finals - allergies/ immuno diseases Flashcards by Luke Lloyd

_ aka canker sores

common, _ relationship

unknown pathogenesis - immune-mediated process

most common in children and young adults

possible triggers = stress, local trauma, menstrual cycle, tomatos

recurrent aphthous ulcerations

familial relationship

minor, major, herpetiform variations

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_ aphthous ulcerations

most common form with the fewest recurrences, shortest duration of lesions

almost exclusively occur on _ site

minor aphthous ulcerations

nonkeratinized moveable mucosa

buccal/labial mucosa, ventral tongue, floor of mouth, soft palate

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1-5 painful ulcers: preceded by erythematous macule with prodromal symptoms

erythematous halo - central area of ulceration and red halo, round to oval ulcer 3-10mm

heal without scarrying 7-14 days

minor aphthous ulcerations

most common, fewest recurrences, shortest duration of lesion

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_ aphthous ulcerations

longer duration per episode, 1-3cm ; heal in 2-6 weeks often with scarring

1-10 lesions - labial mucosa, soft palate, tonsillar fauces

major aphthous ulcerations

Complaint will sometimes be sore throat, not so much the intraloral pain

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_ aphthous ulercations

greatest number of lesions and most frequent recurrences

individual lesions small 1-3mm

any oral mucosal surface

herpetiform aphthous ulcerations

Most unique and least common
- Most frequent ulcerations (continuous)
Small!

Moveable tissue non keratinized tissue location is most common
But these herpetiform aphthous ulcerations can occur anywhere

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herpetiform aphthous ulcerations superficial resemble primary HSV

heal in 7-10 days, but recurrences tend to be closely spaced

another way to distinguish?

Recurrent herpes - no because it is on attached gingiva and palate

Primary herpes - acute out break and then heals - systemic health declines and patient feels like sick

Herpetiform aphthous ulcerations - have had some previous and not as much as an urgency - coming and going weeding out

if really can’t dx - then do exfoliative cytology

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recurrent aphthous ulcerations

dx? tx?

dx - based on clinical presentation - histopathology non-specific - just to rule other things out

tx - topical high potency corticosteroids (Betamethasone dipropionate, Clobetasol propionate)

Only need to apply until the pain it gone (immune response over) - need a lot of applications because saliva will take it off - If no erythema - the corticosteriod won’t probably work bc immune response is over

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multisystem disorder (like Celiac disease) with oral aphthous-like ulcerations

abnormal immune process triggered by an environmental or infectious Ag in a genetically predisposed individual (pesticides)

Behcet’s syndrome

highest prevalence in Turkey, Japan, and Eastern Mediterranean countries

much less frequent in US

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Behcet’s Syndrome classic triad

oral ulcerations (similar to aphthous ulcers) - 75% of cases, occur in 99% cases - soft palate and oropharynx - back of oral cavity

genital ulcerations - 75% of cases

ocular disease - 70% of cases - posterior uveitis - conjunctivitis, corneal ulceration, arteritis,

also hace cutaneous lesions, arthritis, CNS, cardio, GI, muscular, Pulmonary, renal

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Behcet’s syndrome

dx- based on clinical presentation and positive _ test

pathergy test - 20 G needle and sterile saline - inject subq and see if there is a response

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Behcet’s Syndrome

topical or systemic immunosupprussive and/or immunomodulatory therapy - early aggressive therapy for severe cases

Px - generally good; relapsing/remitting course

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unknown etiology; appears to represent an abnormal immune rxn

most often in adults
non-necrotizing granulomatous inflammation, presenting as persistent non-tender swelling

lips most common site, may involve any oral or perioral location - if have GI problem then it is probably Crohn’s

orofacial granulomatosis

Cheilitis granulomatosa - only lip involvement

melkersson-rosenthal syndrome - non-tender lip sweelingm Bell’s palsy, fissured tongue

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type of oral granulomatosis

non-tender lip swelling
Bell’s palsy
fissured tongue

Melkersson-Rosenthal syndrome

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superficial vascular ectasia(dilation) , vasculitis, edema, leaky

non-necrotizing granulomas (may be sparse)

no evidence of foreign material and special stains to rule out specific infection

orofacial granulomatosis

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orofacial granulomatosis

Pt’s require thorough medical eval

remove sources of inflammation, then _ works best

Px?

intralesional corticosteroids work best - multiple injections may be necessary

Px - good, primarily a cosmetic problem

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unknown etiology, necrotizing granulomatous process with vasculitis
uncommon but well recognized disease

Inflammation of vessels , usually response to inhaled Ag
Upper and lower airway - lungs, main thing is renal(kidney) involvment

Wegener’s Granulomatosis aka Granulomatosis with Polyangiitis

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generalized Wegener’s or Classic Wegener’s

what systems are affected

upper and lower resp tracts

renal-kidney

limited Wegener’s which systems affected

upper and lower resp tracts

Without rapid renal - may overtime develop renal but currently no renal involvment

Superficial Wegener’s

which systems affected

skin and mucosa

This is oral mucosa and skin - we will probably see this version

Epistaxis - acute bleeding from nose, purulent discharge, pain, nasal obstruction

destruction of nasal septum

dry cough, hemoptysis, dyspnea, chest pain

proteinura, RBC casts

oral manifestations?

