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OPT Allergies
| Term | Definition |
|---|---|
| transient lingual papillitis | enlargement of fungiform papilla on dorsal tongue |
| localized form of transient lingual papillitis | one enlarged fungiform papilla on anterior tongue |
| diffuse form of transient lingual papillitis | many enlarged, painful fungiform papilla; sometimes with fever and lymphadenopathy |
| 'papulokeratotic variant' of transient lingual papillits | diffuse and asymptomatic enlargement of fungiform papillae; most likely frictional hyperkeratosis |
| recurrent apthous stomatitis/ulceration (RAS/RAU) | oral ulcers mediated by CD8 T-cells |
| 1. antigenic stimulus 2. immunodysregulation 3. decreased mucosal barrier | 3 pathologic mechanisms of apthous stomatitis |
| simple apthosis | most common type of RAS; self-limiting without other disease processes |
| complex apthosis | patients that have several apthous ulcers with significant disease and recurrences |
| minor apthous stomatitis | mildest form of RAU; a couple of outbreaks each year, usually in adolescents |
| major apthous stomatitis | large ulcers with long healing time and a later onset |
| herpetiform apthous stomatitis | numerous small ulcers like herpes but not on gingiva or systemic symptoms |
| Behcet syndrome | systemic vasculitis with irregular oral ulcers on soft palate, genital ulcers, and ocular problems |
| sarcoidosis | multisystem granulomatous disorder, probably autoimmune; lungs and lymphoid tissues are most affected -oral involvement of mass or papules is seen first in 2/3 of patients |
| Heerfordt syndrome | acute form of sarcoidosis; parotid gland enlargement, facial nerve paralysis, uveitis and fever |
| orofacial granulomatosis | variety of clinical presentations that show non-specific granulomatous inflammation; called Melkersson-Rosenthal syndrome when with facial paralysis and fissured tongue |
| Wegener granulomatosis | necrotizing granulomatosis lesions of respiratory tract; effects in kidneys and vasculitis |
| classic/generalized Wegener granulomatosis | fatal kidney involvement after initial respiratory infection |
| limited Wegener granulomatosis | disease stays localized to respiratory tract without renal lesions |
| 'superficial' Wegener granulomatosis | only have skin and oral mucosal lesions |
| strawberry gingivitis | early manifestation of Wegener granulomatosis |
| PR3-ANCA | antibodies detected in 90% of patients with Wegener's and can be used to monitor disease activity |
| stomatitis medicamentosa | mucosal reactions to systemic drugs |
| anaphylactic stomatitis | IgE mediated erythema and ulceration 24 hours after exposure to drug |
| fixed drug eruptions | reactions that reappear at same site after taking drug |
| lichenoid drug reactions | mucosal changes from systemic drug that mimic lichen planus |
| pemphigus-like drug reactions | mucosal desquamation and bullae formation like pemphigus |
| pemphigoid-like drug reactions | mucosa comes off in sheets and mimics pemphigoid |
| lupus erythematous-like drug reactions | fever, flu-like symptoms and lupus-like changes |
| nonspecific vesiculoerosive or apthous-like lesions | nonspecific mucosal changes due to drug reaction |
| allergic contact stomatitis | long list of agents that cause hypersensitivity reaction; {from artificial cinnamon flavoring} |
| perioral dermatitis | inflammatory reaction around mouth from antigen or corticosteroid cream |
| lichenoid contact reaction to dental restorative materials | reaction adjacent to old, corroding amalgam fillings |
| angioedema | diffuse edematous swelling of soft tissue; minor trauma can precipitate reaction |
| IgE-mediated type I hypersensitivity reactions | most common cause of angioedema; mast cells degranulate and histamine is released |
| angiotensin-converting enzyme (ACE) inhibitors | drug used to treat hypertension that also causes angioedema due to increased levels of {bradykinin} |
| angiotensin II receptor blockers | drugs developed to avoid inhibition of bradykinin breakdown and angioedema |
| activation of complement pathway | mechanism of causing angioedema; can be hereditary or acquired |
| type I complement pathway | inherited from decreased {C1 esterase inhibitor} that enhances complement pathway |
| Type II complement pathway | normal C1-INH levels but enzyme does not work |
| acquired type of C1-INH deficiency | can be seen in lymphoproliferative diseases that inhibit C1-INH |
Created by:
aharnold
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