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allergies Flashcards

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1
Q

what is the clinical term for canker sores?

A

Recurrent Aphthous Ulcerations

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2
Q

what are the causes of canker sores

A

Common; familial relationship

Unknown pathogenesis; Immune-mediated process

Most common in children and young adults

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3
Q

what are the common “triggers” of recurrent aphthous ulcerations?

A

stress, local trauma, menstrual cycle

immune dysregulation; allergy/contact rx

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4
Q

list the 3 forms of recurrent aphthous ulcerations

A

Minor

Major

Herpetiform

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5
Q

what is the most common variation of aphthous ulcers? what are its characteristics?

A

Minor Aphthous Ulcerations

Almost exclusively occur NON-KERATINIZED mucosa

Fewest recurrences; shortest duration of lesions

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6
Q

where are minor aphthous ulcerations commonly found?

A

buccal and labial mucosa
ventral tongue
floor of mouth
soft palate

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7
Q

list the morphological characteristics of minor aphthous ulcers

A

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

Round to oval ulcer; 3-10mm diameter

ERYTHEMATOUS HALO

Heal without scarring 7-10 days

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8
Q

list the characteristics of major aphthous ulcers

A

Larger than minor aphthae; 1-3 cm diameter

Longer duration per episode; heal in 2-6 weeks often with SCARRING

1-10 lesions per episode

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9
Q

what are the most common sites for major aphthous ulcers?

A

labial mucosa, soft palate, tonsillar fauces

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10
Q

which form of aphthous ulcers have the highest rates of reoccurrence and present with the largest number of lesions?

A

Herpetiform Aphthous Ulcerations

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11
Q

characteristics of Herpetiform aphthous ulcers:

A

Individual lesions small (1-3mm), with many present per episode

occur on ANY oral mucosal surface

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12
Q

healing characteristics of herpetiform aphthous ulcers:

A

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

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13
Q

how are Recurrent Aphthous Ulcerations treated?

A

Respond well to topical high –potency corticosteroids

Applied early in course of disease; thin film, multiple times per day

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14
Q

T/F: once an Aphthous ulcer has lost its erythematous border, a corticosteroid steroid will not speed healing

A

True

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15
Q

__________ syndrome is a multisystem disorder with oral aphthous-like ulcerations

A

Behcet’s Syndrome

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16
Q

which ethnic groups are at highest risk for Behcet’s syndrome?

A

Highest prevalence in Middle East and Japan; much less frequent in US

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17
Q

classic triad of Behcet’s syndrome:

A

Oral ulcerations
Genital ulcerations
Ocular disease

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18
Q

describe the oral lesions of Behcet’s syndrome:

A

First manifestation in up to 75% cases
Occur in 99% cases
Commonly involve soft palate and oropharynx
Variable size, ragged borders, large zone erythema

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19
Q

T/F: the genital lesions of Behcet’s syndrome resemble the oral lesions

A

true

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20
Q

what are the characteristics of the “ocular disease” present in Behcet’s syndrome?

A

Posterior uveitis

conjunctivitis, corneal ulceration, arteritis, etc.

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21
Q

how is Behcet’s syndrome diagnosed?

A

Based on clinical presentation

Positive PATHERGY test

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22
Q

Treatments & prognosis for Behcet’s syndrome:

A

Topical or systemic immunosuppresive or immunomodulatory therapy; early aggressive therapy for severe cases

Prognosis: generally good; relapsing/remitting course

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23
Q

Orofacial Granulomatosis seems to represent a abnormality in what?

A

abnormal immune reaction

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24
Q

clinical characteristics of Orofacial Granulomatosis lesions

A

non-necrotizing granulomatous inflammation, presenting as persistent non-tender swelling

