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BDS4 > Oral Med > Flashcards

Oral Med Flashcards

1
Q

Define xerostomia and hyposalivation

A

Xerostomia: dry mouth as result from

  • absent/red. salivary flow
  • change in saliva composition
  • unknown reason

Hyposalivation: objective red. salivary secretion due to red. salivary gland function

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2
Q

Functions of saliva

A 
Lubrication: swallowing, speech
Defence, antimicrobial properties
Taste
Digestion: amylase (starch), lipase (fat)
Lavage, buffering
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3
Q

Complications dry mouth

A 
Dental: caries, depapillated tongue
Oral soft tissue disease
GIT dryness
Dysphagia
Dysphonia, hoarseness 
Psychological 
Nutritional, taste alteration
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4
Q

Aetiology of dry mouth

A 
Dehydration/red. fluid intake
Habits: mouth breathing
Medications 
Salivary Gland Disease
Systemic Disease
Change in oral perception due to
- nerve damage
- Alzheimer’s 
- stroke
Psychological 
Age
Idiopathic
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5
Q

Salivary gland diseases possibly leading to dry mouth

A 
Infection: viral (mumps), bacterial 
Obstruction
- meal time syndrome 
- mucocele, ranula
Damage: 2ry to cancer Tx
Tumours
Degernatiive: autoimmune destruction (Sjögren’s)
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6
Q

Systemic diseases possibly leading to dry mouth

A 
Sjögren’s
DM
Liver disease
Amyloidosis 
Sarcoidosis 
Thyroid disease
HIV-related 🙀
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7
Q

Discuss sialadenosis

A 
Sialosis
Unspecific gland enlargement 
Non-painful
Aetiology unknown 
- factors
— eating disorder
— medication 
— alcohol abuse
— nutritional deficiency 
— DM
— pregnancy
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8
Q

Discuss sialadentitis and sialolithiasis

A

Sialadentitis

  • enlargement 1/+ glands due to infection/inflammation/obstruction
  • parotid, submandibular
  • conditions: mumps, Sjögren’s, sarcoidosis

Sialolithiasis

  • stones/calculi in glands causing pain + swelling
  • submandibular
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9
Q

Classification of salivary gland tumours

A

Benign

  • nonepithelial
  • epithelial

Malignant

  • nonepithelial
  • epithelial
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10
Q

Types of benign epithelial salivary gland tumours

A 
Pleomorphic adenoma 
Warthin tumour 
Monomorphic adenoma 
Oncocytoma
Intraductal papilloma 
Sebaceous neoplasms
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11
Q

Discuss pleomorphic adenoma and warthin tumour

A

Pleomorphic Adenoma
- most common tumour
- tail of parotid; minor glands H palate + U lip
- variable, diverse histological patterns of epithelium and connective tissue
- incomplete capsule: complete removal difficult = recurrence high
— radiotherapy common Tx following removal to kill cells
- slow growing + asymptomatic

Warthin tumour

  • smooth, soft, parotid mass
  • multicystic, well encapsulated
  • recurrence low (5%); malignancy rare
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12
Q

Types of benign non-epithelial salivary glands tumours

A 
Haemangioma 
Neural sheath tumour 
Angioma 
Lymphangioma (cystic hygroma)
Lipoma
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13
Q

Discuss haemangioma

A

Benign non-epithelial salivary gland tumour

Vascular tumour
Usually parotid, sometimes submandibular
Solid mass cells + multiple anastomosing capillaries replace acinar structure

Rapid growth b/w 1-6/12, slowly red. until 12y

Dark red, lobulated, unilateral, compressible, asymptomatic mass

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14
Q

Types of malignant epithelial salivary gland tumours

A 
Mucoepidermoid carcinoma
Adenoid cystic carcinoma 
Carcinoma ex-pleomorphic adenoma 
Clear/basal cell carcinoma
Squamous cell carcinoma 
Epithelial-myoepithlial carcinoma 
Salivary duct carcinoma 
Lymphoepithelial carcinoma 
Sialoblastoma
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15
Q

Discuss mucoepidermoid carcinoma

A

Malignant epithelial salivary duct tumour
Most common malignancy of parotid 8%

Mucous + epidermal cells

Grading: ratio epidermal cells inc.
- low: non aggressive, good prognosis 
- int.
- high: aggressive, high change metastasis regional lymph nodes
— may resemble SSC
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16
Q

Discuss adenoid cystic carcinoma

A

Malignant epithelial salivary gland tumour
2nd most common malignancy tumour
Most common malignancy submandibular

Slow growing, painless mass
Locally invasive 
Metastasis 
- regional lymph nodes uncommon 
- distant (lungs) common
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17
Q

Discuss carcinoma ex-pleomorphic adenoma

A

Malignant epithelial salivary gland tumour
Arises from incomplete removal of pleomorphic adenoma

2-4% all salivary gland malignancies

Sudden rapid growth otherwise stable/slow mass
Aggressive natural Hx + poor prognosis
Metastasis: regional + distant common

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18
Q

Types of tumour-like lesions of salivary glands

A

Necrotising sialometaplasia
Lymphoepithelial Hyperplasia/benign lymphoepithelial lesions
Cystic lymphoid hyperplasia (AIDS)
Salivary gland cysts

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19
Q

Discuss necrotising sialometaplasia + lymphoepithelial hyperplasia

A

Tumour-like lesions of salivary glands
Necrotising sialometaplasia
- benign, self-healing lesion minor glands
- mistaken for malignancy
— single, unilateral painless/slightly painful lesion H palate
- aetiology: unknown
— response to ischaemic necrosis of salivary tissue

Lymphoepithelial hyperplasia

  • discreet mass/diffuse enlargement of part/whole parotid
  • occasionally bilateral
  • slow-growing, may be painful
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20
Q

Most common 2ry cause of xerostomia

A

Sjögren’s syndrome

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21
Q

What is Sjögren’s? Aetiology

A

Multisystem autoimmune disease

Aetiology: unknown

  • virus triggering immune reaction
  • genetic susceptibility
  • gender predisposition: hormones (90% F >50y)
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22
Q

What is Sjögren’s syndrome characterised by?

A

Inflammation of exocrine glands w/ lymphocytic infiltration of lacrimal + salivary glands leading to xerostomia + xerophthalmia (sicca complex)

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23
Q

Compare 1ry and 2ry Sjögren’s

A

1ry (Sicca): dry eyes + mouth

2ry: connective tissue disease (rheumatoid arthritis) + dry eyes and mouth

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24
Q

General symptoms + signs of Sjögren’s

A

Dry mouth/eyes/skin/mucous membranes
Fatigue/fibromyalgia
Rheumatoid arthritis/connective tissue disease
Raynaud’s phenomenon

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25
Q

What is Raynaud’s phenomenon?

A

Condition in which spasm of capillaries causes extremities to change colour (white -> blue) and become painful
Usually response to cold

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26
Q

Oral signs + symptoms of Sjögren’s

A

No saliva pooling
Dry, atrophic mucosa
Sticky/glassy mucosa
Cracked lips

Oral burning sensation
Oral soreness

Sialadenitis: swelling, pain, fever
Oral candidiasis

Inc. DMF
Cervical + incisal decay pattern

Denture wearing difficulty

Dysohonia, dysphasia, dysgeusia
Halitosis

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27
Q

Discuss potential systemic complications/involvement of Sjögren’s

A

Haematological

  • autoimmune haemolytic anaemia
  • idiopathic thrombocytopenia purpura
  • non-hodgkin’s lymphoma

Respiratory: interstitial fibrosis
Renal: renal tubular acidosis
Nervous: cranial/peripheral neuropathy

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28
Q

Classification criteria for Sjögren’s

A

1: ocular symptoms (subjective)
2: oral symptoms (subjective)
3: ocular signs (objective)
4: histopathology (objective)
5: salivary gland involvement (objective)
6: serum auto-Ab (objective)

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29
Q

What auto-Ab are involved in Sjögren’s?

