Oral Medicine

Question 1

Name the 4 categories of medcinies used in Oral Medicine (OM)?

Answer 1

Anti-microbial - virals, fungals and biotics
Topical Steroids - inhaled and mouthwash
Dry mouth medication - benzdamine wash
Others - carbamazepine

Question 2

Name the 5 classification of medicines?

Answer 2

General Sales
Pharmacy Medicines
Prescription only Medicines
Controlled Drugs
Medical Devices

Question 3

What is the definition of a licensed medication?

Answer 3

A medicine that has been proven in evidence to the MHRA to have efficacy and
safety at defined doses in a child and/or adult population when treating specified
medical conditions
Clinical trial data provided
Post licence surveilence via MHRA

Question 4

What is the defintiion of an unlicensed medication?

Answer 4

Medicines that have not had evidence of efficacy submitted for the condition under
treatment

Will be ‘licenced medicines’ – but for another condition
Use is at the discretion of the treating physician
Patient must be informed that medicine is being used ‘off-licence’
Patient must be given PIL specific to the condition under treatment

Question 5

Name antimicrobials used for OM? and what they treat?

Answer 5

virals - primary herpetic gingivostomatosis, recurrent herpetic lesions and shingles
- aciclovir
fungals - Acute pseudomembranous candidiasis and acute erythematous candidiasis
- miconazle
- fluconazole
- nystain

Question 6

Name topical steroids used for OM? and what they treat?

Answer 6

Betamethasone mouthwash
Beclomethasone Metered Dose Inhaler

Both used for
- Treating aphthous ulcers
- Treating Lichen planus

Question 7

What is the definition of a medical devices?

Answer 7

‘Medical device’ means any instrument, apparatus, implement, machine, appliance, implant, reagent for in vitro use,
software, material or other similar or related article, intended by the manufacturer to be used, alone or in combination, for
human beings, for one or more of the specific medical purpose

• diagnosis, prevention, monitoring, treatment or alleviation of disease,
  • diagnosis, monitoring, treatment, alleviation of or compensation for an injury,
  • investigation, replacement, modification, or support of the anatomy or of a physiological process,
  • supporting or sustaining life,
  • control of conception,
  • disinfection of medical devices
  • providing information by means of in vitro examination of specimens derived from the human body

Question 8

Medical devices include dry mouth treatments - name 5 types of treatments?

Answer 8

Salivix pastilles
Saliva orthana
Biotene Oral Balance
Artificial Saliva DPF
Glandosane

Question 9

Name 6 other medicines used in OM?

Answer 9

Tricyclic Antidepressants
Gabapentin/Pregabalin
Azathioprine
Mycophenolate
Hydroxycholoroquine
Colchicine

Question 10

What needs to be considered before any drug is prescribed or drug is reccomended?

Answer 10

Clinical indication
Licenced or unlicensed for this use
Dose and route of administration
Important warnings for the patient
Drug interactions and cautions
Treatment duration and monitoring

Question 11

What to include on a presciption?

Answer 11

Patient’s name, Address, Age (under 18)
Patient identifier – DoB, CHI Number
Number of Days treatment
Drug to be prescribed
Drug formulation and Dosage
Instructions on quantity to be dispensed
Instructions to be given to the patient
Signed – identifier of Prescriber

Question 12

What are the rules and regulation on prescrption validity?

Answer 12

Six months from date issued
More than one item on a script
More than one repeated dispensing occasion

Question 13

Tips for writing a prescription?

Answer 13

Key Patient information MUST be legible
AVOID abbreviations – write full instructions in INK
Only legal requirement is for dentist to SIGN prescription – this confirms all the
other information is correct and has been checked.
Essentially the SAME information for Private
– GDC number usually added

Question 14

What are the advantages of written instruction for the patient?

Answer 14

Stressed patient may not remember instructions
Language issues may prevent proper understanding
Multilingual options, large print options
Contact number for Patient Issues with the medicine
Legal protection if post-treatment course questioned

Question 15

What advice should you give to your patient after prescribing the drug?

Answer 15

Take drugs at correct time and finish the course
Unexpected reactions: STOP! and contact prescriber
Known side-effects should be discussed e.g. Metronidazole and alcohol
Keep medicines safe: especially from children

Question 16

Types of drugs for mucosal disease?

Answer 16

Non-steroid topical therapy
- inconvientient lesions with discomfort
Steroid topical therapy
- disabling immunologically driven lesions

Question 17

Non-steroid topical therapy for mucosal diease? - Name 4?

Answer 17

Chlorhexidene mouthwash
- dilute 50% with water if needed
Benzdamine mouthwash or spray
- green things help! Useful topical anaesthetic/pain relief
OTC remedies such as Igloo, Listerine, Bonjela
Anything else the patient finds helpful!
- check that it is not harmful though – bleach, aspirin!

Question 18

Steroid topical therapy for mucosal diease? - Name 3?

Answer 18

Hydrocortisone mucoadhesive pellet
Betamethasone mouthwash
Beclomethasone Metered Dose Inhaler (MDI/Puffer) -
- CFC-free preparations, e.g. ‘Clenil Modulite’

Question 19

How does it work - hydrocortisone mucoadhesive tablet?

Answer 19

allow tablet to dissolve over the ulcer

Question 20

How to use betamethasone mouthwash?

Answer 20

Unlicenced product
• Supply patient with a tailored information leaflet

Use Betnesol tabs 0.5mg
- 1mg 2 tablets
- 10mls water 2 teaspoons water
- 2 mins rinsing
- Twice daily
Refrain from eating/drinking for 30 min after use
DO NOT SWALLOW
Do not rinse after use

Question 21

What must be included on betamethasone mouthwash PIL?

Answer 21

Licenced for other medical conditions
Explain dose range and frequency of use
Explain hazards of exceeding the standard dose
Add any known side effects – small oral candida risk
Add special instructions

Question 22

How to use beclomethasone medical device?

Answer 22

Unlicenced product
- Supply patient with a tailored information leaflet
Dental Prescribing 50mcg/puff device
- Position device correctly – exit vent directly over ulcer area
- 2 puffs
- 2-4 times daily
- Don’t rinse after use
Must be a pressurised device

Question 23

What must be included on beclomethasone medical device PIL?

Answer 23

This is an accepted and proven effective treatment for the oral condition
Licensed for other medical conditions – asthma and COPD
Instruct to discard the manufacturer’s PiL
Explain dose range and frequency of use
Explain technique used for oral lesions – different from use for lung conditions
Add any known side effects – small oral candida risk
Add special instructions

Question 24

Systemic drugs used in OM, only for specialists?

Answer 24

Disease modulator
- colchine
Steroid
- prednisilone (ulcers) 30mg for 5 days
Immune suppressants:
- hydroxychloroquine - lichen planus
- azathioprine
- mycophenolate
Immunotherapy:
- adalimumab
- enterecept

Question 25

Systemic use of steroid risk - side effects?

Answer 25

If prolonged course – or repeated short courses over many months • 3 months continuous • Gaps of 2 weeks or less between ‘pulses’ of prednisolone. Adrenal suppression – steroid dependency – don’t stop suddenly – taper dose Cushingoid features Osteoporosis risk – bone prophylaxis – Calcium supps and bisphosphonates - DEXA bone density scan may be needed from time to time Peptic ulcer risk – Proton Pump Inhibitor prophylaxis Mood/Sleep alteration and mania/depression risk – can be very quick onset

Question 26

What preparation do patients need for systemic immunomodulatory treatmets?

Answer 26

Must ensure that immunosuppression will not harm the patient Pre-existing medical condition not yet detected Screening for: Blood borne virus screen - Hep B, Hep C, HIV • FBC • Electrolytes • Liver Function tests • Thiopurine Methyltransferase (TPMT) - Only for Azathioprine use • Zoster antibody screen • EBV • Chest X-Ray - Evidence of previous/active TB • Cervical Smear up to date • Pregnancy test

Question 27

What must be included when planning immunomodulatory treatment?

Answer 27

Needs full consent from patient - Alternative treatments tried or discussed Patient information given and patient reviewed to discuss this - Short term risk – acute drug reaction - Long term risk – cancer risk increased – Azathioprine and skin cancer especially - Effective Contraception to be used and any pregnancy planned with clinical care team Treatment outcome understood by patient and clinician - Complete remission, acceptable level of symptoms - Trial treatment – perhaps 6 months then reassess benefit/need for treatment

Question 28

What are the differential diagnoses of oral white lesions? 5 examples?

Answer 28

Hereditary Smoking/frictional Lichen planus - lupus erythematosus - gvhd Candidal leukoplakia Carcinoma

Question 29

What does a typical white spot lesion look like?

Answer 29

Thickening of the mucosa or keratin - Less visibility of blood Less blood in the tissues - vasoconstrictor

Question 30

What is the definition of Leukoplakia?

Answer 30

A white patch which cannot be scraped off or attributed to any other cause No histopathological connotation - it is a clinical description Diagnosis of exclusion 1 - 5% become malignant

Question 31

Name 4 types of leukoplakia?

Answer 31

Fordyce's spots Smoker's Keratosis Frictional Keratosis Hereditary Keratosis

Question 32

What is the link between smoking and leukoplakia?

Answer 32

Smokers are six times more likely to have “leukoplakia" Low malignant potential of the lesion - But higher oral cancer risk overall!

Question 33

Name 3 types of infective leukoplakia?

Answer 33

Candidosis - pseudomembranous acute (thrush) - denture associated (chronic) Herpes Simplex

Question 34

When should you refer a white spot lesion?

Answer 34

Most are benign If RED and WHITE concentrate on the RED part If the lesion is becoming more raised and thickened If the lesion is ‘without cause’ - lateral tongue - anterior floor of mouth - soft palate area

Question 35

Why are red spot lesions red?

Answer 35

Blood flow increases - inflammation - dysplasia Reduced thickness of the epithelium

Question 36

What is the definition of Erythroplakia?

Answer 36

Atrophic or non-keratotic end of the spectrum A red patch which cannot be attributed to any other cause More of a concern for malignancy than leukoplakia

Question 37

Why does a red/blue lesion look like it does? explain why?

Answer 37

Fluid in the connective tissue - Dark – slow moving blood – varicosities - veins or cavernous haemangioma Light Blue – clear fluid - saliva (mucocele), Lymph (Lymphangioma)

Question 38

Name 2 types of vascular hamartomas?

Answer 38

Haemangioma - capillary - cavernous

Question 39

What is thw defintion of a lymphangioma?

Answer 39

Lymphangioma - most are cavernous Tongue - cystic hygroma

Question 40

Name 3 types of connective tissue diseases?

Answer 40

Large vessel Disease - giant cell (temporal) arteritis Medium Vessel Disease - polyarteritis nodosa - kawasaki disease Small vessel Disease - granulomatosis with Polyangiitis

Question 41

What are the 3 types of mucosal pigmentations?

Answer 41

Exogenous stain Intrinsic Pigmentation Intrinsic foreign body

Question 42

Name the 4 examples of exogenous stains for mucosal pigmentation?

Answer 42

Tea coffee chlorhexidine Bacterial overgrowth

Question 43

Name the 4 examples of intrinsic pigmentation for mucosal pigmentation?

Answer 43

Reactive Melanosis/melanotic macule Melanocytic naevus Melanoma Effect of systemic disease - paraneoplastic phenomenon

Question 44

Name the 1 examples of intrinsic foriegn body for mucosal pigmentation?

Answer 44

Metals

Question 45

Name the differential diagnoses for brown/black lesions - localised and generalsied?

Answer 45

Localised: - Amalgam - Melanotic Macule - Melanotic naevus -Malignant Melanoma - Peutz-Jehger’s syndrome - Pigmentary incontinence - Kaposi’s sarcoma Generalised: - Racial/familial - Smoking - Drugs - Addison’s disease (Raised ACTH conditions)

Question 46

Name 2 types of melanin pigmentation?

Answer 46

Racial pigmentation Melanotic macule

Question 47

What questions to think about when deciding whether to refer for mucosal pigmentations?

Answer 47

Is it easily explained? - Racial - Smoking - Medicines Is it increasing in size, colour or quantity? Any NEW systemic problem? Do I have an EXISTING radiograph showing it to be amalgam?

Question 48

What is the ateiolog of mucosal inflammation?

Answer 48

trauma - physical or chemical infection - viral, bacterial or fungal immunological can be remalignant or melignant

Question 49

How to decide whether something is a melanoma? questions?

Answer 49

Variable pigmentation Irregular outline Raised surface Symptomatic - Itch - bleed

Question 50

What is the purpose of a biopsy?

Answer 50

identifies or excludes malignancy identifies dysplasia identifies other disease, e.g. lichen planus

Question 51

When must you biopsy?

Answer 51

if unexplained

Question 52

When should a patient be referred to oral medicine?

Answer 52

Patients with abnormal and/or unexplained changes to the oral mucosa - Practitioner threshold will vary with experience If there is concern about dysplasia risk - Appearance of lesion - Risk site - Risk behavior - Family history

Question 53

When should you NOT refer a patient to Oral Medicine?

Answer 53

Asymptomatic VARIATIONS of NORMAL mucosa Benign conditions the practitioner has diagnosed that: - Are asymptomatic - Do not have potentially malignant risk - For which there is no treatment If unsure – consider clinical photography to - Monitor area until next check up - Send to specialist for an opinion

Question 54

When should a mucsoal lesion be refered to oral medicine for an opinion?

Answer 54

ANYTHING the dentist thinks is might be cancer or dysplasia - 2 week Cancer referral pathway for actual malignancies - NICE and SIGN Head & Neck cancers guidelines Any SYMPTOMATIC lesion that has not responded to standard treatment - Hospital referral criteria - SDCEP guidance Any BENIGN lesion that the patient can’t be persuaded is not cancer…..

