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 ESAP™2021
Endocrine Society's
Endocrine Self-Assessment Program
Questions, Answers, and Discussions

Lisa R. Tannock, MD, Program Chair Mark Gurnell, MBBS, MA Roberto Salvatori, MD
Professor of Medicine {Med Ed), PhD, FRCP Professor of Medicine
Chief, Division of Endocrinology Professor of Clinical Endocrinology Medical Director.

and Molecular Medicine & Clinical SubDcan .Johns Hopkins Pituita ry Center
University of Kentucky and University of Cambridge, Johns Hopkins University
Department of Veterans Affairs Wellcome Trust-MRC Institute
of Metabolic Science & Aniket Sidhaye, MD
Barbara Gisella Carranza Leon, MD School of Clinical Medicine Assist ant Professor of Medicine

Assistant Professor of Medicine .Johns Hopkins University

Division of Diabetes, Endocrinology, Steven B. Magill, MD, PhD
and Metabolism Associate Clinical Professor of Medicine Savitha Subramanian, MD
Vanderbilt University Medical Center Endocrinology, Diabetes, and Metabolism Associate Professor of Medicine
Medical College of Wisconsin University of Washington

Alice Y. Chang, MD, MSc

Assistant Professor Sarah E. Mayson, MD Anand Vaidya, MD, MMSC
Division of Endocrinology, Associate Professor of Medicine Associate Professor of Medicine
Diabetes, and Nutrition Director of the Endocrinology Brigham and Women's Hospital
Mayo Clinic Fellowship Program Harvard Medical School
Division of Endocrinology,

Dima Lutfi Diab, MD Metabolism, and Diabetes Thomas J. Weber, MD

Associate Professor of Clinical Medicine University of Colorado School of Medicine Associate Professor of Medicine
University of Cincinnati Division of Endocrinology,
Kevin M. Pantalone, DO, FACE Metabolism, and Nutrition

Nazanene H. Esfandiari, MD Staff Endocrinologist Duke University Medical Center

Associate Professor Director of Diabetes Initiatives

University of Michigan Department of Endocrinology Abbie L. Young, MS, CGC, ELS(D)

Cleveland Clinic Medical Editor

Mathis Grossmann, MD, PhD, FRACP

Professor of Medicine Deepika Reddy, MD

University of Melbourne Associate Professor of Medicine

Austin Health Division of Diabetes, Endocrinology,

and Metabolism
University of Utah Healthcare

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On the Cover: Left: PhotJqruph of tf:e cytopotholcg.<. findin,ls ot cribriform-mornlcr

vorial"'.t ot pop.liar; t•1yroiG ccncet sh::iwing hypercellularity, a cribr'f:Jro, p □ttem,
Mon..les, pew'ior n;,cleor c;earing, □ nri tl-e otisen:e o! co:loid in t~e backgro~rid.
Upper righl: Pituitary MRi S"lawlng a 1.4-cm pituitary rnocroodenomo with moss effect on
the-right coli-errio!JS slmis b,rt without chiosrnotlc con1pces~ion in a potient with ocromegoly.
Lower right: X-roy showing marked subperiosteol onC endosteal cortical thickening of
bilate,al femoral Ciophyses, wh:ch is ch □ rrKwristic of p;ogcessive ::llophy5eol dy~p·oslo
OVERVIEW • 'lecog11ize c::,;ical mc::-,ifestat:cms of cndocr'ne
The f-ndocrine SEclf-As,;ec.,;1~1em f)roqror'. (1-'SAF"'') is n end '11eta::iolic disorciers ord select oc:1c:,g c,::-rer,t
'.;elf-i;'.,:,dy rur·ic:.1lurr nin1fir, :1t ,Jh\n;1(:inr1::, .scckiny ir1i1::1I opticms fo1· diognoo<s, :---1w;agement, ond the:-cipy.
c crt:licolion or tCCCf tific.1lic·: in c•;doc·inolo(Jy, oro9·arn ~ ·dentify ,;sk focto1·s fm u 1 doclne a 0:d rnetabok
dircctoro interested in a testing and troini119 instrument, disor(,p:·s 0nd deve:op strm:eg,es ~er prevent:o,,.
and cl:nicioris si:np:y wontins o sd'-ossessmcnt oriel nrcod • ::vo:uc.1le crid:xr:ne o·od meton:::ilic 1~anifestat:c,r,s o~
review of e".docrinolcgy. ESAP 2021 is available ::o both syste'Y!'c c'sord1.1 rs.
rrint a:,d oni:ne fc:;-crwts. It consi.:;ts of .120 bra:,d-11ew • ~Jse exist:ng ·csourccs percciniri(J lo dir1icil
mu:tip:--choice quest:;ns in di areas of endou:nology, guideli;,es o:,d tre:Jtmcnt ·ecornr.,encc.1'.icns for
diabetes, c:--,d "'etabolisrn. T";ere is extersive discussion er:docr:ne ard related :-ietobolic disorclci·s to gu:dc
of each co:-rec: on.,;,ver, a corrprehensive sylloOus, and diogr,::isis a:,d t:-eatrnent.
refNP''.::es. f-SAf-' ic, 11pcJated nnr:,::illy wicb new q~estiors
ond new sylluous rr:ulcriols. TARGET AUDIENCE
ES/,P is composc:::I of two key components: the hitk:: lSA"-' is u self study c.uriculu;n ninwd ot phys:cirn1s
o:oline :nteractive n•odule :me the ;:irinted book. Up:::,n scs::king init'::il ccrtikot'::;n o- rcccrlificulion ..,
purc:,ose. leon,ers will ini1 :ally receive access to the or:ine end::icr:nology, vogro:--r :lirecto1·s in:crcotcd in u tc-.;U·:(J u•'.(,
n:ociule. To use L.SA~' as a true se:f--ossessrnent tool, tcainil".:_:J i:ostru':lent. ar,d clinicians s:".loly wcnting a se·1
lec:-ncrs are strongly e1KOLll"cgecl to corr::Jlete tbe onli 0;e assessment and brcod revievv o~ er,docr:nolofJY-
i ~teroctive self-cs.sf!ssment :nodule fi:-st Oefore c::;ntirdng
sP·{-;;trK:ywi11a 1hP pri:'ted nnok; the online 1~:::idule >;1ay be STATEMENT OF INDEPENDENCE
occesseo al cUurntion.0ridocr'nc.orq. As a prov:der of Cf.E oc:redited ::iy the A:crec:tation
Co,,nci· for ConlimJi>'.g :v1edicol Fduc:Jticn; the E:,docr:~e
ACCREDITATION STATEMENT Soc'cty hos o :Joi icy of cn.s-1ririy thot thf! untent o:,d q.1olity

,~❖
::,e [:1doc:·ine Soc::e:y :s accredited l::y of this oducation::il oc:ivity c.1re :Jak1·;ccd, :ndep<'ndf:n1
fr1e .Accrec:tatlon Cou :cil for Cc:-,tinu:ng
0 object:ve, and sc:e.-,tifically r'gorous. T•;c sc:c•:lilic rnnlent
fJiedic:al i::JucotiM to provide contnuir:g 'i!ACCMEJ
rn
ACU(Ull; WI; I'
of this activity vvos develoi:;ec uncer tho supcrvio'on of t·;c
r'ledico: educatic:, for physicio~s. (0',IM[-IWMIIJN
[ndccrine Soc:e1y's ESAD ;:;oculty V\lorKi11g Grc~m.
Tc'e Frdocr:ne Soc:e:y :,as received
Acce:Jiccl.ion with Commf!ncJoticr. T".e Fndocrine Society DISCLOSURE POLICY
dcsig•;atcs this crio'.,rin(,: rno!.er::,I for c, m:1ximum of 40.0 The fc::ulty, COIT'~ittee rne~ners, ::md stcff wf:-.:, are:,:
A.MA P,'iA Cotcgory 1 crc,dits ". Physicians should cairn poS:tion to co,,trol the conten~ of this activity ore recJired
only the credit co:nmens~ro:e with ~~,c cxtc-;t cf their lo d'.sc:)se tc: thf! F·odoc:rinf! Soc:ety anci to leo:ne•s any
parfrioa:ior, in the activity. re·cvunt 1 im.mc:1.11 re:oliorr;hi,,(.s) oft:,e ino:viou:JI or spol.se/
port11cr thoc hove occut·cd wd::n th-: ios:. ': 7 P10ntns wich
MAINTENANCE OF CERTIFICATION :Jny cornr:iercial intNcst(s) whose' prnd,:cls or st:"vir:es
s~:cessfol co!T'pletion ot this ore related :o the CME cortent. F:nancbl ·elations hips
Crv'.F act:vity, which :ncl~des are def-:ned by rer:l,merat:on :n or,y amount •rom t:-,c
p(,ri:ci,)mior'. in thf! o:cvoluotior. commercial inte:-est(s) :n :r:e form o~ grants: resec~ch
::o,·1ooner1t, cnublcs the support; consu:ting fees: salary; cwnersf:ip i:,tecest (eg,
po!<'ciocmt to cam :.,o to 40 MOC po'nts in the An~e·icon stocks, stock op;ons, ::ir owreship in:erest exc:c::Jing
Board of lr,tecnol Medici:oe·s (.AB·M) Mo'ntcncncc of diversi"Ged mutual furds); honorario or cc';er payments
Certification Uv10C) ;:,rogr:Jm. :tis tf.e CM': activity ror pmlicip:.1tio,i iri spenkNs' bure011s, advisory boa 0 ds, or
provider"s responsibility to submit participant :omp:etion boards of ci'rectors: v oth:· firiuncicl bf!nf!fit~·,. Thf! .ntent
in~c:-matior: to the Accedi:ction Council foe Cor>tinuing ::if tf.:s disclosure is not to prevent CME: plur1,:e,s with
Medical Educatio:-, fo1·the pJrpose c'. gro,;ting .AOIM MOC relevcnt fi:--.oncial rebtio:.sf.:ps from 1~lannin9 or cc,:iveri':(J
rrerlit. conte'lt, bc1t mther t::a pcov:de learners wit!--, in•ormot:e; lhol
allows them :c rr:akc: their own judgmer,ts of w:s,e:rer these
LEARNING OBJECTIVES fino:-,cioi relations';ips may f;aw: influenceO the edtxaticnol
ES!',P 2022. vvil· C":::>W :e::irrc~s to osscss their l(J1ow!edgf! activ;ty with :--sgarci tc expositon or conclusior:. :he
'.Jf all aspects o~ e:odocr:nology, dicbctcs, Olld mctobolism, FnrJocr••of! Society hes •eviewed all c:sc:osures and resolvcc
dpon cornplet:on of this ed,xa::0110: activity, lec·ncrs will nr monuye'd o·I iof'rtified ;_crf:::::ts of i~te:est, os opplicablc.
:::ie ab:e to: ; he fo":JWinq foc.1lty rf!ro:-ted re:evm1t financiol
rcloc:vnsh:o(s): Alice Y. Chong, MD, MSc, is c site
investigator and on the advisory board for clinical POLICY ON UNLABELED/OFF-LABEL USE
trial for Millendo Therapeutics. She is also on the The Endocrine Society has determined that disclosure of
national advisory board for Corcept Therapeutics. unlabeled/off-label or investigational use of commercial
Roberto Salvatori, MD, receives grant funds from product(s) is informative for audiences and therefore
Roche, and he is on the advisory board of Pfizer and requires this information to be disclosed to the learners
NovoNordisk. He serves as a clinical trial investigator at the beginning of the presentation. Uses of specific
for Novartis, Chiasma, OPKO, Strongbridge Biopharmo, therapeutic agents, devices, and other products discussed
Corcept Therapeutics, and Crinetics Pharmaceuticals. in this educational activity may not be the same as those
Savitha Subramanian, MD, serves on the advisory board indicated in product labeling approved by the Food and
for Sanofi. Anand Vaidya, MD, MMSC, is a consultant Drug Administration {FDA). The Endocrine Society requires
for Selenity Therapeutics, HRA Pharma, and Orphagen that any discussions of such "off-label" use be based on
Pharmaceuticals. Thomas J. Weber, MD, is a consultant for scientific research that conforms to generally accepted
Ultragenyx Pharmaceutical and Pharmacosmos, He is also standards of experimental design, data collection, and
a primary investigator for Ultragenyx Pharmaceutical. His data analysis. Before recommending or prescribing any
s pause is an editor for Nivalis Therapeutics and a primary therapeutic agent or device, learl'lers should review the
investigator for AstraZeneca. Kevin M. Pantalone, DO, is a complete prescribing information, including indications,
consultant for AstraZeneca, Bayer, Corcept Therapeutics, contraindications, warnings, precautions, and adverse
Eli Lilly, Merck, and Novo Nordisk and a speaker for events.
AstraZeneca, Merck, and Novo Nordisk. He has received
research support from Bayer, Merck, and Novo Nordisk. PRIVACY AND CONFIDENTIALITY STATEMENT
The following committee members reported no The Endocrine Society will record learner's personal
relevant financial relationships: Lisa R. Tannock, MD; information as provided on CME evaluations to allow for
Barbara Gisella Carranza Leon, MD; Dima Lutfi Diab, MD; issuance and tracking of CME certificates. The Endocrine
Nazanene H. Esfandiari, MD; Mathis Grossmann, MD, Society may also track aggregate responses to questions in
PhD, FRCP; Mark Gurnelt, MBBS, MA (Med Ed), PhD; activities pnd evaluations and use these data to inform t he
Steven B. Magill, MD, PhD; Deepika Reddy, MD; ongoing evaluation and improvement of its CME program.
Aniket Sidhaye, MD; Sarah E. Mayson, MD. No individual performance data or any other personal
The medical editor for this program, information collected from evaluations will be shared with
Abbie L. Young, MS, CGC, ELS(D). reported no relevant third parties.
ti nancial relationships.
The Endocrine Society staff associated with the ACKNOWLEDGMENT OF
development of content for this activity reported no COMMERCIAL SUPPORT
relevant financial relationships. This activity is not supported by educational grant(s) or
other funds from any commercial supporter.
DISCLAIMERS
The information presented in this activity represents the AMA PRA CATEGORY 1 CREDIT
opinion of the faculty and is not necessarily the official (CME) INFORMATION
position of the Endocrine Society. To receive a maximum of 40.0 AMA PRA Category 1
Credits. participants must complete the online interactive
USE OF PROFESSIONAL JUDGMENT: module and activity evaluation located at education.
The educational content in this self-assessment test relates endocrine.org. Participants must achieve a minimum score
to basic principles of diagnosis and therapy and does not of 70% to claim CME credit. After initially completing the
substitute for individual patient assessment based on module, if participants do not achieve a minimum score of
the health care provider's examination of the patient and 70%, they hove the option to change their answers and make
consideration of laboratory data and other factors unique additional attempts to achieve a passing score. Learners also
to the patient. Standards in medicine change as new data have the option to clear all answers and start over.
become available.
METHOD OF PARTICIPATION
DRUGS AND DOSAGES: This enduring material is presented online and in print
When prescribing medications, the physician is advised to format. The estimated time to complete this activ ity,
check the product information sheet accompanying each including review of material. is 40 hours. Participants
drug to verify conditions of use and to identify any changes must achieve a minimum score of 70% to claim CME credit
in drug dosage schedule or contraindications. and MOC points. After initially completing the module{s),

4 ESAP 2021
if po, Udpot·ls do r•ot achieve o mh:num sccrc :::,f 70%,
t".ey :.ave the option to change their answers anci make
additiona: :1tter:1p1c; to achieve o passing score. Pa~ticipo,..,ts
a:so have the op:ict' to clear all answers and s:ar: ove.

SYSTEM REQUIREMENTS
:o complete this oc:,ivity, omtiripnnts m11s, have access to
a cor'f'p11ler or mol:ile device with an lnterne: conriectio'l
and use on uo to dote Web browser. In adrJ:tion, coo¼:ies
md J:Jv::iscript muse be cr·ubled in t•,e browser's options.

LAST REVIEW DATE: t'-:ovember 2020

ACTIVITY RELEASE DATE:Ja,,:ary 2021

ACTIVITY EXPIRATION DATE: December 31, 2023

(dutc ufll;:· which chis etxlurirg mntf:riol is no lon~er
certified iot .AJu1A PRA Co:cgory 1 Credits (l'ld AFW'.11
Medical Krowledge MOC pointsj

r- or aciestions abou: cor12:,t or ob:cining ChiE c:edi: or

MOC points, please contac: the E:-,docr:ne Sociely at
:-, ttp://eci .-ca:: on.endocrire.org/co1;tact.

5
 Laboratory Reference Ranges
f{e!e·er1ec 1:;c•ges var_v c'17ocg labo,·(;tc;-ie:;. ; he :,s1(cd rr!(,ra1u' rnoJc~ S'"1C'Jlc oe 'Jseci v1:ien 1r1terp,et:r:::,
btor□ rnry v:Jh.::::s presented '7 C:SN''" Ccnvent:c•:1al units are ii:,ted fit·,;•, with SI Jnics ,,, ::,c:e1-,thes<c 0,.

