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Oral Pathology > Dermatology > Flashcards

Dermatology Flashcards

1
Q

White Sponge Nevus: Etiology

A

Inherited condition due to mutations in keratin 4 and keratin 13

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2
Q

White Sponge Nevus: Inheritance Pattern

A

Autosomal dominant

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3
Q

White Sponge Nevus: When do signs appear?

A

Childhood to adolescence

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4
Q

Clinical Appearance of White Sponge Nevus

A

Symmetrical, thickened, white, corrugated/velvety, diffuse plaques

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5
Q

Location of White Sponge Nevus

A

Most often affecting the bilateral buccal mucosa; can be found at other intra-or extraoral sites

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6
Q

Symptoms of White Sponge Nevus

A

Asymptomatic

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7
Q

Clinical Differential Diagnosis for White Sponge Nevus

A

White sponge nevus, morsicatio buccarum, hereditary benign intrepithelial dyskeratosis, leukoedema

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8
Q

Treatment/Prognosis for White Sponge Nevus

A

Benign condition that does not require treatment

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9
Q

Keratoacathoma: Describe

A

Self-limiting epithelial proliferation on the skin.

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10
Q

Keratoacanthoma: Causes

A

Sun damage, HPV 26/37, trauma, immunosupression, tar exposure

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11
Q

What is Keratoacathoma mistaken for? Why?

A

Mistaken for SCC both clinically and histologically but is BENIGN

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12
Q

Population affected by keratoacathoma

A

> 45 years old; male predilection

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13
Q

Location affected by keratoacathoma

A

95% occurs on sun-exposed skin; 8% found on outer edge of vermillion boarder

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14
Q

Clinical Apperance of Keratocathoma

A

Presents as firm, non-tender, well-demarcated, sessile, dome-shaped nodule with central keratin plug

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15
Q

Growth Pattern of Keratoacanthoma

A

Rapid growth occurs to 1-2 cm in 6 weeks
Stabilizes in size at 6 weeks
Involutes in size at 6 weeks

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16
Q

Treatment for Keratoacanthoma

A

Surgical excision due to similarity with SCC, cyrotherapy or ablative techniques are typically recommended

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17
Q

Recurrence rate for Keratoacahtoma

A

4-8% recurrence after excision

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18
Q

Seborrheic Keratosis: Describe

A

Benign proliferation of the epidermal basal cells.

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19
Q

Location of Seborrheic Keratosis; where does it not occur?

A

More common on sun exposed skin
Does not occur in mouth

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20
Q

When does Seborrheic Keratosis appear?

A

Begins to develop in 30’s and are more prevalent with increasing age

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21
Q

Clinical Appearance of Seborrheic Keratosis

A

Sharply demarcated pigmented lesion; “stuck on” appearance

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22
Q

How does a seborrheic keratosis start out?

A

As a flat lesion and gradually enlarges and elevates

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23
Q

Saborrheic Keratosis Surface Texture

A

Fissured, pitted, verrucous, or smoth

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24
Q

Treatment For Seborrheic Keratosis

A

Benign lesion, consider referral to dermatologist for further evaluation and potential biopsy if showing any concerning characteristics
ABCDE (Signs concerning for melanoma)

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25
Q

Deratosis Papulosa Nigra: Describe Clinical Appearance and location

A

Multiple small dark papules scarred peri-orbital and zygomatic region

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26
Q

Dermatosis Papulosa Nigra: When do these lesions develop?

A

Begin to develop at adolescence

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27
Q

Dermatosis Papulosa Nigra: Inheritance pattern

A

Autosomal dominant inheritance

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28
Q

Population affected by Dermatosis Papulosa Nigra

A

Most commonly affects black population

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29
Q

Treatment/Prognosis for Dermatosis Papulosa Nigra

A

Benign condition; no treatment indicated

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30
Q

Leser Trelat Sign: Define

A

Paraneoplastic cutaneous marker of internal malignancy with the hallmark finding being an abrupt eruption of multiple seborrheic keratoses

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31
Q

Symptoms & TIme frame for Leser-Trelat Sign

A

Arise in a short period of time and are associated with pruiritus (itching)

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32
Q

Leser-Trelat Sign is associated with

A

Internal Malignancy

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33
Q

How does Leser-Trelat Sign resolve?

