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FPP-MSS > Skin Patho Day 2 > Flashcards

Skin Patho Day 2 Flashcards

1
Q

Telogen effluvium

A

Stress=more hair in telogen phase than normal and shed

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2
Q

Alopecia areata

A

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

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3
Q

Anagen effluvium

A

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

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4
Q

Acne Vulgaris

A

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

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5
Q

Propionibacterium Acnes

A

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

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6
Q

What is normal treatment for acne?

A

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

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7
Q

What is systemic treatment for acne?

A

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

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8
Q

Tinea Versicolor

A

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

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9
Q

Acne rosacea

A

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

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10
Q

Tuberous Sclerosis

A

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
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11
Q

Vitiligo

A

T cell autoimmune disease–> destruction melanocytes –> depigmentation

  • acquired
  • hair sometimes affected (poliosis)
  • acral/eyes/knees/elbows
  • Use topical corticosteroids, then UV
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12
Q

Oculocutaneous Albinism

A

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

  • diffuse
  • eye issues (decreased acuity, nystagmus)
  • increased skin cancer chance
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13
Q

Ephelides

A

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

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14
Q

Cafe au lait macules

A

Uniform macules/patches; multiple=sign of neurofibromatosis

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15
Q

Neurofibromatosis 1 (NF1)

A

“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
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16
Q

Solar lentigo

A

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

Later in life and bigger than ephelides

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17
Q

Dermal melanocytosis (Mongolian Spots)

A

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
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18
Q

Congenital Melanocytic Nevi

A

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

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19
Q

Piebaldism

A

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

  • depigmented patches/white forelock
  • Stable compared to vitiligo; i.e. at birth present
20
Q

Waardenburg Sx

A

Multiple gene mutations (usually PAX)–> abnormal melanocytes

  • achromia (white skin or hair)
  • deafness
  • heterochromia irides
  • dystopia canthorum
21
Q

Port-Wine Stain

A

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

22
Q

Sturge Weber Sx

A

mosaic GNAQ gene defects

Port wine stain V1

Calcifications of cerebral cortex (tram track)–> seizures

Glaucoma

Developmental delay

Migraine headaches

23
Q

Infantile Hemangioma

A

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

24
Q

What does PHACE stand for?

A

P=posterior fossa issues

H=hemiangiomas

A=arterial anomolies

C=cardiac issues

E=eye issues

S=midline issues

*will not follow dermatomes

25
Q

Hypohidrotic Ectodermal Dysplasia (HED)

A

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
26
Q

What are some general side effects of topical corticosteroids?

A

Hypopigmentation, hypertrichosis, skin atrophy, telangiectasia (all reversible)

Striae (irreversible)

Acne/perioral dermatitis (on face)

Glaucoma/cataract risk

*sometimes may be systemic!

27
Q

What do the differnt classes of corticosteroids mean?

A

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

Class VII (hydrocortisone) least potent

28
Q

Ointment pros and cons

A
  • Generally more potent than cream form and is preferred
  • PROS: occlusive barrier, better penetration, moisturizing
  • Cons: greasy, patient non-compliance
29
Q

Cream pros and cons

A

Pros: better patient compliance

Cons: less potent for same steroid, can sting on open skin

30
Q

Lotion/solution/foam Pros and Cons

A

Pros: good for scalp and hair-bearing areas

Cons: stinging

31
Q

Gel pros and cons

A

Pros: good for intraoral use

Cons: drying, stinging

32
Q

What is the concept of the fingertip unit?

A

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

33
Q

Psoriasis

A

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

34
Q

Psoriasis Arthritis

A

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

35
Q

Psorasis Treatment

A

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

36
Q

Types of Psoriasis

A

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

37
Q

Lichen Planus

A

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)
38
Q

Treatment Lichen Planus

A
  1. Topical steroids/antihistamines
  2. UV and oral corticosteroids; metronidazole, griseofulvin, antimalarials, acitretin, mycophenolate mofetil, methotrexate, cyclosporin
39
Q

Atopic Dermatitis

A

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)

40
Q

Complications of Atopic Dermatitis (Eczema)

A

Infection, poor sleep, failure to thrive

41
Q

Pathogenesis of Atopic Dermatitis

A

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

42
Q

Treatment for Atopic Dermatitis

A

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

43
Q

Seborrheic Dermatitis

A

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)

44
Q

Treatment Seborrheic Dermatitis

A

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)

45
Q
A

FPP-MSS (6 decks)

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