Lec 3: Pigmented Lesions Flashcards
What gives lesions color?
Blood
melanin
foreign material
Pigmentation Caused By Blood (2)
Intrascular: blanches
Extravascular: does not blanch
Diascopy tests for
whether a lesion is vascular (inflammatory) or nonvascular (nevus) or hemorrhagic (petechia or purpura).
Hemangioma
Not present at birth
Tumor of infancy that has rapid growth and endothelial cell proliferation
Gradual involution
Venus malformation
Present at birth and persist through life
Anomalies of blood vessels without endothelial proliferation
Hemangioma treatment
Will regress on their own
Systemic corticosteroids may help reduce size
Venus malformation
Small lesion: no treatment
Large lesions: sclerosing agent and later resection
STURGE-WEBER ANGIOMATOSIS
Born with vascular malformation of face known as port wine stain
Non-hereditary
Leptomeningeal angioimas on ipsilateral cerebral cortex may cause
convulsive disorder or mental retardation
port wine stain + meningeal angiomas + seizures + mental retardation
STURGE-WEBER SYNDROME
PORT WINE STAIN (NEVUS FLAMMEUS):
vascular malformation seen in 0.3-1.0% of newborns
STRUGE-WEBER ANGIOMATOSIS treatment
Flashlamp pulsed dye laser can improve esthetics of facial/oral port wine nevi
Mental retardation/epilepsy may require neurosurgical treatment
varix is? common in? loss of what? blanch or non-blanch? common location? treatment?
Abnormally dilated and tortuous veins
Common in older adults
Loss of connective tissue tone supporting vessels
Usually blanch, but will not if thrombosis occurs
Common location: sublingual varix
Txt: none needed. May be removed for esthetics
Firm, nontender, blue-purple nodule describes a
varix
KAPOSI’S SARCOMA caused by? seen in? appears? occur on? treatment?
Vascular neoplasm
Caused by human herpesvirus 8 (HHV-8)
Seen in association with HIV
Painless blue-purple macules/plaques on surface of skin
Oral lesions generally occur on the palate
Treatment: Chemotherapy or Radiation therapy
SUBMUCOSAL HEMORRHAGE is a ? leads to? examples?
Bruise from minor trauma Leads to extravasated erythrocytes PETECHIAE ECCHYMOSIS HEMATOMA
PETECHIAE
very small hemorrhages into skin, mucosa, serosa
ECCHYMOSIS
blood accumulation greater than 2 cm
HEMATOMA
accumulation produces a mass
Keratinocytes histology? most common in? function? amt of cytokeratins increase as?
are stratified squamous epithelial cells. Most common cell in epidermis. Function is to produce intermediate filaments called cytokeratins. Amount of cytokeratins increases as the cells move upward.
melanocytes produce
melanin
Langerhans cells are
antigen presenting
Merkel cells are
neuroendocrine cells involved in tactile sensation
Oral mucosa and skin contain __ distinct cell types in surface epithelium
4
Children Love Getting Sun Block
Stratum Corneum Stratum Lucidum Stratum Granulosum Stratum Spinosum Stratum Basale Dermis
Melanocytes synthesize ____ & inject it into _____
melanin; keratinocytes
Melanocytes synthesize melanin pigment in _____.
melanosomes
Is melanin more present in keratinocytes or melanocytes?
keratinocytes
Number of melanocytes per unit area of skin varies from one part of body to another but is independent of ___. Differences in skin color are due to differences in the _____ .
race; number of melanin granules in keratinocytes
Melanin granules accumulate above region of ____ ___to protect genetic material from damage by ____ radiation.
keratinocyte nuclei; ultraviolet
Ephelis
Freckle
Ephelis–present region of
increased melanin production
Ephelis receptor?
Melanocortin-1-receptor gene (MC1R)
Ephelis more pronounced after?
sun exposure
Oral Melanotic Macule-Brown, mucosal discoloration due to?
increased melanin production
Oral Melanotic Macule-shape?
FLAT = Not thickened or raised
Oral Melanotic Macule unlike epelis because
not related to sun exposure
Oral Melanotic Macule has potential for premalignant?
