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Chapter 9: Allergies and Immunologic Diseases

front 1 Clinical Features localized variant involve one to several fungiform papillae mildly painful, elevated, red-yellow papules occur on anterior dorsal surface of tongue generalized variant involves many fungiform papillae sensitive, enlarged, erythematous occur on tip and lateral dorsal surface of tongue papulokeratotic variant diffuse involvement of fungiform papillae asymptomatic, parakeratotic white-yellow papules occur on tip and lateral dorsal surface of tongue Histopathologic Features focal areas of exocytosis or ulceration proliferation of small vascular channels mixed inflammatory cellular infiltrate hyperparakeratosis with bacterial colonization	back 1 transient lingual papillitis
front 2 Tender, yellow-pink papule on the dorsum of the tongue.	back 2 transient lingual papillitis, localized
front 3 Multiple painful white papules on the lateral dorsum and tip of tongue.	back 3 transient lingual papillitis, generalized
front 4 Clusters of asymptomatic, elevated, yellow papules on the dorsolateral surface of the tongue.	back 4 transient lingual papillitis, papulokeratotic

front 5 What is the treatment and prognosis for transient lingual papillitis?	back 5 resolves without therapy topical corticosteroids or anesthetics may be used to reduce pain or duration
front 6 Clinical Features one of the most common oral mucosal pathoses (20%) T cell–mediated immunologic reaction with production TNF-α appear to be initiated by some antigenic stimulus may be associated with systemic disorders three clinical variations: mild, moderate, herpetaform occur most in children and young adults (80% before 30 years) Histopathological Features central zone of ulceration covered by fibrinopurulent membrane increased vascularity of connective tissue mixed inflammatory cellular infiltrate	back 6 recurrent aphthous stomatitis
front 7 Clinical Features fewest recurrences and shortest duration arise on nonkeratinized mucosa, especially buccal and labial yellow-white, fibrinopurulent membrane with erythematous halo between 3 and 10 mm in diameter heal in 7 to 14 days without scarring one to five lesions at a time disproportionately painful	back 7 minor aphthous ulceration
front 8 Clinical Features largest lesions and longest duration measure 1 to 3 cm in diameter yellow-white ulceration with red halo take from 2 to 6 weeks to heal and may cause scarring occur most on labial mucosa, soft palate, tonsillar fauces onset after puberty	back 8 major aphthous ulceration

front 9 Clinical Features greatest number of lesions and most frequent recurrences measure 1 to 3 mm in diameter up to a hundred present at once superficial resemblance to primary HSV infection may coalesce into larger irregular ulcerations heal within 7 to 10 days occur on nonkeratinized, movable mucosa female predominance, with onset in adulthood	back 9 herpetiform aphthous ulceration
front 10 Erythematous halo encircling a yellowish ulceration of the soft palate on the left side.	back 10 minor aphthous ulceration
front 11 Two ulcerations of different sizes located on the maxillary labial mucosa.	back 11 minor aphthous ulceration
front 12 Single ulceration of the anterior buccal mucosa.	back 12 minor aphthous ulceration

front 13 Large, deep, and irregular ulceration of the posterior buccal mucosa. Note extensive scarring of the anterior buccal mucosa from previous ulcerations.	back 13 major aphthous ulceration
front 14 Large, irregular ulceration of the soft palate.	back 14 major aphthous ulceration
front 15 Numerous pinhead ulcerations of the ventral surface of the tongue, several of which have coalesced into larger, more irregular areas of ulceration.	back 15 herpetiform aphthous ulceration
front 16 Aphthous ulcerations that heal within 1 to 2 weeks and recur infrequently.	back 16 simple aphthosis

front 17 Aphthous ulcerations that occur in multiples and develop continuously.	back 17 complex aphthosis
front 18 How is recurrent aphthous stomatitis diagnosed?	back 18 No laboratory procedure provides definitive diagnosis; the diagnosis is made from the clinical presentation and from exclusion of other diseases.
front 19 What is the treatment and prognosis for recurrent aphthous stomatitis?	back 19 topical corticosteroids (e.g. dexamethasone, fluocinonide) for mild disease potent corticosteroids (e.g. triamcinolone, clobetasol) for major disease in resistant cases, systemic corticosteroids may be required for control complex aphthosis demands thorough evaluation for systemic disease
front 20 Large ulceration of the left anterior buccal mucosa. Same lesion after 5 days of therapy with betamethasone syrup used in a swish-and-swallow method. The patient was free of pain by the second day of therapy. The ulceration healed completely during the next week.	back 20 major aphthous ulceration