Lipid Values
Higt: :irn<ty hpoar::;tein iHDL) dlO'r~t,:,rol ·:·•,ycoii-s:imt:lc1\;,1g i:-r,m,,noglocu:,n- ---eo,J.LG% ol :Jmc: m.L:vily
----- .,GG mgf'.1~ {SI: >l.5S cr:tT10:1l.) '':;i:Oce:o;;ir'.os<c !; PU) anl.:JoC1eo --- - <.2.0 IIJ/,r,. [SI: < 7.0 klL:1I ;
- L0-60 cr·g/dL (S:. 1.Q4- l.55 :r;mo:iL) '":>ycox1ne I;,) :1ree) --- .. ,. . .-Q 8 1.8 nglr:: (SI; 10 30 ).~.17 ;,1110"(1 /
-- - -- - -- - -- - -- - - -- - <40 mg/.ic {'.'ii: d.0,1 ~;mo•/LJ '.>1y:-oxi·1e F,l {lolol)
I-rec 1:1yrc"Jx:11e (T_1; ''ldcx - 4-12
--------- <:CO mg/al {SI: <2.59 ·uno·/1) "'."ri·rnk:~1-,ycoi,:nc '.T-,) (free) -2..3-4.7. pglr:1L (SI: J.5:'-0.4':i CIT'oliL:
Luw--• 100-129 •r;g/dl. /;': 7.:09 :l.:l4 rrmri/L) Tri,cd::icry"or--ne :·:·,: i:ot:JI: - 70-2JC 112/dl. (SI· 1.0S-3 GB prml1L;
F:ordrrlirs,• hi-;h UO 159 rrglrll (S : 3.37 -4.~2 1,mo'/L)
Hi-;1 ··---- ---- 160-18') 1,qldL ('~1: 4.lL-4.98 n:rno::u
Very h:s•1 __ ,,___ -------------- 2~90 r:19/dl. ;s1: ~4.92 mmoi.J
"wn-1 JC'- ~:•olc<,lc!:o:
CJptirr:.J,- - - .. - -- .. - .. - ---- ---- -- - ---- - <'30 l":'19/dl :s1. <3 ..'.'/ fllr'lO:/~] Endocrine Values
□ o,derF'1c-h19I' ------ U0-1':,'3 :ng/C~ iSI: 3.37-<l..; 7 mrno'/: J

High- -------------- ~240 r:1y/dl (SI: ~f,./ ✓ rnrin:/~I Scrum

1::im: chJlt>,-Cc,o·
<700 n10/dl \SI: <:i.~8 rrwm:/~]
FJo•(b'•,(' h;gr 200-2:3'J mg.Id~ 1SI: 518-6.~9 rnrw:!:_I A.:kalir.e :,hcspra:::1,.e (Joce-~pedi•L:
Hic;h -- 2cLLO !"'lgidl \S:: e:6.22 mr:m,/c.l •
0
'.,1 pglc. (pre1~·1erm,-JULsul f~r;7t,•c1:
:,,_L'. µ9!~ 1µ0~'.r•1eno:,m,:;ol fi~1"1:,:f')
Op'.lll'GI < lC,O mc_;tdl. !S:. <1./0 m1":'d/c.J r,r,U,o~Le•:eoio•1(i 6'i ? .1.0 rgl:J: (5" 2 n 7.":~:3 11,1d'...) (c1C'.1lt rc1U't>);
Bo·der··•,e-h:gf: 158- '. 99 l'lg/a~ {SI: : J0-2.h r;ir•,d/~) JC ?00 icgk:. (SI· 1.:Y:C-6.98 rmo:/L) {ouull te·Dale;
I1igh-- -- -- - -- ---- -- - ---- ---- - 20Q-,l99 t":lg/CL {SI: 2.~6-5.64 r'1r:idl:.j Anti1'<JIINi:in ro1T1::ine -- ---- 0.7- ~9.0 ,,gl1:1L :s:: 5.0- '. :'5.7 cmoliL.:
Very t,igh - -- -- - -- - -- - -- .,., ________ 2c':JOO rn:]ldL \S· -~5.6'.' rnr1~,11: 1 (1,cile, >12years];
0.9-9.5 i,g/mL (SI: 6.4- 57 .9 P'H.JI/L\ (:'e1TcJle, J.:,H !.., ycc:rsi
Apolipapcotein 13 --------------- ----- 5C 110 rng/dL \SI: Ci.5-1.1 9/~j <1.0 r:g/ml. (S,; <7. l pnw/l.) {fer:ne >4b years)
ca:citrnil' ---- ---- - -- -------<10 pg!t":lL ;s1: <'1.6/ µr:10·/c.) :busul ,role):
Hematologic Values <S pg/n'~ {SI: <L:H p:,,ul/L: (L>u~:..,I, f~rn::·ej;
,-,;130 pg,lnL (:C:·: .c::37.96 p·r,olil; f:icuk cnI.~:<1r1 iic-:'l,sior,, rnalr):
Haptn::loCin ----··--· ····--·--· '30-20S mg/:;i~ iSI: 3QG- 2GO'.) ~;q/L) eo,90 py/r'1L :s1: :.76.78 prndl'. j \cc:-:k calcium i1·,fus'o1·, fo:irnle;
HcrrillUU'l--------------------------41 'Yo-50% {SI: JA1.-0.':,l) {rm:"): C:..,•Lir:ocr•1bryo:iir: c1ti:1e11 -------- <2.5 rg!mL (Si: <2 5 µg/L)
JS')t,.L5c,,, {51 0.35-0.43; ffeni:;,;el ::::t:ro·r:og•an''l A --------- <93 :1gh:~ ISi: <93 p91t.;
f lecr:oglooin A,, -- 4.0%-5,()% {20-::0E n:mo·hno:) -~.,r~irc"tcrcne ---53- ~SSO n9/dL :s1: 1.5.J- 45.DB ~mo:/l.) {> 18 years)
I 1e~'oglobin - ---- _;_J,8-1/.L g.1G'.. !SI: U8-172. :,;/I) {mc·c): C::inc::i-::npir ::,CT':) - --·- ---- ---- ---- "'. 2-t,0 pg/ml {'.;I: 2 2 -13.2 p1-~o-1L;
12.1-1:l.~ t;,'dL (SI: 121-lSl g_lL) (1trnale) Ccirtiscl (8 MAi -- -- - -- - ---- - -- - -- b-Lb ,-19/dl {SI: J.J/.::J-029./ :1r10:IL)
lnle.-:-1ulio,1t1I nC'rrr:illi;,~d rafr1 ·--0.3-1.2 Cons,! (4 ?,,1;- ---L-14 ~g/dL :s1- ':J5.L-c'86.2 ·ir:10·/I)
C- prptide -- ----- -C.9 <.? ·1gi,n:. (:"·: 0.30 ·1 .4? ~ri,,:/1)
~30-450 x 103/~L (S:: lSS-430 x lO"iL.: L-re□ ctivce :.irc'.e,n -- O.f: :!.1 rnc;/1 \SI' 7.62-29.52 11,10'/L)
" -- - -- - -- - ---- ---6.J-7.9 gidL /SI: 63- 79 911.! C·o~:,-li·1kcid H-'.eiopeptidc or ~y;,P I cn"aqcn --
flel,cu:,xyte cour·: "- O.':'%- "'.5S1, of :ed bbo~ :d:s '.SI: 0.003-2.0:t:,; C:.4 )4.7 r.T,OI R[~,tmno! ,,roe (1,ulc;:
wr:tt b:CL}d <.:e:: COL::1t - - .. --- ,1 !:,00-1:.00J/pL (S·: 4.S- J. l Ox 10'1L: G./ \'::.O i,crol BCC/mmo' ~",?□' (ten,ole;
Ochydroepic:,1d•ostero11e ~u·iott> iJf I[/\- S!
Thyroid Va!ues ?c,t:er·: Age lcrno:e
1,:·,t:00lcbU"'1 ·----- - 3-il2 n:,;/rn[ iSI: .1 4? :1,yL.; lot:cr ,u~gpry r,m: 18-2'::! ye::ics 4,1-3?.2 µc_;!dl.
ru:Jiuuct1ve ,,xl1·ie '.wul•T;('nt: < 1.0 nqlmL \S" <1.0 pg1L;1
T•1y,09ld.tll'''I □ l'CICoJies -------,AO IU_i--r,~ [SI: .c::4.0 klUili
T:1y,o:r•;pi,• {TSl-•j -------0.S-5.~• cr"'.JIL (:;i: 0.2 11-6./8 µrno·/L) {SI: ~ 76 9.C::' p~:ol/l !

6 I'
 f\1tit>1;'. /\gr ~er:1ole l·i'.clr:: Pa'.ientAge Male

-10-49 ve□ rs l8--2,;.4 1;g/:;i~ 48-Z'14 11(]/dl 11-hyems lHi-31\1 r1y/n1L iH.:i-3,11 rglmL

>60 yeurs 2':J-Hl c1g/dL 1::.3-19/ 1:9/m'- 1l3 797 n,;/n1L

l:C.I: 0.41-4.2~ µrnol/L; (SI: J GB-3.5:_;: pmol/L) :s: l".3-.12.9 ·1rno·/I) :s:: 14-8 38.9 n·nol/L;
Joecxyco1t'costcr0nc <lO n;,;/dl :s1: <0.::JG nmcllU ::<lB )'UffS] 'IOG 777 ng/r•1L ·1 O:i /17 "lg/crl

~,2S-Dit-ydroxyvitc11i1·, D,- 16 65 cglrr;:_ ISI: 4::_ fi- lG:J.G p1'1cll:_J (SI: 1.3.9-3[; CJ Grrol/1) {SI: U.'J-36.3 nrnd/l)
Lstn::dio: --------------- 10-40 p::Jml (SI: :':6.7 !.46.8 p•r:oliL; [male). ;JS-261 n:;;(1T1L
J..:). '. 80 pgkr~ (SI: 36.7-660.8 ;:;r-10:/L) (foli:c<1lc•, for'Hlil'): {SI: l2.B-34.2 nrnol/L! ISi: 12.8-34.2 ·1rr,ol/'...i
10:.J-300 PSirT',. {SI: 3E7.1--1 J..Sl.J pr,--ol/LJ (riidcyc:C', frT,alc): 46-:JO years ?.1-246 rglm'... 91-2L6tig/ml

40-200 pg1:nL (SI: HG,8-734,2 prio:/'...) 1:c1te □ I. fe1,Gle); (SI: J..:.9-.32:.2 nmol/L) (~I: a9-32.2 rmo:/Ll
<7::l ;:g/,n'- (SI: </3_'1 pMo:/L) {p::ist1;1enop::ius<i:, '.emale) 84-233 rgl1-:1L 84- 233 :19/cr.L
·:0-6:) pgicr''- (SI: 37.0-2?::...9 pr:101/ .I ::r-ale):
17-20'.) pg!ml :s:: 6/.9 7:':9.6 fYr:oliL) (pre1-:1encpac1sal fe•wle\: 5C-6C years 78 no n9/rnl 10-no pg/IT.:...
7-40 ps;frnL [SI: 2S.9-1!.7.9 prio:11) (pm;L•r:er•op:..,~sa: Je,,;ale) {S:· 10.2-28.8 "lmri·/:) :s: 10.2-28.<' riln::il/L;
u-- ;:;r.:oorotc-;'n ----- ------------- ---- ---- · li1-65 yea:s 72-207 n9/ml 7) 707 n9/r:1L

~ollic:e-stb·,c1laticg horr10:1e {rSf I/ --- :sI: 9.4- 27 1 n:-rcl/L) {'J: 9.rl 77.1 rwo:,'I)

1.0-13.0 mlU/1":lL (S:: 1.0--1.3.'.J ·U/~1 l;n □ lc;: 66-/0 yec:·s 67 19'.: ng/rd_ 67-19~ n::/ml

<3.0 rn:J(r:1L {SI: <3.0 IU/l/ (:,rq,~i::c-i:ty, fer1c::e1: {SI. 8.8-Lb.li nmcl/L) {SI: 8.8-25 S r,1,01/L)

7.0 17.0 rn:~/n1L :s:. L.0-12.:.J ,J/c.) :toll,cula~, fern,:ei: 71. 75 vr:ur:; 62 184 :1gh:.. C2 184 :1g1mL

4 0-16-~ rr·u/rnl ;s,: 4.0-36.0 :J!:...J (1":li:xycle, fe1":lale): iSI: 8.l-2'1.1 tll'lOlf:_) !SI: 8. l- 2"-.l nmol/L:

LC-<J.O rr,IU/IT1: {SI: ':.O :'! C IU/L) (·utc'O' 'er:1ole): 76-80 years S7 l 77 rg!:,,:_ :J/-172. :ig/cr::_

>JC rnlU/rr'... (S·: >30 ·u/1) {postmcrwpod<;l.l' itcn'ale: 1SI: 7.5 n.s nr'lo:/L] (SI: /.':,-22.S rn'lcl/:.)

r:e<, '.atty adds -----------------10.6 : 3.0 f'lg/dl (SI: J.ti-C./ :•mo:1L; >80 years 53-162 r(]rl'fll 52-162 pg,\n:...

Gastri'1- <10'.: ~g/ml. (S·· <.lJC ng/L; (SI: 6.9-21.2 rmo:11.) (S:: 6.9-21.2 ,m10:!:...]
Growt'l h::irl'.10,;e iGI 11--0.01-:J.9 7 ng/ril \S·: O.Ol J 97 1:9/~.l (·r:ulc'); 2.5-4.8 ,r:gJL

0.01-3.61 :ig/1":lL \S:: 0.0~-3.61 µ;:)IL) {fem:J:el lrbJli:'-------·-··· -- ---- - -- - -- - -- ~-4-lL.J ~IU/1,L {SI: 9.7 97.7 pmol/L)
H:..,rr:ocy~1e:•1e ----------- --- - -- - -- - -------d.76 rng/L {SI: :o13 µ'T,ol/l j l:;let-cell L11'.'.ibcdy assay --- ---- - 2 J~verJe :)iabetes Fourdat'on uf'its

f) Humon ~:1orionic goncdat:api:i (fl-1:CG)-· I utr:i•:i;in:, ho,moPe {LH)--- :.C-9.0 mll,/r-1l_ :s: 1,0-9.0 IU/L/ lmo:cl;

<.1.0 mlU/rnL (SI: <3.:J IU/L; {nonp•e~'lart forrici:e): <1.:l ,T"U/rnl (S·: <'.'..0 IU/L) (prepubercy, fe:r,ale):
>25 IT,::J/ml ISi: >25 IJIL) ind:rntes o posit.,ve preg:iar:cy test 1.0-18 0 rnllJkr~ {SI: ;_ 0-18.J IU/L) (fo••icu-m. fecr:cile):
p-Hydroxy:::utyratc • ----------<3.0 Mg/dL {SI: <288.2 pr1ol/'...) 20.0-8:J.0 mlU/ml (SI: 70.0-8::J.O IU/L) {MiCcyde. ~er-ic:c-i);

17-f lydroxypregnen::iloric 79 189 ,19/,JL (SI: 0.8/-'.::.69 rn":lol/,.) ◊.5-18.C rnlU/m~ (SI: O,:i HU ·d/'-i \:-Jts'nl. female):

1. 7o:-Hyd:oxyorosestemne <22C n:,/dl \SI: <6.67 r··r:ol/L) Im LI'"( l":7:Jle): _,,30 r:11\.:/rnL {SI: >30- IU/L/ {pc5trnr:Gop'."1u~aL ft'r:1o·ej

<80 ,,gfdL (SI: <.2.42 nrnol!L! (fcllic1.:lm, fcmalc): ',4et□ r:ep'lrires {pl::ismo f ,act:orated)
<!Sb :ig/(.:_ (S!: <8.E4 nr:10:/L) {IL teal, female): f,:etcnepl:rine - --------------------d9 pf!(l'fll (SI. <0.30 n'f:o:/:_J

<"31 ng/dL (SI: <1,5G '1tr-olil.) (pos:me:1ooaLsol, fcmc'c) Nurmecal'ephl"i!'.e - ---- ---- ---- - ------ <165 pg/ml {SI: <0.90 n,ro:/L)

/ 5 f·'ydroxyvit:Jcr,:n l) ---- <2C ng/rd. [SI: <49.9 :srr:ol/L/ (defic:c-rcy): 7:'i g ort;: gluc.ose toleraPce te5t blcod glucose vah.:es------·

2.1 79 n;,/n''- (SI: 51.-1-/Lt\ ncr~ol/L/ (:ns-iffde:icy;: 60 ': JO r:19/dL {SI: 3.3-S.6 'T,\l'Ol/l.; jfcs:irg;:
3J-8C nf)/t7"1: (SI: 74 9-199./ nrnol:L; [o::1,i1m· ,evels); <200 mg/rll {SI: <11.l rr:rro·/L) (::. l:oJr::

>8C ng/rnL [S·: >199.7 m:ol/l) (:oxicity ::,oss·l::le) <'..4C rng/dl {SI: <7.B mrrd/l) (2 h::iu•·l: betwee1·, :l40-2CO r19/&.
,nhib;'1 6----···------------------- l:'i 30:J ;;gli'lL :s, lb-300 :1g/L) (SI: 7.8- 1::...1 mmo!(~) is co1si:for(~tJ :rnpui,ed glucose tolerc:nce cr

::isulidike growth fact:,r 1 (IGF-1) ;)redio(:r-i:es. Greote, 1:hcn 2:JC mgkll (SI: 11.: in:MltL; :so sign
f-'ot.e:it Age ~emole of :;i:obet.t>s l:lellitus.
13 Jc'O''S 170-6,'.:) .,g/ml 50-g o•·al g·ucose toler::ince le$t lo" ges:at'o1·,al di:-;C::e'.tc5
{SI: 2:'...2-70.9 crolil.) 1SI: n 3-83.8 "1110'/I) < 1,'10 ,r••;_i/dL (S:: <7 8 mrriO!/:,J (1 ·mur)

138-4-12 cg/1'7L '.47-527 i,g/nL 100 9 o:ril t;IU(_:;)se c0:era11:e trst '.or gesw1.:orol rli,1bdc'~ --

