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As a third-year dermatology resident about to graduate, I embarked on a four-week elective in Botswana that would prove to be one of the most educational and enriching experi-ences of my life. I had worked in underserved inner-city clinics in the United States as well as rural villages in Latin America, but I had never been to Africa. I had no idea how much I would learn — about dermatology, about global health, and about myself.

During my month in Gaborone, Botswana in 2014, I treated more than 20 patients a day. I saw adults and children, inpatients and outpatients. Many patients presented with mundane diagnoses — atopic der-matitis, folliculitis, etc., but several others suffered from conditions that were much more difficult to diagnose and/or manage. The high rate of HIV and dearth of resources added extra elements of complexity. Initially, functioning as the only dermatologist there felt a bit unnerving. What if I didn’t know something? What if I made a mistake? These fears quickly transformed into appreciation for both my training up to that point as well as for the opportunity to have full responsi-bility for my patients. This autonomy inspired me to study vigorously, talk to colleagues in other specialties, read slides, and submit teledermatology consults for difficult cases.

I saw patients I will never forget. The resident who rotated before me biopsied a growing mass on a patient who had been diagnosed with dermatomyositis; the result was subcutaneous T cell lymphoma. With the help of Carrie Kovarik, MD, director of the dermatology program at Prince Marina Hospital in Botswana, we arranged for the patient — (who was initially very angry and upset with us for making this grave diagno-sis) — to get the appropriate workup and treatment with oncology. On one of my con-sults, I evaluated a pregnant woman with HIV and eclampsia on her way to an emergent C-section. She had noticed pink papules scattered all over her body. My differential was wide and included varicella and gono-coccemia. While awaiting biopsy and culture

results, she was placed on isolation precautions. After only a few days, her baby girl died due to necrotizing enterocolitis; because the patient was in isolation, she never even got to hold her. Another memo-rable patient was a 10-year-old boy with flat warts all over his face and scalp. He had been tested for HIV but never received the result. It was positive, but his mother refused to allow us to inform him or arrange counseling. These heartbreaking cases and the ethical issues they raised forced me to examine my own ideas of morality and cultural biases.

Of course there were many inherent challenges and frustra-tions. The pace of work in the hospi-tal was slower than we expect in the United States. Many areas of the hos-pital lacked soap and running water. Charts were usually illegible and often lacked important information. Rarely did the dispensary have all the medications on formulary. We worked closely with one of the pharmacists for several months just to obtain liquid nitrogen. Treatments and tests that we take for granted in the United States were a luxury in Botswana. These difficulties reminded me how fortunate we are to live and practice in the United States, and they also helped outline some of the potential areas that could be targeted to improve care.

In addition to seeing patients, I tried to teach as much as possible. I precepted students and medical officers in clinic, I participated in morning report cases, and I gave talks at Princess Marina Hospital and at our outreach sites about various dermatologic topics. I spent evenings with residents from other specialties discuss-ing their experiences in global health and their perceptions of the healthcare system in Botswana. I travelled to beautiful parks and witnessed some of the most amazing

natural wonders I have ever seen. I made friends with some of the locals and learned about their lives and culture.

The University of Pennsylvania-Botswana partnership program has created a unique

Spring 2015

Tswana’s ways: a resident’s rememberance A resident’s four-week elective in Botswana as part of an AAD Resident International Grant, prepares her for a career in the world of dermatology

Official Publication of the Residents/Fellows Committee, American Academy of Dermatology

A resident at Prince Marina Hospital in Botswana injects lidocaine prior to performing a biopsy of a dermatology patient with suspected sub-acute cutaneous lupus erythematous (SCLE). Photo courtesy Christa Slaught, MD.