A

Treatment of underlying malignancy

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34
Q

Melasma: AKA

A

Mask of Pregnancy

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35
Q

Melasma: Describe

A

Acquired, symmetrical hyperpigmentation of sun-exposed skin of the face and neck

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36
Q

Cause of Melasma

A

UV light exposure and hormonal influences (hence association with pregnancy)

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37
Q

Can Melasma occur in males?

A

Yes but it less common

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38
Q

Population affected by Melasma

A

Mainly affects medium/dark complexioned patients

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39
Q

Clinical Features of Melasma

A

Brown or gray macules

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40
Q

Sites affected by Melasma

A

Midface, forehead, upper lip, chin, mandibular ramus region, rarely arms

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41
Q

Treatment for Melasma

A

Treatment unnecessary but may be desired for esthetics

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42
Q

What are some esthetic treatment options for melasma?

A

First line is combination cream
Laser therapy, light therapy, microdermabrasion
Avoidance of UV, sunscreen
Lesions may resolve after parturition

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43
Q

Potential for malignant potential of melasma

A

No malignant potential

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44
Q

Other names for actinic lentigo

A

Age spot, liver spot, solar lentigo

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45
Q

Describe actinic lentigo and what causes it

A

Pigmented lesion of the skin associated with UV exposure

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46
Q

Population affected by actinic lentigo

A

Typically seen in older adults
Most commonly affects fair complected individuals

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47
Q

What part of the body does actinic lentigo not occur?

A

The mouth

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48
Q

Actinic lentigo: Clinical Features

A

Uniformly pigmented macule well-demarcated, but irregular borders

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49
Q

Common sites of actinic lentigo

A

Face, dorsal of hand, shoulders, upper back

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50
Q

Actinic Lentigo: Treatment and Prognosis

A

-Benign lesion that does not show malignant transformation
-Can be removed or treated for esthetic reasons
-Sunscreen for prevention

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51
Q

Developmental types of nevi

A

Nevus Flammeus

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52
Q

Acquired types of nevi

A

Mole

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53
Q

Three less common types of nevus

A

Halo Nevus
Spitz Nevus
Blue Nevus

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54
Q

Define Halo Nevus

A

Nevus with a strong inflammatory reaction

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55
Q

Define Spitz Nevus

A

Primarily occur in children, histologically can be mistaken for melanoma

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56
Q

Define Blue Nevus

A

Nevus with a blue hue

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57
Q

Nevus Flammeus is better known as

A

Port wine stain

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58
Q

Define Nevus Flammeus

A

Congential dermal capillary vascular malformation

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59
Q

How does the nevus flammeus occur?

A

Lesions may occur independently or as a component of Sturge-Weber Syndrome

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60
Q

Sturge Weber Syndrome is _______ condition

A

Developmental condition; not hereditary

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61
Q

Sturge-Weber Sydnrome affects what parts of the body?

A

Skin, brain and eyes

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62
Q

Sturge-Weber Syndrome Major Features

A

Convulsive disorder, intellectual disability, migraines, stroke-like episodes, glaucoma

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63
Q

Acquired Melanocytic Nevus: Cause

A

Acquired

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64
Q

When do acquired melanocytic nevus occur?

A

Not at birth, rarely begin to devolop over age 40 and show regression in later decades (5-7th decades)

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65
Q

Clinical features of acquired melanocytic nevus

A

-Well circumscribed macules, papules or nodules
-Almost always <1 cm in diameter
-Range in color from skin colored to pink, brown and black/blue

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66
Q

Melanocytic nevus that are greater than 1 cm could be what three things?

A

Congenital nevus, atypical nevus, or melanoma

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67
Q

Treatment for Acquired Melanocytic Nevus

A

About one third of melanomas develop from a pre-existing nevus, so clinicans should take care in examining any moles that a patient notes have changed

68
Q

Common Premalignant and malignant skin lesions (4)

A

Cutaneous melanoma
Basal cell carcinoma
Actinic keratosis
Cutaneous SCC

69
Q

“A” in Melanoma

A

Asymmetry due to its uncontrolled growth pattern

70
Q

“B” in Melanoma

A

Border irregularity (often with notching)

71
Q

“C” in Melanoma

A

Color variegation (which varies from shades of brown to black, white, red, and blue, depending on the amount and depth of melanin pigmentation)

