Oral Medicie YR4

Question 1

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

Answer 1

Anti-microbial - virals, fungals and bioticsTopical Steroids - inhaled and mouthwashDry mouth medication - benzdamine washOthers - carbamazepine

Question 2

Name the 5 classification of medicines?

Answer 2

General SalesPharmacy MedicinesPrescription only MedicinesControlled DrugsMedical 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 conditionsClinical trial data providedPost 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 treatmentWill be ‘licenced medicines’ – but for another conditionUse is at the discretion of the treating physicianPatient 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- aciclovirfungals - 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 mouthwashBeclomethasone Metered Dose InhalerBoth 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, forhuman 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 pastillesSaliva orthanaBiotene Oral BalanceArtificial Saliva DPFGlandosane

Question 9

Name 6 other medicines used in OM?

Answer 9

Tricyclic AntidepressantsGabapentin/PregabalinAzathioprineMycophenolateHydroxycholoroquineColchicine

Question 10

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

Answer 10

Clinical indicationLicenced or unlicensed for this useDose and route of administrationImportant warnings for the patientDrug interactions and cautionsTreatment duration and monitoring

Question 11

What to include on a presciption?

Answer 11

Patient’s name, Address, Age (under 18)Patient identifier – DoB, CHI NumberNumber of Days treatmentDrug to be prescribedDrug formulation and DosageInstructions on quantity to be dispensedInstructions to be given to the patientSigned – identifier of Prescriber

Question 12

What are the rules and regulation on prescrption validity?

Answer 12

Six months from date issuedMore than one item on a scriptMore than one repeated dispensing occasion

Question 13

Tips for writing a prescription?

Answer 13

Key Patient information MUST be legibleAVOID abbreviations – write full instructions in INKOnly 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 instructionsLanguage issues may prevent proper understandingMultilingual options, large print optionsContact number for Patient Issues with the medicineLegal 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 courseUnexpected reactions: STOP! and contact prescriberKnown 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 discomfortSteroid 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 neededBenzdamine mouthwash or spray - green things help! Useful topical anaesthetic/pain reliefOTC remedies such as Igloo, Listerine, BonjelaAnything 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 pelletBetamethasone mouthwashBeclomethasone 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 leafletUse Betnesol tabs 0.5mg - 1mg 2 tablets - 10mls water 2 teaspoons water - 2 mins rinsing - Twice dailyRefrain from eating/drinking for 30 min after useDO NOT SWALLOWDo not rinse after use

Question 21

What must be included on betamethasone mouthwash PIL?

Answer 21

Licenced for other medical conditionsExplain dose range and frequency of useExplain hazards of exceeding the standard doseAdd any known side effects – small oral candida riskAdd special instructions

Question 22

How to use beclomethasone medical device?

Answer 22

Unlicenced product - Supply patient with a tailored information leafletDental Prescribing 50mcg/puff device - Position device correctly – exit vent directly over ulcer area - 2 puffs - 2-4 times daily - Don’t rinse after useMust 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 conditionLicensed for other medical conditions – asthma and COPDInstruct to discard the manufacturer’s PiLExplain dose range and frequency of useExplain technique used for oral lesions – different from use for lung conditionsAdd any known side effects – small oral candida riskAdd special instructions

Question 24

Systemic drugs used in OM, only for specialists?

Answer 24

Disease modulator- colchineSteroid- prednisilone (ulcers) 30mg for 5 daysImmune suppressants:- hydroxychloroquine - lichen planus- azathioprine- mycophenolateImmunotherapy:- 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 doseCushingoid featuresOsteoporosis risk – bone prophylaxis – Calcium supps and bisphosphonates- DEXA bone density scan may be needed from time to timePeptic ulcer risk – Proton Pump Inhibitor prophylaxisMood/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 patientPre-existing medical condition not yet detectedScreening 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 discussedPatient 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 teamTreatment 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

HereditarySmoking/frictionalLichen planus- lupus erythematosus- gvhdCandidal leukoplakiaCarcinoma

Question 29

What does a typical white spot lesion look like?

Answer 29

Thickening of the mucosa or keratin- Less visibility of bloodLess 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 causeNo histopathological connotation- it is a clinical descriptionDiagnosis of exclusion1 - 5% become malignant

Question 31

Name 4 types of leukoplakia?

Answer 31

Fordyce’s spotsSmoker’s KeratosisFrictional KeratosisHereditary 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 benignIf RED and WHITE concentrate on the RED partIf the lesion is becoming more raised and thickenedIf 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- dysplasiaReduced thickness of the epithelium

Question 36

What is the definition of Erythroplakia?

Answer 36

Atrophic or non-keratotic end of the spectrumA red patch which cannot be attributed to any other causeMore 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 haemangiomaLight 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 cavernousTongue- cystic hygroma

Question 40

Name 3 types of connective tissue diseases?

Answer 40

Large vessel Disease- giant cell (temporal) arteritisMedium Vessel Disease- polyarteritis nodosa- kawasaki diseaseSmall vessel Disease- granulomatosis with Polyangiitis

Question 41

What are the 3 types of mucosal pigmentations?

Answer 41

Exogenous stainIntrinsic PigmentationIntrinsic foreign body

Question 42

Name the 4 examples of exogenous stains for mucosal pigmentation?

Answer 42

TeacoffeechlorhexidineBacterial overgrowth

Question 43

Name the 4 examples of intrinsic pigmentation for mucosal pigmentation?

Answer 43

Reactive Melanosis/melanotic maculeMelanocytic naevusMelanomaEffect 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 sarcomaGeneralised:- Racial/familial- Smoking- Drugs- Addison’s disease (Raised ACTH conditions)

Question 46

Name 2 types of melanin pigmentation?

Answer 46

Racial pigmentationMelanotic macule

Question 47

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

Answer 47

Is it easily explained?- Racial- Smoking- MedicinesIs 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 chemicalinfection - viral, bacterial or fungalimmunologicalcan be remalignant or melignant

Question 49

How to decide whether something is a melanoma? questions?

Answer 49

Variable pigmentationIrregular outlineRaised surfaceSymptomatic- Itch- bleed

Question 50

What is the purpose of a biopsy?

Answer 50

identifies or excludes malignancyidentifies dysplasiaidentifies 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 mucosaBenign conditions the practitioner has diagnosed that:- Are asymptomatic- Do not have potentially malignant risk- For which there is no treatmentIf 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 guidelinesAny SYMPTOMATIC lesion that hasnot responded to standard treatment- Hospital referral criteria- SDCEP guidanceAny 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 epitheliumlamina propriagross types - lining, masticatory, gustatorymicroscopic - non-keratinised - keratinised - orthokeratosis or parakeratosis

Question 56

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

Answer 56

Keratinised - palateNon-keratinised - cheek

Question 57

What are the compartments of the oral mucosa?

Answer 57

STratumCorneumGranulosumSpinosumBasalLamina ProperiaCornified, 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 layersErosion - partial thickness lossUlceration - fibrin on surfaceOedema - intracellular - intercellular (spongiosis)Blister - vesicle or bulla

Question 60

How do age and nutritiona ffect the oral mucosa?

Answer 60

Age - progressive mucosal atrophyNutritional 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 timingBlack hairy tongue - hyperplasia of papillae - bacterial pigmentFissured tongue (scrotal tongue)

Question 62

What are the symptoms of geographic tongue?

