Med IV Exam 3 - Derm 1

the shedding of dead skin cells from the outer layer of skin = skin peeling

desquamation

desquamation follows what skin rxn

first degree sunburn

this sx is a sign of systemic disease like SJS/TEN, TSS, scarlet fever, etc

desquamation

acute inflammatory skin dz. varies from mild self limiting rash to life threatening form. can be major or minor type based on findings. SJS/TEN used to be considered apart of this dz

erythema multiforme (EM)

this dz is caused by infxous dz, vaccines, and meds. assoc with HSV, mycoplasma pneumoniae, less commonly HBV, EBV, covid 19.

erythema multiforme

90% of minor EM cases are caused by

HSV, called herpes assoc erythema multiforme

pt has target lesions with three concentric zones of color change = red rim, clearance zone, and central blister or erosion. mostly seen on acral surfaces (hands feet elbows knees). recurrence is not uncommon if caused by HSV.

EM

how to definitively dx EM

skin bx

how to tx EM

self limiting, tx sx with PO and topical steroids (prednisone, triamcinolone), suppression therapy with antivirals like acyclovir, valacyclovir if recurrent dz from HSV

severe life threatening skin rxn. sx begin with fever and flu like sx and become atypical targeted lesions = painful necrosis, blistering, and detachment of epidermis. there needs to be 2+ mucous membranes involved. complications = dehydration, sepsis, PNA, multi organ failure

SJS and TEN

what % of the body surface is affected in SJS

<10% BSA

what % of the body surface is affected by TEN

>30% BSA

at what % of the body surface is affected when SJS and TEN overlap

10-30% BSA

SJS and TEN is mostly aused by

oral or rarely topical meds, like sulfonamides (bactrim), NSAIDs, allopurinol, anticonvulsants (carba, phenobarbital, phenytoin, VPA, lamotrigine). meds are #1 cause, and infxn is #2

pt has raised purpuric target like lesions with only 1-2 zones of color change. they have pain on eating, swallowing, and urinating depending on mucus membrane involved.

SJS and TEN

tracheobronchial mucosa, conjunctiva, genital, and urethral mucosa involvement in SJS & TEN result in

scarring and stricture formation

how to tx SJS and TEN before meds

in acute care environment (ICU/burn unit). admit if mucosal involvement interferes with hydration and nutrition, or if inc blistering. manage open lesions like second degree burns. if you stop the medication before blistering occurs then your outcome of dz will be better. delaying dx results inc morbidity and mortality

how to tx SJS and TEN with meds n stuff

nutritional and fluid support. can give

• hi dose systemic steroids before blistering

• IVIG to dec mortality

  • cyclosporine (also used to tx organ rejection post txp)

• etanercept

how to differentiate b/w EM SJS and TEN

SJS affects <10% BSA, extensive oral and genital mucosal involvement. drug exposure common in SJS NOT EM. Nikolsky sign in SKS/TEN

what is Nikolsky sign

skin sloughing when touching skin. seen in SJS/TEN

how long does EM usually last

2-6 wk. can recur

prognosis of SJS/TEN

mortality rate of 30% in cases with >30% BSA

what do we use to predict mortality in SKS/TEN

ABCD-10 and SCORTEN severity of illness scales

exotoxin mediated illness caused by bacterial infxn from GAS, MSSA, or MRSA. sudden and toxicity occurs early = life threatening illness and multi organ failure

TSS

this dz is classically assoc with tampon use, but any foci harboring toxin producing staph aureus can cause it. can be in nasopharynx, bone, vag, rectum, abscess, or wound. strep infxns can also cause it like necrotizing fasciitis, thru pyrogenic erythrotoxin hat stims massive release of cytokines that mediate shock. mortality rates inc now (staph 15%, strep 80%)

TSS

pt has high fever, vomiting, watery diarrhea. sore throat and myalgias. diffuse macular erythematous rash with non purulent conjunctivitis, causing desquamation of palms and soles.

staph TSS

invasion of skin/soft tissue, ARDS, AKI. skin rash and desquamation may not be present.

strep TSS

how to dx TSS

staph blood cx can be (-) bc sx are from toxin, not invasive organism. strep has a 60% (+) blood cx. leukocytosis seen

how to tx staph TSS

remove sources of toxin. rapid dehydration, antistaphylococcal abx like penicillinase resistant PCNs (diclox) if MSSA. clinda added to inhibit toxin production

how to tx strep TSS

beta lactams like PCN G + clinda. IVIG

hair loss that affects any part of the body. alopecia areata, androgenic alopecia. determine follicular marking (scarring = no follicle vs non scarring = intact follicle forms)

alopecia

hair loss where follicles are permanently destroyed by inflammation = scar tissue formation and irreversible hair loss.

