Dermatology Flashcards
1
Q
White Sponge Nevus: Etiology
A
Inherited condition due to mutations in keratin 4 and keratin 13
2
Q
White Sponge Nevus: Inheritance Pattern
A
Autosomal dominant
3
Q
White Sponge Nevus: When do signs appear?
A
Childhood to adolescence
4
Q
Clinical Appearance of White Sponge Nevus
A
Symmetrical, thickened, white, corrugated/velvety, diffuse plaques
5
Q
Location of White Sponge Nevus
A
Most often affecting the bilateral buccal mucosa; can be found at other intra-or extraoral sites
6
Q
Symptoms of White Sponge Nevus
A
Asymptomatic
7
Q
Clinical Differential Diagnosis for White Sponge Nevus
A
White sponge nevus, morsicatio buccarum, hereditary benign intrepithelial dyskeratosis, leukoedema
8
Q
Treatment/Prognosis for White Sponge Nevus
A
Benign condition that does not require treatment
9
Q
Keratoacathoma: Describe
A
Self-limiting epithelial proliferation on the skin.
10
Q
Keratoacanthoma: Causes
A
Sun damage, HPV 26/37, trauma, immunosupression, tar exposure
11
Q
What is Keratoacathoma mistaken for? Why?
A
Mistaken for SCC both clinically and histologically but is BENIGN
12
Q
Population affected by keratoacathoma
A
> 45 years old; male predilection
13
Q
Location affected by keratoacathoma
A
95% occurs on sun-exposed skin; 8% found on outer edge of vermillion boarder
14
Q
Clinical Apperance of Keratocathoma
A
Presents as firm, non-tender, well-demarcated, sessile, dome-shaped nodule with central keratin plug
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
16
Q
Treatment for Keratoacanthoma
A
Surgical excision due to similarity with SCC, cyrotherapy or ablative techniques are typically recommended
17
Q
Recurrence rate for Keratoacahtoma
A
4-8% recurrence after excision
18
Q
Seborrheic Keratosis: Describe
A
Benign proliferation of the epidermal basal cells.
19
Q
Location of Seborrheic Keratosis; where does it not occur?
A
More common on sun exposed skin
Does not occur in mouth
20
Q
When does Seborrheic Keratosis appear?
A
Begins to develop in 30’s and are more prevalent with increasing age
21
Q
Clinical Appearance of Seborrheic Keratosis
A
Sharply demarcated pigmented lesion; “stuck on” appearance
22
Q
How does a seborrheic keratosis start out?
A
As a flat lesion and gradually enlarges and elevates
23
Q
Saborrheic Keratosis Surface Texture
A
Fissured, pitted, verrucous, or smoth
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)
25
Deratosis Papulosa Nigra: Describe Clinical Appearance and location
Multiple small dark papules scarred peri-orbital and zygomatic region
26
Dermatosis Papulosa Nigra: When do these lesions develop?
Begin to develop at adolescence
27
Dermatosis Papulosa Nigra: Inheritance pattern
Autosomal dominant inheritance
28
Population affected by Dermatosis Papulosa Nigra
Most commonly affects black population
29
Treatment/Prognosis for Dermatosis Papulosa Nigra
Benign condition; no treatment indicated
30
Leser Trelat Sign: Define
Paraneoplastic cutaneous marker of internal malignancy with the hallmark finding being an abrupt eruption of multiple seborrheic keratoses
31
Symptoms & TIme frame for Leser-Trelat Sign
Arise in a short period of time and are associated with pruiritus (itching)
32
Leser-Trelat Sign is associated with
Internal Malignancy
33
How does Leser-Trelat Sign resolve?
Treatment of underlying malignancy
34
Melasma: AKA
Mask of Pregnancy
35
Melasma: Describe
Acquired, symmetrical hyperpigmentation of sun-exposed skin of the face and neck
36
Cause of Melasma
UV light exposure and hormonal influences (hence association with pregnancy)
37
Can Melasma occur in males?
Yes but it less common
38
Population affected by Melasma
Mainly affects medium/dark complexioned patients
39
Clinical Features of Melasma
Brown or gray macules
40
Sites affected by Melasma
Midface, forehead, upper lip, chin, mandibular ramus region, rarely arms
41
Treatment for Melasma
Treatment unnecessary but may be desired for esthetics
42
What are some esthetic treatment options for melasma?