72
Q

“D” in Melanoma

A

Diameter greater than 6 mm (which is diameter of pencil eraser)

73
Q

“E” in Melanoma

A

Evolving (lesions that have changed with respect to size, shape, color, surface, or symptoms over time”

74
Q

Cause of Cutaneous Melanoma

A

May arise de novo or from pre-existing benign melanocytic lesion such as acquired nevus

75
Q

Clinical Features of Cutaneous Melanoma

A

ABCDE

76
Q

Treatment for Cutaneous Melanoma

A

-Based on Clark’s Classification and TMN staging
-Surgical excision
-Immunotherapy
-Tyrosine Kinase Inhibitors for lesions with KIT mutations

77
Q

Basal Cell Carcinoma: Describe

A

Epithelial malignancy arising from the basal cell layer of the skin and its appendages

78
Q

Most common skin cancer and most common of all cancers overall

A

Basal Cell Carcinoma

79
Q

Location of Basal Cell Carcinoma

A

80% occur on the skin of the head and neck

80
Q

Cause of Basal cell carcinoma

A

Cumulative UV exposure

81
Q

Clinical Features of Basal Cell Carcinoma

A

Locally invasive, slowly spreading tumor

82
Q

What are three types of clinical presentations for basal cell carcinoma?

A
  1. Papule with shiny surface, telangiectasia and central ulcerative necrosis
  2. Gray-black papule with erosion giving the appearance of a melanocytic lesion
  3. Erythematous poorly defined plaque with erosions
83
Q

What are are basal cell carcinoma lesions in young patients associated with?

A

Nevoid basal cell carcinoma syndrome

84
Q

Treatment for Basal cell carcinoma

A

Surgical excision (may or may not use Mohs), topical chemotherapeutic agents

85
Q

Prognosis for basal cell carcinoma

A

Recurrence is uncommon
Metastasis is exceptionally rare

86
Q

Actinic Keratosis: Describe

A

Precancerous lesion of the skin

87
Q

Cause of Actinic Keratosis

A

UV Radiation
Radiation causes mutations in the p53 tumor suppressor gene

88
Q

Actinic Keratosis is the skin equivalent of

A

Oral dysplasia

89
Q

Clinical features of actinic keratosis

A

White/gray/brown/red
Irregular scaly patches, vary in color

90
Q

Population affected by Actinic Keratosis

A

> 40 years of age, no gender predilection
Affects 50% of all light skinned adults

91
Q

Describe sandpaper appearance of Actinic Keratosis

A

Roughened texture

92
Q

Describe keratin horn appearance of actinic keratosis

A

Arising from central area

93
Q

Histology of Actinic Keratosis

A

Some degree of epithelial dysplasia + solar elastosis

94
Q

Treatment of Actinic Keratosis

A

Removal of lesion to prevent progression to SCC (cyrotherapy, curettage, excision, topical chemotherapeutic agents, laser excision or ablation)

95
Q

How often does actinic keratosis undergo malignant transformation over 2 year period

A

10%

96
Q

What are topical chemotherapeutic agents?

A

Efudex, Carac, Aldara

97
Q

Cutaneous Squamous Cell Carcinoma: Describe

A

A malignant tumor of keratinocytes of the skin.

98
Q

Cutaneous Squamous Cell Carcinoma: Cause

A

UV Exposure -> genetic mutations (particularly p53 tumor suppressor mutation)

99
Q

Second most common skin cancer in the US

A

Cutaneous Squamous Cell Carcinoma

100
Q

Clinical Features of Cutaneous Squamous Cell Carcinoma

A

Small, firm, dull-red nodule, +/- ulceration, frequently with elevated rolled borders

101
Q

Histology of Cutaneous Squamous Cell Carcinoma

A

Same as oral SCC

102
Q

Treatment of Cutaneous Squamous Cell Carcinoma

A

Depends on TNM staging -> surgical excision, radiation, topical agents

103
Q

Ectodomeral Dysplasia: Define

A

Group of inherited disorders defined by the failure to develop 2 or more ectodermal derived anatomic structures

104
Q

What structures are affected by ectodermal dysplasia?

A

Skin, hair, nails, teeth, sweat glands

105
Q

What is the most well known ectodermal dyslpasia syndrome?

