Disease and Defense Unit 3-Derm Flashcards
Identify the structure and list the functions of the skin
-skin is the largest organ: covers 2m^2 SA, weighs 4kg.
Structure:
-Epidermis, Dermis, Adnexal Structure, Subcutaneous Fat, Regional variation of Skin
1-stratum corneu: top layer that flakes off
2-stratum granulosum: has filagrum that breaks down into natural moisturizing factor (protects skin)
3-stratum spinosum: has tiny spinous processes=desomosomes (keep skin together)
4-stratum basalis: basal layer, stem cells of epidermis that cause skin to regenerate.
every 28 days new cells in basal layer that gradually mature and then slough off
-keratinocyte: normal skin cell
melanocytes: pignment cells
-langerhans cells: antigen presenting cells of skin (initiate immune response, allergic response, etc.)
-keratohyalin granules
Functions:
- decoration/beauty
- barrier: physical, light, immunologic
- vitamin D synthesis
- water homeostasis
- thermoregulation
- insulation/calorie reservoir
- touch/sensation
Identify Fitzpatrick skin types.
1. Hair: red/blonde Eyes: blue/green Skin: white Freckles: +++ Sunburn: always Tan: 0
2. Hair: blonde/brown Eyes: light-med. Skin: fair Freckles: ++ Sunburn: easily Tan: minimally
3. Hair: brown Eyes: medium to dark Skin: light brown Freckles: + Sunburn: initially Tan: gradually
4. Hair: med-dark Eyes: dark Skin: moderate brown Freckles: 0 Sunburn: minimally Tan: tans well
5. Hair: Dark Eyes: Dark Skin: dark brown Freckles: 0 Sunburn: Rarely Tan: Dark Tan
6. Hair: Dark Eyes: Dark Skin: Black Freckles: 0 Sunburn: Never Tan: Always Tan
Differentiate between melanin in dark and light skin.
- eumelanin: black to brown pigment
- pheomelanin: yellow to red-brown pigment
- light skin: melanosomes distributed in clusters above the nucleus in keratinocytes. smaller.
- dark skin: melanosomes distributed individually through the cytoplasm. larger melanosomes
albinism: due to defect in tyrosine kinase gene in melanin production
vitiligo: autoimmune disorder against melanocyte. acquired depigmentation. microscopic finding is complete absence of melanocytes. seen in periorificial and acral locations. depigmented patches, macules (not raised area of skin)
screen for autoimmune, hypothyroid, etc. Treat with topical steroids, UV stimulation, etc.
Identify the functions of the different layers of the epidermis and cells in this region.
Epidermis:
-stratified squamous epithelial layer
Dermis:
-underlying connective tissue layer, includes papillary layer (loose connective tissue, under epidermis) and reticular layer (deeper, dense, connective tissue)
Adnexal structures:
-apocrine/eccrine/sebaceous glands, hair, nails
Subcutaneous fat:
-made of adipocytes
Regional variation of skin:
-thick skin on soles/palms, is hairless
Vitamin D Synthesis:
-can get it from 7 dehydrocholesterol and UVB sunlight, OR from diet.
Describe the proteins involved in cell attachments. Keratinocytes Stratum Basalis Stratum Spinosum Stratum Granulosum Stratum Lucidum Stratum Corneum
Keratinocytes
- form barrier layer
- synthesize keratin, intracellular fibrous protein of skin
- involved in cycle of proliferation, differentiating, programmed cell death
- epidermis renewed by mitosis of these cells in 28 day cycles
Stratum Basalis (germinativum)=Basal Layer
- single layer keratinocytes, stem cells of epidermis
- attached via hemidesomsomes (attach basal lamina of dermal-epidermal junction)
- defects/antibodies cause issues such as bullosa pemphigoid, collagen 7 issues cause dystrophic epidermolysis bullosa, laminin 5=Junctional EB
- Desmosomes attach keratinocytes to each other,
- antibodies in desmosomes: autoimmune blistering diseases such as pemphigus vulgaris. acquired antibodies to desmoglein
- congenital defects in Keratin 5 and 14 cause Epidermolysis bullosa simplex
Straum Spinosum:
- prickly/spiny appearance due to desmosomes
- intracellular adhesion depends on tonofilament-desmosome interaction in distribution sites
- synthesis of involucrin and membrane coating granules begins here
Stratum Granulosum:
- cells have granules
- keratohyalin granules have profilaggrin (filaggrin cross links keratin monofilaments and is impt. for barrier in skin)
- filaggrin is mutated in dry skin conditions
Stratum Lucidum:
- under light microscope, thin light staining band seen in thick skin
- cells have no nuclei/organelles
Stratum Corneum:
- outermost layer
- keratinocytes have lost nuclei and organelles and cell is filled with keratin
- desmosomes connect tightly packed adjacent cells
Distinguish regional variation of skin with regard to skin thickness and adnexal structures. Papillary Layer Reticular layer Apocrine sweat glands Eccrine sweat glands Hair Nails Sebaceous Glands
Papillary Layer:
- where attaches to epidermis, impt. differentiation/development
- capillary network supplies epidermis, has defense cells, has Meissner’s corpuscles
Reticular Layer:
- collagen/elastic fibers that give strength/flexibility
- has epidermal derivatives
- path for major blood vessels, thermoregulation, nerve tracts, Pacinian corpuscles
Apocrine Sweat Glands:
- sweat glands in axillary, pubic, perineal regions
- milky, viscid, carb-rich secretion (initially odorless, becomes odor with bacteria)
- functions in puberty, ducts empty into hair follicles above sebaceous glands
Eccrine Sweat Glands:
- traditional sweat glands
- watery enzyme rich secretion, isotonic, hypotonic as Na+ resorbed
- thermoregulation
Hair:
- pilosebaceous unit develops in utero
- hair is central medusa of keratin, cortex cuticle of hard keratin
- pigment from melanocytes at hair base
- arrector Pili contracts and makes the hairs stand up
Nails
Sebaceous Glands:
- oil glands secrete sebum (mixture of lipids)
- develop with hair follicles, empty secretions onto upper 1/3 of follicles
- accelerates at puberty
Recognize how abnormal structure and function of the epidermis is reflected in disease.
Recognized.
describe skin lesions using proper terminology, and approach to the skin exam.
see handout from small groups
Approach to skin exam:
- sytemic approach (pattern recognition)
- adequate lighting
- Universal precautions
- good hand washing/gloves when appropriate
- ensuring that patient is comfortable with amount of skin being exposed at a time
Examine entire skin surface:
- pt in gown
- looking for: lesions that may accompany presenting complaint, unrelated but important incidental findings
- don’t forget scalp, mouth, eyes, nails
morphology: flat, raised, rased scaly, fluid filled, redness, purpura, thinning or loss, gangrene, eschar
macule: flat area of color change less than 1 cm
patch: flat area of color change, greater than 1 cm
papule: discrete, solid, elevated body 1cm, broader than thick. surface change.
nodule: firm, well defined. dermal or subq. >1cm
scale: secondary feature to classify papules/plaques. scale/crust
crust: dried blood serum, purulent exudate forms on skin surface. thick or thin, dried fluid.
vesicle: fluid filled cavity/elevation. form just bleow epidermis 1cm
pustule: circumscribed elevation that has puss.
Identify common causes of irritant and allergic contact dermatitis.
Irritant Contact Dermatitis:
- not immunologically mediated, results from direct cytotoxic effect.
- single or repeated exposure
- most common type of contact dermatitis
- can be done by strong irritants (damage skin, have labels) or weak irritants (“harmless” on own, but frequent contact may damage)
- may burn more than itch
- soap and water, skin products, perfumes, wool, raw foods, body secretions, friction
Allergic Contact Dermatitis:
- requires exposure to allergen, immune response, development memory T cells
- type 4 delayed type hypersensitivity reaction 24-48 hrs after exposure, but can be longer
- patch testing
- nickel sulfate (most frequent allergen), fragrance, neomycin sulfate, bacitracin
List common clinical associations and clinical presentation of atopic dermatitis.
Atopic Dermatitis
- skin disease that may begin at any age, most common before age 5
- 7-17.2% prevalence in children
- associated with xerosis (dry skin), atopy (asthma, allergic rhinitis)
- stages of infantile, child, adult
- must have itchy skin + 3 or more of: (history of involvement of skin creases, personal history of asthma/hay fever, history of dry skin in last year, flexural eczema, onset of under 2 years of age)
- pathogenesis: barrier disrupted skin, filaggrin mutation, strep as super antigen, elevated IgE, eosinophilia, TH2 type cytokine immune response
Recognize the clinical presentations and different patterns of psoriasis.
