Lec 4: Red Lesions Flashcards
Vesicle vs. Ulcer
A vesicle may eventually lose the overlying epithelium and then present as an ulceration
EPIDERMOLYSIS BULLOSA defect in?
Defect in the attachment mechanisms of the epithelial cells
EPIDERMOLYSIS BULLOSA cure?
No cure
EPIDERMOLYSIS BULLOSA management?
supportive
EPIDERMOLYSIS BULLOSA–Vesicles and bullae due to?
minor trauma
EPIDERMOLYSIS BULLOSA–oral lesions? (2)
Bullae may heal with scarring; restricted opening
Hypoplastic teeth
VIRAL DISEASES onset?
acute
VIRAL DISEASES symptoms?
May have malaise, fever, lymphadenopathy
Lymphadenopathy not present with?
recurrent herpes and zoster
Viral diseases all have?
vesicle stage
Viral diseases multiple___
ulcers
Spread predominantly through infected saliva or active perioral lesions
Adapted best to the oral, facial and ocular areas
Developed nations show 20% exposure at age 5 and 50-60% at adulthood
Herpes simplex 1
Adapted best to genital zones
Transmitted through sexual contact, typically involving the genitalia
Herpes simplex 2
Primary infection? occurs at? symptomatic or asymptomatic?
Initial exposure of individual without antibodies to virus
Typically occurs at young age
Often asymptomatic or subclinical
Latency? most common?
Virus taken up by sensory nerves
Most common site for HSV-1 is trigeminal ganglion
Recurrent? affect the? usually symptomatic or asymptomatic?
Reactivation of the virus
Affect the epithelium supplied by sensory gangilion
Usually symptomatic
Primary Herpetic Gingivostomatitis
Lymphadenopathy present
Multiple vesicles and ulcers anywhere in oral cavity, pharynx, and perioral skin
May present subclinically
Primary Herpes
Numerous pinhead vesicles develop
Lesions enlarge slightly and develop central ulceration
In primary herpes, Sometimes yellow fibrin covers the ulcers, which may?
coalesce
Primary herpes involves
keratinized and non-keratinized mucosa
In Primary herpes, the gingiva is always enlarged and..
painful and extremely red
Primary Herpes treatment?
Acyclovir (Zovirax)
Adults: 200mg
resolves in 10-14 days
HERPES SIMPLEXRECURRENT HERPES aka
cold sore and fever blisters
Prodrome: tingling, burning, paresthesia
RECURRENT HERPES occur in? appears on?Lymphadenopathy present?
small clusters;
Appears on On vermilion border, perioral skin and keratinized oral mucosal surfaces; Recur in same location each time; NO
HERPETIC WHITLOW (HERPETIC PARONYCHIA): due to? common in what profession?
Due to self-innoculation in children. Used to be common in dentists before gloves.
HERPES GLADIATORUM (SCRUMPOX): common in
wrestlers and rugby players
CHRONIC HERPETIC INFECTION: seen in?
immunocompromised hosts
TZANCK CELL?
free floating epithelial cell
Recurrent Herpes treatment? (2)
Medication most effective if taken at prodrome
RX: Valacyclovir (Valtrex)
Rx: Acyclovir
HEREPES ZOSTER (SHINGLES)-zooster represents a?
recurrence
Herpes Zoster (Shingles)-unilateral or bilateral?
Unilateral distribution
Herpes Zoster (Shingles) follows peripheral?
nerve distribution
Herpes Zoster (Shingles)–prognosis?
Post-herpetic neuralgia: chronic severe pain in nerve distribution after lesions resolve
INFECTIOUS MONONUCLEOSIS etiology?
Epstein-Barr virus (EBV, HHV-4)
EBV also associated with:
Burkitt’s lymphoma
Nasopharyngeal carcinoma
Hairy leukoplakia
INFECTIOUS MONONUCLEOSIS– Laboratory features?
Leukocytosis
Lymphocytosis with atypical T lymphocytes
Positive serology
INFECTIOUS MONONUCLEOSIS–oral mucosa?
Erythematous
Petechiae on palate
Ulcers without vesicles, later in disease
HAND, FOOT AND MOUTH DISEASE etiololgy?
coxsackievirus, group A
HAND, FOOT AND MOUTH DISEASE lesions?
Vesicles and ulcers throughout oral cavity
Macules and vesicles on hands and feet
HERPANGINA etiology?
coxsackievirus, group A
HERPANGINA-lesions?
Similar to HFM, but confined to posterior oral cavity
Soft palate, uvula, tonsillar pillar
MEASLES (RUBEOLA)–Viral infection caused by a member of the?
paramyxovirus family
MEASLES (RUBEOLA)–spread through?
respiratory droplets
MEASLES (RUBEOLA)–appearance signs?
Koplik’s spots
“Grains of salt”
AUTOIMMUNE DISEASES onset? progressive? These diseases cannot be cured but can be?
Gradual onset: weeks to months; progressive; controlled with corticosteroids
Treatment of Non-Microbial Mucositis with Corticosteroids
Topical Steroids
Systemic Steroids
Intralesional Steroids
Treatment of Non-Microbial Mucositis with Corticosteroids–Topical Steroids?
Mouthrinse
Dexamethasone
Triamcinolone acetonide
Ointment
Treatment of Non-Microbial Mucositis with Corticosteroids–Systemic Steroids?
Prednisone: 30-60 mg A.M. x 5 days, followed by 5-20 mg A.M. QOD
Treatment of Non-Microbial Mucositis with Corticosteroids–Intralesional Steroids?
Triamcinolone acetonide, inject 10-40 mg
EROSIVE LICHEN PLANUS–cause?
Immune abnormality involving T lymphocytes
Lichenoid drug reactions
Graft-versus-host reactions
Erosive Lichen Planus: Oral Lesions–appearance? vesicles are? bilateral or unilateral?
white striae along periphery;
Vesicles are rare;
Bilateral; focal or generalized
PEMPHIGUS VULGARIS–etiology?
autoantibodies to intercellular protein in desmosomes
PEMPHIGUS VULGARIS–type of blisters?
Fragile blisters rupture easily forming painful ulcers
PEMPHIGUS VULGARIS-sign? Large areas of skin or mucosa involved; usually?
Nikolsky sign sometimes present; multifocal