A

Auto-Ab to Ro/SSA and La/SSB auto-Ag

Act against auto-Ag in lacrimal and salivary glands

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30
Q

Classification criteria for 1ry and 2ry Sjögren’s

A

1ry

  • symptomatic: any 4/6 +ve incl. histopathology and/or serum
  • asymptomatic: any 3/4 objective measurements +ve

2ry

  • systemic disease +
  • 1/2 subjective measurement +
  • 2/3 from ocular signs, histopathology, salivary gland involvement
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31
Q

Serious complications of Sjögren’s

A

Lymphoma
- 40x greater risk
- 10% SS pt develop non-Hodgkin’s lymphoma
Heart Block newborns
- maternal Ab cross placenta
Eye damage + Vision loss
- corneal ulcers due to unTx dry eyes + infection

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32
Q

Ix useful for Dx Sjögren’s

A

Salivary Assays (sialometry)

  • whole unstim. salivary flow
  • parotid/submandibular stim. flow

Bloods: specific auto-Ab (not all pt)
X-ray: sialograph
US
L lip minor gland biopsy (gold standard)

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33
Q

Tx/management of Sjögren’s/dry mouth

A

No cure
Regular appt; OHI, F- m/w
Tx/prevent candidiasis

Diet

  • inc. H2O intake; esp. eating, speaking
  • red. sugar
  • avoid: caffeine, alcohol, fizzy drinks, tobacco

Stim. saliva: sugar free gum/sweets
Artificial saliva products: personal preference
Humidifier: esp. at night

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34
Q

Non/pharmacological management methods for Sjögren’s

A

Pharmacological

  • parasympathetic nervous system agonist: pilocarpine
  • only v severe cases
  • many adverse effects: GIT, CVS, respiratory, GU (inc. urination)

Non-Pharmacological

  • acupuncture
  • electrostimulation: IO neural stim, (US approved)
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35
Q

Differentiate b/w ulcer and erosion

A

Erosion: partial loss skin/mucous membrane
Ulcer: total loss of epithelium

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36
Q

Define atrophy and plaque

A

Atrophy: loss of thickness

Plaque: raised uniformed thickening skin/mucous membrane w/ defined edge

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37
Q

Classification of oral ulcerative diseases by aetiology

A 
Local
- trauma: chemical, electrical, thermal, radiation
- recurrent aphthous stomatitis 
Systemic
Infective
- bacterial: TB, ANUG, syphilis 
- viral: VZV, HSV, CAV, HIV, EBV
- fungal: histoplasmosis, aspergillosis, candidiasis
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38
Q

Cutaneous systemic diseases causing oral ulcers

A 
Erosive lichen planus
Pemphigoid 
Pemphigus
Erythema multiforme 
Dermatitis herpetiformis
Epidermolysis bullosa
Linear IgA disease
Chronic ulcerative stomatitis
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39
Q

Blood diseases potentially causing oral ulcers

A

Anaemia
Leukaemia
Neutropenia
Myelodylastic syndrome

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40
Q

GI and CT diseases causing oral ulcers

A

GI

  • coeliac
  • Crohn’s
  • ulcerative colitis

CT

  • SLE/DLE
  • Wegner’s granulomatosis
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41
Q

Drugs/Tx and malignancies potentially causing oral ulcers

A

Drugs/Tx

  • cytotoxic drugs
  • radiotherapy
  • nicorandil (cardiac)

Malignancy

  • SSC
  • lymphoma
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42
Q

Classification of oral ulcers by recurrence

A 
Recurrent
- aphthae
- erythema multiforme 
Persistent: 2ry to systemic disease
Single episode
- trauma 
- infective 
- drug 
Single persistent: neoplastic
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43
Q

Types of recurrent oral ulcers

A 
Recurrent aphthous stomatitis 
- major
- minor 
- herpetiform 
Smoking related aphthous stomatitis 
Associated w/ Behçet’s disease
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44
Q

Compare minor, major, herpetiform RAS

A

Age: 10-19; <10; 20-19
No.: 1-5; 1-10; 5-20
Size: <10mm; >10mm; 0.5-3mm
Shape: oval; irregular/oval; round, may coalesce
Colour: grey base, erythematous border; grey base, +/- indurated edge; yellow base, erythematous base
Site: non-keratinised (B mucosa); any (fauces); non-keratinised (V tongue, FoM)
Duration: 1-2/52; 2-12/52; 1-2/52
Scarring: N; Y; N

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45
Q

Discuss Behçet’s disease

A

Chronic autoimmune disease
- affects small blood vessels
Triad: oral ulcers, genital lesions, recurrent eye inflammation
- oral ulcers indistinguishable from RAS

Clinical
- ulcers: oral, genital (50%), skin
- skin: spots, sores, lesions, ulcers, red patches, lumps
- eye: uveitis (50%), retinal vasculitis
— floaters, haziness, loss of vision
— pain, inflammation
- joint inflammation: pain, swelling

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46
Q

Management of oral ulcers

A 
Eliminate local aggravating factors 
Control infection
Control pain
Promote healing 
Prevent recurrence
Assess response
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47
Q

General + local predisposing factors for candidiasis

A

General

  • broad spectrum AB
  • corticosteroids
  • cytotoxics
  • poorly controlled DM
  • xerostomia
  • nutritional deficiency
  • immunosuppression

Local

  • trauma: ill fitting denture
  • smoking
  • red. saliva flow
  • carb rich diet
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48
Q

Discuss impact of drug therapy in candidal infections

A

Broad spectrum ABs, immunomodulators, xerogenic agents

ABs: alter commensal microflora
- Candida controlled by competition for dietary substrates + epithelial cell adhesion

Xerogenic: red. salivary flushing + antifungal components

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49
Q

Discuss impact of DM on candidal infections

A

Related to glycemic control
- poorly controlled = higher Candida carriage

Contributory 
- red. salivary flow
- lower pH
- inc. salivary glucose 
= inc. growth + colonisation
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50
Q

Discuss immunodeficiency + haematological factors related to candidal infections

A

Immunodeficiency

  • candidiasis may be 1st presentation
  • cell-mediated + humoral immunity in prevention + elimination of fungal infections
  • candidiasis: >60% HIV, >80% AIDS

Haematological

  • blood group H Ag acts as R for C. Albicans
  • H Ag inc. blood type O
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51
Q

Discuss impact of diet on candidal infections

A

Protein energy malnutrition

Fe, folate, VitA/B12/C deficiency
Red. host defence + mucosal integrity
= hyphal invasion + infection

CHO rich: inc. candidal adhesion to epithelial

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52
Q

2 acute candidal infections

A

Pseudomembranous candidiasis

Erythematous candidiasis

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53
Q

Discuss pseudomembranous candidiasis

A

Detachable confluent creamy-white/yellowish patches on mucosa
- tongue rare; depapillated if occurs
Wiped off: erythematous, occasionally bleeding base
Plaques: desquamated epithelial cells, necrotic material, fibrin, fungal hyphae
Usually asymptomatic

Found in immunocompromised
- HIV: oesophageal candidiasis; dysphagia, odynophagia, chest pain
Freq. associated angular cheilitis

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54
Q

Management of pseudomembranous candidiasis

A

Improve OH
Tx systemic: immunosuppression, DM, anaemia, hypothyroidism
Live active yoghurt
Topical
- CHX m/w
- nystatin suspension
- miconazole gel; interactions, systemic absorption

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55
Q

Discuss erythematous candidiasis

A

Characterised by erythematous patches +/- pain
Common: D tongue + palate, occasionally B mucosa
Associated: chronic broad spectrum AB + corticosteroids, HIV

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56
Q

Discuss chronic hyperplastic candidiasis

A

Pre-malignant condition

  • Candida prod. nitrosamines -> malignant transformation
  • unTx: 5-10% dysplasia, may develop OSCCh

Chronic hyperkeratosis in which Candida identified
Common: middle age M smoker
Asymptomatic

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57
Q

Clinical findings of chronic hyperplastic candidiasis

A

B mucosa towards commissures w/ bilateral distribution
White to erythematous raised lesions
- don’t rub off
Nodular/speckled (inc. risk malignancy) or homogenous plaque-like
Possible angular cheilitis