Answer 62

Sensitive with acidic/spicy foodsIntermittentMuch 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 sensationThe cause is unknown, but it may be partly a genetic trait. Aging and environmental factors may also contribute to the appearanceIs 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) surfaceWhat 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 hygienecertain 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 mucosaIncreasing in size’rubbery’ consistencyTrauma from teethUnsightly

Question 71

What is the definition of a pyogenic granuloma?

Answer 71

granulation tissue – mixed inflammatory infiltrate on fibro-vascular backgroundany mucosal site response to traumaNot a granuloma, not pyogenicother names- gingiva – aka vascular epulismost frequent site- gingiva, during pregnancypregnancy epulis

Question 72

Name the 5 causes of mucosal ulcerative reactions?

Answer 72

TraumaImmunologicalInfectionsGICarcinoma

Question 73

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

Answer 73

Immunological:- aphthous ulcers- lichen planus- Lupus- vesiculo-bullous- Erythema multiformeGI:- Crohn’s- UC

Question 74

What are the differential diagnoses for single episode oral ulceration?

Answer 74

Trauma1st episode of Recurrent Oral UlcerationPrimary Viral infectionsOral Squamous Cell Carcinoma

Question 75

What are the differential diagnoses for Recurrent Oral Ulceration?

Answer 75

Aphthous ulceration- minor, major, herpetiformLichen PlanusVesiculobullous lesions- pemphigoid, pemphigus- angina bullosa haemorrhagica- erythema multiformeRecurrent viral lesion – HSV, VZVTraumaSystemic 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 ulcersCrohn’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

CommonUsually single episode - can be recurrent if cause not removedNormal or abnormal epitheliumHealing - 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/branchOften Hard palate- lesion recurs in the same place- patient often aware of prodrome and vesiculation which bursts- PAIN suggests Herpes ZOSTER rather than simplexTreat 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 syndromeDiagnosis 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 mucosaAre there systemic symptoms? - consider infection – herpes group, coxsackie groupAlways 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 steroidsThis is the commonest type of recurrent oral ulceration- One is a nuisance, many more at once can be disablingThe 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 usefulUsually 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 weeksCan coalesce into larger areas of ulcerationNOTHING 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 diseasesLichen Planus

Question 89

How to diagnose Behcet’s disease?

Answer 89

Many who don’t meet the criteriaDiagnosis - 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 RASSystemic immunomodulation where multisystem involvement: - Colchicine used ‘off label’ often a first treatment - Azathioprine/Mycophenolate - Biologics – infliximab and othersManaged 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 infectionsGenetic predispositionSystemic diseasesStressMechanical injuriesHormonal level fluctuationsMicroelement 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 absAllergy 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 B12Refer for investigation if Coeliac positive - endoscopy and jejunal biopsyAvoid 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 B12Refer for investigation if Coeliac positive - endoscopy and jejunal biopsyAvoid 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’ GuidanceNon-Steroid Topical Therapy - for inconvenient lesionsSteroid 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 peculiaritiesNOT related to growth (present since birth) then largely a genetic component:- consider allergy testing as well as bloodsTreatment:- 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 investigationsAfter topical trreatmentIf no good result has been achievedIf patient under 12 YO

Question 100

What is the defintion of oral thrush?

Answer 100

Caused by candidaCan 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

ImmunosuppressionEndocrine disordersNutritional deficiencyAntibioticsSteroidsFemaleExtremes of ageHospitalisationSmokingHigh 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 damageDental prosthesisChanges to commensal flora

Question 104

Name the topical and systemic treatment of oral thrush?

Answer 104

Topical:- nystatin - miconazoleSystemic:- fluconazole- targeted therapy

Question 105

Explain how to use nystatin suspension?

Answer 105

1ml QDSKeep in mouth for as long as possibleContinue for 48 hours after resolvedLow risk for inters

Question 106

Explain how tonuse miconazole oral gel?

Answer 106

2.5 ml QDS - gold in mouth after foodContinue for 7 days after resolvedUse 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 systemsCYP3A4:- statins - Ca ch blocker- tacrolimus- carbamazepine- midazolam CYP2C9- warfarin- sulphonylureas - phenytoin

Question 109

Name the contraindications of miconazole?

Answer 109

Liver dysfunctionCoadministration with drugs that are metabolised by CYP3A4Substrates known to prolong QT interval - astemizole, cisapride, dofetilide, mizolastine, pimozide, quinidine, sertindole and terfenadineErgot alkaloidsHMG-CoA reductase inhibitors - simvastatinTriazolam and oral midazolam

Question 110

Explain how to take fluconazole?

Answer 110

50-200mg capsules50-5ml oral suspensionIV avaliable 50mg once a day for 7-14 days100mg if immunocompromised

Question 111

Name the 6 contraindications of fluconazole?

Answer 111

Mod inhib of P3A4 and 2C9Strong inhib of 2C19AlfentanilAmitriptylineBenzodiazepinesCitalopramClopidogrelWarfarin

Question 112

How importance is drug resistance to antifungal?

Answer 112

A growing problemsMost common in azoles

Question 113

Explain a dentists role in antimicrobial stewardship?

Answer 113

Don’t start antibiotics without bacterial infectionUse local guidelinesDocument everything such as indication, duration, dose and routeReview 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 mouthOral discomfortTaste disturbanceDifficulty chewingDifficulty swallowingDifficuly speakingHalitosis

Question 115

Advice for toothbrushing?

Answer 115

At least twice a daySmall headed brushMedium texture filamentSoft brush if very soreToothpaste between 1350-1550 ppm FlWater if toothpaste is unworkable

Question 116

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

Answer 116

Twice daily brushingGloves with toothpaste Small circular motionsStart on outer surfaces then move to inner surfacesSpit out toothpaste after brushingAvoid rinsing

Question 117

How can a nurse care for a patients denture?

Answer 117

Cleanse denture after mealsCleaned and removed overnight Ensure denture fits wellAdhesive if necessary

Question 118

How can a nurse care for a patients soft tissue?

Answer 118

Glove and run finger over tissuesRenew gause on cleansingCan use cleaning stock if gause not goodRecord mouth condition

Question 119

How can a nurse care for a patients lips?

Answer 119

Moisten with waterApply saliva replacementOr apply aqueous cream BP

Question 120

What to implement for a dry or coated mouth patient?

Answer 120

At least 4 x a dayReview medicinesGently remove coating, debris and plaque Maintain hydrationStimulate saliva

Question 121

Which 5drug types cause dry mouth?

Answer 121

OpoidsAnticholinergics AntidepressantsDiureticsOxygen

Question 122

Explain how to manage dry mouth?

Answer 122

Treat underlying causeReview medicationGood oral hygieneDietary adviceRegular dental checksRegular sips of waterLubricate cracked lipsSaliva substitutesSaliva stimulants

Question 123

What does saliva consist of?

Answer 123

6.8-7.4 pHWaterMucin-principal active componentElectrolytesEnzymesProteins

Question 124

Name saliva stimulants?

Answer 124

Sugar free chewing gum or sweetsFrozen fruit juices or lolliesOrganic acids such as salivix pastilles

Question 125

Describe and name artificial replacement saliva?