front 21 Clinical Features chronic ocular inflammation and orogenital ulcerations systemic vasculitis caused by an abnormal immune process usually arises in the third and fourth decades increased prevalence and worse clinical course in men oral lesions similar to aphthous ulcers often herald onset genital lesions (papules, vesicles, pustules, etc.) in 75% of cases positive skin “pathergy” self-limiting and nondeforming arthritis ocular involvement (uveitis, conjunctivitis, etc.) in 70% of cases vascular disease often presents as thrombophlebitis variable gastrointestinal disease (pain, anorexia, diarrhea, etc.) CNS involvement (paralysis, dementia) in 10% to 25% of cases Histopathological Features leukocytoclastic vasculitis similar to aphthous stomatitis	back 21 Behçet syndrome
front 22 Diffuse erythema surrounding numerous irregular ulcerations of the soft palate. Oral ulcerations often herald the onset of this disease.	back 22 Behçet syndrome
front 23 Numerous irregular ulcerations of the labia majora and perineum as part of a disease characterized by chronic ocular inflammation and orogenital ulcerations.	back 23 Behçet syndrome
front 24 Sterile pustule of the skin that developed 1 day after injection of saline. This reaction is termed cutaneous pathergy.	back 24 Behçet syndrome

front 25 From a diagnostic standpoint, one of the most important skin manifestations in Behçet syndrome is the presence of positive “pathergy.” What does this refer to?	back 25 One or 2 days after the oblique insertion of a needle under sterile conditions, a tuberculin-like skin reaction or sterile pustule develops.
front 26 No laboratory finding is diagnostic of Behçet syndrome. What In an attempt to standardize diagnoses, five definitive criteria have been developed. What are they?	back 26 recurrent oral ulceration, plus and two of the following: recurrent genital ulcerations eye lesions skin lesions positive pathergy test
front 27 What is the treatment and prognosis for Behçet syndrome?	back 27 most treatment is symptomatic until the disease goes into remission old or female patients have a better prognosis than male or young ocular lesions or CNS involvement mandate more aggressive therapy systemic medications include azathioprine, colchicine, corticosteroids orogenital ulcerations respond to topical or intralesional corticosteroids relapsing and remitting pattern, with attacks lessening after 5 to 7 years
front 28 Clinical Features arises prior to age 50, with predilection for females and blacks acute cases exhibit fever, fatigue, anorexia, or weight loss chronic cases exhibit pulmonary symptoms affects lungs, lymph nodes, skin, eyes, and salivary glands chronic, violaceous, indurated skin lesions ("lupus pernio") scattered, tender erythematous nodules ("erythema nodosum") ocular involvement (25%) often appears as anterior uveitis salivary gland involvement results in enlargement and xerostomia submucosal masses, isolated papules, granularity, or ulcerations occur on buccal mucosa, gingiva, lips, tongue, and palate Histopathological Features granulomatous inflammation aggregates of epithelioid histiocytes surrounding rim of lymphocytes scattered Langhans' or foreign body type giant cells laminated, basophilic, calcified lysosomes ("Schaumann bodies") stellate inclusions of trapped collegen ("asteroid bodies")	back 28 sarcoidosis

front 29 Violaceous indurated plaques of the right malar area and bridge of nose.	back 29 lupus pernio (sarcoidosis)
front 30 Multiple erythematous macules of the hard palate. Oral lesions are uncommon in this disease, but may be normal in color, brown-red, violaceous, or hyperkeratotic.	back 30 sarcoidosis
front 31 Erythematous macules with central hyperkeratosis of the lower labial mucosa. Oral lesions are uncommon in this disease.	back 31 sarcoidosis
front 32 Labial minor salivary gland demonstrating granulomatous inflammation characterized by circumscribed collections of histiocytes, lymphocytes, and multinucleated giant cells.	back 32 sarcoidosis

front 33 Multinucleated giant cell with intracytoplasmic asteroid body, a stellate inclusion consisting of entrapped fragments of collagen.	back 33 sarcoidosis
front 34 A clinical syndrome associated with acute sarcoidosis consisting of erythema nodosum, bilateral hilar lymphadenopathy, and arthralgia.	back 34 Löfgren syndrome
front 35 A clinical syndrome associated with acute sarcoidosis consisting of parotid enlargement, anterior uveitis of the eye, facial paralysis, and fever.	back 35 Heerfordt syndrome (uveoparotid fever)
front 36 How is sarcoidosis diagnosed?	back 36 The diagnosis is established by clinical and radiographic presentations, the histopathologic appearance, and negative tests for casative organisms. Elevated serum angiotensin-converting enzyme (ACE) levels supports the diagnosis, but is reported in only 60% of patients with the disease. In the past, the Kveim test, was performed by intradermal injection of a sterilized suspension of human sarcoid tissue.

