ESAP 2018 ENDOCRINE SELF-ASSESSMENT PROGRAM QUESTIONS, ANSWERS, DISCUSSIONS ENDOCRINE BS Seen —ESAP” 2018 Endocrine Society’s Endocrine Self-Assessment Program Questions, Answers, and Discussions Kristien Boolaert, MD. ‘Readerin Endocrinology Center for Endocrinology, Diabetes, and Metabolism University of Birmingham Barbara Gisella Carranza Leon, MD Assistant Professor of Medicine Division of Diabetes, Endocrnoiogy, and Metabolism Vanderbilt University Mecical Center ‘Stephen Clement, MD Mecical Director, Endocrine Services Inova Fairfax Hospital Kathryn MeCrystal Dahir, MD Assistant Professor of Medicine Division of Endocrinology ender University Medical Conter ‘Thomas W. Donner, MD. Associate Professor of Medicine Division of Endocrinology, Diabetes, and Metabolism Johns Hopkins University Endoorine Society Usa R. Tannock, MD, Program Chair Professor of Medicine Chief, Dirision of Endocrinotogy ‘and Molecular Medicine University of Kentucky and Department of Veterans Affairs ‘Marie Freel, MB, ChB, PhD Consuttant Endocrinologist (Queen Eilzabeth University Hospital Glasgow, United Kingdom (Mimi Hu, MD Associate Professor Department of Endocrine Neoplasia land Hormonal Disorders University of Texas MD Anderson Cancer Center Michael 8. rwig, MD Associate Professor George Washington University ‘Jacqueline Jonklaas, MD, PhD Professor Division of Endocrinology and Metabolism Georgetown University Steven Magi, MD, PhD ‘Associate Clinical Professor of Medicine Endocrinology, Diabetes, and Metabolism ‘Medical College of Wisconsin 2055 L Street NW, Suite 600, Washington, DC 20036 1-888-ENDOCRINE * www.endocrine.org Deepika Reddy, MD Assistant Professor Division of Diabetes, Endocrinology, ‘and Metabolism University of Utah Healthcare Roberto Salvatori, MD Professor of Medicine Medical Director, dehns Hopkins Pituitary Center Johns Hopkins University Savitha Subramanian, MD Associate Professor of Medicine University of Washington ‘Anand Vaidya, MD, MMSC Assistant Professor of Medicine Brigham and Women's Hospital Harvard Medical Schoo! Corrine Welt, MD Professor of Medicine University of Utah Schoo! of Medicine Abbie L. Young, MS, CGC, ELS(0) Medical Editor ENDOCRINE BS SOCIETY tuaenn = “Te Endocrine Society isthe words ages. oldest, and most active organization working to advance the erica! practice a endocrinology and hormone esearch. Founded 11916, the Society now has more han 1,000 lot members aes arange of ‘scipines. The Socely hss sered an iteration reputation for excaloce nthe ual of ts pescreviewed journals, educational resoucse, meetings and programs that Imgrove pubic eath trough the pracce and sence of endocrinology. Visits a ther Publications: ‘eveaton endocrine. preesendoctine og endoctne.ra “To statements and opinions exressed|i tis pubiaton are those of he nd auhors ‘and do rok nccossary rie th vews ofthe Endoerne Society The Endocrine Sit not reeponabie or lable any way forthe carey ofthe rfarmaton fray ers, cisions Inaccuraces, for ny consequenosearing throm, With respect to ay uss mentioned ‘tha readers adie refer tothe appropriate mecca erature and the product rormation caer provided by the manufactur very appropiste dosage, method and ation (tadninraton, and ober rdevatiformaton. In alinstances, Ms the responsi fhe ‘rear pyacon or ctor heath care professors, ying on independent expsence and ‘experte, aswel as knowledge fhe patient to deterine the best teatant forthe patent PERNISSIONS: For pomision to reuse materi plese acess hpy/wiw copyr@htcom cor const the Copyright Clearance Garter ne. (CCC), 222 Rosewood Ove, Danvers | Ma01823, 078-750-8400, CCC is aron-cr-roi cganzation tat provides Scenes anc reaitaton for a vary of ves. For mre ntrmatio, individ or efor purest, ‘nase cortact Member Services by telephone a 202-871-9646 or 888-365-6762; eal inioendosine org or st he cine store at wer endocrne.o/sto, copyigtt ©2018 by the Endocrine Sect, 2055 L Sree NV, Sit 600, Westington 100.2006, Aliht eserved. No pata this pubiton may be reprodod,storedin retiova sytem, pstedon the Iter, or rane in any fr, by ay means, econ ‘mechanical photocopying, recog, oF ctherwise, without writen permission oe pulse TRANSLATIONS AND LICENSING: Right 1 tana and raprocice Endocrine Society ‘pubicatons international are extended through aieensing agreement on flr pati ‘ations To request rights for aloea ection, please contact Ray Thibodeau, Contnt Ed Net LL, by one (USA 267-895-1758 a -mal ry tibodeau@contentenet com. Igen:976-1-878205-81-1 LUbrary of Congrats Corr Number: 2017951680 ‘On the Gover: Lot: Xray ofthe ight em showing aras ef tral cortical thickening that cause a *bsoking”o“tarng” fc achacent to areas of transverse rectus, which evry ‘vole and propagate medal and utmatay leas to a complete ature Ici: PEECT showing fuorodeonyehcose-aid salt metastatic disease the ight scapula, several i, horacourba vrata, pois, the right vertebra Body ofS, andthe {aoum ia patent wih radoiodne rfactor cleontsted hye cancer Fight Unennanced CT ofthe ackenal ands showing mutple nnpigmertad noes ager ‘han 10 mmin elaneterin oth acrenals in a pation wih bie macrorolar acronal yperlaiOVERVIEW ‘The Endocrine Self-Assessment Program (ESAP")is a selt- study curriculum aimed at physicians seeking intial certification ‘or recertification in endocrinology, program cirectors interested in a testing and training instument, and clinicians simply wanting a sel-assessment and a broad review of endocrinology. ESAP 2018 is available in both print and online formas. It Consists of 120 brand-new multiple-choice questions in all areas ‘of endocrinology, ciabetes, and metabolism. There is extensive clscussion of each correct answer, @ comprehensive sylabus, and references. ESAP is updated annually with new questions and new syllabus materials. ESAP is composed of two key components: the initial online interactive module and the printed book. Upon purchase, learners wil initialy receive accass to the online module. To use ESAP as a true self-assessment tool, learners are strongly encouraged to complete the online interactive self-assessment module frst before continuing self-study with the printed book; the online module may be accessed at education enclocrine.org, ACCREDITATION STATEMENT ‘The Endocrine Society is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical ‘education for physicians. The Endocrine ‘Society has received Accreditation with ‘Commendation. The Endocrine Society designates this enduring material for a maximum of 40.0 AMA PRA Category 1 Crecits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity 1A (CME activity, which includes participant to earn up to 40 MOC points in the American responsibility to submit participant completion information to MAINTENANCE OF CERTIFICATION Stowe compton hi aa occ meres — ERY Corporat enable the far orn accn: AB Hahtorane of Certeaton (406) progam ts the CME ety rovers th Arto Coa fr Contr Mesa Education fore purpose of ganing Aa HOC eet LEARNING OBJECTIVES ESAP 2018 will allow learners to assess thei knowledge of all aspects of endocrinology, diabetes, and metabolism, Upon completion of this educational activity, learners will be able to: ‘+ Recognize clinical manifestations of endocrine and ‘metabolic disorders and select among eurrent options for diagnosis, management, and therapy. + Identity risk factors for endocrine and metabolic disorders and develop strategies for prevention. + Evaluate endocrine and metabolic manifestations of systemic disorders, * Use existing resources pertaining to clinical guidelines ‘and treatment recommendations for endocrine and related metabolic disorders to guide diagnosis and treatment, ‘TARGET AUDIENCE ESAP is a self-study curriculum aimed at physicians seeking intial certification or recertification in endocrinology, program irectors interested in a testing and traning instrument, and clinicians simply wanting a self-assessment and a broad review of endocrinology. ‘STATEMENT OF INDEPENDENCE ‘As a provider of CME accredited by the Accreditation Council for Continuing Medical Education, the Endocrine Society has a policy of ensuring that the content and quality ofthis educational activity are balanced, independent objective, and scientifically rigorous. The scientific content of this activity was developed under the supervision of the Endocrine Society's ESAP Faculty Working Group, DISCLOSURE POLICY The facuity, committee members, and staff who are in position to control the content ofthis activity are required to disclose to the Endocrine Society and to learners any relevant financial elationship(a) ofthe individual or spouse/ partner that have occurred within the last 12 months with any commercial interest(s) whose products or services are related to the CME content. Financial relationships are {defined by remuneration in any amount from the commercial interest(s) in the form of grants; research support; consulting ‘ees; salary; ownership interest (eg, stocks, stock options, fr ownership interest excluding diversified mutual funds); honoraria or other payments fr participation in speakers! bureaus, advisory boards, or boards of directors; or other financial bonofits. The intent of this disclosure is not to prevent CME planners with relevant financial relationships {rom planning or delivering content, but rather to provide learners with information that allows them to make their own judgments of whether these financial relationships