Answer 125

Mucon or carboxymethylcellulose based Short duration of actionAvoid acidic products - glandosaneNeutral pH- AS saliva Orthana- Biothene Oralbalance gel- BioXtra gel- Saliveze

Question 126

Which saliva replacements can a dentist prescribed on the NHS?

Answer 126

GlandosaneSalivezeSalivix pastillesSalivox 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 lesions10-30% skin lesions

Question 129

Name the 3 different types of Lichen Planus

Answer 129

ReticularErosive/atrophicUlcerative

Question 130

What is the histopathological findings of lichenoid reaction?

Answer 130

Chronic inflammatory cell infiltrate Saw tooth rete ridgesBadal cell damagePatchy acanthosis Parakeratosis

Question 131

What is the histopathological findings of licehn planus?

Answer 131

OrthokerstosisWedge shaped hypergrabulosisDermal epidermal Junction obscured lymphocytesVacuoles at basal laterLuck band of lymphocytes under epidermisCivatte bodies - dead keratinocytes

Question 132

What does the histopathological findings tell us?

Answer 132

Lymphocyte activationOverreaction to normal triggerVirus umplicated in immune upregulation but NOT as a cause of LP - hep C or herpesSometimes has external triggers - medicines or amalgam

Question 133

What are the 8 aetiologices of lichen planus

Answer 133

AutoimmuneViralGenetic predispositionPhysical and emotional stressTrauma - scraped or after surgery an isomorphic response (koebnerisation)Localised skin disease - herpes zoster - isotopic responseContact allergy - amalgamDrugs - gold, quinine, beta blockers and ACE inhibitors

Question 134

What are the symptoms of lichen planus?

Answer 134

Often noneMay 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

SkinScalpGenitalsHairNails

Question 136

What are the 5 main sites for oral LP?

Answer 136

Biccal mucosaGingiva - desquamative gingivitisTongue- lateral or dorsumLipsPalate

Question 137

Describe buccal lichen planus?

Answer 137

CommonestCan be found anywhere - ant at commisure- mid- post around 3rd molarMainly an incidental findingEasy to biopsy

Question 138

Describe gingival lichen planus?

Answer 138

Found in isolationTermed desquamative gingivitis- similar to gingival pemphigoid and to plasma cell gingivitis - clear histologicalVery erythematous appearance to the gingivaPatchyReticular pattern more commonOral 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 smoothLateral 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 lipBiopsy hard?Looks soreErythema

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 inhibBeta blockersDiuretics - bendroflu and frusemideNSAIDs DMARDsRare - phenothiazines

Question 143

Name 3 types of DMARDs?

Answer 143

PenicillamineGoldSulphasalazine

Question 144

What are the discriminative characteristics of a lichenoid drug reaction?

Answer 144

Widespread lesionBilateral and mirrorsPoorly 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 drugHow bad is the discomfort from the symptoms If significant symptoms - may need to find alternative medicationDiscuss 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 triggerPatch 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

CompositeGlassGold - low palladium alloyBonded crown

Question 149

Srmamentarium for amalgam removal?

Answer 149

DamHigh vol suctionPPIAvoid during preg

Question 150

Explain the overall lichen planus management for the patient?

Answer 150

Remove any cause- medicines- dental restorationsBiospy- unless a good reason not toBlood 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 - benzdamineAvoid 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 - ClobetasolTopical tacrolimus mwHydroxycholorquineSystemtic immumodilators - azathioprine and mycophenolate

Question 153

What are the histological findings of lupus erythematosis?

Answer 153

Basal vacuolar damageAtrophic epitheliumMelanophageIntense lymphocytic infiltrate

Question 154

Describe lichen like lesions?

Answer 154

Underlying disease needs considerationGVHD common after stem cell transplantLupus lesion can be- only in mouth - discoid lupus no auto abs- mouth and elsewhere (systemic ANA/Ro/dsDNAIf oral symptoms only treat like lichen llanjs

Question 155

Name 5 vesiculobulloua conditions?

Answer 155

Erythema multiformPemphigusPemphigoidAngina Bullish HaemorrhagiaBullous lichen planus

Question 156

What is the defintion of Pemphigoid?

Answer 156

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

Question 157

Name 3 different forms and presentations of Pemphigoid?

Answer 157

Bullous pemphigoid - skinMucous membrane pemphigoid - all mucous membranes Cicatritial pemphigoid - mucosal with scarring

Question 158

Describe the histopathogy of pemphigoid?

Answer 158

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

Question 159

Describe how Pemphigoid is seen with immunofluorescence?

Answer 159

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 160

What is a symblepharon?

Answer 160

Pemphigoid that is present on the eye

Question 161

Non-oral locations of Pemphigoid?

Answer 161

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 162

How to manage Pemphigoid?

Answer 162

SteroidsImmune modulating drugs- azathioprine- mycophenolate

Question 163

What is the defintion of Pemphigus?

Answer 163

Commonest form is vulgarisIntraepithelial bullaeClinically:- more common in females and over 50s- genetic with ashkenazi JewsSites:- skin- mucosaThey blister, then burst and then it spreads

Question 164

Describe Pemphigus histopathologically?

Answer 164

Supra-basal split with tzank cells

Question 165

Describe Pemphigus using immunofluorescence?

Answer 165

Very greenBasket weave pattern - around each epithelial cellC3 and IgG in Pemphigus vulgaris

Question 166

How to treat Pemphigus?

Answer 166

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

Question 167

Explain 2 different types of immune mediated disease?

Answer 167

HypersensitivityImmunogenic

Question 168

How many types of hypersentivitiy?

Answer 168

5

Question 169

Name the 2 types of immunogenic immune mediated disease?

Answer 169

Cell mediatedAntibody mediated

Question 170

Name 3 types of local immunological oral disease?

Answer 170

Aphthous ulcersLichen planusOrofaxial granulomatosis

Question 171

Name 6 systemic diseases with local oral effects?

Answer 171

Eythema multiformPemphigusPemphigoidLupusSystemic sclerosisSjogren’s syndrome

Question 172

Type 3 Hypersensitivity example?

Answer 172

Erythema multiform

Question 173

Name 3 examples of cell mediated immunity?

Answer 173

Aphtous ulcersLichen PlanusOrofaxial Granulomatosis

Question 174

Name 2 examples of antibody mediated immunity?

Answer 174

PemphigusPemphigoid

Question 175

Immunological skin diseases?

Answer 175

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

Question 176

Explain the mechanism of immunological skin disease?

Answer 176

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 177

How do cells of the epidermis adhere to eachother?

Answer 177

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

Question 178

Explain the mechanism of action for immunofluorescence?

Answer 178

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

Question 179

Explain the difference between direct and indirect immunofluorescence?

Answer 179

Direct:- antibody mediated tissue disease- antibody bound to tissues - targeted in DIFIndirect:- 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 180

What is the defintion of erythema multiforme?

Answer 180

Acute onset - more menSkin - show target lesionsMucosa - show ulcersFor young males it is recurrent within a short period

Question 181

What is the aetiology of erythema multiforme?

Answer 181

Immune complex?- drugs- herpes simplex- mycoplasma

Question 182

What specific sites do erythema multiforme target?