Question 55

What is the oral mucosa made up of?

Answer 55

stratified squamous epithelium lamina propria gross types - lining, masticatory, gustatory microscopic - non-keratinised - keratinised - orthokeratosis or parakeratosis

Question 56

Different parts of the mouth which are keratinised and non-keratinised?

Answer 56

Keratinised - palate Non-keratinised - cheek

Question 57

What are the compartments of the oral mucosa?

Answer 57

STratum Corneum Granulosum Spinosum Basal Lamina Properia Cornified, Maturation, Progenitor

Question 58

Name the 3 reactive chnages of the oral epithelium?

Answer 58

Keratosis - nonkeratinised site (parakeratosis) Acanthosis - hyperplasia of stratum spinosum Elongated rete ridges - hyperplasia of basal cells

Question 59

Name the 5 mucosal reactions of the oral mucosa?

Answer 59

Atrophy - reduction in viable layers Erosion - partial thickness loss Ulceration - fibrin on surface Oedema - intracellular - intercellular (spongiosis) Blister - vesicle or bulla

Question 60

How do age and nutritiona ffect the oral mucosa?

Answer 60

Age - progressive mucosal atrophy Nutritional deficiency - iron or B group vitamins - atrophy - predisposes to infection

Question 61

Name 3 types of benign tongue conditions? Dorsal surface

Answer 61

Geographic tongue - 1-2% of population - less in children - desquamation - varied pattern and timing Black hairy tongue - hyperplasia of papillae - bacterial pigment Fissured tongue (scrotal tongue)

Question 62

What are the symptoms of geographic tongue?

Answer 62

Sensitive with acidic/spicy foods Intermittent Much worse in young children

Question 63

What is the aetiology of geographic tongue?

Answer 63

None! Something else is causing the trouble - Haematinic deficiency (B12, Folate, Ferritin) - Parafunctional trauma - Dysaesthesia

Question 64

How to manage a black hairy tongue?

Answer 64

Sucking on a peach stone

Question 65

What is the definition of a fissued tongue?

Answer 65

Fissured tongue is a benign condition characterized by deep grooves (fissures) in the dorsum of the tongue. Although these grooves may look unsettling, the condition is usually painless. Some individuals may complain of an associated burning sensation The cause is unknown, but it may be partly a genetic trait. Aging and environmental factors may also contribute to the appearance Is there another disease process there? - Candida - Lichen planus

Question 66

What is the defintion of glossitis? And possible investigations?

Answer 66

What is Glossitis? - Glossitis can mean soreness of the tongue, or more usually inflammation with depapillation of the dorsal surface of the tongue (loss of the lingual papillae), leaving a smooth and erythematous (reddened) surface What investigations are needed? - Haematinics - Fungal cultures

Question 67

What is the definition of black hairy tongue?

Answer 67

is a condition of the tongue in which the small bumps on the tongue elongate with black or brown discoloration, giving a black and hairy appearance.

Question 68

What is the aetiology of black hairy tongue?

Answer 68

smoking, xerostomia (dry mouth), soft diet, poor oral hygiene certain medications

Question 69

What is the aetiology of glossitis?

Answer 69

Often caused by nutritional deficiencies - Fe - B - Infection - others

Question 70

When should you refer a swelling to Oral Medicine?

Answer 70

Symptomatic (pain is a feature of salivary gland malignancy!) Abnormal overlying and surrounding mucosa Increasing in size 'rubbery' consistency Trauma from teeth Unsightly

Question 71

What is the definition of a pyogenic granuloma?

Answer 71

granulation tissue – mixed inflammatory infiltrate on fibro-vascular background any mucosal site response to trauma Not a granuloma, not pyogenic other names - gingiva –  aka vascular epulis most frequent site - gingiva, during pregnancy pregnancy epulis

Question 72

Name the 5 causes of mucosal ulcerative reactions?

Answer 72

Trauma Immunological Infections GI Carcinoma

Question 73

Name the differential diagnoses for immunological and GI mucosal ulcerative reactions?

Answer 73

Immunological: - aphthous ulcers - lichen planus - Lupus - vesiculo-bullous - Erythema multiforme GI: - Crohn's - UC

Question 74

What are the differential diagnoses for single episode oral ulceration?

Answer 74

Trauma 1st episode of Recurrent Oral Ulceration Primary Viral infections Oral Squamous Cell Carcinoma

Question 75

What are the differential diagnoses for Recurrent Oral Ulceration?

Answer 75

Aphthous ulceration - minor, major, herpetiform Lichen Planus Vesiculobullous lesions - pemphigoid, pemphigus - angina bullosa haemorrhagica - erythema multiforme Recurrent viral lesion – HSV, VZV Trauma Systemic disease – Crohn’s Disease ulceration

Question 76

Describe the difference between Crohn's ulcers and aphthous ulcers?

Answer 76

Aphthous-type ulcers: - haematinic deficiency associated - behave like aphthous ulcers Crohn's specific ulcers: - linear at the depth of the sulcus - full of Crohn’s associated granulomas - persist for months – intralesional steroids help

Question 77

Explain what to include for an Oral Ulceration History?

Answer 77

Where? Size & Shape? Blister or ulcer? How long for? - more than 2 weeks? Recurrent? - same site? different Sites? Painful?

Question 78

Explain how to describe/examine an ulcer?

Answer 78

Margins? - flat? raised? rolled? Base? - soft? firm? hard? Surrounding tissue - inflamed? normal? Systemic Illness?

Question 79

What is the definition of traumatic ulceration?

Answer 79

Common Usually single episode - can be recurrent if cause not removed Normal or abnormal epithelium Healing - remove cause - heal in about 2 weeks

Question 80

Describe a recurrent herpetic lesion? - location and treatment

Answer 80

Ulceration limited to one nerve group/branch Often Hard palate - lesion recurs in the same place - patient often aware of prodrome and vesiculation which bursts - PAIN suggests Herpes ZOSTER rather than simplex Treat with systemic ACICLOVIR - prophylactic if a severe problem

Question 81

Describe recurrent aphthous stomatitis (RAS)? severity? diagnosis?

Answer 81

Severity: - minor - major - herpetiform - Behçet’s syndrome Diagnosis by : - history - examination

Question 82

What is the general rule for recurrent self-healing ulcers?

Answer 82

Those affecting exclusively the non-keratinized mucosa are inevitably aphthae.

Question 83

The overall summary of Oral Ulceration?

Answer 83

Not all ulcers are aphthous! Is the lesion on keratinized or non-keratinized mucosa Are there systemic symptoms? - consider infection – herpes group, coxsackie group Always look for a traumatic cause - primary – sharp edge on a tooth/appliance - secondary – parafunction rubbing mucosa against the teeth

Question 84

What is the definition of an Aphthous Ulcer?

Answer 84

- Immunologically generated RECURRING oral ulcers - Follow a set pattern depending upon the ulcer type - Genetically driven with environmental modification - Multifactorial environmental triggers and variable expression - Ulcer experience may change as ‘risk factors’ change over life

Question 85

Describe the characteristics of a minor aphthous ulcers?

Answer 85

- Less than 10mm diameter - Last up to 2 weeks - ONLY affect NON-Keratinised mucosa - Heal without scarring - Usually a good response to topical steroids This is the commonest type of recurrent oral ulceration - One is a nuisance, many more at once can be disabling The ULCER FREE PERIOD is a good guide to morbitity – longer ulcer free + less morbidity

Question 86

Describe the characteristics of a major aphthous ulcers?

Answer 86

- Can last for months - Can affect ANY part of the oral mucosa - keratinised OR non keratinised or both - MAY scar when healing - Poorly responsive to topical steroids - intralesional steroids often more useful Usually LARGER than 10mm - may get smaller ulcers too – diagnose from the worst ulcer

Question 87

Describe the characteristics of a herpetiform aphthae ulcer?

Answer 87

- Rarest form of Aphthous ulcers - Multiple small ulcers on non-keratinized mucosa - Heal within 2 weeks Can coalesce into larger areas of ulceration NOTHING to do with herpes viruses - in the early stages looks like primary herpetic gingivostomatitis - in HSV get KERATINISED epithelium involved – not in herpetiform aphthae

Question 88

What cause Oral and Genital Ulceration?

Answer 88

Behçet’s Disease (mainly) Vesiculobullous diseases Lichen Planus

Question 89

How to diagnose Behcet's disease?

Answer 89

Many who don’t meet the criteria Diagnosis - three episodes of mouth ulcers in a year - at least two of the following: genital sores, eye inflammation, skin ulcers, pathergy

Question 90

What is the definition of Behcet's Disease? and where can it effect?

Answer 90

PRIMARILY a Vasculitis – inflammation of blood vessels - Oral & genital ulceration - Eye disease - snterior or posterior uveitis – can lead to loss of vision in 20% - Bowel ulceration – iliocaecal area – pain and cramping - Heart and lungs - Brain - Joints

Question 91

How to manage a patient with Behcet's Disease?

Answer 91

Treat local oral disease or RAS Systemic immunomodulation where multisystem involvement: - Colchicine used ‘off label’ often a first treatment - Azathioprine/Mycophenolate - Biologics – infliximab and others Managed with help of Rheumatology - also National specialist treatment centres

Question 92

Name the 7 predisposing factors for Recurrent Aphthous Stomatitis (RAS)?

Answer 92

Viral and bacterial infections Genetic predisposition Systemic diseases Stress Mechanical injuries Hormonal level fluctuations Microelement deficiences

Question 93

What to remember for Aphthous ulcers?

Answer 93

Damage happen before the ulcer appears - treatment is most effective in ulcer rpodrome period

Question 94

What tests to carry out when investigating aphthous ulcers?

Answer 94

Blood test: - haematinic deficiencies Iron B12 or folic acid - coeliac disease - TTG (tissue transgutaminase) - if TTg +ve anti-glidain and anti-endomysial abs Allergy tests - contact or immediate hypersensitivty - food additives E210-E219 - benzoate - sorbate - cinnamon - chocolate

Question 95

Explain the treatment of a recurrent Aphthae?

Answer 95

Management: Correct blood deficiencies - ferritin (iron), folic Acid, vit B12 Refer for investigation if Coeliac positive - endoscopy and jejunal biopsy Avoid dietary triggers - SLS containing toothpaste – (Sensodyne Pronamel and Kingfisher are SLS free) Dietary triggers - identified from testing - empirical dietary avoidance – use FOOD MAESTRO app to help with identifying foods

Question 96

Explain the treatment of a recurrent Aphthae?

Answer 96

Management: Correct blood deficiencies - ferritin (iron), folic Acid, vit B12 Refer for investigation if Coeliac positive - endoscopy and jejunal biopsy Avoid dietary triggers - SLS containing toothpaste – (Sensodyne Pronamel and Kingfisher are SLS free) Dietary triggers - identified from testing - empirical dietary avoidance – use FOOD MAESTRO app to help with identifying foods

Question 97

What drugs can be prescribed for aphthous ulcers?

Answer 97

In dental practice follow SDCEP ’Drugs in Dentistry’ Guidance Non-Steroid Topical Therapy - for inconvenient lesions Steroid Topical Therapy - for disabling lesions

Question 98

Why do chuildren get aphthous ulcers?

Answer 98

Periods of rapid growth – very few before this - 8-11 years and 13-16 years - feet usually grow first so look for ‘new shoe sign’ Treatment - usually respond to 3/12 iron supplements – always check the diet for peculiarities NOT related to growth (present since birth) then largely a genetic component: - consider allergy testing as well as bloods Treatment: - issues with Betnesol under age 12 - licence - issues with Betnesol if child unable to spit mouthrinse out reliably

Question 99

When should you refer an Aphthous ulcer case?

Answer 99

After simple investigations After topical trreatment If no good result has been achieved If patient under 12 YO

Question 100

What is the defintion of oral thrush?

Answer 100

Caused by candida Can be associated with dentures causing denture stomatitis

Question 101

What species of candida causes oral thrush?

Answer 101

Candida albicans

Question 102

Name the 10 host factors that predispose you to developing oral thrush?

Answer 102

Immunosuppression Endocrine disorders Nutritional deficiency Antibiotics Steroids Female Extremes of age Hospitalisation Smoking High carb diet

Question 103

Name the 5 intraoral factors that predispose you to oral thrush?

Answer 103

Poor oral hygiene Salivary gland dysfunction Oral mucosal damage Dental prosthesis Changes to commensal flora

Question 104

Name the topical and systemic treatment of oral thrush?

Answer 104

Topical: - nystatin - miconazole Systemic: - fluconazole - targeted therapy

Question 105

Explain how to use nystatin suspension?

Answer 105

1ml QDS Keep in mouth for as long as possible Continue for 48 hours after resolved Low risk for inters

Question 106

Explain how tonuse miconazole oral gel?

Answer 106

2.5 ml QDS - gold in mouth after food Continue for 7 days after resolved Use gel to brush dentures

Question 107

What treatment is advised for angular cheilitis?

Answer 107

Miconazole - antifungal - bacteriostatic vs gram positive - topical - with mild steroid

Question 108

Name the drug interactions of Miconazole?

Answer 108

Inhjbits the metabolism of drugs metabolised by the CYP3A4 and CYP 2C9 enzyme systems CYP3A4: - statins - Ca ch blocker - tacrolimus - carbamazepine - midazolam CYP2C9 - warfarin - sulphonylureas - phenytoin

Question 109

Name the contraindications of miconazole?

Answer 109

Liver dysfunction Coadministration with drugs that are metabolised by CYP3A4 Substrates known to prolong QT interval - astemizole, cisapride, dofetilide, mizolastine, pimozide, quinidine, sertindole and terfenadine Ergot alkaloids HMG-CoA reductase inhibitors - simvastatin Triazolam and oral midazolam

Question 110

Explain how to take fluconazole?

