Skin Patho Day 2

Question 1

Telogen effluvium

Answer 1

Stress=more hair in telogen phase than normal and shed

Question 2

Alopecia areata

Answer 2

Autoimmune condition; lose patches of hair –patchy hair –nail pits –treat for topical corticosteroids

Question 3

Anagen effluvium

Answer 3

Losing hair from meds (chemotherapy); regrows when meds are stopped

Question 4

Acne Vulgaris

Answer 4

Caused by onset of puberty –more sebum, more keratin in hair follicles causes comedone (plugging) and P. acnes causes inflammation response

Question 5

Propionibacterium Acnes

Answer 5

Anaerobic gram + bacteria that lives in hair follices and causes acne Uses glycerol by hydrolyzing sebum Releases proinfalmmatory mediators, porphyrins, lipases

Question 6

What is normal treatment for acne?

Answer 6

RETINOIDS: regulate hyperproliferation of keratinocytes, anti inflammatory BENZOYL PEROXIDE: oxidizes and kills P. acnes, decreases inflammation; chemolytic effect against sebum ANTIBIOTICS: clindamycin, erythromycin

Question 7

What is systemic treatment for acne?

Answer 7

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

Question 8

Tinea Versicolor

Answer 8

Due to malassezia spp (fungi) –truncal oval/round scaly patches –can be hyper or hypopigmented

Question 9

Acne rosacea

Answer 9

Vascular hyperactivity –easy blushing, reddened face –overgrowth sebaceous glands=bumpty skin, papules, pustules

Question 10

Tuberous Sclerosis

Answer 10

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

Question 11

Vitiligo

Answer 11

T cell autoimmune disease–> destruction melanocytes –> depigmentation

• acquired
• hair sometimes affected (poliosis)
• acral/eyes/knees/elbows
• Use topical corticosteroids, then UV

Question 12

Oculocutaneous Albinism

Answer 12

Autosomal dominant/recessive–> defect in tyrosinase –> decreased melanin production

• diffuse
• eye issues (decreased acuity, nystagmus)
• increased skin cancer chance

Question 13

Ephelides

Answer 13

Freckles, from sun exposure; marker UV damage so increase chance cancer

Question 14

Cafe au lait macules

Answer 14

Uniform macules/patches; multiple=sign of neurofibromatosis

Question 15

Neurofibromatosis 1 (NF1)

Answer 15

“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

Question 16

Solar lentigo

Answer 16

Age spots; tan/dark brown macules due to UV sun exposure

Later in life and bigger than ephelides

Question 17

Dermal melanocytosis (Mongolian Spots)

Answer 17

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

Question 18

Congenital Melanocytic Nevi

Answer 18

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

Question 19

Piebaldism

Answer 19

Autosomal dominant due to mutation KIT proto-oncogene–> impaired migration melanocytes

• depigmented patches/white forelock
• Stable compared to vitiligo; i.e. at birth present

Question 20

Waardenburg Sx

Answer 20

Multiple gene mutations (usually PAX)–> abnormal melanocytes

• achromia (white skin or hair)
• deafness
• heterochromia irides
• dystopia canthorum

Question 21

Port-Wine Stain

Answer 21

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

Question 22

Sturge Weber Sx

Answer 22

mosaic GNAQ gene defects

Port wine stain V1

Calcifications of cerebral cortex (tram track)–> seizures

Glaucoma

Developmental delay

Migraine headaches

Question 23

Infantile Hemangioma

Answer 23

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

Question 24

What does PHACE stand for?

Answer 24

P=posterior fossa issues

H=hemiangiomas

A=arterial anomolies

C=cardiac issues

E=eye issues

S=midline issues

*will not follow dermatomes

Question 25

Hypohidrotic Ectodermal Dysplasia (HED)

Answer 25

**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

Question 26

What are some general side effects of topical corticosteroids?

Answer 26

Hypopigmentation, hypertrichosis, skin atrophy, telangiectasia (all reversible) Striae (irreversible) Acne/perioral dermatitis (on face) Glaucoma/cataract risk \*sometimes may be systemic!

Question 27

What do the differnt classes of corticosteroids mean?

Answer 27

Class I (clobetasol propionate, halobetasol propionate, etc.) most potent Class VII (hydrocortisone) least potent

Question 28

Ointment pros and cons

Answer 28

* Generally more potent than cream form and is preferred * PROS: occlusive barrier, better penetration, moisturizing * Cons: greasy, patient non-compliance

Question 29

Cream pros and cons

Answer 29

Pros: better patient compliance Cons: less potent for same steroid, can sting on open skin

Question 30

Lotion/solution/foam Pros and Cons

Answer 30

Pros: good for scalp and hair-bearing areas Cons: stinging

Question 31

Gel pros and cons

Answer 31

Pros: good for intraoral use Cons: drying, stinging

Question 32

What is the concept of the fingertip unit?

Answer 32

Fingertip unit: med from fingertip to distal interphlangeal joint (.5 g, will cover palm for BID)

Question 33

Psoriasis

Answer 33

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

Question 34

Psoriasis Arthritis

Answer 34

20%-30% pts; sausage digits, pencil in cap

Question 35

Psorasis Treatment

Answer 35

Needed to stop inflammation loop ## Footnote **Localized:** topical corticosteroids, retinoids, coal tar, calcineurin inhibitors, vitamin D analogs **Systemic:** UV, methotrexate, cyclosporine, acitretin, TNF alpha block, IL 12/23

Question 36

Types of Psoriasis

Answer 36

**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

Question 37

Lichen Planus

Answer 37

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)

Question 38

Treatment Lichen Planus

Answer 38

1. Topical steroids/antihistamines 2. UV and oral corticosteroids; metronidazole, griseofulvin, antimalarials, acitretin, mycophenolate mofetil, methotrexate, cyclosporin

Question 39

Atopic Dermatitis

Answer 39

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)

Question 40

Complications of Atopic Dermatitis (Eczema)

Answer 40

Infection, poor sleep, failure to thrive

Question 41

Pathogenesis of Atopic Dermatitis

Answer 41

Skin disrupted by allergens, microbes and scratching; Th2 is activated acutely and Th1 chronically

Question 42

Treatment for Atopic Dermatitis

Answer 42

**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

Question 43

Seborrheic Dermatitis

Answer 43

**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)

Question 44

Treatment Seborrheic Dermatitis

Answer 44

**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)