Lumps on the Lids PDF - Benign and Malignant Lesions

Benign lesions Milia: small, raised, round and pearly white/yellowish cystic lesions ○ Protein and keratin deposits are the “ingredients” of milia under the epidermis of the skin ○ Bigger in size than acne ○ Acne: pores of the epidermis are clogged; not...

Benign lesions Milia: small, raised, round and pearly white/yellowish cystic lesions ○ Protein and keratin deposits are the “ingredients” of milia under the epidermis of the skin ○ Bigger in size than acne ○ Acne: pores of the epidermis are clogged; not milia ^ ○ Associations: Infants: can be congenital and disappears fast Adults: trauma- laser surgery, cuts on the skin, medications: steroids, oily creams, any skin conditions can trigger milia ○ Milia en plaque: associated with systemic diseases such as Lupus, frágil loose skin disease (?) ○ Sun factor: continuous exposure to the sun (hours and hours and has a triggering factor) ○ Usually one or two can be asymptomatic, if it is more- cosmetic factor ○ Treatment: child: no tx needed b/c it disappears; pediatrician adult: incision of skin w/ sharp needle or blade and expression and antibiotic oint. Also cryotherapy but more rare ○ Prevention: avoid one of the factors ^ creamy cosmetics and sun** ○ Sebaceous cysts: “oily”cysts ○ Infundibulum of hair follicle gets inflamed/seb glands/gland of Zeis ○ Causes: #1: Seb glands/ Gland of Zeis clogged; will be superficial cyst How to distinguish it** has its yellow lipid color #2: Deep: AKA Epidermal inclusion cyst  skin on top; will not see yellow inside because it is deeper ○ Most likely secondary to: 1st) clogged Glands of Zeis then 2nd) infundibulum of hair follicle = deeper cyst ○ Treatment (if patient desires): cosmetic superficial: clean area w/ alcohol, incise cyst surface w/ needle, express w/ 2 Q-tips, then apply antibiotic oint. 1x F/U Deep: refer for excision; if not reassurance ○ Like a pimple Sudoriferous cyst/ Hidrocystoma ○ Cavity filled with water (water-filled cyst)* ○ On lid margins but not oily. It is a fluid cyst of Gland of Moll, so it is transparent/adenoma (benign tumor) of eccrine (larger in size and anywear in lid)/apocrine sweat glands (smaller in size and always in lid margin) ○ Cause: surgeries or growth by temperature; cold minimizes the size ○ Easy to pop them off; easier than sebaceous cysts ○ Tx: excision/laser ○ Verrucae (warts) ○ Usually from viral origin ○ Type of papilloma of squamous origin ○ Thickening of squamous cells of epidermis ○ Gradual onset- smaller become bigger ○ Many appearances: planar (flat)- they do look like skin tags, vulgaris (something that looks like cauliflower appearance), pedunculated (two extensions in one), cutaneous horn (things that are sticking out- typical verrucae- ex: holding two fingers up) ○ HPV #6 &#11 ○ If in lid margin can cause a viral conjunctivitis ○ Treatment: 1-5% that it can progress to squamous cell carcinoma Patient education, reassurance Change to malignancy If on lid margin and patient has conjunctivitis: refer for excision Other treatments: cryosurgery, laser ○ Verrucae Vulgaris ○ Verrucae Plana “flat wart” ○ Pedunculated Verrucae ○  Cutaneous horn ^ Squamous Cell Papilloma ○ Most common benign lesion of the eyelid Not life threatening ○ Age: 60-65 ○ Race: White ○ Sex: Males>females ○ Upper eyelid: Occurs more ○ Lower eyelid: Occurs less ○ UV exposure, radiation Tx, skin cancer hx, immunosuppressive drugs, chemicals ○ Actinic keratosis or Keratocanthoma can be a precursor** ○ Red nodule, crusted, raised, scaly plaques of keratin rapidly progressing and leading to destruction of tissue and impaired lid function/ with or without a central depression/ crater ○ Metastases to orbit and systemic organs  ○ Tx: Biopsy and excision w/ reconstruction Mohs surgery Laser ablation (photothermal ablation) Cryotherapy Radiation: PDT, Photochemical dissociation ○ Sebaceous cell carcinoma ○ A highly aggressive malignant neoplasm that arises from the meibomian glands, glands of Zeis, and from the sebaceous glands of the caruncle and eyebrow ○ Recurrence rate ○ Metastasis high ○ Accounts for up to 5% of all eyelid