Answer 110

50-200mg capsules 50-5ml oral suspension IV avaliable 50mg once a day for 7-14 days 100mg if immunocompromised

Question 111

Name the 6 contraindications of fluconazole?

Answer 111

Mod inhib of P3A4 and 2C9 Strong inhib of 2C19 Alfentanil Amitriptyline Benzodiazepines Citalopram Clopidogrel Warfarin

Question 112

How importance is drug resistance to antifungal?

Answer 112

A growing problems Most common in azoles

Question 113

Explain a dentists role in antimicrobial stewardship?

Answer 113

Don't start antibiotics without bacterial infection Use local guidelines Document everything such as indication, duration, dose and route Review clinical diagnosis and the need for the pt to continue the dose 48 hours after symptoms go

Question 114

Name 7 types of oral symptoms?

Answer 114

Dry mouth Oral discomfort Taste disturbance Difficulty chewing Difficulty swallowing Difficuly speaking Halitosis

Question 115

Advice for toothbrushing?

Answer 115

At least twice a day Small headed brush Medium texture filament Soft brush if very sore Toothpaste between 1350-1550 ppm Fl Water if toothpaste is unworkable

Question 116

How can a nurse care for a patients teeth if they can't?

Answer 116

Twice daily brushing Gloves with toothpaste Small circular motions Start on outer surfaces then move to inner surfaces Spit out toothpaste after brushing Avoid rinsing

Question 117

How can a nurse care for a patients denture?

Answer 117

Cleanse denture after meals Cleaned and removed overnight Ensure denture fits well Adhesive if necessary

Question 118

How can a nurse care for a patients soft tissue?

Answer 118

Glove and run finger over tissues Renew gause on cleansing Can use cleaning stock if gause not good Record mouth condition

Question 119

How can a nurse care for a patients lips?

Answer 119

Moisten with water Apply saliva replacement Or apply aqueous cream BP

Question 120

What to implement for a dry or coated mouth patient?

Answer 120

At least 4 x a day Review medicines Gently remove coating, debris and plaque Maintain hydration Stimulate saliva

Question 121

Which 5drug types cause dry mouth?

Answer 121

Opoids Anticholinergics Antidepressants Diuretics Oxygen

Question 122

Explain how to manage dry mouth?

Answer 122

Treat underlying cause Review medication Good oral hygiene Dietary advice Regular dental checks Regular sips of water Lubricate cracked lips Saliva substitutes Saliva stimulants

Question 123

What does saliva consist of?

Answer 123

6.8-7.4 pH Water Mucin-principal active component Electrolytes Enzymes Proteins

Question 124

Name saliva stimulants?

Answer 124

Sugar free chewing gum or sweets Frozen fruit juices or lollies Organic acids such as salivix pastilles

Question 125

Describe artifical saliva?

Answer 125

Mucon or carboxymethylcellulose based Short duration of action Avoid acidic products - glandosane Neutral pH - AS saliva Orthana - Biothene Oralbalance gel - BioXtra gel - Saliveze

Question 126

Which saliva replacements can a dentist prescribed on the NHS?

Answer 126

Glandosane Saliveze Salivix pastilles Salivox Plus pastilles

Question 127

At what age does lichen planus usually affect?

Answer 127

30-50 years old

Question 128

What percentage of skin and oral cases are there.

Answer 128

50% oral lesions 10-30% skin lesions

Question 129

Name the main types of Lichen Planus and their

Answer 129

Cutaneous - skin Reticular - commonest Erosive - premalignant Desqamative attached gingivae Descriptors - Atrophic/Ulcerated/ Plaque

Question 130

What is the histopathological findings of lichenoid reaction?

Answer 130

Chronic inflammatory cell infiltrate Saw tooth rete ridges Badal cell damage Patchy acanthosis Parakeratosis

Question 131

What is the histopathological findings of licehn planus?

Answer 131

Orthokerstosis Wedge shaped hypergrabulosis Dermal epidermal Junction obscured lymphocytes Vacuoles at basal later Luck band of lymphocytes under epidermis Civatte bodies - dead keratinocytes

Question 132

What does the histopathological findings tell us?

Answer 132

Lymphocyte activation Overreaction to normal trigger Virus umplicated in immune upregulation but NOT as a cause of LP - hep C or herpes Sometimes has external triggers - medicines or amalgam

Question 133

What are the 8 aetiologices of lichen planus

Answer 133

Autoimmune Viral Genetic predisposition Physical and emotional stress Trauma - scraped or after surgery an isomorphic response (koebnerisation) Localised skin disease - herpes zoster - isotopic response Contact allergy - amalgam Drugs - gold, quinine, beta blockers and ACE inhibitors

Question 134

What are the symptoms of lichen planus?

Answer 134

Often none May relate to thinning of epithelium - sensitive to hot and spicy food - burning sensation in the mucosa

Question 135

What other body parts can LP affect?

Answer 135

Skin Scalp Genitals Hair Nails

Question 136

What are the 5 main sites for oral LP?

Answer 136

Biccal mucosa Gingiva - desquamative gingivitis Tongue- lateral or dorsum Lips Palate

Question 137

Describe buccal lichen planus?

Answer 137

Commonest Can be found anywhere - ant at commisure - mid - post around 3rd molar Mainly an incidental finding Easy to biopsy

Question 138

Describe gingival lichen planus?

Answer 138

Found in isolation Termed desquamative gingivitis - similar to gingival pemphigoid and to plasma cell gingivitis - clear histological Very erythematous appearance to the gingiva Patchy Reticular pattern more common Oral hygiene is essential to settle the lesion - plaque driven - especially interdentally Biopsy can be difficult - risk of damage to attachment area - adherent attached mucosa damaged lifting from bone

Question 139

Describe tongue lichen planus?

Answer 139

Dorsum usually idiopathic - loss of papillary becoming smooth Lateral may be drug/amalgam trigger - amalgam most likely in isolated lesion - look at tongue rest position - contact amalgam? Easy biopsy but painful

Question 140

Describe lip lichen planus?

Answer 140

On the lip Biopsy hard? Looks sore Erythema

Question 141

What is it called if the cause is known for oral lesion?

Answer 141

Lichenoid reaction to...

Question 142

Medications which can cause LP?

Answer 142

ACE inhib Beta blockers Diuretics - bendroflu and frusemide NSAIDs DMARDs Rare - phenothiazines

Question 143

Name 3 types of DMARDs?

Answer 143

Penicillamine Gold Sulphasalazine

Question 144

What are the discriminative characteristics of a lichenoid drug reaction?

Answer 144

Widespread lesion Bilateral and mirrors Poorly response to standard steroid treatment

Question 145

How to manage lichenoid drug reactions?

Answer 145

Benefit of the drug vs the risk of stopping the drug How bad is the discomfort from the symptoms If significant symptoms - may need to find alternative medication Discuss with GP

Question 146

What is the defintion of amalgam contact sensitivity LP?

Answer 146

Is it the amalgam, Mercury or something else as the trigger Patch test to the allergen

Question 147

How to manage an amalgam related lichen planus lesion?

Answer 147

If asymptomatic do nothing Any replacement will lose tooth tissue

Question 148

Which materials to replace amalgam with?

Answer 148

Composite Glass Gold - low palladium alloy Bonded crown

Question 149

Srmamentarium for amalgam removal?

Answer 149

Dam High vol suction PPI Avoid during preg

Question 150

Explain the overall lichen planus management for the patient?

Answer 150

Remove any cause - medicines - dental restorations Biospy - unless a good reason not to Blood test - haematinics - fbc - if lulus suspected autoantibody screen for ANA, Ro and dsDNA

Question 151

What treatment would be recommended for mild intermittent lichen planus lessons?

Answer 151

Topical OTC remedies - chlorhexidine - benzdamine Avoid SLS containing toothpaste

Question 152

What treatment would be recommended for a persisting synthetic lichen planus lesion?

Answer 152

Topical steroids - beclomethasone inhaler - betamethasone rinse Higher strength steroid - skin steroid cream - Clobetasol Topical tacrolimus mw Hydroxycholorquine Systemtic immumodilators - azathioprine and mycophenolate

Question 153

Graft vs host disease

Question 154

What are the histological findings of lupus erythematosis?

Answer 154

Basal vacuolar damage Atrophic epithelium Melanophage Intense lymphocytic infiltrate

Question 155

Describe lichen like lesions?

Answer 155

Underlying disease needs consideration GVHD common after stem cell transplant Lupus lesion can be - only in mouth - discoid lupus no auto abs - mouth and elsewhere (systemic ANA/Ro/dsDNA If oral symptoms only treat like lichen llanjs

Question 156

Name 5 vesiculobulloua conditions?

Answer 156

Erythema multiform Pemphigus Pemphigoid Angina Bullish Haemorrhagia Bullous lichen planus

Question 157

What is the defintion of Pemphigoid?

Answer 157

A subepithelial antibody attack Thick walled blisters - persist to be seen - clear or blood filled

Question 158

Name 3 different forms and presentations of Pemphigoid?

Answer 158

Bullous pemphigoid - skin Mucous membrane pemphigoid - all mucous membranes Cicatritial pemphigoid - mucosal with scarring

Question 159

Describe the histopathogy of pemphigoid?

Answer 159

Sub epithelial split - epithelial/CT tissue junction Hemi-desmosomes involved at basement membrane

Question 160

Describe how Pemphigoid is seen with immunofluorescence?

Answer 160

Linear staining along the basement membrane C3 and IgG detected in this area in 'standard' pemphigoid IgA occasionally found - linear staining with C3 is 'Linear IgA disease' - granular IgA and C3 deposits is seen in 'dermatitis herpetiformis'

Question 161

What is a symblepharon?

Answer 161

Pemphigoid that is present on the eye

Question 162

Non-oral locations of Pemphigoid?

Answer 162

Oral and skin lesions - bullous on skin - mucous mem usually mouth, eye or genitals (needs specialist) Scarring is a feature in some cases - cicatritial pemphigoid

Question 163

How to manage Pemphigoid?

Answer 163

Steroids Immune modulating drugs - azathioprine - mycophenolate

Question 164

What is the defintion of Pemphigus?

Answer 164

Commonest form is vulgaris Intraepithelial bullae Clinically: - more common in females and over 50s - genetic with ashkenazi Jews Sites: - skin - mucosa They blister, then burst and then it spreads

Question 165

Describe Pemphigus histopathologically?

Answer 165

Supra-basal split with tzank cells

Question 166

Describe Pemphigus using immunofluorescence?

Answer 166

Very green Basket weave pattern - around each epithelial cell C3 and IgG in Pemphigus vulgaris

Question 167

How to treat Pemphigus?

Answer 167

It affects the mucosa and skin Rarely see intact bullae - intra epithelial blisters Can be fatal without disease - complications of treatment are major cause of death

Question 168

Explain 2 different types of immune mediated disease?

Answer 168

Hypersensitivity Immunogenic

Question 169

How many types of hypersentivitiy?

Answer 169

5

Question 170

Name the 2 types of immunogenic immune mediated disease?

Answer 170

Cell mediated Antibody mediated

Question 171

Name 3 types of local immunological oral disease?

Answer 171

Aphthous ulcers Lichen planus Orofaxial granulomatosis

Question 172

Name 6 systemic diseases with local oral effects?

Answer 172

Eythema multiform Pemphigus Pemphigoid Lupus Systemic sclerosis Sjogren's syndrome

Question 173

Type 3 Hypersensitivity example?

Answer 173

Erythema multiform

Question 174

Name 3 examples of cell mediated immunity?

Answer 174

Aphtous ulcers Lichen Planus Orofaxial Granulomatosis

Question 175

Name 2 examples of antibody mediated immunity?

Answer 175

Pemphigus Pemphigoid

Question 176

Immunological skin diseases?

Answer 176

Skin and oral.mucosa.share many antigens and epitopes - blistering skin conditions can also affect the mouth

Question 177

Explain the mechanism of immunological skin disease?

Answer 177

Auto-antibody attack on skin compartments causing loss of cell to cell adhesion - causing splits in the skin - fill with inflammatory exudate - form vesicles or blisters

Question 178

How do cells of the epidermis adhere to eachother?

Answer 178

Via desmosomes and hemidesmosomes 2 proteins - desmoglein (VIP) and desmocollin

Question 179

Explain the mechanism of action for immunofluorescence?

Answer 179

A fluorescein molecule is attached to an engineered antibody, that when binds fluorescence and becomes active

Question 180

Explain the difference between direct and indirect immunofluorescence?

Answer 180

Direct: - antibody mediated tissue disease - antibody bound to tissues - targeted in DIF Indirect: - circulating antibody not yet bound to the tissue - detected by immunofluorescence from a plasma sample - not always useful for diagnosis - often good for monitoring disease activity

Question 181

What is the defintion of erythema multiforme?

Answer 181

Acute onset - more men Skin - show target lesions Mucosa - show ulcers For young males it is recurrent within a short period

Question 182

What is the aetiology of erythema multiforme?

Answer 182

Immune complex? - drugs - herpes simplex - mycoplasma

Question 183

What specific sites do erythema multiforme target?

Answer 183

Lips and anterior part of the mouth Heals in 2 weeks Very painful - unable to eat or drink

Question 184

What os erythema multiforme relation to Stevens Johnson syndrome?

Answer 184

Can be involved with Stevens-Johnson syndrome - sevre multisystem involvement - skin, conjunctivae, nose, pharynx, mouth and genitals

Question 185

What is the treatment for erythema multiforme?

Answer 185

Oral lesions: Urgent medical therapy: - systemic steroids of up to 60mg per day - systemic aciclovir Encourage fluid - possible I Encourage analgesia If recurrent: - prophylactic acyclovir daily - allergen test for triggers Mycoplasma infective agent

Question 186

What is the defintion of angina bullous haemorrhagica?

