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Oral Path 2, Exam 4 > Mucocutaneous Conditions > Flashcards

Mucocutaneous Conditions Flashcards

1
Q

Inappropriate production of antibodies by the host directed against host tissue (autoantibodies)

A

Pemphigus vulgaris

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2
Q

What do the autoantibodies destroy in Pemphigus vulgaris?

A

Desmosomes

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3
Q

Role of desmosomes

A

Bond epithelial cells together

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4
Q

Where can Pemphigus vulgaris be seen clinically?

A

Skin and oral lesions

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5
Q

What is important about the oral lesions in Pemphigus vulgaris

A

“First to show, last to go” (first to show - hardest to treat)

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6
Q

Describe the oral lesions in Pemphigus vulgaris

A

Superficial, ragged erosions and ulcerations

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7
Q

Patients with Pemphigus vulgaris show a ____ ____ sign

A

Positive Nikolsky

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8
Q

Nikolsky sign

A

Inducing a bulla by applying firm, lateral pressure to normally appearing skin

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9
Q

What is really important in management of Pemphigus vulgaris

A

Plaque control

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10
Q

What is characteristic of skin involvement of Pemphigus vulgaris

A

Flaccid cutaneous bulla

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11
Q

Normal tissue adjacent to the ulceration or erosion in Pemphigus vulgaris should be sampled in a biopsy. What for? Where is the sample taken?

A

For direct immunofluoresent and light microscopic evaluation. Sample at the periphery, not the ulcerated center

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12
Q

2 histological features of Pemphigus vulgaris

A
  1. Intraepithelial clefting above the basal layer (SUPRABASILAR)
  2. Acantholysis (breakdown of spinous layer)
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13
Q

A technique that uses fluorescent-labeled antibodies to detect specific targets

A

Immunofluorescence

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14
Q

What is DIRECT immunofluorescence used to detect?

A

Autoantibodies bound to patient’s tissues

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15
Q

What is INDIRECT immunofluorescence used to detect?

A

Antibodies circulating in the blood

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16
Q

Autoantibodies in Pemphigus vulgaris will bind desmosomal components ( desmoglein ___ & ___)

A

1 & 3

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17
Q

Treatment for Pemphigus vulgaris

A
  1. Systemic corticosteroids
  2. OHI
  3. Prophy 3-4x per year
  4. SOFT toothbrush
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18
Q

Why do topical corticosteroids show little effect in Pemphigus vulgaris?

A

Because Pemphigus vulgaris is a systemic disease

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19
Q

Prognosis for Pemphigus vulgaris

A

Fatal if not treated (SEVERE infection, loss of fluids/electrolytes, malnutrition due to mouth pain)

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20
Q

What may lead to mortality in Pemphigus vulgaris?

A

Complications of long-term steroids

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21
Q

Condition that resembles Pemphigus vulgaris due to blister formation, but is 2x as common as Pemphigus vulgaris?

A

Mucous Membrane Pemphigoid (MMP)

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22
Q

Another name for Mucous Membrane Pemphigoid

A

Cicatricial (scarring) Pemphigoid

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23
Q

Are patients with Mucous Membrane Pemphigoid older or younger than patients with Pemphigus Vulgaris?

A

Older

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24
Q

Does Mucous Membrane Pemphigoid have a male or female predilection?

A

Female

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25
Q

Where is scarring typically seen in patients with Mucous Membrane Pemphigoid

A

Skin, Symblephreron (conjunctiva), oral mucosa (rare)

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26
Q

Why might you see intact intraoral blisters in patients with Mucous Membrane Pemphigoid?

