5 Things to Know About Managing Obesity in Clinical Practice · 2017-11-10 · 5 Things to Know About Managing Obesity in Clinical Practice Taraneh Soleymani, MD, FTOS Assistant Professor

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

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Prenatal Screening in 2017—The DOs and the DON’Ts

Joseph R. Biggio, MDUniversity of Alabama at BirminghamMaternal Fetal Medicine and Genetics

Disclosures

• No financial conflicts to report

Learning Objectives

• Discuss differences between cfDNA screening and conventional screening

• Review performance and limitations of cfDNAscreening 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

• Maternal age should not be sole factor in offering diagnostic test• Aneuploidy screening or diagnostic testing should be offered to all women early in pregnancy

Integrated Screening

• A combination of 1st and 2nd trimester screening tests• 11-‐13 weeks: NT, PAPP-‐A• 15-‐17 weeks: AFP, hCG, estriol, & inhibin

• Final result provided once Quad screen completed

• All testing combined into a SINGLE result

Malone et al., NEJM, 2005;; 353:2001-11


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68 69

8185 86

95

NT Triple Quad NT + PAPPA + hCG

PAPPA + Quad

NT + PAPPA + Quad

Detection Rate for 5% Screen Positive Rate

Integrated tests

Non-‐Invasive Prenatal Testing (NIPT)OR

Non-‐Invasive Prenatal Screening (NIPS)OR

Cell-‐free DNA Screening for Aneuploidy

Placenta Maternal plasma Maternal blood cells

•Cell-free fetal AND maternal DNA fragments in maternal plasma •Placenta→ Fetal DNA•Reliably detected >10 weeks gestation•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

Using cf-DNA screening in your practiceThe DOs and the DON’Ts

The DOs

1. Provide patients with appropriate pre-‐test and post-‐test counseling

2. Refer patients who receive a high-‐risk result for counseling and possible diagnostic testing

3. Order AFP only, NOT a QUAD, in the second trimester for assessment of NTD risk in patients who have had cf-‐DNA screening

4. Offer cf-‐DNA to high risk groups as an option for screening

The DON’Ts1. Don’t tell patients that cf-‐DNA will detect all chromosome

abnormalities and that their fetus is normal if the result is normal

2. Don’t order cf-‐DNA screening in low-‐risk groups just so the patient can finder out gender earlier

3. Don’t order microdeletion panels as part of cf-‐DNA screening

4. Don’t ignore ’No call’ or ‘equivocal’ results; refer patients for counseling and further evaluation

5. Don’t use cf-‐DNA as a replacement for diagnostic testing, especially in the setting of U/S abnormalities

6. Don’t order a targeted U/S in AMA patients if the patient has a low-‐risk cf-‐DNA result and there are no other indications for scan.


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DO order AFP only, NOT a QUAD, in the second trimester for assessment of NTD risk in patients who have had cf-‐DNA screening

Origins of Maternal Serum Screening

• Neural tube defects–1970s elevated AFP in amniotic fluidàserum• Brock et al, 1973; Wald et al, 1974

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

AFP• Elevated– Disruption of fetal-‐maternal-‐placental barrier– Placental vascular damage– Impaired integrity of fetal skin

• Disorders– Neural tube defects– Ventral wall defects– Dermatologic disorders – Congenital nephrosis

AFP for NTD and VWD

• Unclear incremental benefit with modern US for NTD detection–Questionable need in severe lesions–Potential role for distal or difficult to visualize lesions• 9 out of 12 missed cases of NTD, AFP not done—Racusin et al, Am J Perinatol, 2015

• 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-risk groups just so the patient can finder out gender earlier

WHAT IS THE APPROPRIATE POPULATION FOR CELL-FREE DNA TESTING?


