Oral medicine

Question 1

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 ?

Answer 1

Keratin is formed from the basal layer

Question 2

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)

Answer 2

Keratinised stratified squamous epithelium

Question 3

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?

Answer 3

Melanin

Question 4

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)

Answer 4

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.

Question 5

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)

Answer 5

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

Question 6

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 ()

Answer 6

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)

Question 7

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)

Answer 7

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

Question 8

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) -

Answer 8

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

Question 9

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?

Answer 9

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

Question 10

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

Answer 10

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.

Question 11

Name 4 histological features of lichenoid reactions

Answer 11

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

Question 12

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

Answer 12

Angular cheilitis

Question 13

Name 2 microorganisms involved in this condition. (2)

Answer 13

Staphylococcus aureus
candida albicans

Question 14

What type of sample should be taken in this case?

Answer 14

A swab of the commissures of the mouth

Question 15

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

Answer 15

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

Question 16

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

Answer 16

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

Question 17

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

Answer 17

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)

Question 18

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

Answer 18

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

Question 19

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

Answer 19

Desquamative gingivitis

Question 20

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

Answer 20

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)

Question 21

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)

Answer 21

Pemphigus, Pemphigoid, Lichen planus, plasma cell gingivits

Question 22

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)

Answer 22

Plaque build up
Smoking
poor overhanging restorations
Partial dentures
SLS toothpaste

Question 23

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)

Answer 23

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.

Question 24

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)

Answer 24

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

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

Question 25

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

Answer 25

Direct immunofluorescence & histopathology

Question 26

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)

Answer 26

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

Question 27

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

Answer 27

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)

Question 28

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

Answer 28

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.

Question 29

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

Answer 29

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

Question 30

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

Answer 30

Alcohol Smoking, Betel quid (paan) HPV

Question 31

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)

Answer 31

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

Question 32

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)

Answer 32

**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.

Question 33

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)

Answer 33

None - paliative Radiotherapy, Chemotherapy, combination of both Immunotherapy

Question 34

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?

Answer 34

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

Question 35

What is an erosion?

Answer 35

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

Question 36

What is an ulcer?

Answer 36

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.

Question 37

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

Answer 37

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/.

Question 38

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

Answer 38

* Infections * Dehydration and malnutrition * Problems wearing dentures * Can affect speech and mastication

Question 39

What can cause recurrent apthous stomatitis? (7)

Answer 39

- 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

Question 40

How can we treat recurrent apthous stomatitis?

Answer 40

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)

Question 41

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)

Answer 41

An intense stabbing pain which extends along the course of branch affected - maxillary or mandibular usually Unilateral Lasts 5-10 seconds

Question 42

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?

Answer 42

Idiopathic Vascular compression of the trigeminal nerve.

Question 43

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)

Answer 43

OPT to rule out dental cause Trigeminal nerve reflex testing MRI

Question 44

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?

Answer 44

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

Question 45

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)

Answer 45

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

Question 46

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?

Answer 46

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

Question 47

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)

Answer 47

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)

Question 48

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)

Answer 48

* 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.

Question 49

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

Answer 49

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

Question 50

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?

Answer 50

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

Question 51

Intra-oral manifestations of herpes?

Answer 51

Fluid filled vesicles that rupture. Oral ulceration (Primary herpetic gingivostomatitis/ Herpes labialis)

Question 52

Three causes of vesicles?

Answer 52

Erythema multiforme, Pemphigoid, Pemphigus, angina bullosa haemorrhagica

Question 53

2 groups (virus) that cause oral ulceration?

Answer 53

Herpes simplex, Coxsackie virus, EBV, Varicella Zoster virus

Question 54

Give 2 causes of Coxsackie oral lesions?

Answer 54

Herpangina, Hand foot and mouth

Question 55

disorders caused by epstein bar virus.

Answer 55

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

Question 56

How herpes labialis forms? (4)

Answer 56

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. 2. Latency - Virus stays dormant in the ganglion 3. 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. .

Question 57

Diagnose

Answer 57

acute pseudomembranous candidosis

Question 58

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

Answer 58

Local: oral steroid/Inhalers with steroids Nutritional deficiencies Broad spectrum antibiotics dry mouth Medical- HIV, Poorly controlled diabetes

Question 59

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)

Answer 59

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.