may have influenced the educational activity with regard to exposition ‘or conclusion. The Endocrine Society has reviewed all disclosures and resolved or managed all identified conflicts of interest, as applicable. ‘The following faculty reported relevant financial ‘olationship(s: Thomas W. Donner, MD, isa study site principal investigator for Novo Nordisk. Mim! Hu, MD, is @ primary investigator for AstraZeneca. Michael Irwig, MD, served as male hypogonadism faculty for Medscape. ESAP 2018 3Roberto Salvatori, MD, receives grant support from [National Institutes of Health and the Department of Defense; ie a reviewor for the National Institutes of Health; and is ‘an investigator for Prizer Novartis, Chiasma, Milendo ‘Thorapeutics, and Strongbridge Biopharma, Savitha ‘Subramanian, MD, receives grant support from lonis: Pharmaceuticals. Anand Vaidya, MD, recelved grant support {rom the National Institutes of Health and the Doris Duke ‘Charitable Foundation. Corrine Welt, MD, isa writer for UpToDate and a consultant for Takeda, The following faculty members reported no relevant financial relationships Kristien Boetaert, MD; Barbara Gisella Carranza Leon, MD; Stephen Clement, MD; Kathryn Dahir, MD; Marie Freel, MD: Jacqueline Jonklaas, MD, PhD; Stoven Magill, MD; Deepika Reddy, MD; and Lisa R. Tannock, MD. “The medical editor for this program, Abbie L. Young, MS, CGC, ELS(0), reported no relevant financial relationships, ‘The Endocrine Society staf associated with the development of content for this activity reported no relevant ‘financial relationships. DISCLAIMERS ‘The information presented in this activity represents the ‘opinion ofthe faculty and is not necessarily the official position of the Endocrine Society. USE OF PROFESSIONAL JUDGMENT: ‘The educational content inthis self-assessment test relates, 10 basic principles of diagnosis and therapy and does not substitute for individual patient assessment based on the health care provider's examination ofthe pationt and Consideration of laboratory data and other factors unique to the pationt. Standards in medicine change as new data become available. DRUGS AND DOSAGES: |When prescribing medications, the physician is advised to ‘check the product information sheet accompanying each drug to verlty conditions of use and to identity any changes in drug dosage schedule or contraindications. POLICY ON UNLABELED/OFF-LABEL USE ‘The Endocrine Society has determined that disclosure of unlabeled/of-label or investigational use of commercial product(s) is informative for audiences and therefore requites this information to be disclosed to the learners at the beginning of the presentation. Uses of spectic therapeutic agents, devices, and other products ciscussed In this educational actvity may not be the same as those indicated in product labeling approved by the Food and Drug ‘Administration (FDA). The Endocrine Society requires that any discussions of such “off-label” use be based on scientific 4 ESAP 2018 research that conforms to generally accepted standards of experimental design, data collection, and data analysis. Before recommending or prescribing any therapeutic agent or device, learners should review the complete prescribing information, including indications, contraindications, warnings, procautions, and adverse events, PRIVACY AND CONFIDENTIALITY STATEMENT ‘The Endocrine Society will record learner’s personal information as provided on CME evaluations to allow for isauance and tracking of CME certificates. The Endocrine Society may aiso track aggregate responses to questions in activites and evaluations and use these data to inform the ‘ongoing evaluation and improvement ofits CME program. No individual performance data or any other personal information collected from evaluations will be shared with third parties ACKNOWLEDGMENT OF COMMERCIAL ‘SUPPORT This activity is not supported by educational grants) or other funds from any commercial supporter. AMA PRA CATEGORY 1 CREDIT (CME) INFORMATION To receive a maximum of 40.0 AMA PRA Category 1 Credits, participants must complete the online interactive module ‘and activity evaluation located at education endocrine.org Perticipants must achieve a minimum score of 703% to claim CME credit. After intialy completing the module, it participants do not achieve a minimum score of 70%, they have the option to change their answers and make additional attempts to achiave a passing score. Learners also have the option to clear all answors and start over. METHOD OF PARTICIPATION “Ths enduring material Is presented online and in print format “The ostimated time to complete this activity, including review of material, is 40 hours. Participants must achieve @ ‘minimum seare of 709% to claim CME credit and MOC points. ‘After initially completing the module(s),f participants do ot achieve a minimum score of 70%, they have the option ‘to change their answors and make additional attempts to achieve a passing score, Participants also have the option to Clear all answers and start over. ‘SYSTEM REQUIREMENTS ‘To complete this activity, participants must have access to a ‘computer or mobile device with an Internet connection and tuce an up-to-date Web browser. In addition, cookies and ‘Javascript must be enabled in the browser's options. LAST REVIEW DATE: Septomber 2017ACTIVITY RELEASE DATE: March 14, 2018 ACTIVITY EXPIRATION DATE: Apri 30, 2020 (date after which this enduring material Is no longer certified for ‘AMA PRA Category 1 Credits and ABIM Medical Knowledge MOC points) For questions about content or obtaining CME credit or MOC points, please contact the Endocrine Society at http:/education. endocrine org/contact. ESAP 2018 5Laboratory Reference Ranges Reference ranges vary among laboratories. Conventional units ae listed first with SI units in parentheses, Lipid Values High donety lipoprotein (HDL) cholosterot 60 moi. (1.55 mmoUL) 0-60 mala. (1.04-1.55 mov) += <0 gil (1.04 mmol) sty lipepeoten (LDL) cholesterol ~<100 mg/dl. (<2 59 mma) — 100-128 mg/l. (2.59-9.94 mot) (20-159 mg/d. (837-412 mmovL) 160-189 m/l. (4.14-4.60 mmol) 180 mg/L (24.82 mmol) Optimal <190 mg/Al (<3.87 mmol) Bordedine-igh ~ = 190-159 mg/d (3:37-4:12 mmo) Hon 2240 mg/d (26.22 mmol) ‘Tota cholester! Optimal <200 mpi. («5.18 memo) Bordertine-high ~ 200-259 ma/al. 6.18-6.18 mov) High 240 mld. (26.22 mmoVL) Tigycerdes 150 ma (<3.88 merit) 150-189 mg/L. (.68-5.16 mmol} 100-499 mpl (6. 18-12.92 meno} 500 moja. (412.95 molt) ~ 230 mafdl (1.07 uo) Apoipoprotein 8 50-410 maja. (05-11 g/L) Hematologic Values Erytvocyte sedimentation rate meen 020 mma Haptoglobin 30-200 mg/l. (00-2000 mg/t) Hematocrt-——~ —-41%-50% (041-051) (ale 5%-45%6 (.35-0.45) (female) Hemoglobin A 4.094-5.6% 20-38 mmovmo) Hemegltin- 198-172 gf (198-172 gL (malo, 12.1-1541 gf (121-151 g/t) emale) International normalized rat Mean corpuscular volume (MCV) Plateet count Protein ota) Roticulooyte count nite biood cell count 0842 80-100 ym* (80-100 iL) 150-450 x 10%}A. (150-450 « 1071) 9-79 gid (68-79 9) 0.5%-1.5% of rd blo calls 0.005-0.018) 4500-11,000/pL (4.5-11.0 10%) ‘Thyroid Values: ‘Thyoglobulin---3-42 ng/ml @-42 po/L) (after surgery and radioactive ioxine toatment:<1.0 ng/ml [1.0 voit ‘Tryroglobutn antbodtes ~ ‘Tayrotropin TSH) 4.01U/m (240K) 05-50 mis, “Thyoid-stinuating immunoglobulin 120% of basal activity Tyroneronidase (TPO) antibodies <2.0 UimL (<2. KUL) Thyroxine 7) (hoo) (06-18 ngia. (10:30-28.17 pov) Thyroxine (7) (ota ~ 5.5125 pod. (04.02-213.68 amo/t) Free thyroxine (7) indx “ilodathyronine 7) (reo) Tlodotnyronine (, (ota Triodothyronine (T, reverse Tilodotnyronine upta Radioactive iodine uptake: 412 2.0-4.2 pgm (3.59-5.45 pri) 70-200 ng/L (1.08-9.08 nail) 10-28 agi. (0.15-0.37 reno) resin 2556-389 396-1686 (6 hours): 159%-30% (24 hours) Endocrine Values, Serum Aldosterone 21 ng. (111.0-882.5 pmol) Alkane phosphatase 50-120 UML (0.84-2.00 pat) Aaline phosphatase (bore-spectc) ~ 20 9) (adit male); ‘14 yi (oremencpausal femal); «22 poi. (postmencpausa femal) Androstenedione -----65-210 ng (2.27-7 83 nm) (adult male, 0-240 ng/dl. 279-838 nmol) (adult female) ‘Artimuteran hormone 07-19.0 ng/mL 6 0-195.7 pmol) (rato, >12 years: 0.9-95 ng/mL (64-67.9 pmol) (femal, 18-45 years 1.0 ngiml. (<7.1 pei) female, >45 years) Caetonin. 16 pom. («4.87 pmo) (basal, male << poyml. (2.34 pmoVL) (basal, emai), £120 pg/mL. -87.98 pro) (peak calcum intsion, male 80 pg/mL (26.28 pal (peak caeium infusion, female) CCarcinoembryenie antigen 25 ngimt (25 pa) CChromagranin A~ -<88 ng/me (03 p91) Corticosterone-—-—--- 63-1560 ng/l. (1.53-45.08 meV} (>18 years) Coticotopin (ACTH 10-60 pgiml.(22-13.2 pmol) Cortisol (6 AM 6-25 pola. (197-9-889.7 nmoVt) 2-14 yall. (55.2-386.2 nmol) C-peptide -0.9-4 ngiml. (030-442 nmol) CC-oactve protein 0.83.1 mai (7.62-28.52 nmoVt) Crosslinked N-tolopoptide of type 1 collagen ~ 5.4:24.2 nmol BOE/mmel creat (mae 16.2-19.0 nmol BCE/mmel creat (erate) DDetycroepiandrosteronesuifate (OHEA-S) Patient Age. Female Mae 18-29 years 44-922 g/dL 89-457 pola (0,19-9.00 pmolt)(2.41-12.38 pmolA) 30-39 years 31-228 old 65-934 pala. (0.64-6.78 pmol) (.76-8.05 ymovt) 40-49 years 18-284 g/dl 48-284 volo (049-651 pmol) (1.80.61 umol) 6 ESAP 2018Patent Age Female Maio 5059 years 15-200 p9/d. 35-179 g/dL (041-542 umolL) (085-4.85 pmol) 60 years 1SAST gd 25-131 pole. (0.41-4.25 mol) (068-85 ymotL) Deoxycartcosterone -<1O gid. (<0:30 nmol [18 years) +,25:Ditydroxyvitamin D, 16-85 pai. (41.6-160.0 pmol) Estradiol 10-40 py/mt. (8.7-146.8 pmol) (rate); 10-180 pg/mL. (6.7-€60.8 pmol oliculr, ferme) 100-300 p/m. (867.1-1101.8 pmoVly (mideyce, female; 40-200 pg/mL (146.8-738.2 pmol) (tea, eal) <20 pg/mL. (<73.4 pmoUL) (pestmenopaueal, eal) Estrone 10-60 pail (37.0-221.9 pmol) (mate) 17-200 pa/mi.