Answer 186

Commonest oral blistering condition Blood blisters in mouth: - buccal mucosa and soft palate - rapid onset - 1 hr then burst Painless Iniated by minor trauma or eating Heal with no scar within days

Question 187

Give a brief overview of how to treat and what tests for angina bullish haemorrhagica?

Answer 187

Non specific ulceration DIF and IFF negative No defects Chlorhex MW May recur

Question 188

How to manage angina bullish haemorrhagica?

Answer 188

No treatment Reassure patient that is benign Explain known triggers

Question 189

Why are mucosal lesions more frequent in children?

Answer 189

Clinical issues traditionally related to immunological immaturity

Question 190

Name the 2 types of congenital oral mucosal lesions?

Answer 190

Hereditary Developmental defects

Question 191

Name the 6 types of acquired oral mucosal lesions?

Answer 191

Traumatic Drug-related Chronic inflammatory Hyperplastic Neoplastic Infective

Question 192

What is the defintion of white sponge naevus?

Answer 192

Hereditary Inherited as autosomal dominant condition . Defect in keratin gene 4 and 13. Uncommon

Question 193

Name the clinical features of white sponge naevus?

Answer 193

•White, soft, irregularly thickened, no defined borders •Bilateral •Genital tissues can also be affected •Often misdiagnosed with candidosis

Question 194

Name the histopathology of white sponge naevus?

Answer 194

•Uniform acanthosis •Hyperparakeratosis • Intracellular oedema •No dysplasia, no inflammation

Question 195

How to manage white sponge naevus?

Answer 195

Reassurance

Question 196

Name 3 developmental defect oral mucosal lesions?

Answer 196

Fordyxe's granules Foliate papillae Geographic tongue

Question 197

Describe the clinical features of fordyce's granules?

Answer 197

▪Ectopic sebaceous glands ▪Association with hormonal changes in puberty? ▪Bilateral, most commonly on buccal mucosa

Question 198

Describe the clinical feattures of folaite papillae?

Answer 198

▪Pinkish soft nodules ▪Bilateral, ventral tongue ▪Lymphoid tissue, sometimes inflamed/hyperplastic

Question 199

Describe the clinical features of geographic tongue?

Answer 199

▪Dorsum of tongue ▪Irregular, smooth, red areas (depapillated) with sharply-defined edge ▪Recurrent, migrates

Question 200

Describe the histology of geographic tongue?

Answer 200

▪Thinning of epithelium at centre, mild hyperplasia at periphery ▪Epithelium infiltrated by neutrophils

Question 201

Explain how to manage geographic tongue?

Answer 201

reassurance. If symptomatic exclude heamatological deficiencies. Median rhomboid glossitis generally not seen in children

Question 202

Name 3 traumatic oral mucosal lesions?

Answer 202

mucocele traumatic ulcer frictional keratosis

Question 203

Describe the clinical fearues of frictional keratosis?

Answer 203

▪Pale and translucent or white/dense with rough surface

Question 204

Describe the histology of frictional keratosis?

Answer 204

Epithelial hyperplasia, with thick granular cell layer and hyperorthokeratosis ▪Scattered subepithelial lymphocytes

Question 205

Describe the clinical features of traumatic ulcer?

Answer 205

Mechanical, thermal or chemical trauma ▪Inflammation levels and clinical features vary ▪Yellowish floor of fibrin slough often present

Question 206

Describe the histology of traumatic ulcers?

Answer 206

Non-specific ulceration. See RAS ▪Destruction of epithelium ▪Tissue infiltration by neutrophils

Question 207

Describe the clinical features of a mucocele?

Answer 207

▪Most commonly on lower labial mucosa ▪Overlying mucosa is intact and healthy typically circular ▪Firm or fluctuant and bluish

Question 208

Describe the histology of a mucocele?

Answer 208

▪Damage to duct of salivary gland ▪Mucin and macrophages surrounded by compressed connective tissues ▪No epithelial lining

Question 209

Name a drug-induced oral mucsoal lesion?

Answer 209

Chemo-induced stomatitis Aspirin burns

Question 210

Name 3 types of inflammaotry oral mucosal lesions?

Answer 210

Orofacial granulomatosis erythema multiforme recurrent apthous stomatitis

Question 211

Describe the clinical features for recurrent aphthous stomatitis?

Answer 211

▪Idiopathic, but systemic factors known to modulate the severity of disease ▪Onset in childhood, but peak in adolescence Minor Major Herptiform

Question 212

Describe the histology of recurrent aphthous stomatitis?

Answer 212

▪Initial lymphocitic infiltration? ▪Destruction of epithelium ▪Tissue infiltration by neutrophils ▪Dilated vessels

Question 213

Explain the management for a mucocele?

Answer 213

Reassurance/excision if symptomatic or interferes with oral functions

Question 214

What should be excluded when dealing with recurrent aphthous stomatitis?

Answer 214

Extraoral involvement should be excluded, e.g. GI (coeliac disease, Crohn’s), genital/ocular (Behcet’s).

Question 215

Describe the clinical features for erythema multiforme?

Answer 215

▪Mostly HSV-related, drug-induced ▪Cutaneous erythema or “target” lesions ▪Ulceration of outer lip with bleeding, crusting. ▪Intraorally irregular fibrin- covered erosion and erythema ▪Ddx with HSV-1 infection

Question 216

Describe the histology of erythema multiforme?

Answer 216

▪Necrosis of keratonocytes ▪Epithelial infiltration by inflammatory cells ▪Intraepithelial or subepithelial vesiculation

Question 217

Describe the clinical features for orofacial granulomatosis?

Answer 217

▪Swelling of the lips ▪Mucosal nodularity (cobblestoning) ▪Mucosal tags ▪Gingival hyperplasia ▪Aphthous oral ulcers ▪Children more likely to develop Crohn’s disease

Question 218

Describe the histology for orofacial granulomatosis?

Answer 218

Granulomas containing multinucleated giant cells ▪Lymphoedema

Question 219

What are possible differential for orofacial granulomatosis?

Answer 219

DDx with sarcoidosis and tubercolosis. Primary TB of the oral cavity is rare,?more common in children than adults

Question 220

Name 3 inflammaotry oro mucosal diseases rarely seen in children?

Answer 220

Oral Lichen Planus • Mucous Membrane Pemphigoid • Pemphigus vulgaris

Question 221

Describe the clinical features for oral lichen planus?

Answer 221

▪White striae and/or mucosal atrophy, and/or erosions, and/or plaques ▪Desquamative gingivitis in isolation or in combination with above ▪Bilateral lesions

Question 222

Describe the histology for oral lichen planus?

Answer 222

Basal membrane thickening Band-like lymphocitic infiltrate Colloid bodies, apoptotic basal cells

Question 223

Describe the clinical features for mucous membrane pemphigoid?

Answer 223

▪Bullae, sometimes intact, can appear as blood blisters. If ruptured raw ulcer ▪Desquamative gingivitis ▪Conjuctival involvement ▪Cutaneous involvement less prominent than bullous pemphigoid

Question 224

Describe the histology for mucous membrane pemphigoid?

Answer 224

•Separation of full thickness of epithelium from CT •Linear deposition of IgG and C3/C4 along basal membrane. •Auto-antibodies bind along basal membrane indirect immunofluorescence assay •CT infiltrated with inflammatory cells

Question 225

Describe the clinical features of pemphigus?

Answer 225

▪Fragile vesicles/bullae ▪Ruptured vesicles ▪Nikolsky’s sign positive ▪Widespread cutaneous involvement

Question 226

Describe the histology for pemphigus?

Answer 226

•Acantholysis •Intraepithelial vesicles. •‘Chickenwire’ deposition of IgG and C3/C4 within the epithelium. •Anti-desmoglein3 antibodies bind intercellular substance in direct immunofluorescence assay

Question 227

Deswcribe the clinical features for epydermolysis bullosa?

Answer 227

▪Subepithelial bullae leading to severe scarring after minimal trauma. ▪Type VII collagen defect. ▪Autosomal recessive

Question 228

Name 3 hyperplastic forms of oral mucosal lesions?

Answer 228

Vascular malformation Giant cell epulis Pyognic granuloma

Question 229

Describe the clinical features for a pyogenic granuloma?

Answer 229

▪Soft, red polypoid swelling ▪Most commonly gingival but not exclusively

Question 230

Describe the histology for a pyogenic granuloma?

Answer 230

•Granulation tissue •Dilated blood vessels in oedematous CT •Dense infiltration by neutrophils NO GRANULOMAS, NO PYOGENIC BACTERIA

Question 231

Describe the clinical features of a giant cell epulis?

Answer 231

▪Soft, violaceus swelling ▪Central gingival segments Related to resorption of deciduous teeth?

Question 232

Describe the histology for giant cell epulis?

Answer 232

•Subepithelial clusters of giant cells in fibro- vascular tissue

Question 233

What to exclude when dealing with a giant cell epulis?

Answer 233

Need to exclude central GCG and underlying hyperparathyroidism

Question 234

Describe the clinical features of vascular malformation?

Answer 234

Purple nodular lesion ▪Blanches upon pressure

Question 235

Describe the histology for a vascular malformation?

Answer 235

•Capillary: small vessels and vasoformative tissue •Cavernous: large blood filled sinusoids

Question 236

Name 2 pigmentary chnages ivolved with oral mucosal lesions?

Answer 236

Puetz-Jeghers syndrome Addison's Disease

Question 237

Name the clinical features of Peutz-Jegher's syndrome?

Answer 237

Clinical features ▪Intestinal polyposis ▪Mucocutaneous pigmented lesions appearing during childhood

Question 238

Describe the histology for Addison's disease?

Answer 238

•Mild acanthosis •Melanin in basal layer

Question 239

Describe the clinical features for warts?

Answer 239

HPV 2, 4 •White or pinkish, raised •Sessile or pedunculated •Often multiple •Mainly secondary to self inoculation

Question 240

Describe the histopathology of warts?

Answer 240

•Papillary processes of hyperplastic epithelium with acanthosis, hyperkeratosis, hyperplastic basal cell layer •Connective tissue core •Koilocytes often present

Question 241

Describe the clinical features for pseudomembranous candidosis?

Answer 241

•Acute •Thick white pseudomembranes of various sizes •Erythematous background •Often idespread

Question 242

Diseases that cause immunocompromisation and lead to oral mucosal lesions?

Answer 242

HIV/AIDS

Question 242

How are viruses transmitted?

Answer 242

Exchange of blood products Sexual transmission Perinatal infection

Question 243

MoA of HIV?

Answer 243

Retrovirus - group VI (baltimore) Infects activated T cells and macrophages vis the envelope glycoprotein Transferred by dendritic cells via DC-SIGN, then migrate to lymph nodes to transfer the CD4 T cells

Question 244

How does HIV infect T cells?

Answer 244

HIV gp120 binds T cells through CCR5/CXCR4 and CD4

Question 245

How does HIV infect macrophages?

Answer 245

HIV gp120 binds macrophages through CCR5 and CD4

Question 246

What infections are diagnostic for acute HIV infection?

Answer 246

Pyrexia Skin rash Haedache Diarrhoea Oropharyngitis Oral mucosal erythema

Question 247

What infections are diagnostic fir ARC asymptomatic seropostive HIV?

Answer 247

Lymphoadenopathy Persistent pyrexia Diahorrea Weight los Fatigue and malaise

Question 248

What infections are diagnostic for AIDS?

Answer 248

Kaposi's sarcoma NH lymphoma Thrombocytopenia Neurologival diseases

Question 249

What drug is Pre-exposure prophylaxis of HIV?

Answer 249

Trivada - emtricitabine

Question 250

When will HIV/AIDS related oral lesions occur?

Answer 250

May occur during mild immunodeficiency and prior to severe opportunistic infections Evidence suggests that patient s with oral.lesikns may progress to AIDS more rapidly compared to patients without

Question 251

Why can oral lesions occur?

Answer 251

Immunodeficiency

Question 252

Name 5 oral mucosal lesions strongly associated with HIV?

Answer 252

Candidiasis: - erythematous, pseudo and angular cheilitis Hairy leukoplakia Kaposi sarcoma NH lymphoma Perio disease: linear gingival erythema, necrotising gingivitis and periodontitis - more commonly seen due to immunosuppressant therapy

Question 253

Describe candidiasis in HIV patients?

Answer 253

Mild immunodeficiency If psuedomem, indicative of acture immunosuppression - widespread oropharyn and oesoph Can persist for month Erythamtous Hyperplastic

Question 254

Describe linear gingival erythema in HIV patients?

Answer 254

Red band involving the free gingival margin - not plaque induced - hypermedia due to vasoactive cytokines

Question 255

Describe hairy leukoplakia in HIV?

Answer 255

Not pre malignant White patches that can't be removed Lateral border of the tongue Vertical white folds with hair like surface Smooth

Question 256

Describe the histopathology of hairy leukoplakia?

Answer 256

Acabthotic parakerarinsed epithelium Finger like keratin projections on the surface Band of ballon cells in prickle cell layer Secondary candidal infections Swollen cells are EBV+ (koliocytes), EBV demonstration essential for diagnosis

Question 257

Describe Kaposi sarcoma in HIV patients?

Answer 257

Most commonly associated with HIV HHV8 Involves skin and mucosal surfaces Red purple patch - becomes nodular

Question 258

Describe the histopathology of Kaposi sarcoma?

Answer 258

Early lesions consit of proliferating endothelial cells, extravasated blood cells, haemosiderin and inflamm cells Late lesions have a more predominant vascular component and atypical spindle cells

Question 259

Describe non-hodgkins lymphoma in HIV patients?

