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Oral Medicine and Diagnosis > Vesiculobullous and Ulcerative Lesions part 1 > Flashcards

Vesiculobullous and Ulcerative Lesions part 1 Flashcards

1
Q

oral lichen planus seen _____ frequently than cutaneous lichen planus

A

more

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2
Q

which type of lichen planus is more persistent and more resistant to tx

A

oral lichen planus

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3
Q

what ages get lichen planus

A
  • occurs in 4th-8th decades
  • mean age in 5th decades
  • rare in children
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4
Q

what is the incidence of lichen planus

A

-3-4% incidence; 25% with oral lesions have concomitant skin lesion
- 0.5-1% cutaneous incidence; 50% also have oral lesions
- white females (60%)

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5
Q

what are the frequency of sites of lichen planus

A
  • bilateral and often quasi-symmetric distribution
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6
Q

what is the oral site frequency of lichen planus

A
  • buccal mucosa
  • tongue
  • gingiva
  • lips
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7
Q

what are the skin sites in LP

A
  • forearm
  • shin
  • scalp
  • genitalia
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8
Q

what is the pathophysiology of LP

A
  • autoimmune disease; t-lymphocytes attack langerhan cells in epithelium of affected areas
  • causes chronic inflammatory lesions with varying episodes of intensity
  • not infectious
  • not hypersensitivity
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9
Q

what is the etiology of LP

A
  • NSAIDs - ibuprofen and naproxen
  • various medications for heart disease and HTN, and RA - hydrochlorothiazide
  • hep C and other types of liver disease
  • vaccines - Hep B, various flu vaccines, COVID vaccine uncertain
  • food allergens
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10
Q

what are instigating factors for LP

A
  • co-morbidities such as DM
  • alcohol, tobacco
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11
Q

what is the clinical presentation of LP

A

erythematous
- ulcerated
- keratotic triations
- episodic pain to severe discomfort

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12
Q

what are the clinical symptoms for LP

A
  • asymptomatic
  • itching
  • episodic pain
  • severe discomfort
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13
Q

what are the clinical types of LP

A
  • reticular
  • erosive
  • patch
  • bullous
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14
Q

what is the most common LP

A

reticular

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15
Q

what is the most painful LP

A

erosive

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16
Q

what LP stimulates dysplasia

A

patch

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17
Q

what LP is clinically similar to diseases of greater morbidity

A

bullous

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18
Q

how is reticular LP described clinically

A

lacy
- striated
- wickham striae

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19
Q

where is erosive LP seen

A
  • buccal and labial mucosa
  • tongue laterodorsum
  • gingiva
  • palate
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20
Q

describe the clinical presentation of erosive LP

A
  • large, irregular atrophic erythematous patches diffuse outlines
  • progress to ulcerations, pseudomembranous cover
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21
Q

what are the symptoms of erosive LP

A
  • epsidoic pain to severe discomfort
  • symptoms may persist weeks or longer
  • symptoms result in weight loss, nutritional deficiencies and depression
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22
Q

what is the DDX for LP

A
  • lichenoid dysplasia
  • contact stomatitis
  • lichenoid reaction
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23
Q

what are the treatment goals for lichen planus

A
  • there is no cure
  • reduce length and severity of symptoms
  • resolve oral mucosal lesions
  • reduce risk of malignant degeneration to squamous cell carcinoma
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24
Q

what are the tx issues with LP

A
  • maintain good OH because good OH reduces symptom severity
  • OH is difficult to accomplish during active disease
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25
Q

what are the medications used to treat LP

A
  • oral anesthetic rinse - 1% dyclonine solution
  • antibiotics
  • antifungals with steroid- nystatin with triamcinolone
  • corticosteroids
26
Q

what is the treatment regimen with topicals for LP and why is it used

A
  • 4-6 week course
  • most popular, best success with steroid carriers
27
Q

what is the mild treatment regimen for LP

A
  • cortisone 5% ointment
  • triamcinolone 0.1% ointment
28
Q

what is the moderate treatment regimen for LP

A
  • cortisone 10% ointment
  • fluocinonide gel 0.05%
  • dexamethasone 0.05% ointment
29
Q

what is the potent treatment regimen for LP

A
  • clobetasol 0.05% ointment/gel
  • halobetasol 0.05% ointment
30
Q

what is the difference between steroid carriers and bleaching trays

A

need to border mold the impressions so tray extends to mucobuccal folds with steroid carriers

31
Q

what is the treatment regimen for intra lesion steroid injections for LP

A
  • 12 mg/week dexamethasone for 8 weeks
  • 5-10 mg/wek triamcinolone PRN
32
Q

what is the treatment regimen for systemic steroids with LP

A
  • prednisone 2-3 weeks
  • loading dose 0.5-1mg/kg/day (40-80 mg/qd)
  • need tapering down regimen
33
Q

what is the treatment regimen for methotrexate

A
  • 10-20 mg once weekly for 4-12 weeks
34
Q

what other medications are used to treat LP

A
  • hydroxychloroquine (plaquenil)
  • thalidomide
  • calcineurin inhibitors
  • dapsone
35
Q

what is the issue with thalidomide

A
  • bad history when used in pregnancy for anxiety, morning sickness headache
  • thalidomide babies had lack of appendage development or other aplasias such as ears or malformed kidneys
36
Q

what is the contemporary use for thalidomide

A

inflammatory mucocutaneous diseases

37
Q

what is hydroxycholoroquine used for

A

disease modifying anti RA drug (DMARD), anti malarial, anti COVID
- relieve inflammation, swelling, stiffness and joint pain