- affects 2% of population
- positive FH in 36% of psoriasis patients
- impacts life quality
Subtypes:
- chronic plaque disease
- guttate: red, drop-like lesions on skin
- erythroderma: an inflammatory skin disease with erythema and scaling that affects nearly the entire cutaneous surface
- pustular psoriasis
- psoriatic arthritis occurs in 5-20% of patients
Comorbidities:
- Arthritis
- Crohns
- persistent low grade inflammation favors insulin resistance, obesity, metabolic syndrome (have accelerated atherosclerosis due to inflammation)
- cardiovascular disease: if in 40’s have 2x’s higher risk of heart attack.
- mild psoriasis raises risk by 20% for people in 40’s
Compare and contrast the clinical presentations of atopic dermatitis and psoriasis.
Atopic Dermatitis:
- common, majority before age 5
- 7-17.2% in children prevalence
- associated with xerosis, history of atopy (asthma/rhinitis)
- 3 stages: infantile, childhood, adults
- must have itch skin + (itch first then rash. often involves eyelids with adults involves dry skin. hyperlinearity of the palm)
- barrier disrupted skin, filaggrin mutations
- staph acts as super antigen
- elevated IgE
- eosinophilia
- TH2 type cytokine immune response
Psoriasis:
- affects up to 2% of the population
- positive FH in 36% of psoriasis patients, impacts quality of life
- Clinical subtypes: chronic plaque disease, guttate, erythroderma, pustular psoriasis, psoriatic arthritis
- comorbidities: arthritis, chrohns, inflammation=insulin resistance, obesity and metabolic syndrome, cardiovascular disease
- trat locally or widespread + psoriatic arthritis
Recognize the common clinical location of seborrheic dermatitis and stasis dermatitis. Identify the causes of seborrheic dermatitis and stasis dermatitis.
seborrheic dermatitis:
- clinical presentations: demarcate patches (thin plaques) with pink/orange-yellow erythema
- characterized by “greasy scales”
- infancy and post puberty when sebaceous glands active
- adults: scalp, diffuse and fine, facial involvement=symmetric (eyebrows, nasolabial folds, ears), chronic, extensive in HIV and parkinsons
- infants: cradle cap, 1 week after birth, can be thick scale, inguinal folds/axillae
- pathogenesis: yeast (normal flora), may be linked to imbalance, immune response possibly to M. furfur
- treat in infants with bathing, ketocanozole cream, hydrocortisone cream. treat in adults with OTC shampoo, ketoconazole shampoo/cream, steroids (topical), calcineurin inhibitors.
Stasis dermatitis:
- pathogenesis: chronic venous insufficiency of lower extremities due to lower extremity edema
- complicating factors: dryness, itching, allergic contact, 58-86% of pts. with leg ulcers, irritant dermatitis due to wound exudates
- treat: compression, elevation, exercise, vascular surgery, topical steroids, avoiding allergens
- located: epidermis and dermis
- morphology: erythematous papules and thin plaques with scale
Compare and contrast the clinical presentations of cellulitis and stasis dermatitis.
Dermatitis
- morphology: erythematous papules and thin plaques with scale
- location of inflammation: epidermis and dermis
Cellulitis
- morphology: warm, tender, erythematous patches or plaques
- location of inflammation: dermis and subQ tissue
Recognize the similarity of drug eruptions and viral exanthems.
- Drug eruptions differential diagnosis = viral exanthem
- EBV, Enterovirus, Adenovirus, Early HIV, Parvovirus B19, CMV
- Viral infections enhance risk of drug eruption: almost 100% of patients with mono will get an exanthematous eruption if give ampicillin.
- HIV patients are susceptible to drug eruptions
Treatment
- discontinue medication
- eruption should resolve after 1-2 weeks, supportive therapy for pruritus with topical steroids/antihistamines
- may take 3 months to resolve completely
Acknowledge the difference between immediate type hypersensitivity reactions and
delayed type hypersensitivity reactions in the skin (urticaria vs. ACD)
Immediate Hypersensitivity (Urticaria):
- shows dermal edema with eosinophils +/- neutrophils
- treat with antihistamines
- hives/wheals, each lesion lasts 6 weeks
Delayed Hypersensitivity (ACD):
- type 4 delayed type hypersensitivity rxn
- requires contact exposure to allergen, immune response, development memory T cells
- delayed 24-48 hours or longer
Describe the physiology, histology and function of and be able to recognize the structural components
of the dermis.