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58
Q

Management of chronic hyperplastic candidiasis

A

Biopsy: risk malignant transformation 15%
FBC: Fe, folate, B12, glucose, TFT
Remove predisposing: smoking

Topicals not effective
2-4/52 oral fluconazole

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59
Q

Discuss chronic erythematous candidiasis

A

Denture stomatitis
Chronic erythema of mucosa beneath fit surface acrylic denture
- excludes saliva from mucosa + allow candidal overgrowth
- 65% denture wearers

Associated: poor denture/OH + ill fitting denture
Usually asymptomatic; except angular cheilitis

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60
Q

Clinical findings + management of chronic erythematous candidiasis

A

Clinical

  • marked erythema of P mucosa w/ sharply defined margin
  • relief area present -> underlying spongy, granular change
  • mistaken for acrylic hypersensitivity

Management

  • OH
  • eliminate trauma: tissue conditioner
  • miconazole gel applies to fit surface
  • no resolution = systemic or not compliant
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61
Q

Discuss angular cheilitis + aetiological factors

A

Symmetrical erythematous tissue @ angles of mouth/commissures

Elderly denture pt w/ denture stomatitis
Red. OVD + maceration of skin by saliva
C. Albicans, Staph. aureus, B-haemolytic Strep

Aetiology

  • red. haematinics: B12/folate/Fe
  • malabsorption: OFG, Crohn’s
  • immunosuppression
  • DM
  • xerostomia
  • ABs
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62
Q

Management of angular cheilitis

A 
Remove predisposing 
Correct OVD
Improve denture/OH
Address fissuring
Tx IO Candida 
Miconazole gel on corners of mouth
Chronic: trimovate cream (AB, antifungal, steroid)
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63
Q

Discuss medium rhomboid glossitis + chronic mucocutaneous candidiasis

A

Median rhomboid

  • chronic candidal infection w/ atrophy filiform papillae
  • asymptomatic diamond shaped smooth area ant. circumvallate papillae
  • associated smoking + corticosteroids
  • may have kissing lesion on palate

Chronic mucocutaneous

  • chronic candidal infections involving skin, nails, mucous membranes
  • associated w/ rare congenital conditions
  • aetiology: impaired cellular immunity
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64
Q

Discuss polyenes

A

Antifungal: fungicidal through interacting w/ ergosterol in membrane

Nystatin

  • inhibit ergosterol synthesis
  • no but absorption
  • adverse: irritation, sensitisation, nausea

Amphotericin

  • binds fungal membrane ergosterol; disrupt membrane
  • no gut absorption
  • IV: severe systemic infections
  • adverse: mild GI disturbance
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65
Q

Discuss azoles

A

Antifungals; fungostatic (have to remove predisposing too)
Inhibit lanosterol demethylase = prevent ergosterol synthesis
Resistance rising

Types

  • imidazoles
  • triazoles
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66
Q

Discuss imidazoles

A

Antifungals
Miconazole
- topical gel; mucosa, denture (inc. compliance)
- AB activity
- gut absorption: interaction w/ warfarin, statins

Ketoconazoles

  • rarely used
  • hepatotoxic
  • nonspecific: inhibit testosterone + cortisol synthesis
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67
Q

Discuss triazoles

A

Antifungals

Fluconazole
- better toxicity profile cf ketoconazole
- expensive
- contraindications: pregnant, breast feeding
- interactions: benzodiazepines, Ca channel blockers, warfarin, cyclosporin
Itraconazole
Vorticonazole

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68
Q

Define vesicle + bulla

A

Vesicle: small, fluid filled blister <5mm
Bulla: large, fluid filled blister >5mm

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69
Q

Clinical features of primary herpetic gingivostomatitis

A

HSV1
Prodromal: fever, malaise

Clinical 
- multiple herpetic oral ulcers
— 2-3mm vesicles erupt keratinised tissues
— rupture -> widespread painful ulcers; heal 7-10d
- diffuse gingivitis 
- cervical lymphadenitis 
- fever, malaise
- severe
— lip erosions
— lymphadenopathy  
— pharyngotonsilitis
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70
Q

Dx + management 1ry herpetic gingivostomatitis

A

Dx: clinical, possible viral culture

Management

  • supportive
  • antiviral if severe
  • CHX m/w; prevent 2ry bacterial infection
  • fluid intake
  • analgesic, antipyretic
  • prevent spread/limit contact
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71
Q

Discuss recurrent herpes labialis

A

Cold sores
40% pt experience recurrence

Prodrome: tingling/burning
Reactivation
- HSV1 dormant in DRG
- breakdown in local/systemic immunosurveillance
- trigger: UV, immunosuppression, trauma, post-op, infection, menstruation
Clinical
- vesicular eruption -> breakdown crusting lesion
- vesicles enlarge, coalesce, weep, rupture (2-3d), crust, heal (10d)

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72
Q

Prevention of recurrent herpes labialis

A

Suncream; red. freq.
Topical acyclovir/penciclovir
Severe/freq.: systemic prophylactic acyclovir

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73
Q

Discuss herpetic whitlow

A

HSV recurrence involving skin
Acquired from pt saliva

Highly infective
Intensely painful

Management

  • analgesic
  • elevation, splinting
  • systemic antiviral
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74
Q

Discuss erythema multiforme

A

Mucocutaneous blistering condition
Mucosal erosions + lip blistering w/ skin lesions
T3 hypersensitivity

Aetiology

  • drugs: NSAID, anti-epileptic, barbiturates, antifungals
  • infection: HSV, Hep, HIV
  • systemic: SLE, pregnancy, malignancy
  • idiopathic 50%
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75
Q

Clinical features of erythema multiforme

A

Sites: extremities, mucous membranes

Oral
- bullae on erythematous base
— breakdown rapidly -> irregular ulcers, bleed, crust
- lips freq.; swollen, bloody, crusted
- gingiva rare

Skin

  • erythematous macules + papules
  • target/iris: central pale area surrounding by oedema + bands of erythema
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76
Q

Discuss chickenpox

A

VZV/HHV3

Condition of children (90%)
Itchy maculopapular rash
- back, chest, face, limbs
- maculopapular -> vesicular -> pustular 
Initial site URT; droplet infection

Oral: erythematous ulcers of palate/fauces/uvula

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77
Q

Discuss shingles

A

Recurrence of VZV

Affect single dermatome, unilateral
Predilection for CN5/7
- oral/skin lesions if V2/3 affected
Occasionally underlying immunosuppression
- likely VZV lays in DRG or cranial nerve ganglion from childhood
- progressive + disseminated

Prodrome: pain, parathesia
Vesicles on erythematous base, scab, heal w/o scar

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78
Q

Discuss post-herpetic neuralgia and Ramsay-Hunt syndrome

A

Complications of VZV

Post-herpetic neuralgia

  • severe shooting pain
  • constant burning

Ramsay-Hunt

  • VZV affect geniculate ganglion CN7
  • ipsilateral LMNL; total paralysis
  • vesicular rash EAM
  • loss of taste ant. 2/3 tongue
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79
Q

Management of VZV

A

> 50y: antiviral (inc. risk PHN)

Commence within 72h rash

  • dec.: duration, pain severity + duration
  • red. neural damage; red. risk PHN

CNV1 assessment
Analgesics

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80
Q

Conditions caused by EBV

A

HHV4

Infectious mononucleosis 
Oral hairy leukoplakia 
Non-Hodgkin’s lymphoma 
Burkitt’s lymphoma 
Nasopharyngeal carcinoma
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81
Q

Discuss infectious mononucleosis

A

EBV

Kissing disease of teenager; salivary spread

Clinical

  • fever, malaise, weight loss
  • lassitude
  • generalised tender lymphadenopathy
  • pharyngitis
  • faucial oedema
  • cream tonsillar exudate
  • oral petechia: H/S P junction
  • gingival bleeding, ulcers
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82
Q

Dx + management of infectious mononucleosis

A

Dx: Paul Bunnell+; monospot+

Management

  • symptomatic
  • maintain fluid
  • antiseptic m/w
  • analgesic
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83
Q