See TSWANA’S WAYS on p. 3

3 Resident Jeopardy!

4-5 Boards’ Fodder: Disorders of Hypopigmentation

6 Race for the Case

7 AM15 Resident Events

8 Message from the Chair

Inside this issue

75918-R1-V1

Spring 2015 • p. 3www.aad.org/DIR Directionsesidencyin R

opportunity for dermatology resi-dents to learn about dermatologic diseases they might never otherwise encounter, as well as the challenges and benefits of establishing and pro-viding meaningful, long-lasting care in a developing country or under-served area. I will be forever grateful to the AAD and the UPenn partner-ship for allowing me to participate in this incredible rotation. I hope that by sharing my experience, I will inspire my peers to see the value in contributing to or developing similar programs.

To learn more about the AAD’s Resident International Grants go to: www.aad.org/residentgrant.

Rachel Schleichert, MD, is a procedural dermatology fellow at the Skin Institute of South Florida and cosmetic dermatologic surgery fellow at Hollywood Dermatology.

TSWANA’S WAYS from p. 1

Resident using a dermatoscope to examine for typical nail changes seen in dermatomyositis and to instruct a University of Botswana medical student on the dermatologic manifestations of dermatomyositis. Photo courtesy Christa Slaught, MD.D R

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Resident Jeopardy 2015: “this is their moment”Are you ready for Resident Jeopardy 2015? It’s happening Saturday, March 21, from 2-5 pm in Room 303 of the Moscone Center in San Francisco.

Resident Jeopardy entertains while also providing you with the ability to assess core competencies and identify knowledge gaps to bet-

ter prepare you for the board exam and life after residency.

“Our residents take such pride in being the best of the best,” said David Peng, MD, this year’s director of the session. “They were each top of their class in medical school, they study their rear ends off as residents. Resident

jeopardy is a great chance for them to be recognized. It gives them a chance to shine and represent not only their respective residency programs, but also our field. We have the best and brightest. And this is their moment.”

And now (cue dramatic music), here are your 2015 teams!

Team Name: Institution: Team Members:EB Ac-quiz-ita University of Minnesota Kevin Gaddis, MD, PGY3 & Ronnie Hamrick, MD, PGY4

Miracle College of Georgia Medical College of Georgia Morgan Wenner, MD, PGY3 & Jessica Burgy, MD, PGY3

Rash Decisions McLaren Oakland Hospital Ivy DeRosa, MD, PGY3 & Cynthia Chen-Lazzaro, MD, PGY4

Chili Buns Wake Forest Baptist Health Jacqueline DeLuca, MD, PGY4 & Robin Lewallen, MD, PGY3

East Carolina University Brody School of Medicine, Tanner Parrent, MD, PGY4 & East Carolina University Ryan Harris, MD, PGY4

The Woolly Bears UCSF Dermatology Residency Roberto Ricardo-Gonzalez, MD, PGY4 & Iris Ahronowitz, MD, PGY4

The Dermcats University of Arizona Drew Kurtzman, MD, PGY4 & Christie Alexander, MD, PGY2

Made in Detroit Henry Ford Alison Tisack, MD, PGY2 & Swati Kannan, MD, PGY3

A strategy for winningDirections asked Erik Domingues, MD (left), who along with Vincent Criscione, MD (right) was one half of the winning University of Massachusetts team in last year’s Resident Jeopardy competition in Denver), what contributed to their success in 2014. He offered these pearls.

1. Turn your board studying into Jeopardy studying.

2. Make Sima Jain, MD, your best friend.

3. Stay calm and jeopardy on.4. Forget about everything else in

the room and focus on the task at hand.

5. Most importantly, have fun!

Follow @AADMtgs on Twitter!

#AAD15

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boards’ fodderDisorders of Hypopigmentation by Gina Chacon, MD, and Meredith Hancock, MD

Meredith Hancock, MD, is a PGY-3 at Marshfield Clinic, Saint Joseph’s Hospital dermatology residency, Marshfield, Wisconsin.

Gina Chacon, MD, is a PGY-3 at Marshfield Clinic, Saint Joseph’s Hospital dermatology residency, Marshfield, Wisconsin.