First line is combination cream
Laser therapy, light therapy, microdermabrasion
Avoidance of UV, sunscreen
Lesions may resolve after parturition
43
Potential for malignant potential of melasma
No malignant potential
44
Other names for actinic lentigo
Age spot, liver spot, solar lentigo
45
Describe actinic lentigo and what causes it
Pigmented lesion of the skin associated with UV exposure
46
Population affected by actinic lentigo
Typically seen in older adults
Most commonly affects fair complected individuals
47
What part of the body does actinic lentigo not occur?
The mouth
48
Actinic lentigo: Clinical Features
Uniformly pigmented macule well-demarcated, but irregular borders
49
Common sites of actinic lentigo
Face, dorsal of hand, shoulders, upper back
50
Actinic Lentigo: Treatment and Prognosis
-Benign lesion that does not show malignant transformation
-Can be removed or treated for esthetic reasons
-Sunscreen for prevention
51
Developmental types of nevi
Nevus Flammeus
52
Acquired types of nevi
Mole
53
Three less common types of nevus
Halo Nevus
Spitz Nevus
Blue Nevus
54
Define Halo Nevus
Nevus with a strong inflammatory reaction
55
Define Spitz Nevus
Primarily occur in children, histologically can be mistaken for melanoma
56
Define Blue Nevus
Nevus with a blue hue
57
Nevus Flammeus is better known as
Port wine stain
58
Define Nevus Flammeus
Congential dermal capillary vascular malformation
59
How does the nevus flammeus occur?
Lesions may occur independently or as a component of Sturge-Weber Syndrome
60
Sturge Weber Syndrome is _______ condition
Developmental condition; not hereditary
61
Sturge-Weber Sydnrome affects what parts of the body?
Skin, brain and eyes
62
Sturge-Weber Syndrome Major Features
Convulsive disorder, intellectual disability, migraines, stroke-like episodes, glaucoma
63
Acquired Melanocytic Nevus: Cause
Acquired
64
When do acquired melanocytic nevus occur?
Not at birth, rarely begin to devolop over age 40 and show regression in later decades (5-7th decades)
65
Clinical features of acquired melanocytic nevus
-Well circumscribed macules, papules or nodules
-Almost always <1 cm in diameter
-Range in color from skin colored to pink, brown and black/blue
66
Melanocytic nevus that are greater than 1 cm could be what three things?
Congenital nevus, atypical nevus, or melanoma
67
Treatment for Acquired Melanocytic Nevus
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
Common Premalignant and malignant skin lesions (4)
Cutaneous melanoma
Basal cell carcinoma
Actinic keratosis
Cutaneous SCC
69
"A" in Melanoma
Asymmetry due to its uncontrolled growth pattern
70
"B" in Melanoma
Border irregularity (often with notching)
71
"C" in Melanoma
Color variegation (which varies from shades of brown to black, white, red, and blue, depending on the amount and depth of melanin pigmentation)
72
"D" in Melanoma
Diameter greater than 6 mm (which is diameter of pencil eraser)
73
"E" in Melanoma
Evolving (lesions that have changed with respect to size, shape, color, surface, or symptoms over time"
74
Cause of Cutaneous Melanoma
May arise de novo or from pre-existing benign melanocytic lesion such as acquired nevus
75
Clinical Features of Cutaneous Melanoma
ABCDE
76
Treatment for Cutaneous Melanoma
-Based on Clark's Classification and TMN staging
-Surgical excision
-Immunotherapy
-Tyrosine Kinase Inhibitors for lesions with KIT mutations
77
Basal Cell Carcinoma: Describe
Epithelial malignancy arising from the basal cell layer of the skin and its appendages
78
Most common skin cancer and most common of all cancers overall
Basal Cell Carcinoma
79
Location of Basal Cell Carcinoma
80% occur on the skin of the head and neck
80
Cause of Basal cell carcinoma
Cumulative UV exposure
81
Clinical Features of Basal Cell Carcinoma
Locally invasive, slowly spreading tumor
82
What are three types of clinical presentations for basal cell carcinoma?
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
What are are basal cell carcinoma lesions in young patients associated with?