(62.9-739.6 pmol oremenopausal femal) 7-40 lil. @5:8-147.9 pmoUL) (postmenopausal femal) @-Fetopetein- = -<6 ng/ml (<6 yo) Follicle-stmulating hormone (FSH). — 1.0-180 miUimL (1.0-13.0 UA} (mate 60 mL/min per 1.73.m? S:Hydroxyindole acetic acd 2-9 mg/24 h(10.5-47-1 pi/8) ledine fandom) S100 ug {1 Ketosteroids 6.0-21.0 mg24h 20.8-72.9 pmol (mae), ‘40-17.0 mg/24h (13.9-58.0 uml) (female) Metanepivine fractionation Metanepiine ——~ Noretanephrine: <10 ug/28 n ~<400 24 h (2028 nmol 2900 4924 h (4914 row 1000 y9/24h (<5260 nmol) 450-1150 mOsnvkg (150-1150 mmoVkg) -<40 mg/24 h (456 mmole) 19-13 g/24h (29.1-42.0 mous) 17-77 mEgi28 (17-77 omoleh 8 ESAP 2018Sodum. rie asia 40-217 mEg/24h (40-217 mmo -<800 me/24 h (<4.7 mmol Saliva ‘Cortisol salivary), mcg <0.13 pic (<3.6 mot) ‘Semen Semen analyse 220 nillon spermvimb; >60% motility acm ACE inhibitor orticotrapin _angotensin-converting enzyme inhibitor alanine aminovaneteras0 aspartate aminotransferase body mass indox central nervous system ‘computed tomography -dehydreopiandrostorone enycroepiandrosterone sulfate sdeoxyribonuclee acid duahenesgy xray absorptiometry Food and Drug Acinistation fine-needle aspiration biopsy ‘olcle-stmuiatng hormone “growth hornene ‘grovth hormone-reieasing hormone ‘oenadotropin-elasing hormone human chosionie gonadotropin high-density ipoprotein human immunedeficioncy virus coenzyme A reductase inhibitor oF ESAP 2018 910 ESAP 2018—QUESTIONS ENDOCRINE SELF-ASSESSMENT PROGRAM 2018 Part I‘A 59-year-old man with an 18-year history of diabetes mellitus is being treated with insulin glargine and metformin, He has had longstanding hypertension, hyperlipidemia, and renal insufficiency, but no previous heart attack or stroke. His review of systems is negative. He stopped smoking cigarettes 2 years ago. He asks for recommendations to help him reduce his risk of a cardiovascular event. Both his father and patemal uncle have diabetes and developed coronary artery disease requiring stenting. His medication regimen is as follows: insulin glargine, 36 units at bedtime; metformin, 500 mg twice daily; atorvastatin; lisinopril; hydrochlorothiazide; and amlodipine. (On physical examination, his blood pressure is 138/82 mm Hg and pulse rate is 88 beats/min. His height is 73.5 in (186.7 cm), and weight is 247 Ib (112 kg) (BMI = 32.1 kg/m’). Eye examination reveals bilateral retinal microaneurysms. On cardiac examination, he has a regular rate and rhythm, a loud S,, no S,, and no murmurs. ‘There are no carotid bruits. His abdomen is obese with no striae or renal bruits. On neurologic examination, there is symmetric decreased light touch and vibration sense in both feet. Laboratory test results: Hemoglobin A, = 8.3% (4.0%-5.6%) (67 mmolimol [20-38 mmol/mol]) Fasting glucose ~ 142 mg/dL (70-99 mg/AL) (SI: 7.9 mmoVL [3.9-5.$ mmoVL]) Serum urea nitrogen = 31 mg/aL (8-23 mg/dL) (St: L1.1 mmol/L (2.9-8.2 mmoV/L}) Creatinine = 1.8 mg/dL (0.7-1.3 mg/aL) (St: 159.1 wmoVL [61.9-114.9 wmol/L)) Estimated glomerular filtration rate = 40 mL/min per 1.73 m (60 mL/min per 1.73 m?) Liver function, normal You decide to add therapy. Which of the following is the best agent for this patient? Premeal aspart insulin Glipizide ‘Acarbose Sitagliptin Liraglutide moow> You are asked to evaluate a 24-year-old man who collapsed during an outdoor music festival 3 days earlier. Since his arrival at the hospital, he has developed intractable hypoglycemia, which has required a continuous 10% dextrose infusion. He has no notable medical history. He takes no regular prescribed medications, but he did consume amphetamines while at the music festival, His mother has type 2 diabetes mellitus treated with glibenclamide and metformin, On physical examination, he is alert and oriented. He is centrally obese with some purple striae over his abdominal wall and inner thighs. His height is 70 in (177.8 cm), and weight is 224 Ib (101.8 kg) (BMI = 32.1 kg/m’), His blood pressure is 148/99 mm Hg, and pulse rate is 90 beats/min. Laboratory test results (on 10% dextrose infusion): Sodium = 135 mEq/L (136-142 mEq/L) (SI: 135 mmoV/L [136-142 mmoVL]) Potassium = 4.2 mEq/L (3.5-5.0 mEa/L) (St: 4.2 mmoVL [3.5-5.0 mmoVL)) Serum urea nitrogen = 14 mg/dL (8-23 mg/dL.) (SI: 5.0 mmoV/L [2.9-8.2 mmol/L]) Creatinine = 0.9 mg/AL.(0.7-1.3 mgldL) (SI: 79.6 urnoV/L [61.9-1149 ymoV/L]) Glucose = $3 mg/al (70-99 mg/dL (SI: 2.9 mmol/L [3.9-5.5 mmoV/L]) Insulin = 0.2 ulUlmL (1.4-14.0 ulUimL) (SI: 1.4 pmoVL.[9.7-97.2 pmoVL}) C-peptide = 0.1 ng/mL (0.9-4.3 ng/mL) (St: 0.03 nmoV/L 0.30-1.42 nmoVL)) B-Hydronybutyrate= 0.12 mg/aL. (<3 mg/dL) (Sk: 11.5 pmoV/. [<300 jmoV/L]) TSH~ 1.4 m{UML (055.0 mIU/L) Free T,= 1.2 ng/4L.(0.8-1.8 ng/dL) (SI: 15.4 pmol/L (10.30-23.17 pmol/L) Early morning serum cortisol = 24 yg/dL (5-25 pg/L) (SI: 662.1 nmol/L [137.9-689.7 nmoV/L]) ESAP 2018—QUESTIONS 11CT of the abdomen is shown (see image). Which of the following tests is most likely to reveal the cause of this patint’s hypoglycemia? ‘ACTH stimulation test Arterial calcium stimulation test Urinary toxicology sereen Plasma sulfonylurea screen Serum IGF-2 to IGF-I ratio moop> You are asked to consult on a 43-year-old woman with a history of hypocalcemia. Sensorineural hearing loss was diagnosed at birth, This has progressed to 90% hearing loss and she requires multiple hearing aids. During evaluation for a syncopal event 10 years ago, she was noted to have hypocalcemia. At that time, her total calcium concentration was 5.3 mg/dL. (8.2-10.2 mg/dL) (SI: 1.3 mmol/L [2.1-2.6 mmol/L}). She has since been on calcium and calcitriol supplementation. ‘When she is fatigued or when she forgets to take her calcium supplements, she occasionally notes diffuse pedal spasms and “Charlie horses” running up and down her legs. She has no perioral nutnbness or other paresthesias and she has had no seizures or arrhythmias since she has been on supplementation. Other medical problems include hypothyroidism and a history of ovarian cysts. Ultrasonography has documented that she has small kidneys. Both her daughter and her granddaughter have renal anomalies. She also reports a stillborn birth at 26 weeks’ gestation due to renal dysplasia. On physical examination, she is well nourished. Her height is 63 in (160 cm), and weight is 141 Ib (64.1 ke) (BMI = 25 kg/m’). Her blood pressure is 108/60 mm Hg, and pulse rate is 83 beats/min. Neck examination reveals a small, firm thyroid gland, She has brisk reflexes. Her examination findings are otherwise unremarkable. Her current medications include calcitriol, 0.25 meg daily; calcium carbonate, 1000 mg twice daily; and levothyroxine, 75 meg daily. Laboratory test results Serum total calcium = 80 mg/dl (8.2-10.2 mg/dL) (Sk: 2.0 mmoVL [21-26 mmoVL}) Tonized calcium = 3.73 mg/dL. (4.60-5.08 mg/dL) (SI: 0.93 mmol/L [1.2-1.3 mmoVL)) Phosphate = 4.0 mgidl (2.3-4.7 mp/dL) (Sk: 1.3 mmoVL[0.7-1.5 mmoV/L]) Serum ereatinine = 0.99 mg/dL. (06-1.1 mg/dL (SI: 87.5 pmol/L. [53.0-97.2 umoVL)) Alkaline phosphatase = 77 U/L (50-120 U/L) (SI 13 wkavL[0.84-2.00 pkav/L]) PTH = 16 pg/ml (10-65 pa/mL) (Sk: 16 ng/L [10-65 ng/L) Urinary calcium = 35 mg/24 h (100-300 mg/24 h) (SI: 0.9 mmoVd [2.5-7.5 mmolid}) Which of the following is the most likely cause of her hypocalcemia? Abnormality in the calcium-sensing receptor Abnormal parathyroid development PTH resistance Autoimmune destruction of the parathyroid glands Wilson disease moOm> ‘A43-year-old woman with a history of hypertension and gastroesophageal reflux disease returns to see you 1 year after sleeve gastrectomy. You initially met her 2 years ago for evaluation and management of her medically complicated obesity. After a complete evaluation, you recommended she undergo bariatric surgery. ‘The patient was reluctant to have Roux-en-Y gastric bypass because her sister had multiple complications after the same procedure. The patient instead elected to have a sleeve gastrectomy, and her BMI decreased from 44 to 28 kg/m’. The patient is pleased with her weight loss, but reports dysphagia with solids and epigastric pain. Also, she frequently feels nauseated and has had | episode of vomiting, 42 ESAP 2018—QUESTIONSOn physical examination, her vital signs are stable, abdomen is soft, bowel sounds are present, and there is no focal tenderness. Given her symptoms, which of the following should be performed next? Esophageal pH testing Upper gastrointestinal series ‘Abdominal ultrasonography Abdominal CT Gastric emptying study ronm> 422. yearold woman comes fo you fo follow-up of androgen insensitivity. The patient was found to have female genitalia at birth despite amniocentesis demonstrating a 46,XY karyotype. An elevated testosterone level was documented. At age 12 years, she underwent vaginal reconstruetion/dilatation. The family elected not to have the patient undergo orchiectomy and the gonadal tissue remained in the abdomen. As an adult, the patient has Not chosen to undergo orchiectomy based on her fear of decreased libido and her belief that the risks of malignancy are lower than those reported. On physical examination, her blood pressure is 110/80 mm Hg, Her height is 69 in (175.3 