Discuss oral hairy leukoplakia

A

Risk

  • immunocompromised
  • potent oral/inhaled corticosteroids
  • transplant pt

Clinical

  • demarcated corrugated white lesion
  • lat. border tongue

Management: control immunosuppression

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84
Q

Discuss measles

A

Paramyxovirus

Acute, contagious infection

Clinical
- fever, rhinitis, cough, conjunctivitis
- maculopapular rash
- Koplik’s spot; 1-2d pre-rash
— B/L mucosa, soft P
— irregular patchy erythema w/ tiny central white specks

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85
Q

Importance of Koplik’s spot

A

Pathognomonic of measles

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86
Q

Discuss mumps

A

Paramyxovirus

Painful swelling major salivary glands
— usually asymmetrical
Respiratory spread

Clinical

  • headache, nausea, fatigue
  • dry mouth, trismus
  • joint pain
  • pyrexia
  • mild abdominal pain
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87
Q

General features of hand, foot + mouth disease

A

CAV16 mainly
1ry childhood, highly infectious

Prodrome: mild systemic upset

Triad: macular + vesicular eruptions hands, feet + oropharyngeal mucosa

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88
Q

Oral + dermatological clinical findings + management of hand, foot + mouth disease

A

Oral

  • multiple shallow painless ulcers/vesicles
  • pharynx, S palate, B mucosa, tongue
  • rarely req. dental opinion
  • no lymphadenopathy, gingiva spared

Skin

  • erythematous macules + vesicles hands + feet
  • may be deep + blister
  • transient: 1-3d

Management

  • supportive
  • antiseptic m/w
  • self resolving
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89
Q

Discuss herpangia

A

CAV2/4/5/6/8
Childhood

Clinical: mild
- sudden onset pyrexia + pharyngitis 
- oral: 2d
— multiple papules, vesicles, ulcers on S palate + fauces
— salivary glands: swelling, pain

Management

  • no active Tx
  • self resolving: 10d
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90
Q

Clinical features of HPV

A

Human papillomavirus

HPV2/4: most commonly cause mucosal warts

Butcher’s warts: hands, fingers (HPV7)
Verruca vulgaris (HPV2/4)
- white warty lesions w/ granular surface (cauliflower appearance)
- auto-inoculation from fingers: L mucosa, palate, lingual frenum
Condyloma acuminatum (HPV6/11/60)
- soft pink papillary lesion
- venereal contact: labial + lingual mucosa
- multiple lesions

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91
Q

Management of HPV

A

Tx all sites simultaneously
May resolve spontaneously

Surgical excision
Cryotherapy
Laser Tx
Medical Tx: inc. immune system

92
Q

Discuss Kaposi’s sarcoma

A

Cancer of endothelium (blood vessels)
Associated HHV8

Site: skin, eye, mouth, nose, mucosa
Clinical
- reddy-blue/purple macules/nodules
- may ulcerated

Pathognomonic of AIDS

Tx: ART

93
Q

Discuss affect of haematinic deficiencies on oral mucosa

A

Clinically mild B12/folate/Fe deficiency -> generalised epithelial atrophy + depapillation D tongue
Altered epithelial metabolism -> abnormal structure + keratinisation
Filiform papillae sensitive -> soreness, red. taste, ulcer, candidiasis

94
Q

Oral conditions associated w/ haematinic deficiencies

A 
Glossitis 
- smooth, depapillated (Fe)
- raw, beefy (B12, folate)
Angular cheilitis, candidiasis
Recurrent Oral Ulceration
- B12/Fe/Folate in 20%
- typically normal Hb +/- altered MCV
Burning mouth 
Plummer-Vinson syndrome
95
Q

Discuss Plummer-Vinson syndrome

A

F

Characterised by

  • Fe anaemia
  • post-cricoid web
  • glossitis

Inc. incidence oropharyngeal carcinoma

96
Q

Effects of malnutrition on mucosa

A

Protein Energy Malnutrition

  • impairment of non/specific immunity
  • ascorbate deficiency
  • inc. blood + saliva free corticosteroids

Retinol/Zn

  • diminished cell mediated immunity
  • early breakdown oral mucosa integrity

Ascorbic Acid

  • impaired phagocytosis
  • altered Ab response to viral Ag
97
Q

Oral signs of alcoholism

A

Sialosis (nonspecific gland enlargement)
Erosion (2ry reflux)
Liver cirrhosis signs: easy bruising, prolonged bleeding
Malnutrition

98
Q

Discuss bulimia nervosa

A

Obsessive control of weight
- repeated bouts of over eating then purging

Typically young F, 20s

Clinical

  • weight: normal range
  • hypokalaemia: repeated vomiting
  • sialosis
  • erosion
  • Russel’s sign: calluses D hand
  • ulcers S palate
  • angular cheilitis
99
Q

Risk factors + clinical signs acute necrotising ulcerative gingivitis

A

Risk

  • poor plaque control
  • malnutrition
  • smoking
  • stress
  • immunocompromised

Clinical

  • punched out ulcers tip of interdental papilla; readily bleed
  • necrotic slough covering interdental papilla
  • lymphadenopathy
100
Q

Aetiology + predisposing factors of necrotising stomatitis

A

Noma

Aetiology: bacterial

  • porphyromonas gingivalis
  • fusobacterium nucleatum
  • prevotella intermedia

Predisposing

  • poverty, proximity to livestock
  • poor OH
  • measles
  • malaria
  • PEM + vit(A,B)/Zn deficiency
  • disease: AIDS, VZV, CMV
101
Q

Clinical features of noma

A

Necrotising stomatitis

Putrid odour
Rapid devastating necrotising destruction of soft/hard tissues

Acute

  • oedema
  • cheek perforation
  • 2ry infection -> rapid death

Chronic

  • fibrous scar
  • oral strictures
  • trismus
  • dental malposition (tooth movement)
  • salivary incontinence
102
Q

Discuss VitC deficiency

A

Essential collagen synthesis cofactor

Clinical
Initial: enlargement + keratosis follicles -> cork screw hairs
Later
- blood vessel proliferation around follicles + interdental papilla
- gingival hyperplasia w/ haemorrhage
- tooth mobility + exfoliation
- cutaneous bleeding + purpura

103
Q

Causes of Zn deficiency

A

Moderate

  • malabsorption
  • deficient diet
  • chronic renal disease
  • sickle cell disease

Severe

  • acrodermatitis enteropathica
  • post-penicillamine Tx
104
Q

Clinical signs of Zn deficiency

A

General

  • diarrhoea, lost appetite
  • lethargy, depression
  • pustular bullous dermatitis
  • alopecia
  • retarded growth
  • hypogonadism
  • poor wound healing

Oral

  • delayed wound healing
  • hypogeusia
  • angular cheilitis
  • candidal superinfection
  • perioral psoriasiform
  • erythema migrans
105
Q

What is coeliac disease?

A

Genetically determined chronic inflammatory small intestine disease due to gluten sensitivity

106
Q

Clinical findings of coeliac disease

A

General

  • malabsorption w/ chronic diarrhoea
  • weight loss
  • abdominal distension
  • fatigue
  • childhood anaemia
  • LP exacerbation

Oral

  • recurrent oral ulceration
  • dental hypoplasia
  • glossitis, burning mouth
  • angular cheilitis
107
Q

Occult manifestations of coeliac disease

A 
Metabolic bone disease
Fe/folate deficiency 
Infertility 
Autoimmune disease: Sjögren’s, DM
Malignancy: SCC, NHL
108
Q

Disease dental hypoplasia seen in coeliac disease

A 
96%, children 83% adults
Enamel defects; symmetrically + chronologically distributed 
Mild enamel defects
- rough surface
- horizontal grooves
- shallow pits
109
Q

What is Crohn’s disease? Aetiology

A

Chronic aggressive inflammatory bowel disease
Discontinuous (‘skip lesions’) pattern of transmural inflammation
Affect whole GIT w/ large ulcerations + occasional granulomata

Aetiology: unknown

  • genetic: NOD2
  • environmental: enteric microflora, nutrition
  • host immune response
110
Q

Oral features of Crohn’s

A 
Gingival swelling + mucosal tags
Cobblestone mucosa; ulcerated fissures
Lip swelling: diffuse, soft, non-tender
Angular cheilitis
Persistent irregular ulcers, ROU
111
Q

What is orofacial granulomatosis?