front 37 What is the treatment and prognosis for sarcoidosis?	back 37 symptoms may resolve spontaneously within 2 years (60%) intervention is recommended for progressive disease corticosteroids remain first-line therapy resistance and relapses are common resolution may not occur even with treatment (10% to 20%) patients may die of pulmonary, cardiac, or CNS complications (4% to 10%)
front 38 Clinical Features primarily affects adults, but can occur at any age nontender, persistent swelling involving lips may be combined with facial paralysis and fissured tongue intraoral lesions including edema, ulcers, and papules tongue may develop fissures, edema, paresthesia, or erosions gingiva can develop swelling, erythema, or pain buccal mucosa often exhibits a cobblestone linear hyperplastic folds may occur in the sulcus Histopathological Features edema in superficial lamina propria dilation of lymphatic vessels scattered lymphocytes fibrosis in long-term lesions noncaseating granulomatous inflammation granulomas clustered around scattered vessels	back 38 orofacial granulomatosis
front 39 The variant of orofacial granulomatosis in which there is nontender, persistent swelling of the lips combined with facial paralysis and a fissured tongue.	back 39 Melkersson-Rosenthal syndrome
front 40 The variant of orofacial granulomatosis in which there is nontender, persistent swelling of the lips in isolation.	back 40 cheilitis granulomatosa (of Miescher)

front 41 Nontender, persistent enlargement of the upper lip. This patient did not present with facial paralysis nor a fissured tongue.	back 41 cheilitis granulomatosa (orofacial granulomatosis)
front 42 Persistent enlargement of the lower lip. This patient also presented with numerous furrows on the dorsal surface of the tongue.	back 42 Melkersson-Rosenthal syndrome (orofacial granulomatosis)
front 43 Note numerous furrows on the dorsal surface of the tongue. This patient also presented with persistent enlargement of the lower lip.	back 43 Melkersson-Rosenthal syndrome (orofacial granulomatosis)
front 44 Hyperplastic mucosa noted bilaterally in the mandibular mucobuccal fold with elongated ulcerations in the base of these folds.	back 44 orofacial granulomatosis

front 45 Clusters of granulomatous inflammation around scattered vessels. The inset illustrates the histiocytes and multinucleated giant cells within the granulomas.	back 45 orofacial granulomatosis
front 46 How is orofacial granulomatosis diagnosed?	back 46 Based on histopathologic demonstration of granulomatous inflammation that is associated with negative special stains for organisms and no foreign material.
front 47 What is the treatment and prognosis for orofacial granulomatosis?	back 47 first goal of management is discovery of initiating cause intralesional delayed-release high-concentrate triamcinolone prognosis is highly variable; some lesions resolve spontaneously
front 48 Diffuse enlargement of the upper lip. Same patient after intralesional triamcinolone injections.	back 48 orofacial granulomatosis

front 49 Clinical appearance before local therapy. Significant resolution after intralesional corticosteroid therapy.	back 49 orofacial granulomatosis
front 50 Clinical Features wide age range (mean, 41 years), 90% in Caucasians necrotizing granulomatous lesions of respiratory tract (limited) may also exhibit necrotizing glomerulonephritis (generalized) may exhibit lesions of the skin and mucosa (superficial) nasal drainage, sinus pain, nasal ulceration (URT involvement) dry cough, hemoptysis, dyspnea, chest pain (LRT involvement) proteinuria and red blood cell casts (renal involvement) florid and granular ginvival hyperplasia ("strawberry gingivitis") oral ulcerations (usually diagnosed at a later stage) salivary gland enlargement Histopathological Features mixed inflammation centered around blood vessels heavy neutrophilic infiltration, necrosis, and nuclear dust inflammatory cellular infiltrate pseudoepitheliomatous hyperplasia and subepithelial abscesses prominent vascularity with extensive red blood cell extravasation	back 50 Wegener granulomatosis
front 51 Florid and granular gingival hyperplasia with hemorrhagic and friable bulbous projections ("strawberry gingivitis").	back 51 Wegener granulomatosis
front 52 Hyperplastic and hemorrhagic mucosa of the facial mandibular gingiva on the left side. This red, bumpy surface is responsible for the strawberry-like appearance	back 52 Wegener granulomatosis