cm), and weight is 147 Ib (66.8 kg) (BMI = 21.7 kg/m"). On skin examination, she has no axillary or pubic hair. Her breasts are Tanner stage 5. No masses are noted on abdominal examination, Pelvic examination reveals a vaginal length of 1.5 cm. Which of the following tests is the most important for follow-up in this patient who does not desire gonadectomy? ‘Abdominal ultrasonography a-Fetoprotein measurement hCG measurement ‘Testosterone measurement Bone density scan roam> A 67-year-old woman who was diagnosed with Hashimoto thyroiditis 3 years ago presents to the clinic with a 4-week history of progressive confusion and cognitive decline. Her husband reports dramatic deterioration in her symptoms over the preceding 5 days with disorientation, falls, and inability to perform routine tasks. Her appetite has been poor and she has lost 11 Ib (5 kg). Her medical history includes celiae disease and hypertension. She smokes 20 cigarettes daily but does not drink alcohol. She follows a gluten-free diet, and her medications include levothyroxine, 100 meg daily; aspirin; sertraline; and a thiazide diuretic. On physical examination, her height is 66 in (167.6 cm) and weight is 123 Ib (55.8 kg) (BMI = 19.9 kg/m). Her blood pressure is 124/78 mm He, and pulse rate is 92 beats/min. She is afebrile. She is disorientated and agitated. She has a coarse tremor of the upper and lower limbs. There is no palpable thyroid enlargement. Neurologic examination reveals tremor and ankle clonus with bilateral hyperreflexia and normal plantar responses. Her gait is unsteady and her speech is slurred. Laboratory test results: ‘Complete blood cell count, normal Renal, liver, and calcium profile, normal (C-reactive protein = <3.0 mg/L (0.8-3.1 mg/L) (SI: <28.57 nmol/L. [7.62-29:52 nmol/L]) ‘TSH=23 mIUML (0.5-5.0 mIU/L) Free T, = 1.4 ng/L (0.8-1.8 ng/dL) (SI: 18.02 pmoV/L [10:30-23.17 pmol/L]) ‘TPO antibodies = 260 IU/mL. (<2.0 1U/mL) (Sk: 260 KIU/L [<2.0 KIL/L]) Urine dipstick and microscopy: normal Cerebrospinal fluid examination: elevated protein concentration, no oligoclonal bands, otherwise normal Urine and blood bacterial cultures: no growth after 48 hours Cerebrospinal fluid bacterial cultures: no growth ESAP 2018—QUESTIONS 13Cerebrospinal fuid viral PCR: negative for herpes simplex types 1 and 2, varicella zoster, cytomegalovirus, Epstein-Barr virus, adenovirus, enterovirus, and polyoma virus Serology for HIV and syphilis: negative ‘Vasculitis screen: negative Chest radiography and brain CT do not reveal any abnormalities. She is admitted to the hospital and started empirically on broad-spectrum antibiotics and acyclovir. Twenty-four hours following admission, she has 3 brief tonic-clonic seizures, and electroencephalography shows diffuse slow-wave activity, Brain MRI is unremarkable. ‘Anticonvulsant agents are initiated, She remains confused with periods of agitation after 72 hours. Which of the following is the best next step? Increase the levothyroxine dosage to 125 meg daily Start high-dosage glucocorticoid treatment Recommend treatment with plasmapheresis, Start treatment with intravenous immunoglobulins Start treatment with liothyronine (T;) POOD> ‘A.20-year-old man presents to the emergeney department with diabetic ketoacidosis. Type 1 diabetes mellitus ‘was diagnosed at age 10 years, and he has a history of moderate glycemic control. His insulin regimen consists of insulin glargine, 30 units each moming, and insulin aspart, 8 to 10 units with each meal. He uses insulin pens for both glargine and aspart. He keeps his insulin aspart pen on his person. The unused box of insulin aspart pens, as well as his insulin glargine, is kept in the refrigerator at his house. His blood glucose values usually range from 150 t0 200 mg/dL. (8.3-11.1 mmol/L). ‘One week before admission, he noticed that his blood glucose started to inctease to the range of 250 to 300 mg/dL (13.9-16.7 mmol/L), with no change in his diet or his usual insulin doses. Over the next 5 days, he took ‘multiple additional doses of insulin aspart, 10 units at a time. His glucose transiently dropped by 20 to 30 mg/dL. (.1-1.7 mmol/L) with each dose, but would return to the range of 250 to 300 mg/dL within 3 hours. On the day before admission, he noticed worsening fatigue, polyuria, and polydipsia. He never tests his urine for ketones. ‘There is no sign of infection or other precipitant. He had a previous episode of diabetic ketoacidosis 7 ‘months ago for which no cause was found. He states that he does not use recreational drugs and has not recently consumed alcohol. He was under the care of a pediatric endocrinologist until age 18 years, but he has not seen an ‘endocrinologist since then. His primary care physician prescribes his insulin. Which of the following is the most important next step? ‘Identify an endocrinologist who takes the patient’s insurance and is willing to see him Initiate insulin pump therapy Initiate continuous glucose monitoring Change from insulin glargine to insulin detemir [Ask the patient how the insulin was initially stored after picking it up from the pharmacy roa 8 ‘A 67-year-old man with a history of prostate cancer is referred for evaluation of osteoporosis. He underwent prostatectomy 6 years ago and started leuprolide. One year ago, leuprolide was stopped and abiraterone with prednisone, $ mg daily, was started because of progression to lymph nodes. He has no history of fractures or height loss. He does not eat much dairy, nor does he take calcium or vitamin D supplements. ‘On physical exemination, his blood pressure is 119/67 mm Hig and pulse rate is $5 beats/min. His height is 71 in (180 em), and weight is 257 Ib (116.8 kg) (BMI = 35.8 kg/m’), There is no evidence of cushingoid features or kyphosis. Laboratory test results: ‘Serum urea nitrogen = 39 mg/dL (8-23 mg/dL) (SI: 13.9 mmoVL [2.9-8.2 mmol/L}) Creatinine = 1.8 mg/dL. (0.7-1.3 mg/dL) (St: 159.1 pmoVL (61.9-114.9 umol/L]) 414 ESAP 2018—QUESTIONSEstimated glomerular filtration rate = 28 mL/min per 1.73 m? (260 mL/min per 1.73 m') Calcium = 9.6 mgidL (82-10.2 mg/AL) (SI: 2.4 mmol/L [2.1-2.6 mmol/L) Phosphate = 4.0 mg/dL. (2.3-4.7 mgidL) (SI: 1.3 mmol/L (0.7-1.5 mmol/L]) Albumin = 3.9 g/dL. (3.5-5.0 gidL) (SI: 39 giL [35-50 g/L]) ‘Total testosterone = <20 ng/L. (300-900 ng/dL) (SI: 0.7 nmol/L (10.4-31.2 nmoV/L]) 25-Hydroxyvitamin D = 16 ng/mL (25-80 ng/ml. [optimal]) (SI: 39.9 nmol/L [62.4-199.7 nmol/L) Bone mineral density as determined by DXA is shown (see table), Rogion TSe0re LiLa spine: 28 Left total hip 7 Letttemoral neck [17 Right total hip 20 Right fomoral neck _|-2.2 Bone scan is negative for bone metastases. After repleting vitamin D stores and recommending calcium supplementation, which of the following is the best recommendation now? ‘A. Stop prednisone B. Initiate denosumab C. Initiate teriparatide D. Initiate alendronate E._ Initiate zoledronic acid A previously healthy 20-year-old African American man comes to clinic for a follow-up visit. He was hospitalized for treatment of diabetic ketoacidosis 4 months ago, Laboratory test results at hospital admission Plasma glucose = 748 mg/dl (70-99 mg/dL) (Sk: 41.5 mmol/L 3.9-5.5 mmol/L]) Bicarbonate = 10 mEq/L (21-28 mEq/L) (St: 10 mmol/L. (21-28 mEq/L) 22 mE (3-11 mEq/L.) 2 mg/dL (0.7-1.3 mg/dL.) (SI: 194.5 pmol/L [61.9-114.9 wmolL)) Estimated glomerular filtration rate = 34 mL/min per 1.73 m? (260 mL/min per 1.73 my “Moderate ketones present in the serum No obvious cause of the diabetic ketoacidosis was found. He was treated with intravenous fluids and a continuous insulin infusion, The acidosis resolved and he was discharged on basal-bolus insulin, The total insulin dose at the time of discharge was 1.0 units/kg per day. He received diabetes education and has modified his diet. He has lost 22 Ib (10 kg) since hospital discharge. The insulin doses have been gradually reduced over time. He is now administering 12 units of insulin glargine at bedtime and 3 units of insulin aspart before breakfast and dinner (he only eats 2 meals per day). The 2-week average glucose value is 107 mg/dL (5.9 mmol/L}. The fasting glucose values range from 79 to 106 mg/dL. (4.459 mmol/L). He has no other medical problems. He does not have hypertension or dyslipidemia, He does not drink alcohol or smoke cigarettes. His mother, 2 of his 4 siblings, and other maternal relatives have a history of diabetes, (On physical examination, his height is 73 in (185 em) and weight is 242 Ib (110 kg) (BMI = 31.9 kg/mm). His blood pressure is 122/83 mm Hg, and pulse rate is 82 beats/min, He has central weight distribution, There is evidence (of acanthosis nigricans. The cardiac, lung, abdominal, and neurologic findings on examination are all normal, ESAP 2018—QUESTIONS 15Current laboratory test results (fasting): Hemoglobin A,,= 5.8% (4.0%-5.67) (40 mmol/mol [20-38 mmol/mot)) Creatinine = 1.3 mg/dL. (0.7-1.3 mg/dL) Sk: 1149 pmol (619-1149 umoVL) Estimated glomerular filtration rate = >60 mL/min per 1.73 m° 60 mL/min per 1.73 m*) Electrolytes, normal ‘TSH, normal C-peptide = 3.2 np/mL (0.9-4:3 ng/mL) (SI: 1.06 nmol/L. [0.30-1 42 nmol/L) Glucose ~ 124 mg/dL (70-99 mg/d.) (SI: 6.9 mmoV/L [3.9-5.5 mmol) Glutamic acid decarboxylase antibodies, undetectable Which of the following is the best next step in treating this patient's diabetes? Stop insulin aspart and start empagliflozin Stop insulin aspart and start glimepiride Stop all insulin and start metformin