1sl: 18.1-:i/.9 n,rcl!L) 1SI: 19.3·59.0 m101/L/ <9S rns/dL. (SI: <:d cr~n,ol/l.: {fcs:irg;:
20 year> ':77 3fl" n:,/n1L :32-~'.,7 rg/r:1L <180 rng/dL :sr <i'..l.O l":ll'lcll'...) (1 hourJ:
(SI: '16.0 5'.:l.3 n,ncl/L) (S·: J7.3-59.9 rcr:ol/L\ <1:i'i r-1t;!dl (SI: <8.C n•mo:/LJ \:!. Pour):
-d4ll rn:,/dl :s1: </.5 'f:ri'OI/L) (31:o:ir:
 H:ond pH-
Colciun :1.7 187 rng/'J: \SI: 21-7.6 r:md/~l
P:..,•ql•,y,oi-., t:orrnonr related pr::,-;:e·n (?THrP) 4.20 5.02 m11/r: ISi: :.7 1.3 r·unn·/1)
•------------c:~.2 ns;/rnL {SI· <.1 P, nrn,,:11) :rndr;: --- 22.-?S 1cc'q/l (SI:// )R rnri,,:11)
<'..0 ngh:. [SI' ,;3_2 nmoliL) (lo'"curn, fe---r,clic;: CD, ce·I co:.inl -- 5JC-1!.0:J/µL {S:· 0.5-: 4x 10"/L/
2.0-2:::.o ng/r;~ {SI: 6.4-03.f: nrio:/~) \lciteal, fenwle): c,10,·de------ 96- :i06 nEq/~ iSI: 9E-- ~:]6 mr10:/l;
,:;~.~ ngh•~ 1SI: :S:5-5 nmol/l.) (r,ostni:iocousal, te:-rale): Cwotiri:; kirasc;- - -- - -- - ---- - -- - -- - -- 5J-2GO Uil \SI: S.84-3.JL ~k::it/l/
>lO:J n-;i,r,L :s1: >31.B ,1r10:1u {ev:denct> of ov0lotory ade::,00:vl Crc~r.ti1-,i'le --- ---- ---- ---- - C:,7 L.J 171gf::;, {SI: Gl.9-1 '.4.9 ~rr:oliL, i:T'alc-i1;
PDinsuk, ---------- ----- 2.6.S-1/6.4 Vi;/mL {SI: 3J)-.c0.0 vnol/l; O.G-1.: 'l·,g/o~ (SI: (:.::l.0-:j/,L Jr10:1~1 \fomc:e)
PrclaC:1:1 ----------- -- 4 }3 rig/ml {SI: :.J.l/-~.00 1:rrnl/l; {r'1c:e); ~erritin ----- -- ::::-200 ,:g/i,)I. :s, 33./-~,19.~ f:t'l'ol!L)
4-3'.J ng/rnl :s1: 0 ·17-1.30 nT,r:1/: I ;r:rl'lludoti,•g fN•1n:e); >4.0 ·1g/rni. (S·: .:C) :Jg/L)
10 70:l 'lq/crL :s:: 0.43-8.7:J 1mol/L) (lr:nafr1g fo1calr) .. ·---·-·--·--·-- 70·99 T,!"]/dl :s1: 3.9 55 'T:rr•0II[)
P rcst::itc-speci f:c c::11:-;en (PS/\; ----------- v-Glu'.arnyltransfero~c - ------------- 2-3C :JI~ {SI: 0.G3-0.5C µkatl~1
<2..0 c1gi~l. (SI: <2.Q :Jg/l.) {,;4'., yeo:s; !:or: - ---- - -- - -- 50-~5C pg;dl :s1: 9.0-26.2 prncll~J \n □ le):
<2..8 :igh-,L !SI: <2.8 ,1g/l) {'.".5Cl yews:: 3:0-US f.g/:J, (SI· 6.3 26.0 pr-ol1L: {fornalcil
<3.8 ng/:.,L ISi: <3.8 Jgil) {,06'..) yeo,s;: Lactate dehyC::oge:--,:ise -- --------- 100-2CO U/l !SI: :l,7--3.3 .J~ot/c)
<:d ,19/,nL \SI: <5.c' :ig/l) !:,;/0 yeu<"s:: -- :>.4-L0./ 1~·1gidl !!:>I: 0.ti-2.::S rnmo:/:...J
<7.0 ·1g/rnl ISi: <:7.0 ,iq!I) {<79 y\'urs;; I 1p,,sci 10· 7:': u/~ ISi: 0.17-1.22 ..1kat/L)
<7.7 ng/ml tSI: <:.7.?. ;1qil) (;,80 yrors/ f~ogr,,,-s ,lri 1.5 ~.:'l rngkil {SI: 0 f, 0.9 r:l/'10:11 )
Kcr:n □ ct:v:ty, p· □ s1,ci, scdium rcclc-~c,. arnbcilatory - Osr1Jlal.-c:,1---- ---------- 27:i-29!:- rrCsnV~S \SI: 275-295 rr1,ol/kq)
0.6-4.3 c•gJ1-r~ per h 2.:!-4.7 rr1g!JL {SI: 0 7- LS rnr10:1l;
'1er:'n, di:ect co:Kertr □tor -- - •--- .. -- 4.44 pg,tl'L {SI: '.)_ J .. J..(> ;Jrw:/:_J l·otuss::w1 -- - -- - ---- ---- - -- - -- - -- - -<i.5-5.0 r:1[q/~ [SI: 3.5-5.0 r:w101/l/
Sex :1ormone--b:n.-:iing gloou:'n (S! mc,1 - - -- - -- - -- - -- - - 1.1--6.7 p:J.lrnl. Pi-::,•J.:omb;n t.:T'e - 8.3- lC.8 s
{Sl.18-GQ ~n•ol/l.) (1·rro:e): ~erL~' ,wca 1;1trcgcr, ----------- 8-13 mg/c;:_ [SI: 2.9- 8 2 m1T101iL)
2.2.-1,;.o Jg/ml(::;,: LO- ~30 1-,mcl!~J :te~,cile; Sudiu,1: - - 136-.:.,1:!. rnl::q/L (S·: UG-.:.,1:!. rnmol/l)
t..: -Subu,1it of pitLit:Jry g·yc.of::roteiP ·10(n10,1es 7 ro·:sf1=rr:11 sul-Jr(;Cio·: -- 1'1%-:>0%
<L!_ ns;ln1L ::::1: <.1.2 µg/L) 7r1wo•,in I <0.6 ngh:~ 1SI: <0.6 µg/L)
0.8 ll.("; ng/dl (SI: f:.O?, 0.1.;. rrno:11) d15rg/rnl (S::-d'..:'::19/lj
17r: :'iO years, forrolc or· o:nl c\:;trogrn): -- 3.5-7.0 Mf]/dL {SI: 2C8.2-410,:1 vn1l/l)
0.8-10.0 nq/dl :s:: 0,03-0..'.lS 'llTlO'/L)
i2C:-:'>O year~. ferrale no~ on ore:' estrogen); Urine
83.C- 257.C rigl::iL !SI: 2..88-8.92 nmol/L) (crnle 20-29 yE>c~J- Alb0rnir- - ---- ---- ---- --- 30--300 µgi:T'g er eat {SI: 3.4- JJ.9 ;,g/mol creotl
72.0- 235.0 r,g/dL {SI: 2.50-8.15 nm:,1/L) (:T' □ le 30- 39 yeocs):
61,2-213.C: r,g/;:il {SI: f.12- 7.::i9 nrnol/L) (rr:ole 40-49 yeo:s)· /:.ldcstercrif--- ------------------- 3-LO µ;_:ifL.1 h (S:: 8.3-5GA 1-,mol!d)
SO.'.J-190.'.J nglc;\_ {SI: L7 4- 6.59 nm::,I/L\ (~•ale so.r_;9 yeo's). [~h:.,u•d Lie <:'.1 µy/14 :1 :s:. <3:l.2 rim::,l/dj witn orcl so:J:u1-~
1\0.C- H:i8.C rigl:J:.. {SI: : 3!:l-5.83 rnncl!L) (cr~ale liO-bc.' yea:·s/ lon(.;,ng :·on1irr:wd wil·1 24-h%: uri1-ury so(.;,ur•1 >2CO r•1E:.,j
7c'sto~tero,:e {f·ee/----- 9.0-30.0 1-,;;1dl :s, l:.31- 1.04 ,m10:1u :rn::le): c:1:1il,rr 100 300 nig/74 I' (SI: 7.5 7.5 rnmo·/d)
D 3 ; 9 n9!dl (SI: O.Cl-0.07 ninl:I/U (1errule) Cr::c·cho·a1·nirc- fn::d:onotio1
30(1 9(;0 nntdl (10.4 :':1.7 rwol/1) (rnr1r); N:xri:Jtensive m:rmal rcmges:
8-EO n~/dl (0.3-2.l nmo·/LJ (fci"fla<e] Doe,omic1e---------------- ---<4:JC pg/24 h (S:: <261C nr:10:/d]
Vito:nir fJ,, ··········-------- - 180-914 p§/ri1l \S:· 133-(i7!. pT,olll: Ep,nepbci11e -<21 µg/24 h iSI: <~ l5 nrr10:/d)
Noce:,i1-,eprri1x· -- -- - ---- ---- ---- - --<20 µg/24 h (SI: <473 nr:ioVd;
Chemistry Values ::JL0-i240 rigi2,1 h ;s:. 10./-6,1.b l';JMOlid;
A:on·ne amicio:.rcm.sferase---- ----- J.::Hl: U!L :s1: C:.17-0,C? :ikat/L/ '.:'.ortiso: ------------------ --------- 4-',0 µ,;/24 h (SI: 1.:.- US nmol/d;
/',:cu:)1ir'------------ ------------------- .. ·-2.5-5.0 gldL (S·: 3:>-SO g!L) Cortiso· iu::ow"19 c~xum1ctho:,r;nc su;:prcssio,1 test \low-d:•se
A:.,y•u~<c --.. 76 1:17 lJ/l {SI: C.4~ ;.70 ,1lc.1LiL) 2. ::iciv, 2 :r'-:, d(fry) <'.:! :Jg/?4 h :s: <J7.C, 1mol/d/
".sr,u:'tal1= arq•qr:tror;sforos,, - 20-48 UiL {SI: Ci.:33 0,20 1•katll l Creahir:<c---- ····---·: G-2.0 -;/2..1 h (5·: 8.8-~7 7 ITllllOlin;
Rico:bcT,01:e ---· ----- 21-28 r·1Eq/~ [SI: 2~ -2.8 rimcl/L) :o:orrv•r1,lur r,1tr.1iion rntc" (cs-;:1riate::i) -------s,60 mL/r1in oer 1.73 r1'
Bilir-ii"J'n itotol) --·-- 2.3-1.2 rr:g/J~ 1SI: 5.1-20.5 u1·d/:_j 5-Hydroxyii-.,iolr n,,•t~ ::Kid----- 2-9 :T'g/2L h {SI: 10.3-47 . .:. ,.m,olia)
Glorn.; gosr5 - ---- ---- - -- - .. ·- >100 j.;g/~
"o,, crter·ol :ilooc: 80 ~20 1-c1r:1 I lg ISi: "'.O.G-13.3 kf'ol '. 7 -K:!"lost'crc,ids - 6.0-2~.0 r·1gi24 h (S·· 2.0.S- 7 2.9 vr:olh) (:nc:c-i):
?er:,. mte<,~: blJCJ:C J\-,-45 cr··T' ,lg (S, 4.7-6.0 ki-'ol 4 Q-~7.0 nq/24 h 1SI: lJ.9-59.0 :Jricl/dJ !femc:e)

8 ESAP 202l.
~/c~am:p1rinc frncboraticn DAA---· ·· - ----------d:ial ('ntc•gy x-my c:bs;:;rpt:anelry
N:::irmotcMivc nwmi:il mnges: FD/\--- -- - ---- --------------Foo<l and Drug N.imi11;s'.rc:tiori
Mc:un,;phrin(• ········ 0.261 i;g/24 h [SI: <l 323 ·w10·/d) {P1:1:o); FGF-23 -- - ---- ---- --------- fibrab·aM ;,;rowch factor 23

<18C µs/2111 (<913 nrnol/dJ \femc·e) -- - ---- -·------------fine ncr:dle aspirat:or:

l',;or1i,etonephrine ------- -age ar·d oex depencC'n-;: FSH - - -- - - '.oilide-st1T,-ilotin:,i ·10:rno:,e

Tate: metonc,pi'rir.c! ---- ---- ---- - -- - ---- ---- tlgc □ Pd sex decendcr: GH •--.,- growth ho·n•oce
8smo:ality - - --------1S0 -1 J..SC mCJsn:lkg (S:: 150- _;_130 mmol/kq) (;HR- ---------------- g:·owth l·,om1one--relea~:ni:i hor·r:or•e
Oxabte -------------------------- .. - - <4C mg/7.4 r: ;s1: <.i56 nno·/dJ
f'h::,sph:.i:e---------------------V.9 1.3 gi24 h (S:: 29.1-42.0 rr1,al/d) iinRH ---- ---- ------- - go'la::wtcop,n- releasir19 hormon1c
Po1ossitm -------------------- i7-77 :r,Lq/24 :1 \S:: 17-77 mrrolid/ hC:Cc ------------------ h,w1a:1 chori:Jnic go:imlotroplri
Sodium - -------------~O-Ll/ 1'7Eq/2.~ r {SI: 4C-217 rnrnol/c) HDL ·- ·--------------------Ligl'-::lecsity lipop:oteh

Uric m:'d ····· --------------<800 ~~g/24 h {'.;I: <4.7 rirrnl/::i) HIV--······ • ..,___ h:.1r:1a·1 ir11mun;:;def:ce:1r::y vircs
3-nydr()xy-3-•1'.ethylg:'Jtcry•

Saliva coenzyne 1\ red1..,aasc inhibitor

Ccrtiso1 {salivary), r:1icinig•,t ---------···<O. 11 11~/dl :s: <3.6 ,1rm:!:..1 :GF-J.-
'---1)'--- ------ ---- ---- - ---- ---··------------------·-···10,v ('(\'d1-y l.co;:ro1e:n

Semen :..H -----------· ----- - ••-· --------------· lute: C1i1irg horrn,'ne

S('men w1u:y~.s--------- ------ >20 million soerrn,tnL >50% 1Y1c:ilitv MCV ------------------------- •······meori COTL.:scubrvo•:Jr:ir
!v'·9S ---- - mew-'0dcbenzylgu::1riio·1•·
l,(;:i,I -··-· • -----··----------·- rragretic resanc:-ice imogin-;
HPI 1 insuliri •···-- -- r:eJcr::,, pracam•ne ci(lgecJ:Jrr: 'nsulin
PCSK9 ir•1ib:tor---- pr::1protcin c:,rwer:a~e SLbHsin/kexir: S inf1ibitor
PCT oosi1ro•1 emissi::,n to1'1cgrc:phy
Abbreviations
PSA-- pro~lote-~aec.ific ant:gen
i\C'. H --------·· f'l H-------- - ······--··---------··--··- -p<::rrihyruid horrn::,ne
ACE inl'.ibitor-------·-··· - - -::,cigiatrnsir-canvHting erzvT,c irhib::o· ::>THr~'----------- --- ·· -- oara'.hyroid ho:mor:r re·uted p,ole::i
ALT--------- ---- ---- - -- - ---ci:onir:e :J'T'in::rcrarsferr,~r SC::LT-2 ir>iib:tor -------- --- sodi,u:1-glucase co:rc1spcr~cr 7 inhioi:~,r
,AST -- - asaartciie c::T':na:ransfer::isc SHRG -- ---- sex bormone-b:nd'1q c;·ob-1lif'

- - -- - - Oo:iy rn::;ss inc:ex T, .,. - ---- ---- --·---- triiodothyrr:ni10

aMI ···-·-
CNS-----·-·-·-· --------- central nervotis systeri T" ---··--· - ---- -•------- t\-yoxirc-
CT-----------------·-·· •· ----------LOmputec tor:iograohy -:-ro antibodies•·· ____ ---------- thyro::,eroxidose ortibod;es

dehyde"oepic :1dr::,ster::,ne 'Rf 1---·------------·--· •----- l·1yrolropi11-releos,ng bor:1--.ore

DrlE.ll.. -S ------ ---------------· ---· • -- dr:<iydrcc;,irmdr oscerni'.e su lfote ~RAb ____ ., --------- ·---·---· ·· · ------ TSH-receptor antibodies

UNA------- - ------------------------··-··-· droxyriborwdeic ac:d TSH ------------ chyrot:op:n

DPf'-,1 inhibitor --- ---- ---- -·-- -----------;:J:ce;:iticyl-pcpt'da:,c .e. ir:hib::o:- VLDL---- -- - --------·--------------------·--very low (;ef'sily lipopcote·'l
 ENDOCRINE
SELF-ASSESSMENT
PROGRAM
2021

Part I

10 FSAP 2021-QUESTIONS
i•:i A 44 ·year-old woman with type 2 diabetes mellitus rrea~Pd with insulin presents wi:h wo:·sening hirsutism.
Ji_ Sl::c i.ws a history of polycyst\c ovary sy1:<lron:e and \Yas previously treated with an om'. contraceptive and
S!-)i.::·o::whctonc with good contr;); ofhypernndrogenism. She stopped taking hoth of these medications 3 years
ago. Type 2 G'.abete~ was dLignosed 7 yea;es ;i,go and wa:; ini~ia'.ly ~1Ta~e<l with n1etformin. Two years ago, her
1-:cmoglobin A: .. !eve'. was docu:::e11tPd to he fU% (67 mmol/mol), and a basal· bolus insu:ir: regime:: was startPd.
Over the pas: year, despite <lm'.blii~g her ins1rlin <loses and goo<l adherence :o her hsulin regi1~1en, her hee.1oglohin
A1c level ~1as ris<:':1 co 9.6% (B 1 :11mol/mol). Conrodtantiy, s}::c :'1as r.ot'.ced wo'."sening hdr growth u:1 her face
and chest. 1n the p;1sr 2 :110nths, she has alw h,1.<l worsening lower-extremity edema, amenorrhca1fa:igue, and
ger.e:-allzed ,waknf!ss.
On p~1ysic'a1 examination, her blood pressure i.s 180/96 mm Hg a:1.d pulse ra:e is 79 beats/min. Her height is
6-'1 in (162.5 un;, and weigh': ls 250 '.l:: ( [ 13.4 kg) (BM1 = 4.-1 kg/m 2). She has moon facies and ;l dorsocervical h;.11np.
Ti.1cre are tcrn'.na: hairs on her face and chest, :ncstly :·emoved by shaving. She has thkk violaceous striae on her
a'.,domrn, proximal :nus2'.e weakness, and diffuse ecchymoses scattered over her arms and legs.

Labo:·atory test :·esu'.ts:

Mo:t1'.t1g st21 ;i:1; ccr:isol ld:nwi;1g overr.ighl ~ mg (kxamethaso:J.e = J7.8 11g/dL (SI: 1042 ..S nmol/L)
L"rlP:My fr(cf rortis,)l = 1923 ,"g/24h (<4-50 vg/24 h) (SI: 5313 :1rn,1/d r1 :-138 nmo[/c])
Rar.dorr: ACTH= <5 pg/mL (10-60 pg/mL! (SJ: d.1 pnoliL f2_2-13.2 pn:ol/L:)
'J'o~?J ~estostcr0nc - 182 r.g/dL (8-60 ng/dL) (SI: 6.3 nmol/L [0.3-2.! :inol/L)j
DHEA-S - 1,:90 µg/d~, (18-·244 :Jg/dLl (S:: 40.38 :tncl/L [:J.49-6.61 ..1.r:101/Lj)

Which of the following ls the most likely cause of this patient's current presentation?
A. $urrep:itious use of eXOtjenous g1ucocortcoids
B. Adrenocortkal adenom,1
C Adrenocortic;i,1 c1tdnoma
D. NPurce1~docrine lumor
E, l';'i,,,c•y pipacnte<l co<lular adrenocorticsl diseaSe

2 A 7:-year-old woman is r~.ferred for man~grn:~nt of o~teoporosis, which ·was ~la~nosed at age 6~ ~'e,i:s v,;he1:
she nad a DXA scan revea~mg T-scores of -3.2 m the right femoral neck and-2.9 m the left total ;np. She tool\
a:endronate fo:· 1 year and stoppeC. C.ue to the development of osteonecrosis of the jaw. She has :10t tried any othe:·
c11edi.ca:Jo:1.s. She went throui3h nahl:al menopansP at age 10 yearn ,i:n<l has not taken eslrogen. She- has nu his~ory of
fragility fo:.cti;:es, ki<lney stones, or parathyroid disease,
Physical examination reveals a 2-cm area of exposed yellow bone in the right upper maxilla.

La'..loratory test results:

.:'.erum ca'.cium - 8.6 mg/dL (8.2.-10.2 mg/dLi (Sl: Z,2 rcrcol/L [2.1-2.6 mmol/L];
Sen:m pbos/:1.a1e .- 3J) rr:.g/ dI.. (2.3-4.7 mg/ dLj (SI: 1.0 mr:101/L [0.7- 1.5 n::n::ol/L:)
Serur:i creatinine - 0.9 mg/dL (0.6-l.'. n1g/dl) (SI: 79.6 wnol/L :s3.0-97.2 r-mol/L])
Glomern!ar filffation raie (es:,imated) = 72 ml./min per !.73 m1 (>60 mL/min per L1/3 m2}
Serum intac1 PTH = 60 _'.1g/nL (10-65 ;1g/mL} '.SI: 60 Hg/L [10 6.5 ng/L];
Sc"rm:1 7.':i-hydr:wyvi.laai.in D = 26 ng/mL (30 80 ng/mL [opti:nal]) (SJ: 64.9 nmol/L 174.9-199.7 nmol/L;)
Sm1m ,llbt,mb. = 3.5 g/dL (3.5-5.0 g/dL) (SJ: 35 g/L (35-50 g/L;)
Scrum alkaline phosphatase - 110 lliL (50- J20 U/L) (SI: L84 µkat/L [0.84-2.00 1Lbt/L])

A second DXA s2a11 reveals declining bone m:.neral density i.n both h:ps_, with T-scores of -.3.S in the righ: fe1:1cral
neck and -32 in the ieft to~al hip.
Which of the following should be recommended in addition to adequate calcium and vitamin D
supplementation?
A. Raloxifene
B. Zoledronic acid
C. Denosumab
D. Romosozumab
E. T eriparatide

3 An 83-year-old woman with a 25-year history of type 2 diabetes mellitus presents for follow-up. Her
hemoglobin A1, level was approximately 6.5% (48 mmol/mol) for many years. Over the past 12 months, it
has risen to greater than 8.0% (>64 mmol/mol). The patient reports that her diet is poor. She eats cake and cookies,
especially at bedtime, although this is not substantially different from what she has done for years. She reports
being in her usual state of health except for fatigue, lightheadedness, occasional loose stool, and unsteadiness on h er
feet. Review of her medical record reveals a 20-lb (9.1-kg) weight loss over 3 years. Current'medications for blood
glucose control are sitagliptin and metformin.
On physical examination, she is a frail elderly woman who needs help with ambulation. Her blood pressure
is 131/71 mm Hg, and pulse rate is 84 beats/ min. Her height is 64 in (162.6 cm), and weight is 117.5 lb (53.4 kg)
(BMI = 20 kg/m2). Examination findings are normal.

Laboratory test results:

Hemoglobin A1, = 8.4% (4.0%-5.6%) (68 mmol/mol [20-38 mmol/mol])
Sodium= 132 mEq/L (136-142 mEq/L) (SI: 132 mmol/L [136-142 mmol/L])
Potassium= 4.2 mEq/L (3.5-5.0 mEq/L) (SI: 4.2 mmol/L [3.5-5.0 mmol/L])
Chloride= 96 mEq/L (96-106 mEq/L) (SI: 96 mmol/L [96-106 mmol/Ll)
Carbon dioxide= 26 mEq/L (22-28 mEq/L) (SI: 26 mmol/L [22-28 mmol/L])
Serum urea nitrogen= 16 mg/dL (8-23 mg/dL) (SI: 5.7 mmol/L [2.9-8.2 mmol/L])
Creatinine = 0.62 mg/dL (0.6-1.1 mg/dL) (SI: 54.8 fJ.ffiol/L [53.0-97.2 fJ.ffi□l/L])
Glucose= 342 mg/dL (70-99 mg/ dL) (SI: l 9.0 mmol/L [3.9-5.5 mmol/L])

Which of the following is the best next step in this patient's management?
A. Initiate insulin therapy
B. Measure fructosamine
C. Perform abdominal CT
D. Add glimepiride
E. Measure serum somatostatin

4 A 56-year-old woman is referred for cardiovascular risk management. She has a history of moderate
hypercholesterolemia. Despite multiple attempts, she has been unable to take statins for many years because
of muscle aches. She has no major concerns or other medical problems. Medications include ezetimibe, 10 mg daily,
and aspirin, 81 mg daily. She does not smoke cigarettes or drink alcohol. Family history is notable for premature
cardiovascular disease in her 49-year-old brother (nonsmoker) who underwent placement of 2 coronary stents. Her
mother, who had a 40 pack-year history of cigarette smoking, had coronary bypass surgery at age 74 years.
On physical examination, she is an anxious-appearing woman in no acute dist ress. Her blood pressure is
132/84 mm Hg. Her height is 63 in (160 cm), and weight is 178 lb (80.9 kg) (BMI = 31.5 kg/m 2}. The rest of the
examination findings are normal except for abdominal adiposity.

