allergies Flashcards

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
Q

where in the mouth would you expect to find orofacial granulomatosis lesions?

A

Lips most common site; may involve any oral mucosal or perioral location

Edema and swelling of other parts of face can be seen

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26
Q

what are the 2 forms of Orofacial Granulomatosis?

A

Cheilitis granulomatosa:
- Involvement of the lips alone

Melkersson-Rosenthal syndrome

27
Q

characteristics of Melkersson-Rosenthal syndrome:

A

non-tender lip swelling
Bell’s palsy
fissured tongue

28
Q

Microscopic features of Orofacial Granulomatosis:

A

Superficial vascular ectasia, vasculitis, edema

Non-necrotizing granulomas

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

29
Q

how is Orofacial Granulomatosis diagnosed & treated?

A

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
Q

_________________ is Granulomatosis with Polyangiitis

A

Wegener’s Granulomatosis

31
Q

characteristics of Wegener’s Granulomatosis:

A

Uncommon; well-recognized disease

Unknown etiology; necrotizing granulomatous process with vasculitis

32
Q

what areas are affected by Wegener’s Granulomatosis?

A

Can affect upper airway, lungs, kidneys, skin and mucosa

33
Q

what are the 3 types of Wegener’s Granulomatosis and what areas do they effect?

A

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
Q

what are the clinical manifestations of Wegener’s Granulomatosis?

A

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
Q

Microscopic appearance of Wegener’s Granulomatosis:

A

Poorly formed granulomas, mixed inflammation

Subepithelial hemorrhage

Vasculitis

36
Q

what antibodies are used to diagnose Wegener’s Granulomatosis?

A

c-ANCA (cytoplasmic) – most useful

p-ANCA (perinuclear) – also seen in other systemic vasculitides

37
Q

prognosis for Wegener’s Granulomatosis:

A

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
Q

During an allergic reaction to systemic drugs, a _________ relationship may be acute or delayed

A

temporal

39
Q

what are the common clinical characteristics of oral lesions due to allergic reactions to drugs?

where are these lesions most commonly located?

A

mucosal ulceration and erosion with variable erythema and white striae

Most common sites: buccal mucosa, labial mucosa, ventro-lateral tongue

40
Q

what is a fixed drug reaction?

A

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

41
Q

what is a Lichenoid drug reaction?

A

medication induced mucosal alterations which mimic appearance of lichen planus

42
Q

how are Allergic Reaction to Systemic Drugs DIAGNOSED?

A

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
Q

what are the treatment options for Allergic Reaction to Systemic Drugs?

A

Discontinue responsible medication in conjunction with pt. physician (replace with alternate drug)

+/- Topical corticosteroids

44
Q

what are the clinical characteristics of Allergic Contact Stomatitis?

A

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

May be asymptomatic; burning, itching, stinging

45
Q

name some of the causes for Allergic Contact Stomatitis:

A

Foods, flavoring agents, gum, candies, oral hygiene products, cosmetics, dental gloves and rubber dam material, metals, denture materials, impression materials, etc.

46
Q

how is Allergic contact stomatitis Diagnosed?

A

Identification of temporal relationship between contact with agent and oral changes

Patch testing

47
Q

name the 3 types of Allergic contact Stomatitis:

A

1) Dentrifice-Related Sloughing
2) Oral Mucosal Cinnamon Reaction
3) Lichenoid Amalgam Reaction

48
Q

characteristics of Dentrifice-Related Sloughing:

A

Toothpaste can cause widespread desquamation of the superficial layers of epithelium

Minimal/mild erythema

Associated with sodium lauryl sulfate

49
Q

treatment for Dentrifice-Related Sloughing:

A

No treatment necessary; harmless process

Switching to a bland toothpaste will result in resolution

50
Q

causes of Oral Mucosal Cinnamon Reaction:

A
  • Contact reaction to ARTIFICIAL CINNAMON flavoring
  • Clinical distribution varies by medium of delivery
    A) Toothpaste = diffuse, gingiva
    B) Chewing gum/candy = localized
51
Q

clinical presentation of Oral Mucosal Cinnamon Reaction:

A

Erythema with overlying shaggy hyperkeratosis

Pain and burning are common symptoms

52
Q

T/F: the lesions caused by an Oral Mucosal Cinnamon Reaction will normally resolve within ONE WEEK after discontinuing use

A

true

53
Q

what type of allergic reaction is associated with old amalgam restorations undergoing corrosion and release of metallic ions?

A

Lichenoid Amalgam Reaction

54
Q

where are lichenoid amalgam reaction lesions usually found?

A

Limited to mucosal surfaces directly in contact with the restoration (buccal mucosa, ventral and lateral tongue)

55
Q

characteristics of Lichenoid Amalgam Reaction lesions:

A

Mucosal alterations mimic lichen planus, however are localized

May be white or erythematous, +/- peripheral striae

56
Q

how are Lichenoid Amalgam Reaction lesions treated?

A

Smooth, polish, recontour old amalgam

Replace amalgam with non-metallic restoration (composite resin, porcelain crown)

57
Q

__________ is a diffuse edematous swelling of soft tissue

A

Angioedema

58
Q

name the 3 types/causes of Angioedema:

A

1) IgE mediated hypersensitivity reaction
2) Angiotensin-converting enzyme (ACE) inhibitors
3) C1 esterase inhibitor (C1-INH) deficiency

59
Q

what type of Angioedema is most common? what are its major causes?

A

most common = IgE mediated hypersensitivity reaction

Contact reaction: foods, cosmetics, drugs, etc.
Physical stimuli: heat, cold, exercise, sun exposure

60
Q

Excess ___________ due to Angiotensin-converting enzyme (ACE) inhibitors will cause Angioedema

A

bradykinin

61
Q

Clinical features of Angioedema:

A

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
Q

how is Angioedema Diagnosed?

A

Based on clinical presentation, possibly in conjunction with known trigger

Evaluation for adequate functional C1-INH

63
Q

how is Angioedema treated?

A

Oral antihistamine, IM epinephrine, IV corticosteroids

Prevention

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