Gynecologic Robotic Surgery: Choosing the Right Indications And

5 Things to Know About Managing Obesity in Clinical Practice

Taraneh Soleymani, MD, FTOS Assistant Professor Department of Nutrition Sciences University of Alabama at Birmingham [email protected]

5 Things to Know About Managing Obesity in Clinical Practice

Educational Objectives

 Participant will be able to identify and describe the stages of obesity  Participant will be able to describe obesity treatment modalities  Participant will be able to prescribe dietary interventions for weight management  Participant will be able to prescribe physical activity for weight management  Participant will be able to prescribe SMART lifestyle goals for weight management

Outline

1. Staging of obesity  World Health Organization classification of obesity 2. Obesity treatment modalities  Lifestyle modification  Pharmacotherapy  Bariatric surgery 3. Dietary intervention for weight loss  Calorie  Composition 4. Prescribe physical activity  Acute weight loss  Weight maintenance 5. SMART lifestyle goals  Importance in clinical practice

Select References - Jensen MD. 2013 AHA/ACC/TOS Guideline for the Management of Overweight and Obesity in Adults. Circulation. 2014 Jun 24;129(25 Suppl 2): S 102-38. - Ard JD. Nutrition Interventions for Obesity. Med Clin North Am. 2016 Nov:100(6):1341-1356 - Soleymani T. Weight Maintenance: Challenges, Tools and Strategies for Primary Care Physicians. Obes Rev. 2016 Jan;(1):81-93. - Jakicic JM. Effect of Exercise on 24-month Weight Loss Maintenance in Overweight Women. Arch Intern Med. 2008 Jul 28;168(14):1550-9. - Johnston BC. Comparison of Weight Loss Among Named Diet Programs in Overweight and Obese Adults: A Meta-analysis. JAMA. 2014 Sep 3;312(9):923-33. - Alamuddin N. Management of Obesity. J Clin Oncol. 2016 Dec 10;34(35):4295-4305. - Courcoulas AP. Weight Change and Health Outcomes at 3 Years After Bariatric Surgery Among Individuals with Sever Obesity. JAMA. 2013 Dec 11;310(22):2416-25. Prenatal Screening: Biggio UAB Progress in OBGYN 2017

Disclosures

• No financial conflicts to report Prenatal Screening in 2017— The DOs and the DON’Ts

Joseph R. Biggio, MD University of Alabama at Birmingham Maternal Fetal Medicine and Genetics

Learning Objectives

• Discuss differences between cfDNA screening and conventional screening • Review performance and limitations of cfDNA screening compared to conventional screening for common aneuploidies and all chromosome abnormalities • Identify key components of informed consent as well as pre- and post-test counseling

ACOG Practice Bulletin #163 Integrated Screening • A combination of 1st and 2nd trimester • Maternal age should not be sole screening tests factor in offering diagnostic test • 11-13 weeks: NT, PAPP-A • • 15-17 weeks: AFP, hCG, estriol, & Aneuploidy screening or diagnostic inhibin testing should be offered to all • Final result provided once Quad screen women early in pregnancy completed • All testing combined into a SINGLE result Malone et al., NEJM, 2005; 353:2001-11

1 Prenatal Screening: Biggio UAB Progress in OBGYN 2017

Detection Rate for 5% Screen Positive Rate 95 Non-Invasive Prenatal Te st ing (N IPT)

85 86 OR 81 Non-Invasive Prenatal Screening (NIPS)

68 69 OR

Integrated tests Cell-free DNA Screening for Aneuploidy

NT Triple Quad NT + PAPPA + NT + PAPPA + Quad PAPPA + hCG Quad

Placenta Ma terna l pla s ma Ma terna l blood c ells

•Cell-free fetal AND maternal DNA fragments in maternal plasma Using cf-DNA screening in your •Placenta→ Fetal DNA practice •Reliably detected >10 weeks gestation The DOs and the DON’Ts •Gone by 2 hr postpartum •Blood cells, soft tissue, tumors→ Maternal DNA •Fetal DNA: 5-25% (~15%) total cell-free DNA