Answer 259

AIDA and severely immunocompromised patients Associated with EBV

Question 260

Name 4 less commonly oral mucosal lesions with HIV?

Answer 260

Bacterial infections Salivary glabd disease Oral ulceration Viral infections

Question 261

Describe HSV and VZV infections in HIV?

Answer 261

More severe and higher recurrence

Question 262

Describe the HPV infection in HIV patients?

Answer 262

6,11 and 16 Venereal war Transmitted via oro genital contact Multiple white/pink nodules Fuse forming sessile or pedunculated papillary lesions

Question 263

Describe the histopathology of HPV in HIV patients?

Answer 263

Induce hyperplastic changes rather than ballooning degeneration Fibrovascular core covered by stratified squamous epithelium with - hyperpladtiv basal cell layer - acanthosis - parakeratosis Koilocytes

Question 264

Describe atylical ulceration in HIV patients?

Answer 264

Oropharyns most commonly affected Associated with CMV infection - can also be aphthous stomatitis

Question 265

Describe salivary gland disease in HIV patients?

Answer 265

Salivary gland enlargement - mainly parotid Xerostomua Lymphocyte infiltration Lympho-epothelial cysts Enlargement of intraparotid nodes as part of P

Question 266

How is Oral cancer classified?

Answer 266

International Classification of Disease for Oncology - ICD-O

Question 267

What makes classification of cancer difficult?

Answer 267

Makes comparison difficult Makes epidemiology difficult Makes treatment planning difficult

Question 268

Name the 2 distinct disease patterns for oral cancer?

Answer 268

Oral Cavity Cancer (OCC) Oro-Pharyngeal Cancer (OPC)

Question 269

Describe the epidemiology of OCC?

Answer 269

2.5 per 100,000 pop (2012) Almost HALF (48.7%) in south central Asia Male 2:1 Female Incidence not increasing worldwide - Decreasing in men, increasing in women - Linked to reduction in tobacco use Scottish Cancer Registry - 10% increase 2001-2012

Question 270

Name the 6 common sites for mouth cancer?

Answer 270

Floor of the mouth Lateral border of the tongue Retromolar regions Soft and hard palate Gingivae Buccal mucosa

Question 271

Name the 3 higher sites for SSC in drinkers and smokers?

Answer 271

FoM Lat. border of the tongue Soft palate

Question 272

Name the 8 sites of oral cancer?

Answer 272

Lips Palate Tonsils FoM Other throat Tongue Oropharynx Gums

Question 273

Describe the epidemiology for OPC?

Answer 273

1.4 per 100,000 pop Most in North America and south central Asia Male 4.8:1 Female Rates rapidly rising, especially in High Income areas (North America) - Linked to rising HPV epidemic Scottish Cancer Registry - 85% increase 2001-2012 – highest increase for any cancer

Question 274

Name the 5 main risk factors and their associations to Oral Cancer? - how much does each RF multiply the risk of OC?

Answer 274

Smokers who don’t drink x2 risk - Increases with quantity, duration and frequency of tobacco use - Fewer cigarettes for longer duration worse than high number, short term - Smoking risks were generally greater for larynx cancer Drinkers (3-4 drinks/day) x2 risk - Never smoked population - Frequency more important than duration – more drinks each day key - alcohol drinking for oral cavity and pharyngeal cancers Smoke and Drink x5 risk - Increases with frequency and duration of smoking and alcohol consumption - No safe lower limit Betel quid (paan) x3 risk - mixture of substances including areca nut with or without tobacco wrapped in a betel leaf and placed in the mouth Socioeconomic Status x2 risk - Even without other risk factors - Low educational attainment

Question 275

Name the 3 risk factors that have not been confirmed as certain to increase the overall risk of Oral cancer?

Answer 275

Family History - 1st degree relative with H&N cancer may be important Oral Health - Early data suggests poor oral health may be associated with an increased cancer risk – small effect Sexual Activity - a slight increased risk for oropharyngeal cancer with: - six or more lifetime sexual partners - four or more lifetime oral sex partners - early age (<18 years) of sexual debut (INHANCE)

Question 276

What are the benefits of reducing smoking and alcohol intake?

Answer 276

Benefits seen between 1-4 years Risks reduced and reached a similar level to those who had never smoked after 20 years of quitting. In contrast, the risk effects associated with quitting heavy alcohol consumption take 20 years to begin to emerge.

Question 277

What are the benefits of improving SE status?

Answer 277

Socioeconomic status - SE status is on a par with smoking and alcohol in terms of magnitude (two-fold increased risk) - specifically low educational attainment and low income. - These risks were not fully explained by smoking and alcohol consumption ('the cause of the cause’) - have a more direct effect associated with socioeconomic circumstances

Question 278

What are the benefits of reducing poor diet choices?

Answer 278

- There is limited new evidence in relation to dietary factors beyond confirming that a high intake of fresh fruits and vegetables were associated with reducing by half the oral cancer risk - Obesity was not associated with an increased oral cancer risk - young people (aged 30-years or less) oral cancer was more likely in those who self-reported a low body mass index (BMI)

Question 279

Name 4 potentially malignant lesions?

Answer 279

White lesions (leukoplakia) Red lesions (erythroplakia) Lichen planus - Candidal Leukoplakia - Chronic Hyperplastic Candidiasis Oral Submucous Fibrosis

Question 280

Describe the epidemiology of white lesions in OC?

Answer 280

incidence 0.2 - 4% - wide variation in different populations - Reliability of data not clear malignant change - varied reports, most under 4% - period prevalence 2.5% in 10 years, 4% in 20 years Most oral carcinomas in UK arise in initially clinically normal mucosa Most cancer in high incidence areas (e.g. India) from potentially malignant lesion Worldwide leukoplakia is 50 to 100 times more likely to progress to cancer than clinically normal mucosa

Question 281

Name 3 types of descriptions of white lesions?

Answer 281

Homogenous Erosive Non-homogenous on atrophic background

Question 282

How does erythroplakia compare to leukoplakia?

Answer 282

much less frequent than leukoplakia much higher risk of cancer greater dysplasia risk - Up to 50% already be carcinoma no good follow-up studies available

Question 283

What are the common characteristics of dysplasia and the new categorisation of severity?

Answer 283

Based on: - Cellular Atypia - Epithelial Architectural Organisation New categorisation - Low grade - high grade - carcinoma-in-situ

Question 284

Describe the histological low grade of oral mucosal dysplasia?

Answer 284

Easy to identify that the tumour originates from squamous epithelium Architectural change into lower third Cytological atypia or dysplasia may not be prominent Shows a considerable amount of keratin production Evidence of stratification Well formed basal cell layer surrounding the tumour islands Tumour islands are usually well defined and are often continuous with the surface epithelium Invasion pattern with intact large branching rete pegs ‘pushing’ into underlying CT (Where there is architectural change into middle third, depending on the level of cytological atypia will be classified into low grade or high grade)

Question 285

Describe the histological high grade of oral mucosal dysplasia?

Answer 285

Show little resemblance to a normal squamous epithelium Architectural change upper third Usually show considerable atypia Invade in a non-cohesive pattern with fine cords, small islands and single cells infiltrating widely through the CT Mitotic figures are prominent and many may be abnormal Degree of differentiation used to predict prognosis

Question 286

Describe the histological carcinoma in situ of oral mucosal dysplasia?

Answer 286

Theoretical concept Cytologically malignant but not invading Abnormal architecture - Full thickness (or almost full) - Severe cytological atypia Mitotic abnormalities frequent

Question 287

Name the histoloigcal prognostic facors which give information on survivability?

Answer 287

Pattern of Invasion - Bulbous rete pegs infiltrating at same level is considered of a better prognosis than widely infiltrating small islands and single cells Depth of Invasion - Risk of metastases for a tumours greater than 4mm was 4x greater than for a tumour less than 4mmm Perineural Invasion - Is seen in up to 60% of OSCCs but is most significant when a tumour is seen within a large nerve at a site some distance from the main tumour mass Invasion of Vessels - Widely thought to be associated with lymph node metastaes and a poor prognosis

Question 288

Describe the Field Cancerisation concept?

Answer 288

Multiple primaries possible over time - up to 15 to 20 in some patients Concept of “field cancerisation” - high cancer risk in 5cm radius of original primary - that’s most of the mouth/pharynx Synchronous or metachronous lesions - Can occur at the same time as the primary or at later times

Question 289

Name the multiple variables for clinical cancer staging of OC?

Answer 289

site size (T) spread (N&M)

Question 290

Describe the different varying change of cancer prognosis/survivability?

Answer 290

1/3 patients present at stage I/II - Stage I - 80% cure rate - Stage II – 65% cure rate - Later than this 5 year survival <50%, cure <30% - If untreated, with metastases, survival is about 4 months Surgery, Radiotherapy and Chemo/Immunotherapy all used - Choice will depend on patient choice and health/prognosis - Tumour location, size and nutitional status all important For resectable tumours, primary surgery offers the best outcome - Post surgical radiotherapy or chemotherapy

Question 291

Describe the aetiology, behaviour and prognosis of Lip cancer?

Answer 291

Lower lip - non-healing ulcer or swelling Aetiology - Sunlight UV-B - smoking Behaviour - slow growth - local invasion - rarely metastasise to nodes Good prognosis as early detection

Question 292

How is OC detected?

Answer 292

Difficult to do – a judgement from experience - Use the  'Oral Cancer Recognition Toolkit’ - Developed jointly by Cancer Research UK and the British Dental Association

Question 293

What are the advantages and disadvantages of OC screening?

Answer 293

Benefits vs Harm Undetected lesions vs False positive Cost of Screening vs Cost of disease Cost of Screening vs Disability from disease

Question 294

Name the 5 OC screening tools?

Answer 294

HPV16 screening Toluidene blue VELscope Photodynamic Diagnosis (PDD) Clinical judgement of experienced clinician

Question 295

Describe what and how toluidine blue is and used?

Answer 295

false positive in inflammatory lesions ? 50 % false negatives good for invasive disease, but usually clinically evident

Question 296

Describe what and how VELscope is and used?

Answer 296

Autofluorescence of tissues with blue light - Loss of fluorescence equates to ‘change’ - Change may be cancer but can be other changes Published work ‘thin’ - May well work, but evidence not yet adequate

Question 297

Explain the duty of Primary care dentistry in OC screening/detection?

Answer 297

Part of General CPD requirement now Dentist has opportunity for PRIMARY PREVENTION in patients attending for regular oral care Dentist must be familiar with and competent in: - Smoking cessation advice - Alcohol reduction advice - Healthy diet promotion There is a GDC expectation that a dentist will do this as part of ‘good patient care’ rather than any particular remuneration Dentist has to make decision about their referral threshold for potentially malignant lesions Monitor with photographs and education Remove local factors where ulcer may be due to trauma, then review 2 WEEK RULE for referral to clinic for the hospital Patient must be initially seen within this time 62 day referral to treatment time for cancer patients

Question 298

What is the definition of precancerous lesion?

Answer 298

An altered tissue in which cancer is more likely to form

Question 299

What is the defintiion of precancerous condition?

Answer 299

A generalised state associated with an increased cancer risk

Question 300

Name the 4 types that can't be conisdered leukoplakia?

Answer 300

Tobacco related lesions Smokers keratosis Chronic hyperplastic candidosis Frictional keratosis

Question 301

What is the definition of leukoplakia?

Answer 301

It is a clinical diagnosis It has NO histological connotation Epithelial dysplasia may or may not be present Non-homogeneous types are more likely to be dysplastic

Question 302

Describe the epidemiology of leukoplakia?

Answer 302

- Incidence ? 0.2 – 10% but wide variation in different parts of the world. 6 x commoner in tobacco users. Male > Female world wide but only marginally so in the west. More common in the “elderly.” - Malignant change in 3 -28% - Period prevalence - how many in what time? 2.5% in 10 years, 4% in 20 years (West) ? % in Far east and Africa

Question 303

Name the clinical predictors of malignancy?

Answer 303

Clinical appearance - very variable Non-homogeneous Verrucous, speckled, Ulcerated, leuko-erythroplakia

Question 304

Describe the molecular progression of oral cancer?

Answer 304

The development of oral cancer involves the progressive accumulation of 6 -10 genetic alterations in an epithelial cell leading to uncontrolled proliferation and clonal expansion. A genetic progression model based on chromosomes frequently identified as showing Loss of Heterozygosity (LOH) in oral carcinogenesis suggests: - Normal mucosa experiences a LOH at 9p: leads to predysplastic lesion. - Predysplastic lesion experiences an additional LOH at 3p, 17p :leads to dysplasia. - Dysplastic lesion experiences further LOH at 11q,13q and 14q leads to carcinoma-in-situ. - C-I-S lesion experiences a further LOH at 6p,8,4q which leads to invasion

Question 305

What is the definition of hyperplasia?

Answer 305

Increased cell numbers Architecture regular stratification altered compartment size NO cellular atypia

Question 306

What is the definition of hyperplasia?

Answer 306

Increased cell numbers Architecture regular stratification altered compartment size NO cellular atypia

Question 307

What is the definition of hyperplasia of stratum spinosum (acanthosis)

Answer 307

Architecture - increased maturation compartment

Question 308

What is the definition of basal cell hyperplasia?

Answer 308

increased basal cells

Question 309

What is the definition of low grade (mild hyperplasia)

Answer 309

Architecture - change in lower third Mild - cytological atypia

Question 310

What is the definition of high grade (mod/severe dysplasia)

Answer 310

Architecture - change into middle/upper third Marked cytological atypia Possibility of numerous abnormal mitoses

Question 311

What is the definition of oral candidosis?

Answer 311

Opportunistic fungal infection of the oral cavity. - Oral rarely in itself painful - Oesophageal may be in HIV

Question 312

How do people aquire candida?

