may have trigeminal
neuralgia.
If the patient had trigeminal neuralgia due to MS or a brain tumour what symptoms might they experience? 1 for MS, 2 for brain
tumour. (3 Marks)

A

MS: intention tremor/loss of proprioception,
Brain Tumour: Diplopia, memory loss

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46
Q

A patient enters your surgery and you suspect after your initial examination that they may have trigeminal
neuralgia.
What is the 1st line drug management for trigeminal neuralgia?

A

Carbamazepine modified release 100mg 2x daily, (20 capsules 1 tablet twice daily)

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47
Q

A patient enters your surgery and you suspect after your initial examination that they may have trigeminal
neuralgia.
What investigation/tests would you take before giving the medical management and why? (3 marks)

A

Blood tests - FBC, LFT (liver function test), U&E (urea and electrolytes)

Side effects of carbamazepine -
Sodium reduced (can get hyponatraemia)
Liver function reduced (thrombocytopenia/ neutropenia/ pancytopenia)

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48
Q

A patient enters your surgery and you suspect after your initial examination that they may have trigeminal
neuralgia.
Give 3 side effects of the medical intervention selected for trigeminal neuralgia? (carbamazepine)

A
  • Blood dyscrasias/disorders
  • Thrombocytopenia
  • Neutropenia
  • Pancytopenia
  • Electrolyte imbalances (hyponatreamia)
  • Neurological deficits
  • Paraesthaesia
  • Vestibular problems
  • Liver toxicity
  • Skin reactions (including potentially life threatening)

Liver dysfunction
Nausea/vomiting/ dizziness.
Dry mouth & swollen tongue.

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49
Q

A patient enters your surgery and you suspect after your initial examination that they may have trigeminal
neuralgia.
What are the 2 indications for surgical treatment of trigeminal neuralgia

A

If approaching the maximum tolerable dosage & ineffective
If younger patients (would have to be on the medication for the rest of their life)
If medical intervention is contraindicated
Medication is causing side effects

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50
Q

A patient enters your surgery and you suspect after your initial examination that they may have trigeminal
neuralgia.
Name one type of surgery that can be carried out?

A

Microvascular decompression

  • Destructive Central Procedures
  • Radiofrequency thermocoagulation
  • Retrogasserian glycerol injection
  • Balloon compression
  • Stereotactic Radiosurgery
  • Gamma knife = targeted radiation at the trigeminal ganglion to kill trigeminal nerve cells
  • Destructive Peripheral Neurectomies = Only performed as a last resort after trial local anaesthesia
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51
Q

Intra-oral manifestations of herpes?

A

Fluid filled vesicles that rupture.
Oral ulceration

(Primary herpetic gingivostomatitis/ Herpes labialis)

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52
Q

Three causes of vesicles?

A

Erythema multiforme, Pemphigoid, Pemphigus, angina bullosa haemorrhagica

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53
Q

2 groups (virus) that cause oral ulceration?

A

Herpes simplex, Coxsackie virus, EBV, Varicella Zoster virus

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54
Q

Give 2 causes of Coxsackie oral lesions?

A

Herpangina, Hand foot and mouth

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55
Q

disorders caused by epstein bar virus.

A

Hairy leukoplakia, Glandular fever (infectious mononucleosis), Burkitt’s lymphoma

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56
Q

How herpes labialis forms? (4)

A

3 STAGES:
1. Primary infection
HSV1 enters the body via mucous membrane or abraded epithelium, replicates in epithelial cells and travels along the nerve and infects the trigeminal ganglion.

  1. Latency - Virus stays dormant in the ganglion
  2. Reactivation - due to Stress/ Infection /Sunlight/Fatigue/ Immunosupression
    causing
    = virus travels back along nerve and causes secondary infection

Herpes labialis lesion in upper- infected maxillary branch. Lesion in lower- infected mandibular branch.
.

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57
Q

Diagnose

A

acute pseudomembranous candidosis

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58
Q

Name local and medical conditions that might cause this?associated with this clinical presentation.

A

Local:
oral steroid/Inhalers with steroids
Nutritional deficiencies
Broad spectrum antibiotics
dry mouth

Medical- HIV, Poorly controlled diabetes

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59
Q

The patient has attended with generalised white plaques that scrape off easily and leave an erythematous base.

Discuss the advantages and disadvantages of a mouth Swab + oral rinse (4)

A

Swab -
Adv: site specific
Dis: easily contaminated& uncomfortable,

Rinse -
Adv Records the whole mouth and can separate healthy organisms.
Disadv: it is not site specific and some patients find the rinse difficult to do.
It is a quantifiable amount but difficult to standardise.

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60
Q

What to ask pathologist for when sending sample (1)

A

Culture (using saubraunds agar)
Check sensitivity to antifungals

For antifungals
Helps you select an antigual
If candida globrata (use Nystatin- globrata is resistant to azole )
Otherwise- Miconazole or fluconazole

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61
Q

The patient has attended with generalised white plaques that scrape off easily and leave an erythematous base
Fluconazole reacts with many drugs. Name 2 drug interactions and the effects the interaction would have (2)

A

Warfarin- Increases the anti coagulant effect of warfarin and is classed as a severe interaction as it can increase likelihood of a catastrophic bleed as it increases INR. Statins- Increased risk of Hepatotoxicity.

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62
Q

The patient has attended with generalised white plaques that scarape off easily and leave an erythematous base.
What information is required on a lab sheet for sample? (8)

A

o Patient details – Name, address, DOB, CHI, telephone number
o GDP and GMP details – Name, address, contact number
o Patient medical, drug, dental and social history
o Clinical description of the problem
o Provisional diagnosis
o Test previously done and test required to be done e.g. culture, viral, ESR
specimen site and type
o Antibiotic use previous, currently and resistance o Date and time of sample
o Referring clinician name, signature

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63
Q

The patient attends with this lesion on their cheek diagnose and give justification.

A

Minor aphthous ulcer
Diameter= <1cm
Shape= red margins with yellow fibrinous base.
Location - Non keratinised mucosa

Ask about history to find out how long the ulcer has been there (should last <2 weeks )

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64
Q

The patient attends with this lesion on their tongue, diagnose this and give justification.

A

Herpetiform aphthous ulcers
Diameter <2mm.
Shape- mutliple small ulcers that could coalesce into a large area of ulceration.
Location= Non keratinised mucosa.

Duration- from history should last about 2 weeks.

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65
Q

The patient attends with this lesion on their tongue diagnose and give justification

A

Major apthous ulcer
Diameter >1cm
Shape- red eryethematous border with fibrinous yellow exudate in the centre.
Location- Keratinised/ non keratinised mucosa

From history- Duration >2 weeks but we refer to oral med for biopsy due to risk of oral cancer.

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66
Q

2 investigations for apthous ulcers

A

Haematinics
FBC- looking for coeliac disease (TTG)
Allergy test

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67
Q

From FBC + told normal values- diagnose anaemia type

A

Microcytic- below normal value- caused by iron deficiency/ thalassaemia
MCV < 90FL

Normocytic- within normal values- caused by bleeding.

Macrocytic- bigger than normal cells - B12 or foliate deficiency.
MCV>90FL

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68
Q

What common conditions cause microcytic anaemia but require further blood tests?

A

Iron deficiency,
Thalassaemia
Anaemia of chronic disease

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69
Q

3 topical treatments available for apthous ulcers - not brand name (3)

A

Chlorohexidine mouthwash (0.2%)
Benzydamine mouthwash (0.15%
Betamethasone mouthwash (1mg (2 soluble tablets twice ad ay)
Beclomethasone inhaler (50mg )

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70
Q

Mid age female complaining of burning mouth with diffuse erythema (1)

***CHECK PAST PAPER

A

Oral dysaesthesia

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71
Q

Male mid age, dull throbbing pain in maxillary region, made worse by bending over (1)

A

Sinusitis

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72
Q

Unilateral episodic pain lasting up to 20 mins, nose dripping + worse when shaking head (1)

A

Chronic Paroxysmal Hemicrania

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73
Q

Elderly + sharp shooting pain in right cheek when biting + lacrimation (1)

A

Trigeminal neuralgia

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74
Q

Temporal pain, weakness of shoulder muscles (1)
(also associated with scalp tenderness and pain in the jaw muscles when eating and relief when jaw rested)

A

Giant cell ateritis (accompanied by shoulder girdle weakness)

what is it?
inflammation of the temporal artery - restricts blood flow to the associated structures (masseter)

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75
Q

Patient presents with a pigmented tongue. List some local causes (5)

A

Smoking,
Medication - hydroxychloroquine,
Chromogenic bacteria causing black hairy tongue
Melanoma
Melanotic macule

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76
Q

Patient presents with a pigmented tongue. List some systemic causes (6)

A

Racial,
Lead poisoning,
Addison’s,
Kaposis sarcoma,
Haemochromatosis

cushings = raised ACTH

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77
Q

What is lichen planus?

A

An immunomediated chronic inflammatory mucocutaneous disease affecting the lining of the mouth and skin.
Patients who suffer from severe lichen planus have an increased risk of 1% of developing oral malignancy in a 10 year period.