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• Appropriate Populations:• AMA• Prior affected• Abnormal screen • Ultrasound abnormality• Robertsonian translocation involving 13 or 21

• Pre- and post-test counseling• Need more information for multiples

Comparison of prenatal screening and diagnostic test options

Test Detection rate for DS

(%)

Screenpositive rate

(%)

PositivePredictive Value (%)

First trimester screen 80 5 ~3

Sequential/Integratedscreen

93 5 ~4-‐6

Cell-‐free DNA screen 99 1-‐9

(in cludes no cal l /test

fai lu res)

40-‐88%

Chorionic Villus Sampling >99 1 (in cludes mosaicism)

Amniocentesis >99 0.2 (in cludes mosaicism)

Adapted from SMFM Consult Prenatal aneuploidy screening with cfDNA. Am J Obstet Gynecol 2015.

Test Comparison: High vs Low Risk

• Prevalence 1 in 1,000–10 will have aneuploid fetus

• Detect 10 aneuploid • 9 false positive

PPV=10/19=53%

• Prevalence 1 in 100–100 will have aneuploid fetus

• Detect 99 aneuploid• 9 false positive

PPV=99/108=92%

In a population of 10,000 womenDetection rate 99.7%, false positive rate 0.1%

DON’T ignore ’No call’ or ‘equivocal’ results; refer patients for counseling and further evaluation

“No call” results (screening failure)

• Not reported, indeterminate, or uninterpretable results

• Occurs in 1-‐8% of patients• 50-‐60% of repeat screens will provide a result

No result significance

• Uninterpretable results associated with• Aneuploidy• Vanishing twin• Maternal malignancy• Mosaicism• 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• Genetic counseling• Targeted ultrasound• Repeat cfDNA testing consideration• 50% get interpretable result• Gestational age and options considerations

• Offer diagnostic testing

DON’T tell patients that cf-‐DNA will detect all chromosome abnormalities and that their fetus is normal if the result is normal

DON’T use cf-‐DNA as a replacement for diagnostic testing, especially in the setting of U/S abnormalities

Current cf-‐DNA platforms: Conditions routinely screened for

• Down syndrome• Trisomy 18 (Edward syndrome)• Trisomy 13 (Patau syndrome)• Sex chromosome aneuploidy (most labs)• Turner syndrome• Klinefelter syndrome• XXX• XYY

Limitations of cf-‐DNA for detection of chromosome abnormalities

• Proportion of chromosome abnormalities due to common trisomies (13,18, 21) depends on population risk, especially maternal age• Ranges from 60-‐75%

• Cannot differentiate mode of inheritance and recurrence risk• Non-‐disjunction trisomy• Translocation• Mosaic

53%

13%

5%

8%

5%

16%

T21T18T13TurnerSex trisomyOther

Distribution of chromosome abnormalities: Livebirths, Fetal death >20

weeks, TOP for anomalies

Adapted from Wellesley et al. , Eur J of Hum Gen, 2012

1st Trimester/Integrated Screening vs cf-‐DNA: Performance in a high-‐risk cohort

• 68,990 screen-‐positive• 26,059 (38%) diagnostic testing• 2,993 (11.5%) abnormal result•83.1% (n=2487) Trisomy 13, 18, 21, sex chromosome aneuploidy—DETECTABLE•16.9% (n=506) UNDETECTABLE—mosaic, triploid, translocation, marker, other

Norton et al, Obstetrics & Gynecology, 2014


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Distribution of chromosome abnormalities (n=2,993)

53%

17%

5%

8%

5%3% 3% 1%

5%T21T18T13SCAMosaicRare trisomyTranslocationTriploidyOther

16.9% 1st Trimester/Integrated Screening vs cf-‐DNA: Performance in a high-‐risk cohort

• 2% of screen positive patients had an abnormal result not detectable by cf-‐DNA

Norton et al, Obstetrics & Gynecology, 2014

1st Trimester/Integrated Screening vs cf-‐DNA: Population-‐based performance

• California prenatal screening program 2009-‐12• All singletons with either 1st or Integrated result

• Karyotypes tracked through California Chromosomal Defect Registry

Norton et al, AJOG, 2016


• cf-‐DNA detection modeled• Trisomy 13, 18, 21 and sex chromosome aneuploidy—DETECTABLE

• Mosaic, triploidy, other trisomy, translocations, other rearrangements—UNDETECTABLE