Answer 312

Majority of normal population are healthy carriers Most common isolate is C. albicans

Question 313

Name 5 candidal virulence factors?

Answer 313

Adherence Switching mechanisms Germ tube formation Extracellular enzymes Acidic metabolites

Question 314

Name the local predisposing factors for candidal infections?

Answer 314

Smoking Dentures Local corticosteroids Xerostomia Topical antimicrobials

Question 315

Name the general predisposing factors for candidal infections?

Answer 315

Extremes of age Endocrine disease - Diabetes Immunodeficiency - Steroid use, HIV Nutritional deficiency - iron Antibiotics

Question 316

Name the classification of oral candidosis?

Answer 316

Acute Pseudomembranous - Sudden local/systemic immunosuppression Chronic Erythematous - Longstanding & persisting issue - e.g. below poor fitting dentures, HIV, median rhomboid glossitis and antibiotic Chronic Hyperplastic

Question 317

How to diagnose oral candidosis?

Answer 317

Laboratory tests - Differentiate from commensal - Only by QUANTIFIABLE assay - Culture and sensitivity to inform treatment - Multiple sites usually - Smear/microscopy occasionally

Question 318

How to diagnose candidosis via lab?

Answer 318

Swab (mucosa or denture ) Whole saliva/Oral rinse - Growth onto selective agar Oral rinse - Patient rinses with 10ml of PBS. Inoculate onto selective agar on spiral plater. - Has the advantage of being a “Quantitative technique”

Question 319

How to identify candidaosis in the lab?

Answer 319

Direct microscopy Germ Tube test Physiological tests - Carbohydrate fermentation - Carbohydrate and nitrogen assimilation Commercial systems - API 20C systems

Question 320

How to identify candidaosis in the lab?

Answer 320

Direct microscopy Germ Tube test Physiological tests - Carbohydrate fermentation - Carbohydrate and nitrogen assimilation Commercial systems - API 20C systems Biopsy - Essential for diagnosis of hyperplastic candidosis. - PAS stain Direct smear

Question 321

Name the 5 candida species?

Answer 321

C. albicans C. glabrata C. tropicalis C. krusei C. dubliniensis

Question 322

Describe the principles of management for candidal infection?

Answer 322

Correction of predisposing factors OH, diet, trauma, steroid inhaler hygiene Identify underlying illnesses Antifungal agent Co-infection with other microorganisms?

Question 323

Name different categories of antifingal drugs?

Answer 323

Polyenes - Nystatin - Amphotericin Imidazole - Miconazole - Clotrimazole Triazoles - Fluconazole - Itraconazole

Question 324

Explain the treatment regimes for oral candidosis?

Answer 324

Topical Therapy (lengthy courses required) - Nystatin (pastille, suspension, cream and ointment) - Amphotericin (not available in the UK) - Miconazole Systemic treatment (often preferred) - Fluconazole - Itraconazole

Question 325

What is the definition of miconazole?

Answer 325

- Imidazole antifungal - Not absorbed systemically - Available as a cream, ointment, patch or a gel - Don’t use gel for skin lesions (orange!) - Cream/ointment available with hydrocortisone - Available without prescription Slow release adhesive preparation available ACTIVE AGAINST STAPHYLOCOCCI as well as Candida

Question 326

Name the types of systemic antifungals and their treatment regimes?

Answer 326

Fluconazole - 50mg capsules taken once daily - 14 day course Itraconazole - 100mg capsule - 14 day course - 100mg twice in once daily for Pseudomembranous candidiasis

Question 327

Name 3 antifungals that have resistance?

Answer 327

C. glabrata C. kruseii C. dubliniensis

Question 328

Name the disease that come from Human herpesvirus/

Answer 328

Herpes simplex virus (HSV) - Primary herpetic stomatitis - Herpes labialis (recurrence) Varicella-Zoster Virus (VZV) - Chickenpox - Zoster (recurrence) Epstein-Barr Virus - Infectious mononucleosis Cytomegalovirus (CMV) HHV8 - Kaposi’s sarcoma

Question 329

Explain the virion replication cycle?

Answer 329

Virus attachment and entry Uncoating of virion Migration of acid to nucleus Transcription Genome replication Translation of virus mRNAs Virion assembly Release of new virus particles

Question 330

Effect of viral infections on host cells?

Answer 330

Cell death (cytopathic effect) Latent infection Hyperplasia Transformation

Question 331

Explain the lifecycle of HSV, VZV associated leison?

Answer 331

Intranuclear oedema (glass-appearance of nuclei) at basal cell layer “Ballooning degeneration” : Keratinocytes swelling and loss of attachment. Cells can be multinucleated with eosinophilic intranuclear inclusions and eosinophilic cytoplasm Progressive cell swelling (cells are large and clear) Rupture of infected cells and release of viral particles to non-infected cells

Question 332

Explain how to diagnose human herpesvirus?

Answer 332

Laboratory investigations available: - Antigen-specific IgG or IgM serum titres - PCR - Immunofluorescence, immunocytochemistry on affected tissue - Virus isolation from lesion and cultivation

Question 333

Describe the apperance of primary herpetic stomatosis?

Answer 333

HSV-1 - Incubation period: 5-7 days - Intraoral vesicles - Vesicles on lips and crusting due to exudate coagulation - Generalized gingival inflammation Extra-oral involvement: - peri-oral - fingers (herpetic whitlow) - eyes Symptoms - Pain - Dysphagia - Dehydration - May be associated with fever, lymphadenopathy, - Pharyngitis in adolescents Recurrent infection: - Occur in the same location, unilateral and recur 2-3 times a year on average - Most commonly on lips, but can involve other perioral tissues - Erythematous areas papules vesicles ulcers - Intraoral mucosal involvement is less common. - Chronic ulcers in immunocompromised individuals

Question 334

Describe the apperance of chickenpox and recurrent zoster infection

Answer 334

VZV - Prodromes: fever, fatigue, pharyngitis - Small ulcers (rarely intact vesicles) mainly on soft palate and fauces - Intraoral lesions may precede skin lesions Recurrent infeection (Zoster) - Prodromes: pain and parasthesia - Unilateral vesicular eruption following distribution of sensory nerves, e.g. divisions of the trigeminal nerve, geniculate ganglion of facial nerve (Ramsay Hunt syndrome). - Intraoral vesicles rupture quickly - Cutaneous lesions clear within 3 weeks. Pain may persist (post-herpetic neuralgia)

Question 335

Describe the managment for HSV-1 and VZV mild infections?

Answer 335

Symptomatic relief : - Hydration - Rest - Pain relief - Antimicrobial mouthwashes (chlorhexidine 0.2%, H2O2 6%) Mild infection of the lips in healthy individuals: - Aciclovir cream 5% every 4 h - Penciclovir cream 1% every 2 h

Question 336

Describe the managment for HSV-1 and VZV severe and immunocompromised infections?

Answer 336

Severe infections in non-immunocompromised patients: - 200 mg Aciclovir tabs or oral suspension, 5 times daily, 5 days - Prophylaxis: aciclovir 400mg twice daily (in liaison with specialist) Immunocompromised patients: - 400mg Aciclovir tabs or oral suspension, 5 times daily, 5 days - Both adults and children Immunocompromised with severe infection: - Refer to specialist/GP for treatment Shingles: - 800mg Aciclovir tabs or oral suspension, 5 times daily, 5 days, within 72 h onset of rash - Not in children - Refer to specialist/GP

Question 337

Describe the apperance of infectious mononucleosis?

Answer 337

EBV: - Long incubation period (4-6 weeks) - Prodromes: severe fatigue, malaise and anorexia (10-15 days) - Main symptoms: fever, pharyngitis and generalized lymphoadenopathy (cervical nodes) Diagnostic features: - Paul-Brunell test + - Raised anti-EBV antibodies. - If above are negative consider CMV and toxoplasmosis. - Possible oral signs: tonsilar exudate, palatal petechiae

Question 338

Describe the apperance of CMV?

Answer 338

Mostly subclinical If symptomatic, clinically similar to infectious mononucleosis Large, shallow ulcers (Cytomegalovirus-associated ulceration) in immunocompromised individuals. Histopathology: Non-specific ulceration but CMV+ inclusion bodies present at ulcer floor.

Question 339

Describe the apperance of hand-foot and mouth disease?

Answer 339

Coxsackie Virus (A): - Incubation period is 4-7 days. Highly infectious. - Small ulcers (rarely intact vesicles) causing little pain mainly on buccal, labial, lingual and palatal mucosae - Vesicles and ulcers on hands and feet (occasionally oral ulcers or skin rash in isolation) - No gingivitis, no lymphadenopathy, no systemic upset - Self-limiting (7 days)

Question 340

Describe the apperance of herpangina?

Answer 340

Coxsackie A and B strains: - Prodromes: muscular pain, nausea, malaise. - Small ulcers mainly on palate, uvula, tonsils - Associated with fever, dysphagia and oropharyngitis - Self-limiting (8-10 days)

Question 341

Describe the apperance of measles?

Answer 341

Koplik’s spots - Prodrome of measles (2-4 days before measles cutaneous rash). Appear mostly on buccal mucosa (opposite molars). White spots against an erythematous background.

Question 342

Describe the apperance of warts?

Answer 342

HPV 2,4: - White or pinkish, raised but mostly sessile - Similar to squamous cell papilloma, but more rounded and sessile - Often multiple - Mainly children affected, secondary to self inoculation

Question 343

Describe the apperance of squamous papilloma?

Answer 343

More common in individuals >20 of age Exophitic, peduncolated Distinctive branched structure, finger-like processes, white or pinkish Up to 20 mm in diameter

Question 344

Describe the apperance of condyloma acuminatum?

Answer 344

HPV 6, 11, 16: Venereal wart HIV infection manifestation Transmitted via oro-genital contact Multiple white/pink nodules. Fuse forming sessile or pedunculated papillary lesion.

Question 345

Describe the management of oral mucosal HPV-related lesions?

Answer 345

Diagnosis - Clinical - Biopsy (excisional if possible) Treatment - Reassurance and monitoring - Cryotherapy - Surgical excision

Question 346

Describe the histopathology of oral mucosal HPV-related lesions?

Answer 346

HPVs induce hyperplastic changes rather than “ballooning degeneration” Fibro-vascular core covered by stratified squamous epithelium with - hyperplastic basal cell layer - acanthosis - hyperortho/parakeratosis Koilocytes

Question 347

Name the 2 categories for diagnosis of infections? And their options?

Answer 347

Clinical features - history - exam Laboratory tests - microscopy - culture - mass spec - nucleic acid amp - immuno tests

Question 348

Describe what sampling and testing involves?

Answer 348

Culture and sensitivity: - swab - mouth and related sites Whole saliva Aspirate Smear Biopsy Blood

Question 349

How to decide if infection need treatment?

Answer 349

Active symptoms: - directly related to the infectious agent Consequences of infection: - local - systemic

Question 350

How to decide appropriate treatment for infection?

Answer 350

Culture and sensitivity test - always preferred Best guess Experience Side effect profile Cost

Question 351

What is the defintion of staphylococcal infection

Answer 351

Uncommon as an acute problem- immunocompromised Very common as chronic mixed infection (related angular cheilitis) Topical treatment sufficient If systemic indicated- consider narrow spectrum

Question 352

What is the defintion of scarlet fever?

Answer 352

Exotoxin mediated mucocutaneous manifestations

Question 353

Name the 4 clinical features of scarlet fever?

Answer 353

Incubation period of 2-4 days Prodromes: nausea, malaise, vomiting, pharyngitis and lymphoadenopathy Macular erythema Oral mucosa erythematous and oedematous Dorsum tongue covered by white thick coating with enlarged fungiform papillae

Question 354

What are the clinical features of tuberculosis?

Answer 354

Chronic, painless and irregular ulcer Covered by yellowish exudate Surrounding tissue indurated with inflamm Localisation- tongue, palate gingivae, and lips Assoc subman and services lymphoadenopathy

Question 355

What isnthe histopathology of tuberculosis ?

Answer 355

Granukomas containing muktinuc giant cells - mycobacteria not always identifiable

Question 356

What are the oral manifestations of syphilis?

Answer 356

Primary - chancre Secondary - mucosal patches and blisters Latent Tertiary - gumma, CV and CNS complications

Question 357

What is the defintion of gonorrhea?

Answer 357

Second most common STI Oral lesions result of progenitor contact Non-specific oral presentation: - multiple ulcers - erythema - white pseudomembranes - painful pharyngitis - lymphoadeno

Question 358

What are the clinical features of actinomycosis?

Answer 358

Cerviofacial most common form Painful and slow growing hard swelling Absfesses and draining sinuses Discharge yellow purulent material

Question 359

What are the histopathologucal features of actinomycosis?

Answer 359

Colony of actinomyces in centre Dense collection of inflamm cells Surround by wall of fibrous tissue

Question 360

What is the definition of sicca syndrome?

Answer 360

Partial Sjögrens findings

Question 361

What is the definition of primary and secondary sjogrens syndrome?

Answer 361

Primary - no connective tissue disease Secondary - connective tissue disease - SLE, Rheumatoid Arthritis, Scleroderma

Question 362

Name 4 types of auto-immune disease related to sjogrens?

Answer 362

Question 363

Describe the background of Sjogrens Syndrome - spread? gender? systemic? genetic? environemnt?