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78
Q

What are the histological features of lichen planus. (5)

A

Chronic inflammatory cell infiltrate (lymphocytic band hugging the basement membrane)
Saw tooth rete ridges
Basal cell damage
Patchy ancathosis
Parakeratosis

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79
Q

WHat are the types of lichen planus? (6)

A

PPBREA
Papular- White plaques
Plaque- plaques arranged in lines
Bullous- development of fluid filled vesicles and bullae with skin lesions projecting from the surface
Reticular- spider web like lacy white lines
Erosive (ulcerative)
Atrophic- white bluish plaques with central superficial atrophy

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80
Q

Give some features of the lichen planus disease?

A

30-50yo,
1% malignant potential, Recurrence

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81
Q

What are the causes of lichen planus?

A

Stress,
Immunomediated,
Idiopathic,
Amalgam,
SLS allergy,
Plaque build up (Desquamative gingivitis),
Medications (NSAIDS, Anti-hypertensive, Anti-malarials, Anti-diabetics, Sulphonamides, Penicillamine)
Haematinic deficiency

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82
Q

What special investigations are used for lichen planus patients and when? (2)

A

Biopsy all lesions- to distinguish between lichen planus and a lichenoid lesion (lichenoid lesion has an increased risk of cancer) and provide a definitive diagnosis.

ALWAYS Biopsy in: smoker, symptomatic lichen planus or the erosive type lesions.
High risk area (floor of the mouth/lateral border of tongue)

Analyse with Direct Immunofluorescence (DIF)

Blood tests
LP more symptomatic in px with haematinic deficiency
- Haematinincs
- FBC

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83
Q

Patient presents with lichen planus. How do we treat them?

A

Take clinical photographs and refer to Oral medicine
Where:
Asymptomatic- observe/ remove cause

Symptomatic-
Identify & remove causative agent (e.g. amalgam/ OHI
MILD- chlorohexidiene m/w. Benzdamine m/w. Avoid SLS toothpaste.
PERSISTING- Beclomethasone MDI 0.5mg/ puff -2 puffs 2-3 x daily
Betamethasone rinse- 1mg/10ml/ 2min/twice a day.

May Biopsy white patch.

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84
Q

What do you see on a histological image of Pemphigus

A

Tzank cells,
Supra-basal split: antibodies have attacked the desmosomes- causing fluid between the cells & then thinning of the cells and loss of epithelium.

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85
Q

Discuss the features of the Pemphigus disease.

A

There is mucosa erosion and mucosal surface loss. Loss of epithelial covering leads to fluid loss (protein and electrolyte imbalance) and infection risk

S - superficial, S - serious, S - steroids,

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86
Q

What causes pemphigus?

A

Autoimmune: type II hypersensitivity reaction where (iGG) antibodies attack the desmosomes responsible for cell to cell adhesion.

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87
Q

How do we treat patients with pemphigus?

A

Topical- betamethasone mouthwash 0.5mg 3xday. (sdcep 500mg dissolvable tablets 4xdaily)
High dose steroids,

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88
Q

Order the salivary gland tumours by incidence

A

Pleomorphic adenoma (75%),
Warthin’s tumour (15%),
Adenoid Cystic Carcinoma (5%)
Mucoepidermoid Carcinoma (3%),
Acinic Cell carcinoma (<1%)

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89
Q

What are the histological features of a pleomorphic adenoma?

A

Incomplete fibrous tissue capsule
Duct like structures
Myoepithelial cells (looks like muscle cells and can contract- moving saliva through the duct)
Mixed tumour- Epithelium in ducts &
Myoepithelial cells (looks like muscle cells and can contract- moving saliva through the duct)
Myxoid (loose ground tissue) and chondroid areas (looks a bit like cartilage tissue)

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90
Q

What histological feature is related to recurrence of a pleomorphic adenoma? (2)

A

Non/poorly encapsulated which makes it harder to remove & more likely to recurr

myxoid tissue - jelly like and hard to remove in entirety

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91
Q

What are the histological signs of Warthin’s tumour? (3)

A

– Cystic spaced lined by 2x layers of pink epithelium and lymphoid tissue between

– Distinctive epithelium

– Can have germinal centres developing

(Fully Encapsulated so less difficulty with removal)

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92
Q

How are salivary gland neoplasms diagnosed? (3)

A

Fine needle aspirate- not enough tissue for a proper diagnosis but tells you if its benign or malignant.
followed by;
Core biopsy (more tissue)

Incisional biopsy - sample of tissue

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93
Q

Histology of adenoid cystic carcinoma?

A

No capsule present and the tumour can be tubular/ cribiform architecture (swiss cheese) or solid in nature.

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94
Q

What features of a parotid swelling would make you suspicious of malignancy? (7)

A

Localised swelling- firm mass
Painless
Fast growing
Attached to underlying structures
assymetry of gland
Obstructionof the gland
Late stage will have pain and possible facial palsy.

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95
Q

Describe how you would manage Desquamative gingivitis (4 Marks)

A

Confirm diagnosis and any underlying conditions (manage these appropriately)
Blood test
Immunofluorescence assay

Treat underlying cause
Allergy to SLS- Use SLS free toothpaste.
Improve oral hygiene (Plaque aggravates the lesions),
Topical steroids -Betamethasone rinse or rmeter dose inhaler (MDI; or Steroid cream in (gum shield),
Topical tacrolimus (immune modulator, rinse or cream),
Systemic immunosuppression if required (rarely needed)

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96
Q

Arthur is a 68 year old retired mechanic who presents at your practice after an absence of 2 years. He is partially
dentate in the upper and lower arch and wears upper and lower acrylic prostheses. These prostheses were well
fitting when provided by you 2 years ago. He now complains that the upper prosthesis no longer fits well and is
uncomfortable. On examination the upper prosthesis does not seat fully in the edentulous regions. In addition,
there are numerous early to moderately deep primary carious cavities. Periodontal examination reveals no
periodontal pockets greater than 3-4 mm and minimal bleeding on probing. Radiographic examination confirms no
obvious peri-radicular radiolucencies. To the contrary, there are large radio-opacities in relation to the roots of
several teeth. There is minimal periodontal bone loss. In relation to his medical history he says he is taking
medication for Paget’s disease.
Describe the anatomical changes, pathology and incidence behind the reason why the denture no longer fits? (4
marks)

A

Paget’s is a disease of disturbed bone turn over - deposition and resorption can occur at the same time. The bone becomes soft and deformed. Then calcifies in the deformed shape.
This causes
Bone swelling - i,e, dentures don’t fit
Pain
Swelling.

Can affect one bone (monocytic) or many bones (polycytic)

Presenting as:
ill fitting dentures (bone has swollen)
presents as bone swelling/enlargement and thus the dentures don’t fit.
Migration of teeth (increased jaw size)

Treating these patients:
Extraction- softening stage will cause bleeding. Sclerotic stage can cause dry socket.
Patient may be on anti resorptive (MRONJ risk)
Dense bone is harder to LA.

incidence:
>40
M>F

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97
Q

Arthur is a 68 year old retired mechanic who presents at your practice after an absence of 2 years. He is partially
dentate in the upper and lower arch and wears upper and lower acrylic prostheses. These prostheses were well
fitting when provided by you 2 years ago. He now complains that the upper prosthesis no longer fits well and is
uncomfortable. On examination the upper prosthesis does not seat fully in the edentulous regions. In addition,
there are numerous early to moderately deep primary carious cavities. Periodontal examination reveals no
periodontal pockets greater than 3-4 mm and minimal bleeding on probing. Radiographic examination confirms no
obvious peri-radicular radiolucencies. To the contrary, there are large radio-opacities in relation to the roots of
several teeth. There is minimal periodontal bone loss. In relation to his medical history he says he is taking
medication for Paget’s disease.
Why could Arthur have developed dental caries? (2 marks)

A

Polypharmacy and xerostomia in aging population, Diet and lifestyle factors - increased sugar intake, Non-fitting
denture acting as plaque trap, Reduced manual dexterity for OH

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98
Q

Arthur is a 68 year old retired mechanic who presents at your practice after an absence of 2 years. He is partially
dentate in the upper and lower arch and wears upper and lower acrylic prostheses. These prostheses were well
fitting when provided by you 2 years ago. He now complains that the upper prosthesis no longer fits well and is
uncomfortable. On examination the upper prosthesis does not seat fully in the edentulous regions. In addition,
there are numerous early to moderately deep primary carious cavities. Periodontal examination reveals no
periodontal pockets greater than 3-4 mm and minimal bleeding on probing. Radiographic examination confirms no
obvious peri-radicular radiolucencies. To the contrary, there are large radio-opacities in relation to the roots of
several teeth. There is minimal periodontal bone loss. In relation to his medical history he says he is taking
medication for Paget’s disease.
Account for the most likely cause of the radio-opacities on the radiograph. (1 mark)

A

Paget’s caused hypercementosis

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99
Q

Arthur is a 68 year old retired mechanic who presents at your practice after an absence of 2 years. He is partially
dentate in the upper and lower arch and wears upper and lower acrylic prostheses. These prostheses were well
fitting when provided by you 2 years ago. He now complains that the upper prosthesis no longer fits well and is
uncomfortable. On examination the upper prosthesis does not seat fully in the edentulous regions. In addition,
there are numerous early to moderately deep primary carious cavities. Periodontal examination reveals no
periodontal pockets greater than 3-4 mm and minimal bleeding on probing. Radiographic examination confirms no
obvious peri-radicular radiolucencies. To the contrary, there are large radio-opacities in relation to the roots of
several teeth. There is minimal periodontal bone loss. In relation to his medical history he says he is taking
medication for Paget’s disease.