A

Hypohidrotic ectodermal syndrome

106
Q

What type of inheritance causes ectodermal dysplasia?

A

X-linked inheritance

107
Q

Describe lyon hypothesis when it comes to ectodermal dysplasia

A

Females have a lesser phenotype because half of the x chromosomes express the normal gene

108
Q

How are eccrine glands affected in ectodermal dysplasia?

A

Reduced eccrine glands causing heat intolerance

109
Q

How is hair, nails, skin and eyes affected in ectodermal dysplasia?

A

Fine sparse hair, fine wrinkling, and hyperpigmentation around the eyes, dystrophic/brittle nails

110
Q

Midlface ____ occurs in ectodermal dysplasia?

A

Midface hypoplasia

111
Q

How are salivary glands affected by ectodermal dysplasia?

A

Hypoplastic or absent salivary glands

112
Q

How are teeth affected in ectodermal dysplasia?

A

Oligo or hypodontia -> reduced number of teeth
Incisor crowns: tapered or conical, pointed
Molars: reduced in diameter
Rarely no teeth

113
Q

Treatment for Ectodermal dysplasia

A

Replacement of missing teeth, increased preventative care for xerostomia related caries

114
Q

Peutz Jeghers Syndrome: Inheritance pattern

A

Autosomal dominant inherited condition with an STK11 Mutation

115
Q

Key features of Peutz Jeghers Syndrome

A

Freckle-like lesions of the hands
Perioral skin
Oral mucosa in conjunction with intestinal polyposis and predisposition to develop cancer

116
Q

Peutz-Jeghers Syndrome: When do pigmented lesions develop?

A

Early childhood

117
Q

Describe oral lesions and where they are located in peutz-jeghers syndrome

A

1-4 mm brown to blue-gray macules, occur on vermillion, labial and buccal mucosa and tongue

118
Q

Where do skin lesions occur in peutz-jeghers syndrome?

A

On the extremities

119
Q

Describe peutz-jeghers syndrome’s lesions compared to true freckles

A

Lesions do not wax and wane with sun exposure like a true freckle does

120
Q

Describe intestinal polyps that occur in peutz-jeghers syndrome

A

Hamartomatous intestinal polyps throughout the GI tract that are not premalignant

121
Q

Define Hamartoma

A

Benign growth of normal tissue

122
Q

What are other GI findings in peutz-jeghers syndrome

A

Intussusception (telescoping) of the bowel
While the intestinal polyps are not premalignant, 33 percent of patients develop GI malignancy by 60 years of age

123
Q

Treatment of Peutz-Jeghers Syndrome

A

Dentists can be screeners for this condition, characteristics pigmentation arise in childhood before patient is at significant risk for syndrome associated malignancy

124
Q

Once peutz-jeghers syndrome is diagnosed, describe treatment

A

Pigmented lesions do not require treatment, they are benign
Patient should be monitored by GI doctor for malignancy and intussusception

125
Q

Ehlers-Danlos Syndrome: Define

A

A group of inherited connective tissue disorders resulting in the abnormal production of collagen

126
Q

Inheritance pattern of ehlers-danlos syndrome

A

Autosomal dominant

127
Q

How are joints and skin affected in ehlers-danlos syndrome

A

Hypermobility of the joints, easy bruising, elasticity of the skin

128
Q

What type of scarring occurs with ehlers-danlos syndrome?

A

Papyraceous scarring (resembling crumpled cigarette paper)

129
Q

Oral manifestations of ehlers-danlos syndrome

A

Gorlin SIgn: touching the tip of the tongue to the nose
TMJ subluxation
Pulp Stones

130
Q

Treatment of Ehlers-Danlos syndrome

A

Classical type usually normal lifespan
TMJ subluxation treated as normal

131
Q

Marfan Syndrome: Describe

A

A multisystem connective tissue disorder due to a mutation in the fibrillin-1 gene

132
Q

Marfan Syndrome Inheritance Pattern

A

Autosomal dominant

133
Q

Marfan syndrome effect on body size

A

Tall, thin body habitus

134
Q

Cardiovascular system effects on marfan syndrome

A

Risk of aortic aneurysm aortic dissection, valve malformations

135
Q

Marfan syndrome effects on eyes

A

Early onset glaucoma, retinal problems, lens problems

136
Q

Skeletal complications associated with marfan syndrome

A

Scoliosis

137
Q

Oral cavity effects on marfan syndrome

A

High arched palate
Dental crowding

138
Q

Treatment for marfan syndrome

A

Ideal dentition achievable through prosth and ortho

139
Q

Systemic Sclerosis: Describe

A

Immunologically mediated pathogenesis involving abnormal interactions among vascular tissue, connective tissue and immune cells.