Stop all insulin and instruct the patient to continue diet treatment alone Continue the current insulin regimen PonDD> 10 ome ‘consult on a 69-year-old woman with a history of high serum calcium noted on routine laboratory testing over the past 2 years. She reports a progressive decline in her health, including an unintentional 25-Ib (11.4-kg) weight loss, constipation, and joint pain. She had a dry cough for the last few years, which improved with steroid nasal spray. She takes no over-the-counter supplements, specifically no calcium or vitamin D. She has been avoiding dairy products. Her other medical problems include gastrointestinal reflux and hypertension. There is no family history of calcium or parathyroid disorders. Her current medications include valsartan, carvedilol, amlodipine, pantoprazole, and furosemide. (On physical examination, she is a thin woman. Her height is 66.5 in (168.9 cm), and weight is 137 Ib (62.3 kg) (BMI = 21.8 kg/n?). Her blood pressure is 148/61 mm Hg, and pulse rate is 62 beats/min Laboratory test results: ‘Serum total calcium = 12.2 mg/dL (8.2-10.2 mg/dL) (Sk 3.1 mmol [2.1-2.6 mmoVL}) Ionized calcium = 6.17 mgidL (4.60-5.08 mg/dL) (Sk 1.5 mmol/L [1.2-1.3 mmoV/L}) Phosphate = 3.5 mg/dL (2.3.4.7 mg/dL) (Sk 1.1 mmol/L [0.7-1.5 mmol/L) ‘Serum creatinine = 2.39 mg/dL (0.6-1.1 mg/dL) (SI: 211.3 umoV/L [53.0-97.2 umoVL)) Estimated glomerular filtration rate = 32 mL/min per 1.73 m* (260 mL/min per 1.73 m?) PTH = 12 pg/mL (10-65 pg/mL) (SI: 12 ng/L [10-65 ng/L) PTHrP =2.9 pg/mL (14-27 pg/mL) (SI: 2.9 ng/L [14-27 ng/L) Magnesium = 2.7 mg/dL (1.5-2.3 mg/dL) (Sk: 1.1 mmol/L [0.6-0.9 mmol/L) 25-Dihydroxyvitamin D = 30 ng/ml (25-80 ng/mL. [optimal]) (Sl: 74.9 nmoV/L (62.4-199.7 nmoVL]) 1,25-Dihydroxyvitamin D = 84.9 pg/mL. (16-65 pg/mL) (SI: 221.7 pmol/L [41.6-169.0 pmoVL}) CT of the abdomen and chest shows ehronic-appearing interstitial Jung disease and scattered lymph nodes most pronounced in the abdomen (see images). 46 ESAP 2018—QUESTIONSIn addition to intravenous fluids, which of the following should be prescribed? Cinacalcet, Denosumab Zoledronate Prednisone Raloxifene Pooe> 11 Aés2ezeolt woman presents wth hypertension (180100 mm Hg), hirsutism, and hypokalemia (potassium = 3.1 mEq/L [3.1 mmoV/L)). A 7-cm adrenocortical carcinoma with invasion of the inferior vena cava is identified. She has numerous metastases to the liver and lungs, hypercortisolism causing Cushing syndrome, and biochemical hyperandrogenism. Laboratory test results: Urinary free cortisol ~ 1750 pg/24b (4-50 yg/24 h) (ST: 4830 nmolld [11-138 nml/d)) 0.6 ngimL per h (06-43 ng/mL perb) 4.0 nga (4.0-21.0 ng'dL) (Sk: ESAP 2018—QUESTIONS 171 ‘A 64-year-old woman is referred for possible lipid-lowering therapy. She notes that “high cholesterol” was detected 15 years ago. Medical nutrition therapy was offered, and she was prescribed atorvastatin at that time (dosage unknown) but she did not start it. She has a history of biopsy-proven primary biliary cirrhosis that is ‘treated with ursodiol and has been stable over many years. She takes no other medications. She walks 3 to 4 miles several times a week and does Pilates twice a week. She does not smoke cigarettes, and she drinks 3 alcoholic ‘beverages weekly. In reviewing her family history, you learn that her father had a myocardial infarction and 2-vessel coronary artery bypass grafting at age 51 years and died after his second myocardial infarction at age 64 years. A paternal uncle died at age 42 years after a massive myocardial infarction, The patient has 2.adult daughters ‘who are reportedly healthy. On physical examination, her blood pressure is 120/72 mm Hg. Her height is 64 in (162.5 em), and weight is 128 Ib (58.2 kg) (BMI = 22 kg/m?). There are no xanthomas or other remarkable findings. Laboratory test results (sample drawn while fasting) Total cholesterol = 270 mg/dL (<200 mg/l. foptimal]) (Sk: 6.99 mmoV/L [<5.18 mmoVL}) LDL cholesterol = 163 mg/dL (<100 mg/L [optimal]) (SI: 4.22 mmol/L [<2.59 mmol/L) ‘Triglycerides = 89 mg/dL (<150 mg/aL [optimal] (SI: 1.01 mmoV/L [<3.88 mmol/L) HDL cholesterol = 89 mgicl (60 mg/AL. [optimal] (SI: 2.31 mmol/L (1.55 mmoVL)) Non-HDL-cholesterol = 181 mg/dl. (<130 mg/AL [optimal]) (Sk: 4.69 mmol/L [<3.37 mmoVL) ‘Apolipoprotein B= 132 mg/dL. (50-110 mg/dL) (SI: 1.32 g/L [0.5-1.1 wL}) Lipoprotein(a) = 14 mg/dL (<30 mg/dL) (SI: 5.14 mol/L [£1.07 wmol/L}) Hemoglobin A, ,= 5.9% (4.0%-5.6%) (41 mmoV/mol [20-38 mmot/mol)) ‘TSH = 3.2 mIUIL (0.5-5.0 mIUIL) Liver function, normal According to the 2013 American College of Cardiology/American Heart Association atherosclerotic cardiovascular disease risk calculator, her calculated 10-year risk is 4.2%. Which of the following should you recommend as the best next step in this patient's, management? No medication needed, recommend low-fat diet Colesevelam Ezetimibe Astatin Metformin moOp> 144 54-year-old man is referred to you after a low serum testosterone concentration (120 ng/L. [4.2 nmoV/L}) was identified during the workup of new-onset erectile dysfunction. He has noted no change in weight and no new headache pattem. He has no history of hypertension or diabetes mellitus. ‘On physical examination, his blood pressure is 128/75 mm Hg. His height is 69 in (175.3 em), and weight is 177 Ib (80.5 kg) (BMI = 26.1 kg/m). Examination findings are normal. Testes are 10 mL bilaterally. Formal visual field testing shows a mild bitemporal defect. Laboratory test results: 0 mIU/mL. (1.0-9.0 mIU/mL) (SI: 2.0 1U/L [1.0-9.0 IU/L) FSH = 4.2 mIU/mL (1.0-13.0 m[UimL) (Sk: 4.2 1U/L [1.0-13.0 1U/L]) = 81 ng/mL (4-23 ng/mL) (SI: 3.5 nmoVL [0.17-1.00 nmoV/L) 1 gid (5-25 g/dL) (SI: $79.3 nmoVL [137.9-689.7 nmoV/L]) ‘TSH, normal IGF-1, normal 48 ESAP 2018—QUESTIONSPituitary MRI shows a 2.3 x 2.2-cm solid mass with suprasellar extension (see image). The optic chiasm is displaced upwards. Which of the following is the most appropriate next management step? Measure macroprolactin Start therapy with bromocriptine or cabergoline Refer to neurosurgery Start testosterone therapy Measure a subunit moom> 4B Nonaressked to sec 25-year man with history of intermittent hyperalemia and kidney stones. He was first noted to have high calcium levels on routine blood work as a teenager, but this resolved on subsequent testing. Over the last 8 years, his serum calcium has ranged from 10.2 to 11.3 mg/dL (2.6-2.8 mmol/L). Although he states that he currently takes no calcium, vitamin A, or vitamin D, he does frequent health food stores for other supplements. He reports at least 5 episodes of kidney stones in the last 2 years, Otherwise he feels well, his weight has been stable, and he has not experienced night sweats or fatigue. A recent chest x-ray was normal. His medical history is otherwise unremarkable and he takes no medications. There is no family history of calcium disorders. Laboratory test results: Serum total calcium = 10.7 mg/dL (8.2-10.2 mg/dL) (SI: 2.7 mmol/L (2.1-2.6 mmolL}) Tonized calcium = 5.1 mg/d. (4.60-5.08 mg/dL) (SI: 1.3 mmoV/L [1.2-1.3 mmoV/L]) Phosphate = 2.9 mg/dL. (2.3-4,7 mg/dL) (SI: 0.9 mmoV/L [0.7-1.5 mmoV/L]) ‘Magnesium = 2.4 mg/AL (1.5-2.3 mg/dL) (SI: 1.0 mmol/L [0.6-0.9 mmoV/L]) ‘Serum creatinine = 1.94 mg/dL. (0.6-1.1 mg/dL) (SI: 171.5 wmoVL [53.0-97.2 moV/L]) PTH =7 pe’mL (10-65 pg/mL) (SI: 7 ng/L [10-65 ng/L) PTHsP = <15 pg/mL (14-27 pg/mL) (SI: <1.5 ng/L [14-27 ng/L]) 25-Hydroxyvitamin D = 24 ng/mL ({optimal] 25-80 ng/mL) (ST: 59.9 nmoV/L [62.4-199.7 nmol/L]) 1,25-Dihyéroxyvitamin D = 112 pg/mL (16-65 pg/mL) (SI: 291.2 pmol/L [41.6-169.0 pmol/L]) 24,25-Dihydroxyvitamin D = <0.3 ng/mL (1.6-9.1 ngimL) Angiotensin-converting enzyme = 11 U/L (9-67 U/L) Which of the following is most likely the cause of this patient's hypercalcemia? ‘Overingestion of over-the-counter cholecaleiferol Sarcoidosis Lymphoma Inactivating mutation in the CYP244I gene Inactivating mutation in the CASR gene Foom> 1G AS7yeatld man with a history ot hypertension, severe osteoarthritis, chronic fatigues, hypothyroidism, type 2 diabetes mellitus, and obesity comes to see you for assistance with weight loss. His diabetes is managed with a multiple daily injection regimen, and his last hemoglobin A, measurement was 7.0% (53 mmol/mol). The patient has severe osteoarthritis in both knees, which limits his activity. For the past 12 months he has been using an electric wheelchair because of severe pain when he stands. On physical examination, his height is 67 in (170 em) and weight is 273 Ib (124 kg) (BMI ~ 42.8 kg/m) His blood pressure is 130/85 mm Hg, and pulse rate is 84 beats/min, Pulmonary and cardiovascular examination findings are unremarkable. He has reduced range of motion and crepitus bilaterally on knee examination Given his current BMI, an orthopedic surgeon deemed that he was not a surgical candidate for knee replacement at this time, The surgeon has agreed to operate once his BMI is below 40 kg/m?, which corresponds to a body weight Jess than 253 tb (<115 kg). During your evaluation, the patient tells you he is interested in a weight-loss program that will help him quickly achieve weight loss, so he can proceed with knee replacement as soon as possible. ESAP 2018—QUESTIONS 19Which of the following treatment recommendations would you suggest? Very low-calorie diet Low-carbohydrate diet Lorcaserin Phentermine Liraglutide moog 17 ‘48-year-old woman with a 26-year history of type 1 diabetes mellitus follows