cance ○ 10-15% mortality rate but can go up to 40% ○ Lid location: has gone to the second place? ○ Dx by clinical appearance/ hx and histological study ○ Age: 60-65 ○ Sex: Females* ○ Population: 85% ○ Always in the upper lid ○ May have a variety of clinical appearance looks like chalazion painless bump firm nodule that resembles a chalazion multiple chalazion that recurs after excision? Sebaceous cell carcinoma*** (boards ?) remember: unilateral, recurrent and resistant: RED FLAG ○ May develop to: a plaque-like thickening of the tarsal plate/lid margin with destruction of lid function and presence of lid inflammation, madarosis  ○ Treatment: wide surgical excision with microscopic monitoring of the margins is the procedure of choice extremely aggressive carcinoma Mohs’ micrographic surgical excision may be used BUT radiation tx may be considered alone or as an adjunct to surgical excision proton beam radiation x-rays ***use of Mitomycin C ○ Malignant Melanoma ○ Cutaneous malignant melanoma is an invasive proliferation of malignant melanocytes ○ Spindle melanocytic cells and epithelioid melanocytic cells ○ Nodular vs. non-nodular types Nodular lesion may present as a markedly pigmented or somewhat pigmented or amelanotic nodule Associates: size and appearance Differential- nonmalignant pigmented nevi (comping or intradermal) that affect the eyelids ○ 1% of all eyelid malignancies ○ Malignant melanoma and deaths from all cutaneous cancers Most common tumor that causes the most deaths ○ Changing cutaneous moles, excessive sun exposure, and sun sensitivity, family hx ○ Age: ~50 y/o ○ Race: White race ○ Sex: Males ○ Last 5 years new trends include younger females < 50 y/o ○ Dx- clinical appearance examination / excisional biopsy / and histopathological examination  Biopsy: punch (take a sample of lesion), exicisional (take the whole lesion out), incisional (take sample of more suspicious area) Excision: whole lesion, surrounding skin and tissue below ○ Nodular lesion may present as a markedly pigmented or somewhat pigmented or amelanotic nodule Associations: size and appearance Differential - nonmalignant pigmented nevi (compound or intradermal) that affect the eyelids Abnormal Pigmented Abnormalities Nevi of Ota ○ Hamartoma (congenital/acquired) of dermal melanocytes/Epidermis and early dermis Hamartoma- cells of the tumor has the same histology of the organ that it grows on ○ Accumulation of pigment (melanocytes) ○ Easy to recognize by its color Blue or gray patch on the face – at birth or around puberty ○ Distribution of the first two branches of the trigeminal nerve ○ Unilateral* or bilateral ~70% are unilateral ○ What part of the eye structures does it cover? Uvea, sclera, eyelids Greater risk of chorodial melanoma - but it occurs in only as many as 4% of prominent cases  ○ ○ Signs Increased pigmentation in the eyelid and/or sclera/iris Iris may be darker No associated symptoms DDx: ocular melanosis has the same ocular melanocyte and pigment distributions as well as the risks but there is no pigment in the lids Ocular melanosis: episcleral and uveal hyperpigmentation w/o pigment in the lids ○ Tx Most patients have no subsequent related problem Few will develop intracranial neoplasia Observation- yearly eye examinations with dilated ophthalmoscopy Also should have an initial neurology assessment and yearly F/U Dilate patients q 6mo. Because they are at risk for choroidal melanoma Poliosis ○ Premature, localized discoloration of the lashes and eyebrows (it may involve any hairy area of the body) ○ Caused by or classically associated w/ several systemic genetic and autoimmune syndromes Vogt-Koyandagi-Harada Syndrome (VKH) Bilateral granulomatous panuveitis with or without extraocular manifestations affecting young adults Can affect uvea with choroidal depigmentation/ONH/retina and lens Originally classified as two separate entities: ○ Vogt-Koyandagi Syndrome - uveitis, alopecia, poliosis, cutaneous as well as perilimbal vitiligo (also known as Sugiura’s sign)- look at picture, and dysacusia (lose high  pitched sounds hearing problems so everything sounds distorted) ○ Harada’s