Lo, Lancet 1997;350:485-487

The DON’Ts The DOs 1. Don’t tell patients that cf-DNA will detect all chromosome abnormalities and that their fetus is normal if the result is 1. Provide patients with appropriate pre-test and normal post-test counseling 2. Don’t order cf-DNA screening in low-risk groups just so the patient can finder out gender earlier 2. Refer patients who receive a high-risk result for 3. Don’t order microdeletion panels as part of cf-DNA counseling and possible diagnostic testing screening 3. Order AFP only, NOT a QUAD, in the second 4. Don’t ignore ’No call’ or ‘equivocal’ results; refer patients trimester for assessment of NTD risk in patients for counseling and further evaluation who have had cf-DNA screening 5. Don’t use cf-DNA as a replacement for diagnostic testing, especially in the setting of U/S abnormalities 4. Offer cf-DNA to high risk groups as an option for 6. Don’t order a targeted U/S in AMA patients if the patient screening has a low-risk cf-DNA result and there are no other indications for scan.

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Origins of Maternal Serum Screening

• Neural tube defects DO order AFP only, NOT a QUAD, in the –1970s elevated AFP in amniotic second trimester for assessment of NTD risk fluidàserum in patients who have had cf-DNA screening • Brock et al, 1973; Wald et al, 1974

• Aneuploidy screening a result of serendipity and ingenuity • Merkatz et al, 1984

AFP AFP for NTD and VWD • Elevated – Disruption of fetal-maternal-placental barrier • Unclear incremental benefit with modern US – Placental vascular damage for NTD detection – Impaired integrity of fetal skin – Questionable need in severe lesions • Disorders – Potential role for distal or difficult to – Neural tube defects visualize lesions – Ventral wall defects • 9 out of 12 missed cases of NTD, AFP not – Dermatologic disorders done—Racusin et al, Am J Perinatol, 2015 – Congenital nephrosis • US identifies most VWD

DO offer cf-DNA to high risk groups as an option for screening

DON’T order cf-DNA screening in low- WHAT IS THE APPROPRIATE risk groups just so the patient can finder POPULATION FOR CELL-FREE out gender earlier DNA TESTING?

3 Prenatal Screening: Biggio UAB Progress in OBGYN 2017

Comparison of prenatal screening and diagnostic test options

Te st Detection Screen Positive rate for DS positive rate Predictive (%) (%) Value (%) • Appropriate Populations: First trimester screen 80 5 ~3 Sequential/Integrated 93 5 ~4-6 • AMA sc reen • Prior affected Cell-free DNA screen 99 1-9 40-88% • Abnormal screen (includes no call/test failures) • Ultrasound abnormality Chorionic Villus Sampling >99 1 (includes mo sai ci sm) • Robertsonian translocation involving 13 or 21 Amnioc entesis >99 0.2 • Pre- and post-test counseling (includes mosaicism) • Need more information for multiples Adapted from SMFM Consult Prenatal aneuploidy screening with cfDNA. Am J ObstetGynecol 2015.

Test Comparison: High vs Low Risk In a population of 10,000 women Detection rate 99.7%, false positive rate 0.1%

• Prevalence 1 in 100 • Prevalence 1 in 1,000 – 100 will have – 10 will have DON’T ignore ’No call’ or ‘equivocal’ results; aneuploid fetus aneuploid fetus refer patients for counseling and further • Detect 99 aneuploid • Detect 10 aneuploid evaluation • 9 false positive • 9 false positive