How are you going to manage his clinical care? Describe the treatment you would provide and treatment you
would seek to avoid? (6 marks)

A

We will manage:
Prevention:
OHI (Toothbrushing/ Interdental cleaning/Fluoride use)
Diet advice

Disease control:
Perio:
BSP S3 step 1= Education, OHI, risk factor management, PMRP, 6 point pocket chart Plaque and gingival scores.
Caries:
Caries removal and restore
May need RCT if caries is extensive.

New dentures- Need to inform the patient that they will have to be frequently remade due to Paget’s.

Monitor:
More prone to malignancy = osteosarcoma (this is more common In young so when symptoms occur in older patients consider padgets)

Treatment you would seek to avoid = Extractions
Go through Osteolytic and osteoscleroitic phases
- During osteolytic phase = bleed a lot after XLA
- During osteoscleroitic phase = dense and harder to XLA = more prone to dry socket
- risk of Medication Related Osteonecrosis of the jaw as they are on bisphosphonates
- more prone to infection

They should be referred to a specialist for this treatment.

We need to regularly monitor this patient & Reassess.

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100
Q

You decide Arthur needs to have extraction of a lower molar which does not have a radio-opacity associated with
its root and you are aware he is taking bisphosphonates. What precautions would you take when you extract the
tooth? (7 marks)

A

OHI
Achieve Primary intention closure,
Use an atraumatic extraction technique,
Advise patient to contact the practice if they have any pain/tingling/numbness
Avoid raising flaps.
Review healing after 8 weeks
Refer to a specialist if complications develop,

NO CHX unless other clinical reason (Sdcep)

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101
Q

Name a life-threatening Vesicullo-bullous disease (1 mark)

A

Pemphigus vulgaris

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102
Q

Name 2 methods of testing for pemphigus and describe the histology of a positive result (4 marks)

A

Direct Immunofluorescence: basket weave appearance,
H&E staining microscopy: tzank cells, supra-basal split, acantholysis

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103
Q

How is pemphigus managed?

A

Topical/systemic steroid - beclometasone inhaler/prednisolone,
Analgesics

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104
Q

3 year old Child attends with blisters on gums - What is the likely diagnosis?

A

Primary Herpetic Gingivostomatitis.

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105
Q

3 year old Child attends with blisters on gums - How might the blisters appear

A

Fluid filled vesicles found on the gingivae/tongue/lips/buccal and palatal mucosa.
Will rupture causing ulceration covered by yellow membranes.
Lasts 10-14 days.

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106
Q

3 year old Child attends with blisters on gums - What other signs and symptoms may be present? (6)

A

Fever
Headache
Ulcers on lips. gingiva and extra-oral mucosa
Severe oedematous marginal gingivitis
Sore mouth with no desire to eat, chew or swallow.
Halitosis

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107
Q

3 year old Child attends with blisters on gums - What is the likely cause of the blisters?

A

primary herpetic gingivostomatitis = Initial infection of the Herpes Simplex virus I

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108
Q

3 year old Child attends with blisters on gums
It has been diagnosed as Primary herpetic gingivo-stomatitis - How do we manage this?

A

Reassurance- the lesions will heal spontaneously in 1-2 weeks.
Advise infectious nature to patients eyes / immunocompromised.

Treatment
Bed rest
Soft diet/ hydration
Paracetamol (antipyrexic & analgesic)
Antimicrobial gel or mouthwash if too sore to brush(Chlorohexidine)
Refer to specialist if too sore for patient to eat or drink (may need topical acyclovir)

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109
Q

3 year old Child attends with blisters on gums
It has been diagnosed as Primary herpetic gingivo-stomatitis. What future issues may this virus cause? (2)

A

Secondary infection- herpes labialis (cold sores)
Bell’s palsy (inflammation of the facial nerve)

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110
Q

Patient attends with generalised white plaque that scrapes off easily and leaves an erythematous base.
What is your diagnosis?

A

acute pseudomembranous candidiasis

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111
Q

What two medical conditions might we see in patients with hairy leukoplakia ?

A

HIV, EBV

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112
Q

Patient attends with generalised white plaque that scrape off easily and leave an erythematous base
What to ask pathologist for when sending sample (1)

A

if Hairy leukoplakia take a biopsy and ask for a Special stain for EBV

Candida = PAS stain from biopsy if candida not resolved after antifungals

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113
Q

A patient presents at your practice with a large brown/grey discoloured swelling.
Give 3 causes of localised pigmentation (brownish grey) in the mouth.

A

Local-
Amalgam tattoo due to macrophages and granulation tissue surrouding the amalgam.
Pigmented incontinence linked with chronic inflammation.
Vascular malformation (Haemangioma)
Macule- flat due to increased melanin production
Naevus (raised)- due to increased melanocytes

General-
Racial/familial
Smoking (leakage of melanocytes & submucosal fibrosis)
Medications (contraceptive pill/ iron tablets)
Addison’s disease- reduced cortisol and aldosterone from adrenaline glands causes brown patch due to the increased ACTH.

114
Q

A patient presents at your practice with a large brown/grey discoloured swelling.
What is a haemangioma?

A

A developmental overgrowth/collection of tiny blood vessels that burst their walls creating a venous lake.

These are commonly found on the inside of the lip/edge of the tongue & trauma can cause bleeding.

115
Q

A patient presents at your practice with a large brown/grey discoloured swelling.
Name two types of haemangioma

A

Capillary- superficial so bright red in colour
Cavernous- Deep so appear bluish under the skin

116
Q

A patient presents at your practice with a large brown/grey discoloured swelling.
What is the histological difference between the 2 types of haemangioma

A

Capillary: groups of smaller vessels, most of which are capillaries. Held tightly together by connective tissue.

Cavernous: larger, dilated vascular blood spaces filled with slow moving rapidly deoxygenating blood (not closely packed)

117
Q

Patient attends and we suspect they have trigeminal neuralgia.
Name 2 clinical investigations would you do?

A

OPT- to rule out dental case
MRI- to rule out any space occupying lesions
Trigeminal nerve reflex testing
Blood: FBC, haematinics, blood glucose, U&ES (for carbamazepine)

118
Q

Patient attends and we suspect they have trigeminal neuralgia.
How does trigeminal neuralgia occur?

A

idiopathic
Vascualar compression from the blood vessel as the nerve exits the brainstem.

Demyelination of the trigeminal nerve??

Multiple sclerosis
Space occupying intra-cranial lesion

119
Q

Patient attends with suspected trigeminal neuralgia
What 2 neurological disorders that may give rise to this type of pain

A

Multiple Sclerosis
Brain tumour compressing on trigeminal nerve

120
Q

What is the first line drug management for trigeminal neuralgia ?

A

Carbamazepine modified release- 100mg 1 tablet twice daily.

121
Q

What blood tests would you have to do before giving carbamazepine? (3)

A

Must check: FBC, LFT, Urea &Electrolytes for reduced Na (causes hyponatraemia)

122
Q

What are the 2 indications for surgery to treat trigeminal neuralgia ?

A

No improvement of condition with carbamazepine and had been tried for substantial period
Young patient

Medical intervention ineffective,
Medical intervention contraindicated
Medication causing side effects

123
Q

Name one type of surgery used to treat trigeminal neuralgia

A

Classical TG consider;
* Microvascular decompression (MVD)
- Preferred surgical treatment where possible

  • Destructive Central Procedures
  • Radiofrequency thermocoagulation
  • Retrogasserian glycerol injection
  • Balloon compression
  • Stereotactic Radiosurgery
  • Gamma knife = targeted radiation at the trigeminal ganglion to kill trigeminal nerve cells
  • Destructive Peripheral Neurectomies = Only performed as a last resort after trial local anaesthesia
124
Q

What are the side effects of carbamazepine? (5)

A

Blood dyscrasias (Thromocytopenia/ Neutropneia/ Pancytopenia)
Electrolyte imbalances (Hyponatraemia)
Liver toxicity
Skin reactions
Ataxia (similar to being drunk)

125
Q

What muscles are examined in a patient with temporomandibular disorder?

A

Masseter, temporalis,
(lateral pterygoid- palpating behind the maxillary tuberosity)
medial pterygoid-)

126
Q

Name some common causes of TMD

A

Stress, parafunction, occlusal discrepancies, trauma.

127
Q

What nerves supply the TMJ?

A

auriculotemporal
masseteric
posterior (deep) temporal nerve

128
Q

What are the signs and symptoms of TMJ dysfunction?

A

pain, stiffness, limited opening, deviation on opening,
click, crepitus, locking, headache.

129
Q

What are the mechanisms of a bite splint?

A

Minimise parafunctional habits
Improves mastigatory muscle function
Minimise load on TMJ
Eliminate occlusal interference (stabilising occlusion )

130
Q

What is arthrocentesis?

A

Where you inject into the superior compartment of the TMJ to wash the joint (breaks fibrous adhesion and washes away inflammatory exudate) to increase lubrication.
It is carried out under LA.

Used for patients with anterior dislocation without reduction.