Answer 182

Lips and anterior part of the mouthHeals in 2 weeksVery painful - unable to eat or drink

Question 183

What os erythema multiforme relation to Stevens Johnson syndrome?

Answer 183

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

Question 184

What is the treatment for erythema multiforme?

Answer 184

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

Question 185

What is the defintion of angina bullous haemorrhagica?

Answer 185

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

Question 186

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

Answer 186

Non specific ulcerationDIF and IFF negativeNo defectsChlorhex MWMay recur

Question 187

How to manage angina bullish haemorrhagica?

Answer 187

No treatmentReassure patient that is benignExplain known triggers

Question 188

Why are mucosal lesions more frequent in children?

Answer 188

Clinical issues traditionally related to immunologicalimmaturity

Question 189

Name the 2 types of congenital oral mucosal lesions?

Answer 189

HereditaryDevelopmental defects

Question 190

Name the 6 types of acquired oral mucosal lesions?

Answer 190

TraumaticDrug-relatedChronic inflammatoryHyperplasticNeoplasticInfective

Question 191

What is the defintion of white sponge naevus?

Answer 191

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

Question 192

Name the clinical features of white sponge naevus?

Answer 192

•White, soft, irregularly thickened, nodefined borders•Bilateral•Genital tissues can also be affected•Often misdiagnosed with candidosis

Question 193

Name the histopathology of white sponge naevus?

Answer 193

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

Question 194

How to manage white sponge naevus?

Answer 194

Reassurance

Question 195

Name 3 developmental defect oral mucosal lesions?

Answer 195

Fordyxe’s granulesFoliate papillaeGeographic tongue

Question 196

Describe the clinical features of fordyce’s granules?

Answer 196

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

Question 197

Describe the clinical feattures of folaite papillae?

Answer 197

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

Question 198

Describe the clinical features of geographic tongue?

Answer 198

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

Question 199

Describe the histology of geographic tongue?

Answer 199

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

Question 200

Explain how to manage geographic tongue?

Answer 200

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

Question 201

Name 3 traumatic oral mucosal lesions?

Answer 201

mucoceletraumatic ulcerfrictional keratosis

Question 202

Describe the clinical fearues of frictional keratosis?

Answer 202

▪Pale and translucent or white/dense withrough surface

Question 203

Describe the histology of frictional keratosis?

Answer 203

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

Question 204

Describe the clinical features of traumatic ulcer?

Answer 204

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

Question 205

Describe the histology of traumatic ulcers?

Answer 205

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

Question 206

Describe the clinical features of a mucocele?

Answer 206

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

Question 207

Describe the histology of a mucocele?

Answer 207

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

Question 208

Name a drug-induced oral mucsoal lesion?

Answer 208

Chemo-induced stomatitisAspirin burns

Question 209

Name 3 types of inflammaotry oral mucosal lesions?

Answer 209

Orofacial granulomatosiserythema multiformerecurrent apthous stomatitis

Question 210

Describe the clinical features for recurrent aphthous stomatitis?

Answer 210

▪Idiopathic, but systemic factors known to modulate the severity of disease▪Onset in childhood, but peak in adolescenceMinorMajorHerptiform

Question 211

Describe the histology of recurrent aphthous stomatitis?

Answer 211

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

Question 212

Explain the management for a mucocele?

Answer 212

Reassurance/excision if symptomatic or interferes with oral functions

Question 213

What should be excluded when dealing with recurrent aphthous stomatitis?

Answer 213

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

Question 214

Describe the clinical features for erythema multiforme?

Answer 214

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

Question 215

Describe the histology of erythema multiforme?

Answer 215

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

Question 216

Describe the clinical features for orofacial granulomatosis?

Answer 216

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

Question 217

Describe the histology for orofacial granulomatosis?

Answer 217

Granulomas containingmultinucleated giant cells▪Lymphoedema

Question 218

What are possible differential for orofacial granulomatosis?

Answer 218

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

Question 219

Name 3 inflammaotry oro mucosal diseases rarely seen in children?

Answer 219

Oral Lichen Planus• Mucous Membrane Pemphigoid• Pemphigus vulgaris

Question 220

Describe the clinical features for oral lichen planus?

Answer 220

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

Question 221

Describe the histology for oral lichen planus?

Answer 221

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

Question 222

Describe the clinical features for mucous membrane pemphigoid?

Answer 222

▪Bullae, sometimes intact, can appear as bloodblisters. If ruptured raw ulcer▪Desquamative gingivitis▪Conjuctival involvement▪Cutaneous involvement less prominent thanbullous pemphigoid

Question 223

Describe the histology for mucous membrane pemphigoid?

Answer 223

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

Question 224

Describe the clinical features of pemphigus?

Answer 224

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

Question 225

Describe the histology for pemphigus?

Answer 225

•Acantholysis•Intraepithelial vesicles.•‘Chickenwire’ deposition of IgG and C3/C4within the epithelium.•Anti-desmoglein3 antibodies bindintercellular substance in directimmunofluorescence assay

Question 226

Deswcribe the clinical features for epydermolysis bullosa?

Answer 226

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

Question 227

Name 3 hyperplastic forms of oral mucosal lesions?

Answer 227

Vascular malformationGiant cell epulisPyognic granuloma

Question 228

Describe the clinical features for a pyogenic granuloma?

Answer 228

▪Soft, red polypoidswelling▪Most commonly gingivalbut not exclusively

Question 229

Describe the histology for a pyogenic granuloma?

Answer 229

•Granulation tissue•Dilated blood vessels inoedematous CT•Dense infiltration byneutrophilsNO GRANULOMAS, NOPYOGENIC BACTERIA

Question 230

Describe the clinical features of a giant cell epulis?

Answer 230

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

Question 231

Describe the histology for giant cell epulis?

Answer 231

•Subepithelial clusters of giant cells in fibro-vascular tissue

Question 232

What to exclude when dealing with a giant cell epulis?

Answer 232

Need to exclude central GCG andunderlying hyperparathyroidism

Question 233

Describe the clinical features of vascular malformation?

Answer 233

Purple nodular lesion▪Blanches upon pressure

Question 234

Describe the histology for a vascular malformation?

Answer 234

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

Question 235

Name 2 pigmentary chnages ivolved with oral mucosal lesions?

Answer 235

Puetz-Jeghers syndromeAddison’s Disease

Question 236

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

Answer 236

Clinical features▪Intestinal polyposis▪Mucocutaneous pigmented lesionsappearing during childhood

Question 237

Describe the histology for Addison’s disease?

Answer 237

•Mild acanthosis•Melanin in basal layer

Question 238

Describe the clinical features for warts?

Answer 238

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

Question 239

Describe the histopathology of warts?

Answer 239

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

Question 240

Describe the clinical features for pseudomembranous candidosis?

Answer 240

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

Question 241

Diseases that cause immunocompromisation and lead to oral mucosal lesions?

Answer 241

HIV/AIDS

Question 242

How are viruses transmitted?

Answer 242

Exchange of blood productsSexual transmissionPerinatal infection

Question 243

MoA of HIV?

Answer 243

Retrovirus - group VI (baltimore)Infects activated T cells and macrophages vis the envelope glycoproteinTransferred 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

PyrexiaSkin rashHaedacheDiarrhoea OropharyngitisOral mucosal erythema

Question 247

What infections are diagnostic fir ARC asymptomatic seropostive HIV?