PPV=99/108=92% PPV=10/19=53%

“No call” results (screening failure) No result significance • Uninterpretable results associated with • Not reported, indeterminate, or • Aneuploidy uninterpretable results • Vanishing twin • Maternal malignancy • Occurs in 1-8% of patients • Mosaicism • 50-60% of repeat screens will provide a result • Low fetal fraction • Increased risk of aneuploidy • 20-25% prevalence Pergament et al, O&G 2014; Norton et al, NEJM, 2015

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• Follow-up DON’T tell patients that cf-DNA will detect all • Genetic counseling chromosome abnormalities and that their fetus • Tar get ed u l t r as o u n d is normal if the result is normal • Repeat cfDNA testing consideration • 50% get interpretable result DON’T use cf-DNA as a replacement for • Gestational age and options considerations diagnostic testing, especially in the setting of • Offer diagnostic testing U/S abnormalities

Current cf-DNA platforms: Limitations of cf-DNA for detection of Conditions routinely screened for chromosome abnormalities

• Down syndrome • Proportion of chromosome abnormalities due to common trisomies (13,18, 21) depends on • Trisomy 18 (Edward syndrome) population risk, especially maternal age • Trisomy 13 (Patau syndrome) • Ranges from 60-75% • Sex chromosome aneuploidy (most labs) • Cannot differentiate mode of inheritance and • Tu r n er s y n d r o m e recurrence risk • Klinefelter syndrome • Non-disjunction trisomy • XXX • Tr an s l o c at i o n • XYY • Mosaic

Distribution of chromosome 1st Trimester/Integrated Screening vs cf-DNA: abnormalities: Livebirths, Fetal death >20 Performance in a high-risk cohort weeks, TOP for anomalies • 68,990 screen-positive 16% • 26,059 (38%) diagnostic testing T21 5% T18 • 2,993 (11.5%) abnormal result T13 8% 53% Turner • 83.1% (n=2487) Trisomy 13, 18, 21, sex 5% Sex trisomy chromosome aneuploidy—DETECTABLE Other 13% • 16.9% (n=506) UNDETECTABLE—mosaic, triploid, translocation, marker, other Adapted from Wellesley et al., Eur J of Hum Gen, 2012 Norton et al, Obstetrics & Gynecology, 2014

5 Prenatal Screening: Biggio UAB Progress in OBGYN 2017

Distribution of chromosome abnormalities st 16.9% (n=2,993) 1 Trimester/Integrated Screening vs cf-DNA: Performance in a high-risk cohort 1% 3% 3% T21 5% 5% T18 • 2% of screen positive patients had an T13 abnormal result not detectable by cf- SCA 8% Mosaic DNA 5% 53% Rare trisomy Translocation 17% Triploidy Other

Norton et al, Obstetrics & Gynecology, 2014

1st Trimester/Integrated Screening vs cf-DNA: 1st Trimester/Integrated Screening vs cf-DNA: Population-base d performance Population-base d performance • cf-DNA detection modeled • California prenatal screening program 2009-12 • Trisomy 13, 18, 21 and sex chromosome • All singletons with either 1st or Integrated aneuploidy—DETECTABLE result • Mosaic, triploidy, other trisomy, translocations, other • Karyotypes tracked through California rearrangements—UNDETECTABLE Chromosomal Defect Registry • Performance adjusted for condition-specific • No-call rate • Detection rate • “No-call” as “screen positive” also modeled Norton et al, AJOG, 2016 Norton et al, AJOG, 2016

Distribution of chromosome abnormalities 1st Trimester/Integrated Screening vs cf-DNA: 22% Population-based performance % “No- DR cf-DNA % detected % detected T21 Call” by cf-DNA by 1st/Int 3% 15% 1% T18 T21 (n=1275) 3.3 99.2 95.9 92.9 T13 3% T18 (n=336) 10.3 96.3 86.3 93.2 49% SCA T13 (n=143) 12.5 91.0 79.7 80.4 Rare trisomy 10% 45, X (n=161) 17.2 90.3 74.5 80.1 Translocation Other SCA (n=95) 17.2 93.0 76.8 58.9 6% Triploidy Other (n=601) 4.3 0 0 53.7 13% Other All (n=2575) 5.0 70.7 70.7* 81.6 *“No-call” results treated as normal Adapted from Table 2 Norton et al, AJOG, 2016