A

Predominantly labial swelling associated w/ granulomatous inflammation
Continuum
- overt Crohn’s chronic granulomatous cheilitis Melkerson-Rosenthal syndrome

112
Q

Clinical features of orofacial granulomatosis

A

Non-tender recurrent lip/lower face swelling
- eventually becomes persistent
Lymphadenopathy

Angular cheilitis 
Ulceration 
Vertical labial fissures
Mucosal tags
Tongue fissuring
113
Q

Management of orofacial granulomatosis

A 
Spontaneous remission unusual 
Diet: exclude benzoate, cinnamon 
Corticosteroids
Topical tracolimus 
Thalidomide
Adalimumab
114
Q

Discuss Peutz-Jeghers syndrome

A

Rare, autosomal dominant
Multiple small perioral + vermillion freckles
Pigmented spots: IO, extremities, nasal + rectal mucosa
- no risk of melanoma
Hamartomatous intestinal polyps: abdominal pain + rectal bleeding
- risk internal malignancy: gut, breast, genital

115
Q

Discuss black hairy tongue

A

Localised oral pigmentation

Aetiology

  • elongation of filiform papillae
    • extrinsic staining
    • overgrowth pigment prod. bacteria/fungi

Associated

  • smoking
  • antiseptic m/w
  • ABs

May alternate w/ white hairy tongue

Management

  • reassure + info
  • OH
  • smoking cessation
  • tongue brushing: avoid over brushing
  • oxidising m/w
116
Q

Discuss amalgam tattoo

A

Aetiology

  • XLA amalgam filled tooth
  • removal amalgam filling

Site

  • mandibular gingiva
  • alveolar mucosa

Slate grey, black/blue macules
No elevation
No size change; margins may blur

Histology

  • lamina propria: fine granular black/brown pigment encases elastic fibres + basement membrane fo superficial capillaries
  • within cytoplasm of histiocytes
117
Q

Discuss graphite tattoo

A

2nd most common exogenous cause localised oral pigmentation

Ant. palate children

Biopsy: mandatory to rule out malignancy

  • abundance granulation tissue
  • destruction of labial cortical bone 1s
  • residues of solid black granules

Histology

  • mild chronic inflammatory cell infiltrate
  • multinucleate giant cells
  • solid granules consistent w/ pencil graphite
118
Q

Management of amalgam/graphite tattoo

A 
X-ray: amalgam in tissue
Reassure: not health hazard
Observation 
Excision: clinical doubt 
Q-switched ruby laser: shatters particles
119
Q

Discuss metallic salt deposition

A

Metallic sulphide deposition along gingival margin
- bismuth, Pd, mercuric salts
Salts in crevicular fluid precipitate as sulphides by H2S from bacteria
Pd/Burton’s lines: linear grey/black lines along gingival margin

120
Q

Discuss oral melanotic macule

A 
F>M
Benign, localised areas of pigmentation 
Focal inc. melanin prod.
Uniformly flat black/brown macule
Distinct borders, <5mm

Site

  • any mucosal surface; OC rare
  • lip lesion; reaction to sun damage

Management

  • benign
  • remove: Dx, avoid long term follow up
  • lip: monitored if no suspicious feature
121
Q

Discuss oral melanoma

A

Rare: 1-2% all melanomas

Site

  • palate common
  • any site
  • lips, gingiva

Clinical

  • darkish brown/black; 30% amelanotic
  • irregular poorly defined borders
  • irregular colour distribution
  • thickening
122
Q

Prognosis of oral melanoma

A

Poor: 5-20% 5yr survival

Late Dx
Early metastasis; rich blood + lymphatics
- lungs
- liver
- lymph node
Aggressive histology 
Difficult local clearance
123
Q

Discuss ecchymosis

A

Brushing
Red/blue
Hx: trauma
Spontaneous: underlying platelet/coagulation disorder

124
Q

Discuss varices

A

Abnormal venous dilation
Site: lip, sublingual

Clinical 
- painless
- blue, lobulated
- blanch
- thickened + hard
— thrombosis w/ calcified phleboliths

Management

  • observation
  • excision
  • sclerotherapy, laser ablation
125
Q

Aetiology of Peutz-Jegher’s syndrome

A

Mutated LKB1 gene on chromosome 19

Codes serine-threonine kinase

126
Q

Management Peutz-Jegher’s syndrome

A

No Tx req.
- no melanoma transformation

Counselling + monitoring

Risk internal malignancy: gut, breast, genital

127
Q

Discuss racial pigmentation

A

POC; 5% Caucasian

Mostly gingiva (1s), any mucosa poss
Generalised
A/symmetrical

128
Q

Discuss betel nut pigmentation

A

Areca nut pigmentation mucosa + teeth
Yellow/orange/brown

Risks

  • TSL
  • staining
  • lichenoid reaction
  • submucous fibrosis
  • epithelial dysplasia
  • OSCC
129
Q

Discuss paan use

A

Combination: betel nut, leaf, slaked lime, spices, tobacco
All carcinogenic
Severe attrition

130
Q

Management of betel nut/paan user

A

Info
Cessation advice
NRT
Biopsy if req.

131
Q

Discuss post-inflammatory hyperpigmentation

A 
Post-mucosal irritation + inflammation 
- inc. pigmentation during healing phase 
Usually generalised
Common: chronic LP B mucosa 
Histology: melanin drop out
132
Q

Discuss mediation related hyperpigmentation

A

Many medications + mechanisms
Mechanisms
- IO inflammatory reaction
- stim. melanin: arsenic combine w/ thiols groups
- react w/ melanin: phenothiazines + minocycline

S:

  • palate
  • B mucosa
  • gingiva

Management: drug cessation

133
Q

Examples of drugs causing hyperpigmentation

A

Blue-Grey

  • chloroquine
  • minocycline
  • fluoxetine
  • amiodarone

Brown

  • bleomycin
  • busulphan
  • cyclophosphamide
  • minocycline
  • doxycycline
  • aziodthymidine
  • propranolol
134
Q

Discuss Addison’s disease

A 
1ry adrenal insufficiency 
- autoimmune
- infection: HIV, TB, sarcoidosis 
Adrenal cortical atrophy + insufficiency 
- dec. cortisol + aldosterone

Hyperpigmentation: 2ry melanocyte stim. by inc. ACTH
Streaks/patches of blue/black pigmentation (water spaniel)

Management: steroid replacement therapy

135
Q

Clinical features of Addison’s disease

A 
Cutaneous bronzing sun exposed sites
- hyperpigmentation scars + flexures
Genital pigmentation 
Vitiligo 
Hypotension
Hypoglycaemia
Salt craving
Weight loss, lethargy 
Nausea, vomiting
136
Q

Discuss Cushing’s disease

A 
Aetiology: inc. ACTH secretion from ant. pituitary gland
Clinical
- cataract
- hypertension
- hirsuitism
- hyperglycaemia
- skin thinning
- ulcers
- hyperpigmentation
137
Q

What is Nelson’s syndrome?

A

Condition following removal both adrenal glands due to Cushing’s syndrome
Macro-adenomas develop which prod. ACTH

138
Q

Discuss McCune-Albright syndrome and hyperthyroidism

A

Albright
- genetic disorder; mutation of GNAS gene
- affect: bone, skin, endocrine system
- clinical
— fibrous dysplasia
— cafe au lait macules
— hyper-functioning endocrine; Cushing’s, hyperthyroidism

Hyperthyroidism

  • tachycardia
  • heat intolerance
  • palmar sweating
  • weight loss, inc. hunger
  • diarrhoea
139
Q

Discuss lichen planus; epidemiology, aetiology, symptoms

A

Epidemiology

  • 1-4% popn.
  • 0.5-2% oral
  • oral chronic: 4-25y
  • skin: 18/12

Aetiology

  • immunologically mediated
  • cytotoxic T cell
  • basal keratinocytes targeted; Ag unknown
  • related: stress, spice, DM, liver disease

Symptoms

  • asymptomatic
  • pain/discomfort w/ spice/citrus
  • aesthetics concerns
140
Q

Discuss oral LP

A

Reticular: white lines, asymptomatic
Erythematous/Atrophic: superficial redding due to mucosal thinning
Erosive/Ulcerative: painful, chronic
Symmetrical: skin + oral

S: B mucosa, tongue, gingiva
- palate rare

141
Q

What is Koebner phenomenon?