- dermis is tough, elastic support structure below epidermis and above subQ tissue
- has BV, nerves, cutaneous appendages (hair, sweat glands/ducts, etc. adnexal structures: hair follicles, sebaceous glands, sweat glands)
- 1-4mm thick (dermis)
- epidermis is thickness of paper, has no blood vessels, depends on DERMIS for nutritional support
- 2 zones of dermis: papillary (beneath the epidermis), reticular (deeper tissue)
- dermal matrix is collagen + elastic fibers + ground substance
Structural Components:
- layers of epidermis, dermis, fatty tissue
- has interlocking dermoepidermal junction
- downward projections of epidermis are epidermal rate, they interdigitate with dermal papillae (interlock=strength, increases SA. fingerprints on hands)
- dermis made mostly of collagen/elastic fibers, ground substance
Describe the synthesis of and distinguish between the types of collagen relevant to the skin
- collagen provides all tensile strength of skin, body makes many different types.
- protocollagen is made intracellularly in fibroblasts. has 3 chains in alpha-helix at 68 nm intervals. forms Gly-X-Y structure (X=proline, Y=hydroxyproline)
- synthesized collagen proteins are secreted, assembled into collagen extracellularly
Collagen 1:
->85% of the dermis, major part of bone
Collagen 3:
-fetal dermis
Collagen 4:
-found in basement membrane in dermoepidermal junction. prominent around vessels and explains vascular fragility in ED syndrome
Collagen 7:
-anchors fibrils used by body to attach dermis to epidermis
- collagen=resiliency.
- elastic fibers are much smaller than collagen
- collagen=large eosinophilic (pink) bundles and elastic are argyrophilic (silver loving, stain well with Verhoff-Van Gieson stain)
- solar elastosis: acquired disorder of sun exposure. degeneration of elastic fibers. collagen bundles become dystrophic and clump.
- IMPORTANT CLUE UNDER THE MICROSCOPE and informs age of person.
- inherited forms of elastic disorder: PXE (pseudoxanthoma elasticum). caused by mutation in gene for multi drug resistance complex. elastic fibers become enlarged, tangled, calcified, purple-blue on histology, plucked chicken appearance of skin.
List the components and describe the function of the ground substance of the dermis.
- ground substance is a gelatinous material intercalated btw. collagen bundles, elastic fibers, appendage structures of dermis
- made of glycosaminoglycans: hyaluronic acid, dreamt sulfate
- capable of absorbing >10,000x’s their weight in H2O
- “pie filling” made of long chains of sugar molecules.
- this + fibronectins = gel-like mass that functions as a sponge
- helps nourish the epidermis by allowing for water based environment for diffusion
- renewed by fibroblasts
- Restylane
Describe the pathophysiology of and identify disorders associated with defects in collagen and elastin.
Scurvy:
- lack of vitamin C means collagen doesn’t hold desired strength
- acquired abnormality of collagen production
- minor wounds don’t heal, hair grows abnormally, blood vessels are fragile, teeth fall out
EDS (ehlers-danlos syndrome):
- 4 major clinical features: skin hyper extensibility, joint hyper mobility, tissue fragility, poor wound healing
- due to abnormally formed collagen. example of disordered collagen production due to genetic defects
Describe the pathophysiology and recognize the clinical manifestations associated with disorders of
the vascular supply and innervation of the skin.
vascularity: epidermis, subcutaneous, capillaries
sudden removal of epidermal scale
verruca
leukocytoclastic vasculitis
Nerves
Vascular!
- epidermis=no blood supply, gets nutrients from diffusion from ground substance
- has superficial and deep vascular plexi
- cutaneous vascular system important for wound healing, control of homeostasis, modulation of inflammation/leukocyte trafficking.
- capillary structures of skin are in the uppermost papillary dermis (suprapapillary plate)
- sudden removal of epidermal scale (Auspitz sign) causes trauma to capillaries of the suprapapillary plate, results in pinpoint bleeding. doesn’t violate rule of no BV in epidermis
- verruca: benign, virally induced neoplasms (growths) that require increased blood supply. appear as brownish, thromboses capillary structures in center of verruca
- leukocytoclastic vasculitis: some type of insult results in formation of immune complexes. most common cause=strep but can come from allergies, cryoglobulin production, etc.
- due to the precipitation of immune complexes in the walls of vessels (type 3 gell and coombs reaction pattern)
- presents as palpable purport due to neutrophils attaching to vessel walls and degranulating. damages RBC, promotes fibrinoid deposits.
Nerves!