disease - bilateral exudative uveitis accompanied by pleocytosis of cerebrospinal fluid and neurological signs ○ Due to the overlapping of signs and symptoms, it was changed to Vogt-Koyandagi-Harada Syndrome Age: 20-50 y/o (~40 y/o is the common age) Race/Skin complexion: Dark; Latins, African Americans, Asians, Native Indians Gender- Females only*** An association with HLA-DR1 and HLA-DR4 4 stages of VKH ○ Prodromal stage: early stage, photophobia, blurry vision ○ Uveitic stage: uveitis symptoms ○ Chronic stage: deafness, poliosis presents **** ○ Chronic recurrent stage: end stage, ONH (glaucoma), lens (cataracts), retina (neovascularization) Poliosis associated with vitiligo occurs in CHRONIC STAGE ** ○ Perilimbal vitiligo ^^ Tuberous sclerosis An inherited genetic neurocutaneous disorder in which tumors (usually hamartomas) develop in multiple organs (Common to find in the skin and back of the eye); also de novo mutations Inheritance ** Mutation TSC1 and TSC2, tumor suppressor genes by regulating mTORC1 (protein complex) activity 1 of 6000 children Multiple organs (discoloration) (Mainly found in Skin #1, Retina #2, Brain #3)/ Peculiar ash leaf skin discoloration + skin growths (bumps on the skin) CNS tubers ○ Accumulation in the astrocytes in the brain that start off small, then grow bigger that can compress on the side of  the ventricles in the brain and causes symptoms such as extreme HA and seizures Cardiac myxomas ○ Tumors in the heart, in the common area which is L atrium Kidney tumors (angiolipomas) leading to kidney disease and kidney failure and in extreme cases, death Retinal astrocytic hamartoma ○ ○ Accumulation of astrocytes ○ Looks like bright yellow lesion, cauliflower-like Waardenburg syndrome Group of genetic conditions - hearing loss and changes in coloring (pigmentation) of the hair, skin, and eyes Very pale/light color eyes or distinctive hair coloring ○ Distinctive characteristics: Hair has a white stripe and have light eyes or heterochromia Piebaldism Absence of melanocytes in certain area of the skin and hair Patches of skin and hair that are lighter than normal ○ A little vitiligo and more white extensive in hair  ○ ○ May also be associated with localized inflammatory process of the lids May have damage to the hair follicles so check the lids Medications can also cause: starts from fluramet. (Antibiotic), anti-cancer agents ○ Associated with vitiligo ○ Precursor to skin cancer so be careful Extensive poliosis and extensive vitiligo can cause skin cancer Chloasma ○ AKA Melasma or the mask of pregnancy when present in pregnant women ○ Tan or dark skin patches that are usually around the cheeks, above the lips, neck, forehead ○ -lasma term is used for pregnant women ○ More common in women especially while taking hormonal therapy Can also appear in men if taking hormones ○ UV light: triggering factor that makes patches worse ○ Dark complexion - race: Native Americans, Indians, African Americans, Latinos ○ Tx (has asked in boards) Hydroquinone (inhibits tyrosinase: an amino acid that is produced for melanin production)- cream, lotion, gel, or liquid Tretinoin (Vitamin A) and corticosteroids Triple therapy (Hydroquinone + Tretinoin + Corticosteroids) Dermabrasion w/ laser ○ Vitiligo ○ Loss of skin melanocytes that causes areas of skin depigmentation of varying sizes (little area or ○ Affects skin and mucous membranes and the inner part of the eye ○ Generalized (whole body is affected), segmental (one side of the body is affected- L or R), localized (specific area such as the cheek is affected) ○ Cause is unknown but the most common conviction is autoimmune disease ○ Sun and chemical triggering ○ Complications: skin, eye, ear ○ Need to get sun to even skin tones ○ Treatment Topical corticosteroids (often combined with calcipotriene under UV exposure (vitamin D + UV B light and /or Psoralen while in UV therapy (PUVA)— P comes from Psoralen and UV-A light (more effective than calcipotriene) PUVA is the first line of treatment for vitiligo ****** For severe widespread pigment loss, residual patches of normal skin may be permanently bleached Surgical skin-grafting ○