Vitiligo Heterogeneous group of disorders with various genetic backgrounds, exogenous and intrinsic triggersFunctional melanocytes absentClinical: amelanotic macules and patches with surrounding nl skin. Discrete margins, convex borders. Usually asymptomatic. Predilection for face (periorificial), dorsal hands, nipples, axillae, umbilicus, sacral, anogenital areas. + isomorphic Koebner phenomenon.Localized:

- Focal: not clearly segmental- Unilateral/segmental: do not cross midline, children (15-30%) > adults (5-10%)- Mucosal: only mucous membranes

Generalized: (90% of cases)- Vulgaris/non-segmental: widely-distributed, scattered - Acrofacial- Mixed

Universal: complete depigmentationAssociated (adults): adult-onset AI-DM, AI-thyroid , LE, RA, Addison’s disease, pernicious anemia; +/- halo nevi, AA, lichen sclerosisAPCED (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy) syndrome: AR, AIRE gene, predisposed to vitiligo and AI destruction of endocrine cells. Failure to delete autoreactive T cells à AI disease

HEREDITARY HYPOMELANOSIS

Disease Genetics / Pathophysiology / Histology Clinical Features

Oculocutaneous Albinism (OCA)

Diffuse pigmentary dilution

40% of cases are OCA1(A + B)

50% of cases are OCA2

Melanocytes present

OCA1AAR, TYR geneno tyrosinase activity (tyrosinase negative)

At birth white hair, milky white skin, blue-gray eyes; with age hair may yellow slightly, skin remains white, melanocytic nevi remain amelanoticExtreme UV light sensitivity, high risk for skin cancers (SCC especially)Reduced visual acuity most severe in OCA1A, some legally blind

OCA1BAR, TYR gene↓ tyrosinase activity (tyrosinase positive)

Yellow OCA: little to no pigment at birth. Hair becomes yellow with age (pheomelanin requires less tyrosinase)Minimal pigment OCA, platinum OCA, temperature-sensitive OCA: little to no pigment at birth. Develop some pigment in by 2nd decade. Burn without tanning. Amelanotic or pigmented melanocytic nevi possible.Temperature-sensitive: in puberty, arm hairs à light reddish-brown, leg hairs à dark-brown. Mutated tyrosinase loses activity at 35˚C (like Siamese cat)

OCA2AR, OCA2 gene (prev P)Transmembrane transporter, role in organelle pH regulation, tyrosinase trafficking/processingtyrosinase positive

Broad clinical spectrum. Mild to mod pigmentary dilution. Little to no ability to tan. Pigmented melanocytic nevi/lentigines develop in sun-exposed skin. Brown OCA phenotype: African descent, light brown hair and skin, irides gray to tan at birth, do not sunburn.1% of pts with PWS/AS also have OCA2; del + mutation 15q (with OCA2/P gene)

OCA3AR, TYRP1 gene (melanocyte specific)Eumelanin synthesis via tyrosinase stabilization

Rufous OCA: skin type III–V, red–bronze skin, ginger-red hair, blue/brown irides

OCA4SLC45A2 gene (prev MATP)Transmembrane transporter role in tyrosinase processing and intracellular trafficking of proteins to melanosome

Most common in Japanese (25% of pts), China (10-20%), India (~10%), < 5 % in Caucasians

Variable phenotype; hair from white to yellow-brown, +/- increased pigment in hair/skin with age

OA1 Severe decrease in visual acuity, hypopigmentation of the retina, +macromelanosomes in the eyes and skin; skin is normally pigmented overall

Piebaldism AD, KIT proto-oncogene à tyrosine kinase transmembrane receptors on melanocytes; functional receptor required for nl melanocyte migration (from neural crest and postnatally); Histo: no melanocyctes in amelanotic skin/hair follicles; hyperpigmented areas with abundance of melanosomes

Present at birth. Leukoderma favors central anterior trunk, mid-extremities, central forehead, midfrontal scalp (à white forelock in up to 90% pts; absence does not exclude dx); distinctly irregular in shape, well-circumscribed, milk-white; nl pigment and hyperpigmented areas within leukoderma. Poliosis of eyebrows, eyelashes common.Must exclude Waardenburg syndrome via eye exam, hearing exam

