Skin Patho Day 2 Flashcards
Telogen effluvium
Stress=more hair in telogen phase than normal and shed
Alopecia areata
Autoimmune condition; lose patches of hair –patchy hair –nail pits –treat for topical corticosteroids
Anagen effluvium
Losing hair from meds (chemotherapy); regrows when meds are stopped
Acne Vulgaris
Caused by onset of puberty –more sebum, more keratin in hair follicles causes comedone (plugging) and P. acnes causes inflammation response
Propionibacterium Acnes
Anaerobic gram + bacteria that lives in hair follices and causes acne Uses glycerol by hydrolyzing sebum Releases proinfalmmatory mediators, porphyrins, lipases
What is normal treatment for acne?
RETINOIDS: regulate hyperproliferation of keratinocytes, anti inflammatory BENZOYL PEROXIDE: oxidizes and kills P. acnes, decreases inflammation; chemolytic effect against sebum ANTIBIOTICS: clindamycin, erythromycin
What is systemic treatment for acne?
ANTIBIOTICS: tetracyclines, erythromycin, bactrim, penicillins –doxycycline=pill esophagitis, photosensitivity –minocycline=drug hypersensitivity sx, lupus, hepatitis ORAL CONTRACEPTIVES: block androgen production by decreasing free testosterone; good for all acne but causes nausea, vomitting, abnormal menses, weight gain, breast tenderness, thrombophlebitis, HTN ISOTRETINOIN: for severe nodular acne; 1 mg/kg/day BID x 5 mo
Tinea Versicolor
Due to malassezia spp (fungi) –truncal oval/round scaly patches –can be hyper or hypopigmented
Acne rosacea
Vascular hyperactivity –easy blushing, reddened face –overgrowth sebaceous glands=bumpty skin, papules, pustules
Tuberous Sclerosis
Autosomal dominant genetic disorder (TSC1 or TSC2); majority mutations denovo
- 3 or more hypopigmented macules (ash leaf)
- angiofibromas/fibrous plaque
- Shagreen patch
- Periungual fibromas
- H – hamaratomas in CNS and skin
- A – angiofibromas
- M – mitral regurgitation
- A – ash leaf spots
- R – cardiac Rhabdomyomas
- O – autosomal dOminant
- M – mental retardation
- A – renal Angiomyolipoma
- S – seizures, shagreen patches
Vitiligo
T cell autoimmune disease–> destruction melanocytes –> depigmentation
- acquired
- hair sometimes affected (poliosis)
- acral/eyes/knees/elbows
- Use topical corticosteroids, then UV
Oculocutaneous Albinism
Autosomal dominant/recessive–> defect in tyrosinase –> decreased melanin production
- diffuse
- eye issues (decreased acuity, nystagmus)
- increased skin cancer chance
Ephelides
Freckles, from sun exposure; marker UV damage so increase chance cancer
Cafe au lait macules
Uniform macules/patches; multiple=sign of neurofibromatosis
Neurofibromatosis 1 (NF1)
“Von Reckling Hausen’s disease”; autosomal dom. or de novo
- cafe au lait macules, axillary/inguinal freckling, soft/rubbery papules
- Plexiform neurofibromas=bag of worms
Solar lentigo
Age spots; tan/dark brown macules due to UV sun exposure
Later in life and bigger than ephelides
Dermal melanocytosis (Mongolian Spots)
Blue/grey patches over lumbosacrum spots in infants
- on butt, will eventually fade; blue color because melanocytes are too low in dermis
- If in other spots, may persist
Congenital Melanocytic Nevi
1 cm –> 20 cm, risk of transformation to melanoma/neurocutaneous melanosis
A=asymmetry
B=border irreg
C=color weird
D=diameter >6mm
E=evolution/change
Piebaldism
Autosomal dominant due to mutation KIT proto-oncogene–> impaired migration melanocytes
- depigmented patches/white forelock
- Stable compared to vitiligo; i.e. at birth present
Waardenburg Sx
Multiple gene mutations (usually PAX)–> abnormal melanocytes
- achromia (white skin or hair)
- deafness
- heterochromia irides
- dystopia canthorum
Port-Wine Stain
Dilated BV present at birth, darken and thicken (increase in VEGF or VEGFR2)
V1=opthalmic branch, to eyes
V2=maxillary branch
V3=mandibular branch and sometimes oral mucosa
Sturge Weber Sx
mosaic GNAQ gene defects
Port wine stain V1
Calcifications of cerebral cortex (tram track)–> seizures
Glaucoma
Developmental delay
Migraine headaches
Infantile Hemangioma
Proliferating endothelial like cells visible in 1 mo of life
Most common vascular tumor
Pallor around white patch at birth; grows 3-9 months and disappears
Need tx if above eye or PHACE
What does PHACE stand for?
