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skin and mucosal dx 1 Flashcards

1
Q

Ectodermal dysplasia
 what fails to develop? examples?
inheritance pattern?

A

 Two or more ectodermally derived structures fail to develop
 Hair, skin, nails, teeth, sweat glands, salivary glands
 AD, AR, X-linked inheritance

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2
Q

Ectodermal dysplasia
 Clinical features of the most common form:
 sex?
 sweat?
 hair?
 Salivary glands?
 Teeth?

A

 Hypohidrotic ectodermal dysplasia (most common form):
 Male predominance
 Reduced number of sweat glands → cannot regulate heat (resemble infection in neonates)
 Sparse hair, reduced eyebrows, eyelashes
 Salivary glands may be hypoplastic or absent
 Teeth – hypodontia, abnormal shape

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3
Q

ecto dysplasia tx

A

Genetic counseling, prosthetic appliance

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4
Q

likely dx?

A

ED

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5
Q

White sponge nevus
 Defect in?
inheritance?
 mutation?

A

 Defect in the normal keratinization of oral mucosa= hyperkerstosis
 AD inheritance
 Keratin 4, Keratin 13 mutation

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6
Q

White sponge nevus
 Clinical features:
 Usually appear when?
 app?
 MC location?
 other locations?
 Treatment:

A

 Usually appear at birth, early childhood
 Symmetrical, thickened plaques
 White, corrugated appearance
 MC buccal mucosa bilaterally
 Ventral tongue, labial mucosa, soft palate, alveolar mucosa, FOM
 Treatment: none

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7
Q

likely dx? dif?

A

white sponge nevus
dif: cheek biting, leukoedema, LP, candidasis

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8
Q

likely? dif?

A

white sponge nevus
dif: cheek biting, leukoedema, LP, candidasis

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9
Q

white spoong nevus histo

A

hyperkeratosis and acanthosis at low power and peri-nuclear condensation of keratin tonilfilaments

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10
Q

what is this?

A

white sponge nevus biopsy: peri-nuclear condensation of keratin tonilfilaments

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11
Q

Ehlers-Danlos syndrome
 def
 genes involved?

A

 Connective tissue disorder, production of abnormal collagen
 Many genes involve

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12
Q

Ehlers-Danlos syndrome
 Clinical features: skin, joints, bruising, Gorlin sign?
 Type VIII ?

A

 Hyperelasticity of the skin, cutaneous fragility
 Hypermobility of joints – remarkable flexibility
 Patients may bruise easily
 Gorlin sign: touch the tip of the nose with tongue! (50% of patients)
 Type VIII – rare type, periodontal disease

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13
Q

Ehlers-Danlos syndrome tx:
depends on?
mild type?

A

 Treatment: Depends on subtype
 Mild type: compatible with normal life span

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14
Q

Peutz-Jeghers syndrome
 inheritance?
 Mutations?

A

 AD inheritance
 Mutations in tumor-suppressor gene – STK11

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15
Q

Peutz-Jeghers syndrome
 Clinical features:
 Pigmented lesions where?
 Intestinal?
 Increased frequency of?
 Intraoral lesions where?

A

 Pigmented lesions on periorificial areas (mouth, nose, anus, genital region) and extremities
 Intestinal polyps – may develop into adenocarcinoma (like gardner syndrome)
 Increased frequency of other malignancies
 Intraoral lesions: buccal mucosa, labial mucosa, tongue

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16
Q

Peutz-Jeghers syndrome tx

A

patients should be monitored for tumor development

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17
Q

likely dx? dif?

A

preutz jaeger
dif: oral melanotic macules

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18
Q

Epidermolysis bullosa
 dx type?
 cause?
 Defect in?

A

 Mucocutaneous disease, several types
 Genetic mutation
 Defect in attachment mechanisms of epithelial cells

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19
Q

Epidermolysis bullosa
 what can develop from low-grade trauma?
 Result in? causing?
 forms?
 Oral signs?

A

 Vesicles and bullae develop from low-grade trauma
 Result in erosions and ulcerations that cause scarring
 Minor forms and severe forms
 Oral: gingival erythema, recession, loss of vestibule depth

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20
Q

Epidermolysis bullosa bullae structure

A
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21
Q

Epidermolysis bullosa tx

A

wound care, antibiotics, surgery
 Recommend noncariogenic diet (soft foods), atraumatic oral hygiene procedure

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22
Q

histo of?

A

Epidermolysis bullosa or pemphigoid

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23
Q

likely?

