U3 medicine - dermatology pt 2

actinic keratosis

2nd most common dermatology diagnosis

firm, rough keratotic papule with erythematous base

found in sun exposed/sun damaged areas

precursors to Squamous Cell Carcinoma (SCC)

--> around 30% go on to become a SCC

leukoplakia

is an actinic keratosis on mucous membrane/sides of tongue

20-40% progress to SCC if untreated

more aggressive

causes - sun, smoking, chronic irritation

actinic keratosis treatment

cryotherapy: can cause hypopigmentation

photodynamic therapy (PDT) - field treatment

topical treatments

-5-fluorouracil

-Imiquimod (Aldara)

-aasers, chemical peels, ED&C

if unsure biopsy lesion to rule out SCC

seborrheic keratosis

incredibly common, oval slightly raised 'stuck on' tan/brown/black sharply demarcated dry papule ¨

lesar trelat sign - sudden appearance of numerous SKs can be a sign of internal malignancy

treatment: Cryotherapy or curettage

nevus

mole or freckle

benign, symmetric, even pigmentation

new nevi appearing after 30 in sun protected areas is suspicious

blue nevus

blue color caused by pigmented melanocytes in the dermis

beckers nevus

can be present at birth or appear with puberty

occurs mostly in moles

ABCDE rule

Assymetry

Border irregularity

Color

Diameter > 6mm

Evolving

5-10% of population has at least 1 atypical nevus

increased atypical nervus increases your chance for melanoma

atypical nevi treatment

biopsy via shave or punch method

completely excise with 5mm margins if severely atypical

moderately atypical lesions may be excised or monitored

benign growths

ephelides and lentigines

ephelides

freckles

-flat brown macules found in sun exposed areas or due to genetics

lentigines

sun spots

-flat brown macules in sun exposed areas

-due to photoaging

-doesn't fade

basal cell cancer

most common skin cancer

locally invasive, rarely metastasizes

mostly presents on sun-exposed areas

risk factors

-rlderly males

-sun damage

-fair skin

-previous skin injury

-thermal burn

lesion that won't heal and keeps bleeding

types of BCC

Nodular = most common

Superficial = least aggressive Sclerosing = most aggressive Pigmented = can be confused with melanoma clinically

BCC treatment

surgical excision

electrodessication and curettage (ED & C)

>superficial and nodular only; leaves scarring

Moh's surgery

>cosmetically sensitive areas; 98% cure rate

Imiquimod cream (Aldara)

>superficial only, only 70% effective

Radiation

Vismodegib (Erivedge) >chemotherapeutic agent, oral ¤ >teratogenic

merkel cell carcinoma

physical exam

-solitary, rapidly growing, pink-red nodule

-mostly older adults with extensive actinic damage

-commonly on the head and neck

aggressive growth

-40% have distant metastases, 18% survival

-70% survival at 5 years if lesion <2cm, no metastases

treatment

-wide excision, SLNB (sentinel lymph node biopsy), radiation

paget disease

mammary paget disease

-resembles nipple eczema (unilateral)

-hyperpigmented in SOC

-manifestation of underlying intraductal mammary carcinoma

extramammary paget disease

-resembles eczema; usually in genitalia

-manifestation of intraepidermal carcinoma or GI cancer

squamous cell carcinoma

2nd most common skin cancer

can arise from an actinic keratosis

can metastasize (4-5%)

common on sun-exposed areas and genitalia, oral mucosa and in areas of chronic trauma or inflammation

risk factors

-sun exposure, fair skin, HPV infection, radiation exposure, sunburns

types of SCC

bowens disease = SCC in situ

keratoacanthoma (KA) = appear suddently and grow rapidly

treatment of SCC

-Mohs surgery

-surgical cxcision

-ED &C

-radiation therapy only in patients who are not good candidates for surgery

-very high cure rate with early treatment

melanoma

malignancy that originates from melanocytes in skin

half develop in pre-existing nevi, rest on previously normal appearing skin

most common cancer in women age 25-29

rsk factors

-atypical nevi, fair skin, FMH, sunburns (risk doubles if more than 5 sunburns or 1 blistering sunburn)

with early detection and treatment cure rate for melanoma is about 90%

prognosis for distant metastatic disease is extremely poor, with median survival of 6-9 months and 5 year survival rates of less than 20%