Question 60

What to ask pathologist for when sending sample (1)

Answer 60

Culture (using saubraunds agar) Check sensitivity to antifungals **For antifungals** Helps you select an antigual If candida globrata (use Nystatin- glob**r**ata is **r**esistant to azole ) Otherwise- Miconazole or fluconazole

Question 61

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)

Answer 61

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.

Question 62

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)

Answer 62

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

Question 63

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

Answer 63

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 )

Question 64

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

Answer 64

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.

Question 65

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

Answer 65

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.

Question 66

2 investigations for apthous ulcers

Answer 66

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

Question 67

From FBC + told normal values- diagnose anaemia type

Answer 67

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

Question 68

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

Answer 68

Iron deficiency, Thalassaemia Anaemia of chronic disease

Question 69

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

Answer 69

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

Question 70

Mid age female complaining of burning mouth with diffuse erythema (1) ***CHECK PAST PAPER

Answer 70

Oral dysaesthesia

Question 71

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

Answer 71

Sinusitis

Question 72

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

Answer 72

Chronic Paroxysmal Hemicrania

Question 73

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

Answer 73

Trigeminal neuralgia

Question 74

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)

Answer 74

Giant cell ateritis (accompanied by shoulder girdle weakness) what is it? inflammation of the temporal artery - restricts blood flow to the associated structures (masseter)

Question 75

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

Answer 75

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

Question 76

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

Answer 76

Racial, Lead poisoning, Addison’s, Kaposis sarcoma, Haemochromatosis cushings = raised ACTH

Question 77

What is lichen planus?

Answer 77

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.

Question 78

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

Answer 78

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

Question 79

WHat are the types of lichen planus? (6)

Answer 79

PPBREA **P**apular- White plaques **P**laque- plaques arranged in lines **B**ullous- development of fluid filled vesicles and bullae with skin lesions projecting from the surface **R**eticular- spider web like lacy white lines **E**rosive (ulcerative) **A**trophic- white bluish plaques with central superficial atrophy

Question 80

Give some features of the lichen planus disease?

Answer 80

30-50yo, 1% malignant potential, Recurrence

Question 81

What are the causes of lichen planus?

Answer 81

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

Question 82

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

Answer 82

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

Question 83

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

Answer 83

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.

Question 84

What do you see on a histological image of Pemphigus

Answer 84

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

Question 85

Discuss the features of the Pemphigus disease.

Answer 85

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,

Question 86

What causes pemphigus?

Answer 86

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

Question 87

How do we treat patients with pemphigus?

Answer 87

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

Question 88

Order the salivary gland tumours by incidence

Answer 88

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

Question 89

What are the histological features of a pleomorphic adenoma?

Answer 89

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)

Question 90

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

Answer 90

Non/poorly encapsulated which makes it harder to remove & more likely to recurr myxoid tissue - jelly like and hard to remove in entirety

Question 91

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

Answer 91

– 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)

Question 92

How are salivary gland neoplasms diagnosed? (3)

Answer 92

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

Question 93

Histology of adenoid cystic carcinoma?

Answer 93

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

Question 94

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

Answer 94

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.

Question 95

Describe how you would manage Desquamative gingivitis (4 Marks)

Answer 95

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)

Question 96

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)**

Answer 96

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

Question 97

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)

Answer 97

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

Question 98

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)

Answer 98

Paget’s caused hypercementosis

Question 99

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)

Answer 99

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.

Question 100

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)

Answer 100

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)

Question 101

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

Answer 101

Pemphigus vulgaris

Question 102

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

Answer 102

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

Question 103

How is pemphigus managed?

Answer 103

Topical/systemic steroid - beclometasone inhaler/prednisolone, Analgesics

Question 104

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

Answer 104

Primary Herpetic Gingivostomatitis.

Question 105

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

Answer 105

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.

Question 106

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

Answer 106

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

Question 107

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

Answer 107

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

Question 108

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

Answer 108

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)

Question 109

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)

Answer 109

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

Question 110

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

Answer 110

acute pseudomembranous candidiasis

Question 111

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

Answer 111

HIV, EBV

Question 112

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

Answer 112

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

Question 113

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

Answer 113

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.

Question 114

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

Answer 114

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.

Question 115

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

Answer 115

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

Question 116

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

Answer 116

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)

Question 117

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

Answer 117

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)

Question 118

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

Answer 118

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

Question 119

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

Answer 119

Multiple Sclerosis Brain tumour compressing on trigeminal nerve

Question 120

What is the first line drug management for trigeminal neuralgia ?