140
Q

What is deposited in systemic sclerosis? Where?

A

Dense collagen deposited throughout the body in extraordinary amounts: mainly skin, but every organ affected.

141
Q

Population affected by systemic sclerosis

A

Women affected 3-5x more than men, occurs in adults

142
Q

How is opening affected by systemic sclerosis

A

Microsomia -> limited opening due to collagen deposition in the perioral tissues

143
Q

Oral manifestions of systemic sclerosis

A

Loss of attached gingiva and recession
Dysphagia (due to lingual collage deposition)
Xerostomia
Widening of PDL
Generalized resportion of the mandible

144
Q

Describe Raynaud phenomenon in systemic sclerosis

A

Vasoconstriction in cold weather

145
Q

Describe how figures are affected in systemic sclerosis

A

Resportion of terminal phalanges, flexion contractures (claw-like fingers)
Skin: Diffuse, hard and smooth texture

146
Q

Diagnosis of Systemic Sclerosis

A

Serum lab testing for Anti-topoisomerase I antibodies

147
Q

Overall treatment for systemic sclerosis

A

Systemic medications like penicillamine to prevent collagen production, systemic steroids have little effect and photochemotherapy some benefit for the skin

148
Q

Oral treatment for systemic sclerosis

A

-May need collapsible dental appliances to replace teeth
-Surgical correction of open bite caused by condylar resportion if necessary

149
Q

Describe Prognosis of systemic sclerosis

A

-Fibrosis of lungs, heart, kidneys, GI tract -> organ failure within 3 years of dx

150
Q

“C” in CREST

A

Calcinosis cutis (calcium deposits in the skin)

151
Q

“R” in CREST

A

Raynaud phenomenon (vasospasm in cold weater causing less blood to flow to digits)

152
Q

“E” in CREST

A

Esophageal dysfunction (due to abnormal collagen deposition)

153
Q

“S” in CREST

A

Sclerodactyly (Claw like deformity of the fingers due to abnormal collagen deposition in the dermis)

154
Q

“T” in CREST

A

Telangiectasia (superficial, dilated capillaries)

155
Q

Describe Telangiectasia

A

Vascular lesion caused by dilation of a small, superficial blood vessel
-Visible dilated small blood vessels
-Blanch with light pressure

156
Q

Describe Petechiae

A

Round, pinpoint area of hemorrhage

157
Q

Describe Purpura/Ecchymosis

A

Non-elevated area of hemorrhage, larger than a petechia

158
Q

Population affected by CREST

A

Female predominance
50-70 years old

159
Q

Diagnosis for CREST

A

Serum lab testing for anticentromere antibiodies

160
Q

What is less severe and has a better prognosis than systemic sclerosis?

A

CREST

161
Q

Treatment for CREST

A

Monitored for increased risk of pulmonary hypertension and primary biliary cirrhosis (more than 10 years after diagnosis)

162
Q

Hereditary Hemorrhagic Telangiectasia: Describe

A

Autosomal dominant disorder in which genetic mutations results in decreased blood vessel integrity

163
Q

Clinical Features of Hereditary Hemorrhagic Telangiectasia

A

Oral lesions are most dramatic and easily identifiable
Telangiectatic vessels of vermillion zone of lips, tongue, buccal mucosa
Periodontal vascular malformations
Epistaxis
AV Fistulas: Lungs, liver, brain

164
Q

Overall treatment for Hereditary Hemorrhagic Telangiectasia

A

Electrocautery, cryosurgery, laser ablation
Progesterone, estrogen therapy
Antibody therapy against endothelial growth factor

165
Q

Dental treatment for hereditary hemorrhagic telangiectasia

A

Antibiotic prophylaxis until pulmonary AV fistula has been ruled out

Oral Pathology (7 decks)

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