a basal-bolus insulin injection regimen with insulin glargine at bedtime and premeal insulin lispro. She asks whether one of the newer long-acting insulins would improve her glycemic control. She adjusts insulin lispro doses on the basis of the carbohydrate content of her meals and her measured glucose level. She has tried to maintain tight control sinee her diagnosis. Diabetes complications have been limited to stable, mild background retinopathy. She measures glucose levels 6 t08 times daily, always boluses before meals, and closely assesses the carbohydrate content of her meals, Her hemoglobin A,, measurement today is 7.3% (4.0%-5.6%) (SI: 56 mmol/mol [20-38 mmol/mol]). Data downloaded from her glucose meter for the past 2 weeks show average premeal glucose levels of 132 mg/dL (7.3 mmoV/L) and average postmeal glucose levels of 168 mg/dL (9.3 mmol/L), with moderate glucose variability. Seven percent of the readings are below 70 mg/dL (<3.9 mmolL). ‘Switching her regimen from insulin glargine to insulin degludec would be expected to result in reduced: Postmeal glucose Hemoglobin A,, Nocturnal hypoglycemia Frequency of injections Microvascular complications room 1 8 ‘A 21-year-old woman presents to the adult clinic for transition of care with a history of congenital adrenal hyperplasia. She has no medical records but reports that she was diagnosed at age 2 months when she required genitoplasty for fused labia. She has been maintained on hydrocortisone, 15 mg in the morning and 10 mg, in the evening. She has never required mineralocorticoids. She underwent menarche at age 12 years and has had regular menstrual eycles, On physical examination, her blood pressure is 148/90 mm Hg and pulse rate is 63 beats/min, Her height is 62 in (157.5 cm), and weight is 172 Ib (78.2 kg) (BMI = 31.5 kg/mm’), She has acne scars and hyperpigmentation, but no hirsutism. She has no supraclavicular or dorsal cervical adiposity. Breast development is Tanner stage 5. Abdominal examination reveals no striae. Pelvic examination reveals Tanner stage 5 pubic hair development and no masses. Laboratory test results: ‘Testosterone = 183 ng/dL. (8-60 ng/AL) (SI: 6.35 nmoVL [0.3-2.1 nmol/L]) Androstenedione ~ 1090 ng/dlL (80-240 ng/AL) (SI: 38.06 nmoV/L [2.79-8.38 nmol/L]) DHEA-S = 165 jg/dL (44-332 ugidL) (SI: 4.47 pmol/L [1.19-9.00 umoV/L]) I7-Hydroxyprogesterone = 857 ng/dl. (<285 ng/dL) (SI: 26.0 nmol/L [<8.64 nmoV/L}) 11-Deoxycortisol = 22,400 ng/L (<33 ng/dL) (Sk: 647.4 nmoV/L [£0.95 nmoVL) 11-Deoxyeorticosterone = 484 ng/dL (<10 ng/dL) (Sk: 14,6 nmoVL [<0.30 nmol/L}) Progesterone = 1.5 ng/mL ( D4 A 2yeold man witha history of congenital hypogonadotropic hypogonadism is transferring his endocrine care to your practice. Hypogonadism was diagnosed at age 15 years when he demonstrated no signs of pubertal development. At that time, his testicular volumes were 5 mL each and he had a normal sense of smell. Genetic testing revealed a mutation in the GINRHR gene. Puberty was induced with GnRH therapy, which he received for several years, He has been self-administering intramuscular testosterone esters since starting college. ‘The patient is sexually active with a female partner. He reports a normal libido and erectile function and has no gynecomastia. He is somewhat bothered by changes in his mood several days before his scheduled testosterone injection. He is curious as to whether he is fertile but does not desire children in the next few years. His only current medication is testosterone cypionate, 150 mg intramuscularly every 2 weeks. Laboratory test result ‘Total testosterone 7 days afler an injection = 380 ng/dL. (300-900 ng/L) (SI: 13.2 nmol/L [10.4-31.2 amolL]) On physical examination, his blood pressure is 110/67 mm Hg. His height is 71 in (180 cm), and weight is 170 Ib (77.3 kg) (BMI = 23.7 kp/m:). Testes are 8 mL bilaterally without any masses, and he is well viilized. Which of the following would you recommend next? Obtain a baseline semen analysis Increase the dosage of the testosterone cypionate Reassess his reproductive axis after stopping testosterone for 4 months Switch to transdermal testosterone Switch to hCG therapy moop> 92% 29-yeat-old man presented with severe thyrotoxicosis | year ago. His presentation was complicated by severe orbitopathy and underlying schizophrenia for which he had recently stopped taking his prescribed medications. His endocrinologist recommended that he undergo thyroidectomy, but he clected to be treated with antithyroid medications, He initially required 60 mg of methimazole daily to control his hyperthyroidism. His thyroid status has varied considerably while on treatment with periods of both undertreatment and overtreatment. However, recently he has been euthyroid while taking 5 mg of methimazole daily. The patient would now like to begin a trial off antithyroid agents to see if he can remain euthyroid. He currently has no symptoms of hyperthyroidism, except for some anxiety. He takes risperidone for his schizophrenia, He takes cholecalciferol for itamin D deficiency, but he often forgets doses. (On physical examination, his height is 69 in (175.3 cm) and weight is 136 Ib (61.8 kg) (BMI = 20.1 kg/m), His blood pressure is 108/76 mm Hg, and pulse rate is 88 beats/min. He has moderate proptosis, but no signs of active ophthalmopathy. His thyroid gland is slightly enlarged, but he has no bruit. His deep tendon reflexes are normal. He exhibits restlessness and paces the room during his visit. His thyroid function test results at the time of diagnosis and current values are shown (see table). 22 ESAP 2018—QUESTIONS‘Measurement Time of Assessment [At Diagnosis Now 73H) 000% miu 1.6 miviL Free, 37.0 ng/al (90.1 pmov)_[1.5 ng/a (19.3 pmav) Total Ts 3800 ngia. (12.3 nov [140 ng/al (2.2 nmoVL) Thyroid-stimulating immunoglobulin | 400% 280% Reference ranges: TSH, 055.0 miU: fee T, 08-18 ng (St:10.90-28.17 pmol} oa, 70-200 gic (Gi 1198-8.09 mov thyroiestmulatng mrmunoglobuin, 120% of basal acy. Which of the following factors most directly predicts the likelihood that this patient will experience relapse of his Graves disease while off antithyroid medication? Vitamin D deficiency Initial requirement for 60 mg methimazole Variable adherence to taking medications Orbitopathy Current thyroid-stimulating immunoglobulin titer moom> 23 ‘A32-year-old man has a 12-year history of type | diabetes mellitus. Insulin pump therapy was initiated 7 years ago. He has had reasonable glycemic control, with hemoglobin A, levels ranging from 6.6% to 7.5% (49-58 mmol/mol) over the last 4 years. He has background retinopathy. The total insulin dose per day is 32.6 units; 34% is basal insulin and 66% is bolus and correctional insulin. He takes simvastatin, 20 mg daily. He has 4 to 6 beers per week and does not smoke cigarettes. He is raining fora half marathon, scheduled in 3 months. He runs between S and 12 miles in the late afternoon, 6 days per week. He usually leaves his insulin pump on when he trains and does not adjust the rate daring the activity. His glucose values are in the range of 113 to 160 mg/dl. (6.3-8.9 mmol/L) immediately after ‘most of his runs, He has noted that hypoglycemia occurs 5 to 12 hours after some of the more strenuous runs. He does not have hypoglycemia unawareness, and there has never been a paramedic call to treat severe hypoglycemia. He is able to treat these noctural hypoglycemic episodes, but he would like to avoid them if possible. On physical examination, his height is 72 in (183 cm) and weight is 174 Ib (79.1 kg) (BMI = 23.6 kg/m) His blood pressure is 112/72 mm Hg, and pulse rate is 56 beats/min. Examination findings are normal except for several tiny dot hemorrhages noted in the left eye. Laboratory test results: Hemoglobin A,,~ 7.1% (4.0%-5.6%) (54 mmoVmol [20-38 ramot/mol}) Creatinine = 1,0 mg/dL (07-13 mg/dL.) (SI: 88.4 ymoVL. (61.9-114.9 ymoV/L]) Estimated glomeruar filtration rate =>90 mLimin pr 1.73 m? (>60 mLimin per 1.73 m) Electrolytes, normal Which of the following is the best treatment option for this patient? Ingest carbohydrates to increase glucose to >170 mg/dL (>9.4 mmol/L) before each strenuous run Lower the basal insulin rate by 50% before each strenuous run ‘Skip the premeal bolus for the meal after the run Lower the basal rate for 7 hours after each strenuous run, starting at bedtime Remove the pump before each run and restart the pump after the run moom> ESAP 2018—QUESTIONS 23D4 vox asked to evaluate a 60-year-old postmenopausal woman for osteoporosis, which has worsened despite pharmacotherapy. Her first fracture was an elbow fracture in elementary school when she fell ‘on the playground. Her medical history is remarkable for back pain secondary to degenerative disease. Her dental history is extensive, She lost her first baby tooth at age 4 years, and she has recently had loosening of her permanent teeth, She has had significant dental work for caries, abscesses, and cracked teeth, At age 55 years, @ screening bone density assessment showed a femoral neck T score of -2.7 and an invalid result in the spine due to artifact from her arthritis and slight scoliosis. She was prescribed weekly risedronate because of additional risk factors for fracture, including a family history of hip fracture and personal history of spontaneous and recurrent metatarsal stress fractures. Follow-up bone densitometry 2 years later showed a 3% decline in hip bone mineral density