Waardenburg Syndrome (WS)

Absence or minimal numbers of melanocytes

WS1AD, PAX3 gene

White forelock is most frequent pigment abnormality (20-60% pts)Leukoderma similar to PiebaldismHeterochromia irides (partial/extorial or complete) in ≥ 20%Synophrys (confluent, bushy eyebrows), broad nasal rootDystopia canthorum. Hearing impairment in up to 37% (unilat/bilat)

WS2AD, MITF gene, (also SOX10)

Similar to WS1 (except no dystopia canthorum), deafness more common

WS3 (Klein-Waardenburg)AD, PAX3 gene

Similar to WS1, with upper limb abnormalities (hypoplasia, syndactyly)Dystopia canthorum

WS4 (Shah-Waardenburg)AD, EDNRB or SOX10 gene

Similar to WS1 (except no dystopia canthorum or broad nasal root)Hirschsprung diseaseRarely CNS dysfunction, neonatal hypotonia, arthrogryposis (related to SOX10)

Tiez Syndrome AD, MITF gene (allelic to WS2) Diffuse pigmentary dilution of skin/hair, deafness, hypoplasia of eyebrows. Blue eyes without nystagmus or photophobia.

DISORDERS OF MELANOSOME BIOGENESIS

Disease Genetics / Pathophysiology / Histology Clinical Features

Hermansky Pudlak Syndrome (HPS)

AR, 9 subtypes

Most subtypes have mutations in genes encoding biogenesis of lysosome-related organelles complexes 1-3 (BLOC1/2/3 genes); à involved in lysosome-related organelles (LRO), eg, melanosomes formation.

Exception is HPS2, mutation in AP3B1 gene à involved in protein sorting to lysosomes and LRO, associated with antigen presentation, secretion of lytic granules in cytotoxic T cells

Pigmentary dilution of the skin, hair, eyes; variable, depending on mutation and ethnicity (HPS1 and 3 in Puerto Ricans). ↑ pigmentation with age.Nystagmus and reduced visual acuity similar to albinism, NMSCSystemic symptoms due to organelle dysfunction:

- Bleeding tendency (on EM: absence of dense bodies in platelets)- interstitial pulmonary fibrosis à cause of early death (30-50 y)- granulomatous colitis (ceroid lipofuscin accumulation in lysosomes)- renal failure, cardiomyopathy (less common)

HPS2: recurrent bacterial infection due to neutropenia, abnl cytotoxic T-cell function

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boards’ fodderDisorders of Hypopigmentation (cont.) by Gina Chacon, MD, and Meredith Hancock, MD

Boards’ Fodder

In addition to this issue’s Boards’ Fodder, don’t for-get to download the new Board’s Fodder online exclusive from www.aad.org/DIR, where a new chart is published each quarter. The latest online Boards’ Fodder is Herbal supplements in Dermatology by Josh Weingartner, MD and Anne Miller, MD.

To view, download, or print every Boards’ Fodder ever published, both in print and online, check out the com-plete archives at www.aad.org/BFarchives.

DISORDERS OF MELANOSOME BIOGENESIS (cont.)

Disease Genetics / Pathophysiology / Histology Clinical Features

Chédiak–Higashi Syndrome (CHS)

AR, LYST gene (lysosomal trafficking regulator) à protein regulating fission/fusion of lysosome-related organelles

OCA with silvery-gray hair, photophobia, nystagmus, ocular hypopigmentation, hyper/hypopigmentation, bleeding diathesis (diminished function of platelet granules), progressive neurologic dysfunction, severe immunodeficiency. Giant LRO (including melanosomes, platelet dense granules, PMN granules); peripheral smear for screening

DISORDERS OF MELANOSOME TRANSPORT AND/OR TRANSFER

Griscelli Syndrome (GS) GS1AR, MYO5A gene à myosin Va, key role in transfer of melanosomes to keratinocytes

Diffuse pigmentary dilution of skin, silvery-gray hair due to pigment clumping in melanocytes (GS1/2/3). Neurologic impairment (MYO5A also found in neurons).