A

Feature of LP

Lesion in areas of inc. friction; flexures, O line

142
Q

Discuss extra-oral forms of LP

A 
Cutaneous
- flexure surfaces wrists + shins
- symmetrical, bilateral 
- koebner phenomenon 
- wickham’s striae: surface network fine white lines
- purple pruritic polygonal papules + plaques 
— red -> violaceous
— flat topped
— few mm

Nails: 10%

  • longitudinal pitting + grooving
  • reversible
  • possible onycholysis

Lichen planopilaris: scarring alopecia

143
Q

Discuss vulvovaginal-gingival syndrome

A 
Severe variant of LP
Often unrecognised
Usually ulcerative + symptomatic 
- desquamation of vulval, gingival + gingival mucosa 
Progressive vulval disease -> scarring
Malignant transformations reported
144
Q

Histological features of LP

A 
Subepithelial band of inflammatory cells
- lymphocytes 
Basal cell liquefaction/degeneration 
\+/- hyperkeratosis
Saw tooth rete ridges in epidermis
145
Q

Management of LP

A

No cure

  • red. inflammation + pain
  • prevent complications

Asymptomatic: reassure, GDP review

Symptomatic
- remove provoking 
- red. irritation: spice, acid
- OH
— desquamative gingiva may prevent OH
— alternative OH; alcohol free corsodyl
146
Q

Medications for LP management

A

Corticosteroids: 1st line

  • topical/systemic
  • risk suppression HPA
Topical Calcineurin inhibitors 
- protein in synthesis IL2
— viral for T-cell activation 
- cyclosporine 
- tacrolimus
- pimecrolimus
147
Q

What is lichenoid reaction?

A

Condition clinically + histologically similar to LP w/ identifiable aetiology
No pathognomonic histology

Uni/bilateral
May be ulcerative
Dx: withdraw drug

148
Q

Clinical features of lichenoid reaction

A

Clinical

  • soreness similar to LP esp. erosive
  • indistinguishable from LP
  • asymmetric; if due to local cause
  • more likely erosive + palate/tongue

Oral Contact Hypersensitivity Reaction

  • sensitised to DM component
  • Au, bisGMA, Am, Hg, Ni
  • S: mucosa in direct contact
  • patch test+
149
Q

Histology of lichenoid reaction

A

Similar to LP

Infiltrate may be deeper + less defined
Poss more plasma cells + eosinophils 
Perivascular infiltrate possible 
Colloid bodies + basal cell Ab in epithelium 
Consider bale basal cell liquefaction
150
Q

Management of lichenoid reaction

A

Drug Hx + T relationship important
Patch test if local
Withdraw drug
As LP until resolution

151
Q

Discuss discoid lupus erythematous

A

Chronic indolent disorder
Cutaneous + oral

Aetiology

  • autoimmune
  • may be precipitated by drug/environment/viral/hormonal
  • auto-Ab + cell mediated immunity against cellular components
152
Q

Cutaneous + oral features of DLE

A 
Cutaneous 
- sun exposed sites
- 1/+ oval plaques on face/scalp/hands
- well demarcated red, atrophic scaly plaques 
— w/ keratin plugs in dilated follicles 
- generalised telangiectasia 
- scarring -> alopecia + pigmentation

Oral

  • less well demarcated erythematous ares surrounded by fine white striae
  • may ulcerate; active or in those progress to SLE
  • bilateral on L/B/alveolar mucosa, vermillion border
  • palate: SLE
153
Q

DLE histology

A

Ortho/parakeratosis
Liquefaction of basal layer
Hyalinisation of subepithelial connective tissue
Chronic inflammatory infiltrate in subepithelial tissue
Irregular acanthosis
Civatte/colloid bodies
Keratotic plugging

154
Q

Management of DLE

A

Oral: LP

Cutaneous

  • chloroquine + potent topical steroids
  • sunblock useful but not sufficient
  • others: cytotoxics, dapsone, thalidomide, retinoids
155
Q

Discuss graft v host disease

A

Common, serious complication follow allogeneic bone marrow transplantation
- within 6-24/12 post-BMT
Graft lymphocytes against recipient host cells

Risk

  • poorly matched graft
  • old donor/recipient
156
Q

What is graft v leukaemia affect?

A

Ability of donor immune cells to eliminate/keep underlying disease in long term remission

157
Q

Clinical features GvHD

A 
May be asymptomatic 
Burning oral discomfort
- lesions: reticular/ulcerative/erosive
Salivary gland involvement -> oral dryness
- superficial palatal + labial mucocele 
Red. opening following sclerotic GvHD
158
Q

Management of GvHD

A

Topical analgesic: lidocaine, benzydamine
Corticosteroids: betamethasone m/w, fluocinonide/clobetasol gels
Tacrolimus ointment

Regular monitoring as OSCC inc. risk

159
Q

What is pemphigus vulgaris?

A

Chronic organ specific autoimmune blistering disease

Aetiology: T2 hypersensitivity
- circulating + bound IgG auto-Ab against desmosome adhesins
— dissolution of cell-cell adhesion
- diet: garlic, onion, leaks, mustard
- medication: thiol containing drugs; penicillamine, captopril

160
Q

Clinical features of pemphigus vulgaris

A

Nikolsky sign: blisters rapidly breakdown -> erosions
Desquamative gingivitis (60%)
Fragile blisters; slow healing
Dysphagia, odynophagia

Oral

  • bullae fragile + short lived
  • large shallow non-healing ulcers
  • S: P, B mucosa, gingiva

Cutaneous

  • large, non-healing erosions + ulcers
  • 3-4/12 post-oral lesions
  • frank blisters rare
161
Q

Ix and histological features of pemphigus vulgaris

A

Ix

  • biopsy of para-lesional and/or normal tissue
  • routine histology
  • blood for indirect immunofluorescence

Histology
- intraepithelial clefting + acantholysis
- intact bullae: clumps of acantholytic cells (Tzank cells)
- keratinocytes immunofluorescent+
— auto-IgG against desmoglein 3 in desmosomes in supra/basal keratinocytes

162
Q

Management of pemphigus vulgaris

A

Systemic corticosteroids: prednisolone, deflazacort
Steroid sparing: azathioprine, cyclosporine, mycophenolate mofetil
Topical: potent corticosteroids
IV Ig
Plasmaphoresis

163
Q

What is mucous membranes pemphigoid?

A

Chronic rare autoimmune blistering disease
Aetiology: unknown
Affects middle age-elderly; F>M

Circulating + bound Ab against basement membrane zone
- BP180/230 Ag in hemidesmosomes

164
Q

Clinical features of mucous membrane pemphigoid; oral, ocular

A

Predominately mucosa, skin rare
Full thickness epithelium lifts off connective tissue
Large, tense bullae (blood filled) -> chronic, painful erosion

Oral

  • S: any, lip rare
  • nikolsky+
  • blister rupture rapidly -> irregular pseudomembrane-covered painful erosions
  • desquamative gingivitis
  • chronic soreness, bleeding, dysphagia
  • scarring uncommon
Ocular 
- lead to blindness 
- chronic conjunctivitis 
- blurring, irritation, photophobia
- excess tears
- unilateral -> bilateral within 2y
- repeated fibrosis leads to scarring
— symblepharon, entropion, trichiasis, blindness
165
Q

Other sites of mucous membrane pemphigoid

A

Skin: rare 30%

  • scalp: scarring alopecia
  • face, neck, L trunk

Genital: 30%; sexual + urinary dysfunction

Larynx + oesophagus: infreq.