12 ESAP 2021-QUESTIONS
Laborato;y test resu;ts (sample drawn while fasting):
Tou,l choieste,ol ~ 211 ,a,/,IL ('200 '"f/di. [op1i,nsl]! (SL 5.46 mmol/L c,S.18 mmo'/; I)
Trislyn•·:-ldes"' BO rag/,IL (<:50 mg/d~ '.oplinal]) (Sl: : A'! mmol/l f< 1.70 mr.10!/:.,))
'."":DT. c!wlesu-ro; = 55 ::ng/d.:... (>60 mg/CL [op':i:-na:]) (S:: L42 mmo!/:, '.> 1.55 :-n:-nol/Ll
::. Di chobte~ol = l 30 mg/dl. (<100 mg/d~ [optimalD (SJ: 3.37 mmol/L '. d .. 59 mmo:IL])
:\lon-HDL choles:erol - 156 mg/dl. (<'.30 mg/dL rO?timallJ (~l: ,:.04 mmol/L [ dJ7 :n:uML:)
.:..ipprotein (2) = 26 mg/dL (:;30 :ng/dL) (Sl: 0.93 ;mw;/L [:o:1.07 v.moliL;)
:--1er:1cglobin A:, - SY:6 (4.0%-·5.6X.) (:B mmol/rr:ol r20-3S mmol/r:wll)
Creatir.ine - 0.S4 rr:g/ dL {0,6-- l .1 mg/ dL) (SI: 74.3 :.u:iol/L [Sj,0---97. 2 1~mol/L;)
TSH = L8 mlU/L (D.S. 5.0 mlU/L)

Shf' is lE1willing to try statin therapy agai:--.. Using the Ame1ican College of Cardiology/ Ame1ican He2rt Associa.tion
risK calculator, you c1'.n1fate her JO-year cndiovJscuiar risk to be 2.5%. Jiow<:'wr, hased on he:· family hist::iry, you
are concerned t~iat this tool m~derescimate.s her risk.

Which of the following is the best next test in the evaluation of this patient's cardiovascular
disease risk stratification?
A. Apolipoprotein B 1c1.easure1:1ent
n. Apolipopro:ein A-1 meas:irement
C, C:2:--otisi intirna medi;i thickness
D. Coronary cl!lerycaldum scoring
E. St:-css cchocar<liography

A 66-year-old man is referred for management of type 2 diabetes md'.itus. He has hacl type 7: diahetes for
5 16 years, and bis regimen was trans'.tioned to multiple daily injections '.US00 regular ir..sctlin) 4 years ago. Tbe
dosage cfUS00 has been titrated over the past few years, but despite 175 units ofU500 :cgdar insulir.. 3 times daily
(total daily lh,se = 525 units), his blood glucose remains subopdmally comrcllcd witJ:: a hcr:wglobin A1c level of9,7%
(83 rnmol/mol).
The pa dent's BM [ is .s7 kghn\ and he reports tha: his lifestyle is sedentary. His comorbidities i:ich:dc coror.ary
a.:-tery disease status post coronary artery bypass grafting 8 years ago, obstructive sleep apnea! hypertension,
hypcrli.pidemia, and stage 4 chronic .kidney <lisf!ase \'-'1th microalh'.lminuri,t Tiis diabetes is ;:omp:icaled by
'.le'.lropa-:-hy, ,,vhkh is cum.,ntly well controlled with gab1,pentin, His wife repo:-ts th2t while he ls adherent to
bis insulin regimen and pofr:t-of-carc blood glucose checks, he does not foliow thf! dietary recommenda.tions
he has :·e;:eived from nutrition counseling. He snacks frequently and generally consurnes farge portions of food,
particularly carbohydrates.
Current medkations are atorvastatin, US00 regular insulin, gabapentin, 1-isinopril, and amlo<lipiae.

Laboratory test resu:ts:

Hc:noglobin A1, "'9.7% (4.f)% 5,6%) (83 umw:hnol '.20-38 ;n;no:/moU)
Serum c~eatinine - 2.4 rr.g/dL (0,7-1.3 mg/dL) (SI: 21:U 1rrr.ol/L [61.9-: l •1.9 i,:.mol!L:)
Estitmted glomernlar filtrat'.on rate - 27 mL/r:li:1. per L73 m 1 (>60 mJ./mb pe: 1.7.'I ;u 1 )

Which of the foflowing is the best next step in this patient's management?
A. AddanSGLT-2l,1hibitor
B. bcreas~ the <los.ige ofT500 regular insulin
C Add piogcitazone
D. AdJ a Gl..,P 1 receplor agonist
E. AJd metti.mnin

ESAP 2021
,--, A 46-year-old man presents with gn,dual-or.set fati13ue, decreased libido, ,md erec:-ile dysfur.ction over the last
() 12 mor.ths. He reports a significanl akohol history and consumes an averng1c of.'.\ standard drinks per day. His
father 0ied ofhe2:-t faH1ee al age 63 years. He ha.s ?. sons aged ?.3 and 18 years. On review of systems, he descrihes
occasinna'. join, ;:iairi. in his hands and knees.
On ;Jhy~ica: examin~tio:1, he has a tnned aµpearance. His height is 68 in (173 cm), and weight is '. SS lb
(83.9 kg) (BMl =- 28 kg/m 2). Waist circumference is 41 in (104 c:n). Blood pressure is 152/85 mm Hg, and rcstir.g
pulse rate is 70 beats/min. There is no evidence of arthropathy, and findi:1gs on cardiac examino.tion are normal.
His liver is palpable 2 cm below the righ: costi margin. There is no clinical visual field defect, and he has full range
of eye r.1ovemems. The:e is no palpable gynecomastia, and testes a:·e 18 mL bila:erfuly.

Laboratory tes: results (san:ple <lrnwn ,;t 8 AM while fasting}:

':0:2.l lcstostc'f0Ec"' ;67 ng/dL (300 900 ng/dL) (Sl: 5.8 :1.mo.i/~ '.10.4- 31.2 ::imol/LJ)
S!-IBG "'6.6 µg/m'., (1.1-6.7 µg/mLi (SI: 59 P.mol/L [10-60 nmoUL:)
LH - .15 r:nll'/mL (L0-9.0 :nl~J/mL) (SI: 3.5 HJ/'.. [1.0-9.0 llJ/Ll)
PSH,... 23 mHJ/rr,:_, (1.0-- J 3.0 mJU/rnl,} (S:: 2.9 IU/L [1.0-· 13,0 lU/L:)
EemoglcSin"' 16.9 g/dL (lJ.il-17.2 g/CL) (SI: 169 g/L [138-172 g/:'....])
Al:;·= 51 C/T. (10-40 U/L) (Sf: 0.90 µkat/L '.0.17-0.67 µkat/L];
MT"' /0 U/r. (/0- 1r8 lJ/f.) (SJ: 1.17 p.bt/T. [o..:H-0.R0 ;.:},dl,:)
y Glutamyltramforasc = 84 U/L '.2 30 U/L) (SI: L40 ~ac/L [0.ll3 0.50 µkat/L])
Hcmoglobm Ai,"' 6.6% (4.0'!6-5.6%) \49 mmol/mol [20-38 mmoJL;)
Serum elect:olyre~, r.ormal
~l:yroid fourtion, normal
Pro:actm. norn:,iJ

A repcateC tolal testos:.erone n,easure:nent l ,geek later (sample drawn at 8 AM while fasting) is 150 ng/dL
(SJ: 5_2 nmc,1/L;.

Which of the following is the most important test to order now?

A. No forthe:t testing necessary, hypogonadism 1.vill improve wid1 wcigi".t loss and akohol abstinence
B. Pituitary -<lirected MRJ
C. ACTH and cortisol measurements
D. Iron studies
E. Serum ACE rr.easuremem

7 An 82-year-old nan is referred for evah:ation an<l reco;J:1me1~dations regarding a recent vertPbr,i'. frnc:ure.
Approximately 3 weeks ago, he lost his balance and sat down severely onto his buttocks, whlch was
immediately followed by acute onset of midline 1ow back pain. Subsequent piain x rays obtained by his primary
care physician revealed a moderate (-35%) biconcave compression deformity at the sccon,'. lumbar vertebrae. He
has no other his:ory of fractu:-cs as an adult. Hi~ medical history fa notable for hypertension ,1:1d hyperlipidemia.
Family :-listory is positive for osteoporosis in his mother based on history of vertebral fractures and kypbosis. His
medkations indude benaze;,ril, amrvastatin, and a multivitamin.
On physical examination, his blood p:·essure is 135/80 rnr:.1 Hg and pulse ::-ate i.s 95 :heats/min. Hts height is
68 in (172.7 cm), anC weight is 14.:1 lb (64.8 kg) (BMl - 22 kg/m")_ Hls curre::i.t height is .·1 in (7.6 cm) shorttcrthan
his self-reported adult maximum height. He !las te:::.derr.ess to palpation ,ind peru:ssion over :he mid-bmbar spine.
Mi:<l midthorncic kypllosis is also noteC. Rib-to-pPlvis <listance is ciiminished al 1 fi:1.ger'.Jreadth bilateraEy,

l .aboratory lest rcsul::s (scrum):

Cabi.:m - '.J_S mg/dL (EU-10.2 mg/dL) (SI: 2A rnrnol/L [2.1-2.6 mmol/L!)
Phospha:e - 3.5 mg/dL (23-4.7 mg/c'.L) (SI: l. l rnr:101/L (0.7-1.5 mmo:/L])
Cr,i;1::i::1.be - 1.6 :ng/ dL (0.7, L3 rr.g/ CL) (SI: 14 :A ,tmol/L l61..9--11 L.9 µmol/Ll)
A:hmnin"" 4.0 g/dL (3.5-S.0 g/dL) (Sl: 40 g/L l35-50 g/:'....;)
lntac1 r''!:H '°' 70 pg/rnL (10-65 pg/:nL) (SJ: 70 ng/1 :HJ-65 ng/L;)

14 ESAP 2021~QUESTIONS
 2.)-!Tycirox:l-",.-,lta1:1in D = 2."i 1:.g! mL (:10-80 og/ mL ropd:nal1) \SJ; 6V· 1:.n:.ol/ L [74. 9-199 .7 nm;:;l/ LI)
Urinary calcium -2xm,tio1: = .)00 ;ng/?4 '.1 (! 00-:)00 rng/?4 L) '.ST: '/ ,.S mmol/ (1 '.2.S-7 .S rnmo;/ d_l;
Urinarycr-2atin:ne excretion= U. g/24 h (1.0 2.0g/2,1 h) (SI: 10.6 m:c:i.01/(1 [8.8-1'/.'/ n:mol/(l:}

;-)X .A <loruments che following values:

Lumba.r spi1:c ·;·-score (exdudlng L2) ""-1.6
Righ: fomo~al neck T-score - --2.2
Rig'.1t total hip '::-score - --1.8

Given these clinical findings, which of the following is the most appropriate treatment for this
patient's metabollc bone disorder?
A. Suppleme::ual caklum and vitami1: D
B. Supplerne:1tai cakiurn and ,ritamin D anC a::1 or;;.l iJisphosphonate
C, Soppiemeato: calcium and vicamin D and an intcsvenous bispoosphonate
D. Suppleme:J.la: calcium and vilan1in D and teriparatide
E. :\To treatrr:cnt is required

A 30-year.-old woman returns for continued management of type 1 di2bctcs mcllitus and hypothycoi&sm.
8 She feels well .;,:1d }.as no corn::er::.s on review of systems. Diabetes was diagnosed at age 1,: years. She has been
tre,1:-ed wi:l1 bsal-holus insulin fo, the last [ 4 ye.:.:s. She has had rt'asona:Jk i)ycemk cont:·ol, with hemoglobin
A1cJevels ranging from 6.6';6 co 7,.5% : :9-S8 mrno!/rr.ol) over ;-]1e las~ 4 years. Jiabetes--relalcd :nicrovascu:ar
1

20:::qJli:..:ations i;.~chde mild 11onproliferaUve diabetic rf'tlnopathy and pc-:ipherJ! ne1.:ropathy.

Primary hypothyroidism was diagnorn.l 12 years ago and is tre1\ted wich levothyroxine, The levothyroxine
dosage was increased to 175 mcg daily 2 :nord:1s ago. She lah's her medication ,1.s directf!<l, 60 minutes before cat;ng
breakfast, and never misses a dose. She has a history of anemia, which was treated with a 12-n~onth course of iron,
ending 1 year ago, She has 2 bowe: moverr,ents per day and has no abJomimJ L:loating. Hl'r motlier a;,~d siste:· havf'
a history of .hypothyroidism, Her mother has thalassemi2 major.
On pllyslcal examination, her heighl is 67 in (170.2 en:) and weight is 168 lb (76.4 kg) (BM[= 26.3 kg/nd.
Blood pressure is l 12/ 68 rnm Hg, and pulse rate is 72 bea:s/min. There is a slight deficit in se:1sation to l 0-g
monoDfament in each foot

Laboracory tesl results:

Hemoglobin A,, - 7.2% (4.0%-5.6%) (55 mmoYmol [20 J8 mrr,ol/n:ol]i
Creat:nine"' 0.8 mg/dL (0.6-1.1 mg/GL) (SJ: 70.7 p.mol/L [5~\.0-97.2 J,mol/L])
fasting plas:na gh:cose = 92 mg/{iL (70-99 mg/dL) (SJ: 5.1 mmol/L [J.9-3.5 mmo:/U)
Caki-J:cn - 9.0 mg/dL (8.2-10.2 mg/dL) (SI: 2.3 r:u:10]/L [2.1-2.6 mmcl/L])
TSH"' 10.1 ,nlU/L (0.5-.'i.0 mlC:/!..,)
Fr-2e ;, = l.O ng/dL (0.8- t3 ng/2L) (ST: '.2.9 pmol/L [m3G- 23.:7 p:no:/JJ)
Hn:inglobin = 1U: g/dL '.tJ..l-15. l g/dC (SJ: 112 g/L l121-151 g/L])
lron = 28 p.gldL (35 145 J,g/dL; (SJ: S,0 ;mml/J, '.63-26.0 !J.mol/L;)
Mcrn ccrpi.:scu'.ar voiu::nc"" 78 f,ffi 1 (80 100 µn'; {Sl: 78 lL '.R0- l00 f:,])

Which of the following is the best next step in this patient's management?
A. Start iron sulfate ~o be taken sep2rately fron the :evothyroxinc
B, Increase the ievothyroxine dosage w 200 mcg <laily
C. Order hemoglobin electrophoresis
D. Order" celiac enteropathy .i)anel
E, Swiech the time levothi,,oxinc is ad;ninisteced to bedtime
 A 43-year-old woman is referred for a newly diagnosed pituitary macroadenoma. She developed amenorrhea
6 years ago and was told (without any hormonal evaluation) that she had early menopause. She has frequent
headaches and has noted blurry vision that started 4 months ago. MRI shows a very large solid sellar mass (4.2 cm in
maximal diameter) compressing the optic chiasm and most likely invading the left cavernous sinus (see image). On
physical examination, she has bitemporal hemianopsia.

Laboratory test results:

Prolactin"" 37 ng/mL (4-30 ng/mL) (SI: 1.6 nmol/L [0.17-1.30 nmol/L])
Free T 4 = 0.7 ng/dL (0.8-1.8 ng/ dL) (SI: 9.0 nmol/L [10.30-23.17 pmol/L])
TSH = 1.3 mIU/L (0.5-5 mIU/L)
JGF-1 = 112 ng/mL (98-261 ng/mL) (SI: 14.7 nmol/L [12.8-34.2 nmol/L])
Cortisol (8 AM)= 16.8 µg/dL (5-25 µg/dL) (SI: 463.5 nmol/L
( 137.9-689.7 nmol/L])

In addition to starting levothyroxine replacement therapy, which

of the following is the best next step?
A. Measure a-subunit
B. Measure prolactin after dilution
C. Measure macroprolactin
D. Refer to radiation oncology
E. Refer to neurosurgery

A 36-year-old man falls on ice and sustains a right hip fracture. DXA scan shows a Z-score of-3.S in the
spine and -2.7 in the left femoral neck. He reports multiple shoulder and knee dislocations as a child and
adolescent. He also reports easy bruising. He has good dietary calcium intake and does not take any supplements or
medications. He has normal libido. His mother is being treated for osteoporosis.
On physical examination, he has velvety skin and mild thoracolumbar scoliosis. His arm span to height ratio is 0.9.
Laboratory testing documents normal results from a complete metabolic panel (including calcium and
phosphate) and serum 25-hydroxyvitamin D measurement.

Which of the following is this patient's most likely diagnosis?

A. Osteogenesis imperfecta
B. Ehlers-Danlos syndrome
C. Marfan syndrome
D. Hereditary hypophosphatemic rickets
E. Hypophosphatasia

11 A 19- year-old woman with hypothyroidism presents for her yearly follow-up visit. She reports a left neck
-swelling and tenderness that has been psescnt for 4 days. She has had no fever, chills, shortness of breath,
dysphagia, or dysphonia. There is no history of radiation to her head and neck and no family history of thyroid
cancer or laryngeal cancer. She currently takes levothyroxine, 112 mcg daily.
On physical examination, her blood pressure is 103/56 mm Hg and pulse rate is 90 beats/min. Her temperature
is 98.6"F (37'C). There is a visible fullness on the left side of her neck (level II). On palpation, you feel a 3 x 2-cm,
subcutaneous, mildly tender, fluctuant, somewhat mobile mass anterior to the sternocleidomastoid muscle and
under the angle of the mandible. The overlying skin is not erythematous and the lesion is not fixed to the skin. The
thyroid gland is not palpable, and there is no tracheal deviation. The rest of the examination findings are normal.

16 ESAP 2021-QUESTIONS
Laboratory test results:
TSH = 1.4 m!U/L (0.5-5.0 mIU/L)
Calcium= 9.0 mg/ dL (8.2-10.2 mg/ <lL)
(SI: 2.3 mmol/L [2.1-2.6 mmol/L))
Complete blood cell count, normal

Neck CT is ordered (see images).

Which of the following is this patient's most likely

diagnosis?
A. Cervical lymphadenopathy
8. Neck abscess
C. Paraganglioma
D. Thyroglossal duct cyst
E. Branchial cleft cyst

fo:
12 A 40?ear-old won:an is referred evaluation of wo:sening alo_recia ~nd hirst~tism. She has a several-
year history of cycltcal symptoms. 1 he most recent episode of hair loss rs her pnmary concern because
of the severity and lack of response to medication changes. Her medical history is notable for premature ovarian
insufficiency diagnosed 2 years ago when she developed secondary amenorrhea. Concentrations of FSH and total
testosterone were documented to be 65 mIU/mL (65 IU/L) and 61 ng/dL (2.1 nmol/L), respectively. At that time,
she restarted oral contraceptives. Menarche was at age 11 years, and she initially had regular menses, occuning
every 30 to 35 days. She conceived without difficulty at age 24 years.
On physical examination, her height is 62.5 in (158.8 cm) and weight is 149.5 lb (83 kg) (BMl ;= 27 kg/m2).
Her blood pressure is 113/59 mm Hg. Scalp demonstrates male-pattern hair loss without any patches of hair loss.
She has no striae, facial plethora, or dorsocervical or supraclavicular fat pads. There is mild papular acne. Terminal
hair growth is present on the chin only. She is able to rise and walk without difficulty. The rest of her examination
findings are normal.

