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Oral Path > Mucocutaneous Disorders > Flashcards

Mucocutaneous Disorders Flashcards

1
Q

Stages for Evaluation of oral lesions

A 
Recognize tissue alteration
Generate ddx
Ddx procedures
Recommend for tx
Follow up
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2
Q

History of Present illness (HPI)

A 
Onset
Signs and symptoms
Pain
Trauma 
Meds
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3
Q

Classification of Pathology (4)

A
  • developmental (congenital or acquired, parents, features)
  • neoplastic (malignant vs benign)
  • reaction (inflammatory, infectious, traumatic)
  • autoimmune
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4
Q

Mucocutaneous lesions

A

lesions associated with immunocompromised ppl

Vesiculobullous diseases

Atypical of perio associated with HIV

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5
Q

Mucosal Manifestations: atypical forms

A

linear ging erythema, NUG, NUP

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6
Q

Linear ging erythema LGE

A

unusual pattern with persistent generalized band of erythema on margin

non painful, petechia like, bleeding, diffuse

extend from FGM apically

abnormal rxn to irritants, no response to plaque control

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7
Q

NUG

A

rapid onset or destruction
ulceration/necrosis of ging

severe pain, bleeding, malodor

IP ging necrosis, soft tissue craters

mand incisors and max molars

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8
Q

NUP

A

Disease involves bone/tissue

Most severe form, severe immunosuppression

Deep bone pain complaint

Rapid, exposes bone quickly

Cause: anaerobic bacteria, fusobacterium, spirocate

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9
Q

Clinical features of NUP/NUG

A 
Severe ging pain
Profuse bleeding
IP papillae necrotic slough 
Punched out
Malodor, metallic taste
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10
Q

Tx for LGE, NUP, NUG

A

Acute: pain control

Maintenance: decrease pathogens, debride, remove tissue, CHX 2x daily, OH home care, smoking cessation

Abx therapy: narrow spectrum 10-14 days

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11
Q

Necrotizing Stomatitis

A

localized, rapid bone destruction
highly erythematous, halitosis

invasive beyond periodontium (HIV destroyed immunity)

resembles Noma
soft tissue and bone involved

bone sequestration if not treated quick

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12
Q

Kaposi’s sarcoma

A

Solitary lesion first, no blanching
Elevated, painful, bleeding
Common on hard palate

Prev associated with >60, now associated with HIV/AIDS

Associated with HHV 8
malignancy of skin, spread to lungs/liver/GI

most common form of neoplasm in HIV ppl

mouth involved in 30% of cases

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13
Q

Tx for kaposi’s sarcoma

A

not curable

HAART to treat aids to shrink lesion

local lesions treated with Rad or cryosurgery

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14
Q

Non Hodgkin’s lymphoma

A

rapid growing painful ulcerated mass on gingiva or palate

seen in immunocompromised
plasmblastic lymphoma= rare form

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15
Q

Non Hodgkin’s therapy

A

rad or chemo

stabilize dental needs

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16
Q

Vesicular lesions: lichen planus

A

Etiology unknown (autoimmune, CD8+ T cells trigger apoptosis of epi cells)

infiltration of T cells in band into dermis “hugging” basal layer

similar to fungal infection

Cutaneous presentation

“saw tooth” appearance of rete pegs

17
Q

Predisposing factors LP

A

meds, contact hypersens to dent materials, liver disease, genetics, infection, stress, DM, trauma

18
Q

Lichenoid Rxn

A

similar appearance to LP

may be rxn to dent materials

19
Q

Reticular LP

A 
Wickham's Striaie
Most common on B mucosa
bilateral or symmetrical 
can't wipe off
Found on floor of mouth, ventral tongue, gingiva
20
Q

Atrophic LP

A

reticular form, tiny white papules with red background
on buccal
burning sensation

tx: glucocorticoid ointment

21
Q

Plaque like LP

A

not common
dorsum of tongue
white patch with white papules together

tx: none if asymptomatic, associated with candida or burning

22
Q

Erosive LP

A

peripheral ulceration
extensive
painful
result in scarring

tx: glucocorticosteroids, use rinse if extensive, prednisone pills

23
Q

Mucous Membrane Pemphigoid MMP

A

Chronic blistering mucocutaneous autoimmune diseases

Oral cavity most commonly affected (skin, eyes)

Weakens CT attachment
Blisters form in subepi layer
Bulla short lived, leave ulcerated area
Scarring KEY feature

2:1 female to male, adults
oculars lesions 1/3 of cases

undetected circulating auto IgG

good prognosis; significant morbidity

24
Q

Autoimmune attack

A

affects hemidesmosome

linear pattern

epi sloughs off, create bullae

25
Q

Pemphigus vulgaris: etiology

A

Autoimmune, antibodies directed toward desmosome proteins

50% develop oral lesions initially

26
Q

Pemphigus Vulgaris: classification

A

pemphigus vulgaris
pemphigus vegetans
pemphigus erythematous
pemphigus foliaceu

27
Q

Pemphigus Vulgaris: clinical features

A

= painful, shallow, irregular ulcers with friable adj mucosa (intraepi vesicles)

non keratinized sites are initially affected

lateral shearing force will produce slough/vesicle formation (Nikolsky sign)

fatal if not treated

28
Q

Management of Pemphigus

A

Avoid hard, sharp foods

hygiene treatment

29
Q

Medications for pemphigus

A

topical and intralesional corticosteroid drugs

immunosuppressive meds: prednisone, azathioprine, mycophenolate, mofteil, cyclophosphamide

30
Q

Other treatment for pemphigus

A

plasmapheresis and surgery to repair scars

prevent complications like blindness, airway stenosis, esophageal

IV Ig for some cases

31
Q

Erythema Multiforme: etiology

A 
allergic reaction
likely autoimmune condition 
any age 
penicillin/sulfonamides play role 
herpetic infection can occur prior to onset
32
Q

Erythema Multiforme: clinical features

A

“blood crusted”, lips, “targetoid”, “bulls eye” skin lesions

May occur chronically or periodically in cycles

33
Q

Treatment for EM

A

Anti-inflammatory

Steroids are initiated and then tapered

If herpes simplex= antiviral therapy prior to steroid therapy

34
Q

Severe forms of Erythema Multiforme

A

Steven-Johnson syndrome, toxic epidermal necrolysis

Oral Path (3 decks)

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