166
Q

Mucous membrane pemphigoid Dx + Tx

A

Dx
- exam, histology, biopsy + immunofluorescence
— sub-basilar split
- DIF
— homogenous linear IgG/C3 deposits in BMZ along dermo-epidermal junction

Tx

  • often resistant
  • topical corticosteroid: betamethasone, clobestasol
  • systemic corticosteroid
  • dapsone
  • anti-inflammatory AB: doxycycline, minocycline
  • immunosuppressants: azathioprine, cyclophosphamide
167
Q

Discuss bullous pemphigoid

A

Auto-Ab against hemidesmosomes
Elderly

Clinical

  • skin, mouth rare
  • erythema + blisters; last long T
  • large, tense blisters
  • preceded by itchiness
  • erosions, scarring not prominent

Management

  • topical/systemic steroids
  • anti-inflammatory AB, dapsone
  • ocular exam req.
168
Q

Clinical features dermatitis herpetiformis

A

Rare
Chronic pruritic papulovesicular rash

Younger age group
Associated: coeliac disease

Clinical

  • smaller bullae + vesicles (herpetiform appearance)
  • small blisters on urticated base
  • S: bum, elbows, knees
  • oral: superficial transient blisters -> nonspecific tender ulcers
169
Q

Ix + Tx of dermatitis herpetiformis

A

Histology: localised splitting at BMZ
Speckled/granular IgA immunofluorescence involving BM of dermal papillae

Tx: diet restriction + dapsone

170
Q

Discuss linear IgA disease

A

Chronic autoimmune blistering disease
Mucocutaneous
Oral + ocular common

DIF: linear IgA deposits are epithelium CT junction w/ separation at BMZ
Tx: dapsone, steroids

171
Q

Discuss angina bullosa haemorrhagica

A

Aetiology: unclear, old

  • genetic: loose adhesion b/w epithelium + corum of mucosa
  • inhaled steroid: mucosal atrophy -> dec. epithelium elastic fibres
  • DM: vascular fragility

Large, IO blood filled blisters
Feels like choking

172
Q

Clinical features of angina bullosa haemorrhagica

A 
Solitary, large (2-3cm) blood filled blister 
Develop suddenly
S: H+S palate junction 
Burst spontaneously within 24h
Superficial ulcerative area

Resolve: 7-10d
Recur 5-10 episodes over few yr

173
Q

Management of angina bullosa haemorrhagica

A

FBC/coagulation screen

Symptomatic: benzydamine, CHX m/w

Large, intact blisters: incised to avoid respiratory arrest

174
Q

Discuss epidermolysis bullosa

A 
Genetic collagen defect disease
Many forms
- lethalis: incompatible w/ life
- dystrophica: recessive, skin/mucosa fragility 
- simplex: least severe
175
Q

Oral feature of epidermolysis bullosa

A 
Mucosal fragility 
Minor trauma = mucosa separate from CT
Scarring -> severe deformity 
Severe forms
- OH, dental care, eating problematic
176
Q

Discuss epidermolysis bullosa simplex

A

Most common: 92%

Blisters @ sites of friction
- hands, feet common
Multiple types

Dominant: keratin KRT5/14 affected
- keratinisation failure -> red. integrity + ability resist mechanical stress

Management

  • no cure
  • symptomatic + protection
  • topical/systemic corticosteroid
177
Q

Discuss epidermolysis bullosa acquisita

A 
30-40y, F>M
Autoimmune: associated 
- Crohn’s 
- SLE
- amyloidosis 
- multiple myeloma

Trauma -> widespread blistering w/ scarring
Subepidermal blisters
DIF: linear IgG deposits

Tx

  • corticosteroids
  • immunosuppressants
  • dapsone
178
Q

Define pain

A

Unpleasant sensory + emotional experience associated w/ actual/potential tissue damage or described in such terms

179
Q

What is orofacial pain?

A

Pain in area

  • above neck
  • ant. to ears
  • below orbitomeatal line

Incl. OC

180
Q

What chronic pain?

A

Pain persisted >3/12, outlived usefulness
Disease of neuromatrix
Cure unlikely; disability caused can be red.

181
Q

Difference b/w chronic + persistent

A

Chronic: any never go
Persistent: not intractable

182
Q

What are TMDs?

A

Temporomandibular joint disorders
Musculoskeletal disorder involv. MoM and/or TMJ

Incl.

  • myosfacial pain disorder
  • TMJ disc interference; displacement w/ or w/o reduction
  • TMJ degenerative joint disease
183
Q

Risk factors for TMJD

A 
F 18-44
Depression, psychological distress
Exogenous hormones 
Facial trauma
Sleep problems 
Bruxism 
Multiple pain disorders
184
Q

Hx of TMJD

A 
S: uni/bilateral, TMJ area
C: dull, aching, throbbing 
R: pre/post-auricular, MoM
A: stress, clicking, tenderness
T: intermittent/constant
E: opening, chewing, yawning
A: sleep, analgesic 
S: mild-mod.
185
Q

Indicators of TMJ degenerative change

A 
Clicking
Crepitus 
Limited movement, locking
Momentary hesitation 
Sudden inability to fully close
186
Q

Pt self management methods for TMD

A 
Empowerment
Warm joints
Attention to parafunctional habits 
Jaw exercise
Relaxation 
Massage
Simple analgesic
187
Q

Pharmacological TMD management

A 
Analgesics
- opioids 
- NSAIDs
- paracetamol 
Corticosteroids
- iontophoresis 
- intracapsular injection

Antidepressants
Sedatives
Anxiolytics
Muscle relaxants

188
Q

Adjunctive therapies for TMD

A 
Splint
Acupuncture
CBT
Physiotherapy 
Botox
189
Q

What is persistent idiopathic facial pain?

A

Poorly localised pain w/ widespread radiation
Associated w/ repeated unsuccessful dental Tx (XLA) due to belief that is chronic dental pain

Initiation + persistence

  • dental Tx
  • prolonged dental pain
  • severe dental infection
  • stress
190
Q

Associated features and risk factors for PIFP

A

Associated

  • IBS
  • head, neck/backache
  • dysmenorrhea
  • pruritus
  • fatigue
  • sleep disturbance

Risk: F

  • genetic
  • widespread pain
  • passive coping traits
191
Q

Hx of PIFP

A

S: uni/bilateral; no anatomical area, poorly localised
C: dull, nagging, throbbing, aching, sharp
R: H+N, down arms
A: pain, personality change, life events
T: constant/intermittent
E: chewing, dental/stress, cold weather
A: rest, relaxation
S: mod-severe

192
Q

What is atypical odontalgia?

A

Pain associated w/ tooth/edentulous ridge w/o clinical or radiographic finding

193
Q

Hx of atypical odontalgia

A 
S: tooth/edentulous ridge; UP/M most common
O: dental Tx (>80%)
R: well localised, may move tooth 
T: persistent 
S: mod
194
Q

Management of atypical odontalgia

A

Key: convince pt no current dental cause
Stop ongoing dental interventions/XLAs

TCA: amitriptyline, nortryptiline
Gabapentin/pregabalin

195
Q

What is burning mouth syndrome?

A

Idiopathic burning pain/discomfort in pt w/ clinically normal mucosa and in which medical/dental cause excluded

196
Q

Hx of burning mouth syndrome

A

S: lips, tongue, palate (whole mouth)
C: burning, tiring, smarting, annoying, tender
A: dryness, dysgeusia, depression, anxiety, F>50
T: constant/intermittent, worse pm
E: eating, tension
A: eating, rest, distraction
S: mild-mod

197
Q

Pathophysiology of burning mouth syndrome

A

Hormonal

  • menopause: red. gonadal + neuroactive steroids
  • chronic anxiety + stress impair HPA a is = red. adrenal steroids
  • neuroprotective effect lost
  • oral nerve terminal neurodegenerative change

Dysguesia

  • neuropathic changes affect gustatory nervous system (esp. chorda tympani)
  • lose inhibitory control of small fibre afferents (responsible for burning)
  • inhibition of glossopharyngeal nerve lost -> taste phantoms + altered pain/touch
198
Q

Management of burning mouth syndrome

A 
Reassurance: physiological cause
Symptomatic 
- saliva substitute 
- benzydamine m/w
TCA, SSRI
CBT
Allhalipoic acid, gabapentin, clonazepam
199
Q

Hx glossopharyngeal neuralgia

A 
S: unilateral, RHS more common
C: stabbing
R: ear, base of tongue, tonsillar fossa, beneath angle of jaw 
A: syncope, arrhythmias
T: transient, remission may occur
E: swallowing, chewing, speaking, coughing
A: pulling on ear
S: severe
200
Q

Difference b/w 1/2ry glossopharyngeal neuralgia + aetiology

A

2ry has persistent background aching + exacerbations

Aetiology

  • 1ry: nerve compression
    2ry: congenital vascular abnormality/tumour/aneurysm
201
Q

What is Eagle syndrome?