scarring alopecia

hair loss without follicle destruction = hair can potentially regrow if underlying cause is addressed

non scarring alopecia

m/c form of alopecia. genetically determined with men and women affected (m/c in 3rd decade of life). early signs are changes in widows peak and crown of head. extend of loss is unpredictable

androgenic non scarring alopecia

how to tx androgenic non scarring alopecia in men

minoxidil - for men with recent onst <5 yrs w small areas of hair loss. 40% of pts tx bid for a yr will have mod to dense hair growth. finasteride can be added

how to tx androgenic non scarring alopecia in women

topical minoxidil, finasteride (if not of childbearing potential). spironolactone used in premenopausal women, low dose oral minoxidil also safe. platelet rich plasma also used. women who see their hair thinning but have no sx of alopecia should f/u bc >50% hair loss can be lost before clinician notices

patten of female hair loss

retention of anterior hairline with diffuse thinning of vertex scalp and widening of part

transitory inc in telogen (resting) phase of hair growth cycle. latent period of 4 mo with good prognosis

telogen effluvium, a non scarring hair loss

how do pts get telogen effluvium

occurs spontaneously, after pregnancy, or precipitated by an iron def.

pt has excessive shedding of hair without scalp itching or scaling. pts lose >150 hairs/day (nl 70-100).

telogen effluvium

how to dx telogen effluvium

presence of large number of hairs with white bulbs coming out when tugging hair. if iron def is suspected then order iron panel

this dz has an unknown cause and might be an immunologic process. hairless patches are perfectly smooth without scarring. tiny hairs called exclamation hairs are seen. can involve beard, eyebrows, and eyelashes

alopecia areata

alopecia areata is what type of alopecia

non scarring

alopecia of the full scalp

alopecia totalis

alopecia of scalp and body hair

alopecia universalis

alopecia areata is assoc with what autoimmune d/o

hashimotos, addisonsvitiligo, SLE

how to tx alopecia areata

self limiting. intralesional CCS first line tx (triamcinolone), tx with systemic steroids or JAK inhibitors (baricitinib, ritlectinib) but relapse occurs after d/c

condition where pt repeatedly pulls out hair. type of impulse control disorder. patches of hair loss are irregular with short growing hairs always present bc they can’t be pulled out. u/l on ipsilateral side as dominant hand.

trichotillomania

how to maybe tx trichotillomania

NAC

how can scarring alopecia occur

chemical or physical trauma, bacterial or fungal infxn, severe herpes zoster, chronic discoid lupus erythematous, systemic sclerosis, excessive ionizing radiation.

how to tx scarring alopecia

biopsy of active border. dx and tx as early as possible bc irreversible

acquired pigmentary disorder of sun exposed areas. muddy brown macule on the skin, mostly in malar and central facial areas. occurs from inc in melanocyte activity and melanin deposition in skin. sunlight and hormonal influence are common causes. aka mask of pregnancy

melasma

what skin types are at an inc risk of getting melasma

skin types III and greater (medium white skin-black skin) from african, asian, or hispanic descent

how to tx melasma

lightening agents like hydroquinone and tretinoin first line alone or + steroid to dec irritation. chemical peels with glycolic acid second line, laser/light therapy. if preg = topical azelaic acid + UV protection and stopping makeup.

acquired loss of pigmentation involving the face, body folds, and back of hands. fhx sometimes a factor, dz is limited at first, then progresses over years. occurs secondary to absence of epidermal melanocytes = T cell destruction of melanocytes. half of cases occur in pts <20 yrs old

vitiligo

how to dx vitiligo

wood lamp good for white ppl.

how to tx segmented/limited vitiligo

high potency topical steroids (clobetasol, mometasone) first line. or calcineurin inhibitor (tacrolimus)

how to tx widespread vitiligo

narrow band UV B phototherapy

new tx of non segmental vitiligo

ruxolitinib. expensive so not used that much

2 rare autoimmune blistering disorders that aren’t contagious.

pemphigus and pemphigoid

shallow ulcers or fragile blisters that break open quickly.

pemphigus

stronger “tense” blisters that don’t easily open, may have hot, red, itchy hives

pemphigoid

uncommon intraepithelial blistering disease on skin and MM. caused by autoantibodies to adhesion molecules in the skin and MM. bullae appear spontaneously and are tender and painful when ruptured. mostly happens in middle age. can have other forms, where vulgaris begins in mouth in half of cases

pemphigus

insidious onset of thin walled flaccid bullae, crusts, and erosions in crops or waves

pemphigus

this pemphigus lesions first show on oral MMs and scalp

pemphigus vulgaris

what signs are positive in pemphigus

Nikolsky sign, asboe hansen sign

asboe hansen sign

downward pressure on fresh bulla may cause lateral spread

how to dx pemphigus

skin bx shows acantholysis (separation of epidermal cells). light microscopy, direct and indirect immunofluorescence microscopy, and ELISA testing = autoantibodies to intracellular adhesion molecules.