Answer 247

LymphoadenopathyPersistent pyrexiaDiahorreaWeight losFatigue and malaise

Question 248

What infections are diagnostic for AIDS?

Answer 248

Kaposi’s sarcomaNH lymphomaThrombocytopeniaNeurologival 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 infectionsEvidence 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 cheilitisHairy leukoplakiaKaposi sarcomaNH lymphomaPerio 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 monthErythamtousHyperplastic

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 tongueVertical white folds with hair like surfaceSmooth

Question 256

Describe the histopathology of hairy leukoplakia?

Answer 256

Acabthotic parakerarinsed epithelium Finger like keratin projections on the surfaceBand of ballon cells in prickle cell layerSecondary 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 HIVHHV8Involves skin and mucosal surfacesRed 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 cellsLate 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 patientsAssociated with EBV

Question 260

Name 4 less commonly oral mucosal lesions with HIV?

Answer 260

Bacterial infectionsSalivary glabd diseaseOral 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 16Venereal warTransmitted via oro genital contact Multiple white/pink nodulesFuse forming sessile or pedunculated papillary lesions

Question 263

Describe the histopathology of HPV in HIV patients?

Answer 263

Induce hyperplastic changes rather than ballooning degenerationFibrovascular core covered by stratified squamous epithelium with- hyperpladtiv basal cell layer - acanthosis- parakeratosisKoilocytes

Question 264

Describe atylical ulceration in HIV patients?

Answer 264

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

Question 265

Describe salivary gland disease in HIV patients?

Answer 265

Salivary gland enlargement - mainly parotidXerostomuaLymphocyte infiltration Lympho-epothelial cystsEnlargement 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 difficultMakes 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 AsiaMale 2:1 Female Incidence not increasing worldwide- Decreasing in men, increasing in women- Linked to reduction in tobacco useScottish Cancer Registry- 10% increase 2001-2012

Question 270

Name the 6 common sites for mouth cancer?

Answer 270

Floor of the mouthLateral border of the tongueRetromolar regionsSoft and hard palateGingivaeBuccal mucosa

Question 271

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

Answer 271

FoMLat. border of the tongueSoft palate

Question 272

Name the 8 sites of oral cancer?

Answer 272

LipsPalateTonsilsFoMOther throatTongueOropharynxGums

Question 273

Describe the epidemiology for OPC?

Answer 273

1.4 per 100,000 popMost in North America and south central AsiaMale 4.8:1 FemaleRates rapidly rising, especially in High Income areas (North America)- Linked to rising HPV epidemicScottish 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 cancerDrinkers (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 cancersSmoke and Drink x5 risk- Increases with frequency and duration of smoking and alcohol consumption- No safe lower limitBetel 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 importantOral Health- Early data suggests poor oral health may be associated with an increased cancer risk – small effectSexual 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 yearsRisks 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 CandidiasisOral 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 clearmalignant change- varied reports, most under 4%- period prevalence2.5% in 10 years, 4% in 20 yearsMost oral carcinomas in UK arise in initially clinically normal mucosaMost cancer in high incidence areas (e.g. India) from potentially malignant lesionWorldwide 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

HomogenousErosiveNon-homogenous on atrophic background

Question 282

How does erythroplakia compare to leukoplakia?

Answer 282

much less frequent than leukoplakiamuch higher risk of cancergreater dysplasia risk- Up to 50% already be carcinomano 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 OrganisationNew 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 epitheliumArchitectural change into lower third Cytological atypia or dysplasia may not be prominent Shows a considerable amount of keratin productionEvidence of stratificationWell 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 epitheliumArchitectural change upper third Usually show considerable atypiaInvade in a non-cohesive pattern with fine cords, small islands and single cells infiltrating widely through the CTMitotic 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 conceptCytologically malignant but not invadingAbnormal architecture- Full thickness (or almost full)- Severe cytological atypiaMitotic 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 4mmmPerineural 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 massInvasion 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 patientsConcept of “field cancerisation”- high cancer risk in 5cm radius of original primary - that’s most of the mouth/pharynxSynchronous 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 monthsSurgery, 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 swellingAetiology- Sunlight UV-B- smokingBehaviour - slow growth - local invasion- rarely metastasise to nodesGood 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 HarmUndetected lesions vs False positiveCost of Screening vs Cost of diseaseCost of Screening vs Disability from disease

Question 294

Name the 5 OC screening tools?

Answer 294

HPV16 screeningToluidene blueVELscopePhotodynamic 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 changesPublished 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 nowDentist has opportunity for PRIMARY PREVENTION in patients attending for regular oral careDentist must be familiar with and competent in:- Smoking cessation advice - Alcohol reduction advice- Healthy diet promotionThere is a GDC expectation that a dentist will do this as part of ‘good patient care’ rather than any particular remunerationDentist has to make decision about their referral threshold for potentially malignant lesionsMonitor with photographs and education Remove local factors where ulcer may be due to trauma, then review2 WEEK RULE for referral to clinic for the hospitalPatient must be initially seen within this time62 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 diagnosisIt has NO histological connotationEpithelial dysplasia may or may not be presentNon-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 variableNon-homogeneousVerrucous, 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 numbersArchitecture regular stratification altered compartment sizeNO cellular atypia

Question 306

What is the definition of hyperplasia?

Answer 306

Increased cell numbersArchitecture regular stratification altered compartment sizeNO cellular atypia

Question 307

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

Answer 307

Architecture -increased maturationcompartment

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 thirdMild -cytological atypia

Question 310

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

Answer 310

Architecture -change into middle/upper third Marked cytological atypiaPossibility 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 carriersMost common isolate is C. albicans

Question 313

Name 5 candidal virulence factors?

Answer 313

AdherenceSwitching mechanismsGerm tube formationExtracellular enzymesAcidic metabolites

Question 314

Name the local predisposing factors for candidal infections?

Answer 314

SmokingDenturesLocal corticosteroidsXerostomiaTopical antimicrobials

Question 315

Name the general predisposing factors for candidal infections?

Answer 315

Extremes of ageEndocrine disease- DiabetesImmunodeficiency- Steroid use, HIVNutritional deficiency- ironAntibiotics

Question 316

Name the classification of oral candidosis?

Answer 316

Acute Pseudomembranous- Sudden local/systemic immunosuppressionChronic Erythematous- Longstanding & persisting issue- e.g. below poor fitting dentures, HIV, median rhomboid glossitis and antibioticChronic 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 agarOral 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 microscopyGerm Tube testPhysiological tests- Carbohydrate fermentation- Carbohydrate and nitrogen assimilationCommercial systems- API 20C systems

Question 320

How to identify candidaosis in the lab?

Answer 320

Direct microscopyGerm Tube testPhysiological tests- Carbohydrate fermentation- Carbohydrate and nitrogen assimilationCommercial systems- API 20C systemsBiopsy- Essential for diagnosis of hyperplastic candidosis.- PAS stainDirect smear

Question 321

Name the 5 candida species?

Answer 321

C. albicansC. glabrataC. tropicalisC. kruseiC. dubliniensis

Question 322

Describe the principles of management for candidal infection?

Answer 322

Correction of predisposing factors OH, diet, trauma, steroid inhaler hygieneIdentify underlying illnessesAntifungal agentCo-infection with other microorganisms?