Laboratory test results on oral contraceptives:

TSH = 1.4 mlU/L (0.5-5.0 mlU/L)
Total testosterone;= 92 ng/dL (8-60 ng/dL) (SI: 3.2 nmol/L [0.3-2. l nmol/L])
Prolactin = 13.1 ng/mL (4-30 ng/mL) (SI: 0.57 nmol/L [0.17-1.30 nmol/L])
FSH = 24.5 mIU/mL (>30:o mIU/mL [postmenopausal]) (SI: 24.5 IU/L [>30.0 lU/L])
LH = 22.2 mIU/mL (>30.0 mIU/mL [postmenopausal]) (S[: 24.5 [U/L [>30.0 IU/L])
DHEA-S = 701-1g/dL (31-228 µg/dL) (SI: 1.90 µmol/L (0.84-6.78 µmol/L])

Ovarian ultrasonography does not reveal a tumor; the right ovarian volume is 7,7 mL and the left ovarian volume is
2.2 mL.

Which of the following is the best next step in this patient's management?
A. Start spironolactone
B. Prescribe the combined oral contraceptive continuously to eliminate the placebo week
C. Refer for ovarian/adrenal venous sampling
D. Refer to gynecology for right oophorectomy
E. Start leuprolide

ESAP 2021-QUESTIONS 17
 A 36-year-o:d man v,rith a 26• year i1istory n~ type l diabetes me'.litas presencs for a vi.sit Be reports tha: he
13 underwent a coronary artery calcium study ti.1:nuch his emp~oyer, as it was offered for free 1 al;,<l \w brings
the report for yo'Jr interprelalion. T:lc com nary artery c,1.ki'Jrn score is 153, placir:g him at greater than or equal lo
the 75th percenti:e for his age.
He uses a multip:e <lai; y in_;eclion regimen for man21;emen, of ciiahetes .;.nd t~kes no other rr:cdications. His
regimen consists of insdin degludec, 18 uni cs daily, and insulin aspatt vhi ,1 srnar~. pen based on carbohydrate ratios.
He is an 2.vid cyclist and hiker. He does r:ot smoke clgarettes 1 a,-:<l hL' drinks 2 w .1 alcoholic beverages a week. There
is no strong family history of atherosc:erotic ca:·diovascular dise.;.sc.
1
On physical examination, his heigh is 78 in (198 cm) and weight is 204.5 lb (93 kgi (RM1 = 23.6 kg/m ). His
blood pressure is 106/77 mm Hg. Tl:ere is vitiligo on his hands, but the rest of his cxam.inaUon findings are normal,

Laboratory test resu:ts (sample drawn while fasting;:

Total e,_\o:e~1erol"' lSd 1~g/dL (<2CO mg/dL: '.)ptind!) (Sl: i1J19 m;noliL [ <5.18 mmol/L])
Triglycerides= 87 mr,hL (<!50 mg/dL (optima'.]) (Sl: O.S3 mmol/L [<.J:/0 :mno:/1,:)
HDL cholesterol=-- 55 mg/d'., (>60 mg/d:'.... '.optinal]) \ST: l .4:2 m:nol/L [> 1.55 mmo]/Lj)
LDL d:olesterol"' 87 rr..gidL (<100 mg/d[, lop:i:na.'.l) (S:: :U.5 n:n:ol/L [ <2.59 mmo:/L])
Non--llDL 01.olesterol"" ~03 r:ig/<lL (<BO raz!dL lopt;ncaC) (SI: 2.67 mmoi/L: <3.37 mmoV~l)
Lipoprmein (a) - i, n:g/d:, (:,JO mg/dL) (SJ: 0,11 ;rnwi/L '.s1.C7 :.i.mo)L])
Hemog!obb. A;,'""' 6.6% (4.CWi-5.6%) (49 mmol/mvl [J,ll-38 mmo:lo:ol:)
Cre~rimue = 0.7 n,g/:iL (0.7-U n:g/dL) (Sl: 61.9 ?mol/L [61.9-1 H.9 µrno:/L;)
TSH = 2.8 mflJ/L (Q.S-5.0 mt\._:'/L)
Urine ih:min -10-neatinine ratic - 3 r:ig/g neat (<30 mgig creat)

His American College of Cardiology/ American Heart Assoc'.ation ca-r<liovascu}ar risk score is cakula:ed to be 3.9%.

Which of the following ls the best next step in this patient's management?
A, Refer to s dietician for counseling or. a low-cakim:.i di.et
]l Start empagliflozin, 10 mg daily
C. Start atorvastatin, 20 mg daily
D. Start atorvastatin, 5 mg daily
E. Rec.om mend no further thernpy ,r this t'nw

A 37.-year~old white man presen:s for management of diabetes. He reports that type 1 diabetes mellitus was
14 diagnosed when he was a child. l[e has had suboptimal glucose con~rol most of his life, with a hemoglobin A1c
level in the range of 9% lo 11 % (75-97 mmol/:r.:wl). His most recent hemoglobin A10 value is 10.5% (91 mmol/mo1).
JIe has neuropathy, stage 4 chronic kidney disease ,vith macroalbuminuria, and uncontrolled hypertension.
Ile takes insulin tispro 1 5 units at meals, phis s;1pplemental insulin (1 unit per 50 mg/JL blood glucose> 150 mg/ dL
l>8.3 mmol/L]) and 22 units of imulin glargine at bedtime.
He reports that his mother and 2 siblings also have di,1.betes. His mother is on insulin therapy, bul he is not
sure how long she has been receiving ins-:ilin or when she was diagnosed ,v',th diabetes. His mother tol<l him that he
wa~ dagnosed with diabetes shortly after birth and tha:: his 2 sfolings wPre also diagnosed ,vi.th type 1 diabetes in a
similar timcframe.
On physical examination, his helghl is 67 in (170.2 cm), and weight is 142 lb (6'15 kg) (BMI - 22 kg/rr:1l No
:ipohyperrmphy is notc<l a::ound the sites of insulin admi:1'.stratior.. Dccrcasc<l sensation on the plantar as;:,ect of
boll: feet is appreciated with 10- g moeofilament testing,

Hemoglobin A:,"' 10.5% (.:i.0%-5.6%) (91 rr::.mol/mol [20-38 :n:nol/mol;)

Cn~atinine =2.8 rr_g/ ciL (0,7- 1.3 mg/dL) (Sl: 247.3 J,tn(;]/L i 61.9•- l l 4,9 p.:nol/L;)
Ra:l<lom g:uccse"' 275 mg/CL (70-99 n:g/dL) (SL iS.3 mmol/L [3.9-5.5 mrnol/L:)
C-pepdric (dmm simclt~acoaslywid, rnndom giucosci, ,0.2 ng/mL :o.9-4.J ng/n,L) (SL ,0.07 nmol/L [0.30 L•7 oa,o,/; ;)
Gb:r.;.rnic acid 2eca,boxy:c.se antibodies 1 ucdete\.:Uble
ket-ce:1 antibodies, undetec~able

18 ESAP 2021---QUESTIONS
Ordering genetic testing for pathogenic variants in which of the following genes would most
likely confirm this patient's diagnosis?
A. BSCL2
B. HNF'1A
G KCNJ11
D. HNF1A
E. AGPAT2

An 18-ycar-old wo~nau presents with worsening fatigue, swea:ing, and anxiety. She has a history of
15 depression and anxiety and has been treated with ven;afa.xine, 37,5 mg daily, for the past year. Her mother
describes her as always being a "sweaty child," even whe:1 she was younger,
On physical examination, her blood pressure is 1J.)/70 mrr. Hg and pulse rale is 101 beats/min. Her height is
66 i::1 ( ! 67.5 cm), and weight is 160 lb (72.6 kg) (BMl = 26 kg/m 1). She is i:1 no apparent disaess, ar:d there arc no
signs of Cushing syndrome. Heart sounds arc regular without muc!nurs, lungs are clear to auscul::ation, and her
abdomen is soft and nontender. There is no lower-extremily ede:na or t~emor of outstretched hands,

Laboratory Lest resu~ts:

Plasma free mctanephrir.e = :~9 pgh1:L (<99 pgh:r.L) (S[: <0.20 nmol/L f<0.50 nmol/U
Plasma free normctancph:ine = 916 pg/mL (<165 pg/nL) (SJ: 5.0 nmol/I, r<0.90 r,.mol/L])
Crina.(1' meta □ ephrine"' 180 ugn4 h (,185 µg/24 h) (S1: 913 nmo:.!d [<938 n:no!/dl)
1.:rinary 1:orc1etane?hrinc"' 632& µg/24 L (<286 ,1.g/24 h) (SL 34,529 r.mol/d [d.S62 nmol/d1)
Grinary eplnephrine - 4.2 µg/24 h (<21 µ,g/24 L) (SI: 23 mnc~/2 [d 15 nn:ol/d;)
Urinary r.o:epinepbri.ne - 1423 ~-g/2& h {<80 r,g/2,1 h) '.SI: 8416 nmol/d '.<473 nmol/d))

CT of the abdomen and pelvis :-eveals normal findings. Specifically, the adrenal glands have normal :norphology
ar.d there are ::,o abdominal masses.

Which of the following is the best next step in this patient's management?
A. Cessation ofvenlafax:ne for 4 to 6 wceb followed by re;ieated laboratory testing
B. MRJ of the abdor:.1e11 and pelvis
C CT of the chest, mediostinum, ,nd neck
D. Toxicology testing for cocaine and methamphetamines
E. No for6er testing; reassure the p.1.dent that symptoms are not due to a catecholamine-producing tumor

A previous) well 19-yea:-old man presents to the emergency depanment with a 3-week history of an
16 11-lb (5-kg) weight loss, lethargy, palp:tations, an irritating dry cough, an<l prog~·essi:ve left-sided pleuritic
c:les~ pain.
Or. physical examination_, his blood pressure is 110/60 mm Hg and resting pulse rate is 120 beaLs/min and
reglliar. He has a diffuse 30-mg goiter with an audible brait. The:·e is no exophthalmos or orbital inflammation,
He has decreased b::e~th sounds throughout the left hemithorax and marked bitateri 2-in (5.1 cm) gynccomastia,
Testes are 2 mL bilateraEy,

Laboratory test resclts:

TSH"' <0.03 :n:U/L (O.5-5,O mJU/L)
Free 7i\"' 6.3 ng/ dL (0.8-1.8 ng/ dL) (SI: 81.09 pnol/L '.10,30-23.17 pmol/J,:)
Free T1 = 11.,1 pg/mL (2.3--4.2 pg/mL) (SL 17.51 pmol/L [3.i~-6,4S pmo:/L])
Tota.J. testosLernne = 213 Eg/dL (JOQ-9OO ng/dL) (SJ: 7.4 nmol/I [10.4 31.2 nrnol/L;)
Li-I"" -,;G:l mH!/ mL (L0-9.0 nIO/mL) (SI: G.2 PJ/L [1.0-9.0 HJ/LJ;
FSH = <0.7 mJU/mL (1.0-13.0 mJ-:/m!.) (SJ: 0.7 IU/L [LO-:,UI IU/L])
Lactate dehydmgenase = 1374 IU/L (HJ0-200 IC"/L) (SJ: 22.9 rbt/L [1.7-13 ;tka1/L;)
 Chest CT with intravenous contrast is shown (see image).

Which of the following is the most important diagnostic test to

order now?
1

A. ~-hCG measurement
B. TRAb assessment
C. Nuclear medicine thyroid uptake and scan
D. Karyotype analysis
E. Urine androgenic steroid profile

A 32-year-old woman with a 5-year history of suboptimally controlled type 2 diabetes mellitus is
concerned about a right lower-extremity lesion that started small and has grown over time, The lesion is
solitary, not raised, and it itches but does not hurt. Her diabetes regimen includes metformin, glimepiride, and
liraglutide. Additional medications are lisinopril and atorvastatin.
The lesion is located on the right lower extremity, It is erythematous with some
yellowing in the center, with visible blood vessels within the lesion, The border is
regular (see image). No other lesions are observed on careful skin examination.
Her current hemoglobin A1c level is 9.4% (4.0%-5.6%) (79 mmol/mol
[20-38 mmol/mol]).

Which of the following is the most likely diagnosis for the skin finding?
A. Necrobiosis lipoidica diabeticorum
B. Scleroderma diabeticorum
C. Granuloma annulare
D. Diabetic bullae
E. Diabetic dermopathy

A 40-year-old woman presents for follow-up of abnoonal thyroid ftmcti.on test results. Testing was
prompted by the finding of a diffuse goiter on routine neck examination at the patient's annual visit with
her gynecologist. The patient generally feels well, but she does report fatigue and hair loss. Other than 2 normal
pregnancies, she has no notable medical history. She takes a progesterone-only oral contraceptive, but no other
medications or supplements. Her mother has Hashimoto thyroiditis.
On physical examination, there is a diffuse goiter (25 g) without tenderness, asymmetry, or palpable nodules.
Her blood pressure is 135/82 mm Hg, and pulse rate is 84 beats/min. Her height is 68 in (172.7 cm), and weight is
170 lb (77.3 kg) (BMJ = 25.8 kg/m2). The rest of her examination findings are normal.

Laboratory test results:

Six weeks ago:
TSH = 0.22 mIU/L (0.5-5.0 mJU/L)
Today:
TSH = 0.11 mJU/L (0.5-5.0 mIU/L)
Free T4 = 1.5 ng/dL (0.8-1.8 ng/dL) (SI: 19.3 pmol/L [10.30-23.17 pmol/L])
Total T3 = 150 ng/dL (70-200 ng/dL) (SI: 2.3 nmol/L [1.08-3.08 nmol/L])

Which of the1following is the most appropriate next step in this patient's management?
A. Prescribe methimazole
B. Measure TRAb
C. Recommend radioactive iodine therapy
D. Measure TSH and free T 4 again in 3 to 6 months
E. Perform thyroid ultrasonography

20 ESAP 2021-QUESTIONS
 A 44-year-old wo:nan presents wilh a diagnosis of insul'.n-dependent <liabetes. She would liie to establish
19 ca:c with a new endocrinologist She ::.-eports having been diagnosed with gesrntio:rnl diabetes during her
first pregnancy and :equiring insulin therapy to manage hyperglycemia. She continued to require insulin lherapy
, a~er pregnancy. Af'.-er 9 years of multiple daily insulin jnjections, she begar. insulin pump therapy. Her hemog:o::lin
A'., level has typically been arounC: 7.0% (53 mmol/mol), She has mkroalbuminuria and :10r:proliforativc
rerinopathy. Other than diabetes and a BMI of 3l kg/m1 , she bas no o:her health issues.
The patiem's mother also has bsu::n-dcpcndcnt diabetes, ma:1aged with insulin pump tl:erapy. The patient's
daughter was c.iagnosec! vd.th type 2 C:ia'.)e:cs at age 11 years. Her daeghter's regimen co:1sists of metformin, 500 :ng
twice daily; pioglitazone, 15 mg daily; and insdin <lctcmir, 18 unils subcut;rneously at bedtime. The pader.t notes
thac her daughter has always been thin, but since starting insclin therapy 2 years ago, she b,,s gained 15 tb (6.8 k.g).
Her d1rnghter's TIMI is 26 kg/m1 .

Which of the following would confirm the correct diagnosis?

A. Order genetic testing for pathogenic variants in the Hi\/Flil gene
B. Order genetic testing for pathogenic variants in the Gl'K gene
C. Measure C-pcptidc
D. Assess for g:utamic add decarboxylase 65 antibodies
:E. Assess for insulin antibodies

A 4.>-year-old man V1'1th a history of depression saw an ocoiaryngologi.~t for "sinus problems.~ CT of the
20 head showed a sellar mass. MRI confirmed a large sc:lar mass. with suprnseEar extension and displacemem:
of the chiasm. The patient is referred for further evaluatior..

Laboratory ~est results:

Prolactirr"' 30 ng/mL (4-23 ng/mL) (SJ: U mnol/L [0.17- LOO r,mol/L])
Testosterone"" 262 :c.g/Jl (300-900 ng/dL} (Sf: 9J nmoliL [10k3L2 nmol/L:)
Cortisol (8 AM). 19.l eg/dL (5 25 /.g/dL) (Slc 526.9 nmol/C 1137.9-689.7 nmc,JI :)
Serum JGF-1 - 157 ng/mL (98- 261 ng/mL) (SI; 20.6 amo]/L [12.8-34.2 nmol/L])
Pree T, = 1.3 ng/ <lL (0.8- 1.8 ng/ dL) (Sl: 16.7 pmol/J, '.1030-23.17 pmol/LJ
TSH""' 2.S mHJ/L (0.5-5.0 m!C/L)

On physical examination, his blood p:-cssurc is 130/80 mm Hg and pulse rate is 82 beats/min. His height
is 72 in (182.9 cm), and weight is 192 lb (87.3 kg) (BMI"' 26 kg/mt). Visual fieI<l testin1:; shows bitenporaJ
hemi:rnopsia. On review of systems, he reports feeling well overall, His only medirn::ion is fluoxethe 1 20 mg daily.
A nonfunctionir.g pituitary adenoma is diagnosed, Tramsphenoi<l,il surgery is uneventful. He is discharged on
hydrocorti.sone, 15 mg in lhe mo".'ning and 5 mg in the afternoon1 with a plan to measure serum cortisol 1 week
after surgery. On postopera:ive day 6, tbe patient presents to your clinic bemuse lw feels unwell and has nausea and
a head.ache. His vital signs are normal,

Which of the following is the best immediate next step?

A. Perform a pirnilary-directed MRI
B. Adminhter intravenous hydro:::ortisone
C. .Measure so<lium
D, Measure cortisol
E. Refec fo, lumbac puncture

A 67-yea:·-old woman is referred for evaluation of osteoporosis. She has a history of osteopo:'osis
21 documented o:l DXA that was performed 2 years ago. She has had no low-·trauma fractures as an adult.
Following the 0XA scan, alendronatc therapy was initiated. which she has continued to dale. She reports adherence
to the the:'apy and taking the medicctti0n correctly. She recently moved from another state anC underwent another
DXA scan loca.:ly within the past few weeks.
 Medical history is notable for hypertension, hypothyroidism (on a stable levothyroxine dosage for the past
2 years), and osteoarthritis (bilateral hip replacement). Her medications include calcium, 600 mg twice daily;
vitamin D, 800 IU daily; levothyroxine, 75 mcg daily; and hydrochlorothiazide, 25 mg daily. Family history is
negative for osteoporosis or hip fracture. She does not smoke cigarettes or drink alcohol.
bn physical examination, her height is 66 in (167 .6 cm), which is 1 in (2. 5 cm) shorter than her self-reported
maximum adult height. Her examination findings are normal, including normal spinal curvature without kyphosis
and a normal rib-to-pelvis distance of 2 fingerbreadths.

Laboratory test results (serum):

Calcium= 10.4 mg/dL (8.2-10.2 mg/dL) (SI: 2.6 mmol/L [2.1-2.6 mmoi/L])
Phosphate= 3.2 mg/dL (2.3-4.7 mg/dL) (SI: 1.0 mmoi/L [0.7-1.5 mmoi/L])
Creatinine "'0.9 mg/dL (0.6-1.1 mg/dL) (SI: 79.6 µmol/L [53.0-97.2 i,tmoi/L])
Albumin= 4.8 g/dL (3.5-5.0 g/dL) (SI: 48 g/L [35-50 g/Ll)
Intact PTH = 60 pg/mL (10-65 pg/mL) (SI: 60 ng/L [10-65 ng/L))
25-Hydroxyvitamin D = 25 ng/mL (30-80 ng/mL [optimal]) (SI: 62.4 nmol/L [74.9-199.7 nmol/L]}
TSH = 2.1 mIU/L (0.5-5.0 mIU/L)

Previous and current DXA images are shown (see images).