Answer 363

0.2-1.2% (0.5-3 million in the USA) people have this - Half ALSO have another connective tissue disease Mostly women – 10:1 - Diagnostic delay due to late presentations - Lifespan not affected - Risk of neonatal lupus in baby if pregnancy Systemic involvement - Lungs, kidney, liver, pancreas, blood vessels, nervous system - Sometimes general fatigue and chronic pain Speculative Genetic - Genetic predisposition – runs in families, but no specific inheritance - Association with anti-Ro and anti-La seems genetic - low oestrogen risk gives a of getting CT disease – androgens protective? - Incomplete cell apoptosis leads to antigens being improperly exposed - Dysregulation of inflammatory process with dendritic AP cells recruiting Band T cell responses and pro-inflammatory cytokines Speculative Environment - EBV association – weak evidence – may be reactive rather than causative

Question 364

Describe the timeline of Sjorgens Syndrome

Answer 364

Question 365

Name the 4 consequences of Sjogrens Syndrome?

Answer 365

Gradual loss of salivary/lacrimal gland tissue through inflammatory destruction Enlargement of major salivary glands – usually symmetrical - Usually painless Increased risk - Any lymphoma (5% quoted) - Salivary marginal B-cell (MALT) Lymphoma Oral and Ocular effects of loss of saliva and tears

Question 366

Describe how to diagnose Sjogrens Syndrome?

Answer 366

Complex – no single test yet gives ‘the answer’ Balance of probabilities from multiple criteria Different scoring systems in use: - American-European Consensus Group (2002) - ACR-EULAR joint criteria (2016)

Question 367

Describe the diagnosis crietria for AECG of Sjogrens syndrome?

Answer 367

Dry eyes/mouth - Subjective or objective Autoantibody findings Imaging findings Radio nucleotide assessment Histopathology findings FOUR or more positive criteria for diagnosis

Question 368

Describe the diagnosis crietria for ACR-EULAR of Sjogrens syndrome?

Answer 368

Histopathology findings (Weight 3) focus score >1 Autoantibody findings (Weight 3) anti-Ro Dry eyes/mouth (Weight 1) - objective salivary flow - Schirmer test Ultrasound/sialogram now accepted as well (2020) Same exclusion criteria as AECG but also IgG4 disease

Question 369

Describe the oral and eye symptoms necessary to aid diagnosis?

Answer 369

Oral Daily feeling of a dry mouth for >3 months Recurrent swelling of salivary glands as an adult Frequently drink liquid to aid swallowing dry foods Ocular Persistent troublesome dry eyes for >3 months Recurrent sensation of sand/gravel in the eyes Tear substitutes used >3 times day

Question 370

Name the 2 eye tests for Sjogrens Syndrome?

Answer 370

Abnormal Schirmer test <5mm wetting in 5 minutes Fluorescein Tear film assessment

Question 371

Name the oral test for Sjoregns Syndrome?

Answer 371

Abnormal UNSTIMULATED whole salivary flow (UWS) <1.5ml in 15 mins

Question 372

Explain to autoimmunity involved with Sjogrens Syndrome?

Answer 372

What do positive autoantibodies here mean? - NOT CAUSATIVE in the disease process - ASSOCIATED with the clinical pattern - Antibodies possible without disease – need clinical and lab findings Anti-Ro and Anti-La antibodies - Collection of proteins found in the cell - Different ones found in different patients Ro52 (70%), Ro60 (40%) and La48 (50%) Other Autoantibodies? - Other Extractable Nuclear Antigens (ENA) not associated - ANA and RF not associated with Sjögrens

Question 373

Explain the typical findings in a positive labial gland biospy for Sjogrens Syndrome - AECG?

Answer 373

Collection of >50 lymphocytes around a duct = Lymphocytic Focus  Generalised lymphocytic infiltrate is ‘non-specific sialadenitis’ >1 Focus Score (FS) consistent with Sjogren’s Syndrome Thought to be the MOST diagnostic feature on ACR-EULAR criteria

Question 374

Describe the procedure in which to start to process of Sjogrens Syndrome, if suspicious?

Answer 374

First, look in the patient’s mouth - Sjogren’s patients complaining of dryness will have a dry mouth - Early Sjogren’s patients will NOT have a dry mouth, nor complain of one Do the least harmful tests first - UWS in 15 mins - <1.5ml - Anti-Ro antibody - Salivary USS - Baseline MRI of major salivary glands – for comparison for future lymphoma screen If still equivocal do labial gland biopsy - Risk of area of skin numbness following procedure - Informed consent needed LGB and Anti-Ro may be the ONLY positive results in early Sjogren’s

Question 375

Describe the management for a patient suffering with Sjogrens Syndrome?

Answer 375

If patient presenting with a dry mouth and salivary deficit - Gland function is already very low - Oral Health needs paramount – diet, OHI, 5000ppm toothpaste - Symptomatic treatment of oral dryness - Salivary stimulants - pilocarpine? If patient presenting early – NO dry mouth yet – active gland disease - Liaise with rheumatologist – multisystem disease - Consider Immune modulating treatment – hydroxychloroquine, methotrexate

Question 376

Name the 3 categories of complications for patient living with Sjogrens Syndrome?

Answer 376

Effects of Oral Dryness - caries risk, denture retention, infections, functional issues –speech/swallow Salivary enlargement - Sialosis - can occur at any time – usually permanent - Reduction surgery possible but not advised – other health issues Lymphoma risk - Salivary lymphoma may present with unilateral gland swelling at any stage - Increased general lymphoma risk too - Screening? Who should review – generally the GDP with patient awareness

Question 377

Examination of the salivary gland locations?

Answer 377

Extra oral examination - Major salivary glands Intraoral examination - Minor salivary glands - Duct orifices - Fluid expression

Question 378

What is the function of saliva?

Answer 378

Acid buffering Mucosal lubrication - Speech - Swallowing Taste facilitation Antibacterial

Question 379

Name the 5 main causes of a dry mouth?

Answer 379

Salivary Gland disease Drugs Medical Conditions & Dehydration Radiotherapy & cancer treatments Anxiety & Somatisation Disorders

Question 380

How does salivary gland changes with age between 17-90yrs old?

Answer 380

Acinar tissue loss 37% Submandibular 32% Parotid 45% Minor glands

Question 381

Describe in/direct effect on salivation?

Answer 381

Indirect effect - External to the gland Direct Effect - Problems within the gland itself

Question 382

Name 6 drugs that cause indirect salivary problems?

Answer 382

Anti-muscarinic cholinergic drugs - Tricyclic antidepressant - Antipsychotics - Antihistamine - Atropine - Diuretics - Cytotoxics

Question 383

Name the 3 largest influencing drugs on dry mouth?

Answer 383

Antimuscarinic - Amitriptyline 26% reduction Diuretics - Bendrofluazide 10% reduction Lithium - 70% have a significant reduction - Increased caries correlates with drug use

Question 384

Name other medical conditons that can have an indirect effect on salivation? - acute and chronic?

Answer 384

Chronic Medical Problems inducing dehydration - Diabetes – Mellitus & Insipidus - Renal disease? - Stroke - Addison’s Disease - Persisting Vomiting Acute medical Problems - Acute oral mucosal diseases - Burns - Vesiculobullous diseases - Haemorrhage

Question 385

Name 5 direct salivary gland problems?

Answer 385

Aplasia - Ectodermal dysplasia Sarcoidosis HIV disease Gland infiltration - Amyloidosis - Haemochromatosis Cystic Fibrosis

Question 386

What is the defintion of ectodermal dysplasia?

Answer 386

Hair, Nails, Teeth, Salivary & Sweat glands - Hearing and vision may be affected May be limited in effect - Salivary aplasia alone Hypohidrotic – x-linked

Question 387

Describe the symptoms of Sarcoidosis?

Answer 387

Question 388

Haemachromatosis?

Answer 388

HFE gene mutation - 1:10 pop carry

Question 389

Describe radiotherapy effect on salivation?

Answer 389

Radiation effects Graft versus host effects Antineoplastic drugs Radioiodine

Question 390

Describe Challacombe Scale of Mucosal Dryness?

Answer 390

Question 391

What blood tests and other tests can be used to investiagte salivary disease?

Answer 391

Blood tests - FBC - U&Es, - Liver function tests - C-reactive Protein - Glucose - Anti Ro Antibody - Anti La Antibody - Antinuclear Antibody - Complement C3 and C4 Functional Assay– Salivary Flow Tissue Assay – Labial Gland Biopsy Imaging - Plain radiographs – reduced dose – stones - Sialography – contrast to show ducts - MR Sialography – IV contrast - Ultrasound

Question 392

Describe how anxiety and somatisation disorders can cause dry mouth?

Answer 392

‘cephalic’ control of salivation - Inhibition of salivation – anxiety directly causes ‘real’ oral dryness ‘cephalic’ control of perception - Altered perception of reality – normal information coming from the mouth is ‘misunderstood’ by small changes at synapses as it is processed - More often seen with anxiety disorders Anxiety can also inhibit swallowing and can lead to a complaint of ‘too much saliva’!

Question 393

Name 6 forms of somatoform disease that cause dry mouth?

Answer 393

Oral Dysaesthesia TMD pain Headache neck/back pain Dyspepsia Irritable Bowel Syndrome (IBS)

Question 394

Flow rate normal vs abnrmal?

Answer 394

Question 395

Name 5 treatbale causes of dry mouth?

Answer 395

Dehydration Medicines with anti-muscarinic side effects Medicines causing dehydration Poor Diabetes control – type 1 or type 2 Somatoform Disorder – diagnosis of exclusion Management of these should return the patient’s oral comfort

Question 396

Name th 3 treatment options for symptomatic dry mouth?

Answer 396

Sjögren’s Syndrome Dry mouth from cancer treatment Dry mouth from salivary gland disease Treatment options for these cases - INTENSIVE DENTAL PREVENTION - Salivary substitutes - Salivary stimulants

Question 397

Name the 5 categroeis of dry mouth investigations?

Answer 397

Salivary Flow tests – less than 1.5ml unstimulated flow in 15mins Blood tests - Dehydration – U&Es, Glucose - Autoimmune disease – ANA, Anti-Ro, Anti-La (ENA Screen), CRP - Complement levels – c3 and c4 Imaging - Salivary ultrasound – looking for ‘leopard spots’ or sialectasis - Sialography – useful where obstruction/ductal disease is suspected Dry eyes screen - Refer to optician for assessment of tear film (preferred) - Schirmer test – tear flow less than 5mm wetting of test paper in 15 mins Tissue examination - Labial gland biopsy – lower lip – looking for lymphocytic infiltrate and focal acinar disease

Question 398

Describe the dental management of dry mouth?

Answer 398

Prevent oral disease - Caries risk assessment - Candida/staphylococci awareness and reduction – low sugar diet and OHI Angular chelitis Sore tongue Maximal preventative strategy - Diet! - Fluoride - Treatment Planning for a caries risk mouth

Question 399

Name 6 forms of saliva substitiues and their form?

Answer 399

Sprays - Glandosane - Saliva Orthana Lozenges - Saliva Orthana - SST Salivary stimulants - Pilocarpine (Salagen) Oral Care Systems - Oral Balance Frequent sips of water

Question 400

Name the causes of hypersalivation? - True and percieved?

Answer 400

TRUE (rare) – Actual increase in salivary flow - Drug causes - Dementia - CJD - Stroke PERCEIVED (Common) – NO increase in saliva flow Swallowing Failure - Anxiety - Stroke - Motor Neurone Disease - Multiple Sclerosis Postural Drooling - Being a baby - Cerebral Palsy

Question 401

Describe the dental management of excess salivation?

Answer 401

Treat the Cause - Anxiety disorders Drugs to reduce salivation - Anti-muscarinic agents - Botox to prevent gland stimulation Biofeedback training - Swallowing control Surgery to salivary system - Gland removal - Duct repositioning

Question 402

Name the 3 forms of causes for changes in gland size?

Answer 402

Viral Inflammation - Mumps - HIV Secretion retention - Mucocele - Duct obstruction Gland Hyperplasia - Sialosis - Sjögrens Syndrome

Question 403

Name the 7 symptoms of mumps?

Answer 403

Headache Joint pain Nausea Dry mouth Mild abdominal pain Feeling tired loss of appetite Pyrexia of 38C, or above Paramyxovirus Droplet spread Incubation 2-3 weeks 1/3 have no symptoms Symptomatic treatment only

Question 404

What is the defintiion of HIV sailvary disease?

Answer 404

HIV can be a cause of salivary swelling Cause of Unexplained salivary swelling May have NO HIV symptoms when presenting Generally does not improve with treatment Lympho-proliferative enlargement of the glands

Question 405

What is the definition of a mucocele?

Answer 405

Secretion retention - In the duct - Extravasated into the tissues RECURRENT swelling – bursts in days - ‘salty taste’ Common Sites Junction Hard/Soft Palate Lower lip

Question 406

What is the definition of subacute obstruction?

Answer 406

Swelling associated with meals - increases as salivary flow starts - reduces when salivary flow stops Usually SUBMANDIBULAR occ. Parotid Can be slowly progressive – over weeks Eventually fixed & painful Cause – duct obstruction - Usually duct blockage in submandibular - Usually duct stricture in parotid

Question 407

Name the 3 main causes of subacute obstruction?

Answer 407

Sialolith (stones) ‘mucous’ plugging Ductal damage from chronic infection (scarring) (Salivary stones, Duct stricture, Duct dilation, chronic non-specific sialadenitis)

Question 408

Name the 5 investigations for subacute obstruction?

Answer 408

Low dose plain radiography lower true occlusal SIALOGRAPHY – when infection free Isotope scan if gland function uncertain Ultrasound assessment of duct system

Question 409

What is the definition of duct dilation?

Answer 409

Defect prevents normal emptying Micro-organisms grow and lead to persisting and recurrent sialadenits Gland function gradually lost and persisting infection leads to gland removal May follow Recurrent Parotitis of Childhood at age 20-30

Question 410

Describe the management of subacute obstruction?

Answer 410

Surgical sialolith removal if practical Sialography for ‘no stone’ cases – washing effect Consider gland removal if fixed swelling

Question 411

Describe the outcome for subacute obstruction?