No premalignant potential
Hypermelanosis (in oral melanotic macule and freckle)
Hyperactivity of melanocytes
management: Oral Melanotic MaculeSmall unchanging ____ lesions _____ and with ____borders can be followed. Otherwise, biopsy.
nonthickened; uniform in color; regular
Melanoacanthoma–exclusive to? Often demonstrate? Management?
African Americans; Often demonstrate rapid growth; biopsy to rule out melanoma
ACQUIRED MELANOCYTIC NEVUS is proliferation of
nevus cells and melanocytes
nevus refers to
malformation of the skin and mucosa
3 types of nevus
junctional nevus
compound nevus
intramucosal nevus
Oral Melanocytic Nevus Managment
Oral nevus is considered premalignant & should be completely excised
Can melanoma always be distinguished from a nevus from a clinical basis?
NO
CONGENITAL MELANOCYTIC NEVUS: seen in __ of newborns
1%
GIANT HAIRY NEVUS:
extensive hypertrichosis within congenital nevus.
Giant hairy nevus when very prominent can be called (2)
bathing trunk nevus or garment nevus
HALO NEVUS: halo is result of
nevus cells destruction by immune system
BLUE NEVUS–Proliferation of melanocytes deep within the? Seen almost always in the?
CT; palate;
Second most common nevus in the mouth?
Blue nevus
MELANOMA OF SKIN–___ neoplasm?
malignant;
Melanoma of the skin major causative factor?
Damage from UV radiation
Melanoma of skin- is acute or chronic sun exposure of greater importance?
acute
Melanoma of the skin-risk factors?
Fair complexion and light hair
Tendency to sunburn easily
Indoor occupation with outdoor recreational habits
Personal/family history of melanoma
History of dysplastic or congenital nevus
Melanoma–On skin (90%), due to?
acute sun damage
Most common skin cancers–1-3?
1# Basal Cell Carcinoma
2# Squamous Cell Carcinoma
3#Melanoma
Where can melanoma occur?
anywhere
Melanoma Growth Pattern (2)
Radial (horizontal) growth phase
Vertical growth phase
Melanoma Radial Growth Phase- Melanoma cells are present along the epidermal-dermal junction and grow? can remain in this phase for? does melanoma metastasize during this time?
laterally; years; NO
Melanoma Vertical Growth Phase–Melanoma cells grow? can cells metastasize?
downward into the dermis; YES
Melanoma- Four clinicopathologic types exist:
Superficial spreading melanoma
Nodular melanoma
Lentigo maligna melanoma
Acral (mucosal) lentiginous melanoma
The most common type of melanoma
Superficial Spreading Melanoma
Superficial Spreading Melanoma can occur in what population?
young adults
SUPERFICIAL SPREADING: ___ of cutaneous lesions
70%
SUPERFICIAL SPREADING
Macule with variety of colors, may be slightly elevated. Interscapular area of males, back of legs of females
Nodular Melanoma–appears? grows? exists in what growth phase?
Appears as a dome-shaped, darkly pigmented nodule.
Grows rapidly
Exists in the vertical growth phase from the beginning, thus tends to be deeply invasive.
Nodular Melanoma-___% of skin melanomas, 1/3 of these in_____area. No radial growth phase. Usually deeply pigmented, but can sometimes be _____
15; head and neck; nonpigmented
Lentigo Maligna Melanoma associated with?
chronic sun exposure
Lentigo Maligna Melanoma occurs most commonly?
on the face of older adults
-Lentigo Maligna Melanoma typically appears as one or more darkly pigmented nodules arising in a ____
solar lentigo
The most slowly growing melanoma—may remain in the radial growth phase for years is?
Lentigo Maligna Melanoma
Solar Lentigo Clinical Features–> 90% of ____? appearance? occurs on? pigmentation is? no change with exposure to?
Caucasians over 70 yo;
Brown (nonthickened) macule, larger than a freckle.
Occurs on chronically sun-exposed skin especially cheeks and dorsal surface of hands;
Pigmentation is constant; no change with exposure to UV light
LENTIGO MALIGNA: ___% of cases. Develops from _____. Almost exclusive on? growth time?
5-10; precursor lesion; sun-exposed skin of fair-complexioned older adults; Very slow radial growth (15y).
Acral Lentiginous Melanoma most common in?