GS2AR, RAB27A gene à Ras-like GTPase present in melanosomes.

Diffuse pigmentary dilution and silvery hair.Immunodeficiency, hemophagocytic syndrome (RAB27A found in hematopoetic cells). Can be treated with HSCT.

GS3AR, MLPH gene à melanophilin which links myosin Va to Rab27a

Diffuse pigmentary dilution and silvery hair

Elejalde Syndrome Pigmentary findings of GS + severe neurologic dysfunction

TUBEROUS SCLEROSIS COMPLEX AND PIGMENTARY MOSAICISM

Tuberous Sclerosis Complex (TSC)

AD, TSC1 gene à hamartin, TSC2 gene à tuberin(both tumor suppressor genes)Normal # of melanocytes; however, ↓ size and poor melanization of melanosomes

Hamartomas of multiple organs (skin, brain, eye, heart, kidney).White hypomelanotic macules (possibly present at birth), confetti-like/guttate, lance-ovate “ash leaf”; consider in children with ≥ 3 hypomelanotic maculesTriad: facial angiofibromas (“adenoma sebaceum”), seizures, mental deficits

Hypomelanosis of Ito (HI)

Hypopigmentation along Blaschko’s lines, reflects mosaicism characterized by a clone of skin cells with a decreased ability to make pigment. Apparent at birth, during infancy or childhood. The characteristic pattern of streaks and whorls can occur unilaterally or bilaterally. Most common on trunk and limbs. Abnormalities of CNS, eye or musculoskeletal system.

NUTRITIONAL HYPOMELANOSIS

Kwashiorkor Severe protein deficiency Initially, skin erythematous to red-brown color with marked desquamation à hypomelanosis and/or patchy postinflammatory hypermelanosis. Hypomelanosis starts on the face; hair is dry, lusterless, +/- red-brown color

Copper DeficiencySelenium Deficiency

Tyrosinase requires copper Diffuse pigmentary dilution

POSTINFLAMMATORY HYPOMELANOSIS

Secondary to Psoriasis, seborrheic dermatitis, atopic dermatitis, sarcoidosis, lichen sclerosis, lichen striatus, PLC, MF, LEMultiple factors/processes affect skin color; dysregulation caused by inflammation can alter melanosomes biogenesis, melanin production, melanosome transport/transfer to keratinocytes. Severe inflammation can lead to functional loss of melanocytes, even cell death.

Pityriasis Alba Reduced numbers of active melanocytes, decrease in # and size of melanosomes in affected skin

Slightly scaly, round/oval, ill-defined hypopigmented macules/patches. Children/adolescents > adults, more noticeable in darker skin, summer.Early lesions pink à white/dry/powdery with pink borderFace most common site. Wood’s lamp accentuates hypopigmentation

Sarcoidosis Dermal non-caseating granulomas; melanocytes may or may not appear normal. Melanosomes appear normal but ↓ # in keratinocytes.

Circumscribed, poorly marginated papules/plaques +/- induration. Dermal nodules surrounded by hypomelanosis. Most common on extremities, asymptomatic, no secondary changes.

Hypopigmented Mycosis Fungoides (MF)

Histology consistent with MF; decreased melanosomes in keratinocytes. Nl # of melanosomes in melanocytes (= defect in transfer)

Variant of early stage MF; most frequently seen in people with darker pigmentation. Hypomelanotic lesions on trunk/extremities, +/- pruritus. Erythema and infiltration usually present.

Scleroderma Unknown Characteristic leukoderma (sclerotic and non-sclerotic skin) is circumscribed areas of complete pigment loss with perifollicular and supravenous pigment retention. “Salt and pepper.” Seen in overlap syndromes, scleromyxedema.

Lichen Sclerosis (LS) Unknown Genital and extragenital lesions are hypomelanotic +/- epidermal atrophy, follicular plugging, and purpura (anogenital). Extragenital LS may be guttate.