Answer 120

Carbamazepine modified release- 100mg 1 tablet twice daily.

Question 121

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

Answer 121

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

Question 122

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

Answer 122

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

Question 123

Name one type of surgery used to treat trigeminal neuralgia

Answer 123

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

Question 124

What are the side effects of carbamazepine? (5)

Answer 124

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

Question 125

What muscles are examined in a patient with temporomandibular disorder?

Answer 125

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

Question 126

Name some common causes of TMD

Answer 126

Stress, parafunction, occlusal discrepancies, trauma.

Question 127

What nerves supply the TMJ?

Answer 127

auriculotemporal masseteric posterior (deep) temporal nerve

Question 128

What are the signs and symptoms of TMJ dysfunction?

Answer 128

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

Question 129

What are the mechanisms of a bite splint?

Answer 129

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

Question 130

What is arthrocentesis?

Answer 130

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.

Question 131

Give 2 other possible surgical options for treatment of TMJ dysfunction

Answer 131

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

Question 132

What are the histological features of lichen planus?

Answer 132

* 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

Question 133

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

Answer 133

PPBREA **P**apular- White plaques **P**laque- plaques arranged in lines **B**ullous- development of fluid filled vesicles and bullae with skin lesions projecting from the surface **R**eticular- spider web like lacy white lines **E**rosive (ulcerative) **A**trophic- white bluish plaques with central superficial atrophy

Question 134

What can cause lichen planus? (8)

Answer 134

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

Question 135

When do you biopsy lichen planus? (3)

Answer 135

symptomatic/erosive or ulcerative always in a smoker Symptomless on a high risk area

Question 136

How do we manage lichen planus

Answer 136

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)

Question 137

What are the I/O manifestations of herpes?

Answer 137

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

Question 138

Name types of human herpes virus? (5)

Answer 138

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

Question 139

Which cranial nerve does herpes become associated with?

Answer 139

trigeminal nerve

Question 140

Name the common triggers for reactivation of herpes.

Answer 140

stress Illness Fatigue sunlight menstruation immunosuppression

Question 141

What is anaemia?

Answer 141

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.

Question 142

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

Answer 142

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

Question 143

What are the oral signs of anaemia?

Answer 143

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

Question 144

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

Answer 144

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

Question 145

What 3 oral conditions are associated with microcytic anaemia?

Answer 145

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

Question 146

Name the type of anaemia from MCV

Answer 146

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

Question 147

What are the causes of xerostomia?

Answer 147

* 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

Question 148

How can you assess xerostomia intraorally?

Answer 148

* 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)

Question 149

What are the oral signs and symptoms of xerostomia

Answer 149

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

Question 150

How can we manage xerostomia?

Answer 150

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.

Question 151

Name 3 salivary subsitutes

Answer 151

Glandosane-acidic so we avoid it saliva orthana- best as pH neutral adn contains fluoride Biotene Oral balance bioxtra

Question 152

Name 3 sugar subsitutes

Answer 152

Xylitol Manitol Sorbitol

Question 153

List 3 salivary proteins

Answer 153

IgA, PRP, Mucins, Histatin

Question 154

LIst 3 salivary enzymes

Answer 154

lipase, lysozyme, amylase

Question 155

What is sjogren's syndrome?

Answer 155

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

Question 156

What antibodies are linked with? Sjogren's

Answer 156

Anti-Ro and Anti-la

Question 157

What are the investigations used to diagnose Sjogren's

Answer 157

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

Question 158

What gland do we biopsy to investigate sjogren's

Answer 158

Labial gland biopsy

Question 159

What are the histopathological features of Sjogren's ?

Answer 159

* >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

Question 160

Name 4 oral complications of sjogren's disease?

Answer 160

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)

Question 161

What drugs are used to manage Sjogren's

Answer 161

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

Question 162

Where would you commonly find a salivary neoplasm

Answer 162

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 )

Question 163

What are the symptoms of ectodermal dysplasia?

Answer 163

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

Question 164

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

Answer 164

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

Question 165

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

Answer 165

**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

Question 166

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

Answer 166

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.

Question 167

Name and describe the types of orofacial pain syndromes?

Answer 167

**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)

Question 168

Patient attends with denture induced stomatitis What 2 features do you notice about the palatal tissues?

Answer 168

Erythematous and oedema of denture bearing areas hyperplastic papillae Patient complains: Burning sensation/discomfort Bad taste and halitosis of the mouth

Question 169

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

Answer 169

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

Question 170

What causes denture induced stomatitis? Describe what occurs.