A

Because the split is subepithelial

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27
Q

Clinical feature seen in patients with Mucous Membrane Pemphigoid

A

Desquamative gingivitis

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28
Q

Desquamative gingivitis

A

A DESCRIPTIVE TERM - erythema, desquamation, ulceration

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29
Q

What is the most significant aspect of Mucous Membrane Pemphigoid

A

Ocular involvement of symblepheron

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30
Q

What does ocular scarring lead to in patients with Mucous Membrane Pemphigoid

A

Scarring obstructs the orifices of glands that produce tears, resulting in a dry eye

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31
Q

What does ocular dryness lead to in patients with Mucous Membrane Pemphigoid

A

Dryness leads to keratinization of the corneal epithelium, leading to blindness

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32
Q

Term for upper eyelid being turned inward

A

Entropion

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33
Q

Term for eyelashes rubbing against the eye

A

Trichiasis

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34
Q

What must you include in a biopsy for a patient with Mucous Membrane Pemphigoid

A

A generous sample of normal mucosa, 0.5-1.0 cm away from areas of ulceration/erythema

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35
Q

What type of cleft formation is seen in patients with Mucous Membrane Pemphigoid ?

A

SUBepithelial

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36
Q

Subepithelial cleft formation

A

Separation of the epithelium from the connective tissue at the basement membrane zone

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37
Q

What will you see in the immunopathology of patients with Mucous Membrane Pemphigoid

A
  1. Linear deposition of immunoreactants at the basement membrane zone
  2. Positive DIF, Negative IIF (few patients will have circulating autoantibodies)
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38
Q

Treatment for patient with Mucous Membrane Pemphigoid when only oral lesions are present

A

Topical steroids, tetracycline/niacinamide or dapsone, frequent prophy visits (every 3-4 months)

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39
Q

Treatment for patient with Mucous Membrane Pemphigoid if there is ocular involvement

A

Systemic immunosuppressive therapy

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40
Q

Prognosis for patients with Mucous Membrane Pemphigoid

A

Blindness from untreated ocular disease, condition can usually be controlled

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41
Q

Most common of the autoimmune blistering conditions

A

Bullous Pemphigoid

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42
Q

Where is Bullous Pemphigoid primarily seen?

A

Skin

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43
Q

Early symptom of Bullous Pemphigoid? Followed by?

A

Pruritus followed by multiple, tense bullae, blisters on normal or erythematous skin

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44
Q

Describe the transformation of Bullous Pemphigoid lesions?

A

Rupture, crust, heal without scarring

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45
Q

Oral involvement in Bullous Pemphigoid is _____ (common/uncommon), and the bullae rupture ____ (later/sooner) than on the skin

A

Uncommon

Sooner

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46
Q

What is left behind when oral bullae rupture in patients with Bullous Pemphigoid

A

Large, shallow ulcerations with smooth, distinct margins

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47
Q

Is Bullous Pemphigoid seen supraepithelial or subepithelial? What is that similar to?

A

SUBepithelial - similar to Mucous Membrane Pemphigoid

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48
Q

What do you see in the immunopathology of patients with Bullous Pemphigoid

A

Positive DIF AND IIF with immunoreactants deposited at the basement membrane

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49
Q

Treatment for Bullous Pemphigoid

A

Management is similar to cicatricial pemphigoid, but most resolve spontaneously in 1-2 years

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50
Q

When might problems arise in patients with Bullous Pemphigoid

A

With use of immunosuppressive therapy in older patients

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51
Q

Acute onset ulcerative disorder of the skin and mucous membranes in younger patients, most have an unknown etiology

A

Erythema Multiforme

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52
Q

Although most cases of Erythema Multiforme have an unknown etiology, what are some known etiologies ?

A

Preceding infection (viral (herpes), bacterial (mycoplasma pneumoniae)), and Medication related (antibiotics and analgesics)

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53
Q

When do patients with Erythema Multiforme experience prodromal symptoms? What are they?

A

1 week before onset (fever, malaise, headache, cough, sore throat)

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54
Q

2 degrees of severity in patients with Erythema Multiforme

A
  1. EM minor

2. EM major

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55
Q

Where is EM minor seen?

A

Skin (extremities) and Mucosa (oral, conjunctival, genitourinary, respiratory)

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56
Q

What will you see on the vermilion zones of patients with EM minor?

A

Hemorrhagic crusting

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57
Q

2 skin features that you may see in patients with EM minor?

A
  1. Round, dusky-red patches on skin of extremities “targeted lesions”
  2. Bullae with necrotic centers
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58
Q

Oral features seen in patients with EM minor? Which areas are usually spared?