Lupus Erythematosus (DLE, SCLE)

↓ # of melanocytes, epidermal atrophy, vacuolar changes, pigment incontinence

Hypomelanosis/amelanosis associated with cutaneous atrophy/scarring. Hypomelanosis at lesion center often with a rim of hyperpigmentation. Pigment loss can be permanent in chronic scarring DLE, reversible in SCLE.

Abbreviations: Nl: normal, abnl: abnormal, AI: autoimmune, LE: lupus erythematosus, RA: rheumatoid arthritis, AA: alopecia areata, PWS/AS: Prader-Willi syndrome/Angelman syndrome, EM: electron microscopy, PMN: polymorphonuclear cells, HSCT: hematopoietic stem cell transplant, PLC: pityriasis lichenoides chronica , MF: mycosis fungoides, DLE: discoid lupus erythematosus, SCLE: subacute cutaneous lupus erythematosus

References:1. Bolognia, Jean, Joseph L. Jorizzo, and Julie V. Schaffer. “Chapter 66.” Dermatology. 3rd ed. Philadelphia: Elsevier Saunders, 2012. 1023-041. Print. Special

thanks to Erik Stratman, MD.

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Winter 2014 Race for the Case winner

Our winter 2014 Race for the Case Winner is Megan Noe, MD, a 3rd-year resident at the University of Iowa Hospitals and Clinics. In her spare time she enjoys running, crossfit and being an Iowa Hawkeye superfan (her photo submis-sion provided our first clue). “In the resident work room, you will probably find me wrapped in my Hawkeye snuggie sing-ing along to Taylor Swift or sharing the latest viral video with other residents!” she said. Congrats, Megan! Enjoy your coffee!

Visit the Residents and Fellows Resource Center Online at www.aad.org/members/residents-fellows-resource-center

Megan Noe, MD

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1.) What is the name of this condition?

Cutaneous larva migrans (larva migrans cutanea)

2.) What is the most likely culprit causing this condition?

Larva of the animal hookworm Ancylostoma braziliense, which is the most common hookworm in the Caribbean and the most common to affect humans

3.) What is a skin biopsy of this lesion most likely to show?

Histopathology on H&E shows a predominantly spongiotic der-matitis with eosinophils, often with eosinophilic vesicles.

Burrows are also often seen just above the basal layer, which cor-respond to the tracks of the para-site. It is believed that the larva can-not penetrate the basement mem-brane due to its lack of colla-genase enzymes and therefore these empty spaces are limited to the epidermis. Only rarely is the hookworm larva is actually seen on skin biopsy as it is often already advanced much farther

than the visible end of the track seen clinically, into an area of normally appearing skin.

4.) What is the preferred treatment? An anti-helminthic medication

like oral or topical thiabenazole, oral mebendazole, oral albena-zole, or oral ivermectin

Race for the CaseBy Robyn Marszalek, MD

A 65-year-old African-American male presents with a several month history of extremely pru-ritic, circular, clustered plaques on the lower extremities with firmly adherent, depressed, concentric circular crusts and surrounding mild erythema. His past medical history is significant for end stage renal disease on hemodialysis x 2 years, type II diabetes mellitus requiring insulin, COPD, severe coronary artery and peripheral artery disease, rheumatoid arthri-tis managed on prednisone 15mg daily, and recurrent Clostridium difficile colitis s/p bowel resection.1. This condition is classified

under an “umbrella” category which encompasses four clini-cal variants. What is the name of this “umbrella” category?

What are the names of the four conditions in the category?

2. What element(s) in this patient’s past medical history may pre-dispose to this condition?

3. What are histopathologic find-ings that all four clinical vari-ants share?

4. For each clinical variant, what is the primary unique substance seen on histopathology that clinches the diagnosis?

5. What are felt to be cutaneous triggers of this eruption?Respond online today with the

correct answers at www.aad.org/RaceForTheCase for the opportu-nity to win a Starbucks gift card. If you win the coffee gift card we will also publish your mug (face). Good luck! D R

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Robyn Marszalek, MD, is a PGY-4 dermatology resident at Boston University Medical Center.