melanoma

ABCD

asymmetry, border irregularity, color variation, large diameter (greater than 6mm)

lentigo maligna

more common in older patients with heavily sundamaged skin

starts as tan macule and then gradually spreads and darkens, after 5+ years becomes invasive

superficial spreading melanoma

most common form of melanoma

no preference for sun damaged skin

most commonly on upper back (males and females)

multicolored - black, red, brown, blue & white

acral lentiginous melanoma

most common type is dark-skinned & Asian populations ¤

periungual hyperpigmentation

Hutchinson's sign = black discoloration of the proximal nail fold at the end of a pigmented streak

nodular melanoma

smooth, dome shaped tumors on sun-exposed areas

bleeding is usually a late sign

amelanotic melanoma

non-pigmented

pink, erythematous or flesh-colored

melanoma diagnosis

DEPTH is the most important prognostic indicator

breslow depth and ulceration determine the tumor stage

ulceration - top layer of the tumor has begun to break up or pull apart = poorer prognosis

mitoses - increased mitotic rate is associated with declining survival rates

margin Status - did surgeon get clear margins?

melanoma treatment

early stage = surgical excision with 5mm-20mm margin

sentinel lymph node biopsy if 1mm or greater thickness

metastatic disease

-Immunotherapy

>Ipilimumab (Keytruda) and Nivolumab (Opdivo) which activate the immune system to destroy cancer cells, are the first drugs to extend life expectancy in later-stage melanoma

chemotherapy: does not increase overall survival

radiation: palliative

kaposi sarcoma

malignancy of vascular endothelial cells

most commonly presents on skin or mucosa but can also develop in lymph nodes or GI tract

reddish or blue-black macules/patches that spread and coalesce to form nodules/plaques. +/- edema

AIDS-associated

treatment

-excision, radiation therapy, injected chemotherapy, laser ablation

prognosis

-progresses slowly, death usually occurs years later from unrelated causes

-with AIDS patients, nearly all patient die of intercurrent infection.

mycosis fungoides

cutaneous T-Cell Lymphoma

starts on the skin, may remain there for years or progress to systemic disease

itchy localized or generalized erythematous scaly patches/plaques on the trunk

>don’t confuse with eczema, tinea, psoriasis

multiple large punch biopsies to confirm diagnosis

treatment

depends of level of involvement

>topical steroids, topical chemotherapy, UV light phototherapy, systemic chemotherapy, immunotherapy

contact dermatitis

direct skin contact with irritant (bleach) or allergen (poison ivy)

allergic = acquired hypersensitivy to allergen on previously sensitized skin

irritant = substance produces nonspecific inflammatory skin reaction, will be induced in any person if a sufficiently high concentration is used, no previous exposure necessary

treatment

topical steroid

discontinue contact with offending agent

dermatitis medicamentosa

drug rash in response to NSAIDS, antimicrobials, cytokines, anticonvulsants, psychotropic and chemotherapeutic agents

consider in any patient on medications who suddenly develops a symmetric rash

wide range or morphologies

-morbilliform (most common)

-pustular

-urticarial

-pruritis and dysethesia without obvious eruption

prognosis: most are mild, self-limiting and resolve when medication is discontinued

atopic dermatitis

eczema

chronic inflammatory skin disease characterized by pruritis and come/go rash

associated with other allergic conditions such as ssthma, allergic rhinoconjunctivitis, 35% have food allergy

causes: genetic (not completely understood)

risks factors

2+ household smokers,

cat ownership (not dog!) ¨

atopic dermatitis

presents with chronic relapsing pruritis

acute - red/thin scaly plaques

chronic - thick scaly plaques with excoriations

infants: extensor surfaces of arms/legs

children: flexor surfaces of arms/leg

adults: localized

atopic dermatitis

in skin of color, can present as lichenification and prurigo-like lesions with hyperpigmentation

atopic dermatitis

non pharm treatment

-pt education

-repair skin barrier to prevent outbreaks using aquaphor/vaseline, decreasing baths, using allergen free detergents, using cotton clothing, and using a humidifier

-do not do food restriction diet

-consider allergist consult

atopic dermatitis treatment (moderate)

topical steroids

mild - Hydrocortisone 2.5% moderate - Triamcinolone 0.1%

topical immunomodulator

-tacrolimus or pimecrolimus QD

-no risk of atrophy so also good for skin folds

topical JAK inhibitor

-ruxolitinib/opzelura

antihistamines (help with itch/immune response)

