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BDS5 oral disease > ulcers > Flashcards

ulcers Flashcards

1
Q

how can ulcers be classified?

A

single or multiple
recurrent or persistent

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2
Q

what may cause a single recurrent ulcer?

A

trauma or TUGSE
may be infective (multiple ulcers coalesce)

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3
Q

what may cause multiple recurrent ulcers? (9)

A

RAS
Reiter syndrome (reactive arthritis)
MAGIC
PFAPA
smoking cessation
Behcet’s disease
erythema multiforme
recurrent herpes
idiopathic

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4
Q

what may cause a single persistent ulcer? (4)

A

neoplasms
trauma
chronic infections (eg TB, syphilis, fungal)
drugs (esp nicorandil)

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5
Q

what may cause multiple persistent ulcers? (5)

A

dermatological disorders (LP, vesiculobullous conditions)
GI issues
haematological issues
connective tissue disease
drugs

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6
Q

which drugs may cause a single persistent ulcer? (3)

A

(often cause multiple rather than single)
aspirin chemical burn
nicorandil
methotrexate

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7
Q

what is RAS? (name, types, aetiology)

A

recurrent aphthous stomatitis
three types - herpetiform, minor, major
unknown aetiology, modulated by stress

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8
Q

describe herpetiform RAS (age, presentation)

A
  • 20-30yo (young adult)
  • non-keratinised epithelium, esp ventral tongue, soft palate, fauces
  • 0.5-3mm dia, 5-40/crop
  • round (but may coalesce)
  • yellow base with larger erythematous border
  • last 1-2 weeks with no scarring
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9
Q

herpetiform RAS age group

A

young adult (20-30yo)

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10
Q

herpetiform RAS sites

A

non-keratinised
esp ventral tongue, soft palate, fauces

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11
Q

herpetiform RAS ulcer appearance and number per crop

A
  • round (may coalesce)
  • yellow base, large erythematous border
  • <3mm dia, 5-40 per crop
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12
Q

describe minor RAS (age, presentation)

A
  • 10-20yo (teens)
  • non-keratinised epithelium, esp buccal/labial mucosa
  • <10mm dia, 1-5/crop
  • oval
  • grey base with erythematous border
  • last 1-2 weeks with no scarring
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13
Q

minor RAS age group

A

teens (10-20yo)

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14
Q

minor RAS sites

A

non-keratinised epithelium
esp buccal/labial mucosa

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15
Q

minor RAS ulcer appearance and number per crop

A
  • oval
  • grey base with erythematous border
  • <10mm dia, 1-5 per crop
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16
Q

describe major RAS (age, presentation)

A
  • <10yo (children)
  • any surface, esp fauces
  • > 10mm dia, 2-10/crop
  • oval or irregular (esp if long-standing) shape
  • grey base +/- indurated edge
  • last 2 weeks-3 months, with scarring
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17
Q

major RAS age group

A

children <10yo

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18
Q

major RAS ulcer appearance and number per crop

A
  • oval/irregular
  • grey base +/- indurated edge
  • > 10mm dia, 2-10/crop
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19
Q

major RAS site

A

any surface, esp fauces

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20
Q

investigations if pt presents with ulcer (2)

A

bloods - FBC, haematinics, coeliac screen
biopsy if atypical

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21
Q

management steps for RAS (5)

A
  1. eliminate local aggravating factors
  2. topical/local pain relief
  3. anti-inflammatory (topical or systemic)
  4. assess response to therapy
  5. maintenance
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22
Q

examples of topical pain relief for RAS (7)

A
  • Lignocaine 5% ointment or 2% gel
  • Prilocaine 4% max in 10ml
  • Benzocaine 10mg lozenges
  • Bonjela = choline salicylate
  • Difflam MW = benzydamine
  • Cocaine MW = specialist use only (addictive, also for radiotherapy mucositis)
  • Agents that cover mucosa = adhesive gels (Igloo), +/- lidocaine
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23
Q

examples of topical anti-inflammatory therapy for RAS (5)

A
  • Betamethasone (Betnesol) – MW QDS
  • Prednisolone – 5mg MW TDS
  • Fluticasone – spray or nasule MW
  • Clobetasol (Dermovate) ointment mixed 50/50 with Orabase (adhesive topical steroid) OD
  • “Triple” MW = betamethasone, doxycycline and nystatin; TDS (good for herpetiform ulcers but bad taste)
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24
Q

examples of systemic anti-inflammatory therapy for RAS (specialist only) (6)