IIMO
Do.,__
_ _,_ • --u.u~ BMD Young adult Age-matched
,,,,
10
Region g/cm2
% T-score % T-score
:1• •., Ll 0.767 68 -3.0 81 -1.5

·-
I 01S

U IJ
L2 0.848 70 -3.0 83 -1.5

·-
0~

» • c x ■ • s m a
DXA scan performed with machine Brand 112 years ago).
.
"
~ L3
l4
l1-l4
0.852
0.869
0.838
71
73
71
-2.9
-2.7
-2.9
84
86
84
-1.4
-1.2
-1.4

Region BMD, g/cm2 T-score

Ll 0.707 -2.6
L2 0.736 -2.7

...___
L3 0.682 -3.7
........
......... ,___.....
.. .. .. . l4
l1-l4
0.705
0.707
-3.2
-3.1

DXA seem performed with machine Brand 2 (current!.

On the basis of this patient's clinical data, which of the following is the most appropriate next
step in her osteoporosis management?
A. Continue alendronate
B. Discontinue alendronate and administer intravenous zoledronic acid
C. Discontinue alendronate and start teriparatide
D. Perform neck ultrasonography
E. Start ergocalciferol, 50,000 IU once weekly

22 ESAP 2021~QUESTIONS
.· 2 A .-11-yc:u ol<l wonan is :.-efened for evah1atlo:: ,J spe:L, that sw:·:e<l ab01:t 6 mo:1.ths ago, She Jpsnibes
2 - these episodes as shon ar,.d in:.:teasi21g i1: frf'queucy. lkring the speUs, she fcc'.s Jiaphcrelic, has trf'mors,
and is extremely weak. \Vhen asked abon~ lhe timing of tlw episodes in relation tc ea'."i.ng, s'.1.c n.'J.KH'..S 61t t!1ey
usually ha~)pcn 2 hours after meals e.:1d fr.a~ she does not experience speEs wt.en sbe fasts_ She is worried she rnu'.d
have an episode whi;e driving.
At the recommendation of 2 fritnd 1 she t:o,tghc a glucose ;nete. During episodes, her poir_l- of care gh:cc:se
conce:ltrncior. rnges frorr: 40 :o 60 rr:g/dL (2.2 3.3 mmol/.L), Since learning 6a: :,er sym;:,torr.s are ::he co low
g'.ncose readings, she started eating every 2 lo 3 ho,rrs. She is co:~rnned that if she comirn:es eat'.ng '.ike thi5, she
\Viti rega:n the welghr she lost ,dcr :-toux en Y gastric bypass 2 years ago. She lost 100 lb (45.5 kg) after ~urge:·y,
but she ha5 gained 10 b (4.5 kg) b <:he kst 2 ;.~101:th~. Het me:JicatioJ~S i:1el~1de a :nultivila:nin wd iro:1 arnl calcium
cit:·ate.
On physical examinatim:, her b:ood pressure is 12Di72 n~;:n ~g and irnlse ra:e ls 60 beal~imir:. :-le:- height
is 63 ln (160 cm), and weight ls '.70 lb !77J kg) (BMl = 30 kg/ml)_ Si1e is i1: no <lis:ress. Her lungs are clear to
auscdtation bilaterally. On cardiac examim.tionJ her '.1.ea;_t sounJs are rn.mna~, an<l rate and ;hytlm!. a:·e regular. Her
abdomen ls soft anC. nontender.

Which of the following is the best next step in this patient's management?
A. Refer to a dietitian to review her cu:-rent n:ea[ pkn
B. Start oct;eoti<le
C. Start acarbose
D. A<lncil to l:1e hosr,ital for a 72-hou:- fas:
E. Perform an oral g~ucnsr tolerance tes:

A 57-ycar-old ;:na:.1 is fomd 10 have,, new :1-cm righ: ad:·enal lesion on a whole-body surveillance CT
23 scan. Two years ago, he ua<lenwnt allor,e1:ic sterr.-cell transpla:1l for acm:e myeloid lcu',;.emia, which w.is
com:=,lkated by graft-vs-host <li.sea5e and Epstein- fL:: virus infec:io:i. He has longstanding type 2 <liabetes, His
::urrem medicacions arc amitc!.ptyline, atorvast,1tiE, rnetformin, prednisolm:.e, n:nipriC a:1d tacro:lmv.s.
011 ;,hyslul examim.tion, his height is 7 l in ( 1R0 ..1 cm) and weight is 202 b (91.8 kg} (B!VH"' 28 kgim 2). His
'.:>lood pressure is l 4?1/92 mm Hg, and pdse rnte is 76 hess/mi::l and reg:.ila,. Physical examination fin<lings are
otherwise u:1:·emarkabk.

Labora:ory lesl results:

Se1·;im potas5icm ~ 4A mEt,/L (3.5-5.0 rr_Eq/L) (Sl: 4A m;nul/T. :.L5-S.0 rm~wl/L:)
Plasma renin act~vity-s -1.4 ng/ mL per h (0.6-4..:'a ng/::r,:, per h)
Seru:1: aidosterone - 6.2 ng/ dI. (4- 21 ng/ dL) (S~: 172 pron]/'., [ 1l l -S82.S pa)ol/1.])
\,0;1 i.~ol following !-mg dexametbsone-sup;:ircss'.or, test = 1.:) 1n:;/ (1J, (SI: 27 .6 ;unolil.)
P:amra n:etans'phri:ies,,. 82 pg/mL (<99 ;Jg/mL) (SI: 0.42 Emol/L (-di5 nmol/J.])
P:as;n~ ;wnneta:iephrine"' 189 pg/mL (d6S pg/ml) ;s1: 1.03 r,mol/:: . [.d),90 nnwl/Ll)
24· !-101:r 1;rhary stero'.ci profile, within norma'. limi:s

Adrenal CT (triple phase} documems a 3.1-·cm rigl:t ~drcr.al nod,tk wilh a dernicy of 39 Hounsfield units at
baseline, 49 Ho,msfield units 1 :nirn:te after rnntrast1 a:-id 59 Hotnsfield units t 0 mi:rntes afrer contrast.
Whole- L:o<ly PET-CT shows focal increased lncer uptake in the right a<lr,:,'1.al nodctle, but otherwise norr:i.al
physiologic uptake.

Which of the following is the most likely cause of the adrenal abnormality?
A, t\drcnoco:tical adeaoma
B. C-ytomcga'.ovirns adrenafais
C, Pheochromocytoma
D. {IAecasrnsis from un::__nown p1 i.rn,1ry :u:r.1or
E. Secondary lymphoprnlifrrntiw disease

ESAP 2021~QUESTIONS 23
} Aj A 51-ye:ir-old wo1~1a1~ _presenb with swding in the m;dan~erior :.1ecJ< that has been noliceahle for .1 <lays.
i~,,, ¼• This sweEing ls slight.:; ~e1:de1. She haJ a ~imila1 e-;.;isode 2 years ago that imp;-cve<l after ancibiotic
eeatr:ie;;t. The swe'.ling e'.evales wal'. ~u:.1gue prutn:.si();_J or swallowing. Slee ~s otherwise hea'.t~1y, and she cakes :10
:ned;c:itio:1s. Her :n0the1· has a ~1i~t01y u:· hypot~1 yro~dism; :he rest of die frnily L~stury is ur.;-emarka'.:ile.
OE physicd exa:nin,ltior,, her bluoJ rressurc ,~ 124/64 mr'..1 Hg, p-,1Jse :ate is 64 beats/mb, and temperatt.n' is
98.ii'F (3TC), Her height is 66 ir: (167.6 cm), a'.1d weigh~ is 124 lb ;56.2 kg; iB:\11 = 20.0 i.:g/mi;, Sh,:, has a visib'.c
a1:d p2:pable ~nte;-:or neck :nass 1:1easur:ng 2.0 cm, just aL:ovc tte hyoi<l -::,onc Her thyro'.d gland is r.ct cnla:ged.
·;- he:e is no palpable cervical lyr:1.ptaC.tr.opa:hy. He, hca:-t ra~c is regub:", and hir.gs arc clear :o ~uscultation. The rt'
is no :ower-eXtn:''..nity ederr.a.

La'.:loratury test results:

TSH- L2 m'.~J/L (0.S-5.0 m!U/L)
Crilc:um"' 8.5 mg/c'.L (8.2-10,2 mg/dl) (SI: 2.: mrac:.iL [2.1-2.6 mmol/LJ/

~ eek u[trasonograp.hy shows a no::na: thyroid gla:td with nc, evidence of abnormal cerV:ca.l lympha<leJ::op:ithy.
The:·e is a 1.8 x 2.0 x 2.1 err. (_antercposterior x transverse x '.ongitudin:i:) hy;,oe:::hoic rr.ass wH1 posterior acoustic
enha.:.icement i:1 ~he micline anterior Peck with no evidencf' of J:1y so'.id coP1ponicnt above the thyroid gla:1d,

Which of the following is the best next step in this patient's management?
A. !nitiate antibiotic lreatment
:niti.,te [evoll:yrox:'.ae therapy
T-1.
C, Perfoan FNA biopsy of :he 1,iass
D. Refer fo1 excision of the mass
Refer for a Sistr-cmk procedure

25 An 18-year-old woma.n is referred for a secooC op:nion regarding hyperprolactine:nia while on

risperidone to i:r€at schizophrenia. She in:tially sot:ght evalua:.ion when she developed galactorrhea a:id
o'.igomcnorrhca. :V1enarche occurred at age 13 years with nonnai :no:1tl:ly menses until 6e past year when .her
periods occllrred very infregae:1C.y. Her :ast period was 6 months ago. h:itial laboratory testing documented an
elevated prolactin concent:atio:i of 47.3 ng/mL (2.1 nmo)L). Pelvic uitrasonography showed an e:1dometrial lining
of 3 mm, multifollicular appearance, and antral foEide count of 14 on the right ovary consistent with polycystic
ovarian r.1orphology. Ova:"ian volumes were '.ess than 10 mL bilaterally.
Afler fae hyperprolactine::nia was first noted, oral con:raceptlves were prescribed, hut t!ley made her very
t.auseated and were discontinued. A trial of aripiprazole did not nonr.alize her :r,rnhcjn or resofve her symptoms.
Her psychiatrist then tried to switch from risperidone to quetiapine. Afthough her prnfactin normalize<l while on
quetiapine, her psychotic symptorr.s worsene<l, .She is currently back on rispe~idone aml mntinues to have nipple
discharge and arr.enorrhea, which is causing sigrclficimt anxiety,
On physica[ ex:imination, rhere is no terminal hair gro\11111 and only a fe\v r::1ild no:1infiammatory papufar arne
lesions on her foreh0ca<l and cl1eeks,

l .J horarory tesc results:

TSH = 1.7 mlU/L (0.5-5.0 rr:lli/L)
2rolactin"' 50.7 ng/ml (4-30 ng/mL) (SI: 2.2 n:a:ol/L :o.17- LIO nmol/L;)
_:.'SH"" 5.0 mlU/:nL (2.0-12.0 :n'.U/:nL [foJ;ic:1b1 Jr (SI: 5.0 JU/L [2.0-12.0 JU/Ll)
Estradiol ~ 30 pg/mL (10-180 pgh:1L :follirnbr;) \SJ: 1JO. I pmol/L [:~6.?-660,8 pn:ol/'._,;)
Tota'. test::.ste:·one = :n r:g/dL (8-60 ng/dL) (SJ: J .1 nmo;/L [0J-2.1 nmol/Ll)
Fr€e t€stos:€rone = 0.33 ng/clL (0.3- L9 :..g/d;_,) (SI: 0,01 nmo;/L l0,01-0,07 nmo;/L]j
DHEA-S _, 213 r.g/dL (&4-332 jg/dL) (SJ: 5.77 ,.t..-nol/L '.L19-9,00 µ:oo:/L:)

24 ESAP 2021 - QUESTIONS

Which of the following is the best next step in this patient's management?
A. Initiate cabergoline
B. Refer back to her psychiatrist to consider alternative medical options
C. Initiate progesterone for 10 days every 1 to 3 months to induce a period
D. Order pituitary MRI
E. Initiate mctformin to induce ovulation

76 A 36-year-old man presents for follow-up 3 months after commencing medical therapy for a
macroprolaclinoma. Initial symptoms were headaches and a. bitemporal visual field defect, and MRI of
the sella revealed a pituitary macroadenoma with suprasellar extension (see image). He was initially commenced on
cabergoline, 0.25 mg twice weekly, which has been up-titrated at monthly intervals to the current dosage of 0.75 mg
twice weekly. He takes no other medications. His headache and visual symptoms resolved quickly after starting
cabergoline.
On physical examination, his height is 72 in (183 cm) and weight is 198 lb (90 kg) (BMI = 27 kg/ m2) . His resting
pulse rate is 66 beats/min and regular, and blood pressure is 125/75 mm Hg. Visual acuity is 20/20 (6/6) in the right
eye and 20/ 10 (6/3) in the left eye. Formal visual field assessment demonstrates full resolution of the bitemporaI
hemianopia.

Laboratory test results at initial presentation:

Prolactin = 1960 ng/mL (4-30 ng/ mL) (SJ: 85.2 nmol/L [0.17-1.30 mnol/L))
TSH = 1.2 mIU/L (0.5-5.0 mlU/1)
Free T◄ = 1.25 ng/dL (0.8-1.8 ng/dL) (SI: 16.1 pmol/L [10.30-23.17 pmol/Ll)
Cortisol (8 AM)= 15.0 µ,g/dL (5-25 µg/dL) (SI: 413.8 nmoi/L [137.9-689.7 nmol/L])
IGF-1 = 185 ng/mL (106-277 ng/mL) (SI: 24.2 nmol/L [13.9-36.3 nmol/L])
FSH = 0.9 mlU/mL (l.0-13.0 mIU/mL) (SI: 0.9 IU/L [ l.0-13.0 IU/L])
LH = 1.3 mlU/mL (1.0-9.0 mJU/mL) (SI: U lU/ L [1.0-9.0 IU/L])
Total testosterone= 160 ng/dL (300-900 ng/dL) (SI: 5.6 nmol/L [10.4-31.2 nmol/L])

Laboratory test results after 3 months of cabergoline treatment:

Prolactin = 10 ng/mL (4-30 ng/mL) (Sl: 0.43 nmol/L [0.17-1.30 nmol/Ll)
FSH = 2.1 mlU/rnL (1.0-13.0 mlU/mL) (SI: 2.1 IU/L [1.0-13.0 IU/L])
LH = 3.3 mIU/ mL (1.0-9.0 mIU/mL) (SI: 3.3 IV/ L [1.0-9.0 IU/ L))
Total testosterone= 480 ng/dL (300-900 ng/dL) (SI: 16.7 nm.ol/L [10.4-31.2 nmol/L])

MRI of the sella (Tl noncontrast) before and 3 months after commencing treatment is shown (see images).

At initial presentation After cabergoline therapy

ESAP 2021-QUESTIONS 25
Which of the following is the most appropriate management pion?
A Change cabergoline to bromocriptim:
B. Conti..rn.e cabergoline at the current dosage
C Increase the cabcrgL)line dosage
D, Refer for sLereotactic radiosurgery
E, RdCr for transsphcnoidal su:·gery

or
~ 31-year-.old wo~an :.s referred for managem<Cnt gestatior:al <li~bctcs 1:1ellit11s'. Sh~ had gestationa:
27 diabetes with her 1m: pregnancy at age ?,6 yea.-s and was treaced w1tb d1et and glyounde, At 38 weeks
gestation, she delivered a 9 lb 12 oz (4422 g) bahy '::.iy cesarea;_1 delivery. Tb: baby had jaundice a!td hy;JOg!ycemia
at birtli. The patient has a history of obesity. She 1s now a~ 29 weeks' gestation with her second pregr:ancy am!
has again been diagnosed with gestational diabetes. She follows a dfabetes n:eal plan and uses a glucose nwtrr.
Eight days ago, her obstetrician Fescribe<l glyburi<le, 10 mg twice daily. Her mother, 2 sib!lngs, ar:d materna:
grandfather have diabetes.
On physical examinatio:i, he,.- height is 67.5 i1: '.l 71.5 cm) and weight is 208 lh (94.5 kg) (BMJ ""' 32 kg/r'.11).
Blood pressure ls 1?.R/80 m;_n Hg, nd pulse rate is 86 beats/min. A gravid ut<:'rns is plpable, There 1,; trace pedal
edema. Reflexes are nonnal.

Labor;J:tory test results:

Ikmoglobb A1,_ - S.8% (4.0%-5.6%) (40 mmol/n:;:,J '.20-38 ;r.rnol/mol])
Crcatinine - 0.8 mg/ d'., (Q.6-; .1 mg/ dL) (Sl: 70.7 i'IDOl/1. [S3.0-9'/,l µrnol/L;)
Electrolytes, nonna'.

Pi.ngerstick glucose readings (point of care) are shows;1 (.;ee table;,

Doy Breakfast 2-·Hour postbreakfast 2-Hour pastlunch 2-Hour postdirmer

Tuesdny 97 mg/dL (SI: 5.4 rrirnol/l.) 1; 7 mg!cic. (S·: 6.5 n~n,ol/L) 109 :n':::/dl {SI: 6.0 mmol/L) ~31 mg/c:.. (SI: 7.:1 :nr:10:tt.;
W(~rhesday 103 mg/dL (SI: 5.7 mmo:Jl.) 109 '119/c:... (S:: 6.C n'n'.ol,l) ill mSJ/dl {SI: 6.7 mmol/L) :;_35 11g/d:.. (SI: 7.5 rnmo:/1.)
Thursday 102 rng/dL :s1: 5.7 mmo:/1. 1L 2 ,ng/oL [SI: 6.8 O'.ll'OI/Ll 117 rT'\:J!dl {SI: 6.2 mmol/L) 127 'llg/a:.. (51: 7 0 :nrnodL;
Friday 96 mg/dL {SI: 5.3 r:1r101,~.) 118 '119/dL [SI: 6.5 n'mol/L) 103 n:g/dl {SI: 5.7 mmol/L) 121 :ng/dL (Si: 6.7 'Tmol/L)
SoturCay 105 mg!dL (SI: 5.3 rnmol/1.) ll3 :-ng/dL (SI: 6.3 mmol/Ll 114 rrg/dl (SI: 6.3 nmol/Ll 148 mgldL (S:: 8.2 m,;d/L)

After reviewing her adherence to dietary treatment, which of the following is the best next step
in this patient's management?
A. .Start metformin
B, St,1rt insulin lisµro before dinner
C, Start NPH insulin at bedtime
ll Double the dosage of glyburide
E, Stop glyburidc1 start NPH insulin at bedtime and insulin lispro before dinner

28 A 28-year-old woman with Cushing disease undergoes surgery for a pituitary microadrnoma
(0.9 cm in maximal diameter).

Preoperative laboratory test results:

U:inary free cortiso:,,, 153 µg/2'1 b (,t-.':i0 µg/7'1h) ;SI: 422.3 mr.olid [11-138 nmol/dj)
ACTH - 65 pg/rr.L (l0-60 pgh1I.) (S:: l ·U pmol/L [2.2•·112 pmo;/L;)
Pos!· dc,xameth<aso:cie corfool = l .'.\ p.[';/,II. (Sf: .·~58.6 nnol/L;

26 ESAP 2021-QUESTIONS
 Sugery :s cmev::nt:1.:1, On posco:?cr:>.tivc ..lay 2, her morni;,g cortisol coTtcentration is 1'J µgi dL (30.1.J "-moV::J a:,d
she is disd!.argeC c:n no n:ec:icat'.on, fodir.g wdL In 1:,e L-1te cve:::'.ng of postoperative day 5, she presents to a Jocai
eme:·gency deparm:ent witl: m:.1sea 1 vo:niting, a:1d fot(£:11e. The emergency department physi.cix1 ca:!~ for advice.