- nervous tissue of the dermis informs and protects
- know: pacinian corpuscle, meissners corpuscle, free nerve endings
- Free nerve endings: pass through upper dermis and end at dermoepidermal junction. Pain and itch (pruritus-originates info free nerve endings near the junction, C fibers, slow, different sensory modality than pain)
- Pacinian corpuscles: structures with “onion” cross section. involved in pressure/vibration sensation. most concentrated in genital area
- meissner’s corpuscles: “pine cone”. involved fine touch, tactile discrimination. concentrated in digital aspects of digits, esp. finger pulp.
Describe the physiology, histology and function and be able to identify the major adnexal structures of the skin.
-include hair follicles, eccrine glands, apocrine glands, apoeccrine glands, sebaceous glands
Hair follicles: terminal hair (large, thick, coarse, pigmented. pubic, head, beard. start deep) and vellus hairs (small, fine, apigmented, diffusely located). Has an arrestor pili muscle, sebaceous gland, and is made up of the infundibulum, isthmus, martial area.
- primitive ectodermal germ (PEG): due to embryonic induction (of underlying mesenchyme). has 3 bulges; lower, middle, upper (become arrestor pili, sebaceous, and apocrine gland)
- androgenic alopecia: hairs become miniaturized, finer, lie higher in the dermis. 50% of both sexes are affected to some degree. causes ‘pattern baldness’. conversion of testosterone to 5-dihydrotestosterone is what is affected, treated with minoxidil (5 alpha reductase inhibitor)
Describe the pathophysiology and identify disease processes that occur with dysfunction or deficiency of proteins and structural components of the dermis.
Sebaceous Glands
Eccrine Glands
Apocrine Glands
Apoeccrine Glands
Sebaceous Glands:
- oil-secreting glands located in “oily” parts of the body, classic holocrine glands. keep the hairs in good shape.
- sex hormones are required for sebum secretion.
- ACNE is a disorder of the pilosebaceous unit, is multifactorial. the ostia of the pilosebaceous unit is plugged by debris, which leads to oil accumulation.
- blocked pores are comedones, and are open (blackheads) or closed (whiteheads)
Eccrine Glands:
- referred to as sweat glands. function as thermoregulatory
- 3 components: coiled secretory portion (deep), intradermal duct (coiled an straight), intraepidermal portion (acrosyringium)
- even though sweating is mediated by sympathetic portion of the autonomic nervous system, triggered via acetylcholine secretion. can be triggered by stress, drugs can increase ACH secretion and cause sweating.
- atropine poisoning can occur-results in warm, flushed, anhidrotic patient
Apocrine Glands:
- outgrowths of the upper bulge of primitive ectodermal germ (fetal structure)
- remain small, nonfunctional till after puberty. become functional
- have coiled portion deep in the dermis, straight duct, empties into follicle.
- secretion is mostly is done via decapitation where apical portion of the secretory cell cytoplasm. odorless initially, then gets odor from bacteria.
- disorder is Chromohidrosis: apocrine only in origin. mostly on face, axillae, breast, genitals. lipofuscin pigment is responsible for colored sweat.
Apoeccrine Glands:
- hybrid sweat glands that are found in the axilla.
- play role in axillary hyperhidrosis. small diameter like eccrine gland, and larger diameter portion of apocrine gland
- respond to cholinergic stimuli. secrete nearly 10x’s as much sweat as eccrine glands.
- hyperhidrosis is a focal excessive sweating. can be eccrine (clammy hands, sweaty feet, apoeccrine glands). most don’t sweat in sleep-so autonomic dysfunction.
- to determine if someone sweating to the extent of interfering with life=test via an iodine solution application, then sprinkle starch on it and if a purple-black sediment forms, ducts are identified.
- botox blocks
Describe underlying pathology based on skin findings.