131
Q

Give 2 other possible surgical options for treatment of TMJ dysfunction

A
  1. Menisectomy = remove the disc completely
  2. Disc plication = move the disc to correct position
  3. Eminectomy = remove part of the boney eminence
    Others:
  4. High condylar shave
  5. Condylotomy
  6. Condylectomy
  7. Reconstructive procedures
132
Q

What are the histological features of lichen planus?

A
  • Chronic inflammatory cell infiltrate (lymphocytic band hugging the basement membrane)
  • Saw tooth rete ridges
  • Basal cell damage
  • Patchy acanthosis
  • Parakeratosis.
  1. Keratinisation 2. Lymphocytes/macrophages 3. Atrophy/hyperplasia 4. Apoptosis 5. Basal Cell liquefaction leading to colloid bodies 6. Blue band of chronic inflammatory cells
133
Q

What are the different types of lichen planus? (6)

A

PPBREA
Papular- White plaques
Plaque- plaques arranged in lines
Bullous- development of fluid filled vesicles and bullae with skin lesions projecting from the surface
Reticular- spider web like lacy white lines
Erosive (ulcerative)
Atrophic- white bluish plaques with central superficial atrophy

134
Q

What can cause lichen planus? (8)

A

Idiopathic
Drugs (ACE inhibitors/ diuretics/ NSAIDS/ DMARDS/ beta blockers)
Amalgam restorations - contact sensitivity

stress - emotional and physical
systemic viral infections - hep C
trauma to the skin
localised skin disease - herpes zoster
genetic predisposition
contact senssitivity e.g amalgam

135
Q

When do you biopsy lichen planus? (3)

A

symptomatic/erosive or ulcerative
always in a smoker

Symptomless on a high risk area

136
Q

How do we manage lichen planus

A

Asymptomatic and reticular → monitor and reduce risk factor.
If we know the cause- remove them

If symptoms are mild- Chlorohexidine mouthwash/ Benzdamine mouthwash / remove SLS from toothpaste.

If symptoms are persisiting- beclomethasone MDI 50mg puffer or Betamethazone rinse (500mg dissolvable tablet 4x daily)

137
Q

What are the I/O manifestations of herpes?

A

Multiple Vesicles which burst to form round ulcers, 1-3mm.
Affects keratinised and non-keratinised mucosa
Lasts up to 2 weeks

138
Q

Name types of human herpes virus? (5)

A

Herpes simplex (HSV1&2)
Epstein-Barr Virus (HHV4)
Varicella
Zoster
HHV8 ass.w/ Kaposi’s sarcoma,

139
Q

Which cranial nerve does herpes become associated with?

A

trigeminal nerve

140
Q

Name the common triggers for reactivation of herpes.

A

stress
Illness
Fatigue
sunlight
menstruation
immunosuppression

141
Q

What is anaemia?

A

This is the reduction of haemoglobin below normal in the blood meaning the blood has a low oxygen carrying capacity.
This can be due to;
low RBC from reduced production, increased loss
or
dysfunctional RBC’s.

142
Q

What are the general signs and symptoms of anaemia? (10)

A

Lethargy
dizziness
Fatigue
Weakness
Shortness of breath
Increased threat (?)
Noticable paleness and coldness
Loss of consciousness
Low blood pressire
Palpatations

143
Q

What are the oral signs of anaemia?

A

Recurrent oral ulceration,
candida,
glossitis/smooth tongue(iron deficiency),
beefy tongue (VitB12/folate deficiency),
oral dysaesthesia,
mucosal pallor.

144
Q

What are the treatment options for microcytic anaemia? (4)

A
  1. Correct underlying cause:
    - Correct Iron deficiency or thalassaemia.
    - Diagnose and treat any causes of blood loss (chronic)
  2. Provide:
    Iron - via diet advice and supplements advice

For severe cases of microcytic anaemia:
3. RBC blood transfusions

  1. May need erythropoietin replacement (pt with renal function problems - no erythropoietin- kidney not working= red blood cells not produced)
145
Q

What 3 oral conditions are associated with microcytic anaemia?

A

o Recurrent aphthae
o Atrophic glossitis = smooth tongue
o Burning mouth syndrome
o Increased Candida infection - angular cheliitis

o Poor wound healing
o Generalised Mucosal atrophy

146
Q

Name the type of anaemia from MCV

A

Microcytic- below normal value- caused by iron deficiency/ thalassaemia
MCV < 90FL

Normocytic- within normal values- caused by bleeding/ sickle cell anaemia/ chronic disease (diabetes or kidney disease).

Macrocytic- bigger than normal cells - B12 or foliate deficiency. (hypothyroidism or liver disease)
MCV > 90FL

147
Q

What are the causes of xerostomia?

A
  • Local: Mouth breathing, Candida, Alcohol, Smoking, Sialolith
  • Salivary gland diseases: Sjogren’s, CF, HIV, Sarcoidosis, Amyloidosis, Haemochromatosis
  • Drugs: Tricyclic Antidepressants, Antipsychotics, Antihistamines, Diuretics, Atropine, Cytotoxics
  • Dehydrating conditions: Diabetes (1+2), Renal disease, Stroke, Addison’s, Persisting vomiting
  • Radiotherapy and cancer treatments
  • Anxiety and somatisation disorders
148
Q

How can you assess xerostomia intraorally?

A
  • Challocombe scale to test mirror sticking to cheek/ tongue & saliva pooling.
  • salivary flow rate testing unstimulated whole salivary flow over 16 minutes (abnormal <1.5mls in 15 mins)
149
Q

What are the oral signs and symptoms of xerostomia

A

Difficulty- swallowing, speaking, eating, denture control
Tongue fissuring
Altered taste
Halitosis
Increased candida infections
Frothy saliva
Gingivae- loss of architecture and glossy appearance.
Halitosis
INcreased periodontal disease
Increased cervical caries

150
Q

How can we manage xerostomia?

A

Treat the cause: Hydration/ modify drugs/ controlling diabetes/ controlling oral dysaesthesia (meds)/ mouth breathing/ SLS toothpaste

Substitute saliva- Saliva orthana- pH neutral and contains fluoride.

Prevent disease (caries/ candida/ angular cheilitis) through diet advice/ high fluoride toothpaste and OHI. Treat candida.

151
Q

Name 3 salivary subsitutes

A

Glandosane-acidic so we avoid it

saliva orthana- best as pH neutral adn contains fluoride
Biotene
Oral balance
bioxtra

152
Q

Name 3 sugar subsitutes

A

Xylitol
Manitol
Sorbitol

153
Q

List 3 salivary proteins

A

IgA, PRP, Mucins, Histatin

154
Q

LIst 3 salivary enzymes

A

lipase, lysozyme, amylase

155
Q

What is sjogren’s syndrome?

A

A systemic multisystem autoimmune disease

It is a chronic inflammatory and autoimmune disorder
Affects a wide range of organs in the body due to B-cell proliferation destructing exocrine glands.

It particularly affects secretion production at the mucous membranes. This causes dry mouth, reduced tear production and dryness of other body membranes.

There are three types:
Partial sjogren’s (dry eyes OR dry mouth)
Primary ( Sjogren’s without Connective tissue disease)
Secondary (Sjogren’s with a connective tissue disease

156
Q

What antibodies are linked with? Sjogren’s

A

Anti-Ro and Anti-la

157
Q

What are the investigations used to diagnose Sjogren’s

A

Dry eyes
Subjective (Dry eyes >3 months/ feeling. of sand in eyes/ Tear substiutes used >3 times a day)
Objective-Schirmer test <5mm in 5 minutes

Dry mouth-
Subjective (Dry mouth >3 months/ needing to drink liquid to swallow/ recurrent salivary gland swelling)
Objective- Salivary flow test (<1.5ml in 15 minutes)

Auto-antibodies (presence of anti-ro or anti-la)

Histopathology: Focal score >1 lymphocyte focus.

Ultrasound- leopard presentation

sialography - snowstorm appearance

158
Q

What gland do we biopsy to investigate sjogren’s

A

Labial gland biopsy

159
Q

What are the histopathological features of Sjogren’s ?

A
  • > 1 lymphocyte focus (collection >50 lymphocytes)
  • > Acini atrophy.

Minor gland:
*Focal lymphocytic sialadenitis, acinar loss and fibrosis
* Focal collection of lymphocytes 50+ in each collection
Major gland:
* lymphocytic infiltrate which extends to whole lobules § Atrophy of acini
* Duct epithelial hyperplasia which occluded the ducts § Epithelial structures have myoepithelial islands

160
Q

Name 4 oral complications of sjogren’s disease?

A

Oral infection (candida)
Increased caries risk and periodontal disease
Reduced lubrciation affecting (Denture retention/ Speech/Eating)
Sialosis (usually symmetrical)
Functional loss
Salivary lymphoma risk (non-hodgkin lymphoma)

161
Q

What drugs are used to manage Sjogren’s

A

If a patient is presenting with a dry mouth and salivary deficit = Gland function is already very low
* Salivary stimulants – pilocarpine (think side effects)

If patient presenting early – NO dry mouth yet = active gland disease
* Liaise with rheumatologist – multisystem disease
* Consider Immune modulating treatment – hydroxychloroquine, methotrexate – to halt the disease process and prevent symptoms developing in the future

162
Q

Where would you commonly find a salivary neoplasm

A

Parotid 80% of all tumours (15% malignant)
Submandibular 10% of all tumours (30% malignant)
Sublingual 0.5% of all tumours (80% malignant)
Minor 10% of all tumours (45% malignant )

163
Q

What are the symptoms of ectodermal dysplasia?