despite reported adherence to the medication, Daily teriparatide injections were prescribed, and despite adherence to the regimen for the past 18 months, she has sustained additional metatarsal fractures, an winar styloid fracture, and a humerus fracture from lifting her infant granddaughter. Her bone pain has worsened and she now requires a cane. Her current medications include teriparatide, 20 mg daily; calcium carbonate, 600 mg twice daily; and cholecaleiferol, 800 1U daily. Laboratory test results: Calcium = 10.2 mg/dL (2.55 mmol/L) (8.2-10.2 mg/dL) (SI: 2.6 mmoVL [2.1-2.6 mmoV/L]) Phosphate = 4.0 mg/dL (2.3-4.7 mg/L) (Sk: 1.3 mg/dL [0.7-1.5 mmol/L) PTH =55 pg/ml. (10-65 pg/mL) (SI: $5 ng/L [10-65 ng/L.]) ‘Alkaline phosphatase = 27 U/L (50-120 U/L) (SI: 0.5 pkat/L [0.84-2.00 ukavL]) 25-Hydroxyvitamin D = 32 ng/mL (25-80 ng/mL. {optimal]) (SI: 79.9 nmol/L [62.4-199.7 nmol/L) Creatinine = 0,9 mg/dl. (0.6-1.1 mg/dL) (SI: 79.6 mol/L (33.0-97.2 moVL}) Urinary N-telopeptide = 18 nmol BCE/mmol ereat Given her worsening clinical scenario on teriparatide, which of the following options would you recommend now? ‘A. Subcutaneous asfotase alfa B. Subcutaneous denosumab CC. Intravenous zoledronate D. Oral raloxifene E. Nasal caleitonin spray 25 'A47-year-old woman presents to the emergency department with ketoacidosis. Diabetes mellitus was diagnosed at age 35 years. She was initially treated with oral agents, and this regimen was continued ‘with good glycemic control until age 45 years. At that time, she was injured in a motor vehicle crash, Her exercise ‘vas subsequently limited, leading to a 20-Ib (9.1-kg) weight gain and worsening glycemic control, Insulin was recommended, but she refused. Despite maximum dosages of metformin, glipizide, and sitagliptin, her hemoglobin ‘A,, level remained greater than 9% (75 mmol/mol). Five days ago, her physician prescribed canagliflozin, 100 mg aily. In addition to the new medication, the patient initiated a low-carbohydrate diet ( DG Ais-zeurold man is refered by his primary care physician fr lipid management after presenting o the emergency department with atypical chest pain a few weeks ago. Workup was negative for a cardiac etiology of chest pain. He has only recently reinitiated health care after not seeing a physician for 8 years. He recalls being told he had low HDL cholesterol 10 years ago, but he was never prescribed therapy. His primary care physician recently diagnosed hypertension and prescribed nifedipine. He takes no other medications or supplements. The patient does not smoke cigarettes and drinks 1 alcoholic beverage per week. He is adopted and therefore no family history is known, On physical examination, his blood pressure is 130/70 mm Hg. His height is 65.5 in (166.5 cm), and weight is 154 Tb (70 kg) (BMI = 25.2 kg/m’), No hepatosplenomegaly or xanthomas are noted on ex Laboratory test results (sample drawn while fasting): Total cholesterol = 137 mg/dL (<200 mg/dL [optimal] (SI: 3.55 mmol. [ 26 ESAP 2018—QUESTIONSQO A St ye2.0ld woman presents with weight grin, muscle weakness, and insomnia, She describes gaining 25 Ib (11.4 kg) over the last 3 months despite dieting and exercise. During this time, she has also noted difficulty sleeping and not having the strength to elimb stairs, On physical examination, her blood pressure is 154/92 mm Hg and pulse rate is 90 beats/min. Her height is 64 in (162.6 cm), and weight is 200 Ib (90.9 kg) (BMI = 34.3 kg/m’). She has truncal obesity, moon facies, a dorsocervical fat pad, abdominal strze, and proximal muscle weakness Laboratory test results: Urinary free cortisol = 241 yg/24 h (4-50 g/24 h) (SI: 665.2 nmol/d [11-138 nmolid)) Morning ACTH = 75 pg/mL (10-60 pg/mL) (SI: 16.5 pmoVL (2.2-13.2 pmoV/L]) Morning serum cortisol = 43 g/dL (5-25 ug/L) (SI: 1186.3 nmoVL [137.9-689.7 nmol/L) Ing dexamethasone suppression test, AM cortisol = 8.9 g/dL (245.5 nmol/L) ‘8.mg dexamethasone suppression test, AM cortisol = 2.1 pg/dl. (57.9 nmoV/L) Review of her records shows that she underwent an abdominal CT 4 months earlier when she presented with abdominal pain. ‘A 2.4-om right adrenal mass (5 Hounsfield units on unenhanced attenuation) consistent with an adrenal adenoma was noted at that time. Which of the following is the most appropriate next step? Abdominal CT with adrenal washout protocol Chest CT Octreotide scan Brain MRI Adrenal venous sampling roow> 30 You are consulted regarding a 56-year-old woman with a 10-year history of type 2 diabetes mellitus. She has a history of chronic pancreatitis for which she recently underwent partial pancreatectomy. Following the procedure, she continued to experience nausea and epigastric pain with ingestion of food. There is no evidence ‘of gastric outlet obstruction, small-bowel obstruction, or other etiology for her symptoms. Jjunal tube feeds via a gastrostomy-jejunostomy tube are initiated around the clock, She is tolerating this well, and she has reached the goal rate in 24 hours. She is treated with a combination of insulin glargine, 20 units, and supplemental scale (with regular insulin) every 6 hours. The regular insulin daily dose totals 10 to 14 units daily. With this regimen, her blood glucose measurements are in the range of 130 to 160 mg/dL (7.2-8.9 mmol/L). You are consulted regarding insulin management as the surgical team plans to change her to a nighttime tube feeding regimen from 8 PM to 8 AM. Total calories in the nocturnal feeding regimen will be 80% of that in the 24-hour regimen. The surgical team is hoping to discharge her home on this regimen. Which of the following regimens would be most appropriate for treating hyperglycemia associated with tube feeds in this patient? A. Maintain the current regimen of insulin glargine and supplemental scale with regular insulin every 6 hours B, Switch to NPH insulin at the start of tube feeds and use supplemental scale with regular insulin every 6 hours Maintain insulin glargine, 20 units, but use supplemental scale with insulin aspart every 6 hours Stop long-acting insulin and use only insulin aspart every 4 hours ‘Stop long-acting insulin and use only supplemental scale with regular insulin every 6 hours, ron ESAP 2018—QUESTIONS 273 A 32-year-old man seeks further management of advanced papillary thyroid cancer. At age 11 years, he was treated for Hodgkin lymphoma with chemotherapy and mantle radiotherapy. Papillary thyroid carcinoma with neck node involvement was diagnosed 2 years ago (American Joint Committee on Cancer stage T3 NIb MO), ‘and he underwent total thyroidectomy and left lateral compartment neck node dissection followed by radioactive iodine remnant ablation with a 100-mCi dose of "I. Six months after treatment, he developed recurrent left cervical and mediastinal lymphadenopathy, as well as low-volume lung metastases. He has received 3 doses of radioiodine therapy in the last 18 months and has been given a total "'l dose of 550 mCi. He takes levothyroxine, 175 meg daily, and nonsteroidal anti-inflammatory agents for increasing back and left-sided hip pain On physical examination, his height is 71 in (180.3 om) and weight is « ” 172 Ib (78.2 kg) (BMI = 24 kg/m’). His blood pressure is 128/74 mm Hg," " ‘and pulse rate is 68 beats/min. He has a visible thyroidectomy scar but no palpable thyroid enlargement and no palpable cervical lymphadenopathy. Lang fields are clear fo auscultation, and he has tenderness over his, lumbar spine and pelvic bones. Laboratory test results: ‘TSH =<0.01 mIU/L (0.5-5.0 mU/L) Free T,=2.1 ng/aL (27 pmol/L) (0.8+1.8 ng/L) (SI: 27.0 pmol/L [10:30-23.17 pmol/L) Unstimulated thyroglobulin = 738 ng/mL. (<0.1 ng'mL) (Sl: 738 g/L) [<0.1 ng/L) A®'L whole-body single-photon emission CT shows several areas of marked iodine accumulation in the left supraclavicular fossa, the right side of the mediastinum, the right hilum, and the right upper lung (see image). PET-CT shows fluorodeoxyglucose-avid skeletal metastatic disease in the right seapula, several ribs, thoracolumbar vertebra, pelvis, the right vertebral body of LS, and the sacrum (see image). Which of the following is the best next step? ‘An additional 150 mCi dose of "I Systemic chemotherapy with doxorubicin and cisplatin High-dosage glucocorticoids ‘Tyrosine kinase inhibitor therapy Thalidomide therapy ronp> 32 1% old woman seeks treatment for infertility. She and her husband have been trying to conceive for the past year without success. She had axillary and pubic hair development at age 11 years, but had no breast development and never had spontaneous menses. Subsequently, she was treated with hormone replacement therapy (estradiol and progesterone) starting at age 16 years, which induced breast development and menses. She has no anosmia, hirsutism, acne, galactorrhea, headaches, or vasomotor flushes. She does not exercise and has no history ofan eating disorder. ‘On physical examination, her blood pressure is 110/60 mm Hg, Her height is 62.5 in (158.8 em), and weight is 114 Ib G18 kg) (BMI = 20.5 kg/m’). Her breast development is Tanner stage 5, and she has no masses or galactorthea. Pelvic examination demonstrates Tanner stage 5 pubic hair, « small uterus, and nonpalpable ovaries. 