38
Q

what do calcineurin inhibitors do

A
  • anti inflammatory medication primarily used for anti graft rejection
  • pimecrolimus cream
  • tacrolimus ointment
  • psychotic and renal side effects when used systemically
39
Q

what is dapsone

A
  • an antibiotic with anti inflammatory properties
  • can block multiple PGEs and leukotrienes thereby blocking their inflammatory effects
  • potential risk of renal vasculitis
40
Q

what is the risk for untreated LP

A
  • malignant potential risk is 0.1-0.2%
41
Q

which types of LP have the greatest risk of transforming to malignant

A

erosive and ulcerative conditions

42
Q

what are the 3 types of aphthous stomatitis

A
  • minor
  • major
  • herpetiform
43
Q

what is the prevalence of aphthous stomatitis

A

affects 18-27% of the population
- prevalence is about 20%

44
Q

what is the etiology of aphthous stomatitis

A

unknown
- no viral or infectious agent identified
- probbaly is focal immunodysfunction but mechanism is undetermined
- HLA subtype susceptibility is a factor

45
Q

what are the triggers for apthous stomatitis

A

stress/anxiety, hormonal changes, dietary factors, trauma

46
Q

what are human leukocyte antigens and what do they do

A

a system or complex of genes on chromosome 6 in humans which encode cell surface proteins responsible for regulation of the immune system

47
Q

HLA subtype allele mutations permit:

A

dysregulation of the immune system taht affects mucosa and cutaneous tissues and cause outbreaks of aphthous stomatitis

48
Q

in aphthous stomatitis alterations in mucosal membrane barrier permeability may be a factor because of co morbidity associations with:

A
  • HIV/AIDS
  • bone marrow suppression
  • neutropenia
  • gluten sensitivty
  • Chron’s disease
  • ulcerative colitis
  • food allergy
  • behcet disease
  • dietary deficiencies such as iron, zinc and vitamin B12
49
Q

what is the clinical description of aphthous stomatitis ulcers

A
  • recurrent, self limiting, painful ulcers
  • usually restricted to nonkeratinized oral and pharyngeal mucosa- not hard palate or attached gingiva
  • well demarcated ulcers with yellow fibrinous base and erythematous halo
50
Q

describe aphthous minor and when does healing occur

A
  • most common subtype
  • single but more often multiple
  • less than 1cm in diameter
  • oval to round shape
  • healing within 7-14 days
51
Q

describe ahphtous stomatitis major and what is its other name

A
  • sutton disease
  • 1cm or greater
  • single or less commonly several
  • deep
  • to ragged edges with elevated edematous margin
  • may persist for several weeks to months
  • often heal with scarring
52
Q

describe herpetiform aphthous stomatitis

A
  • least common variant
  • grouped superficial ulcers 1-2mm diameter
  • crops of 10-100 lesions
  • lesions coalesce
  • in nonkeratinizaed and keratinized tissues
  • healing within 7-14 days
  • no etiologic role for herpes simplex virus
53
Q

what is the dx for aphthous stomatitis

A
  • usually has diagnostic clinical appearance of focal, well- defined ulcers involving non keratinized mucosa
  • history helpful; a recurrent process
  • positive family history
54
Q

what is the DDX for aphthous stomatitis

A
  • traumatic ulcer
  • chancre
  • recurrent intraoral herpes simplex virus HSV-1
  • cyclic neutropenia
55
Q

what is the treatment for aphthous stomatitis

A
  • symptomatic therapy
  • systemic causative factors should be addressed
  • tetracycline based oral rinses may be helpful
  • corticosteroid therapy- most rational and most consistently effective
  • topical corticosteroids as gels, creams or ointment 4-6 times/ day to early lesions
  • intralesional corticosteroid injections
  • short duration systemic corticosteroids ( low to moderate doses)
  • other immunomodulating drugs may be helpful
  • colchicine sometimes beneficial
  • thalidomide treatment
56
Q

what immunomodulating drugs are helpful in aphthous stomatitis lesions

A
  • dapsone
  • hydroxychloroquine
  • topical tacrolimus
  • amelexanox
57
Q

what dosage of colchicine for aphthous stomatitis

A

0.6-1.2mg/day

58
Q

which form of aphthous stomatitis is more common recurrent form

A

minor

59
Q

how often do minor aphthous stomatitis lesions appear

A

episodic, 1-4 episodes/year
- few lesions, usually minor or herpetiform

60
Q

how often do major aphthous sotmatitis lesions appear

A

almost continuous ulcerations; disabling large or severe lesions

61
Q

what is the difference in AIDS patients with aphthous stomatitis

A

lesions are more severe and may occur on any oral surface

62
Q
A

Oral Medicine and Diagnosis (12 decks)

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