A

Hypodontia and peg shaped teeth
Poor functioning sweat glands
Abnormal nails
CLP
Decreased skin pigmentation
Large forehead
Low nasal bridge
Thin sparse hair
learning disabilities

164
Q

What are the clinical and radiographic signs of Albright’s disease?

A

Genetic condition csuaing the development of areas of fibrous tissue within bone

Usually part of Albrights syndrome:
3 main characteristics:
- Polyostotic fibrous dysplasia
- Melanin pigment (coffee with milk spots)
- Early puberty (especially in girls)

-Autonomous endocrine hyper-function ??

Radiographic
-Regular bone fractures, pain and deformities
-Craniofacial fibrous dysplasia (bone is replaced by fibrous tissue so doesn’t look like normal trabecular bone * Variable, abnormal appearance: Ground glass, orange peel, fingerprint whorl, cotton wool, amorphous (no real appearance – loses trabecular pattern)
Margins blend into adjacent bone and hard to define

165
Q

You have read your patient’s medical records which say they have Paget’s disease.
What are the clinical and radiographic signs of Paget’s disease

A

Clinical:
-Localised Pain or facial palsy from nerve compression
- deafness or blindness
-Focal temperature due to hyperaemia and hypervascularity
-boney swelling size
-Bowing deformities
-Decreased range of motion
-Dentures become ill fitting
-migration of teeth (due to increased jaw size)

Radiographic:
- Patchy and cotton wool appearance from radiolucent areas and radiopaque areas
- Loss of lamina dura
- Hypercementosis
- Migration (due to bone enlargement) and displacement
- Osteoporosis circumscripta
– well defined large lytic lesions
-Radiolucent regions resembling cysts May occur in mature lesions of fibrous dysplasia

166
Q

You have read your patient’s medical records which say they have Cherubism.
What are the clinical and radiographic signs of Cherubism.

A

Clinical-
Painless bilateral enlargement of the jaws
Rounded face and swollen cheeks
Dental malocclusion.

Radiographic-
Mutlilocular radiolucencies delimited by cortical bone and distributed bilaterally in the posterior quadrants of the mandible or maxilla.
Mandible or maxilla replaced with fibrous tissue
Facial sinuses appear obliterated.

167
Q

Name and describe the types of orofacial pain syndromes?

A

Dental
generally gets better or worse over time. Usually acute or subacute (Not chronic)
e.g. Periapical abscess, TMJD pain, pulpitis, Atypical odontalgia (dental pain without dental pathology - Pain free episodes with immense pain that settles spontaneously)

**Non-dental:
**Generally acute infective non-dental pain that gets worse or chronic pain usually caused by a non dental condition.

  1. Persistent idiopathic facial pain (poorly fits into standard chronic symptoms & responds poorly to treatment)
  2. Oral Dysesthesia- Abnormal sesnory perception in absense of an abnormal stimulus. (Burning mouth syndrome/ Dysgeusia/ Touch dysaesthesia/ Dry mouth feeling)
  3. Trimgeminal neuralgia- Intense stabbing pain lasting 5-10s which poorly fits into the standard chronic pain syndromes.
  4. Painful trigeminal neuropathy (continuous/near continuous burning/ pins and needles)
  5. Trigeminal autonomic cephalgias (Cluster headache/ paraoxysmal hemicrania)
168
Q

Patient attends with denture induced stomatitis

What 2 features do you notice about the palatal tissues?

A

Erythematous and oedema of denture bearing areas
hyperplastic papillae

Patient complains:
Burning sensation/discomfort
Bad taste and halitosis of the mouth

169
Q

The patient attends with denture induced stomatitis.
How can this be classified?

A

Newton’s type I- Localised inflammation
Newton’s type II- Diffuse inflammation and erythema confined to the mucosa contacting the denture without hyperplasia
Newton’s type III- Granular inflammation with erythema and papillary hyperplasia

170
Q

What causes denture induced stomatitis?

Describe what occurs.

A

poor denture hygiene
ill-fitting denture
Not removing denture at night
(oral steroids, dry mouth, imunocompromised)

It is the adherence and colonisation of acrylic surfaces cause by co-
aggregation and biofilm formation

171
Q

Patient has attended with denture stomatitis.
What is your 1st line treatment?

A

Local measures first:
Denture Hygiene Instruction
brush palate daily
clean denture thoroughly - soak in CHX or sodium hypochlorite (acrylic only) for 15 mins 2x per day.
Wear dentures as little as possible

No resolution:
2nd line (miconazole/fluconazole/ nystatin)
new dentures made when health restored

172
Q

Patient has attended with denture stomatitis.
What is your 2nd line treatment?

A

Combine the improvement in OH with :
Topical antifungal
Miconazole oromucosal gel (20mg/g) applied 4 times daily after food.
Systemic antifungal- Fluconazole 50mg capsule 1 daily for 7 days.

If contraindicated (so for patients taking warfarin or statins)
Nystatin 30ml oral suspension 1ml after food 4x daily for 7 days.

173
Q

3 herpes group viruses associated with intra oral vesiculation

A

Human Herpes simplex
Group A Coxsackie virus
Epstein Barr virus (EBV)
Varicella zoster virus Cytomegalovirus

174
Q

Name 2 oral mucosal disease caused by Coxsackie viruses

A

Hand foot and mouth disease (ulceration on the gingivae/tongue/cheeks/ palate & macropapular rash on the hands and feet)
Herpangina- vesicles found in the tonsillar or pharyngeal regions.

175
Q

Name 2 oral diseases caused by Epstein-Barr virus (EBV)

A

Infectious mononucleosis
Oral hairy leukoplakia

176
Q

Which cranial nerve does herpes simplex become resident to on lower lip? Nerve
and branch

A

Mandibular division of the trigeminal nerve

177
Q

Name common trigger for reactivation of herpes simplex lesions

A

Stress
Infection
Sunlight
Fatigue
Immunosupression.

178
Q

Your patient attends with Bell’s palsy. What is the aetiology for bell’s palsy?

A

Bell’s palsy is a temporary (can be permanent in rare cases) type of facial palsy/paralysis that has an unknown cause, affecting the excitability of the facial is nerve.
It is ultimately caused by inflammation around the facial nerve and this pressure causes facial paralysis on the affected side
- may have a viral cause (HS1 or other)
- Otitis media- Inflation of the middle ear can apply pressure to the nerve and cause lack of function.
- Penetration from local anaesthetic = temporary BP.

It has unilateral paralysis of the whole side of the face including the eyebrows = stroke doesn’t affect eyebrow

179
Q

Your patient attends with Bell’s palsy.
How do we manage their condition?

A

inform and reassure that the paralysis is temporary.
Protect the eye with an eyepatch until the blink reflex returns (to prevent the eye drying out)

Review + referral if full recovery not achieved within 3 months.

180
Q

Your patient attends with bell’s palsy. How can we differentiate between upper and lower motor neuron disease?

A

Upper motor neuron disease (stroke)
Spasiticity (stiffness of muscle)
Can wrinkle forehead & move eyebrows but cannot move lower portion of the face.

Lower motor neuron disease (facial palsy)
Flaccidity(softened muscle)
Pt cannot wrinkle the forehead/ move eyebrows or move the lower portion of the face.

181
Q

Explain the difference between the upper and lower motor neruon disease?

A

The lower face only has 1 nerve supply so damage to this means there will be facial paralysis. In contrast the upper face is supplied from the same and opposite side of the corticospinal chord. Therefore, paralysis of the upper face is dependent on where the lesion exists (before or after the motor decussation in the medulla)

Upper motor neuron disease occurs in the supra-nuclear lesion whereas a lower motor neuron lesion affects the nucleus of the facial nerve.

UMN lesion interrupts the neural pathway at a level above anterior horn of the spinal cord. (Upper face supply already split so lesion will only block 1 supply)
LMN lesion interrupts the spinal reflexes arc to the muscles (nerve supply for upper face not yet split so this lesion will also cause paralysis of the upper face)

182
Q

List lower motor diseases.
Give possible causes of lower motor neuron disease

A

o MND
o Guillain-Barré syndrome (GBS)
o C.botulism
o Polio
o Bell’s palsy

Trauma/viral infection of ventral horn cells

183
Q

Give possible causes of upper motor neuron disease

A

o Stroke
o Multiple sclerosis
o Traumatic brain injury
o Cerebral palsy
o Spinal cord injury

184
Q

How do we manage Lower motor neuron disease

A

o Distinguish cause of the paralysis through x-rays, history, blood tests
o Reassurance
o Prednisolone to reduce swelling and initial inflammation around the nerve
o Eye protection if the cornea is at risk
o Referral to specialist services if paralysis does not resolve within weeks.

185
Q

On your patient’s medical history form they are taking steroids.
What conditions may require a patient to be on long term steroids?

A

o Severe asthma
o COPD
o Addison’s disease
o Arthritis
o Crohn’s disease
o Lupus
o MS

186
Q

On your patient’s medical history form they are taking steroids.
What are the signs and symptoms of adrenal supression.