So You Think You Can Race?

Why not submit your own Race for the Case feature? Our guidelines are designed for busy residents (are there any other kind?) who wish to share their knowledge, show their com-petitive nature, and have their work published in an AAD publication (and wouldn’t that look good on your CV?). All you need is an interesting case, a few ques-tions and answers, and a few images that you have per-mission to use for publication. While the wheels are still turning inside your head, submit your Race for the Case query to Dean Monti at dmonti@aad.org.

Answers to Winter 2014 Race for the Case

Spring 2015 • p. 7www.aad.org/DIR Directionsesidencyin R

Not to be missed! Events for residents in San Francisco

Move over Zagat! The Sbicca List for San FranciscoA West Coast dermatology resident and foodie provides personal picks and options for residents attending the AAD Annual Meeting 2015.

by Jennifer Sbicca, MD

Make the most out of your time at Annual Meeting and be sure to check out the great courses and events for residents, all happening at the Moscone Center in San Francisco.

Practice Management Symposium for ResidentsThursday, March 19, 7 am - 5:30 pm, Room 3022 Broaden your practice management knowledge as you learn the ins and outs of working in a group, academic, or private setting from well-known, successful dermatologists. Also, be sure to attend a special reception, immediately following the sympo-sium at 5:30 in the 3rd floor foyer of Moscone West. Network with your peers and symposium faculty. Drinks and hors d’oeuvres will be served!

Board Prep for Residents C005 (NEW)Friday, March 20, 9 am - 5 pm, Room 3001Gain hands on experience by taking a “mock certification exam” in the morning and review your results in the afternoon.

AAD Career Networking EventFriday, March 20, 5 pm – 7 pm, Golden Gate Ballroom AMake connections and explore dif-ferent practice setting opportunities.

Resident ReceptionFriday, March 20 5 p.m. – 6:30 p.m, Golden Gate Ballroom BNetwork with fellow residents and meet up with old friends.

Resident Jeopardy S024Saturday, March 2, 2 pm – 5 pm, Room 303Engage in a friendly competition and test your knowledge (see page 3).

Residents and Fellows Symposium S025Sunday, March 22 11 am – 2 pm, Room 122Latest research discoveries!

Boards and Beyond F083Sunday, March 22 1 – 3 pm, Room 3010 (West Bldg.)Hear from successful dermatologists about the boards and life after boards.

High Yield “Power Hour” for Residents F097Sunday, March 22 3:30 pm – 5:30 pm, Room 3005 (West Bldg.)Examine pearls from topics encoun-tered during training.

Young Physicians Pearls and Pitfalls F103Sunday, March 22 3:30 pm – 5:30 pm, Room 2008 (West Bldg.)Receive lessons learned in the first 10 years out from other young physicians.

Board Blitz S039Monday, March 23, 9 am – 12 pm, Room 103 (South Bldg.)Discover key points and tips in pre-paring for the certification exam.

Advanced Self-Assessment of Dermatopathology C025Monday, March 23, 9 am –5 pm, Room 3001 (West Bldg.)Analyze 50 complex dermato-pathol-ogy cases.

For a complete listing of all the ses-sions taking place, be sure to check out the Program online at aad.org.

I’ve lived all over the San Francisco Bay Area: San Francisco (mis-sion district), Oakland, Berkeley, Santa Clara, and Campbell. When Directions in Residency asked for my top ten restaurant suggestions, I put down my fork, picked up my pen and scribbled down my thoughts on local dining.

1. Best and Closest to Moscone Center – Trou Normand and Super Duper Burgers

2. Best Neighborhood Nooks – Frances and Nopa.

3. Best Mexican – Cancun, El Farolito, and Papalote.

4. Best Coffee – Blue Bottle and Tartine

5. Best Asian – Burma Superstar and House of Nanking

6. Best places to impress – Gary Danko and The Slanted Door.

7 Best Vegetarian – Greens and Verbena.

8. Most starred – Benu and Saison

9. Best Dim Sum – Yank Sing. 10. Best Brunch – Foreign

Cinema and Mr. Benjamin.

