finals - allergies/ immuno diseases Flashcards

1
Q

_ 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

A

recurrent aphthous ulcerations

familial relationship

minor, major, herpetiform variations

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2
Q

_ aphthous ulcerations

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

almost exclusively occur on _ site

A

minor aphthous ulcerations

nonkeratinized moveable mucosa

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

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3
Q

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

A

minor aphthous ulcerations

most common, fewest recurrences, shortest duration of lesion

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4
Q

_ 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

A

major aphthous ulcerations

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

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5
Q

_ aphthous ulercations

greatest number of lesions and most frequent recurrences

individual lesions small 1-3mm

any oral mucosal surface

A

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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6
Q

herpetiform aphthous ulcerations superficial resemble primary HSV

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

another way to distinguish?

A

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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7
Q

recurrent aphthous ulcerations

dx? tx?

A

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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8
Q

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)

A

Behcet’s syndrome

highest prevalence in Turkey, Japan, and Eastern Mediterranean countries

much less frequent in US

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9
Q

Behcet’s Syndrome classic triad

A

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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10
Q

Behcet’s syndrome

dx- based on clinical presentation and positive _ test

A

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

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11
Q

Behcet’s Syndrome

tx

A

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

Px - generally good; relapsing/remitting course

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12
Q

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

A

orofacial granulomatosis

Cheilitis granulomatosa - only lip involvement

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

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13
Q

type of oral granulomatosis

non-tender lip swelling
Bell’s palsy
fissured tongue

A

Melkersson-Rosenthal syndrome

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14
Q

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

A

orofacial granulomatosis

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15
Q

orofacial granulomatosis

Pt’s require thorough medical eval

remove sources of inflammation, then _ works best

Px?

A

intralesional corticosteroids work best - multiple injections may be necessary

Px - good, primarily a cosmetic problem

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16
Q

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

A

Wegener’s Granulomatosis aka Granulomatosis with Polyangiitis

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17
Q

generalized Wegener’s or Classic Wegener’s

what systems are affected

A

upper and lower resp tracts

renal-kidney

18
Q

limited Wegener’s which systems affected

A

upper and lower resp tracts

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

19
Q

Superficial Wegener’s

which systems affected

A

skin and mucosa

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

20
Q

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?

A

Wegener’s Granulomatosis

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

21
Q

2 things that can cause saddle-nose deformity

A

syphilis and Wegener’s granulomatosis

22
Q

strawberry gingivitis is very specific for _

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

A

Wegener’s granulomatosis

aka Granulomatosis with Polyangiitis

23
Q

microscopic appearance

poorly formed granulomas, mixed inflammation

subepi hemorrhage

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

A

Wegener’s aka Granulomatosis with Polyangiitis

24
Q

Wegener’s aka Granulomatosis with Polyangiitis

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

A

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

25
Q

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%

A

immunosuppressive therapy

Prednisone and cyclophophamide (steriod sparing) vs. methotrexate

limited and superficial forms may progress to classic WG

26
Q

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

A

ulceration and erosion with variable erythema and white striae

lichenoid appearnace - interlacing white keratioic lines

buccal, labial mucosa and ventrolateral tongue

27
Q

inflammatory alterations that recur at the same site after the administration of a medication

not always present, but recurrent at the same site/location

A

fixed drug eruption

28
Q

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

A

lichenoid drug rxn (unilateral)

more of these rxns than fixed drug ruption

29
Q

how to Dx allergic rxn to systemic drug

tx - discontinue responsible med in conjunction with pt physician - replace with alternate drug

possible topical corticosteroids

A

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

30
Q

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.

A

allergic contact stomatitis

frequency of true allergic rxn appears to be rare

31
Q

mild/barely visible erythema to extensive erythema, edema, erosions, ulcerations, exfoliation

may be asymptomatic or burning, itching, stinging

A

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

32
Q

patch testing?

allergic contact stomatitis

A

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

33
Q

allergic contact stomatitis

3 forms

A

dentrifice related sloughing - product of oral hygiene

oral mucosal cinnamon rxn

lichenoid amalgam rxn

34
Q

dentrifice-related sloughing (allergic contact stomatisis)
toothpaste can cause widespread desquatiom of the superficial epi (like chemical peel)

minimal/mild erythema

associated with _ and _

A

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

35
Q

dentrific- related sloughing

allergic contact stomatisis
tx?

A

none - harmless process

switch to Fl toothpaste

36
Q

erythema with overlying shaggy hyperkeratosis

pain and burning

A

oral mucosal cinnamon rxn

toothpaste - diffuse gingiva

gum/candy- localized

resolution within one week following discontinuation of the cinnamon

37
Q

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

A

lichenoid amalgam rxn allergic contact stomatisis

smooth, polish and recontour old amalgam

replace with composite or porcelain crown

38
Q

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

A

IgE most common

angiotensin-converting enzyme (ACE) inhibitors - excess bradykinin

C1 esterase inhibitor (C1-INH) deficiency

39
Q

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

A

angioedema

IgE hypersens rxn most common

Dx - clinical presentation with known trigger, evaluation for adequate fxnal C1-INH

40
Q

treatment for angioedema

A

oral anti-histamine, IM epinephrine, IV corticosteroids

ACE inhibitor- related and C1-INH deficiency non-responsive to standard tx

prevention