front 53 Deep, irregular ulceration of the hard palate on the left side. These represent late-stage disease; more than 60% of patients will have renal involvement.	back 53 Wegener granulomatosis
front 54 Connective tissue containing proliferation of numerous vascular channels and a heavy inflammatory infiltrate consisting of lymphocytes, neutrophils, eosinophils, and multinucleated giant cells.	back 54 Wegener granulomatosis
front 55 Gingival biopsy specimen showing a mixed inflammatory cellular infiltrate obscured by extensive extravasation of red blood cells.	back 55 Wegener granulomatosis
front 56 The American College of Rheumatology proposed four diagnostic criteria with a minimum of two required for a diagnosis of Wegener granulomatosis. What are these criteria?	back 56 oral ulcerations or nasal discharge nodules, fixed infiltrates, or cavities on chest radiograph abnormal urinary sediment (e.g. RBCs or casts granulomatous inflammation upon biopsy

front 57 What marker is the most useful in the diagnosis of Wegener granulomatosis, seen in 90% to 95% of generalized cases and 60% of the early or localized cases?	back 57 antibodies against proteinase-3 (PR3-ANCA)
front 58 What is the treatment and prognosis for Wegener granulomatosis?	back 58 mean survival of untreated patients with generalized disease is 5 months 80% of the patients are dead at 1 year and 90% within 2 years prognosis is better for the limited and superficial forms first line therapy is oral prednisone and cyclophosphamide prolonged remission is noted in up to 75% of affected patients for maintenance, cyclophosphamide may be replaced with methotrexate relapse rate up to 30%, maintenance therapy is necessary in many patients
front 59 The risk of an adverse reaction is approximately ___% with the use of two medications, ___% with five drugs, and almost ___% with eight or more.	back 59 6%, 50%, 100%
front 60 What is a Type A drug reaction?	back 60 An exaggerated but otherwise expected pharmacologic action of the prescribed medication (e.g. bleeding associated with warfarin).

front 61 What is a Type B drug reaction?	back 61 An idiosyncratic reaction that is not expected, usually arising from immune-mediated effects (e.g. hypersensitivity reactions).
front 62 A reaction of the oral mucosa to the systemic administration of a medication.	back 62 stomatitis medicamentosa
front 63 Several different patterns of stomatitis medicamentosa exist. What are the seven classes of mucosal reactions to systemic drug administration?	back 63 anaphylactic stomatitis intraoral fixed drug eruptions lichenoid drug reactions pemphigoid-like drug reactions pemphigus-like drug reactions lupus erythematosus–like eruptions nonspecific erosive, ulcerative, or aphthous-like lesions
front 64 Clinical Features various patterns of mucosal alterations erythema or aphthous-like ulcerations localized areas of erythema and edema vesiculoerosive lesions of the labial mucosa lupus-, pemphigoid-, or pemphigus-like lesions bilateral and symmetrical lesions are common Histopathological Features nonspecific pattern of subacute mucositis mixed inflammatory cellular infiltrate spongiosis and exocytosis of the epithelium lupus-, pemphigoid-, or pemphigus-like findings DIF for IgG shows annular pattern along basal cell layer ("sting of pearls") may detect circulating antibody ("basal cell cytoplasmic antibody")	back 64 mucosal reactions to systemic drug administration

front 65 Bilateral erosions of lower labial mucosa with intermixed striae. Biopsy revealed lichenoid pattern of mucositis but with numerous plasma cells intermixed with the lymphocytes. Same patient depicted in A after discontinuation of simvastatin.	back 65 allergic mucosal reaction to systemic drug administration
front 66 Irregular area of superficial erosion of the left buccal mucosa. Lesions were also present on the contralateral buccal mucosa and bilaterally on the lateral borders of the tongue. Lesions disappeared after discontinuing allopurinol.	back 66 lichenoid drug reaction
front 67 Large irregular erosion of the right ventral surface of the tongue. The lesion arose secondary to use of oxaprozin, a nonsteroidal antiinflammatory drug (NSAID).	back 67 allergic mucosal reaction to systemic drug administration
front 68 How are mucosal reactions to systemic drug administration diagnosed?	back 68 identify potentially offending medication through detailed medical history and establish a temporal relationship with the mucosal alteration if more than one suspected, start with most recently added if last-introduced drug is not responsible, do serial elimination definitive diagnosis can be made if mucosal alterations resolve after discontinuation of medication and recur on reintroduction presumptive diagnosis usually is sufficient and justified when the mucosal alterations clear after cessation of the offending medication for lupus-like reactions, consider serum evaluation for ANAs dsDNA Ab