A
  • Colchicine – 500ug OD-TDS, least potent (needs monitoring)
  • Corticosteroids, prednisolone – tablet, ulcers tend to recur once stopped
  • Pentoxifylline – 400mg BD, variable efficacy
  • Azathioprine – serious s/e (needs monitoring)
  • Thalidomide (peripheral neuropathy in most, teratogenic)
  • Biologics – infliximab (IV), adalimumab (subcutaneous), various response and immunosuppression
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25
Q

colchicine action/effect (2)

A
  • Inhibits cell-mediated responses, anti-inflammatory
  • Reduces number, size, duration, pain and increases ulcer-free period
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26
Q

infliximab and etanercept drug type

A

anti-TNF (biologic)

27
Q

what is in “triple” MW?

A

bethamethasone (topical steroid)
doxycycline
nystatin

28
Q

which type of RAS is triple MW best for?

A

herpetiform

29
Q

how might smoking be related to ulcers?

A

smoking cessation may allow ulcers to form (multiple recurrent)

30
Q

what is in Difflam MW?

A

benzydamine

31
Q

describe Behçet’s disease (what, demographic, genetic links)

A
  • chronic, relapsing, inflammatory multisystem disease
  • 20-40yo, often more severe in males
  • Silk Road distribution around equator (Turkey, Europe)
  • HLA-D51 and HLA-B21 links
32
Q

pathophysiology of Behçet’s disease (4)

A

Multifactorial
- inflammation set off by infection (eg HSV, Streptococcus) or antigen (eg heat shock protein)
- genetically predisposed individuals
- Th17, IL-17 pathways very active
- Increased PMN activity, significant PMN and lymphocyte infiltration in affected organs

33
Q

features of Behcet’s disease (7)

A
  • oral and genital aphthous-like ulcers
  • uveitis (blurring, pain, floaters) – blindness if untreated (retinal vein occlusion)
  • skin = papulopustular, acne-like and/or erythema nodosum
  • headaches (migraines, brain fog)
  • superficial phlebitis, DVT, PE, aortic aneurysm
  • non-erosive, non-deforming swelling/inflammation of joints
  • IBS-like symptoms (diarrhoea, constipation, bloating, pain)
34
Q

types of Behcet’s disease

A
  • Mucocutaneous = oral, genital + skin lesions
  • Arthritic = oral ulcers + inflamed joints
  • Neurological = ulcers + neurological signs
  • Ocular = ulcers + ocular signs
35
Q

management of Behcet’s disease (3)

A
  • referral to centre of excellence
  • MDT approach
  • oral ulcers treated as per RAS (eg colchicine)
36
Q

describe Reiter syndrome/reactive arthritis (what, cause, demographic) and triad of symptoms

A
  • autoimmune, inflammatory
  • 2-4 weeks after GI infections (Shigella, Salmonella, Campylobacter) or GU infections (esp Chlamydia trachomatis)
  • often adult men
  • triad = non-infective urethritis, arthritis, conjunctivitis with mouth ulcers
  • often circinate lesions on tongue (resembles geographic tongue)
37
Q

management of Reiter syndrome (5)

A

based on symptom severity, 65% self-limiting, 30% needing treatment for chronic symptoms
- NSAIDs mainly
- Corticosteroids – topical, intra-articular or systemic
- Antibiotics for the initiating infection
- DMARDs if NSAIDs ineffective/contraindicated

38
Q

examples of DMARDs (3)

A
  • sulfasalazine
  • methotrexate
  • anti-TNF (etanercept, infliximab)
39
Q

what does MAGIC stand for?

A

Mouth And Genital ulceration
with Inflamed Cartilage

40
Q

describe MAGIC syndrome and symptoms

A
  • relapsing polychondritis and Behcet’s disease (vasculitis)
  • orogenital aphthous ulcers and chondritis
41
Q

what is erythema nodosum?

A
  • tender red bumps, usually found symmetrically on the shins
  • often a sign of another disease, infection or drug sensitivity
42
Q

management for MAGIC syndrome (2)

A

immunosuppressant therapy
topical therapy as per RAS

43
Q

what does PFAPA stand for?