Question 323

Name different categories of antifingal drugs?

Answer 323

Polyenes- Nystatin- AmphotericinImidazole- Miconazole- ClotrimazoleTriazoles- 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)- MiconazoleSystemic 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 prescriptionSlow release adhesive preparation availableACTIVE 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 courseItraconazole- 100mg capsule - 14 day course- 100mg twice in once daily for Pseudomembranous candidiasis

Question 327

Name 3 antifungals that have resistance?

Answer 327

C. glabrataC. kruseiiC. 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 entryUncoating of virionMigration of acid to nucleusTranscriptionGenome replicationTranslation of virus mRNAsVirion assemblyRelease of new virus particles

Question 330

Effect of viral infections on host cells?

Answer 330

Cell death (cytopathic effect)Latent infectionHyperplasia 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 cytoplasmProgressive 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 inflammationExtra-oral involvement:- peri-oral- fingers (herpetic whitlow)- eyesSymptoms- Pain- Dysphagia- Dehydration - May be associated with fever, lymphadenopathy, - Pharyngitis in adolescentsRecurrent 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 childrenImmunocompromised with severe infection:- Refer to specialist/GP for treatmentShingles:- 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 generalizedlymphoadenopathy (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 subclinicalIf symptomatic, clinically similar to infectious mononucleosisLarge, 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 ageExophitic, peduncolatedDistinctive branched structure, finger-like processes, white or pinkishUp to 20 mm in diameter

Question 344

Describe the apperance of condyloma acuminatum?

Answer 344

HPV 6, 11, 16:Venereal wartHIV infection manifestationTransmitted via oro-genital contactMultiple 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/parakeratosisKoilocytes

Question 347

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

Answer 347

Clinical features- history- examLaboratory 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 sitesWhole salivaAspirateSmearBiopsyBlood

Question 349

How to decide if infection need treatment?

Answer 349

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

Question 350

How to decide appropriate treatment for infection?

Answer 350

Culture and sensitivity test - always preferredBest guessExperienceSide 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 daysProdromes: nausea, malaise, vomiting, pharyngitis and lymphoadenopathyMacular erythemaOral mucosa erythematous and oedematousDorsum 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 exudateSurrounding tissue indurated with inflammLocalisation- tongue, palate gingivae, and lipsAssoc 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 LatentTertiary - gumma, CV and CNS complications

Question 357

What is the defintion of gonorrhea?

Answer 357

Second most common STIOral lesions result of progenitor contactNon-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 sinusesDischarge yellow purulent material

Question 359

What are the histopathologucal features of actinomycosis?

Answer 359

Colony of actinomyces in centreDense collection of inflamm cellsSurround 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 diseaseSecondary- connective tissue disease- SLE, Rheumatoid Arthritis, Scleroderma

Question 362

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

Answer 362

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 pregnancySystemic involvement- Lungs, kidney, liver, pancreas, blood vessels, nervous system- Sometimes general fatigue and chronic painSpeculative 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 cytokinesSpeculative Environment- EBV association – weak evidence – may be reactive rather than causative

Question 363

Name the 4 consequences of Sjogrens Syndrome?

Answer 363

Gradual loss of salivary/lacrimal gland tissue through inflammatory destructionEnlargement of major salivary glands – usually symmetrical- Usually painlessIncreased risk- Any lymphoma (5% quoted)- Salivary marginal B-cell (MALT) LymphomaOral and Ocular effects of loss of saliva and tears

Question 364

Describe how to diagnose Sjogrens Syndrome?

Answer 364

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

Question 365

Describe the diagnosis crietria for AECG of Sjogrens syndrome?

Answer 365

Dry eyes/mouth- Subjective or objectiveAutoantibody findingsImaging findingsRadio nucleotide assessmentHistopathology findingsFOUR or more positive criteria for diagnosis

Question 366

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

Answer 366

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

Question 367

Describe the oral and eye symptoms necessary to aid diagnosis?

Answer 367

Oral Daily feeling of a dry mouth for >3 monthsRecurrent swelling of salivary glands as an adultFrequently drink liquid to aid swallowing dry foodsOcularPersistent troublesome dry eyes for >3 monthsRecurrent sensation of sand/gravel in the eyesTear substitutes used >3 times day

Question 368

Name the 2 eye tests for Sjogrens Syndrome?

Answer 368

Abnormal Schirmer test<5mm wetting in 5 minutesFluorescein Tear film assessment

Question 369

Name the oral test for Sjoregns Syndrome?

Answer 369

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

Question 370

Explain to autoimmunity involved with Sjogrens Syndrome?

Answer 370

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 findingsAnti-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 371

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

Answer 371

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

Question 372

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

Answer 372

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 oneDo 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 screenIf still equivocal do labial gland biopsy- Risk of area of skin numbness following procedure- Informed consent neededLGB and Anti-Ro may be the ONLY positive results in early Sjogren’s

Question 373

Describe the management for a patient suffering with Sjogrens Syndrome?

Answer 373

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 374

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

Answer 374

Effects of Oral Dryness- caries risk, denture retention, infections, functional issues –speech/swallowSalivary enlargement - Sialosis- can occur at any time – usually permanent- Reduction surgery possible but not advised – other health issuesLymphoma 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 375

Examination of the salivary gland locations?

Answer 375

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

Question 376

What is the function of saliva?

Answer 376

Acid bufferingMucosal lubrication- Speech- SwallowingTaste facilitationAntibacterial

Question 377

Name the 5 main causes of a dry mouth?

Answer 377

Salivary Gland diseaseDrugs Medical Conditions & DehydrationRadiotherapy & cancer treatmentsAnxiety & Somatisation Disorders

Question 378

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

Answer 378

Acinar tissue loss37% Submandibular32% Parotid45% Minor glands

Question 379

Describe in/direct effect on salivation?

Answer 379

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

Question 380

Name 6 drugs that cause indirect salivary problems?

Answer 380

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

Question 381

Name the 3 largest influencing drugs on dry mouth?

Answer 381

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

Question 382

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

Answer 382

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

Question 383

Name 5 direct salivary gland problems?

Answer 383

Aplasia - Ectodermal dysplasiaSarcoidosisHIV diseaseGland infiltration- Amyloidosis- HaemochromatosisCystic Fibrosis

Question 384

What is the defintion of ectodermal dysplasia?

Answer 384

Hair, Nails, Teeth, Salivary & Sweat glands- Hearing and vision may be affectedMay be limited in effect- Salivary aplasia aloneHypohidrotic – x-linked

Question 385

Haemachromatosis?

Answer 385

HFE gene mutation - 1:10 pop carry

Question 386

Describe radiotherapy effect on salivation?

Answer 386

Radiation effectsGraft versus host effectsAntineoplastic drugsRadioiodine

Question 387

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

Answer 387

Blood tests - FBC- U&Es, - Liver function tests- C-reactive Protein- Glucose- Anti Ro Antibody- Anti La Antibody- Antinuclear Antibody- Complement C3 and C4Functional Assay– Salivary FlowTissue Assay – Labial Gland BiopsyImaging - Plain radiographs – reduced dose – stones- Sialography – contrast to show ducts- MR Sialography – IV contrast- Ultrasound

Question 388

Describe how anxiety and somatisation disorders can cause dry mouth?