28 ESAP 2018—QUESTIONSLaboratory test results: LH= <1.0 mIU/mL (1.0-18.0 mIU/mL) (SE <1.0 1U/L [1.0-18.0 IU/L), FSH = <2.0 m{U/ml (2.0-12.0 mIU/mL) (SI: <2.0 TU/L [2.0-12.0 IU/L) Estradiol = <10 pg/mL (10-180 pg/mL) (SI: <36.7 pmoVL [36.7-560.8 pmol/L) Prolactin = 10 ng/mL (4-30 ng/mL) (SI: 0.43 nmoV/L [0.17-1.30 nmoV/L]) ‘TSH = 1.2 mIU/L (0.5-5.0 mIU/L) Free T, = 0.9 ng/dL. (0.8-1.8 ng/dL) (SI: 11.6 pmol/L [10.30-23.17 pmolL]) Cortisol (8 AM) = 19.9 yo/dL (18 pg/L) (SI: $49.0 nmoV/L [>496.6 nmoV/L]) MRI of the pituitary and hypothalamus is normal, Which of the following is the best treatment for this patient's infertility? .. Estradiol and progesterone Letrozole A B. C. Clomiphene citrate D. E. ). Recombinant FSH ‘Human menopausal gonadotropin BBQ Afr yesrold man is efecto you for management of obesity. Despite attempting lifestyle modifeation for 6 months, he has not lost weight. His primary care physician prescribed phentermine, 37.5 mg daily, and he has been taking this medication for 12 weeks. He reports a 12-Ib (5.5-kg) weight loss since starting phentermine and is happy with the response. His only complaint has been increased insomnia, He has a history of depression and hypertension but is otherwise healthy. His medications include lisinopril, 20 mg daily, and fluoxetine, 20 mg daily. On physical examination, his blood pressure is 148/92 mm Hg and pulse rate is 84 beats/min. His height is (69.7 in (177 em), and weight is 264 Ib (120 kg) (BMI = 38.2 kg/m’). He is healthy appearing. He does not have a rounded face, but he does have acanthosis nigricans on neck examination. There are no abdominal striae. The rest of his examination findings are normal. His last hemoglobin A,, measurement at his primary care clinic 2 days ago was 6.9% (52. mmol/mol). In addition to continuing healthful eating and regular exercise, which of the following is the best recommendation now? Continue phentermine at the same dosage Continue phentermine at the same dosage and add metoprolol, 50 mg twice daily Stop phentermine and continue lifestyle modification Stop phentermine and start lorcaserin, 10 mg twice daily Stop phentermine and start liraglutide, increasing the dosage as tolerated to 3 mg daily moOD> BA. 4 38yesnold man presents to discuss his androgen levels. To years ago, he began weighing program but was not satisfied with his muscle growth. He did some reading online and spoke with several bodybuilders and fitness trainers. He decided to begin a compounded mixture of trenbolone, nandrolone, and testosterone cypionate that he obtained online from another country. He administers this regimen via intramuscular injection once weekly in addition to intramuscular hCG. While on this regimen, the patient has noticed increased muscle mass, less fat mass, and increased libido. His significant other has commented that he is more aggressive at times. The patient goes to the gym 5 to 6 days per week and drinks 4 alcoholic beverages per week. He takes no prescription medications but does take several supplements for bodybuilding. On physical examination, his blood pressure is 137/85 mm Hg. His height is 67 in (170 cm), and weight is, 202 Ib (92 kg) (BMI = 31.6 kg/m”). He is very muscular and has no gynecomastia. Testes are 15 mL bilaterally without masses. ESAP 2018—QUESTIONS 29Laboratory test results: ‘Total testosterone = 918 ng/L (300-900 ng/dL) (SI: 31.9 nmoVL [10.4-31.2 nmoVL]) Bioavailable testosterone = 767 ng/L. (128-430 ng/dL) (SI: 26.6 nmol/L (4.4-14.9 nmol/L) On further questioning, the patient admits to taking something else. Which of the following is he most likely taking? Anastrozole Clomiphene citrate Recombinant FSH Oxandrolone Stanozolol mooD> 3 ‘A 43-year-old woman is referred to you for “treatment-resistant hyperthyroidism.” Her primary care physician diagnosed hyperthyroidism 6 months ago and methimazole was prescribed. Despite escalation of her dosage, she remained biochemically hyperthyroid. Ultimately, the patient decided to discontinue her antithyroid medication, as she felt worse while on therapy. Today, the patient feels well and has no symptoms of hyperthyroidism, On physical examination, her blood pressure is 125/76 mm Hg and pulse rate is 74 beats/min, Her height {63 in (160 cm), and weight is 124 Ib (56.4 kg) (BMI = 22 kg/m’). Her thyroid gland is of normal size and texture, She has no tremor of her outstretched hands and has normal patellar reflexes. She does not take any prescribed medications. She does, however, take several over-the-counter supplements and provides you with a list, which includes large doses of the following: ginkgo, biotin, valerian, and bladderwrack, Serial thyroid function blood test results are shown (see table). ‘Measurement ‘Time of Assessment [E Months Ago [3 Months Ago | 2Months Ago Today (No Therapy) _| (On Mathimazole) | (Increased Methimazole Dosage) | (No Therapy) TSH oor mua [0.01 miu 0.02 mU/L (0.07 mivAL Free, Banga [87 ng/dl 3.3 mg/dl ‘25 ngldl Waspmeny [47.6pmony | 42.5 pmo) (45.0 pouty Total, ‘S00 ng/aL. | 580 ng/L 560 ngial. SiO ng/dl Tramorty [@a7nmovt) | @Snmolt) (@.9nmol} Felerence ranges: TSH, 05-50 miUA; fea T, 08-18 ng/L. (I 10:30-23.17 pmol otal, 70-200 ng (Sk: .08-2.08 nm) Which of the following is the best next step to diagnose this patient's condition? Fecal levothyroxine measurement Repeated thyroid testing after discontinuation of the patient's supplements "| thyroid sean and uptake Urinary iodine measurement , suppression test PoOp> 36° 44-year-old woman with diabetes mellitus is admitted to the hospital with diabetic ketoacidosis. Progress notes from her primary care physician suggest that she has a history of long-term nonadherence to her treatment regimen. Diabetes mellitus was diagnosed 4 years ago, and she was initially treated with metformin and sitagliptin, and then switched to insulin glargine 3 months later. She was given a prescription for premeal rapid-acting insulin, which she has never filled. Her current medications include bupropion; fluoxetine; ‘gabapentin; levothyroxine; phentermine; tapentadol; insulin aspart; and insulin glargine, 15 units every ‘morning. She does not check her glucose levels daily, but when she does, the values are greater than 300 mg/dL. (16.7 mmol/L). 30 ESAP 2018—QUESTIONSShe has been losing weight, but she also notes that she eats infrequently. She is stressed with work and she ‘wonders whether this has contributed to her high blood glucose values. She expresses anger that her boss does not allow her to take breaks to check her blood glucose or to administer insulin injections. The patient states that no cone educated her about her diagnosis or the treatment necessary to improve symptoms. However, review of her medical records shows that she has seen a diabetes educator and that she participated in group diabetes education classes, Her hospital record documents that she requested and has been given opioids daily for abdominal pain, She reports no nausea, Vomiting, or abdominal pain at this time. She states that she does not induce vomiting and does not binge eat. She last saw her endocrinologist 6 months ago, and she has no follow-up appointment scheduled. Review of systems is notable for fatigue, insomnia, reduced pleasure in normal activities, and feeling ‘angry about having diabetes. She expresses having muscle pain “all over.” On physical examination, her blood pressure is 109/72 mm Hg and pulse rate is 78 beats/min. Her height is 662 in (157.5 cm), and weight is 116.5 Ib (53 kg) (BMI = 21.3 kg/m’). Examination findings are normal. Which of the following is the most likely underlying diagnosis? Depression Eating disorder Factitious disorder Narcotic abuse Fibromyalgia ppoee QZ Aiccarold man wih longstanding type 2 diabetes melts presents to discuss his worsening sexual function, Over the past 8 years, his erectile function has gradually declined. Several years ago, he was prescribed tadalafil, 20 mg, as needed for treatment of erectile dysfunction. The medication intially improved his ‘erectile function but this is no longer the case. He has been married for 12 years and has fathered one child. He reporis @ healthy relationship with his wife and has sexual thoughts daily. He reports no depressive symptoms. His current medications are atorvastatin, insulin glargine, lisinopril, and metformin On physical examination, his blood pressure is 134/88 mm Hg. His height is 69 in (175 cm), and weight is 192 Ib (87 kg) (BMI = 28.4 kg/m). Physical examination findings are unremarkable. Testes are 20 mL bilaterally without masses. Laboratory test results: Hemoglobin A,, = 7.3% (4.0%-5.6%) (56 mmol/mol [20-38 mmol/mol]) ‘Total testosterone (8 AM) = 295 ng/L. (300-900 ng/L) (SI: 10.2 nmol/L [10.4-31.2 nmol/L]) Which of the following would you recommend next for treatment of his erectile dysfunction? Alprostadil (intracavernosal injection) Papaverine (intracavernosal injection) Sildenafil (oral) ‘Testosterone cypionate (intramuscular injection) ‘Vacuum constriction device moAp> BG ARtsesreld man is refered to you because of polyuria and polydipsia, He reports dinkng 2103 gallons of water daily and urinating a similar amount, He has had this problem for about 10 years, but it thas become much worse during the past 6 months. He urinates 2 to 3 times at night. He has a history of depression and currently takes fluoxetine. He is otherwise healthy and has no history of head trauma, weight change, cold intolerance, or erectile dysfunction Physical examination findings are normal. His blood pressure is 126/80 mm Hg, and pulse rate is 78 beats/min. His height is 70 in (178 cm), and weight is 215.5 Ib (98 kg) (BMI = 30.9 kg/m. ESAP 2018—QUESTIONS 31