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Impact of the “others” 1st Trimester/Integrated Screening vs cf-DNA: Population-based performance % “No- DR cf-DNA % detected % detected • 2.6-3.3% of screen-positive women have Call” by cf-DNA by 1st/Int an abnormality not detected by cf-DNA T21 3.3 99.2 99.2 92.9 • Raises question of utility of using as a T18 10.3 96.3 96.7 93.2 T13 12.5 91.0 92.3 80.4 reflex test following abnormal 45, X 17.2 90.3 91.9 80.1 conventional screening test Other SCA 17.2 93.0 93.7 58.9 Other 4.3 0 4.3 53.7 All 5.0 70.7 77.1* 81.6 *“No-call” results treated as Screen Positive Adapted from Table 3 Norton et al, AJOG, 2016

cf-DNA detection: Examination in a cohort with diagnostic testing and CMA • cf-DNA detection modeled • 3,140 karyotypes DON’T use cf-DNA as a replacement for • 208 with karyotype changes diagnostic testing, especially in the setting • 173 clinical significant (83%) of U/S abnormalities • 1,037 array CGH • 100 abnormal results • 53 reflected abnormal karyotype • 47 clinically significant with normal karyotype • TOTAL 220 clinically significant abnormalities Shani et al, AJOG, 2016

cf-DNA detection: Examination in a cohort with cf-DNA detection: Examination in a cohort diagnostic testing and CMA with diagnostic testing and CMA % “No- DR% cf-DNA % detected by Call” cf-DNA • 99 (45%) of 220 clinical significant T21 (+mosaic) 6.9 99.2 92.4 changes undetectable with cf-DNA T18 6.9 96.3 89.7 • 42% due to structural anomaly T13 6.9 91.0 84.7 45, X 17.2 90.3 74.8 • 21% due AMA/anxiety Other SCA 17.2 93.0 77.0 Rare trisomy/ 0 mosaic/rearrangement aCGH abnormalities 0 Shani et al, AJOG, 2016 Shani et al, AJOG, 2016

7 Prenatal Screening: Biggio UAB Progress in OBGYN 2017

What if cfDNA screens for “others”? • Some labs offer screening for: • Tr i p l o i d y • Tr i s o m y 1 6 • Tr i s o m y 2 2 DON’T order microdeletion panels as part • Tr i s o m y 9 of cf-DNA screening • Vanishing twin • Specific microdeletion syndromes • 22q, 1p36, 4p, 5p, 8q, 11q, 15q • Genome-wide screening for imbalances >5-7 Mb

Microdeletion screening PPV Microdeletion screening Routine screening by cfDNA not recommended Microdeletion Prevalence PPV* Syndrome • Population-based studies unavailable 22q11 (DiGeorge) 1/4,000 4% 1p36 1/5,000 3% • Majority do not show ultrasound findings 5p (Cri-du-chat) 1/20,000 1% • Are not related to maternal age 4p (Wolf-Hirschhorn) 1/20,000 1% • Are rare 15q (Angelman) 1/21,000 1% • Low PPV 15q (Prader-Willi) 1/23,000 <1%

Zh a o C et a l, PLoSone, 2 0 1 6

Does adding microdeletions help? • Common panel • 22q11 • 1p36 • 15q11.2-q13 DO Provide patients with • 5p15 appropriate pre-test and post- • Represents only 6-11% of clinically relevant deletions test counseling • Reduces residual risk of significant abnormality from 1.7à1.6% Yaron et al, Obstetrics & Gynecology, 2015

8 Prenatal Screening: Biggio UAB Progress in OBGYN 2017

Develop standard approach to counseling

• Pre-test counseling for all patients is imperative • Can be challenging due to •Time constraints •Rapid advances •Patients’ focus on fetal sex