• Performance adjusted for condition-‐specific• No-‐call rate• Detection rate

• “No-‐call” as “screen positive” also modeled Norton et al, AJOG, 2016

Distribution of chromosome abnormalities

49%

13%

6%

10%

3%1%3% 15%

T21T18T13SCARare trisomyTranslocationTriploidyOther

22%1st Trimester/Integrated Screening vs cf-‐DNA:

Population-‐based performance% “No-‐Call”

DR cf-‐DNA % detected by cf-‐DNA

% detected by 1st/Int

T21 (n=1275) 3.3 99.2 95.9 92.9T18 (n=336) 10.3 96.3 86.3 93.2T13 (n=143) 12.5 91.0 79.7 80.445, X (n=161) 17.2 90.3 74.5 80.1Other SCA (n=95) 17.2 93.0 76.8 58.9Other (n=601) 4.3 0 0 53.7All (n=2575) 5.0 70.7 70.7* 81.6

Adapted from Table 2 Norton et al, AJOG, 2016*“No-‐call” results treated as normal


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% “No-‐Call”

DR cf-‐DNA % detected by cf-‐DNA

% detected by 1st/Int

T21 3.3 99.2 99.2 92.9T18 10.3 96.3 96.7 93.2T13 12.5 91.0 92.3 80.445, X 17.2 90.3 91.9 80.1Other SCA 17.2 93.0 93.7 58.9Other 4.3 0 4.3 53.7All 5.0 70.7 77.1* 81.6

Adapted from Table 3 Norton et al, AJOG, 2016*“No-‐call” results treated as Screen Positive

Impact of the “others”

• 2.6-‐3.3% of screen-‐positive women have an abnormality not detected by cf-‐DNA• Raises question of utility of using as a reflex test following abnormal conventional screening test

DON’T use cf-‐DNA as a replacement for diagnostic testing, especially in the setting of U/S abnormalities

cf-‐DNA detection: Examination in a cohort with diagnostic testing and CMA

• cf-‐DNA detection modeled• 3,140 karyotypes• 208 with karyotype changes• 173 clinical significant (83%)

• 1,037 array CGH• 100 abnormal results• 53 reflected abnormal karyotype• 47 clinically significant with normal karyotype

• TOTAL 220 clinically significant abnormalitiesShani et al, AJOG, 2016


Shani et al, AJOG, 2016

% “No-‐Call”

DR% cf-‐DNA % detected by cf-‐DNA

T21 (+mosaic) 6.9 99.2 92.4T18 6.9 96.3 89.7T13 6.9 91.0 84.745, X 17.2 90.3 74.8Other SCA 17.2 93.0 77.0Rare trisomy/ mosaic/rearrangement

0

aCGH abnormalities 0


Shani et al, AJOG, 2016

• 99 (45%) of 220 clinical significant changes undetectable with cf-‐DNA• 42% due to structural anomaly• 21% due AMA/anxiety


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DON’T order microdeletion panels as part of cf-‐DNA screening

What if cfDNA screens for “others”?• Some labs offer screening for: • Triploidy• Trisomy 16 • Trisomy 22• Trisomy 9• Vanishing twin• Specific microdeletion syndromes

• 22q, 1p36, 4p, 5p, 8q, 11q, 15q

• Genome-‐wide screening for imbalances >5-‐7 Mb

Microdeletion screeningRoutine screening by cfDNA not recommended

• Population-‐based studies unavailable• Majority do not show ultrasound findings• Are not related to maternal age• Are rare• Low PPV

Microdeletion screening PPV

MicrodeletionSyndrome

Prevalence PPV*

22q11 (DiGeorge) 1/4,000 4%1p36 1/5,000 3%5p (Cri-‐du-‐chat) 1/20,000 1%4p (Wolf-‐Hirschhorn) 1/20,000 1%15q (Angelman) 1/21,000 1%15q (Prader-‐Willi) 1/23,000 <1%

Zhao C et al, PLoSone, 2016

Does adding microdeletions help?• Common panel• 22q11• 1p36• 15q11.2-‐q13• 5p15

• Represents only 6-‐11% of clinically relevant deletions

• Reduces residual risk of significant abnormality from 1.7à1.6%

Yaron et al, Obstetrics & Gynecology, 2015

DO Provide patients with appropriate pre-test and post-test counseling


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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