Nevoid basal cell carcinoma syndrome
84
Treatment for Basal cell carcinoma
Surgical excision (may or may not use Mohs), topical chemotherapeutic agents
85
Prognosis for basal cell carcinoma
Recurrence is uncommon
Metastasis is exceptionally rare
86
Actinic Keratosis: Describe
Precancerous lesion of the skin
87
Cause of Actinic Keratosis
UV Radiation
Radiation causes mutations in the p53 tumor suppressor gene
88
Actinic Keratosis is the skin equivalent of
Oral dysplasia
89
Clinical features of actinic keratosis
White/gray/brown/red
Irregular scaly patches, vary in color
90
Population affected by Actinic Keratosis
>40 years of age, no gender predilection
Affects 50% of all light skinned adults
91
Describe sandpaper appearance of Actinic Keratosis
Roughened texture
92
Describe keratin horn appearance of actinic keratosis
Arising from central area
93
Histology of Actinic Keratosis
Some degree of epithelial dysplasia + solar elastosis
94
Treatment of Actinic Keratosis
Removal of lesion to prevent progression to SCC (cyrotherapy, curettage, excision, topical chemotherapeutic agents, laser excision or ablation)
95
How often does actinic keratosis undergo malignant transformation over 2 year period
10%
96
What are topical chemotherapeutic agents?
Efudex, Carac, Aldara
97
Cutaneous Squamous Cell Carcinoma: Describe
A malignant tumor of keratinocytes of the skin.
98
Cutaneous Squamous Cell Carcinoma: Cause
UV Exposure -> genetic mutations (particularly p53 tumor suppressor mutation)
99
Second most common skin cancer in the US
Cutaneous Squamous Cell Carcinoma
100
Clinical Features of Cutaneous Squamous Cell Carcinoma
Small, firm, dull-red nodule, +/- ulceration, frequently with elevated rolled borders
101
Histology of Cutaneous Squamous Cell Carcinoma
Same as oral SCC
102
Treatment of Cutaneous Squamous Cell Carcinoma
Depends on TNM staging -> surgical excision, radiation, topical agents
103
Ectodomeral Dysplasia: Define
Group of inherited disorders defined by the failure to develop 2 or more ectodermal derived anatomic structures
104
What structures are affected by ectodermal dysplasia?
Skin, hair, nails, teeth, sweat glands
105
What is the most well known ectodermal dyslpasia syndrome?
Hypohidrotic ectodermal syndrome
106
What type of inheritance causes ectodermal dysplasia?
X-linked inheritance
107
Describe lyon hypothesis when it comes to ectodermal dysplasia
Females have a lesser phenotype because half of the x chromosomes express the normal gene
108
How are eccrine glands affected in ectodermal dysplasia?
Reduced eccrine glands causing heat intolerance
109
How is hair, nails, skin and eyes affected in ectodermal dysplasia?
Fine sparse hair, fine wrinkling, and hyperpigmentation around the eyes, dystrophic/brittle nails
110
Midlface ____ occurs in ectodermal dysplasia?
Midface hypoplasia
111
How are salivary glands affected by ectodermal dysplasia?
Hypoplastic or absent salivary glands
112
How are teeth affected in ectodermal dysplasia?
Oligo or hypodontia -> reduced number of teeth
Incisor crowns: tapered or conical, pointed
Molars: reduced in diameter
Rarely no teeth
113
Treatment for Ectodermal dysplasia
Replacement of missing teeth, increased preventative care for xerostomia related caries
114
Peutz Jeghers Syndrome: Inheritance pattern
Autosomal dominant inherited condition with an STK11 Mutation
115
Key features of Peutz Jeghers Syndrome
Freckle-like lesions of the hands
Perioral skin
Oral mucosa in conjunction with intestinal polyposis and predisposition to develop cancer
116
Peutz-Jeghers Syndrome: When do pigmented lesions develop?
Early childhood
117
Describe oral lesions and where they are located in peutz-jeghers syndrome
1-4 mm brown to blue-gray macules, occur on vermillion, labial and buccal mucosa and tongue
118
Where do skin lesions occur in peutz-jeghers syndrome?
On the extremities
119
Describe peutz-jeghers syndrome's lesions compared to true freckles
Lesions do not wax and wane with sun exposure like a true freckle does
120
Describe intestinal polyps that occur in peutz-jeghers syndrome
Hamartomatous intestinal polyps throughout the GI tract that are not premalignant
121
Define Hamartoma
Benign growth of normal tissue
122
What are other GI findings in peutz-jeghers syndrome
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
Treatment of Peutz-Jeghers Syndrome
Dentists can be screeners for this condition, characteristics pigmentation arise in childhood before patient is at significant risk for syndrome associated malignancy
124
Once peutz-jeghers syndrome is diagnosed, describe treatment
Pigmented lesions do not require treatment, they are benign
Patient should be monitored by GI doctor for malignancy and intussusception
125
Ehlers-Danlos Syndrome: Define
A group of inherited connective tissue disorders resulting in the abnormal production of collagen
126
Inheritance pattern of ehlers-danlos syndrome
Autosomal dominant
127
How are joints and skin affected in ehlers-danlos syndrome
Hypermobility of the joints, easy bruising, elasticity of the skin
128
What type of scarring occurs with ehlers-danlos syndrome?