A

Erythematous patches of oral mucosa that undergo necrosis and result in large, shallow erosions and ulcers with irregular borders (gingiva and hard palate usually spared)

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59
Q

Clinical features of EM major

A

2 or more mucosal sites in conjunction with skin lesions, and ocular involvement that can produce symblepheron

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60
Q

Stevens’-Johnson syndrome

A

At least 2 mucosal sites plus skin involvement

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61
Q

Toxic epidermal necrolysis (Lyell’s disease)

A

Difuse bullous involvement of skin and mucosa

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62
Q

Difference in Stevens’ Johnson syndrome and Toxic Epidermal Necrolysis?

A

Degree of skin involvement and patient age
SJS (< 10% and younger patients)
TEN (>30% and older patients)

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63
Q

Difference in SJS/TEN and Erythema Multiforme

A
  1. SJS/TEN almost always triggered by a drug (rather than infection)
  2. SJS/TEN skin lesions begin as red macules on trunk (rather than extremities)
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64
Q

3 clinical features of SJS/TEN

A
  1. Skin sloughing and flaccid bullae develop within 2 weeks
  2. Patients appear badly scalded - treated in burn unit
  3. Almost all patients have mucosal involvement (esp. oral)
65
Q

How to diagnose EM, SJS, TEN

A

Usually based on clinical presentation (DIF and IIF non-specific)

66
Q

Where are the vesicles seen in the histology of EM, SJS, and TEN?

A

Subepithelial or intraepithelial

67
Q

Treatment for Erythema Multiforme

A

Discontinue causative drug, IV re-hydration, topical anesthetic/analgesic (steroid benefits are controversial)

68
Q

What medication has been implicated in inducing TEN?

A

NSAIDS

69
Q

What medication is avoided in the management of TEN? WHY?

A

Steroids - associated with increased mortality

70
Q

What treatment is seen to be helpful in patients with TEN?

A

IV administration of pooled human immunoglobulins (blocking apoptosis of epithelial cells)

71
Q

Prognosis for EM minor and major

A

Self-limiting in 2-6 weeks, but 20% get recurrences

72
Q

Which has a higher mortality rate, SJS or TEN?

A

TEN

73
Q

If a patient survives SJS or TEN, the ___ heals in 3-5 weeks, _____ lesions take longer, and ____ damage is common

A

Skin
Oral
Ocular

74
Q

2 additional names for Erythema Migrans

A
  1. Geographic tongue

2. Benign migratory glossitis

75
Q

One of the more common oral conditions, occurring in 1-3% of the population - considered a “common oral lesion”

A

Erythema Migrans

76
Q

What is the erythema in Erythema Migrans due to?

A

Atrophy of filiform papillae and shearing off of the parakeratin - remaining epithelium thins and appears red

77
Q

Erythema migrans occurs in 1/3 of patients who already have ____ ____

A

Fissured tongue

78
Q

Clinical feature of Erythema Migrans

A

Wax/Wane and Heal/Develop in different areas

79
Q

Where is Erythema Migrans typically seen

A

Dorsal and lateral anterior 2/3 of the tongue

80
Q

What is Erythema Migrans called when it is seen on other non-keratinized mucosal surfaces?

A

Ectopic Geographic Tongue

81
Q

Multiple, well-demarcated zones of erythema surrounded at least partially by a slightly elevated yellow-white serpentine or scalloped border

A

Erythema migrans

82
Q

Term when Erythema migrans is singular

A

Persistens

83
Q

Histologically, Erythema Migrans is similar to ____

A

Psoriasis

84
Q

Description of Erythema Migrans on a biopsy report

A

“Psoriasiform mucositis”

85
Q

Erythema migrans shows extensive ______ formation in the superficial spinous layer

A

Microabscess (neutrophils)

86
Q

What causes an erythematous macule in Erythema Migrans?