Important Counseling Topics Informed consent • Reasons why patients would choose to accept screening Patients need to know: • To help them, and healthcare providers, prepare • They can decline all screening or diagnostic testing for the birth of a child with special needs for aneuploidy • Because they might choose not to continue a • cfDNA is a screening test pregnancy with a diagnosed condition • What conditions are (and are not) being screened for • Reasons why patients would decline screening • What the accuracy is re: detection rate, false positive • They do not want this information during rate pregnancy and would not do anything differently • The possibility of a “no call” result • They feel the possibility of abnormal results • Their options if results indicate an increased risk or (whether true or false positive) would ruin the are “no call” experience of pregnancy

Post-test counseling Post-test counseling

• Normal results: • Abnormal results: • Should be disclosed by a medical professional • Ideally should be disclosed by the ordering designated to review this information provider • “Low risk”, not “no risk” • Not diagnostic • Patients still have option to have diagnostic • Refer to genetic counseling or MFM specialist testing with expertise in this area for further evaluation

9 Prenatal Screening: Biggio UAB Progress in OBGYN 2017

Post-test counseling 2015 ACOG/SMFM Committee Opinion 640: Cell-free DNA screening for fetal aneuploidy

• “No call” results: • Conventional screening methods remain the • Consider repeat testing depending on GA most appropriate choice for first-line screening for most women in the general • Refer for genetic counseling and further obstetric population due to evaluation • Limited data on cost-effectiveness in low-risk • Offer comprehensive ultrasound evaluation population and diagnostic testing because of an • Option for any women who desires after increased risk of aneuploidy counseling on risks, benefits and limitations

Summary Summary • Microarray abnormalities may represent • Cf-DNA screening for aneuploidy can provide high nearly 50% of the undetected abnormalities, detection rates and low false positive rates for or 25% of the total abnormalities, especially in common chromosome abnormalities the setting of an anomaly • Imperative to remember that these are still screening • Following an abnormal conventional screening tests result, there remains a 2-3% residual risk of a • Patients need appropriate pre- and post-test chromosome abnormality even with a normal counseling cf-DNA result • Current cf-DNA screening is targeted to specific aneuploidies and does not identify 15-20% of karyotype abnormalities

Question to ponder: Questions?

• Why are we doing prenatal screening? • To identify pregnancies at risk for a finite number of well-defined conditions OR • To identify pregnancies at increased risk for any condition associated with adverse perinatal and childhood outcomes

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Pregnancy-Associated and Other Dermatoses of Young Women

Kelly Tyler, MD, FACOG Division of Dermatology The Ohio State University

No Disclosures

• I have no financial interest or other conflict of interest in relation to this program • I have no relevant financial relationships to disclose

Objectives

• Recognize the most common dermatoses of pregnancy • Recognize other dermatoses affecting women of child-bearing age • Discuss bthboth ma terna l an dftld fetal ou tcomes for each pregnancy dermatosis • Describe treatment options for the various pregnancy dermatoses

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Specific Pregnancy Dermatoses: 1. Polymorphic Eruption of Pregnancy (PUPPP, toxemic rash of preg, toxic erythema of preg, late- onset prurigo of preg) 2. Pemphigoid Gestationis (Herpes gestationis, Gestational pemphigoid) 3. Atopic Eruption of Pregnancy (prurigo of pregnancy, prurigo gestationis, early-onset prurigo of pregnancy, papular dermatitis of pregnancy, pruritic folliculitis of pregnancy, eczema of pregnancy) 4. Intrahepatic Cholestasis of Pregnancy (Obstetric cholestasis, cholestasis of pregnancy, jaundice of pregnancy, prurigo gravidarum) 5. Impetigo herpetiformis (pustular psoriasis)