Which of the following is the best next step in this patient's management?
A. Measure; free ·1 ·,
B. Perform a pi.t:Jitary-Cirected MRI
C. l'v1easc:re plas:na AC'l'H
D. AJ.ministe:- hypertonic fluid
E. Start emp::ic glucocorticoid ~herapy

An 18-year-o:d man set'ks evaluation to determine his risl.: for Lype l diabetes mellitus. His pa:·ews
29 accom1:1s1ny him to the appointment. His frater:ul twin brot:1cr developed typtc 1 diabetes at age 16 yea:s.
There is no other family history nf :ype 1 dia'.Je:es.
The patien'.'s r:1cJical Ii is:ory incbdes hypothyroidism with elevated TPO antibodies and rrcent n:onomdeosis
from wbich he has :ccovere<l. Labo;-atory ev,iluation reveals ttat he has c:cva-:-d glu~a:cnic and dt'Gll"l)Oxylase
65 an~ibodics ar.d islet cell an~iboGies, HP a:so has a fasting blood g;ucose concentracion of 89 mg/d[, (,t.9 mm::il/L).
Yoa have a disc:JSSion wit'.1 che pacien~ and his parents abom tte :·:sk of dcvdoping ty~e l Jiabelf'S,

Which of the following factors in this vignette confers the greatest risk that he will develop type
1 diabetes?
A. Pam.:~y I!.iotory of type~ <'.ii'>etes
B. llas~-._:,noto dise,N'
C. ]\1ale sex
;). Rece!'.t histo:·y of rnononudcosi~ infeccio11
V Au:oant\body status

30 :' :)6-y_ear-,,]d rr:an presen:s for managemcn~ of cardiov~scular risk II~ had a~: ST-elevati~n myocardi~l
'.nbrct1011 2 years ago and bad a coronary stcnt placed. He was on low-mtens1ty atorvastatm, 10 mg daily,
before his cnrm:ary even:, as he had deveioped severe royalgias 011 highicr ,1torvastatin dosages and with muitip:c
past a,ten~p1s wich alter:::.ative st:;.tins, ind.uding simvastatin and rnsuvastati:-i. F-ihrate frter:apy was also 2ttc:nptcd,
bul he again dewfoped :ny«lgias. His c'J.rren: Hpid-lowcrir:.g reginen indndes atorvastatin, :o mg daily, and
czcti::nibe, 10 mg daiiy. He sporadic:iJy ta.k.es an over-~be-countcr fah oil St'.p;Jlrment. He has hypertension tre~tcd
witl: lisinopriL He has a ,10 pack-year history of cigarette smoking :aad qui, 2 years ar,o. He drinks 2 to 4 akchoEc
bcverigcs weekly. rte leach a sedentary lifestyle and has mrny dietary i11di.scretions, Hi.s father, fl.OW deceased, haC
cornmry :>.rtery disease and lrn<lerwent coronary artery bypass surgery al age 68 years. His J9-year-old son has
eleva-:-ed trig1yc,:,:'.des.
2
On pl:ysic.;.l examination, his bright is 70 in (177.5 cm) and weigh is 225 lb (102.3 kg) (BMI = 32.3 kg/m ). His
blood pressure is 130/80 mm Hg, Tlie;-o2 ,1::e no skin eruptions, bu:- abdominal adiposi.ty is notrd.

Laboratory test resdts ;sar:1p:c drawn wl~ile fastinr;i:

Toto.! c...'10ksternl ~ 158 mg/dL. (<200 mg/dL [optima11) (SJ: 4.09 mrr.ol/L '. <5,18 mrr:01/L])
Triglycerides ~ 225 rr:g/ dL \ <150 rr.g/ dL ~optimal]) (Sf: 2.54 mr.10VL [d .70 mr:10:/Ll)
HDL d:oles~erol ~ 36 mg/<lL \>60 r:1g/dL [opti.mo.1]) (S:: 053 m:nol/L '.>l..'i5 m:no)/L])
LJL dwksterol,,. 77 :ng/dL \d00 mg/dL '.opti:naCi '.ST: 1.99 mmoi/L l<2.59 mmo;/L])
NcH-E8L c'lolescero~ - 122, :ng/<lL (<130 mg/dL [optimail) (S[: J.16 mmoi/L [d.37 romol/Ll)
Lipoi:rolein (a)= 42 mg/dL (<\G mg/d,/ (SI: :.SO f@ol/L :s:.07 11mo:/U
H~mor:lo:Ji;1 A,,_= 5.9% (4.0%- S,6%) (11l mmol/mo: '.20 ::;8 m:uol/1:w'.;)
fa,1iag gh..:~:)52 = 108 r:1g/ ell.. (70- 99 mg/ clL; (S:: 5.99 :.nmol/L [:1.9-.J.5 mraol/'._,:)
C:eaLlrl1:t = 1.: :ng/:il (0.7-U mg/dL) \S'.: 97.2 :.i.mol/L [61,\i 1H.J ,1.mol/Ll)
TS:-!= IA n:[L/::.., (:J.S-5.0 :nlU!L)

L
In addition to ongoing lifestyle efforts, which of the following is the best next step in this
patient's management?
A. Switch :o rnsuvast;itin
IL Add extend0d-:elf'd)Of' e!Jcin
C. /\Jd colrsevelarn
D. Add purifre<l iros,ipent et~1yl
F. r\dci ddaglutide

31 A 65 year-old woman with a long.,:-.andi:i.g histo:·y of:ype 2 diabetes melHtus seeks recornrnendJtions
cont.:erning he:- bone health. She has no history cf low--trauma fractures. She has hef!:1 on hr.nodi,;lysis
for approximately 4 yc2rs. Diabetes-related rnnplicatiom also include peripherJI neuropathy involvi:1g hf'r '.ower
extrc:nitics. Her medicat'.ons w; !.nsulin glargine once daiiy, ins·Jhn 1-ispro beforf! n:f'J'.s, acorvastatin, metoprdol,
calcium acetate, and gabapemi1;. S.he does not smoke cigarettes or drini{ alcohoL Fa,n.ily hislory is r.egacive for
osteoporosis, inc:uCing no ?arental history of hip fr,;ctu:-e.
Un physical examina.tion, she ls on:y 0.8 i:-i ;2 rm) shorter thai~ her seli"-reponed a<ln:t maximum height She
has a palpable t:lrill over her left forearm ,1rticriovicnous shunt. Her spinal curvature '.s nonnal. There is no palpable
bony tenderness over :he tihias. Then' are no ulcers or lesions on her feet She has absent se:1sation '."o 5.07-g
monofilament testini:: 0;1 ~oth feicL The test of her p'.1ysica.l examination findings are nonco:1tributory.

L,;borJtory tf!st rrslllts (serum;:

C::ilrn:m = 9,8 mg/dL \3.2-10.2 mg/ci.L) (S:: 2.5 mmol/L [2. l-2.6 mmoliLJ.;
Phospha<::e = 5.5 mg/GL '.2.3-4.7 r:1g/dL) (SI: 1.8 mmol/L :o.7-1.5 rr:mo;/L;)
C:reaci:ii:ie = S.9 mg/ dl '.G.6- l.1 .r.ig/dl.) (SI: 786.8 µmol/L [s:rn- 97 ,2 µmol/LJ
Sc~i.:m urear:iuoger. - 25 :ng/dL (8-23 :ng/dL (S1: 8,9 mrool/L '.2.9-8.2 mmol/LJ)
Albmr.in - J.6 g/dL (3.S-5.O g;/d.) (SI: 36 g/L [3.'i-5O g/L]
Alkaline phosphatase - 130 U/L '.50-120 U/L) I_Sl: 2J 7 µkdt/L [0.8'i-2.00 ~Jrnt/~..;}
Intact PTH - .320 pg/mL ('.D-6.'i pg/mL) (S1: 320 ng/L l10-65 ng/Ll)
25-Hydroxyvi1M:1in D "' ~ l ng/ dL (30-80 ng/mL '.optimalJ) (Sl: 27.5 amol/L [7 •1.9-199 .7 umol/L])

DXA documents the fol:owing values:

lxmb,n spine 7--score - -- I.2
Right fe:noral neck T-score.,, -2.0
Right total hip T score "' -1.6
Left proximal one-third radius T-seore = -2.8

Which of the following treatments would best address the patient's underlying bone disorder?
A. Alendronate
R Te:iparatide
C. Cholecikiferol
D. C,kitdol
K Sicvichuner hydrod1luri<le

32 A 69 year•old man is referred by his radiation oncologisl for consideration of testosterone reph:.cement
for ongoing hot ffasbcs, fariglle, and low energy, The patient has nol had low mood or Jepressive
symptoms. He has a history oflocalized, imermediate-ris.i. prostate cancer treated ;,vith defl:-rit'.ve radiotb<C:apy and
12 mor.tn.s of a<'.juvant a:idrogen-deµrivation therapy with a GnRII antago:1ist. Androgen-Ceprivatio:-i thf!~apy
was stopped 6 months ago, and the patien: :s disappoin~ed that he does not feel a:1y bdter. O:her history lndu<les a
provoked pulmon2ry en:boli~r:1 3 years ago treated will; anticoagu'.ation :herapy for 6 mo;1ths.
On physical examination, his heighl i.s 67 in (170,2 cm), and weight ;s 19S lb (8R.6 kg) (Bi'✓.l = .'.\ l kg/n~z), He
has m(_1dest nm:tcnder gynecomastia, :oss of body hair, reduced musd<.: b"Jlk, sc1d l0-mL testes bilaternlly,

2ll ESAP 2021-QUESTIONS

 ::...ab01aco1y test rcsul:~ h.mple d:·awn at 8 AM while fas~ing):
Ser~i;r \()Lal Les:uale:-onc"' 7S n;;/dL \300-900 :1g/dL) (Sl: 2.6 nmol/L ["i0.4-JU r,mo]/L])
LJ-i = .l.1 raHJ/rnJ, (J.0-1.G mlU/mU (S'.: 2.1.iU/L [1.0-9.C lUIL])
PSA = <0.0.-\ :1g/ml, '.tl'.cr,,pemic target, <0.03 ng/:n'.,) (SI: <0.G.') rt/i, [<C.OJ f-'g/L])
Hcm<cgh:!1;u "' 12.0 g/ dL (: 3.f-: 7.2 tJ dL) (SI: : 2G g/:, [138- '. 72 g/f .])

Which of the following is the best treatment to start now?

A. Escradiol gel
B. Long act'.ng :atrnmt:sn'.h,: tes<:osterone
C. T J:noxi'.Cn
D. Tcstostcror:.e gel
E. Venh,fa.xinc

33 A 66-ye;ir-old white wom,m presen:s to you office for diabetes management. Type 2 diabetes mellitus
v.1as diagnosed l S years ago. Her r11;rent treatment regimen consists of 34 units of insulin glargine :ic
bedtir:1e; silaglipti:11 25 mg once daih; and glipizide extended release, 5 mg once daily. She has end-stage renal
disease and hs.s been :·eceiving hcmo<lii; ysis for the past 4 yea:cs. Her diabetes bas alrn been co11:plic<Sted by
reli nop,:thy :mC. neuropathy, She reports lbt her List dilated eye examination W<'S aboul 6 n:.onths <i[';G at wii::-h
~:..me s1 ,1,hle nonp:ol:ferati ve retinepathy ;,vas noted, She lns wel1-co:itrolled hypcrtcr.sion. She iioes r.ot rou:inely
cl1eck her ~loo<l glucose at home, bt:t states that the ff'w tll-aes she has checked it, vak.cs hav(' been in the :ange of
100 to 200 ;ng/CL (S.6-1:.11:.unol/U. She ha~ nol 11Dlke<l any low glucose va'.ucs. She rcpor:~ biurryvisinr: over
the pasl few weeks but has no other sy:nptoms.
On physicJ; exa1;,,ina:-.icm, her b:ood prcss'Jr<:> is 154/86 mm Hg and pulse rnte is 84 '.),:,ats/min. HN heirht
is 64 in (162.6 cm;, Jn<l weigk is 182 Jb (82.7 kg) (BMI =- 3i kg/m 1). She has stasis dermatitis in bo:h lower
extrc:nicies aaci +; pihng p<:':d:?he:·al ede:na. Upcn ai.:scs.1ltalion, her heart has a regular race and rhychc:1, with
a +2/S systo:iL· mumur hest 2.uscu:tated over the right upper Slernal border. Her l:rngs :ire dear lo auscdtatio:1.
''.'hc'."c is :1.0 abdomiml tendern<:'ss or pa.2pable ma~s.
Currcr.t medicalions arc hsinopril, a:nlodipiEe, inm sulfale, and epoetin alfa.

Laior<etory test results:

Hemoglobin r\,,. =6.7% (4Jl%-5.6%) (50 mmol/nc: '.20-38 mrr:ol/mo:])
Hemoglobir. - 3_9 g/dL (17,,J · 1.'i.1 g/d.L) (SJ: 89 g/L [121-151 g/L])
A'.bu..-r,in .,, 3. 7 mg/dL (J.5 5,0 g/(ll ,) (Sl: 37 g/L [35-·50 g/L])
E:e:trolytes, nor:na'.

Which of the following Is the best next step in this patient's mcmogement?
A. C'neck for he1"'.log]obin S variant
fl.Measure fructosaminc
C Reduce the dosage of insulin glargine
D Stop gli?i,ide
E, Me,suce C, peptide

34 A 35-ye2r-old man presents co the e;.nerge:icy department for evah:acior. of progres5ive subs:ernal che~t
;nin over the precl:'ding 5 &y;; and a 2-month history of palp~tations, .,ho:"tness ofbrea~h, <li,iphores:s,
~rcrr:-,ilomness, and 20-lb (9.1--kg) unin~_e;itiom.l weight loss.
On physi:.:al examination, his blood ;>ressur<:> is 14C/90 ml::1 lle; Jr:d pulse rate is 120 lx,a.ts/min. There ;s a
d.iffasc goi~er (30 g) without tenderness or pa:pab~e nodules. He h<es ;1 tine tremor of his Dutstrecd~ed hands,
his ski:1 is warm an<l 1-:::oist, <Sr:<l C:eep ter:d::in rdexes a;-e 3+, He is afebrile, and the rest vf his cx.imina:-icn
f:1::di:1gs are norm,iL
Electro~·ardiogophy shows s:nns tachyca:"di2 withou: ST- or T-wave changes.

l
Laboratory test results:
Complete blood cell count, normal
Complete metabolic panel, normal
Troponin I= <0.05 ng/ mL {<0,6 ng/ mL) {SI: <0.05 µg/L (<0.6 µg/L])
TSH = <0.01 mlU/L (0.5-5.0 mIU/L)
Free T, = 4.2 ng/dL (0.8-1.8 ng/dL) (SI: 54.1 pmol/L [10.30-23.17 pmol/LI)
Total Ti= 510 ng/dL (70-200 ng/dL) (Sl: 7.9 nmol/L [1.08-3.08 nmol/L])
Thyroid-stimulating immunoglobin = 150%of basal activity (~I 20% of basal activity)

CT imaging of the chest with contrast is negative for pulmonary embolism, but reveals a solid, homogenous
anterior mediastinal mass measuring 11.5 x 7.5 x 3 cm (see image, arrow).
The patient is admitted to the hospital and begins
treatment with methimazole, 20 mg twice daily, and
propranolol, 10 mg 3 times daily, witl1 subsequent titration of
propranolol and transition to an extended-release formulation.
The patient's symptoms gradually improve, and his vital signs
normalize over the next 2 days. He plans to pursue treatment
with radioactive iodine (t31I) after hospital discharge.

Which of the following is the most appropriate

initial management of the patient's anterior
mediastinal mass?
A. CT chest imaging in 6 months
B. Mediastinoscopy with biopsy
C. Measurement of serum ~-hCG, a-fetoprotein, and lactate dehydrogenase
D. PET-CT scan
E. Surgical resection via median sternotomy

35 A 23-year-old transgender man with a history of depression is referred for gender dysphoria and gen der-
affirming hormone therapy. He reports first notid11g incongruence between the sex he was assigned
at birth and his gender identity at age 6 years. He recalls preferring playing with boys and dressing like male TV
characters. He experienced significant distress and dysphoria at the onset of puberty, especially with menstruation
and breast development. He did not tell anyone that menstruation had started for 2 years because he was too
embarrassed to discuss it. During a psychology class in his junior year in high school, he had an assignment on
gender dysphoria and learned the language to describe his identity. When moving to the local area 1 year ago, he
shared his identity with his family and socially transitioned in the new city.
He has several goals for gender-affirming hormone therapy. The first is to stop monthly bleeding, which is
emotionally difficult and triggers dysphoria and depression. He has not had any hospitalizations for depression, but
he has presented to the emergency department for evaluation when bleeding was associated with suicidality. He also
desires gender-affirming chest surgery, as he wears a binder. He looks forward to voice deepening and facial hair
development with hormone therapy. He wants to discuss cost-effective options because he cannot afford expensive
testosterone preparations. He has read about the different methods of testosterone treatment and is comfortable
with possible injection therapy. He is now engaged to be married to a cisgender man, and they are interested in
discussing fertility preservation.
On physical examination, his blood pressure is 124/81 mm Hg and pulse rate is 88 beats/min. His height is
66 in (167.9 cm), anJ weight is 199 lb (90.3 kg) (BMI"" 32.1 kg/m2). There are no signs of ,mdrogen excess.

Laboratory test results:

Total testosterone= 16 ng/dL (8-60 ng/dL) (SI: 0.6 nmoVL {0.3-2. t nmol/L])
TSH = 1.7 rn!U/L (0.5-5.0 mlU/L)
DHEA-S = 127 µg/dL (44-332 µg/dL) (SI: 3.4 µmol/L [1.19-9.00 µmol/L])
Fasting glucose= 98 mg/dL (70-99 mg/dl) (SI: 5.4 mmol/L [3.9-5.5 mmol/L))

30 ESAP 2021-QUESTIONS

iI
 Lipid panel, normal
Day 3 FSH = 7.0 mlU/mL (2.0-12.0 mIU/mL [follicular]) (SI: 7.0 IU/L [2.0-12.0 IU/L])
Estradiol = 54 pg/mL (10-180 pg/mL [follicular]) (SI: 198.2 pmol/L [36.7-660.8 pmol/L])

'Which of the following is the best next step?

A. Referral to reproductive endocrinology for controlled ovarian stimulation for embryo cryopreservation
with fiance's sperm
B. Referral to reproductive endocrinology for ovarian tissue cryopreservation now (before initiating hormone
therapy)
C. Initiation of transdennal testosterone
D. Initiation of intramuscular testosterone
a
E. Initiation of GnRH agonist until gender-affirming surgery when ovarian tissue cryopreservation can be
performed

A 58-year-old man is referred for evaluation of severe hypercalcemia. He reports joint pain and mild
36 memory loss. He has no history of fractures or kidney stones. His dietary calcium intake is approximately
600 mg daily, and he does not take any calcium or vitamin D supplements. His family history is negative for
parathyroid or thyroid disease.
On physical examination, he has a palpable 5-cm, mobile, nontender, right-sided central neck mass.

Laboratory test results:

Serum calcium"' 12.5 mg/dL (8.2-10.2 mg/dL) (SI: 3.1 mmol/L [2.1-2.6 mmol/L})
Serum phosphate= 2.0 mg/dL (2.3-4.7 mg/dL) (SI: 0.6 mmol/L [0.7-1.5 mmol/L])
Serum creatinine = 1.4 mg/dL (0.7-1.3 mg/dL) (SI: 123.8 j,lffiol/L [61.9-114.9 ~ol/L])
Serum intact PTH = 233 pg/ml (10-65 pg/mL) (SI: 233 ng/L [10-65 ng/L])
Serum 25-hydroxyvitamin D = 37 ng/mL (30-80 ng/mL [optimal]) (SI: 92.4 nmoI/L [74.9-199.7 nmol/L])
Serum albumin= 3.5 g/dL (3.5-5.0 g/dL) (SI: 35 g/L [35-50 g/L])

Neck CT shows a 5-cm, heterogeneous,

predominantly hypodense lesion in the
right thyroid lobe, with mass effect on the
common carotid artery and trachea, and
no lymph node enlargement or distant'
lesions (see image, arrow).
He undergoes surgical removal of the
neck mass and right hemithyroidectomy,
and the pathology slide is shown (see image).
Surgical pathology reveals nests
of parathyroid tumor cells entrapped
within a thick, irregular capsule, with Neck CT (sagittal view).
adherence to the thyroid gland, with no
foci of transcapsular tumor invasion into
adjacent tissues or definitive lymphovascular invasion.
His calcium and PTH levels normalize 1 month postoperatively, and no residual mass is identified on
subsequent neck CT 6 months later. .