A

Neutrophilic microabsesses lift the keratin which then falls off and leaves the erythematous macule

87
Q

Treatment for Erythema migrans

A

Generally none - maybe a topical steroid if there is sensitivity

88
Q

Purple, polygonal, pruritic papules with Wickham’s striae (lacy white lines)

A

Cutaneous Lichen Planus

89
Q

Mucosal Lichen Planus is typically managed as a ___ ___

A

Chronic condition

90
Q

Lichen Planus (Oral and Cutaneous) has a ____ predilection

A

Female

91
Q

Condition seen on the flexor surfaces of wrists, lumbar region, shins

A

Cutaneous Lichen Planus

92
Q

2 forms of Oral Lichen Planus

A
  1. Reticular (lacy white lines)

2. Erosive (ELP) - erythematous, may ulcerate

93
Q

True/False: Oral Lichen Planus always occurs with skin lesions

A

False - it can occur alone or with skin lesions

94
Q

What is the most common form of oral lichen planus?

A

Reticular

95
Q

What is the most symptomatic form of oral lichen planus?

A

Erosive (esp. with acidic, salty, or spicy foods)

96
Q

Where is oral lichen planus typically seen?

A

Bilateral buccal mucosa, tongue, gingiva (but any intraoral surface and lips)

97
Q

If the dorsal tongue is involved in oral lichen planus, what might it appear as?

A

Patchy keratosis and atrophy

98
Q

What may be superimposed on oral lichen planus?

A

Candida albicans

99
Q

If candida albicans is superimposed, what will happen to oral ulcerative conditions?

A

The conditions worsen

100
Q

What is significant about the rete ridges associated with oral lichen planus?

A

They are absent or pointed (“saw toothed”)

101
Q

For Oral lichen planus, DIF is usually non-specific. What is the exception?

A

To rule out other immune-mediated conditions

102
Q

What can have the same hisology response as lichen planus?

A

Inflammatory response to epithelial dysplasia (especially mild).

103
Q

What kind of diagnosis is oral lichen planus?

A

Clinical

104
Q

What should be ruled out in oral lichen planus?

A

Candidiasis

105
Q

Treatment for reticular lichen planus?

A

None

106
Q

Treatment for erosive lichen planus?

A

Potent topical steroid (NOT systemic)

107
Q

Why would you biopsy an oral lichen planus lesion?

A

If it is suspected to be pre-malignant or malignant

108
Q

Prognosis for oral lichen planus

A

Varies - some well controlled and some difficult to control

109
Q

Topical steroids predispose a patient to _____

A

Candida

110
Q

What is a recurring challenge in patients with oral lichen planus?

A

Candidiasis (due to dry mouth, dentures, ATB, inhaler use)

111
Q

A number of conditions that mimic oral lichen planus (drug reaction, amalgam reaction, mucosal cinnamon reaction, etc.)

A

Lichenoid mucositis

112
Q

Most common collagen vascular/connective tissue disease in the US

A

Lupus erythematosus

113
Q

3 forms of Lupus erythematosus

A
  1. Chronic cutaneous lupus erythematosus (CCLE)
  2. Systemic lupus erythematosus (SLE)
  3. Subacute cutaneous lupus erythematosus (intermediate between CCLE and SLE)
114
Q

What is the appearance of skin lesions for patients with Chronic cutaneous lupus erythematosus

A

Scaly, erythematous patches in sun-exposed areas

115
Q

Describe the healing of Chronic cutaneous lupus erythematosus lesions

A

Heal and then reappear in a different area

May result in atrophy and scarring with hypo/hyperpigmentation

116
Q

Mucosal lesions of Chronic cutaneous lupus erythematosus are essentially identical to ___ ____ __, but seldom occurs without _____ lesions

A

Erosive lichen planus

Skin

117
Q

Form of lupus erythematosus that will wax/wane and has a female predilection

A

Systemic

118
Q

Form of lupus erythematosus that affects women of color more than white women?

A

Systemic

119
Q

What is the initial manifestation of systemic lupus erythematosus

A

Protean manifestation (fever, weight loss, arthritis, fatigue, general malaise)

120
Q

What area of the face is not affected by the butterfly rash associated with systemic lupus erythematosus

A

The nasolabial fold

121
Q

What causes skin lesions to flare in patients with systemic lupus erythematosus

A

UV exposure

122
Q

What is the most significant aspect of the disease in many patients with systemic lupus erythematosus

A

Renal involvement

123
Q

What is another common involvement in patients with systemic lupus erythematosus

A

Cardiac involvement

124
Q

Systemic lupus erythematosus found on the vermilion zones is called ___ ____

A

Lupus cheilitis

125
Q

What may help lead to the diagnosis in CCLE and SLE

A

Subepithelial edema

126
Q

What is characteristic and helps in the diagnosis of CCLE?