Dermrounds.com 6

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Polymorphic Eruption of Preg Epidemiology: • Primiparous woman • 1:160 deliveries • in multiple gestations • Does not usually recur Onset: • Late (3rd Trimester) Description: • Plaques,papules,and microvesicles on thighs and abdomen

Polymorphic eruption of Preg

Labs: • None Treatment: •Topp, Steroids, Prednisone Resolution: • Resolves 7-10 days after delivery

• No fetal consequences

Dermamin.org

Polymorphic eruption of Preg

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Pemphigoid Gestationis

Epidemiology: • 1:50,000 pregnancies Onset: •2nd to 3rd trimester Description: • Plaques, vesicles, bullae, spares striae, involves periumbilical area Treatment: • Top Steroids, Prednisone

Pemphigoid Gestationis

Diagnostic Confirmation:

“BP” ELISA Mayo send out. Serum bullous pemphigoid antibodies 1 and 2 generally elevated.

Biopsy for direct IF (perilesional) in saline or Michel’s (Zeus) media.

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Pemphigoid Gestationis Follow-Up: • 10% infants with bullae, SGA (IgG1 antibody crosses placenta) • Typically will flare with subsequent pregnancies • May flare at delivery, subsequent menstrual cycles, with OCPs ** Patients need to be followed for Graves Disease. ** HLA DR3, 4, association.

Pemphigoid Gestationis

Atopic Eruption of Pregnancy Incidence: • Most common pregnancy dermatosis Diagnosis: • Non-specific pathology, normal LFTs & bile acids • 20% have pre-existing atopic dermatitis • Presents earlier in pregnancy Treatment: Top Steroids

Odermatol.org 15

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Cholestasis of Pregnancy

Occurrence: • Generally, 3rd trimester Description: • Pruritus, excoriations +/- jaundice (10%) Diagnosis: • Check conjugated bili, serum bile acids most specific

Cholestasis of Pregnancy

Treatment: • Narrow-band UVB light therapy, ursodeoxycholic acid Consequences: • Meconium staining, abnormal tracing • Premature labor in 20-60% of patients • Fetal mortality 1-2%

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Impetigo Herpetiformis

Pustular psoriasis of pregnancy

- Psoriasis generally improves during pregnancy but may flare .

- Not triggered by infections etc.

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Impetigo Herpetiformis

Look for thin pustules that coalesce into lakes of pus to develop on a base of erythema

Treatment: Cyclosporine.

PEP PG Prurigo of Cholestasis Impetigo Preg Herpetiformis

Previous -+ in PrevAtopic Derm, Fam history, Psoriasis or history Preg General + in prev Fam hx of Derm pregnancies Psoriasis Early vs Late Late Mid-Late Early Late - (variable) Phys Exam Papules, Plaques, Lichenificatio Jaundice +/-, Thin pustules, plaques in microvesicul n, excoriations, may coalesce STRIAE, no ations, Excoriations pruritus bullae Bullae, without umbilicus findings Labs: - + BP ELISA - + Bilirubin Hypocalcemia + Bile Acids Pathology DIF is H&E may be specific specific http://www.kissesforkatie.org/HealthcareProfess 1st Treatment Top Ster Top Ster Top Ster Light therapy Cyclosporine, ionals.html top steroids if limited 23

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Inflammatory Skin Diseases

Pityriasis Rosea:

Likely viral reaction – HHV6, 7.

Resolves on its own 4-6 weeks. Look for Herald Patch and papulosquamous (red scaly) plaques following relaxed skin tension lines on trunk

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Plaque Psoriasis

Most common type Elbows, Knees, Scalp, Sacrum, Fingernails, Widespread May itch Mild disease on elbows and knees will often respond to topical steroids. Generally improves during pregnancy.

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Inverse Psoriasis

Can be subtle as the only type without scale. The maceration and skin on skin contact prevents the silver coloration.

As opposed to intertrigo, sharply well defined, raised, macerated plaques.