-otc (cetirizine/zyrtec)

-rx (hdroxyzine/atarax)

oral and topical Antibiotics (if infected)

atopic dermatitis treatment (severe)

oral prednisone (short term option)

light treatment: narrow band uvb (3x a week)

injectable dupilumab/dupixent (1st line)

-monoclonal antibody

-sq every 2-4 weeks

-adverse effects: conjunctivitis, increased hsv outbreaks

JAK inhibitors (2nd line)

-rapid improvement, oral

-adverse effects: increased cardiovascular risk (stroke, thrombosis, heart attack), cancer (lung, lymphoma), death, serious infectio

- baricitinib (litfulo), abrocitinib (cibinqo), upadacitinib (rinvoq)

oral immunosuppresive agents

-cyclosporine

>increased risk of malignancy, hypertension, nephrotoxicity

dyshidrosis

recurrent vesicular hand eczema

physical exam

-firm, pruritic vesicles on the palms, soles and lateral/medial aspects of the digits

>vesicles are in tact due to edema in thick acral skin

>"tapioca pudding" appearance

triggers - stress, allergic or irritant contact

dyshidrosis

treatment

exclude allergic or irritant contact dermatitis

same tx as atopic dermatitis

topical steroids, topical immunomodulators, injectable Dupilumab, oral JAK inhibitors

lichen simplex chronicus

circumscribed neurodermatitis

neurological condition where pt constantly scratches area

long-continued rubbing and scratching, more vigorously than a normal pain threshold permits, causes skin to become thickened and leathery with exaggerated skin markings (aka lichenification)

most commonly on neck (back and sides), wrists, ankles

gradual insidious onset

other factors: develop on skin that is the site of another disease, trauma, stress, anxiety

lichen simplex chronicus

treatment

goal: patient to avoid scratching

high potency topical steroid initially (not long term)

steroid tape (Clocortolone/ Cordran tape)

intra-lesional Kenalog

lichen planus

LP

-inflammatory disease of the skin, mucous membranes and hair follicles

>immune reaction mediated by T cells

-acute or chronic

-mucosal LP carries risk of malignancy

-wickham striae (white lines)

-association with Hepatitis C infection

lichen planus

4 P's

purple

polygonal

pruritic

papules

lichen planus

treatment

can be self-limiting, resolved in 8-12 months

superpotent topical or intralesional steroids

phototherapy

treatment for oral lesions

-orabase (benzocaine)

systemic therapy

isotretinoin

acitretin

cyclosporin

pityriasis rosea

mild inflammatory exanthem to subclinical viral infection or medication

salmon-colored papular and macular lesions with fine scale

may be mildly itchy

starts with single 'herald patch' which may persists a week or more before others appear

christmas tree' dermatomal distribution

pityriasis rosea treatment

requires no therapy (may check RPR to rule out syphilis)

topical steroid for itch if needed

disappears spontaneously after 3-8 weeks

psoriasis

common, chronic, recurrent inflammatory disease

common areas: scalp, nails, extensor surfaces of limbs, umbilical region, sacrum

affects 1-3% of world's population

Koebner phenomenon = trauma to skin creates plaque

psoriatic arthiris

involves joints

most commonly affects the distal interphalangeal joint

xray - shows 'pencil in cup' deformity

guttate psoriasis

abrupt eruption following infection

most commonly group A streptococcal pharyngitis

may be acute or chronic

drop-like' numerous salmon pink papules with fine scale

inverse psoriasis

often exclusively involves folds (ears, axillae, groin, intergluteal crease, penis)

mimics candida infection but KOH is negative

pustular psoriasis

sterile pustules that are red and scaly, most commonly on palms and soles

associated with tobacco use

can become generalized if not treated

common nail involvement (oil drop sign)

chronic plaque psoriasis

circumscribed, erythematous, dry, 'silvery' scaling plaques

most common type of psoriasis

plaques on extensor surfaces (elbows, knees, scalp, sacrum)

adherent silvery scale creates pinpoint bleeding when removed = Auspitz sign

psoriasis treatment

first line - topical steroids

vitamin D3 analogue -calcipotriene / dovonex

anthralin and coal tar (not cosmetically elegant)

phototherapy: narrow band UVB, 3 times a week treatment

psoriasis treatment (systemic)