• Reasons why patients would choose to accept screening

• To help them, and healthcare providers, prepare for the birth of a child with special needs

• Because they might choose not to continue a pregnancy with a diagnosed condition

• Reasons why patients would decline screening

• They do not want this information during pregnancy and would not do anything differently

• They feel the possibility of abnormal results (whether true or false positive) would ruin the experience of pregnancy

Informed consentPatients need to know:• They can decline all screening or diagnostic testing for aneuploidy

• cfDNA is a screening test • What conditions are (and are not) being screened for• What the accuracy is re: detection rate, false positive rate

• The possibility of a “no call” result• Their options if results indicate an increased risk or are “no call”

Post-‐test counseling

• Normal results:• Should be disclosed by a medical professional designated to review this information

• “Low risk”, not “no risk”• Patients still have option to have diagnostic testing

• Abnormal results:• Ideally should be disclosed by the ordering provider

• Not diagnostic• Refer to genetic counseling or MFM specialist with expertise in this area for further evaluation

Post-test counseling


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• “No call” results:• Consider repeat testing depending on GA• Refer for genetic counseling and further evaluation

• Offer comprehensive ultrasound evaluation and diagnostic testing because of an increased risk of aneuploidy

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

• Conventional screening methods remain the most appropriate choice for first-‐line screening for most women in the general obstetric population due to • Limited data on cost-‐effectiveness in low-‐risk population

• Option for any women who desires after counseling on risks, benefits and limitations

Summary

• Cf-‐DNA screening for aneuploidy can provide high detection rates and low false positive rates for common chromosome abnormalities

• Imperative to remember that these are still screening tests

• Patients need appropriate pre-‐ and post-‐test counseling

• Current cf-‐DNA screening is targeted to specific aneuploidies and does not identify 15-‐20% of karyotype abnormalities

Summary

• Microarray abnormalities may represent nearly 50% of the undetected abnormalities, or 25% of the total abnormalities, especially in the setting of an anomaly

• Following an abnormal conventional screening result, there remains a 2-‐3% residual risk of a chromosome abnormality even with a normal cf-‐DNA result

Question to ponder:

• 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

Questions?

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Pregnancy-Associated and Other Dermatoses of Young Women

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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

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Objectives

• Recognize the most common dermatoses of pregnancy

• Recognize other dermatoses affecting women of child-bearing age

Di b th t l d f t l t f

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• Discuss both maternal and fetal outcomes 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

f f

4

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)

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Dermrounds.com

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Polymorphic Eruption of PregEpidemiology:

• Primiparous woman

• 1:160 deliveries

• in multiple gestations

• Does not usually recur

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Onset:

• Late (3rd Trimester)

Description:

• Plaques,papules,andmicrovesicles on thighs and abdomen

Polymorphic eruption of Preg

Labs:

• None

Treatment:

• Top Steroids, Prednisone

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Dermamin.org

p ,

Resolution:

• Resolves 7-10 days after delivery

• No fetal consequences

Polymorphic eruption of Preg

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Pemphigoid Gestationis

Epidemiology:

• 1:50,000 pregnancies

Onset:

• 2nd to 3rd trimester

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Description:

• Plaques, vesicles, bullae, spares striae, involves periumbilical area

Treatment:

• Top Steroids, Prednisone


Diagnostic Confirmation:

“BP” ELISA Mayo send out.

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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 GestationisFollow-Up:

• 10% infants with bullae, SGA (IgG1 antibody crosses placenta)

• Typically will flare with subsequent pregnancies

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subsequent pregnancies

• May flare at delivery, subsequent menstrual cycles, with OCPs

** Patients need to be followed for Graves Disease.

** HLA DR3, 4, association.


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Atopic Eruption of PregnancyIncidence:

• Most common pregnancy dermatosis

Diagnosis:

• Non-specific pathology, normal LFTs & bile acids

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Odermatol.org

normal LFTs & bile acids

• 20% have pre-existing atopic dermatitis

• Presents earlier in pregnancy

Treatment: Top Steroids

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Cholestasis of Pregnancy

Occurrence:

• Generally, 3rd trimester

Description:

• Pruritus, excoriations +/-jaundice (10%)

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jaundice (10%)

Diagnosis:

• Check conjugated bili, serum bile acids most specific

Cholestasis of Pregnancy

Treatment:

• Narrow-band UVB light therapy, ursodeoxycholicacid

Consequences:

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• Meconium staining, abnormal tracing

• Premature labor in 20-60% of patients

• Fetal mortality 1-2%

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19

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Impetigo Herpetiformis

Pustular psoriasis of pregnancy

- Psoriasis generally improves during pregnancy but may flare

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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

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develop on a base of erythema

Treatment: Cyclosporine.