P=posterior fossa issues
H=hemiangiomas
A=arterial anomolies
C=cardiac issues
E=eye issues
S=midline issues
*will not follow dermatomes
Hypohidrotic Ectodermal Dysplasia (HED)
X linked recessive issue with ectodysplasin signaling path (EDA-A1, EDAR, EDARADD)
- impaired ability to sweat
- square forehead, frontal bossing
- flattened nasal bridge
- low lying ears
- thin/dry hair and skin
- peg teeth
What are some general side effects of topical corticosteroids?
Hypopigmentation, hypertrichosis, skin atrophy, telangiectasia (all reversible)
Striae (irreversible)
Acne/perioral dermatitis (on face)
Glaucoma/cataract risk
*sometimes may be systemic!
What do the differnt classes of corticosteroids mean?
Class I (clobetasol propionate, halobetasol propionate, etc.) most potent
Class VII (hydrocortisone) least potent
Ointment pros and cons
- Generally more potent than cream form and is preferred
- PROS: occlusive barrier, better penetration, moisturizing
- Cons: greasy, patient non-compliance
Cream pros and cons
Pros: better patient compliance
Cons: less potent for same steroid, can sting on open skin
Lotion/solution/foam Pros and Cons
Pros: good for scalp and hair-bearing areas
Cons: stinging
Gel pros and cons
Pros: good for intraoral use
Cons: drying, stinging
What is the concept of the fingertip unit?
Fingertip unit: med from fingertip to distal interphlangeal joint (.5 g, will cover palm for BID)
Psoriasis
Immune mediated polygenic skin condition
Immune mediated
Triggered by: recent infections, HIV, familial, CV issues
Med triggers: corticosteroid withdrawal, lithium, B blockers, antimalarials, interferons
Koebner phenomenon: development of lesions at injury
Auspitz sign: pinpoint bleeding when scale removed
Psoriasis Arthritis
20%-30% pts; sausage digits, pencil in cap
Psorasis Treatment
Needed to stop inflammation loop
Localized: topical corticosteroids, retinoids, coal tar, calcineurin inhibitors, vitamin D analogs
Systemic: UV, methotrexate, cyclosporine, acitretin, TNF alpha block, IL 12/23
Types of Psoriasis
Plaque: extensor extremities; pink patches/plaques with silver scale
Inverse/flexural: axillae, grain, perineum, chest
Guttate: drop like, 2-10 mm, symmetric trunk/proximal extremities; triggered by group A strep
Pustular: pustules on palsm/soles or generalized
Erythrodermic: generalized redness/variable scaling
Lichen Planus
Idiopathic inflammatory disease of skin/hair/nails/mucous membranes
- Planar, polygonal, pruritic, pink or purple, plaques or papules
- Lower legs, ankles, wrists, genitila (Flexural m.)
- Wickham’s striae –> grayish streaks over papules
- Associations between –> Hep C, B Blockers and other drugs, Hep B vaccines
- Nail Lichen Planus –> thinning nail plates, longitudinal ridging, scarring
- Mucosal Lichen Planus –> oral, genital, esophagus and GI (reticulated=lace pattern white papules, erosive=gingiva or tongue, painful)
Treatment Lichen Planus
- Topical steroids/antihistamines
- UV and oral corticosteroids; metronidazole, griseofulvin, antimalarials, acitretin, mycophenolate mofetil, methotrexate, cyclosporin
Atopic Dermatitis
Assc. with other allergic conditions (mutations in profilaggrin gene, S. aureus and more)
Infant: facial involvement, sparing medface; oozing and crusting; extensor involvement late infancy
Childhood: flexural involvement (wrists, ankles, neck, hands), less crusting
Adults: most outgrow…if not, more chronic and severe; hands or generalized
More sx: lichenification as 2nd change; “Dennie Morgan folds” under eyes; vesicles with secondary viral infection (Herpes Simplex=eczema herpeticum)
Complications of Atopic Dermatitis (Eczema)
Infection, poor sleep, failure to thrive
Pathogenesis of Atopic Dermatitis
Skin disrupted by allergens, microbes and scratching; Th2 is activated acutely and Th1 chronically
Treatment for Atopic Dermatitis
Topicals: corticosteroids, calcineurin inhibitors, antihistamines, bleach baths (new lesions/think skin need weaker meds)
Systemic: UVB; avoid steroids (will get rebound); cyclosporine, methotrexate, mycophenolate mofetil, azathioprine
Seborrheic Dermatitis
Cradle cap; assc. with no other skin conditions
Infantile form: yellow greasy scalp, erythematous intertriginous patches; 2ndarly infected with Candida or strep; dissemination –> scaly papules, patches, plaques
Adult form: yellow red papules scaling; scalp, face (symmetric; forehead, medial eyebrows, nasolabial folds, etc), trunk (presternal; intertriginous)
Treatment Seborrheic Dermatitis
Infantile: Low potency topical steroid (desonide, hydrocrotisone)
ketoconazole, mild shampoos, gentle skin care
Adult: azole, low potency topical steroid, shampoos (zinc pyrithione, tar, selenium sulfate)