Treatment: Low-potency topical steroid, Tacrolimus ointment.

Atopic Dermatitis (AD)

The prevalence of AD is between 15-20% of toddlers and school aged children but decreases with age.

There is an association with the atopic triad: Atopic dermatitis Asthma Allergic rhinitis

There is a defect in skin barrier function and a relative deficiency in lipid ceramide

Psoriasis  Atopic Dermatitis

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Treatment of Atopic Dermatitis (AD)

Moisturization (most important)

Avoid triggers (food allergens, infections, airborne allergens)

Antihistamines

Topical steroids

Contact Dermatitis

Type 4 hypersensitivity reaction: When substance contacts the skin, rash develops 8-48 hours later Rash lasts 7 -28 days Very, very itchy Treatment: Avoidance of substance Oral or topical steroids for flares

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Contact Dermatitis – Nickel

Most common cause of chronic allergic contact dermatitis (up to 10% or more of the population) More common if ears pierced Common sources of exposure: Jewelry (earrings, watches, etc) Clothing (belts, snaps, rivets, etc) Coins, Keys, Eyeglasses Coating items with nail polish not much help Internet for sources of nickel free jewelry

Contact Dermatitis – Fragrance and Preservatives Face, Neck, Hands Common exposures: Shampoo, soap, conditioner, hair products, moisturizer, perfume, deodorant, baby/diaper wipes Very difficult to avoid these substances as even products that say “hypoallergenic” or “dermatologist tested” often have fragrances Allergic patients only react to some fragrances and preservatives

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Contact Dermatitis - Neosporin

Very common, up to 10% of the population is allergic Both Neomycin (most common cause of allergic contact dermatitis from topical medications) and Bacitracin

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Tinea Versicolor

Tinea Versicolor: Scrape for scale, generally on upper body. Treat with pyrithione Zinc otc shampoo tiw to body. Fluconazole if severe

Tinea Corporis

Annular and Acruate plaques with central clearing. Look between toes for confirmation.

Treat with ciclopirox 0.77% cream (B), Clotrimazole 1%, or terbinafine 1% cream (B).

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Ask about known Triggers. If none pinpointed, Titrate cetirizine to 20 mg daily. Can start H2 blocker as well.

If no improvement Refer to derm, can consider further immunosuppres sion

Urticaria

 Itchy, evanescent, and transient wheels  **If greater than 24 hrs in one place, it is not urticaria!!  Common causes include strep infections, drugs, hymenoptera envenomations (wasp/bee stings)  Never scaly  Titrate Antihistamines for treatment.

Acne in pregnancy:

Azelaic Acid (Finacea) – Class B Clindamycin lotion – Class B Benzoyl Peroxide, Sal Acid – Class C Avoid topical retinoids

Orals: Cephalexin TMP/SMX

Tyler, Zirwas. Pregnancy and dermatologic therapy. J Am Acad Dermatol. 2013; 68:663- 71. 48

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Hidradenitis Suppurativa

Underrecognized autoinflammatory disease Affects up to 1% of population.

Strictly involves intertriginous skin with recurrent nodules, pustules, sinus tracts, scarring, purulence and malodor.

Hidradenitis Suppurativa

Treatments:

Topical acne treatments Weight Loss Chronic Antibiotics (Doxycycline 100 mg, clinda/rifampin if not pregnant) Excision and skin grafting

??Adalimumab, infliximab?? Needs referral to dermatology.

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Melanocytic Nevi (Melanoma)

 Pigment darkening normal in pregnancy – estrogen receptor on melanocytes.  If all nevi changing, would defer to after pregnancy  If one nevus is changing, evaluate compare to base line or “s igna ture nevus ” an d if s ign ifican tly different, would recommend biopsying.  Forget the ABCDE, look for “ugly-duckling sign.”