Answer 388

‘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 disordersAnxiety can also inhibit swallowing and can lead to a complaint of ‘too much saliva’!

Question 389

Name 6 forms of somatoform disease that cause dry mouth?

Answer 389

Oral DysaesthesiaTMD painHeadacheneck/back painDyspepsiaIrritable Bowel Syndrome (IBS)

Question 390

Name 5 treatbale causes of dry mouth?

Answer 390

DehydrationMedicines with anti-muscarinic side effectsMedicines causing dehydrationPoor Diabetes control – type 1 or type 2 Somatoform Disorder – diagnosis of exclusionManagement of these should return the patient’s oral comfort

Question 391

Name th 3 treatment options for symptomatic dry mouth?

Answer 391

Sjögren’s SyndromeDry mouth from cancer treatmentDry mouth from salivary gland diseaseTreatment options for these cases- INTENSIVE DENTAL PREVENTION- Salivary substitutes- Salivary stimulants

Question 392

Name the 5 categroeis of dry mouth investigations?

Answer 392

Salivary Flow tests – less than 1.5ml unstimulated flow in 15minsBlood tests- Dehydration – U&Es, Glucose- Autoimmune disease – ANA, Anti-Ro, Anti-La (ENA Screen), CRP- Complement levels – c3 and c4Imaging- Salivary ultrasound – looking for ‘leopard spots’ or sialectasis- Sialography – useful where obstruction/ductal disease is suspectedDry eyes screen- Refer to optician for assessment of tear film (preferred)- Schirmer test – tear flow less than 5mm wetting of test paper in 15 minsTissue examination- Labial gland biopsy – lower lip – looking for lymphocytic infiltrate and focal acinar disease

Question 393

Describe the dental management of dry mouth?

Answer 393

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

Question 394

Name 6 forms of saliva substitiues and their form?

Answer 394

Sprays- Glandosane- Saliva OrthanaLozenges- Saliva Orthana- SSTSalivary stimulants- Pilocarpine (Salagen)Oral Care Systems- Oral BalanceFrequent sips of water

Question 395

Name the causes of hypersalivation? - True and percieved?

Answer 395

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

Question 396

Describe the dental management of excess salivation?

Answer 396

Treat the Cause- Anxiety disordersDrugs to reduce salivation- Anti-muscarinic agents- Botox to prevent gland stimulationBiofeedback training- Swallowing controlSurgery to salivary system- Gland removal- Duct repositioning

Question 397

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

Answer 397

Viral Inflammation - Mumps- HIVSecretion retention- Mucocele- Duct obstructionGland Hyperplasia- Sialosis- Sjögrens Syndrome

Question 398

Name the 7 symptoms of mumps?

Answer 398

HeadacheJoint painNauseaDry mouthMild abdominal painFeeling tiredloss of appetitePyrexia of 38C, or aboveParamyxovirusDroplet spreadIncubation 2-3 weeks1/3 have no symptomsSymptomatic treatment only

Question 399

What is the defintiion of HIV sailvary disease?

Answer 399

HIV can be a cause of salivary swellingCause of Unexplained salivary swellingMay have NO HIV symptoms when presentingGenerally does not improve with treatmentLympho-proliferative enlargement of the glands

Question 400

What is the definition of a mucocele?

Answer 400

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

Question 401

What is the definition of subacute obstruction?

Answer 401

Swelling associated with meals- increases as salivary flow starts- reduces when salivary flow stopsUsually SUBMANDIBULARocc. ParotidCan be slowly progressive – over weeksEventually fixed & painfulCause – duct obstruction- Usually duct blockage in submandibular- Usually duct stricture in parotid

Question 402

Name the 3 main causes of subacute obstruction?

Answer 402

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

Question 403

Name the 5 investigations for subacute obstruction?

Answer 403

Low dose plain radiography lower true occlusalSIALOGRAPHY – when infection freeIsotope scan if gland function uncertainUltrasound assessment of duct system

Question 404

What is the definition of duct dilation?

Answer 404

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

Question 405

Describe the management of subacute obstruction?

Answer 405

Surgical sialolith removal if practicalSialography for ‘no stone’ cases – washing effectConsider gland removal if fixed swelling

Question 406

Describe the outcome for subacute obstruction?

Answer 406

Reformation of stone/obstructionDeformity of duct – stasis & infectionGland damage – low salivary flow, ascending infection

Question 407

What is the definition of silalosis?

Answer 407

Increase in Gland Tissue (Hyperplasia)- Sialosis- Sjögrens Syndrome Major gland enlargementNo identified cause - Alcohol abuse- Cirrhosis- Diabetes Mellitus- Drugs

Question 408

What investigations can be carried out to diagnose Sialosis?

Answer 408

Blood testsGlucoseFBC, U&Es, LFTs, bilirubinBBV screen – HIV, Hep B, Hep CAutoAntibody Screen - ANA, anti-Ro, anti-LaOther investigtionsMRI of major salivary glandsUSS for Sjögren’s changesLabial gland biopsyTear filmSialography – occasionallyPhotography

Question 409

What investigations can be carried out to diagnose Sialosis?

Answer 409

Blood testsGlucoseFBC, U&Es, LFTs, bilirubinBBV screen – HIV, Hep B, Hep CAutoAntibody Screen - ANA, anti-Ro, anti-LaOther investigtionsMRI of major salivary glandsUSS for Sjögren’s changesLabial gland biopsyTear filmSialography – occasionallyPhotography

Question 410

Name 2 types of dental manifestations of systemic disease?

Answer 410

Disruption to the tooth structure formationDisruption to the tooth structure content

Question 411

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

Answer 411

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

Question 412

Name 6 oral mucosal effects from systemic disease?

Answer 412

Giant Cell GranulomaOrofacial GranulomatosisRecurrent Aphthous StomatitisDermatosesImmune Deficiency/Disease - Raised ACTH Addison’sDrug reactions

Question 413

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

Answer 413

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

Question 414

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

Answer 414

Causes thinking and finger-like projections of the bone

Question 415

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

Answer 415

Orofacial GranuolomatosisSjogrens Autoimmune – AddisonsInfections – fungal/viral

Question 416

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

Answer 416

Lichen planus, VB disease

Question 417

What is the definition of immune disease orofacial granulomatosis?

Answer 417

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 avoidedClinical signs:- lip swelling, erythema and crustiness- gingivae erythematous and heavly inflammed

Question 418

What is included for Crohn’s screening?

Answer 418

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

Question 419

Describe the management of orofacial granulamtosis?

Answer 419

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

Question 420

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

Answer 420

Systemic lupus erythematosis (SLE) - erytheamic gingiva and palateSystemic sclerosis (Scleroderma)Sjogrens syndromeMixed connective tissue disease (MCTD)

Question 421

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

Answer 421

Large vessel Disease- Giant cell (temporal) arteritisMedium Vessel Disease- Polyarteritis nodosa- Kawasaki diseaseSmall vessel Disease- Wegener’s Granulomatosis

Question 422

Name 4 forms of acquired immune deficiency?

Answer 422

DiabetesDrug therapyCancer therapyHIV

Question 423

What is the definition of haematinic deficieinces - causes?

Answer 423

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

Question 424

What is the definition of the Parotid gland?

