pigmented lesions Flashcards
what syndrome is associated with hemangioma ?
sturge weber syndrome
what does a hemangioma look like microscopically?
numerous dilated vessels lined by endothelial cells without muscular coat (cavernous hemangioma )
or
endothelial proliferation (cellular/ capillary type hemangiomas)
treatment of hemangioma :
conventional surgery , lazer surgery or cryosurgery
intra-lesional injection of sclerosing agenst such as 1% sodium tetradecy sulfate
clinical apperance of varix?
pathological dilatations of veins in ventral tongue, lower lip, buccal mucosa. gets worse woth old age and does not regress once it begins
usually caused by trauma.
appears as raised blue, red , or purple surface . surface mucosa is lobulated or nodular
some can be blanched, others are not due to formation of intra-vascular thrombi
what is angio-sarcoma ?
-malignant vascular neoplasm that is not related to HIV (differentiates it from kaposi sarcoma )
arising from blood or lymph vessel endothelial cells
what is the site of angio-sarcoma ?
anywhere on the body. oral cavity is a rare site. they appear red , blue , or purple and proliferate rapidly (nodular tumors)
treatment of angiosracoma ?
radical excision
what is kaposi’s sarcoma ? often affected sites?
slowly progressing tumor of vascular origin with no metastasis.
sites: hard palate , facial gingiva
most common neoplastic lesion associated with HIV
Lesions increase in size to become nodular groeths and some will involve whole palate
how does kaposi’s sarcoma appear microscopically?
profliferating spindle cells with mild pleomophism
extravasation of erythrocytes
hemosiderin granules
treatment of kaposi’s sarcoma ?
intra-lesional 1%vinblstine sulfate to eradicate tumor
what is hereditary hemorrhagic telangiectasia ?
multiple round or oval papules measuring less than 0.5 cm in diameter
genetically transmitted disease
lesions represent multiple microaneurysm , owing to weakining defect in adventitial coat of venules
sites affected in HHT?
purple papules on vermillion and mucosal surfaces of the lips as well as on the tongue and buccal mucosa
facial skin and neck are also involved
what is the etiology of oral/labial melanotic macule ? what does it look like ?what are the common sites ? gender predaliction ?
trauma
(can form due to denture too)
lower lip and ginigva <1cm macule with well circumscribed , oval , orirregular outline and often uniform in pigmentation
female
how to differentiate between nevocellular and blue nevus ?
both nevi are due to proliferation of melanocytes
-often have hair protruding from them)
nevocellular nevus arise from the basal layer melanocytes early in life
blue nevus arise from spindle layer which is deeper. the overlying vessels obscure the brown pigmentation and make it appear blue
lesions have no potential to turn to melanoma
lesions are usually asymptomatic and present as a small <1cm , solitary, brown or blue well curcumscribed nodule or macules
treatment of melanoma ?
-ablative surgery with wide margins
-adjuvant radiotherapy is necessary
-recent developments is anti-tumor vaccine adjuvant interferon alpha 2B therapy used to treat primary cutaneous melanomas >4mm in thickness
prognosis is good before apperance of nodular lesions , which indicates invasion into the vertical grwth phase
drugs associated with drug induced melanosis :
-minocycline (tetracycline derivative)
-anti-malarials : chloroquine, hydroxychloroquine, quinoline
phenothiazines
oral contraceptives
cytotoxic medication such as cyclophosphamide and busulfan
what does drug induced melanosis present as?
pigment can be diffuse yet localized to one mucosal surface , often hard palate
lesions are flat
discolorations fades a few months after drug is ceased
what is melasma/ chloasma
acquired systemic melanosis that typically develops on sun exposed areas
used to describe any form of generalized facial hyper-pigmentation
what is smokers melanosis ?
diffuse melanosis of anterior facial maxillary and mandibular gingiva, lateral tongue, floor of mouth , and palate caused by smoking. pigmentation is flat and often irregular
histologically no premalignant potential
examples of endocrinopathic pigmentation ?
addisons disease and pituitary based cushings syndrome . in both , hyper pigmentation is over secreion of ACTH , a hormone with melanocyte stimulation properties
should be suspected whenever oral melanotic hyperpigmentation is accompanied by cutaneous bronzing
apperance of peutz-jeghers syndrome ?
multiple small , pigmented macules oflip, perioral skin and hands and feet . mostly concentrated around lips
<0.5 cm in diamter
basilar melanogensis without proliferation
echymosis presentation:
bright red macule transfer to brwn within a few days .
patients taking anti-coagulants may present with oral ecchymosis , particularly on the cheek or tongue
what is petechia secondary to ?
plarelet deficiencies or aggregation disorders
-autoimmune or idiopathic theombocytopenic purpura
what metals can cause pigmentation inthe oral cavity ?
lead , mercury , arsenic , and bismuth
discoloration is a gray-black line found along the free marginal gingiva
signs and symptoms of metal poisoning , neurologic disorders, intestinal pain and sialorrhea