PEP PG Prurigo of Preg

Cholestasis ImpetigoHerpetiformis

Previous history

- + in PrevPreg

Atopic Derm, General Derm

Fam history,+ in prevpregnancies

Psoriasis or Fam hx of Psoriasis

Early vs Late Late Mid-Late Early Late (variable)

-

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http://www.kissesforkatie.org/HealthcareProfessionals.html

Phys Exam Papules,plaques in STRIAE, no bullae

Plaques,microvesiculations, Bullae, umbilicus

Lichenification, Excoriations

Jaundice +/-, excoriations, pruritus without findings

Thin pustules,may coalesce

Labs: - + BP ELISA - + Bilirubin+ Bile Acids

Hypocalcemia

Pathology DIF is specific

H&E may be specific

1st Treatment Top Ster Top Ster Top Ster Light therapy Cyclosporine,top steroids if limited

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Inflammatory Skin Diseases

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Pityriasis Rosea:

Likely viral reaction – HHV6, 7.

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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

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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.

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

Treatment: Low-potency topical steroid, Tacrolimusointment.

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

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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

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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

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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:

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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

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Contact Dermatitis – Fragrance and Preservatives

Face, Neck, Hands

Common exposures:Shampoo, soap, conditioner, hair products, moisturizer,

perfume, deodorant, baby/diaper wipes

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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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Bacitracin

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Tinea Versicolor

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Tinea Versicolor:

Scrape for scale, generally on upper body. Treat with pyrithione

Zinc otc shampoo tiw to body. Fluconazole if severe

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Tinea Corporis

Annular and Acruate plaques with central clearing.

Look between toes for confirmation.

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Treat with ciclopirox 0.77% cream (B), Clotrimazole 1%, or terbinafine1% 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.

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If no improvement Refer to derm, can consider further immunosuppression

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)

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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

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Avoid topical retinoids

Orals:

Cephalexin

TMP/SMX

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

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Hidradenitis Suppurativa

Underrecognized autoinflammatory disease

Affects up to 1% of population.

Strictly involves intertriginous skin with recurrent

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

Hidradenitis Suppurativa

Treatments:

Topical acne treatments

Weight Loss

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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 b li “ i t ” d if i ifi tl

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baseline or “signature nevus” and if significantly 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

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Axilla,

Breasts

Penis

Scabies

Permethrin 5 % (B) neck down, overnight.

Wash bedclothes in AM.

E i

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Everyone in house needs treated or will reoccur.

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Arthropod:

Look for discrete papules “breakfast, lunch, dinner.”

Very itchy although others in household

i h

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may not itch.

Treatment: Identify arthropod

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The many faces of Lichen Planus

Numerous Types:

Oral

Nail

Annular

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Annular

Hypertrophic

Lichen Planopilaris (Scalp)

Suspected Viral Reaction. Oral disease has an association with hepatitis C.

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Lichen Planus – ClassicThe image part with relationship ID rId2 was not found in the file.

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Lichen Planus – Koebnerization

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Factitial Disease:

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Autoimmune Progesterone Dermatitis

Luteal phase recurrent skin or mucosal disease.

The image part with relationship ID rId2 was not found in the file.

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Polymorphous, can be solely mucosal.

May occur from depo-provera.

Introduction to Topical Steroids:

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

Low: Hydrocortisone 2.5%

Medium: Body –

Topical Steroids You need to know

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Triamcinolone 0.1%

High Potency: Body, thick plaques – Clobetasol 0.05%

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How safe are topical steroids?

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Thank you!

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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.

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