Answer 411

Reformation of stone/obstruction Deformity of duct – stasis & infection Gland damage – low salivary flow, ascending infection

Question 412

What is the definition of silalosis?

Answer 412

Increase in Gland Tissue (Hyperplasia) - Sialosis - Sjögrens Syndrome Major gland enlargement No identified cause - Alcohol abuse - Cirrhosis - Diabetes Mellitus - Drugs

Question 413

What investigations can be carried out to diagnose Sialosis?

Answer 413

Blood tests Glucose FBC, U&Es, LFTs, bilirubin BBV screen – HIV, Hep B, Hep C AutoAntibody Screen - ANA, anti-Ro, anti-La Other investigtions MRI of major salivary glands USS for Sjögren’s changes Labial gland biopsy Tear film Sialography – occasionally Photography

Question 414

What investigations can be carried out to diagnose Sialosis?

Answer 414

Blood tests Glucose FBC, U&Es, LFTs, bilirubin BBV screen – HIV, Hep B, Hep C AutoAntibody Screen - ANA, anti-Ro, anti-La Other investigtions MRI of major salivary glands USS for Sjögren’s changes Labial gland biopsy Tear film Sialography – occasionally Photography

Question 415

Name 2 types of dental manifestations of systemic disease?

Answer 415

Disruption to the tooth structure formation Disruption to the tooth structure content

Question 416

Name 3 forms of systemic diseases that exhibit dental mnifestations in children?

Answer 416

Congenital conditions/infections - Syphilis,TORCH - Ectodermal Dysplasia - perinatal illness Illness/metabolic disorder - Severe childhood illness - Porphria - Cancer treatments Pigmentation from substances in the blood - Bilirubin, tetracycline

Question 417

Name 6 oral mucosal effects from systemic disease?

Answer 417

Giant Cell Granuloma Orofacial Granulomatosis Recurrent Aphthous Stomatitis Dermatoses Immune Deficiency/Disease - Raised ACTH Addison's Drug reactions

Question 418

What is the definition of a ginat cell lesion, in relation to oral medicine?

Answer 418

Peripheral’ and ‘Central’ lesions Check Parathyroid function – could be as a result of excess parathyroid stimulation of osteoclasts - renal failure - hypocalcaemia - parathyroid tumour

Question 419

What is the definition of hyperparathyroidism's effect on the bones?

Answer 419

Causes thinking and finger-like projections of the bone

Question 420

Name 4 systemic illness that cause immunodeficiency throughout life, which show oral manifestations?

Answer 420

Orofacial Granuolomatosis Sjogrens Autoimmune – Addisons Infections – fungal/viral

Question 421

Name 2 forms of skin immune disease that show oral manifestations?

Answer 421

Lichen planus, VB disease

Question 422

What is the definition of immune disease orofacial granulomatosis?

Answer 422

Associated with Dietary Allergens? - Benzoate, Sorbate, Cinnamon, Chocolate (E210-219)  Skin testing not reliable Use dietary exclusion to determine trigger (if any) enzoates found in tomato and tomato products - All things with tomato sauces must be avoided Clinical signs: - lip swelling, erythema and crustiness - gingivae erythematous and heavly inflammed

Question 423

What is included for Crohn's screening?

Answer 423

Parental awareness of importance of altered bowel habit or abdominal pain Growth monitoring at each hospital visit Faecal Calprotectin assay - Unreliable in younger children - Screening test for endoscopy - Good predictor of Crohn’s disease activity

Question 424

Describe the management of orofacial granulamtosis?

Answer 424

Management - 3 month empirical dietary exclusion - Benzoate/cinnamon – unless clear other dietary triggers Topical treatment to angular chelitis/fissure - Miconazole/hydrocortisone cream Topical treatment to lip swelling or facial erythema - Tacrolimus ointment 0.03% - Intralesional steroids to lip - Systemic immune modulation?

Question 425

Name 4 forms of automimmune CT diseases, that show oral manifestations?

Answer 425

Systemic lupus erythematosis (SLE) - erytheamic gingiva and palate Systemic sclerosis (Scleroderma) Sjogrens syndrome Mixed connective tissue disease (MCTD)

Question 426

Name 3 forms of vasculitic CT diseases, that show oral manifestations?

Answer 426

Large vessel Disease - Giant cell (temporal) arteritis Medium Vessel Disease - Polyarteritis nodosa - Kawasaki disease Small vessel Disease - Wegener’s Granulomatosis

Question 427

Name 4 forms of acquired immune deficiency?

Answer 427

Diabetes Drug therapy Cancer therapy HIV

Question 428

What is the definition of haematinic deficieinces - causes?

Answer 428

Poor intake – dietary analysis/reinforcement Malabsorbtion - GI diseases – Coeliac Disease, Crohn’s Disease Blood loss - Crohn’s Disease, Ulcerative Colitis, Peptic ulcer disease, Bowel Cancer, Liver Disease Increased Demand - Childhood growth spurts

Question 429

What is the definition of the Parotid gland?

Answer 429

Largest of major glands Positioned parotid bed anterior to ear overlying mandibular ramus Lower pole extends into postauricular region Intimately associated with facial nerve (VII) Serous gland. Produces thin watery secretion via parotid duct (Stensen’s duct)

Question 430

WHat is the definition of the submandibular gland?

Answer 430

Second largest Situated in submandibular triangle – associated with lower border of mandible, digastric and mylohyoid muscles and marginal mandibular branch of VII Mixed seromucous (80% serous) Expresses secretions via submandibular duct into floor of mouth (Wharton’s duct)

Question 431

What is the definition of the sublingual gland?

Answer 431

Smallest major gland Located in submucosa of floor of mouth Nearby structures: submandibular duct, lingual nerve and lingual artery Predominantly mucous Expels secretions via Bartholin’s duct in floor of mouth

Question 432

Name the 2 categories and 5 types of cells?

Answer 432

Acini: - serous cells - mucous cells - mixed Ducts - Luminal cells: cuboidal/columnar/squamous epithelium - Abluminal cells: myoepithelium and basal cells

Question 433

What is the definition of neoplasia?

Answer 433

A neoplasm is an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissues and persists in the same excessive manner after cessation of the stimuli which evoked the change’ Benign Malignant

Question 434

Describe the epidemiology of salivary gland neoplasms?

Answer 434

Rare - 3/100,000 Commoner in women 75% benign 90% Parotid Commnest parotid and minor- plemorphic adenoma 55% of palatal tumours - minor 50% of minor neoplasms are maligant All sublingual glands are malignant

Question 435

Name the 5 aetiologies of salivary gland neoplasms?

Answer 435

Radiation: nuclear bomb survivors, therapeutic radiation, dental x-rays, ?mobile phones Tobacco smoking: Warthin’s tumour Viruses: EBV & lymphoepithelial carcinoma Familial and genetic Various industrial occupations

Question 436

Describe the differences between Benign and Malignant salivary gland tumours?

Answer 436

Benign - Encapsulated - Slow growing - ‘Rubbery’ consistency - Mobile - Overlying mucosa/skin appears normal - Not invasive Incapable of metastasis Local excision curative Malignant - Unencapsulated - Rapid growth - Dense, firm mass - Fixed - Overlying skin/mucosa ulcerated Invades surrounding tissue including nerves Capable of metastasis Requires more aggressive therapy (surgery +/- radiotherapy)

Question 437

Name 3 investigations for susected salivary gland tumours?

Answer 437

Clinical history and examination Imaging: Radiography/Sialography, Ultrasound, CT, MRI Pathology: Fine Needle Aspiration (FNA), core biopsy, open incisional biopsy, excisional biopsy IMAGING AND PATHOLOGY ARE NOT A SUBSTITUTE FOR ADEQUATE HISTORY AND EXAMINATION

Question 438

Name 5 types of benign epithelial tumoirs of the salivary gland?

Answer 438

Pleomorphic adenoma Warthin’s tumour Basal cell adenoma Canalicular adenoma Oncocytoma

Question 439

Name 5 types of malignant salivary gland tumours?

Answer 439

Mucoepidermoid carcinoma Adenoid cystic carcinoma Polymorphous adenocarcinoma Carcinoma ex pleomorphic adenoma Acinic cell carcinoma

Question 440

What is the definition of a pleomorphic adenoma?

Answer 440

Pleomorphic adenoma is a tumour of variable capsulation characterized microscopically by architectural rather than cellular pleomorphism. Epithelial and modified myoepithelial elements intermingle most commonly with tissue of mucoid,myxoid or chondroid appearance.’

Question 441

Explain the management for a pleomorphic adenoma?

Answer 441

Wide surgical excision recommended due to high rate of recurrence in inadequately excised tumours Excision complicated by lobulated structure, presence of satellite nodules and loose myxoid consistency Enucleation usually results in incomplete excision and recurrences Parotid: optimum technique - superficial parotidectomy with preservation of facial nerve (extracapsular dissection technique developing) Submandibular: resection of gland Minor gland: wide local mucosal excision +/- bone

Question 442

What is the definition of Warthin's Tumour?

Answer 442

A tumour composed of glandular and often cystic structures, sometimes with a papillary cystic arrangement, lined by characteristic bilayered epithelium, comprising inner columnar eosinophilic or oncocytic cells surrounded by smaller basal cells. The stroma contains a variable amount of lymphoid tissue with germinal centres.

Question 443

What is the aetiology of Warthin's tumour?

Answer 443

Exclusively in the Parotid Male predominance Link with smoking

Question 444

Explain the management of Warthin's tumour?

Answer 444

Complete excision is curative (superficial parotidectomy)

Question 445

What is the definition of a Oncocytoma?

Answer 445

Benign tumour of salivary gland origin composed exclusively of large epithelial cells with characteristic bright eosinophilic granular cytoplasm (oncocytic cells).

Question 446

What is the aetiology of a Oncocytoma?

Answer 446

Most in parotid Complete excision curative

Question 447

What is the definition of a canalicular adenoma?

Answer 447

The tumour is composed of columnar epithelial cells arranged in thin, anastomosing cords often with a beaded pattern. The stroma is characteristically paucicellular and highly vascular.

Question 448

What is the aetiology of a canalicular adenoma?

Answer 448

lip commonest conservatice excision curative

Question 449

What is the definition of a basal cell adenoma?

Answer 449

Basal cell adenoma (BCA) is a rare benign neoplasm characterized by the basaloid appearance of the tumour cells and absence of the myxochondroid stromal component present in pleomorphic adenoma.

Question 450

What is the aetiology of a basal cell adenoma?

Answer 450

Mostly Parotid gland Complete excision curative

Question 451

What is the definition of mucoepidermoid carcinoma?

Answer 451

Mucoepidermoid carcinoma is a malignant glandular epithelial neoplasm characterized by mucous, intermediate and epidermoid cells, with columnar, clear cell and oncocytoid features.

Question 452

What is the aetiology of mucoepidermoid carcinoma?

Answer 452

most common saliary gland malignancy Parotid most common, then palate, submand and other minors

Question 453

Exlain the management of mucoepidermoid carcinoma?

Answer 453

Low grade: cystic, lots of mucous cells High grade: solid, few mucous cells, atypia, mitoses++, perineural invasion, infiltrative growth and necrosis. 10 year overall survival rates: low grade 90% intermediate grade 70% high grade 25%

Question 454

What is the definition of an adenoid cystic carcinoma?

Answer 454

Adenoid cystic carcinoma is a basaloid tumour consisting of epithelial and myoepithelial cells in variable morphologic configurations, including tubular, cribriform and solid patterns. It has a relentless clinical course and usually a fatal outcome.

Question 455

What is the aetiology of an adenoid cystic carcinoma?

Answer 455

High grade malignnacy More in female Major glands Distant metastases

Question 456

Explain the management of adenoid cystic carcinoma?

Answer 456

Surgery treatment of choice Wide resection. Extensive surgery often required Clear margins difficult to achieve (mostly impossible) Radiotherapy with wide fields Chemotherapy generally not effective

Question 457

What is the definition of a polymorphous adenocarcinoma?

Answer 457

A malignant epithelial tumour characterized by cytologic uniformity, morphologic diversity, an infiltrative growth pattern, and low metastatic potential.

Question 458

What is the aetiology of a polymorphous adenocarcinoma?

Answer 458

2nd most common intraoral malignant salivary gland Palate most commen Malig in minor

Question 459

Explain the management of polymorphous adenocarcinoma?

Answer 459

Surgical excision with clear margins usually curative Role of radiotherapy not certain

Question 460

What is the definition of Carcinoma ex pleomorphic adenoma?

Answer 460

Carcinoma ex pleomorphic adenoma is defined as a pleomorphic adenoma from which an epithelial malignancy is derived.

Question 461

What is the aetiology of carcinoma ex pleomorphic adenoma?

Answer 461

Usually arises from an untreated benign pleomorphic adenoma present for several years; most arise in the parotid gland Presents as rapid swelling following an extremely long period of slow growth. Slightly more common in women

Question 462

Explain the management of carcinoma ex pleomorphic adenoma?

Answer 462

Extensive surgery with neck dissection is treatment of choice Post operative radiotherapy

Question 463

What is the definition of an acinic cell carcinoma?

Answer 463

Acinic cell carcinoma is a malignant epithelial neoplasm of salivary glands in which at least some of the neoplastic cells demonstrate serous acinar cell differentiation, which is characterized by cytoplasmic zymogen secretory granules. Salivary ductal cells are also a component of this neoplasm

Question 464

What is the aetiology of an acinic cell carcinoma?

Answer 464

Second most common salivary gland malignancy in children

Question 465

Explain the management of an acinic cell carcinoma?

Answer 465

Complete excision required Generally not aggressive but a proportion can metastasise to cervical lymph nodes and lung Recurrence rate as high as 35%