Answer 170

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

Question 171

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

Answer 171

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

Question 172

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

Answer 172

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.

Question 173

3 herpes group viruses associated with intra oral vesiculation

Answer 173

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

Question 174

Name 2 oral mucosal disease caused by Coxsackie viruses

Answer 174

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.

Question 175

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

Answer 175

Infectious mononucleosis Oral hairy leukoplakia

Question 176

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

Answer 176

Mandibular division of the trigeminal nerve

Question 177

Name common trigger for reactivation of herpes simplex lesions

Answer 177

Stress Infection Sunlight Fatigue Immunosupression.

Question 178

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

Answer 178

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

Question 179

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

Answer 179

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.

Question 180

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

Answer 180

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.

Question 181

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

Answer 181

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)

Question 182

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

Answer 182

o MND o Guillain-Barré syndrome (GBS) o C.botulism o Polio o Bell’s palsy Trauma/viral infection of ventral horn cells

Question 183

Give possible causes of upper motor neuron disease

Answer 183

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

Question 184

How do we manage Lower motor neuron disease

Answer 184

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.

Question 185

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

Answer 185

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

Question 186

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

Answer 186

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.

Question 187

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

Answer 187

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.

Question 188

Why are asthmatics more prone to erosion? (3)

Answer 188

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.

Question 189

What is the proper name for burning mouth syndrome?

Answer 189

Oral dysaesthesia

Question 190

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

Answer 190

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

Question 191

What are the causes of oral dysaesthesia?

Answer 191

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

Question 192

What are the signs and symptoms of oral dysaesthesia?

Answer 192

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

Question 193

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

Answer 193

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.

Question 194

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

Answer 194

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

Question 195

How is oral dysaesthesia managed?

Answer 195

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

Question 196

What is the mechanism of action of Chlorohexidine?

Answer 196

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

Question 197

What family of antiseptics does chlorohexidine belong to?

Answer 197

Bisbiguanides

Question 198

What is substantivity?

Answer 198

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.

Question 199

What solution of chlorohexidine is given to patients?

Answer 199

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

Question 200

What are the side effects of chlorhexidine ?

Answer 200

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

Question 201

What are the indications for the use of chlorhexidine?

Answer 201

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)

Question 202

Name the 3 stages in the formation of clots

Answer 202

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)

Question 203

How does aspirin affect clotting?

Answer 203

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)

Question 204

How does warfarin affect clotting?

Answer 204

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

Question 205

How does Apixaban affect clotting?

Answer 205

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

Question 206

How does Dabigatran affect clotting?

Answer 206

This inhibits thrombin (preventing fibrinogen -> fibrin and the formation of the clot ) Dabiga**T**ran

Question 207

How does Rivaroxaban affect clotting?

Answer 207

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

Question 208

Why are aspirin and clopidogrel used in conjuction?

Answer 208

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.

Question 209

What is the pattern of Von Willebrand's disease?

Answer 209

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)

Question 210

How does Von willebrand diease affect bleeding ? (2)

Answer 210

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 )

Question 211

What is a biofilm?

Answer 211

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.

Question 212

What are the stages of colonisation of a biofilm?

Answer 212

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

Question 213

Give 4 methods of identifying the bacteria

Answer 213

* 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.

Question 214

What are the virulence factors for P, gingivalis?

Answer 214

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

Question 215

What are the virulence factors for Candida, albicans?

Answer 215

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.

Question 216

What are the virulence factors for Strep mutans?

Answer 216

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

Question 217

What is the clinical appearance of plasma cell gingivitis?

Answer 217

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.

Question 218

What is the aetiology of plasma cell gingivitis?

Answer 218

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

Question 219

What can worsen the patient's plasma cell gingivitis?

Answer 219

Not removing the causative agent Poor OH Plaque retentive factors

Question 220

How do we manage plasma cell gingivitis?

Answer 220

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)

Question 221

Name 4 dental treatments in which antibiotics are indicated

Answer 221

* 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)

Question 222

Give 5 ways in which antibiotics work?

Answer 222

* Inhibit cell well synthesis * Inhbiti protein synthesis * Inhibit DNA acid replication and transcription * Injure the plasma membrane * Inhibit the synthesis of essential metabolites

Question 223

Give 3 disadvantages of antibiotic use?