A

Adrenal supression is Hypofunction of the adrenal gland (also known as Addison’s disease)

Signs:
Postural hypotension- Low BP (due water & salt depletion)
Weight loss and lethargy - due to loss of fluid
Hyperpigmentation - Overproduction of ATCH (trying to produce cortisol) causes overreaction of melanocytes
Vitiligo (Loss of pigment of patches of skin)

Symptoms :
Dehydration
Weakness
Weight loss.

187
Q

On your patient’s medical history form they are taking steroids. What emergency can be associated with adrenal insufficiency?

A

Addisonian crisis-
If a patient doesn’ thave enough steroids (Cortisol or aldosterone)
Patients don’t have enough fluid or salt- causing them to gradually pee out their blood pressure.

Hypotension
Vomiting
Eventually a coma.

188
Q

Why are asthmatics more prone to erosion? (3)

A

Asthmatic medications place the patient at risk of dental erosion by;
Xerostomia = reducing salivary protection against extrinsic and intrinsic acids
Inhalers can be acidic
Asthmatic patients may also be more prone to GORD which can cause dental erosion.

189
Q

What is the proper name for burning mouth syndrome?

A

Oral dysaesthesia

190
Q

Who is more likley to be affected by burning mouth syndrome? (4)

A

Females > males
Mostly post menopasual women
Aged around 40-60.
haematinic deficiency
Stress and anxiety

191
Q

What are the causes of oral dysaesthesia?

A

Deficiency of Haematinics/ Zinc/ Vit B1/ Vit B6
Fungal and viral infections
Anxiety and stress

192
Q

What are the signs and symptoms of oral dysaesthesia?

A

Burning or nipping feeling in the mouth.
Sensation of dry mouth with increased thirst
Taste changes such as bitter or metallic taste

193
Q

You think the patient could have Oral dysaestheisa. What other differential diagnoses should we consider?

A

Parafunction - can present on tip of tongue and lips
Dental cause (e.g. perio)
Oral infections
symptomatic lichen planus
Xerostomia
Undiagnosed systemic conditions (e.g. diabetes)
Denture problems.

194
Q

You think the patient has oral dysaesthesia. What investigations might you carry out?

A

Blood tests (FBC/ Haematinics/ U&E/ TFT/ LFT/ HbA1c)
Salivary flow rate
Intra & extra-oral examination for parafunctional habits.
Denture assessment.

195
Q

How is oral dysaesthesia managed?

A

Educate and Reassure

Correcting any underlying causes
- treat anxiety
- Nutrient replacement therapy
- treat dry mouth
- Diabetes diagnosis and treatment
- Correcting poorly fitted dentures
- Management of parafunctional habits

Conservative advice
-empower the pateitn and give them control
- staying hydrated
-Benzdamine mouthwash (pain relief)

Pharmacotherapy:
CBT
Gabapentin

196
Q

What is the mechanism of action of Chlorohexidine?

A

It has a diatonic action
One ion binds to the oral surface and one ion to the bacterial cell membrane.

It binds to the microbial cell wall causing cell wall damage (membrane disruption) and interferes with cell wall permeability (osmotic damage) causing the leakage of cell contents which leads to cell death.

:
* +ve charge CHX molecules react with -ve charged clean surface of microorganism and damaged the microbial cell envelope

  • When there is low concentration of bacterial membrane there will be increased permeability
  • When there Is high concentration of the bacterial membrane there will be precipitation of the cytoplasm and resultant cell death which also inhibits absorption from the gut
197
Q

What family of antiseptics does chlorohexidine belong to?

A

Bisbiguanides

198
Q

What is substantivity?

A

Substantivity is defined as the prolonged adherence of the antiseptic to the oral surface and its slow release in effective doses that guarantee the persistence of its antimicrobial activity.

CHX has a great substantivity (~12hours), meaning it is retained in the oral cavity for extended periods of times and provided slow and sustained release of the active ingredient – bisbiguanides.

199
Q

What solution of chlorohexidine is given to patients?

A

0.2% chlorhexidine mouthwash- rinse 10ml for 1 minute twice daily

200
Q

What are the side effects of chlorhexidine ?

A

o Mucosal irritation
o Parotid gland swelling
o Reversible brown staining of teeth and restorations
o Taste disturbances
o Tongue discolouration
o Burning of mouth and gums
o Hypersensitivity and possible anaphylaxis

201
Q

What are the indications for the use of chlorhexidine?

A

o Short term used for candidosis (pseudo and erythematous)
o Cleaning dentures
o Pre +/- post oral and periodontal surgery
o In physically or mentally disabled patients to prevent oral infections when good
OH is difficult to maintain
o Immunocompromised patients
o Management of ANUG, aphthous ulcers, xerostomia and mucositis
o Used as irrigant during RCTs
Checking dental dam seal during RCT
o In high caries risk patients
o OHI patients with jaw fixation (IMF;ORIF)

202
Q

Name the 3 stages in the formation of clots

A
  1. The endothelial injury causes Vasoconstriction (of BV to reduce blood flow & loss)
  2. Platelet aggregation - Platelets become locally active and adhere to one another and adhere to the injured endothelium - Von willebrand factor is released by damaged cells & surface proteins on the Platelets bind to this.
  3. Coagulation cascade - activation of coagulation factors, fibrin plug is formed from platelet releasing chemicals which bind to fibrinogen linking the platelets together (Forming the fibrin plug)
203
Q

How does aspirin affect clotting?

A

It reduces prostaglandin production by inhibiting cyclo-oxygenases (COX-1 and COX-2) preventing thromboxane A2 production.

This inhibits platelet aggregation
& is irreversible for the life of the platelet. (8-9 days)

204
Q

How does warfarin affect clotting?

A

Inhibits vitamin K reductase complex 1- depleting functional vitamin K & reducing clotting factor synthesis (Factors 2/7/9/10 and proteins C&S)

205
Q

How does Apixaban affect clotting?

A

Factor Xa inhibitor which stop sthe production of a fibrin clot by inhibiting the conversion of prothrombin -> thrombin

Apixaban

206
Q

How does Dabigatran affect clotting?

A

This inhibits thrombin (preventing fibrinogen -> fibrin and the formation of the clot )
DabigaTran

207
Q

How does Rivaroxaban affect clotting?

A

Factor Xa inhibitor which stop sthe production of a fibrin clot by inhibiting the conversion of prothrombin -> thrombin

RivaroXaban

208
Q

Why are aspirin and clopidogrel used in conjuction?

A

Aspirin inhibits cycloxoygenase preventing thromboxane A2 production.
Clopidogrel- Blocks the P2Y12 Adenoside Triphosphate receptor on the platelet surface so interfeeres with platelet activation, degranulation and aggregation. (and reduced firbin clot production)

These are used together to treat coronary/cerebral or peripheral artery disease.

209
Q

What is the pattern of Von Willebrand’s disease?

A

It has an autosomal dominant condition with different inheritance patterns.
Type1 - Autosomal dominant (mild- quantitative deficiency VWF)
Type 2- Autosomal dominant (mild qualitative deficiency VWF)
Type 3 = autosomal recessive = severe (deficiency of VWF)

210
Q

How does Von willebrand diease affect bleeding ? (2)

A

Defect of the VW protein on platelets = reduced platelet aggregation
paired with a reduced factor 8 levels.

(VW protein stabilises factor 8 to enable platelet interaction )

211
Q

What is a biofilm?

A

A biofilm comprises of an aggregate of microorganisms, whose cells adhere to one another and embed in a surface. The adherent cells become embedded within a self-produced matrix of extracellular polymeric substances which allows the adherence to a surface.

212
Q

What are the stages of colonisation of a biofilm?

A

Reversible attachment-
Irreversible attachment- reduced production of flaggela gene
Maturation 1- cell clusters embedded in the biofilm
Maturation 2-Colonisation of the bacteria.
Dispersion- of the bacteria.

Niamh - attachment, colonisation, accumulation, complex community

213
Q

Give 4 methods of identifying the bacteria

A
  • Microbiological culture- on a suitable agar material allowig isolationof the bactiera and identification through suitable tests .
  • DNA probes- Label the segment of DNA with chemoluminescent of fluoronescent. When the bacteria is denatured- the labelled DNA will bind to its complementary strand.
  • PCR- Selecting a target sequence of DNA and amplifying it.
  • ELISA- enzyme linked immunosorbant assay- using enzymes to attach to the antibody.
214
Q

What are the virulence factors for P, gingivalis?

A

Host cell tissue adherence and invasion (fimbriae)
Proteases (Degradative enzymes e.g. gingipans)
Endotoxin (LPS)
Metabolic by-products

215
Q

What are the virulence factors for Candida, albicans?

A

Altering the target site to prevent azoles binding
Changing the cell membrane composition to prevent the insertion of polyene into the cell membrane.
Hyphae causing damage to host tissue.
Hydrolytic enzymes- attachment to host cells & causes cell structure.

216
Q

What are the virulence factors for Strep mutans?

A

o Adhesions, glucagon and polysaccharide production
o Biofilm formation
o Acid tolerance- through the acid ATP pup to maintain pH balance and adaptation

217
Q

What is the clinical appearance of plasma cell gingivitis?

A

A clinically as a diffuse, erythematous and papillary lesion of the gingiva, which frequently bleeds, with minimal trauma.
Swelling of the gingiva and the upper lip
A burning sensation on the tongue.

218
Q

What is the aetiology of plasma cell gingivitis?