Methotrexate

-monitor bloodwork

-liver biopsy periodically

-teratogenic

Cyclosporine

-monitor blood pressure and BW (CBC, Cr, Mg, Cholesterol)

Acitretin

- oral retinoin

-monitor BW

-works well with phototherapy

-teratogenic x 3+ years after d/c medication

-cannot drink alcohol

-adverse effects: depression

Apremilast (Otezla)

-selectively inhibits PDE4 which increases intracellular cAMP levels

-side effects: diarrhea, vomiting, headaches, depression

-no blood work monitoring required

-can be less effective than other systemic treatments

psoriasis treatment (biologics)

subcutaneous injections that target psoriasis t cell-mediated inflammatory pathway

most are also effective with psoriatic arthritis

associated with opportunistic infections and lymphoma

bw - check for tb before starting and annually; hbsag, hbcag

tnf-alpha inhibitors (oldest) ¤ entanercept (enbrel), adalimumab (humira)

interleukin 12 and 23 inhibitor ustekinumab (stelara)

interleukin 17 inhibitor ixekizumab (taltz), secukinumab (cosentyx

interleukin 23 inhibitor (newest) guselkumab (tremfya), risankizumab (skyrizi), tildrakizumab (ilumya)

no increased risk of malignancy

melasma

common acquired symmetric hyperpigmentation

sensitivity to hormones

>frequently caused by birth control, pregnancy

> mask of pregnancy

affects the face, worsens with sun exposure

wear spf to prevent worsening

treatment

topical: Hydroquinone, Tretinoin

peels & Lasers

vitiligo

acquired pigmentary anomaly, usually begins in childhood

can be medication-induced

depigmented white patches surrounded by normal or hyperpigented border

diagnosis: wood’s lamp

treatment

-psychological effect

-spontaneous repigmentation 15-25% cases

-non-treatment option if fitzpatrick i and ii

-topical pimecrolimus and tacrolimus, calcipotriene

-narrow band uvb phototherapy 2x/week

-jak inhibitor: topical ruxolitinib/opzelura; oral baricitinib/olumiant

-total depigmentation: monobenzone (if more than 50-80% bsa)

1st degree burn

erythema, tenderness, no bullae

minor epidermal damage

dry, red, painful

2nd degree burn

superficial partial - thickness

-extends to the papillary dermis

-thin-walled blisters, moist, blanching, painful

deep superficial

-extends to the reticular dermis

-thicker-walled blisters that may rupture, erythema & pallor, + pain with pressure

3rd degree burn

white, leathery or charred, dry without sensation

full thickness, destroys epidermis & the dermis

4th degree

significant charring, exposure of muscle or bone, extensive damage to nerves, little to no sensation of pain

destroys the skin and subcutaneous tissue & involves fascia, muscle, bone or other structures

burns

scald burns are the most common type

when burns are caused by electrical energy the skin does not correlate with the extend of clinical injury

labs - HCT, electrolytes, BUN/CR, UA, chest radiography

burn treatment

maintain ABCs

estimate % of burn

manage shock w aggressive fluid resuscitation, NG tube, foley catheter

Sulfadiazine (silvadene) is most common topical burn ointment

complications

-chronic healing wounds can undergo transformation into SCC

lacerations

tearing of soft body tissue, often irregular and jagged, often contaminated

puncture wound

caused by a sharp pointy object (nail, teeth), also prone to infection

pressure ulcer

occur in areas of pressure in patients with limited mobility

result of impaired blood supply caused by localized pressure

mostly in hip, sacrum

complications

-osteomyelitis

-bacteremia

stage 1 pressure ulcer

nonblanching erythema of intact skin

stage 2 pressure ulcer

necrosis, superficial or partial thickness involving the epidermis +/- dermis; shallow ulcer

stage 3 pressure ulcer

deep necrosis; crater ulcer with full thickness skin loss; damage or necrosis can extend down to but not through fascia

stage 4 pressure ulcer

full-thickness ulceration with extensive damage & necrosis to muscle, bone or supporting structures

stasis dermatitis

chronic venous insufficiency leads to edema, stasis dermatitis, hyperpigmentation & ulcerations

varicose veins commonly occur before skin changes

physical exam

-heaviness/aching in legs, aggravated by standing, relieved by leg elevation

treatment

-compression socks

-topical steroids (triamcinolone)