ddx for pemphigus

EM, SJS/TEN, drug eruptions, bullous impetigo, contact dermatitis. **flaccid bullae NOT seen in any of these

how to tx pemphigus

systemic therapy w prednisone ± steroid sparing agent (rituximab, azathioprine, mycophenolate motefil). steroid sparing takes weeks to kick in. secondary infxns occur and are major cause of morbidity and mortality = if no tx then fatal in 5 years

benign pruritic disease characterized by “tense” blisters in flexural areas. goes away in 5-6 yrs, characterized by exacerbations and remissions. in men >60 m/c. before blisters show pt has pruritic urticarial lesions for months. can be induced by meds like furosemide

bullous pemphigoid

how to dx pemphigoid

bx w direct immunofluorescence and ab testing.

how to tx mild dz pemphigoid

ultra potent steroids (fluocinonide)

how to tx widespread dz pemphigoid

systemic steroids (prednisone)

how to tx mild to mod pemphigoid in pt that can’t tolerate steroids

doxy ± nicotinamide

how to tx pemphigoid if mucous membranes are affected

dapsone

how to tx refractory pemphigoid

immunomodulators, rituximab, MTX

small bright red to purple, dome shaped skin lesions that are 0.5-6mm in diameter. several usually present, typically chest and arms with inc number with age. occurs in almost all adults >30 yrs.

cherry angioma/cherry hemangioma/campbell de morgan spots

how to dx cherry angioma

based on appearance, dermoscopic exam shows lesions.

how to tx cherry angiomas

no need tx but if ugly looking or subject to bleeding then do pulsed dye laser or if large then shave removal with cautery.

ddx for cherry angioma

nodular BCC and amelanotic melanoma

this dz seen with extravasation fo RBC into dermis. lesions do not blanch with pressure. purpura >3 mm and petechiae <2 mm are divided into palpable or non palpable

primary cutaneous disorders cause non palpable purpura

trauma, solar (actinic, senile) purpura, steroid induced

clotting disturbances that cause non palpable purpura

thrombocytopenia, clotting factor deficits

thrombi related d/o that cause non palpable purpura

DIC, COVID 19 infxn

vasculitis issues that cause palpable purpura

henoch schonlein purpura (HSP) aka IgA vasculitis

infectious emboli d that cause palpable purpura

acute meningococcemia, disseminated gonorrhea, RMSF

this dz develops on the lower extremity secondary to venous incompetence and chronic edema. hx of varicose veins, DVT, or evidence of vein removal. early findings show mild erythema and scaling assoc with pruritis. initially seen at medial aspect of ankle over distended vein

stasis dermatitis

pts both lower ankles are acutely inflamed and has crusting and exudate. may be complicated by secondary infection and/or contact derm. precedes stasis ulcers

stasis dermatitis

how to tx stasis dermatitis

elevate legs, compression stockings, emollients + mid potency topical steroids. protect legs from injury and chronic edema to prevent ulcers. diuretics to control edema

small dilated blood vessels on surface of skin near MMs. 0.5-1 mm in diameter. seen on face, around nose, cheeks, chin. caused by genetic, venous reflux, and acquired causes.

telangectasias/spider veins

acquired causes of telangiectasia

age related, BCC, chemo, chronic topical steroid use, carcinoid syn, cushing syn, preg, hepatic cirrhosis, rosacea

this type of telangiectasia is a swollen spider like blood vessels slightly beneath skin surface, often w central red dot and deep red extensions. common and benign, in some healthy adults and young kids.

spider angioma

spider angioma is common during

preg. resolves after birth

spider angioma can be indicative of what dz

liver dz like HCV or cirrhosis

localized form of hyperpigmentation. assoc with insulin resistance or hyperinsulinemia. seen in pts with endo d/o like DM, cushings, acromegaly, PCOS, obesity

acanthosis nigricans

acanthosis nigricans results from

long term exposure of keratinocytes to insulin. they have insulin and insulin-like growth factors on surface, insulin binds there and stims proliferation

this dz commonly seen on neck or skin folds. consequence of repetitively used insulin sites. occurs abruptly with malignancy.

acanthosis nigricans

acanthosis nigricans is sometimes assoc with

malignancy, esp adenocarcinoma

how to tx acanthosis nigricans

weight loss thru diet, exercise to reverse the process by red insulin resistance and compensatory hyperinsulinemia. keratocyte agents (salicylic acid, glycolid acid) to improve cosmetic appearance. topical retinoids (adapalene), metformin and rosiglitazone