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25
where in the mouth would you expect to find orofacial granulomatosis lesions?
Lips most common site; may involve any oral mucosal or perioral location Edema and swelling of other parts of face can be seen
26
what are the 2 forms of Orofacial Granulomatosis?
Cheilitis granulomatosa: - Involvement of the lips alone Melkersson-Rosenthal syndrome
27
characteristics of Melkersson-Rosenthal syndrome:
non-tender lip swelling Bell’s palsy fissured tongue
28
Microscopic features of Orofacial Granulomatosis:
Superficial vascular ectasia, vasculitis, edema Non-necrotizing granulomas No evidence of foreign material and special stains to rule out specific infection
29
how is Orofacial Granulomatosis diagnosed & treated?
Patients require thorough medical evaluation Remove sources of inflammation Intralesional corticosteroids work best Multiple injections may be necessary Good prognosis; primarily a cosmetic problem
30
_________________ is Granulomatosis with Polyangiitis
Wegener’s Granulomatosis
31
characteristics of Wegener’s Granulomatosis:
Uncommon; well-recognized disease Unknown etiology; necrotizing granulomatous process with vasculitis
32
what areas are affected by Wegener's Granulomatosis?
Can affect upper airway, lungs, kidneys, skin and mucosa
33
what are the 3 types of Wegener's Granulomatosis and what areas do they effect?
Generalized Wegener’s (Classic Wegener’s) – upper and lower respiratory tract, kidneys Limited Wegener’s – upper and lower respiratory tract Superficial Wegener’s – lesions primarily of skin and mucosa
34
what are the clinical manifestations of Wegener's Granulomatosis?
Epistaxis, pain, nasal obstruction Destruction of nasal septum (saddle-nose deformity) Dry cough, hemoptysis, dyspnea, chest pain Proteinuria, red blood cell casts Large, chronic oral ulcers “Strawberry gingivitis” – pathognomonic Palatal ulcer with oral-antral fistula
35
Microscopic appearance of Wegener's Granulomatosis:
Poorly formed granulomas, mixed inflammation Subepithelial hemorrhage Vasculitis
36
what antibodies are used to diagnose Wegener's Granulomatosis?
c-ANCA (cytoplasmic) – most useful p-ANCA (perinuclear) – also seen in other systemic vasculitides
37
prognosis for Wegener's Granulomatosis:
Prednisone and cyclophosphamide Complete response (remission) is expected in 75% of patients; relapse rate 30% Limited and superficial forms may progress to classic WG
38
During an allergic reaction to systemic drugs, a _________ relationship may be acute or delayed
temporal
39
what are the common clinical characteristics of oral lesions due to allergic reactions to drugs? where are these lesions most commonly located?
mucosal ulceration and erosion with variable erythema and white striae Most common sites: buccal mucosa, labial mucosa, ventro-lateral tongue
40
what is a fixed drug reaction?
inflammatory alterations that recur at the same site after the administration of a medication
41
what is a Lichenoid drug reaction?
medication induced mucosal alterations which mimic appearance of lichen planus
42
how are Allergic Reaction to Systemic Drugs DIAGNOSED?
Biopsy non-specific Detailed medical and clinical history with complete list of Rx and OTC medications If more than one medication suspected, serial elimination of the medications in collaboration with pt. physician Mucosal alterations resolve after discontinue medication (recur on reintroduction)
43
what are the treatment options for Allergic Reaction to Systemic Drugs?
Discontinue responsible medication in conjunction with pt. physician (replace with alternate drug) +/- Topical corticosteroids
44
what are the clinical characteristics of Allergic Contact Stomatitis?
Mild/barely visible erythema to extensive erythema, edema, erosions, ulcerations, exfoliation May be asymptomatic; burning, itching, stinging
45
name some of the causes for Allergic Contact Stomatitis:
Foods, flavoring agents, gum, candies, oral hygiene products, cosmetics, dental gloves and rubber dam material, metals, denture materials, impression materials, etc.
46
how is Allergic contact stomatitis Diagnosed?
Identification of temporal relationship between contact with agent and oral changes Patch testing
47
name the 3 types of Allergic contact Stomatitis:
1) Dentrifice-Related Sloughing 2) Oral Mucosal Cinnamon Reaction 3) Lichenoid Amalgam Reaction
48
characteristics of Dentrifice-Related Sloughing:
Toothpaste can cause widespread desquamation of the superficial layers of epithelium Minimal/mild erythema Associated with sodium lauryl sulfate
49
treatment for Dentrifice-Related Sloughing:
No treatment necessary; harmless process Switching to a bland toothpaste will result in resolution
50
causes of Oral Mucosal Cinnamon Reaction:
- Contact reaction to ARTIFICIAL CINNAMON flavoring - Clinical distribution varies by medium of delivery A) Toothpaste = diffuse, gingiva B) Chewing gum/candy = localized
51
clinical presentation of Oral Mucosal Cinnamon Reaction:
Erythema with overlying shaggy hyperkeratosis Pain and burning are common symptoms
52
T/F: the lesions caused by an Oral Mucosal Cinnamon Reaction will normally resolve within ONE WEEK after discontinuing use
true
53
what type of allergic reaction is associated with old amalgam restorations undergoing corrosion and release of metallic ions?
Lichenoid Amalgam Reaction
54
where are lichenoid amalgam reaction lesions usually found?
Limited to mucosal surfaces directly in contact with the restoration (buccal mucosa, ventral and lateral tongue)
55
characteristics of Lichenoid Amalgam Reaction lesions:
Mucosal alterations mimic lichen planus, however are localized May be white or erythematous, +/- peripheral striae
56
how are Lichenoid Amalgam Reaction lesions treated?
Smooth, polish, recontour old amalgam Replace amalgam with non-metallic restoration (composite resin, porcelain crown)
57
__________ is a diffuse edematous swelling of soft tissue
Angioedema
58
name the 3 types/causes of Angioedema:
1) IgE mediated hypersensitivity reaction 2) Angiotensin-converting enzyme (ACE) inhibitors 3) C1 esterase inhibitor (C1-INH) deficiency
59
what type of Angioedema is most common? what are its major causes?
most common = IgE mediated hypersensitivity reaction Contact reaction: foods, cosmetics, drugs, etc. Physical stimuli: heat, cold, exercise, sun exposure
60
Excess ___________ due to Angiotensin-converting enzyme (ACE) inhibitors will cause Angioedema
bradykinin
61
Clinical features of Angioedema:
Relatively rapid onset of soft tissue swelling Non-painful; pruritis and erythema may be seen Solitary or multiple sites of involvement Commonly affects head and neck region Resolves in 24-72 hours
62
how is Angioedema Diagnosed?
Based on clinical presentation, possibly in conjunction with known trigger Evaluation for adequate functional C1-INH
63
how is Angioedema treated?
Oral antihistamine, IM epinephrine, IV corticosteroids Prevention ACE inhibitor-related and C1-INH deficiency non-responsive to standard tx

oral pathology final (4 decks)

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