A

Glossopharyngeal neuralgia differential
Due to elongation of stylohyoid process (age, trauma) compression CN5/9/1

Clinical

  • shooting pain of throat, ear, jaw
  • pain of tongue base
  • worse on swallowing, turning head
  • tinnitus, hypersalivation, feeling of something stuck in throat

Tx: styloidectomy

202
Q

What is trigeminal neuralgia?

A

Sudden, unilateral, severe, brief, recurrent stabbing pain in 1/+ branches of CN5

Rare: 50-60y

  • M: 108/mil
  • F: 200/mil
203
Q

Hx of trigeminal neuralgia

A

S: CN5; unilateral (97%), RHS (60%)
C: flashing, shooting, sharp, unbearable, terrifying
A: trigger zones, weight loss
T: seconds, remission wks/mnths
E: light touch, eating, talking, spontaneous
A: avoid touch, anticonvulsants, sleep
S: mod-severe

204
Q

Aetiology of trigeminal neuralgia

A

Idiopathic

Aberrant cerebellar artery compressing nerve root @ root entry zone

205
Q

Discuss multiple sclerosis + post. fossa tumours in relation to trigeminal neuralgia

A

MS: demyelination of nerve fibres

  • 1-5% have TN
  • present younger cf TH (20-40)
  • likely bilateral
  • therapy response poor

Post. Fossa Tumours

  • meningiomas, neuromas
  • 2% have TN
  • facial numbness
  • MoM weakness
  • may be constant
206
Q

Pharmacological management options for trigeminal neuralgia

A

Carbamazepine (gold)
Oxcarbazepine
Lamotrigine
Baclofen

207
Q

Discuss carbamazepine use for trigeminal neuralgia

A

70% pt have pain red.
Failure usually due to inc. severity

Inc. dose slowly
- 300-800mg QTD

Adverse

  • drowsiness
  • dizziness
  • nausea, constipation
  • diplopia, blurred vision
  • ataxia
208
Q

What is giant cell arteritis?

A

Granulomatous arteritis affect M/L arteries esp. extracranial branches of carotid
- temporal most freq.

209
Q

Clinical features of giant cell arteritis

A 
Elderly pt new on sent/type of headache
Carotidynia 
Superficial temporal arteries
- thickened 
- tender
- nodular
- erythematous 
Ophthalmic
- diplopia
- blurring 
- amaurosis fugax (temp. loss of vision)
- obscuration
210
Q

Associated features giant cell arteritis

A 
Tongue/jaw claudication whilst chewing
Rare
- necrosis tongue/scalp
- toothache
- trismus 
General
- pyrexia 
- fatigue
- weight loss
Polymyalgia (50%)
Ischaemic limb pain, angina, thoracic + abdominal aneurysm
211
Q

Giant cell arteritis histology

A

Inflammatory cell infiltrate
Giant cells
Thrombus
Arterial wall hyperplasia

212
Q

Management of giant cell arteritis

A

Corticosteroids
Ca + VitD supplements

Visual loss improves in only few pts

213
Q

Causative species + transmission of syphilis

A 
Causative: treponema palladium 
Transmission
- venereal: close contact w/ lesion (main)
- blood: IVDU
- vertical: mother-child
214
Q

Discuss 1ry and 2ry syphilis

A

1ry: 3-4/52 post-infection
- chancres: 1st symptom
— infectious, firm, painless nodule @ inoculation site
— breakdown -> painless sore/ulcer
— resolves spontaneously 2-6/52
— S: genital, oral
- lymphadenopathy: neck, groin, armpits

2ry: 2-6/12
- non-itchy maculopapular rash
- sore throat, several weeks
- condylomata lata
- general
— tiredness, headache
— fever
— weight loss
— patches of hair loss
— joint pain
- followed by latent period; last several years

215
Q

3ry syphilis

A

3-15 post-infection

Gummatous: eyes, heart, liver (any organ)
- gummas: necrotic centre surrounded by inflammation
— painless
— OC: palate
Neurosyphilis: brain, nerves
CV syphilis: blood vessels

Complications

  • blindness, deafness
  • dementia
  • stroke, heart disease
  • paralysis

Potentially life threatening

216
Q

Dx + management of syphilis

A

Dx

  • Hx + exam
  • serology: syphilis Ab
  • swab: sores/ulcers
Management
- referral to GUM
- partners informed
- ABs
— early syphilis: penicillin, doxycycline 
— late: IV penicillin
217
Q

HIV virus + transmission route

A

Lentivirus, retrovirus

Transmission

  • general
  • blood: IVDU
  • vertical: perinatal
218
Q

Pathogenesis of HIV

A

Attach to CD4 R on T helper lymphocytes; gain entry into cell
RNA -> DNA (reverse transcriptase) = viral replication + assembly
Cell lysis -> infect other cells
- cells destroyed or stop functioning

Immune system cells HIV particles and infected cells, lost T cells replace

219
Q

Discuss stage 1 and 2 of HIV infection

A

1: 1ry infection
- lasts few wks
- short, flu-like illness
- 20%: serious enough to consult Dr; Dx missed
- large amount HIV in peripheral blood
- seroconversion: immune system prod. HIV Ab + cytotoxic lymphocytes
— test before seroconversion = false -ve

2: Clinically Asymptomatic
- 10yrs, no major symptoms (lymphadenopathy)
- peripheral blood HIV drops
— remain infectious, Ab detectable in blood
- not dormant: v active in lymph nodes
- many T cells infected + die, lots HIV prod.
- viral load test: measure HIV escapes lymph nodes (accurate to 50copies/mL)

220
Q

Stage 3 and 4 of HIV

A

3: Symptomatic
- immune system loses struggle
— lymph nodes + tissues damaged
— HIV mutates: more pathogenic + stronger -> more T cell destruction
— failure to adequately replace T cells
- symptoms develop as immune system fails

4: AIDS
- immune system more damaged + illness more severe
- Dx: HIV+ pt develops 1/+ opportunistic infection/cancer
- CDCP: CD4 <200/microL

221
Q

What opportunistic infections are diagnostic for HIV?

A 
Pneumocystis carinii 
- most freq.
- pneumocystis carinii pneumonia; rarely disseminates 
CMV
HSV
Toxoplasmosis 
Fungal
Mycobacterium
222
Q

Importance of oral manifestations of HIV

A 
Can indicate HIV
Predict progression HIV->AIDS
Entry/endpoint in therapy/vaccine trials
Determinant of anti-opportunistic infection + anti+HIV therapy
Staging/classification
223
Q

Group 1 oral manifestations of HIV

A

Strongly associated w/ HIV

Candidiasis: erythematous (denture), pseudomembranous (wipe off)
Hairy leukoplakia: corrugated tongue (EBV)
Kaposi sarcoma: HHV8, cancer endothelial cells
PD
- linear gingival erythema
- ANUG (interdental papilla tip), NUP (inc. destruction)
Non-Hodgkin’s lymphoma: singular firm nodule

224
Q

Management of HIV

A

Antiretroviral therapy

  • zidovudine
  • Retrovir
  • tenofovir
225
Q

Effect of ART

A

Inc. CD4, dec. viral load
Oral: red. prevalence of manifestations

Commencing can cause deterioration/reestablishment of opportunistic infections as immune system strengthens and fights again

BDS4 (10 decks)

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