Papyraceous scarring (resembling crumpled cigarette paper)
129
Oral manifestations of ehlers-danlos syndrome
Gorlin SIgn: touching the tip of the tongue to the nose
TMJ subluxation
Pulp Stones
130
Treatment of Ehlers-Danlos syndrome
Classical type usually normal lifespan
TMJ subluxation treated as normal
131
Marfan Syndrome: Describe
A multisystem connective tissue disorder due to a mutation in the fibrillin-1 gene
132
Marfan Syndrome Inheritance Pattern
Autosomal dominant
133
Marfan syndrome effect on body size
Tall, thin body habitus
134
Cardiovascular system effects on marfan syndrome
Risk of aortic aneurysm aortic dissection, valve malformations
135
Marfan syndrome effects on eyes
Early onset glaucoma, retinal problems, lens problems
136
Skeletal complications associated with marfan syndrome
Scoliosis
137
Oral cavity effects on marfan syndrome
High arched palate
Dental crowding
138
Treatment for marfan syndrome
Ideal dentition achievable through prosth and ortho
139
Systemic Sclerosis: Describe
Immunologically mediated pathogenesis involving abnormal interactions among vascular tissue, connective tissue and immune cells.
140
What is deposited in systemic sclerosis? Where?
Dense collagen deposited throughout the body in extraordinary amounts: mainly skin, but every organ affected.
141
Population affected by systemic sclerosis
Women affected 3-5x more than men, occurs in adults
142
How is opening affected by systemic sclerosis
Microsomia -> limited opening due to collagen deposition in the perioral tissues
143
Oral manifestions of systemic sclerosis
Loss of attached gingiva and recession
Dysphagia (due to lingual collage deposition)
Xerostomia
Widening of PDL
Generalized resportion of the mandible
144
Describe Raynaud phenomenon in systemic sclerosis
Vasoconstriction in cold weather
145
Describe how figures are affected in systemic sclerosis
Resportion of terminal phalanges, flexion contractures (claw-like fingers)
Skin: Diffuse, hard and smooth texture
146
Diagnosis of Systemic Sclerosis
Serum lab testing for Anti-topoisomerase I antibodies
147
Overall treatment for systemic sclerosis
Systemic medications like penicillamine to prevent collagen production, systemic steroids have little effect and photochemotherapy some benefit for the skin
148
Oral treatment for systemic sclerosis
-May need collapsible dental appliances to replace teeth
-Surgical correction of open bite caused by condylar resportion if necessary
149
Describe Prognosis of systemic sclerosis
-Fibrosis of lungs, heart, kidneys, GI tract -> organ failure within 3 years of dx
150
"C" in CREST
Calcinosis cutis (calcium deposits in the skin)
151
"R" in CREST
Raynaud phenomenon (vasospasm in cold weater causing less blood to flow to digits)
152
"E" in CREST
Esophageal dysfunction (due to abnormal collagen deposition)
153
"S" in CREST
Sclerodactyly (Claw like deformity of the fingers due to abnormal collagen deposition in the dermis)
154
"T" in CREST
Telangiectasia (superficial, dilated capillaries)
155
Describe Telangiectasia
Vascular lesion caused by dilation of a small, superficial blood vessel
-Visible dilated small blood vessels
-Blanch with light pressure
156
Describe Petechiae
Round, pinpoint area of hemorrhage
157
Describe Purpura/Ecchymosis
Non-elevated area of hemorrhage, larger than a petechia
158
Population affected by CREST
Female predominance
50-70 years old
159
Diagnosis for CREST
Serum lab testing for anticentromere antibiodies
160
What is less severe and has a better prognosis than systemic sclerosis?
CREST
161
Treatment for CREST
Monitored for increased risk of pulmonary hypertension and primary biliary cirrhosis (more than 10 years after diagnosis)
162
Hereditary Hemorrhagic Telangiectasia: Describe
Autosomal dominant disorder in which genetic mutations results in decreased blood vessel integrity
163
Clinical Features of Hereditary Hemorrhagic Telangiectasia
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
Overall treatment for Hereditary Hemorrhagic Telangiectasia
Electrocautery, cryosurgery, laser ablation
Progesterone, estrogen therapy
Antibody therapy against endothelial growth factor
165
Dental treatment for hereditary hemorrhagic telangiectasia
Antibiotic prophylaxis until pulmonary AV fistula has been ruled out