- internal imbalance is in: immune status, nutritional status, metabolic state, organ health, previous insults
- skin offers clues on : immune status, nutritional, metabolic state, organ health, previous insults
- look for details as part of standard exam
- caused by: endogenous pigment, exogenous pigment, metabolic, nutritional, genetic, structural, abnormal signal, infiltration, photo related, autoimmune, allergic
- infection, tumors (on, in, inside body with secondary reaction), parasites. Tick borne diseases (rash, fever, headache). chemicals (external/internal)
Describe skin findings of systemic disease based by organ system and major categories. neurologic endocrine cardiovascular pulmonary hepatic gastrointestinal renal rheum hematology other
Neurologic:
- seborrheic dermatitis: severe form common dandruff. seen parkinson, HIV, cerebral palsy
- neurofibromas: skin pink/tan/brown. compressible papillose. Neurofibromatosis
- angiofibromas in tuberous sclerosis
Endocrine:
- diabetes has acanthosis nigricans
- hyperthyroidism: smooth, warm, moist skin
- hypothyroidism: dry skin, brittle nails, sparse hair, delayed healing
- addisons: increased pigmentation diffusely on skin, palmar creases
- cushings: round face, moon face, buffalo hump, fat in arms, thin skin
Cardiovascular:
- ehler’s danlos: at risk for aortic and valve disease
- endocarditis: splinter hemorrhages, purpura, nail fold lesions
- PHACES syndrome: large facial hemangioma and neck. coarctation of the aorta, atrial and septal defects and abnormal spinal arteries
- marfans: dilation/dissection of aorta
Pulmonary:
- sarcoidosis: hyperpigmented plaques, erosive/ulcerated plaques, granulomatous reactions, hilar lymphadenopathy, renal stones, hepatosplenomegaly
- scleroderma: thickened skin over fingers/hands, skin tightens around mouth, Raynauds. pulmonary hypertension
- tuberculosis: scrufuloderma on neck, lupus vulgaris, cutaneous TB lesions
Hepatic:
- viral hep B and C: lichen planus, vasculitis, cryglubulinemia, pruritus
- porphyria cutanea tarda: blistering lesions on hands with sun exposure, hypertrichosis, atrophic scars, deficiency of uroprhyrinogen and decarboxylase
Gastrointestinal:
- genetic diseases: gardener’s syndrome, muir torre syndrome, peutz jagers
- pyoderma gangrenosum: punched out ulcers that enlarge, IBS associated, NEVER DEBRIDE, can have internal organ lesions
- deficiencies: vitamin A, K, B1, B3, B6, B12, C, Zinc, Iron, Marasmus, Kwashiorkor
- excesses: carotenemia, argyria,
- dermatitis hepetiformis: gluten sensitivity, pruritic pinpoint vesicles on elbows, knees, sarum.
Renal:
- metastatic renal cancer metastasizes to skin, seen as bright red, vascular, enlarging regions
- henoch-schonelin purpura
Rheumatology:
-systemic lupus erythematousus
the 4 that can be diagnosed of the MDSOAPBRAIN are M-malar rash, D-discoid rash, O-oral ulcers, P-photosensitivity
-neonatal lupus: heart block 50% even if asymptomatic
-scleroderma
-deratomyositis: purple, heliotrope rash on eyelids, shawl sign, erythema/dryness/fissuring on palms, cuticle changes, associated with pulmonary fibrosis and genitourinary cancer
Hematology/oncology:
-paraneoplastic skin conditions: nicgricans with tripe palms, cutaneous lymphoma, metastasis to skin common
Other skin signs:
-hair loss, hair abnormalities, ear crease, eye findings, teeth, accessory triages, accessory digit, accessory nipple, skin/texture change, nails
Categorize skin findings as clues to systemic disorders.
Red: infection, inflammation, exogenous pigment. important if unstable vitals, fluids, etc, –>admit
Yellow: don’t miss scleral citrus, could be Gilberts, or exogenous pigment like caroternemia
Blue/grey: circulation, pigment, chemo side effect, cold, deposition disease (argyria)
Sallow: renal disease
Pale: anemia
Flushed: plethoric, habitus, exertion, etc.
Brown: chemo reaction, addison’s, medication side effect
Geometric: likely not internal cause
Location/distribution: patterns tell a story!
Photodistributed: rheumatologic, genetic, medication related
Auto-immune and allergic, endogenous pigment, exogenous pigment, metabolic, nutritional, genetic (structural, abnormal signal), infiltration, photo-related
Diagnose common benign skin tumors in infants and adults.
Describe clinical features of these benign skin tumors.
Vascular Tumors
Vascular tumors:
-cherry hemangioma: primarily on the trunk, a few to hundreds, primary lesion, 1-4mm in size, red and smooth topped. Can be removed with superficial electrodesiccation (if small), may need local anesthesia. Can use Pulse Dye Laser for small lesions
-infantile hemangioma: strawberry hemangioma are benign. stain with Glut-1 a placental antigen. more common in girl, preemies, if mother has chorionic villus sampling. appear by 2 months of age, grow and involute at 10%/year. 50% resolve by 5, 90% resolve by 9. can cause problems based on location (visual field), can distort tissue, can ulcerate, location can let you know if there is internal involvement (airway can compromise air). Moist areas can be tricky-indicate treatment. More than 5 is associated with visceral ones.
Congenital syndromes (PHACES). treatment options: local care, laser, intralesional or systemic steroids, beta blockers.