front 69 What is the treatment for mucosal reactions to systemic drug administration?	back 69 discontinue and replace causative drug and if possible lesions can be resolved with topical corticosteroids If discontinuation is contraindicated, palliative care can be provided
front 70 Clinical Features can be acute or chronic distinct female predominance can be localized or diffuse burning is the most frequent symptom mucosa may be barely red to brilliantly erythematous superficial ulcerations occasionally arise muscosa may be white and hyperkeratotic desquamation of the superficial layers of the epithelium dryness, scaling, fissuring, or cracking of the vermilion border	back 70 allergic contact stomatitis
front 71 Mucosal erythema and vesicles of the lower labial mucosa caused by use of aluminum chloride on gingival retraction cord.	back 71 allergic contact stomatitis
front 72 Erythematous mucosa with superficial epithelial desquamation. This patient reported recently changing brands of toothepaste.	back 72 allergic contact stomatitis

front 73 How is allergic contact stomatitis diagnosed?	back 73 diagnosis of acute contact stomatitis is straightforward due to temporal relationship between agent and resultant eruption diagnosis of chronic contact stomatitis is more difficult, requirring good oral health and elimination of all other possible causes
front 74 What is the treatment and prognosis for allergic contact stomatitis?	back 74 for mild acute cases, simply removal of suspected allergen for severe acute cases, antihistamines and topical anesthetics for chronic cases, topical corticosteroid gel or oral suspension use of plain baking soda or flavor-free toothpaste avoidance of mouthwash, gum, mints, chocolate, cinnamon products
front 75 Clinical Features associated with use of potent corticosteroids on face worsened by exposure to UV light, heat, and wind persistent erythematous papules, vesicles, and pustules occur on skin surrounding the vermilion border may involve perinasal skin (40%) zone of spared skin adjacent to vermilion border most occurs in women between ages of 20 to 45 years Histopathologic Findings chronic lymphohistiocytic dermatitis with spongiosis of hair follicles rosacea-like pattern with perifollicular granulomatous inflammation may be misdiagnosed as sarcoidosis	back 75 perioral dermatitis
front 76 Multiple erythematous papules of the skin surrounding the vermilion border of the lips. Note similar involvement around the nasal orifices.	back 76 perioral dermatitis

front 77 What is the treatment for perioral dermatitis?	back 77 discontinue corticosteroids, cosmetics, facial creams (“zero therapy”) oral tetracycline is "gold standard," except in childhood and pregnancy responds well to topical pimecrolimus or topical erythromycin improvement within weeks, resolution in months, recurrence uncommon
front 78 Clinical Features associated with candy, chewing gum, and toothpaste pain and burning are common in all cases affects gingiva, buccal mucosa, lateral borders of tongue may resemble plasma cell gingivitis enlargement, edema, and erythema hyperkeratosis of surface epithelium Histopathologic Findings acanthotic, often with elongated rete ridges thinning of the suprapapillary plates hyperkeratosis and extensive neutrophilic exocytosis heavy inflammatory cell infiltrate	back 78 contact stomatitis from cinnamon flavoring
front 79 Oblong area of sensitive erythema with overlying shaggy hyperkeratosis. Buccal mucosal lesions often are aligned along the occlusal plane.	back 79 contact stomatitis from cinnamon flavoring
front 80 Sensitive and thickened hyperkeratosis of the lateral and dorsal surface of the tongue on the right side.	back 80 contact stomatitis from cinnamon flavoring

front 81 Left lateral border of the tongue demonstrating linear rows of hyperkeratosis that resemble oral hairy leukoplakia (OHL).	back 81 contact stomatitis from cinnamon flavoring
front 82 Oral mucosa demonstrating significant interface mucositis and deeper perivascular inflammation. Heavy inflammatory cell infiltrate often obscures the epithelium and connective tissue interface.	back 82 contact stomatitis from cinnamon flavoring
front 83 Perivascular inflammatory infiltrate consisting predominantly of lymphocytes and plasma cells, a characteristic feature in localized cases.	back 83 contact stomatitis from cinnamon flavoring
front 84 How is contact stomatitis from cinnamon flavoring diagnosed?	back 84 Based on the clinical appearance and the history of cinnamon use; often biopsies are performed for atypical or extensive cases.