Wegener’s Granulomatosis

oral - large chronic ulcers, “strawberry gingivitis”, palatal ulcer with oral-antral fistula

2 things that can cause saddle-nose deformity

syphilis and Wegener’s granulomatosis

strawberry gingivitis is very specific for _

stays on hard tissue, starts at interdental papilla and spreads latterly

Wegener’s granulomatosis

aka Granulomatosis with Polyangiitis

microscopic appearance

poorly formed granulomas, mixed inflammation

subepi hemorrhage

vasculitis - usually in gingiva - hard to pick up on biospy

Wegener’s aka Granulomatosis with Polyangiitis

even if we think we know Dx, we usually stll do blood test bc _

auto-Ab’s directed against neutrophils have been ID’d in a high percentage of patients (ANCA)

PR3-ANCA (c-ANCA) most useful**

MPO-ANCA(p-ANCA) seen in other systemic vasculitides

prior to _ 95% of Wegener's aka Granulomatosis with Polyangiitis cases died within 5 years, now complete response(remission) is expected in 75% of patients; relapse rate of 30%

immunosuppressive therapy Prednisone and cyclophophamide (steriod sparing) vs. methotrexate limited and superficial forms may progress to classic WG

vast numbers of meds are capable of producing oral mucosal alterations - sometimes acute, other times like 10 years to show up what does the mucosal changes look like

ulceration and erosion with variable erythema and white striae lichenoid appearnace - interlacing white keratioic lines buccal, labial mucosa and ventrolateral tongue

inflammatory alterations that recur at the same site after the administration of a medication not always present, but recurrent at the same site/location

fixed drug eruption

medication induced mucosal alterations which mimic appearance of lichen planus Moves around a little more, not in exact same location Lichen planus is usually bilaterally

lichenoid drug rxn (unilateral) more of these rxns than fixed drug ruption

how to Dx allergic rxn to systemic drug tx - discontinue responsible med in conjunction with pt physician - replace with alternate drug possible topical corticosteroids

biopsy non-specific detailed med and clinical hx with complete list of Rx and OTC if more than one med suspected, serial elimination, muscosal alterations resolve after discontinue med (recur on reintroduction) within 1 month oral mucosa should return to normal

list of agents reported to cause oral mucosal and perioral allergic contact rxns is diverse foods, flavors, gum, candy, OHI products, cosmetics, gloves, rubber dam, metals, dentues, impression materials, etc.

allergic contact stomatitis frequency of true allergic rxn appears to be rare

mild/barely visible erythema to extensive erythema, edema, erosions, ulcerations, exfoliation may be asymptomatic or burning, itching, stinging

allergic contact stomatitis ID of temporal relationship btw contact with agent and oral changes Need to confirm agent that pt was exposed to and oral change Need to keep food dairy - chapstick or anything

patch testing? allergic contact stomatitis

Insert subepidermal needle with various agents - Looking for response - usually red Not perfect test for oral mucosa - because skin is different than oral mucosa

allergic contact stomatitis 3 forms

dentrifice related sloughing - product of oral hygiene oral mucosal cinnamon rxn lichenoid amalgam rxn

dentrifice-related sloughing (allergic contact stomatisis) toothpaste can cause widespread desquatiom of the superficial epi (like chemical peel) minimal/mild erythema associated with _ and _

sodium lauryl sulfate ( foaming agent) and sodium pyrophosphate (plaque reduction)

dentrific- related sloughing allergic contact stomatisis tx?

none - harmless process switch to Fl toothpaste

erythema with overlying shaggy hyperkeratosis pain and burning

oral mucosal cinnamon rxn toothpaste - diffuse gingiva gum/candy- localized resolution within one week following discontinuation of the cinnamon

associated with old amalgam restorations undergoing corrosion and release of metallic ions limited to mucosal surfaces directly in contact with the restoration (buccal mucosa, ventral and lateral tongue) mimic linchen planus but are localized white or erythematous +/- peripheral striae

lichenoid amalgam rxn allergic contact stomatisis smooth, polish and recontour old amalgam replace with composite or porcelain crown

Angioedema - diffuse edematous swelling of soft tissue _ mediated hypersensitivity rxn most common contact rxn - foods, cosmetics, drugs, etc physical stimuli - heat, cold, excersise, sun exposure _ - cause excess bradykinin _ deficificeny - inherited or acquired

IgE most common angiotensin-converting enzyme (ACE) inhibitors - excess bradykinin C1 esterase inhibitor (C1-INH) deficiency

relatively rapid onset of soft tissue swelling non-painful; pruritus and erythema may be seen solitary or multiple sites commonly affects head/neck region (face, lips, tongue, FOM, pharynx, larynx) resolution in 24-72 hours - rapid onset and rapid resolution

angioedema IgE hypersens rxn most common Dx - clinical presentation with known trigger, evaluation for adequate fxnal C1-INH

treatment for angioedema

oral anti-histamine, IM epinephrine, IV corticosteroids ACE inhibitor- related and C1-INH deficiency non-responsive to standard tx prevention