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Circle of Hebra

Location, Location, Location

Interdigital webs, Wrists, Antecubital Fossa Axilla, Breasts Penis

Scabies

 Permethrin 5 % (B) neck down, overnight.  Wash bedclothes in AM.  EiEveryone in house needs treated or will reoccur.

http://www.kissesforkatie.org/HealthcareProfess ionals.html

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Arthropod:

Look for discrete papules “breakfast, lunch, dinner.” Very itchy although others in household may not ihitch.

Treatment: Identify arthropod

http://www.kissesforkatie.org/HealthcareProfess ionals.html

The many faces of Lichen Planus

Numerous Types: Oral Nail Annular Hypertrophic Lichen Planopilaris (Scalp)

Suspected Viral Reaction. Oral disease has an association with hepatitis C. http://www.kissesforkatie.org/HealthcareProfess ionals.html

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Lichen Planus – Classic

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http://www.kissesforkatie.org/HealthcareProfess ionals.html

Lichen Planus – Koebnerization

http://www.kissesforkatie.org/HealthcareProfess ionals.html

Factitial Disease:

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Autoimmune Progesterone Dermatitis

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Luteal phase recurrent skin or mucosal disease.

Polymorphous, can be solely mucosal.

May occur from depo-provera.

Introduction to Topical Steroids:

Courtesy of: http://www.the-dermatologist.com/files/docs/DrugGuide1006.pdf

Topical Steroids You need to know Low: Hydrocortisone 2.5%

Medium: Body – Triamcinolone 0.1%

High Potency: Body, thick plaques – Clobetasol 0.05%

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How safe are topical steroids?

Thank you!

Advanced Reproductive Aging: Pregnancy Risks & Management Strategies Point / Counterpoint

Janet McLaren Bouknight, MD MSCE Associate Professor, Division of Reproductive Endocrinology & Infertility Department of Obstetrics & Gynecology University of Alabama at Birmingham [email protected]

Amelia Sutton, MD PhD Assistant Professor, Division of Maternal Fetal Medicine Department of Obstetrics & Gynecology University of Alabama at Birmingham [email protected]

Educational Objectives

After this session, the participant will be able to:  Counsel women on the decrease in fertility with reproductive aging.  Understand the fertility treatments available to help women of advanced reproductive age conceive.  Recognize the obstetrical risks faced by the “elderly gravida”.

Outline

1. Setting the Stage  Reproductive aging and fertility: What is possible?  Reproductive aging and obstetrical outcomes: What is the risk?

2. REI: Pregnant at 45, why not?  Reproductive aging and loss of ovarian reserve  Fertility treatment to combat age-related fertility decline  Use of Assisted Reproductive Technologies to address aneuploidy risk  Donor oocyte and pushing the reproductive envelope

3. MFM: Pregnant at 45, why run the risk?  Obstetrical risks in women of advanced reproductive age - Hypertensive disorders - Gestational diabetes - Operative delivery - Perinatal mortality  Antenatal care for advanced maternal age patient  Parenting at advanced reproductive age

Select References - Ethics Committee of the ASRM. Oocyte or embryo donation to women of advanced reproductive age: an Ethics Committee Opinion. Fertility and Sterility, 2016, in press. - Female age-related fertility decline. Committee Opinion No. 589. American College of Obstetricians and Gynecologists. Obstet Gynecol 2014;123:719–21 - Sauer MV. Reproduction at an advanced maternal age and maternal health. Fertil Steril 2015; 103: 1136-43. - Paulson RJ, Boostanfar R, Saadat P, Mor E, Tourgeman DE, Slater CC, et al. Pregnancy in the sixth decade of life: obstetric outcomes in women of advanced reproductive age. JAMA 2002; 288:2320-3. - Le Ray C, Scherier S, Anselem O, Marszalek A, Tsatsaris V, Cabrol D, et al. Association between oocyte donation and maternal and perinatal outcomes in women aged 43 and older. Hum Reprod 2012; 27: 896-901.