A

Skin lesions

127
Q

How do you diagnose SLE

A

Criteria by American Rheumatism Association for clinical and lab findings

128
Q

Serum studies show anti-nuclear antibodies in most patients with ____ but it is negative in patients with ____

A

SLE

CCLE

129
Q

Measures the amount and pattern of antibodies in your blood that work against your own body; a non-specific finding (but a screening tool)

A

ANA

130
Q

Deposition of immunoreactants at the basement membrane zone of normal skin

A

Positive lupus band test

131
Q

Positive lupus band tests are non-specific in patients with _____

A

SLE

132
Q

Sunscreen, NSAIDS, and antimalarial drug therapy can all help in the treatment of _____

A

Lupus erythematosus

133
Q

Systemic steroids, immunomodulating agents, and even kidney transplants may be needed for treatment of _____

A

SLE

134
Q

Prognosis for CCLE

A

Good - most resolve, some will transform to CCLE and SLE

135
Q

Prognosis for SLE

A

Worse for men than women
Worse for blacks than whites
Depends on organs affected

136
Q

Most common cause of death in patients with SLE

A

Renal failure

137
Q

Relatively rare condition characterized by inappropriate deposition of dense collagen (replaces/destroys normal tissue)

A

Systemic sclerosis

138
Q

Another term for systemic sclerosis

A

Scleroderma (“hard” “skin”)

139
Q

Diffuse, hard, smooth texture of skin is seen in patients with ____ ____

A

Systemic sclerosis

140
Q

Raynaud phenomenon, Sclerodactyly, and Acro-osteolysis may be seen in patients with ___ ____

A

Systemic sclerosis

141
Q

Patients with this condition are known for having a “mask-like” face, atrophy of alae, and mouse facies (pinched appearance of nose)

A

Systemic sclerosis

142
Q

Systemic sclerosis has a ____ predilection

A

Female

143
Q

Discoloration of the fingers/toes after exposure to changes in temperature or emotional events causing spasm of blood vessels

A

Raynaud’s phenomenon

144
Q

Is Raynaud’s phenomenon specific to systemic sclerosis?

A

No

145
Q

What causes the claw-like deformity (sclerodactyly) of fingers in patients with systemic sclerosis?

A

The collagen deposition

146
Q

Destruction of the digit tips, including bone

A

Acro-osteolysis

147
Q

Why might patients with systemic sclerosis have dysphagia?

A

Due to esophageal involvement

148
Q

Limitation in opening results in ____ in patients with systemic sclerosis

A

Microstomia (Purse-string appearance)

149
Q

Radiographically - widening of PDL, resorption of the posterior ramus/condyle/coronoid/chin, possible root resorption

A

Systemic sclerosis

150
Q

The autoantibodies in systemic sclerosis are directed against _____

A

Scl-70

151
Q

What kind of antibodies are seen in limited cutaneous systemic sclerosis?

A

Anticentromere

152
Q

ACE inhibitors for HTN, esophageal dilation, OHI are used as treatment for ____ ____

A

Systemic sclerosis

153
Q

Prognosis for Systemic sclerosis

A

Death due to internal organ deposition of collagen (worse for cardiac involvement, most death due to pulmonary involvement)

154
Q

CREST Syndrome - what does CREST stand for?

A 
Calcinosis cutis
Raynaud's phenomenon
Esophageal dysfunction
Sclerodactyly
Telangiectasia
155
Q

Milder variant of systemic sclerosis

A

CREST syndrome

156
Q

CREST syndrome has a ____ predilection

A

Female

157
Q

Subcutaneous nodules that are a deposition of calcium salts

A

Calcinosis cutis

158
Q

Treatment for CREST syndrome is similar to ___ ___

A

Systemic sclerosis

159
Q

Which has a better prognosis: CREST syndrome or systemic sclerosis?

A

CREST syndrome

Oral Path 2, Exam 4 (6 decks)

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