Answer 223

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

Question 224

Name 3 antibiotics used in dental treatment and include regime

Answer 224

**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

Question 225

What are the mechanisms of antibiotic resistance?

Answer 225

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.

Question 226

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

Answer 226

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

Question 227

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

Answer 227

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.

Question 228

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

Answer 228

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

Question 229

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

Answer 229

****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.

Question 230

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

Answer 230

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)

Question 231

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

Answer 231

2 out of 10 people in scotland

Question 232

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

Answer 232

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.

Question 233

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

Answer 233

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.

Question 234

What is the histological difference between pemphigus and pemphigoid?

Answer 234

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.

Question 235

How do pemphigus and pemphigoid differ clinically

Answer 235

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

Question 236

How can we investigate pemphigus and pemphigoid?

Answer 236

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. 2. H&E staining fro histopathology

Question 237

How are pemphigus and pemphigoid managed?

Answer 237

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

Question 238

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

Answer 238

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

Question 239

What are the signs and symptoms of oral cancer

Answer 239

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

Question 240

How does cancer spread?

Answer 240

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

Question 241

What is the metastatic cascade?

Answer 241

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

Question 242

What is the TNM grading system

Answer 242

**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.

Question 243

What is necrotising sialometaplasia?

Answer 243

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.

Question 244

What is the aetiology of necrotising sialometaplasia?

Answer 244

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

Question 245

How does Necrotising sialometaplasia appear histologically?

Answer 245

* 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

Question 246

How is necrotising sialometaplsia managed?

Answer 246

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

Question 247

Give 2 differential diagnoses for Necrotising sialometaplasia

Answer 247

Squamous cell carcinoma Salivary gland carcinoma

Question 248

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

Answer 248

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

Question 249

What is a mucocele?

Answer 249

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

Question 250

How does a mucocele appear histologically?

Answer 250

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

Question 251

How do we manage a mucocele?

Answer 251

Excision of the mucocele and associated gland

Question 252

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

Answer 252

A ranula

Question 253

What is orofacial granulomatosis?

Answer 253

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

Question 254

Discuss the aetiology of orofacial granulomatosis?

Answer 254

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

Question 255

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

Answer 255

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

Question 256

How is oral facial granulomatosis managed? (4)

Answer 256

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)

Question 257

Give 6 types of oral candida infection

Answer 257

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)

Question 258

Where does median rhomboid glossitis occur?

Answer 258

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)

Question 259

Give 3 histological features of median rhomboid glossiitis?

Answer 259

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

Question 260

Give 3 methods of testing for candida?

Answer 260

Swab/oral rinse and culture Biopsy lesion for histological testing- use a PAS stain Smear for microscopy

Question 261

What are the virulence factors of candida?

Answer 261

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.

Question 262

Name 5 antifungal agents?

Answer 262

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

Question 263

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

Answer 263

Warfarin and statins

Question 264

What information should be written on a prescription

Answer 264

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.

Question 265

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

Answer 265

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

Question 266

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

Answer 266

HIV 0.3% HepC 3% HepB 30%

Question 267

Name 6 oral lesions associated with HIV

Answer 267

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

Question 268

How is HIV diagnosed and treated?

Answer 268

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

Question 269

What is a fibrous epulis?

Answer 269

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

Question 270

What is the aetiology of a fibrous epulis?

Answer 270

Low grade local chronic irritation

Question 271

How does a fibrous epulis appear histologically?

Answer 271

o Ulceration o Granulation tissue o Metaplastic bone formation

Question 272

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

Answer 272

Fibro-epithelial polyp

Question 273

What is a pyogenic granuloma?

Answer 273

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)

Question 274

How does a pyogenic granuloma appear histologically?

Answer 274

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

Question 275

Name a hereditary white patch

Answer 275

White spongy nevus -Hereditary condition with increased production of keratin

Question 276

How does white spongy nevus appear histologically?

Answer 276

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

Question 277

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

Answer 277

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

Question 278

What factors have resulted in denture induced hyperplasia?

Answer 278

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)

Question 279

How do we manage Epulis fissuratum?

Answer 279

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

Question 280

Name 2 histological features of denture induced hyperplasia?

Answer 280

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

Question 281

How does Dabigatran affect clotting?

Answer 281

This inhibits thrombin (preventing fibrinogen -> fibrin and the formation of the clot ) Dabiga**T**ran

Question 282

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

Answer 282

6 months from the date on the prescription.