-referral to vascular surgeon

-ulcers need chronic treatment

chery angioma

benign vascular papule

due to proliferating endothelial cells (line the inside of a blood vessel)

very common, cause unknown

no treatment needed

infantile hemangioma

benign vascular tumor

treatment

-serial observation

-topical Timolol

-oral Propanolol

-surgery, laser, embolization

purpura

hemorrhagic lesions that result from bleeding within the skin & other small blood vessels

petechiae: pinpoint macules (1-2 mm in size)

ecchymosis: bruise, larger

telangiectasia

visible small, linear broken capillaries

can occur following injury or topical steroid use

can be seen in some skin cancers

no treatment necessary

sclerotherapy, laser treatment

pemphigus vulgaris

etiology not fully understood

mucosal erosions and thin-walled bullae that easily rupture on normal skin and mucous membranes

after bullae rupture they become covered in crusts that take a while to heal and leave behind hyperpigmented patches, no scarring

appear first in the mouth, + odor

Nikolsky sign - pushing a blister causer further separation of the dermis

Paraneoplastic - most commonly non-Hodgkin lymphoma, Chronic, lymphocytic leukemia, sarcoma

treatment

-high-dose oral Prednisone

-if paraneoplastic, most patients die from underlying cancer

bullous pemphigoid

autoimmune disorder or reaction to medication

more common in elderly

common locations: groin, axillae, trunk, thighs, flexor forearms

physical exam

-urticaria (large, tense subepidermal bullae)

-can persist for months or years

diagnosis: Immunofluorescense of normal skin and biopsy on blister edge

treatment

-high dose Prednisone with slow taper

>watch for adrenal insuffiency

-Azathioprine (Imuran)

-topical steroids

Nikolsky sign - pushing a blister causer further separation of the dermis

acanthosis nigricans

hyperpigmented velvet-textured plaque commonly on the posterior neck and/or axillae

commonly associated with Diabetes mellitus

rarely associated with Adenocarcinoma of GI tract

suspect in non-obese aged patient over 40

treatment - weight loss, treat underlying disorder, topical retinoids

dermatitis herpetiformis

itchy papules/vesicles on elbows, knees, buttock, posterior neck, scalp

caused by eating gluten

punch Biopsy

90% have Celiac Disease

labs

tissue transglutaminase

treatment- strict GF diet, oral Dapsone

xanthoma

deposits of lipids in tissue

appear when there is an underlying dyslipidemia

increased cardiovascular risk

diagnosis - full lipid profile, biopsy

treatment - surgery, laser

lipoma

benign subcutaneous fatty tumor

most commonly on the trunk

treatment

-may be left untreated

-surgical excision

epidermal inclusion cyst

benign, round, domeshaped encapsulated lesion with central pore or punctum

20% of adults, cause is unknown

occur on adults - commonly face, neck, trunk

they are more than twice as common in men as in women

treatment: nothing, surgery

in inflamed can use intralesional Kenalog

urticaria

hives

histamine reaction in the skin characterized by a wheal (localized edema), never lasts more than 24 hours

severe itching, stinging or pricking sensation

angioedema, anaphylaxis and hypotension may occur

dermatographism - raised wheal post scratching

causes - 50% idiopathic, medications, cold/heat, foods, stress, infections, menthol, wine (sulfites)

diagnosis - detailed history

urticaria treatment

acute - complete resolution within 6 weeks

antihistamines as needed

chronic - greater than 6 weeks

consider BW (CBC, LFTs, ANA, thyroid/hepatitis screen)

antihistamines daily (linked to dementia)

injectable Omalizumab/Xolair (1x/month)

>black box warning: anaphylaxis

topical steroids have NO role in treatment

consider Allergist referral

pilonidal

most commonly on the upper gluteal cleft in association with a sinus tract, +/- fragments of hairs

more common in men

treatment - refer to colorectal surgeon

hyperhidrosis

excessive production of sweat

usually primary cortical = emotional n

during waking hours only

check thyroid panel

most commonly on axillae, palms/soles

rarely on face

bilateral & symmetric

hyperhidrosis treatment

OTC aluminum chloride antiperspirants (Certain-Dri)

aluminum chloride hexahydrate (Xerac AC, Drysol)

oral glycopyrrolate (anticholinergic)

>questionable if long term use linked to dementia

botulinum toxin injections every 3-6 months