For more on these res-taurant picks, be sure to read the extended story in Annual Meeting

News, onsite and in your email, during the Annual Meeting in San Francisco.

Your new Residents/Fellows Community awaits!

Want to know more about fellowships, treating difficult cases, starting your job search, and more? Check out the Academy’s new community just for AAD residents and fellows at community.aad.org. Log in with your aad.org user ID and password, and join the Residents and Fellows Community. Post and respond to questions; share documents and resources; and access the entire membership direc-tory. Join one of the 17 + discussions happening now!

Jennifer Sbicca, MD is a dermatology resident at the University of Southern California.

Your complimentary subscription to Dialogues in Dermatology just got even better! Accessing Dialogues in Dermatology is now even easier with the new Dialogues app.

• Download and listen to content right from your smart phone or tablet

• Easily track which interviews have been listened to and which are new

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• and much more!

Download the app today at the iTunes or Google Play store.

Why not open a Dialogue? It’s free.

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Brian R. Hinds, MD

Message from the Chair “Strive not to be a success, but

rather to be of value.” –Albert EinsteinBeyond relativity, it seems that

Einstein understood emotional intel-ligence. Value in healthcare has been previously defined as the health out-comes achieved per dollar spent. Value, value, value…say it three times fast, and you will catch a glimpse of the genie of Medicare reform. In January, the US Department of Health and Human Services announced that by 2018, 90 percent of payments will be tied to delivering value! As per-plexing a measurement as the latter sounds, perhaps receiving a medical infusion of value is not necessarily a bad thing. In business [ie. healthcare], value is one characteristic that sets apart two otherwise identical prod-ucts or services [ie. physicians/hospi-tals]. As residents, we should strive to become experts in delivering value to our patients sooner rather than later. From our vantage point — as derma-tologists — this should be an easy application: ensure patients feel com-fortable, sit down face-to-face during clinic visits, listen without interrupting, use patient friendly language, perform timely call-backs, answer questions honestly, etc. I bet many of you prac-tice in this fashion on a daily basis! What about your attendings?

It seems Einstein was onto some-thing: success is measured at the individual level, while value is pro-

jected for others’ benefit. The AAD is equally interested in demonstrat-ing value by addressing the diverse needs of residents/fellows. I can attest that the AAD is honest, sin-cere, and steadfast in its mission to young physicians. In what remains an enigma, the current retention rate of AAD memberships of graduating residents is approximately 80 per-cent. The trend three to four years out slowly recovers to 93 percent retention of young physicians, which is impressive. However, this statistic reflects lost time for young physi-cians to benefit from the panoply of AAD resources at perhaps the most crucial time. The specialty misses out on some of the bright minds, which are desperately needed for dermatol-ogy to navigate future hurdles. To the 2015 graduates: please take advan-tage of the fleeting months of resi-dency, trust in your training, and keep the AAD a central part of your career. It needn’t be lonely in the trenches. Get involved in the AAD and AADA. The value-added service that you will provide as a board certified derma-tologist is unmatched!

It has been an honor and plea-sure serving as chair of the Resident/Fellows Committee, and indubitably, you’re in store for yet another valu-able addition — to this committee — with Nathan Miletta, MD, taking the chair this month.

Spring 2015

Residents / Fellows Committee

Brian R. Hinds, MD, chair 2015

Lindsey Hunter-Ellul, MD, physician reviewer 2016

Lacey Lea Kruse, MD, physician reviewer 2015

Kathryn Beleznay, MD 2015

Nancy Habib, MD 2015

Mark Tye Haeberle, MD 2016

Nathanial R. Miletta, MD 2016

Jenna L. O’Neill, MD 2015

Nishit Sharadchandra Patel, MD, MS 2015

Bethanee Jean Schlosser, MD, PhD 2017

chair, Young Physicians Committee

Thomas E. Rohrer, MD, BOD liaison 2015

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