African-Americans
Melanomas of oral mucosa, palms, soles, nail beds.
Acral Lentiginous Melanoma
Most common in blacks and orally. Develops on palms of the hands, soles of the feet, subungually, and mucous membranes
ACRAL (MUCOSAL) LENTIGINOUS
Melanoma: Treatment?
Treatment is surgical excision.
Radiation therapy is of limited value.
Chemotherapy and immunotherapy are evolving.
Melanoma: Prognosis?
The most important prognostic indicator is the histologic depth of invasion. Melanomas less than 0.75 mm thick have almost 100% 5-year survival.
Melanoma Survival, 10 years-Breslow Depth of Invasion 0.00 to 0.75mm? 0.76 to 1.69mm? 1.70 to 3.59mm? > 3.59mm?
0.00 to 0.75mm 98%
0.76 to 1.69mm 89%
1.70 to 3.59mm 67%
> 3.59mm 43%
Clark Method of Staging-Stage 1?
melanoma in situ (no invasion)
Clark Method of Staging-Stage 2?
tumor in papillary dermis
Clark Method of Staging-Stage 3?
tumor to junction papillary and reticular dermis
Clark Method of Staging-Stage 4?
tumor in reticular dermis
Clark Method of Staging-Stage 5?
tumor in subcutaneous tissue
Clark level 1
96%
Clark level 2
96%
Clark level 3
90%
Clark level 4
67%
Clark level 5
26%
Melanoma- Areas of poor prognosis:
BANS Interscapular area of the BACK Posterior upper ARM Posterior and lateral NECK SCALP
ORAL MELANOMA begins as?
Begins as brown-black macule
Clinical Features of Melanoma
ABCDE Asymmetry Border irregularity Color variation Diameter greater than 6mm Evolving
Benign and malignant melanocytic lesions may be clinically______ in the oral cavity
indistiguishable
The only certain method of excluding malignant melanoma is ______.
excisional biopsy
Melanoma Survival Rates: Oral 5-year?
Oral
5-year: 13-22%
PHYSIOLOGIC PIGMENTATION occurs due to
increased production of melanin
Oral pigmentation is similar in intensity to
skin pigmentation
Gastro-intestinal features where? Intestinal obstruction to due? GI malignancy percentage and age?
Intestinal polyposis (not premalignant) Intestinal obstruction due to intussusception GI malignancy: 33% by age of 60
Oral lesions seen in 90% of the patients found in? size? appearance?
Vermillion zone, labial/buccal mucosa, and tongue
1-4 mm blue-gray macules
ADDISON’S DISEASE is brought on by?
Insufficient production of adrenal corticosteroid hormones (mineralcorticoids, cortisol)
Destruction of the adrenal cortex or pituitary gland dysfunction
ADDISON’S DISEASE
HOW DOES ADDISON’S CAUSE BRONIZING?
Increased adrenocorticotropic hormone (ACTH) stimulates melanocytes (primary, not secondary)
HOW DOES SMOKING CAUSE PIGMENTATION OF THE ORAL SOFT TISSUES?
Stimulation of melanocyte activity by tobacco
MELASMA aka
the mask of pregnancy
Melasma appearance and location
Irregular, symmetric, brown macules on sun-exposed face and lips
Melasma may also occur with use of
oral contraceptives
Drug-Induced Pigmentation (6)
Anti-malarial drugs used for systemic lupus
Anti-psychotic: chlorpromazine, clozapine
Medications for AIDS: AZT
Tetracycline associated hairy tongue
Minocyclines (Minocin): discoloration of bone -> discoloration of oral mucosa; also teeth Chemotherapeutic drugs
NEUROFIBROMATOSIS-clinical appearance? (4)
Multiple “café au lait” freckles
Axillary freckling
Multiple neurofibromas
Lisch nodules
Café au Lait Spots similar lesions seen in
Polyostotic Fibrous dysplasia
Heavy metal pigmentation due to what type of metal?
Arsenic, bismuth, platinum, lead, silver and mercury
LEAD AND BISMUTH: blue-gray line along gingival margin. Lead =
Burton’s line
ARGYRIA aka
chronic silver intoxication
ARGYRIA appearance
diffuse greyish discoloration, especially in sun-exposed areas
X-men!!!