A

Periodic Fever
Aphthous stomatitis
Pharyngitis
Adenitis

44
Q

describe PFAPA syndrome (demographic, s/s)

A
  • Mediterranean and young adolescents (90% present before 5yo)
  • Periodic fevers >40ºC every 3-8 weeks which resolve within a few days, AND: aphthous stomatitis, pharyngitis or adenitis
    (may be related to recurrent infection of tonsil/adenoid)
45
Q

possible treatment for PFAPA syndrome

A

Adenotonsillectomy or tonsillectomy may to lead to complete resolution

46
Q

who manages persistent multiple ulceration secondary to haematological and CT/GI conditions (referral)

A

haematological = via GP
connective tissue or GI = refer to specialist centre

47
Q

examples of dermatological disorders which may cause multiple persistent ulceration (7)

A
  • Lichen planus (relapse + remission)
  • Oral lichenoid lesions
  • Immunobullous (pemphigus, pemphigoid) – no healing between episodes
  • Linear IgA disease
  • Dermatitis herpetiformis
  • Erythema multiforme
  • Epidermolysis bullosa
48
Q

what may ulcers look like if caused by GI issues/IBD?

A

slit-like/linear ulcers in buccal sulci
with hyperplastic folds of mucosa at periphery

49
Q

what haematological conditions may cause multiple persistent ulceration? (4)

A

anaemia (esp haematinic deficiency), dysmenorrhoea
malignancy, leukaemia
other deficiencies (eg vit C)
cyclic neutropenia

50
Q

what may ulcers look like if caused by chronic discoid lupus?

A

linear ulcers with keratotic striae

51
Q

histology of an ulcer (3)

A
  • break in epithelium
  • fibrinous slough
  • granulation tissue in connective tissue
52
Q

describe TUGSE (name, presentation, histology)

A
  • Traumatic Ulcerative Granuloma with Stromal Eosinophilia
  • deep traumatic ulcer, usually on tongue
  • deep inflammation into muscle, leading to degeneration and eosinophil presence
53
Q

what does TUGSE stand for?

A

traumatic ulcerative granuloma with stromal eosinophilia

54
Q

TUGSE common site

A

tongue

55
Q

typical appearance/presentation of traumatic ulcer (2)

A
  • keratotic halo
  • adjacent to cause (eg sharp tooth, occlusal plane)
56
Q

syphilitic ulcer histology (3)

A
  • primary/secondary = dense plasma cell infiltrate
  • tertiary = granulomas
  • antibody stain for Treponeme in intact epithelium
57
Q

herpes virus ulcer histology (3)

A
  • cells appear swollen/ballooned with marginated chromatin, clear centre
  • multinucleated cells (fusion of infected cells)
  • clusters of cell lysis from viral replication = epithelial breakdown
58
Q

what is epidermolysis bullosa? (3)

A
  • group of congenital disorders with skin/mucosal fragility
  • gene mutations
  • many subtypes affecting different layers of skin/mucosa
59
Q

different subtypes of epidermolysis bullosa group (4)

A
  • EB simplex (mildest, keratin mutation)
  • dominant dystrophic EB (mild, type VII collagen in sub-lamina densa)
  • junctional EB (moderately severe, BP180 in lamina lucida)
  • recessive dystrophic EB (severe, type VII collagen)
60
Q

briefly describe EB simplex (3)

A
  • mildest form of EB
  • keratin gene mutation
  • more superficial separation (basal cell layer)
61
Q

briefly describe dominant dystrophic EB (what, age)

A
  • mild form of EB affecting type VII collagen (sub-lamina densa)
  • more in adulthood
62
Q

briefly describe junctional EB (3)

A
  • moderately severe form of EB affecting BP 180 (lamina lucida)
  • widespread involvement
  • normal life expectancy
63
Q

briefly describe recessive dystrophic EB (what, 5 s/s)

A
  • severe form of EB affecting type VII collagen (sub-lamina densa)
  • shortened life expectancy
  • short stature
  • skin cancers, malabsorption
  • severe scarring - oral, hands, feet (mitten deformity)
  • loss of teeth

BDS5 oral disease (26 decks)

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