A

Caused by an allergen (SLS toothpaste/ cinnamon /mint)
Idiopathic
Neoplastic

219
Q

What can worsen the patient’s plasma cell gingivitis?

A

Not removing the causative agent
Poor OH
Plaque retentive factors

220
Q

How do we manage plasma cell gingivitis?

A

Histological sampling to diagnose condition and rule out (Lichen planus/ Gingival pemphigoid/ malignancy) Normal bloods rule out leukaemia)
Preventing exposure to causative agent.

Sometimes- topical steroid (Tacrolimus)

221
Q

Name 4 dental treatments in which antibiotics are indicated

A
  • Prophylactically for infective endocarditis (Valve replacements/
  • Spreading infection (cellulitis/ lymph node involvement/ swelling/ fever/ malaise)
  • Necrotising gingival diseases- if patient is systemically unwell.
  • Sinusitis (if symptomatic treatment is not effective. Lasts longer than 10 days. Fever. Worsening symptoms.
  • Conservatively if there is an oac (OAC increases patient risk of sinusitis- SDCEP)
222
Q

Give 5 ways in which antibiotics work?

A
  • Inhibit cell well synthesis
  • Inhbiti protein synthesis
  • Inhibit DNA acid replication and transcription
  • Injure the plasma membrane
  • Inhibit the synthesis of essential metabolites
223
Q

Give 3 disadvantages of antibiotic use?

A

Antibiotic resistance
Interactions with other medications
Hypersensitivity / anaphylaxis (e.g. penicillin allergy)

224
Q

Name 3 antibiotics used in dental treatment and include regime

A

**Spreading infection **
Pen V (500mg 2 tablets 4x daily for 5 days)

NG or NP
Metrondiazole 400mg 1 tablet 3x daily for 3 days

Sinusitis (if symptomatic treatment is not effective)
Pen V (500mg 2 tablets 4xdaily for 5 days)

prophylaxis
3g amoxycillin 1 hour before treatment

225
Q

What are the mechanisms of antibiotic resistance?

A

a. Enzymatic inactivation
b.Modified target
c.Decreased uptake
d.Increase efflux

Inactiviating the enzymes in the bacteria
Alteration of the target molecules on the bacteria used by the antibiotic
Efflux of the antibiotic
Bacteria blocking entry.

226
Q

You have an asthmatic patient who takes 2 inhalers - What kind of inhalers will these likely be?

A

Short acting beta 2 adrenergic agonist- Salbutamol (blue)
Corticosteroid betamethasone inhaler - Budesonide (brown)

227
Q

You have an asthmatic patient who takes 2 inhalers.
What is asthma?

A

A Reversible airway obstruction due to bronchial hyperactivity in response to a minor stimuli.
This causes inflammation and swelling of the airways mucosa, excessive mucous secretion and smooth muscle airway contraction.

228
Q

You have an asthmatic patient who takes 2 inhalers.
What are the signs and symptoms of asthma?

A

Shortness of breath
Wheezing sound when exhaling
Coughing
Chest tightness or pain

229
Q

You have an asthmatic patient who takes 2 inhalers.
What are the dental impacts of inhalers and what advice should be given?

A

**Increased risk of candida infection (due to the corticosteroid) - get patient to rinse out their mouth after using the inhaler.

Increased erosion (chronic cough at night can cause reflux of gastric acid) - ensure regular dental checkups and use of fluoride

Dry mouth (patient more likely to breathe through their mouth) - ensure correct use of inhalers / use of a spacer and increase fluid intake.

230
Q

You have an asthmatic patient who takes 2 inhalers.
What other considerations should be given when treating this patient?

A

Avoiding Colophony containing fluroide varnish in children who. havebeen hopsitalised with asthma in the last 12 months.

Analgesia- avoid aspirin and other NSAIDs

Their asthma will affect their sedation - IV sedation if worsened by stress
GA type (ASA2)

Asthma attacks-
If pt cannot form a sentence- ambulance
Mild/Moderate use salbutamol inhaler (2 puffs)
Severe- Spacer device (if patient has lost ability to hold their breath for 10s)
Use for 20s to prevent respiratory acidosis- stopping patient rebreathing their own CO2)

231
Q

You have an asthmatic patient who takes 2 inhalers.
What percentage of people in scotaldn are being treated for asthma?

A

2 out of 10 people in scotland

232
Q

You have been given a biopsy of a pottentially malignant lesion.
List 11 histological signs of epithelial dysplasia

A

Cytological changes:
Abnormal variation in nuclear size
Abnormal variation in nucelar shape
Abnormal variation in cell size
Abnormal variation in cell shape
Hyperchromatism- change in nuclei staining due to more DNA material
Atypical mitotic figures

Architectural changes:
How much of the epithelium is involved
Irregular epithelial stratification
Abnormal keratinisation
Loss of epithelial cell cohesion or adhesion
Drop shaped rete ridges.

233
Q

You have been given a biopsy of a pottentially malignant lesion.
How is dysplasia graded?

A

WHO (2005)
Basal hyperplasia (increased basal cells)
Mild dysplasia -Changes in lower third of epithelium (removal of the cause can help it regress)
Moderate dysplasia- change extends to the mid third
Severe dysplasia- change extends to the upper third
Carcinoma in situ- All cells show malignant change but it has not spread to the underlying connective tissue.

234
Q

What is the histological difference between pemphigus and pemphigoid?

A

Pemphigoid- Antibodies attacking the hemi-desmosomes causing separation of the basement membrane and connective tissue. Fluid and inflammatory exudate fills the epidermis. (Thick walled blisters)

Histology:
Subepithelial split with fluid filling the split

Pemphigus- antibodies attack the desmosomes between the cells, allowing fluid between them. This causes the cells to thin and loss of epithelium (Ulcers)

Histology:
Suprabasal split
Tzank cells.

235
Q

How do pemphigus and pemphigoid differ clinically

A

Pemphigoid- Thick walled blisters that persist for some time- Can be clear or blood filled (leakage of RBC if there is damage to the connective tissues)
Pemphigus- mucosal erosion and mucosal surface loss

236
Q

How can we investigate pemphigus and pemphigoid?

A

2x biopsies - 1x perilesional and 1 from anywhere in mucos (can also be perilesional)
Perilesional Biopsy- cannot guarantee the epithelium will still be on the biopsied part of the blister- so we take a biospy from an area close by

1 biopsy = Immunofluorescence- Direct Taken using IgG antibodies. Looking for
Basketweave staining (Pemphigus)
Linear staining along the basement membrane (Pemphigoid)
(can also use but not as useful for diagnosis) Indirect- taken using patient serum and testing for IgG levels.

  1. H&E staining fro histopathology
237
Q

How are pemphigus and pemphigoid managed?

A

Pemphigus-
Fluid intake advice
For symptoms- Benzamine moutwash (Difflam)/ Betamethasone mouthwash (topical steroid)
High dose steroids Prednisolone, immunosupressant and biologics

Pemphigoid-
Fluid intake advice
For symptoms- Benzamine moutwash (Difflam)/ Betamethasone mouthwash (topical steroid)
Immune modulating drugs-azathioprine
High dose steroids

238
Q

What are the risk factors for oral cancer? (6)

A

Tobacco (Smoking/ smokeless)
Alcohol (co-morbiity )
Betel quid
Socioeconomic status
Poor diet and nutrition
Viruses (HPV/ EBV/ HHV-8)

239
Q

What are the signs and symptoms of oral cancer

A

Signs:An ulcer which doesn’t heal after 2 weeks.
Rolled margins /central necrosis.
Speckled erythroleukoplakic appearance
Cervical Lymphadenopathy (enlarged/ firm / non-tender)

Symptoms:
Worsening pain (Dysaestheisa/ paraesthesia/ Neuropathic pain)
Referred pain (to the ear/throat/mandible)
Weight loss (local/ systemic effect)

High risk sites-
Floor of mouth/ lateral border of tongue/ retromolar region/ Soft and hard palate

240
Q

How does cancer spread?

A

Local spread
Lymphatic spread
Haematogeneous invasion (blood & associated with a poor prognosis )
Perineural invasion

241
Q

What is the metastatic cascade?

A
  1. intravasation- cancer cells move into the blood vessels
  2. Survival in circulation
  3. Arrest in organ
  4. Extravasation- exiting the capillaries and moving into the organ.
  5. Survival of cells after extravasation
  6. Persistence of growth

1.local invasion, 2.intravasion, 3.survival in circ, 4.extravasion into normal tx, 5. survival, 6. growth/proliferaiton

242
Q

What is the TNM grading system

A

T- for Tumour size (primary)
TX- size cannot be assessed
T0 (no tumour)
T1(<2cm)
T2(2-4cm)
T3(>4cm)
T4 (>4cm with involvement of antrum/pterygoid muslces/base of tongue or skin)

N- Nodes
Nx- not assessed
N0-No nodes
N1 (single ipsilateral <3cm)
N2a (single ipsilateral 3-6cm)
N2b (multiple ipsilateral 3-6cm)
N2c (bilateral or contralateral <6cm)
N3- lymph node >6cm

**M- Metastasis **
Mx- not assessed
M0- no evidence
M1- distant metastasis present

Scores are combined to give an overall stage of cancer 1-4 increasing in severity.

243
Q

What is necrotising sialometaplasia?