A

Epidermolysis bullosa

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24
Q
A

white sponge nevus

25
Behçet syndrome (Behçet Disease)  Combination of?  Abnormal process? triggeR?  Genetic predisposition?
 Combination of chronic ocular inflammation, oro-genital ulcerations, and systemic vasculitis  Abnormal immune process triggered by an infectious or environmental antigen  Genetic predisposition – HLA-B51
26
Behçet syndrome (Behçet Disease)  Clinical features:  MC age?  Increased prevalence in?  Most patients have what oral sign?  Genital lesions?
 MC 3rd and 4th decade  Increased prevalence in males  Most patients have oral ulcerations: Ulcerations may appear similar to aphthous stomatitis, Usually surrounded by a larger area of erythema (not specific)  Genital lesions: irregular ulcerations
27
Behçet syndrome (Behçet Disease)  Clinical features:  Vascular?  Cutaneous lesions?  Ocular?  Blindness %?  CNS involvement?
 Vascular disease: veins affected more frequently – inflammation, thrombi  Cutaneous lesions: erythematous papules, vesicles, pustules  Ocular involvement: uveitis, conjunctivitis, corneal ulceration, arteritis  Blindness occurs in 25% patients  CNS involvement: includes paralysis and dementi
28
Behçet syndrome (Behçet Disease) tx
may require systemic meds (corticosteroids, immunosuppressants)
29
likely? (pt also presents with conjunctivitis/ corneal ulceration)
Behçet syndrome
30
pt has oral ulcerations and conjuctivitis, likely dx? (35 yo male)
Behçet syndrome
31
Reactive Arthritis/ Reiter syndrome  Likely an?  Genetic predisposition?
 Likely an immunologically mediated disease, triggered by an infectious agent  Genetic predisposition – HLA-B2
32
Reactive Arthritis/ Reiter syndrome  Clinical features:  Prevalent in?  Triad:
 Prevalent in young adult men  Triad:  Urethritis (often first sign)  Arthritis –usually affects joints of lower extremities  Conjunctivitis
33
Reactive Arthritis/ Reiter syndrome  Clinical features:  Oral? where?  Skin lesions?
 Oral: erythematous papules, shallow ulcers (non-specific)  On tongue, buccal mucosa, palate, gingiva  Skin lesions on penis – balanitis circinata: Similar appearance to geographic tongue
34
Reactive Arthritis/ Reiter syndrome tx
NSAIDS for managing arthritis, corticosteroids, immunosuppressants
35
young man with urethritis as well
Reactive Arthritis
36
young male who also has urethrhitis, conjuctivits and joint pain
reactive arthritis
37
Psoriasis  chronic? % affected?  Increased activity?  factors playing a role?  Prevalence of erythema migrans?
 Chronic skin disease, affects 2% of US population  Increased proliferative activity of cutaneous keratinocytes  Genetic and environmental factors may play a role  Prevalence of erythema migrans appears to be higher than general population
38
Psoriasis Clinical features:  Onset during what ages?  Persists for?  MC on? distribution?  app?  Lesions seasonality?
 Onset during 2nd-3rd decade  Persists for years, with periods of exacerbation and inactivity  MC on scalp, elbows, knees – often symmetrically distributed  Well-demarcated, erythematous plaque with silvery scale on surface  Lesions improve during summer and worsen during the winte
39
psoarisis tx
topical corticosteroids for moderate involvement
40
middle aged woman
Psoriasis
41
likely?
Psoriasis
42
Lupus erythematosus  mediated by?  Common?  Systemic lupus erythematosus (SLE)  Chronic cutaneous lupus erythematosus (CCLE)
 Immune mediated condition  Common connective tissue disease in the US  Systemic lupus erythematosus (SLE): multisystem disease: solid organs, cutaneous and oral manifestation  Chronic cutaneous lupus erythematosus (CCLE): primarily affects skin and oral mucosa
43
Lupus erythematosus  Clinical features: (SLE)  sex?  MC diagnosis decade?  signs/symptoms?  common rash?
 Females: 8-10x more common  MC diagnosis in 4th decade  Fever, weight loss, arthritis, fatigue  Butterfly rash (erythematous rash) over malar area and nose (40-50% patients), Sunlight may exacerbate lesion
44
Lupus erythematosus  Clinical features (SLE):  Kidneys?  Cardiac?  Oral lesions? specific? where?
 Kidneys affected (40-50% patients) – may lead to kidney failure  Cardiac involvement - endocarditis  Oral lesions: may appear lichenoid, erythema and ulcerations may be present, often nonspecific (similar app to LP)  palate, buccal mucosa, lips, gingiva
45
dif?
erosive LP CCLE SLE
46
Lupus erythematosus  Clinical features (CCLE):  systemic signs or symptoms  Lesions limited?  Skin lesion?  Oral lesion?
 Few or no systemic signs or symptoms  Lesions limited to skin or mucosal surfaces  Skin lesion: scaly, erythematous patches (sun-exposed skin)  Oral lesions: lichenoid appearance (like LP), Rarely occur in absence of skin lesions
47
Lupus erythematosus  Diagnosis:
 Antibodies directed against double-stranded DNA (70% SLE patients
48
Lupus erythematosus tx  Avoid?  Mild cases may be managed with?  Severe cases  Prognosis depends on?
 Avoid excessive sunlight exposure  Mild cases may be managed with NSAIDS  Severe cases: systemic corticosteroids, immunosuppressive medications  Prognosis depends on organs affected
49
Lupus erythematosus
50
SLE
51
pt has malar rash
SLE
52
Angioedema  def  involves?  MC cause:  Ig involved?  Alternative mechanism:
 Diffuse, edematous swelling of soft tissue  involves subcutaneous and submucosal connective tissue  MC cause: mast cell degranulation → histamine release  IgE-mediated hypersensitivity (drugs, foods, plants, dusts)  Alternative mechanism: ACE inhibitors (0.1 – 0.2%) due to Excess bradykinin
53
Angioedema  Clinical features:  MC where?  ACE-inhibitor associated angioedema: frequently affects where? race?
 Rapid onset of soft, nontender tissue swelling  MC in extremities, also face, neck, trunk, genitals  ACE-inhibitor associated angioedema: frequently affects H&N (Face, lips, tongue, FOM, pharynx, larynx)  3-4x Black patients
54
Angioedema  Diagnosis:
 Clinical presentation and determination of antigenic stimulus
55
Angioedema tx
Allergic: oral antihistamine therapy  ACE-inhibitor: avoid all medications in drug class
56
pt began using captopril for HTN
angioedema
57
angioedema of the lips
58
dif?
erosive LP CCLE SLE

PATH II (32 decks)

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