Bumps and lumps Flashcards
Keratinocytes
Seborrheic Keratosis
What kind of tumor is it?
The sign of Lesser-Trelat is a marker of______.
- Common benign skin tumor of adults
- Clonal expansion of epidermal keratinocytes
Numerous eruptive lesions (sign of Leser-Trelat) may be a marker of internal malignancy.
- Discrete “stuck-on” appearing light to dark brown plaques, velvety or verrucous surface
- ** No treatment necessary
Keratinocytes
Seborrheic keratosis
Subtype
Dermatosis Papulosa Nigra: small, pigmented seborrheic keratoses usually occurring on the face of people with Fitzpatrick skin type V or VI.
Keratinocytes
Actinic (solar) Keratosis
What causes it?
Epidemiology
Most common pre-cancerous skin lesion
Pathogenesis
–Sunlight
–Hereditary (blue eyes, red/blond hair)
What causes similar lesions?
-Arsenical keratosis
-Radiation keratosis
Keratinocytes
Actinic (solar) Keratosis
What is its distribution in the body?
how does the primary lesion looks?
**Photodistribution- face, dorsum of hands, arms
**Arsenical keratoses- anywhere, especially palms
***Radiation keratoses- site of radiation
Primary lesion
–>1-10 mm scaly erythematous irregular papules
–>Variants- hyperkeratotic, pigmented, cutaneous horn
Actinic cheilitis- lip equivalent
Actinic keratosis with **cutaneous horn**
What other skin diseases can have cutaneous horns?
Does Actinic keratosis has the potential to become malignant?
It can become what?
Incidence of AK becoming a SCC
Study results 0.24% to 20%
Best figure: 1-5% lifetime
Spontaneous remission
- 25% in 1 year in 1/3 of patients
- 60% of SCC arise in pre-existing AK
Melanocytes are related to:
What is a Nevi?
Nevi = Moles
Melanoma
Ephelides = Freckles
Lentigo = Sun Spots
Café au lait macule
- Proliferation of melanocytes in the epidermis and/or dermis
- Can be congenital, acquired, sun-induced, atypical, or malignant (melanoma)
- Variants include blue nevi, halo nevi, congenital nevi
- Genetics and sun exposure are contributing factors
- Number of nevi linked to development of melanoma
Atipic (Dysplastic) Nevus
Dysplastic nevi (atypical nevi, Clark’s nevi, nevi with disordered architecture and cytologic atypia) are a subgroup of nevi which have an irregular outline, variable pigmentation, indistinct borders, and can be larger than 6mm in diameter.
Often described as having a “fried-egg” appearance, they typically have a dome-shaped central brown papular component surrounded by a flatter zone of light brown or tan pigmentation. When multiple dysplastic nevi are present in a patient with a family history of melanoma, they herald an increased risk for the development of melanoma in that patient. The presence of a single or few dysplastic nevi outside the context of a family history of melanoma may or may not portend an increased risk for that patient
Examples of atypical nevi
Sporadic Dysplastic nevus syndrome
Familial Atypical Nevi
(FAMMM syndrome)
Familial Atypical Nevi
(FAMMM syndrome)
Risk of developing malignant melanoma from FAMMM:
Blue Nevus
Halo Nevus
Congenital Nevus
- May be solitary or multiple
- May affect any cutaneous surface
- Primary lesion identical to acquired nevi only differ in size- 1 mm to huge (i.e.bathing trunk nevi)
– Presence of dark hairs- no clinical significance
• Complications
– Head, neck, posterior midline- cranial and or leptomeningeal melanocytosis
• Congenital nevi
– 1% of newborns
• Size
– Small (<1.5 cm diameter)
– Intermediate (1.5-20 cm diameter)
– Large (>20 cm diameter) • Treatment
– Highly controversial area
– Elective surgical excision
Most authorities do not recommend
Recommended by some if clinically feasible
– Dermabrasion
• Performed by a minority of authorities
• Risk for Melanoma
– Medium to Large Congenital nevi > 10 cm
• Occur in 1:20,000 newborns
– Calculated potential for malignant melanoma
• Risk 1% per year in large congenital nevi (>20 cm diameter) – Malignant melanoma in congenital nevi
50% appear in first 3 years
60% appear in first decade
Sebocyte:
Sebaceous hyperplasia
Increased size and number of sebaceous glands in the dermis.