A

A benign ulcerative lesion with a surface slough- usually caused by vascular damage to the palatine vessels causing blockage in flow to the minor salivary galnds.

244
Q

What is the aetiology of necrotising sialometaplasia?

A

Small vessel ischaemia with resultant infarction due to smoking/trauma/LA/ bulimia/ infections

245
Q

How does Necrotising sialometaplasia appear histologically?

A
  • Squamous metaplasia of the ducts and acini in the affected lobule
  • Necrosis of the salivary acini
  • ischemic lobular necrosis of seromucous glands,
  • Preservation of intact lobular architecture despite necrosis and inflammation,
  • Accumulation of necrotic debris in the adjacent lobules

The Salivary gland is divided into lobules

246
Q

How is necrotising sialometaplsia managed?

A

Symptomatic management
Conservative management
It will spontaneousy heal (in 6-10 weeks by secondary intention)

247
Q

Give 2 differential diagnoses for Necrotising sialometaplasia

A

Squamous cell carcinoma
Salivary gland carcinoma

248
Q

Patient presents with a swollen lower lip
Give differential diagnoses other than a mucocele?

A

Orofacial granulomatosis
Trauma to the lip causing swelling
Benign fibrous overgrowth
Soft tissue abscess
Squamous cell carcinoma
angio-oedema
hypersensitivity/allergy

249
Q

What is a mucocele?

A

retention = A recurrent swelling in the mucosa filled with saliva whch is caused by obstruction of a minor salivary gland.

or

mucous extravasation cyst (swelling extravasated into the tissues) from damage to a minor salivary gland

250
Q

How does a mucocele appear histologically?

A

A macrophage lined cavity surrounded by granulation tissue and foam cells (macrophages that have injested mucin)

251
Q

How do we manage a mucocele?

A

Excision of the mucocele and associated gland

252
Q

What is a mucocele in the floor of the mouth called ?

A

A ranula

253
Q

What is orofacial granulomatosis?

A

Increase in fluid in the oral and facial soft tissues due to an obstruction of the lymphatic drainage by giant cell granulomas.
This results in swelling .
It is mostly associated iwth a type 4 hypersensitivity reaction but can also be associated with chron’s and sarcoidosis

254
Q

Discuss the aetiology of orofacial granulomatosis?

A

Type 4 Hypersensitivity reactions producing granulomas
Chron’s disease
Sarcoidosis
Allergens to benzoates/ cinnamonaldehdye/ sordid acid / chocolate.

255
Q

What are the signs and symptoms of oral-facial granulomatosis?

A

Erythema of the peri-oral tissues
Buccal cobblestoning
Angular cheilitis
Swollen lips
Fissured lips
Full thickness gingivitis (not plaque related)
Enlarged submandibular duct (stag horning)
Tagging of intra-oral tissues

256
Q

How is oral facial granulomatosis managed? (4)

A

Dietary exclusion for 3 months

Topical treatments:
-miconazole for angular cheilitis
-Tacrilimus ointment for areas of lip swelling and facial erythema to disperse the obstructed giant cells
- Intralesional steroid injections (Triamcinolone)
Systemic immune modulation (Prenisolone pulse for short term/ Azathioprine for long term)

257
Q

Give 6 types of oral candida infection

A

Acute Pseudomembranous = thrush

Atrophic (erythematous lesion)
- acute
- chronic (denture stomatitis)

Hyperplastic/leukoplakia

Angular cheilitis

Median rhmoboid glossitis (symmetrical area on tongue anterior to circumvallate papillae)

258
Q

Where does median rhomboid glossitis occur?

A

This is central papillary atrophy of the tongue.
This affects the dorsum of the tongue anterior to the circumvallate papillae (separates anterior 2/3 and posterior 1/3)

259
Q

Give 3 histological features of median rhomboid glossiitis?

A

Candida hyphae infiltration
Elongated rete ridges
Hyperplastic rete ridges
Polymorphonuclear leukocyte.

260
Q

Give 3 methods of testing for candida?

A

Swab/oral rinse and culture

Biopsy lesion for histological testing- use a PAS stain

Smear for microscopy

261
Q

What are the virulence factors of candida?

A

Altering the target site to prevent azoles from binding
Changing the cell membrane composition to prevent the insertion of polyene into the cell membrane.
Hyphae causing damage to host tissue.
Hydrolytic enzymes- attachment to host cells & causes cell structure.

262
Q

Name 5 antifungal agents?

A

Topical:
* Miconazole
* Nystatin
* Chlorohexidine
Systemic:
* Fluconazole
* itraconazole

263
Q

What medication(s) is/are contraindicated for prescribing azoles

A

Warfarin and statins

264
Q

What information should be written on a prescription

A

Patient:
• Full name
• Address
• CHI
• Date of birth
• Age (If under 12)

Prescriber:
• Name
• Address
• GDC number
• Contact number
• Signature

Drug:
• Name
• Form of preparation
• Strength of preparation
• Dose frequency
• Duration of treatment
• Total quantity of drugs

Date prescription
Score out any residual space.

265
Q

What are the common dosages as written on prescription for 2 antibiotics given for dental infections?

A

Phenoxymethylpenicillin 2x250mg tablets 4x daily for 5 days.
Metrondiazole 400mg 3xdaily for 5 days
(3 DAYS FOR ANUG)

266
Q

What is the rate of infection for HIV exposure, Hep C and Hep B?

A

HIV 0.3%
HepC 3%
HepB 30%

267
Q

Name 6 oral lesions associated with HIV

A

Stage 2 (early or mildly symptomatic)
Herpes zoster flares
Angular cheilitis
Recurrent ulceration

Stage 3 (late or moderately symptomatic)
Candidosis (erythematous)
Hairy leukoplakia
Necrotising ginigvitis / periodoontitis

Stage 4
Kaposi’ sarcoma
Chronic herpes simplex

268
Q

How is HIV diagnosed and treated?

A

Diagnosed:
ELISA antibody test 6-12 weeks post infection
HIV RNA testing

Treatment :
Highly active anti-retroviral therapy (HAARTs) whcih consist of:

Two nucleoside reverse transcriptase inhibitors (NRTIs)
plus a third drug from one of three drug classes:
-integrase strand transfer inhibitor (INSTI)
-non-nucleoside reverse transcriptase inhibitor (NNRTI)
-protease inhibitor (PI)
With a pharmacokinetic (PK) enhancer (also known as a booster), such as cobicistat and ritonavir

269
Q

What is a fibrous epulis?

A

It is a reactive non-neoplastic condition that affects the gingiva as a result of chronic irritation, resulting in a localised fibrous enlargement.

270
Q

What is the aetiology of a fibrous epulis?

A

Low grade local chronic irritation

271
Q

How does a fibrous epulis appear histologically?

A

o Ulceration
o Granulation tissue
o Metaplastic bone formation

272
Q

What do we call a fibrous epulis when it is located on sites other than the gingivae?

A

Fibro-epithelial polyp

273
Q

What is a pyogenic granuloma?

A

Also known as a vascular epulis (if found on the gingivae)

An inflammatory lesion with an overgrowth of granulation tissue .
Soft, deep red/purple swelling that is often ulcerated .
It can haemorrhage spontaneously or with mild truama.
Tends to recur after removal.
It is found on any mucosal site in respond to trauma

Known as a pregnancy epulis if found in pregnant women.

Patient often complains of it bleeding.

Know differentiation with giant cell granuloma (Hour glass. histologically- lots of giant cells)

274
Q

How does a pyogenic granuloma appear histologically?

A

Area of ulceration (loss of epithelium)
Area below the ulcer is highly cellular (Granulation tissue for healing)
There are lots of blood vessels (Vascular)

275
Q

Name a hereditary white patch

A

White spongy nevus
-Hereditary condition with increased production of keratin

276
Q

How does white spongy nevus appear histologically?

A

o Hyperkeratosis
o Areas of mild/variable dysplasia
o Minimal infiltrate of macrophages and melanocytes in basal layer

277
Q

Patient presents with denture induced hyperplasia - Give 2 differential diagnoses?

A

Papillary hyperplasia of the palate- overgrown soft tissue on the palate.
Leaf fibroma - the fibroepithelial polyp has been squashed underneath the denture.

epulis fissuratum

278
Q

What factors have resulted in denture induced hyperplasia?

A

An ill fitting denture causing trauma to the tissues.
This causes an adapative fibroepithelial response with overgrowth of the gingivae.

It commonly happpens if patient wears their temprorary denture long term (alveolar ridge resorbs after extraction so we need to make a new denture to fit the new ridge)

279
Q

How do we manage Epulis fissuratum?

A

Remove the cause to see if it goes away- easing use of the denture.
Use a tissue conditioner to allow the swelling to die down. (e.g. coe comfort)

LA and surgical excision of the fibrous tissue overgrowth

280
Q

Name 2 histological features of denture induced hyperplasia?

A

Hyperplastic epithelium
Hyperkeratosis

o Pseudo-epithelial hyperplasia
o Hyperkeratotic and irregular epithelial cells o Hyperplastic rete ridges

281
Q

How does Dabigatran affect clotting?

A

This inhibits thrombin (preventing fibrinogen -> fibrin and the formation of the clot )
DabigaTran

282
Q

How long is an NHS prescription for a non-controlled drug valid for?

A

6 months from the date on the prescription.

BDS4 Revision (14 decks)

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