Answer 424

Largest of major glandsPositioned parotid bed anterior to ear overlying mandibular ramusLower pole extends into postauricular regionIntimately associated with facial nerve (VII)Serous gland. Produces thin watery secretion via parotid duct (Stensen’s duct)

Question 425

WHat is the definition of the submandibular gland?

Answer 425

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

Question 426

What is the definition of the sublingual gland?

Answer 426

Smallest major glandLocated in submucosa of floor of mouthNearby structures: submandibular duct, lingual nerve and lingual arteryPredominantly mucousExpels secretions via Bartholin’s duct in floor of mouth

Question 427

Name the 2 categories and 5 types of cells?

Answer 427

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

Question 428

What is the definition of neoplasia?

Answer 428

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’BenignMalignant

Question 429

Describe the epidemiology of salivary gland neoplasms?

Answer 429

Rare - 3/100,000Commoner in women75% benign90% ParotidCommnest parotid and minor- plemorphic adenoma55% of palatal tumours - minor50% of minor neoplasms are maligantAll sublingual glands are malignant

Question 430

Name the 5 aetiologies of salivary gland neoplasms?

Answer 430

Radiation: nuclear bomb survivors, therapeutic radiation, dental x-rays, ?mobile phonesTobacco smoking: Warthin’s tumourViruses: EBV & lymphoepithelial carcinomaFamilial and geneticVarious industrial occupations

Question 431

Describe the differences between Benign and Malignant salivary gland tumours?

Answer 431

Benign - Encapsulated - Slow growing - ‘Rubbery’ consistency - Mobile - Overlying mucosa/skin appears normal - Not invasive Incapable of metastasis Local excision curativeMalignant - 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 432

Name 3 investigations for susected salivary gland tumours?

Answer 432

Clinical history and examinationImaging: Radiography/Sialography, Ultrasound, CT, MRIPathology: Fine Needle Aspiration (FNA), core biopsy, open incisional biopsy, excisional biopsyIMAGING AND PATHOLOGY ARE NOT A SUBSTITUTE FOR ADEQUATE HISTORY AND EXAMINATION

Question 433

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

Answer 433

Pleomorphic adenomaWarthin’s tumour Basal cell adenomaCanalicular adenomaOncocytoma

Question 434

Name 5 types of malignant salivary gland tumours?

Answer 434

Mucoepidermoid carcinomaAdenoid cystic carcinomaPolymorphous adenocarcinomaCarcinoma ex pleomorphic adenomaAcinic cell carcinoma

Question 435

What is the definition of a pleomorphic adenoma?

Answer 435

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 436

Explain the management for a pleomorphic adenoma?

Answer 436

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

Question 437

What is the definition of Warthin’s Tumour?

Answer 437

A tumour composed of glandular andoften cystic structures, sometimes with apapillary cystic arrangement, lined bycharacteristic bilayered epithelium, comprisinginner columnar eosinophilic oroncocytic cells surrounded by smallerbasal cells. The stroma contains a variableamount of lymphoid tissue with germinalcentres.

Question 438

What is the aetiology of Warthin’s tumour?

Answer 438

Exclusively in the ParotidMale predominanceLink with smoking

Question 439

Explain the management of Warthin’s tumour?

Answer 439

Complete excision is curative (superficial parotidectomy)

Question 440

What is the definition of a Oncocytoma?

Answer 440

Benign tumour of salivary gland origincomposed exclusively of large epithelialcells with characteristic brighteosinophilic granular cytoplasm (oncocyticcells).

Question 441

What is the aetiology of a Oncocytoma?

Answer 441

Most in parotidComplete excision curative

Question 442

What is the definition of a canalicular adenoma?

Answer 442

The tumour is composed of columnarepithelial cells arranged in thin, anastomosingcords often with a beaded pattern.The stroma is characteristically paucicellularand highly vascular.

Question 443

What is the aetiology of a canalicular adenoma?

Answer 443

lip commonestconservatice excision curative

Question 444

What is the definition of a basal cell adenoma?

Answer 444

Basal cell adenoma (BCA) is a rarebenign neoplasm characterized by thebasaloid appearance of the tumour cellsand absence of the myxochondroid stromalcomponent present in pleomorphicadenoma.

Question 445

What is the aetiology of a basal cell adenoma?

Answer 445

Mostly Parotid glandComplete excision curative

Question 446

What is the definition of mucoepidermoid carcinoma?

Answer 446

Mucoepidermoid carcinoma is a malignantglandular epithelial neoplasm characterizedby mucous, intermediate andepidermoid cells, with columnar, clearcell and oncocytoid features.

Question 447

What is the aetiology of mucoepidermoid carcinoma?

Answer 447

most common saliary gland malignancyParotid most common, then palate, submand and other minors

Question 448

Exlain the management of mucoepidermoid carcinoma?

Answer 448

Low grade: cystic, lots of mucous cellsHigh 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 449

What is the definition of an adenoid cystic carcinoma?

Answer 449

Adenoid cystic carcinoma is a basaloidtumour consisting of epithelial andmyoepithelial cells in variable morphologicconfigurations, including tubular,cribriform and solid patterns. It has arelentless clinical course and usually afatal outcome.

Question 450

What is the aetiology of an adenoid cystic carcinoma?

Answer 450

High grade malignnacyMore in femaleMajor glandsDistant metastases

Question 451

Explain the management of adenoid cystic carcinoma?

Answer 451

Surgery treatment of choiceWide resection. Extensive surgery often requiredClear margins difficult to achieve (mostly impossible)Radiotherapy with wide fieldsChemotherapy generally not effective

Question 452

What is the definition of a polymorphous adenocarcinoma?

Answer 452

A malignant epithelial tumour characterizedby cytologic uniformity, morphologicdiversity, an infiltrative growth pattern,and low metastatic potential.

Question 453

What is the aetiology of a polymorphous adenocarcinoma?

Answer 453

2nd most common intraoral malignant salivary glandPalate most commenMalig in minor

Question 454

Explain the management of polymorphous adenocarcinoma?

Answer 454

Surgical excision with clear margins usually curativeRole of radiotherapy not certain

Question 455

What is the definition of Carcinoma ex pleomorphic adenoma?

Answer 455

Carcinoma ex pleomorphic adenoma isdefined as a pleomorphic adenoma fromwhich an epithelial malignancy isderived.

Question 456

What is the aetiology of carcinoma ex pleomorphic adenoma?

Answer 456

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

Question 457

Explain the management of carcinoma ex pleomorphic adenoma?

Answer 457

Extensive surgery with neck dissection is treatment of choicePost operative radiotherapy

Question 458

What is the definition of an acinic cell carcinoma?

Answer 458

Acinic cell carcinoma is a malignantepithelial neoplasm of salivary glands inwhich at least some of the neoplasticcells demonstrate serous acinar cell differentiation,which is characterized bycytoplasmic zymogen secretory granules.Salivary ductal cells are also a componentof this neoplasm

Question 459

What is the aetiology of an acinic cell carcinoma?

Answer 459

Second most common salivary gland malignancy in children

Question 460

Explain the management of an acinic cell carcinoma?

Answer 460

Complete excision requiredGenerally not aggressive but a proportion can metastasise to cervical lymph nodes and lungRecurrence rate as high as 35%