Presents as a flesh-colored to pink to yellow papule with a central dell
Occurs in “seborrheic” or oily areas
Sebocyte:
Nevus Sebaceous
how does it present at birth?
Most common in the ______.
It has a small risk of ________, a benign or low grade malignant hair follicle tumor.
When is it recommended to remove it?
Developmental “hamartoma” of numerous sebaceous glands focally in the skin.
-Presents as a hairless yellow plaque at birth
Most common on the scalp, can be seen on forehead/face.
- Histology may show other cell lines increased (epidermal overgrowth, ductal hyperplasia)
- Small risk of secondary neoplasia - benign or low grade malignant hair follicle tumors
- Excision at or before puberty recommended by most.
***Hamartoma is a nonneoplastic overgrowth of disorganized tissue indigenous to a particular site.
Fibroblasts
Dermatofibroma
- Benign proliferation of fibrohistiocytic cells in the dermis
- Characteristic histology
- Most common on lower legs of women, shoulder
- Possibly related to exaggerated response to trauma
- No treatment necessary; excision.
Connective Tissue
Acrochordon
All physicians should be able to recognize these benign skin growths. Skin tags commonly occur in areas of rubbing including the neck, axilla and infra-mammary area in women.
No treatment is necessary for these common skin growths as they are benign with no malignant potential. They can, however, be removed if bleeding from irritation or rubbing on clothing. The most common way to remove these lesions is by freezing (cryosurgery) with liquid nitrogen or by cutting them off.
Connective tissue
Accessory Tragus
This is a developemental anomaly of the first branchial arch, presenting at birth, as a small, flesh-colored, exophytic papule on the skin, located anywhere along a line from the anterior tragus to the lateral commissure of the mouth. They may be soft and fleshy, but often contain central cartilage. They are harmless, but are often removed for cosmetic purposes with simple excision. They most commonly occur sporadically, but can be associated with renal disease and certain syndromes (Goldenhar syndrome).
–>Developmental anamoly of the 1st branchial arch
–>Fleshy papule +/- cartilage on face – from tragus to mouth.
–>Solitary or multiple
–> Goldenhar syndrome
Family history of renal disease?
Neural
Neurofibroma
- Soft pink, fleshy or transculscent papule
- “button-hole” sign
- Solitary lesions common
- Numerous lesions associated with neurofibromatosis
Blood vessels:
Cherry Angioma
- Benign proliferation of small dilated vessels in the superficial dermis.
- Trunk/chest/back most common location.
- Increased with age and sun exposure.
- Harmless, no treatment necessary.
Infantile Hemangioma
Its a neoplasm of _______ cells.
What are its phases?
What kind of therapy is useful? Why?
- Neoplasm of the endothelial cells
- Present at or shortly after birth
- Grows rapidly, stablilizes, involutes (doesn’t always “go away”)
- Treatment indicated only for lesions that cause functional impairment or in a cosmetically sensitive area where long-term cosmetic sequelae may be a concern
–Beta blocker therapy
Infantile Hemangioma
Vascular malformation (port wine stains):
-Developmental anomaly of too many small capillaries focally in the skin
Static – no “life cycle” like hemangioma (ie not a neoplastic process).
- Most common on face, extremities
- Flat pink to dark red patch
- If on face in V1-2 distribution, esp bilateral, an be associated with Sturge-Weber syndrome (PWS, seizures, glaucoma, stroke, DD)
Vascular laser can improve cosmetic appearance