front 85 What is the treatment and prognosis for contact stomatitis from cinnamon flavoring?	back 85 disappears within 1 week of discontinuation of cinnamon product patient may benefit from short-term use of a topical corticosteroid
front 86 The vast majority of hypersensitivity reactions to dental restorative materials are to dental amalgam. What component is largely responsible?	back 86 mercury
front 87 Although rare acute reactions to mercury may be seen following placement of amalgam, the vast majority of adverse alterations are associated with older and corroded amalgams. What type of hypersensitivity reactions are these?	back 87 type IV hypersensitivity reaction
front 88 Clinical Features associated with dental restorations can be acute (rare) or chronic buccal mucosa and ventrolateral tongue white or erythematous, with or without peripheral striae no symptoms, but periodic erosion may be noted Histopathologic Findings numerous features of lichen planus hyperkeratotic, atrophic, or ulcerated surface epithelium hydropic degeneration of basal cell layer dense bandlike chronic inflammatory cellular infiltrate	back 88 lichenoid contact reaction to dental restorative material

front 89 Hyperkeratotic lesion with a peripheral radiating pattern on the lateral border of the tongue on the right side; the altered mucosa contacted the amalgams of the adjacent mandibular molar teeth. Appearance of previously altered area of the tongue 14 days after removal of adjacent amalgams. Note total resolution of the mucosal alterations.	back 89 lichenoid contact reaction to dental amalgam
front 90 Radiating pattern of hyperkeratotic striae on the posterior buccal mucosa that contacts a large distobuccal amalgam of the permanent mandibular second molar.	back 90 lichenoid contact reaction to dental amalgam
front 91 How is lichenoid contact reaction to dental amalgam diagnosed?	back 91 Based on (a) the clinical appearance of the lesion, (b) the lack of lesional migration, and (c) the correlation to adjacent dental metal.
front 92 What is the treatment and prognosis for lichenoid contact reaction to dental amalgam?	back 92 acute reactions are self-limiting and resolve within 2 to 3 days for chronic reactions, local measures should be attempted first if unsuccessful, the amalgam in question should be replaced

front 93 A diffuse edematous swelling of the soft tissues, which has also been referred to historically as Quincke disease.	back 93 angioedema
front 94 Angioedema is a diffuse edematous swelling of the soft tissues. What are the potential causes of angioedema?	back 94 allergic IgE-mediated hypersensitivity reactions angiotensin-converting enzyme (ACE) inhibitors hereditary—type I (C1-INH deficiency) or type II (C1-INH dysfunction) acquired—lymphoproliferative or autoimmune
front 95 An unusual pattern of drug reaction that can produce severe forms of angioedema that are not mediated by IgE is the type associated with ACE inhibitors. What is thought to be the cause of this reaction?	back 95 excess bradykinin (ACE degrades bradykinin)
front 96 Clinical Features rapid onset of soft, nontender tissue swelling may be solitary or multiple extremities most common cutaneous sites edema of larynx, pharynx, uvula, or soft palate deeper voice, hoarseness, aphonia, and dyspnea pain is unusual, but itching is common typically resolves over 24 to 72 hours drug-associated form more common in blacks	back 96 angioedema

front 97 Diffuse upper lip swelling that arose rapidly.	back 97 angioedema
front 98 A, Soft, nontender tissue swelling of the face arose relatively rapidly after dental treatment. Facial appearance after resolution of edematous facial enlargement.	back 98 angioedema
front 99 How is angioedema diagnosed?	back 99 for allergic causes, diagnosis is based on clinical presentation in conjunction with the known antigenic stimulus case unrelated to antigenic exposure or medications should be evaluated for the presence of adequate functional C1-INH: type I hereditary—normal C1, low C1-INH type II hereditary—normal C1, normal C1-INH lymphoproliferative—low C1, low C1-INH autoimmune—low C1, normal C1-INH
front 100 What is the treatment and prognosis for angioedema?	back 100 oral antihistamines, IM epinephrine, IV corticosteroids discontinue ACE inhibitors