Which of the following is the best next step in this patient's management?
A. Order sestamibi scintigraphy
B. Order whole-body PET-CT
C. Repeat laboratory tests and neck imaging in 1 year
D. Refer for radiotherapy
E. Refer for chemotherapy

ESAP 2021--~QUESTIONS 31
 37 A 65-year-old man seeks consultation regarding diabetes mellitus that has been exacerbaled by
glucocorticoid treatment. He was admitted to the hospital 2 months ago for evaluation of headaches,
fevers, and left-sided vision impaiIT.1enc He was presumed to have giant-cell arteritis and was initially prescribed
prednisonc, 120 mg daily, which is now being tapered (current dosage 40 mg daily). The plan is to reduce the
dosage by 10% weekly overt.he next 6 months, He has imermittcnt symptoms of paresthesia in his fingers and toes,
b.t he othervd.se feels well. He is up to date on screening laboratorr tests and assessmems, and there is no history of
nephrnpathy.
Before the hospitalization, he was taking metformin, 1000 mg twice daily, and extended-release gHpizide,
6 mg daily. On this regimen, his hemoglobin A1c level ranged from ti.7% to 7.0% (50~53 mmol/ mol) over the
preceding year (before receiving glucocorticoids). While in the hospital, his diabetes regimen was switched to
insulin detemir, 30 units once daily, and insulin aspart, 12 units before meals, with supplemental insulin to be given
on a correctional scale, However, he admits to often missing l dose of aspart daily because he forgets and expresses
di.~sati.sfaction. with the current regimen. His fingerstick blood glucose measurements arc noted as follows:

Fasting"- 100-120 mg/dL /5.6--6.7 mn:ol/L)

Bcfordunch = 178-197 mg/dL (9.9-10.9 rnrnol/T,)
Before dinner - 235-260 mg/dL (B.0-14.4 mmol/L)

Which of the following should be recommended to improve this patient's hyperglycemia?

A. Continue ll!rrent detemir dosage but increase the aspart dose before meals
B. Continue current regimen but increase correctional insulin. scale
C. Continue current regir.1en and add liraglutide once daily
D. Increase both detemi.r and aspart dosages
E. Stop current regimen and start premixed insulin (NPH/regular) twice daily

38 A 46-year-old man with a history of multiple gastrointestinal polyps and Hpomas underwent extensive
abdominal surgery for his polyp burden 3 years ago and now has a colostomy bag. He was recently
diag1~osed with a 5-cr:1 right thyToid nodule. He undergoes FNA biopsy of the thyroid nodule, which is documented
lO be Bethesda IV. Total thyroidecwmy with central neck dissection is performed. The final pathology reveals an
angiuinvasive, well-differentiated follicular carcinoma (5 cm) wit.h oncocytic feati:res in the right thyroid lobe. All
margins are free and 5 of 10 cervical lymph nodes are positive for metastases.
Six weeks postoperatively, he has a radioactive iodine scan while he is hypothyroid,

Laboratory test results:

Thy:-oglobulin, undetectable
Thyroglobulin amibodies"' 1220 IU/mL (~4 lU/mL) (SI: 1220 kIU/L [$4,0 .k!U/L])
TSH"' 240 mili/L (05-5.0 m!U/L)

He receives 100 mCi of radioiodine treatment. His scan after therapy demonstrates an abnormal focus of increased
radioiodine uptake in the midneck that was not seen on a prethernpy 1.iir scan, corresponding to a 10 x 7-mm,
soft-tissue nodule in the anterior aspect of the thyroid cartilage, consistent w'itli a metastatic Dclphian lymph node.
A follow-up recombinant human TSH radioactive iodine scan is negative, ¼i~h undetectable thyroglobulin but
srHl elevated thyroglobulin antibodies of 40 lU/mL (40 kIU/L) 6 montl)s after receiving radioiodin.e treatmenL He
has no palpable mass in his neck, dysphagia, or dysphonia. He currently takes levothyroxine, 200 mcg daily, and
bupropion, 450 mg daily.
Tb.e patient is married and has a 9-year-old son W:th some lei,min~ ditliculties. Family history is nota:ile for
colon polyps in his father and colon cancer in his paternal grandfather,
On physical examination, his blood pressure is l 25/ 68 mm Hg and pulse rate is 70 beats/min. There is a well-
D.caled scar at the base of his neck There ls an ileostomy stoma in Lhe right side of his abdomen. He has no lower-
extremity cden:a. Skin examination shows several skin-colored papules vv:ith slightly rough surfaces aroun<l his lips
and in the nasolabia.l folds.
 La'.)(lratorf tesl resulh:
·;·sH - 0.92 .:-n!C'/L (O,S 5.0 :n'.U/J ,)
''.'hyroglobuli:i "" -,ndttc'ctabk (<; ,0 ngfo1 T.) (SJ: uudeLecta~le '. < I.D µg/L])
·;·nyroglobulin antil:od:es = 10 JU/mi, (<4 HJ/ml.) (S:: 10 :~;;J/L '.~4.0 klt:/1 _:j

In addition to increasing his levothyroxine dosage, which of the following is the most appropriate
next step?
A. Genetic testing for :be BR.AF V6003 som2.tk vari<Ell
R G,cetic testing for a ?TEN gecmlicc psthogeoic ncimt
C. Kidney ultrnsonogrnphy
D. Neck.CT
E. Thyroid .1ltrasonog'."aphy fo'." tbc patient's son

A .12-year-old wo1,1an :·etums for management 0( diabetes mcll.iti.:s. Monogenic diabetes was dag!l.osed
39 at age : 5 years. She was founC to have a pathoge:1'.c variant in the gene encoding hepatic nil clear factor
lo: (HNF1Ai and was the i:1dex case for tl'_onogenic diahetes {J'v10UY type J) in her c.xtcndeJ. fa;.nily, He~ mo:her,
/, of S s1b.Jngs, materni grnndrr.otl1e:: 1 and severa: maternal g'."ea[ aunts rnd uncles have d1abeles.
Jnitially, she was t:·eaced with r,lybw:ide and had excellent glyce:nic co:1trol. During a p'."Cgna:1cy o.t age 26 years,
she st~rteJ insuEn an<l cuntiaued ;.r1.sulin therapy after delivery. She has had reasor:able glyccmic contrcl J.uri2!g
rhe last several years, wit'.1 ~1en10globin A,,- levels :anging frorl'. 6.4% to 7,5% (46-58 :o.mol/mol). She current:y
administers 1.} units of bsu:in Jegbdec ,it hecitime. She uses B il'_sulH-to-·car:)ohydrate ratio o:" I t:nit of b.sulin
aspart per '.4 g carbohydrate (total bobs dose of l6 u:1its/2ay).
She Las not had a di.fated eye examination in lhe ;;isc 2 years. At he: last exam, she was told her eyes appeared
norr:ial. She has no synprn:ns of ncuropo.thy. \'vhen meas1.:red 6 :110:1ths ago, her albumin-lo creatininc ratio was
elevated at 88 :ng/g creadnine. She has never been lreate<l fo:- hypc::te:1sior: or dys~ipidemia, She does net :lave
hypoglyceraia unawa:·eness.
On physical examination, l-:er '.1eight is 69 in (175.3 cm), a:1d weight is '.42 b (64.5 kg) (BMl -~ 21 kg/m 2).
HeT blood pressure is 130/78 mm Hg, and pu:se rate is 56 beatshnin. Pnipheral pulses are strong, She has normal
reflexes and normal sensation fo:: position sense ~nd 10-g monoftla:nellt in each foot

Laborntnry test results:

Elcctrnly1es, norl:rnJ
Hcmog:obtn A1, = 7.4% (t\.0%-5.6%) (57 mmoJmol [20-.~8 m:molimoU
Crca:inim\ = 0,7 mg/ dL (0.6- U :11gidL) '.SI: 6L9 mmoliL [.S3.0-97.2 mrr:ol/ L])
TSH"' 1.64 mlU/L (O.S-'.l.0 :nlU/L)
t\lburein-to-crcatinine rntio = : 03 mg/ g creat (dO mg/g crcat)
Urindys'.s, no whit(' or red blood eds or bacteria

Which of the following [s the best next step in thls patient's management?
A. MonitoT only; :10 therapy :~eeded
B. Start lisir.opril
C. Sta:·t canagliflozin
D. Intensify insulin treatment
E. Sta:: a low-prote:n diet

A 33-year-old woman with hypertension '.s referred for assistance with weight toss. Weight gain has been
40 a problem since she delivered her first child 3 years ago. Before her first pregnancy, he:c weight was 161 lb
(73.2 kg), Twelve months after delivery, ~1er weigh, was 187 lb (85 kg). Her current weight is l 85 lb (84.1 kg),
-:-he patie1~t h;is hef'n ~rying to fo~low diflerent diets, but she is ur.abk tu lose weight She :-eports that her biggest
struggle is cravings. \\!her. she sees sweets or pa~tries, she cannot control l~er cravin~s and cn<'.s up eating. After

l
taking a co:npl,;>t,;> history, il bw ::alori'..' meal plan and an exerc~se prngn:n ,1re recoa1mendcG. The paLem ret\trm
2 weeks later a:1d has not lost any we'.ght. She reports tha: despite her b0csl eifons to foEow her new meal plan,
cnving, are 2. )ig ohstacle,
Her medicatim:s inclwie lcydrnchlorothiazide, 12.5 mg dai'.y.
Cn physkai exaE1i11ation, her blocd pressure is BOi8S 1:1.m Ilg ;,:1d pu~~L' :-ate is '/0 beats/min. Her heig:,t
is 63.5 ;_,i (16'. ..1 err;), and weig~t is 185 lb (84.1 kg) (B.~11 = 32 k~/:n 1'). She is in no d'.stress and does nollook
cushingo'.d, Jle; lungs ac·e dear to au.,cuitat'.on, am: hea:-t sounds J:·e :·egu:ar. Fi:ldings on abdomir:a{ examb.atio::
are unrema;kahle. She has r:.o periphernl ede1:ia.
Her hemoglobin A1c level is 5.4% (4,0%-5.6'.lf,) (36 :nr:10'./mu: [20 38 mmol/mol;;.
Tlw pade:1t agrees :o addir.g a weight-loss nwdication tc he,· prngr.;.m.

Which of the following medications should be recommended for this patient?

A. Lirctglutide
B. N.;.ltrexone/bupropion
C. JV:etformi:1
D. Vi·.ec.teEnine/topi:-arr;ate
J:::. Orlism

Al
~· u
•1 A 20-year-oJd man with hypothyroiCisn:. due :o Hashimoto thyroid,tis on '.ong-1:en:1 levo:hyroxine
:lwrapy presents for rollow-up, He also has cebc drnease trea~ed ·with a glucen-±ree diet. ln:erva; medtcal
history is aornb'.e for a diagnosis of t~xal (partia:l seizu:-es that umet 4 mon;-hs ago, ToCay, the patie:1t reports
fatir;ne and a 5-lb (2.3-ig) weight gain over 3 :11onths, hut he i, mherwi.sc feebg well. Curren~ 1:1.edicatim:.s are
levo~hyroxine, 100 mcg daily, and carbamazqine, '.00 mg l',vice daily. Hr has had no subsequ,;>;:t seizu:-es following
initiacion of antkonvulsant dn:g therapy.
Physical examination is notable fo:: <'.ry ski1:.. His bluod pressu:e is 107/55 mm Hg, and pulse ::ate is
68 beals/min. His heigt-.t is 69 in ( l 75.3 cm;, and weigh is 1)0 lb (OU kg) (B!v~l - 22.1 kghn;'). The rest of h1~
examination findings are norms.I.

Labo:atory tes'.". results:

TSH"' llO m:U/L (0.5-5.D r;1HJ/T.)
I'ree T1 ~ 0.7 !lg/dL (0.8-1.8 Hg/ dL; (Sl: 9.0 pmol/L : lO.YJ-2117 pmol/'._,;)
Ser:1m carbamazepin<2 = S v.g/nL (4· 12. j.tg!!'.lLl (S:: 33.9 r:,mol/L [:7-51 fll11ol/L])

Six months ago, his seni:n TSH value was 2.0 m!U/L

Which of the following is the most likely cause of the change in this patient's thyroid function
tests results?
A. Anti:::onvulsa.nt <lrug th'..'rapy
B. Celiac disease
C. Nonadherence to lcvothyToxine therapy
D, J\"cmhyroi<ld illness sy:1drorr:e
E Weight gain

42 A 56-year~old woman presents with a 1·year history of w0~seni1:g anxi<:'ty, pal;,itations, and swea.ling. Ste
describes episodic anxiety with a feeli11g ofhearc racing and poundb.g, accom;,anied by dren~·~1ing sweats
on her upper body and face. These symploms are not p~ovoked by any physic.ii or emotional trigge::s. The episodes
oc..:ur at ur:pred:nable tim<:'s and resolve ~pontaneoi.:sly within 15 to 60 mir.utes. During syrq)tomatk C:?iso<les,
her b'.ood pressure (assessed ,,t home) raagcs from 15,;/go mm Hg to 210/100 m:n Hg. Pheochromocyto:na is
diagnosed after plasrr.a normetanephrine levels are founC to be 6--fo!d deva:ed, ,md ab6ominal CT imaging reveals
aI1 3-cn left adrenal mass with hi[!,h 2t'.e:l.'.tat\on charactuistics. On ,ev\ew ofhe:-falnily hislory, her father dicC. of a
mctast2tic gastrointestn,,l stromal tumor anC 1:cr :notl--.er and sis:er have !lad breasc c,12:cer.

34 ESAP 202.l~QUESTIONS
 The pathogenesis of this patient's pheochromocytoma is most likely attributoblc to a pathogenic
variant in which of the following genes?
A EFAS! (cn<lmhelial PAS domain protein 1)
B. SVHB (succinale dehy<lrngenase snblE!.it B)
C, RET(,·ctprcto oncoge;ce)
D, TivJFlv1127 (:ranscrn,nbrane IFotein '. 27;
E. VHL (von HippcI-:.,indau 1un:.m suppressor)

-:)
4,;J, -' A 44--year-old womar, p;ese;.cls for Pva'.u,1tion of a goiter. She first noticed enlargement of her thyroid
gla:td 12 r:1omhs ago, and she believes tb:- it hs.s continued to grow, She describes some pressure ove:- her
neck and difficu:ty swaEowi:r:.g. She has bad no weight loss or 11ight sweats. Hypothyroidism was diagnosed a year
ago, and she take~ kv,,thyroxir;e, t 2.S mcg Jaily. Thy:·oi<l ultrasonograph.y reveals hypoechoic thyroid tiss'Je ir; bolh
frtyroiJ lobes an<l a:1 ill-defined, 2.2-cm nodu:e in ll,e left '.ohe. F~A biopsy of'.eft thyroid nodule is non<li,,g:10stic,
A second FNA biopsy of trle nodule is also :1ondiagno~Lic Sh<' Endergoes core biopsy Of the lefr ll,yroid nodule, and
exam'.nation sl~ows e"Xtf'nsive fibrosis w!.t:1 rr.cderm: lynqhoplasrracytit infil:rale a:r:.d no follicular cells. Thyrnizi
'.ymphoma is ;uled out
She bas no notable nsedlrnl or surgical history. She has no know.1~ <lruE allergies, ,ucd her mly medico.lion is
levothyroxine.
On phys'.ca[ ex2mlnation, her ~loo0. press:.ire is 12C/70 inn Hg o.nJ µalse rate is 68 beats/min, Her hdghL
is 63 in (160 cm) and weight is 13C Jb (S9 kc) (B:vll - 23 kg/m 2). She is in no aci:te distress. Her thyr::iid glw<l
is enlarged (3 times r:crmal size), and th<' left lobe is larger than the r'.ght lobe, Tlw g1and does nol move with
sw,dowlng and feels ba:-d. Thc:-e 1~ r;o -;;a'.pab!e cervical lymµhadenopathy. He:.- hear:- rate is reg:ilar, and lu:i.gs ar0
r\p,1r to auscultatio:c. ·;·:1ere is no lown ·ex\ re1;1ity edema. The resc cf the exancirudon ffodi11gs s.re :10rnal.

Laboratory test resu'.ts:

TS~-!= 2.0 rdU/L (0.5·5.0 mf~.:/L)
Ca'.cinm = 8.8 n:g/ dL (8.2· H.1.2 mg/ dL) (Sl: 2.2 mrr:;l/J, : 2.1-2.6 r:nnol/LJ)
Jl'.i'H-= 45 pg/ml. (J0-(;5 Pb/rn:.; (S[:!.5 ng/L [10-6S ng/l ,;)

Whkh of the following is the best next step in thfs patient's management?
A. Pe;.·fonn total thyroidectomy
B. Ir.i.tiate pre<lnisone
C. rnltiale ta:noxife;1
D, Perform ist.hmusect◊:ny with lefl lobecony
E, lncrcasc toe levothy,nxine coscge

44 A 64-year-old woman with a 2O-year h'.story of type 2 diabetes mellitus presents for follow-up. Three
mo:r:.ths ago, her hnnoglobir A,, kvd was 11.0% (97 mmol/moi). She recently retired and has been able
tc eat :)etter, exercise, and take i1~suLn more regularly. Her glycemic control has improved, and her hemoglobin /J·, 1,
!eve! is now 8.5% (69 □ mo!/mo:). ShE' silso repor;-\ a 2O--:b (9.:-kg) weight lo~s ov<'.r the past yea:c,
Hrr ;,rimary concern mday is <li.scomfo:t in her feet that is keej)ing her awake at night. l:le pain started abcut
4 weeks ago and is bilateral and burning i11 natt:re, Ambulation does not signifi:..:ancly worsen the pain.
On physical examination, her 0bo<l ;;ress,1re is 134/82 mm Hg and pulse rate is 88 beats/rain. Her ~1ei!<ht ls
65 in (:65 ce~L ,,nd weight is :755 b (79.8 kg) (B!VIl '""29 kg/m 2).
S',,;.in examination reveals acan~hosis :1igr'.cans. Strengrb '.s preserved in a'.l extrcm'.ties. She has decreased
sensation to pk prkk in both lower extrcmitks 1.,.p to her ankles. The;e is no :notor <lysfonccion, and ankle reflexes
<ere 1+ 0ilatciaEy, BllJteral dorsaEs pecis pulses arc palpable. The rest of the examln2tion fnJi.ngs are normal.

t
Which of the fo!lowlng is the most likely cause of this patient's current prominent symptoms?
A. Vasct:la:- insufficiency
B. D.:abetic polyEe1"rnpa1 hy
C. Rad:culopathy
D, Trea:tl'.ent-in<lucrd ne,1ropa.thy of diabete,;
E. Dia:Jetic nei.:ropat'.~ic cachcxia

or
45 A .H-year-old wom<>n '.s referred because recently diagnosed acromegaly di.;e lo a '. .9-cm pituitary
macroadenomd. She developed symptoms of enlarging himds, sweating! carpal tunnel syndrome, facial
feature chaages, and snoring rh:1t snrted about 9 years ago. Her fa1h<'J is 64 years old a:i.d healthy. She h.as a paternal
cousi1~ will1 acromegaly, another paternal cot:sin (from different unc:e) with a pro:actinoma, and a paternal uncle
(:10w deceased) whom she remembers had ve:-y large h:u1.<ls. She prod,tccs a p'.cture of '."his uncle, who looks frankly
acromcgd!ic. The~e is no fam:ly history of recurrent kid1cey scoacs, "i-iypcrcakemia, panc:·eatic lumors, or cardiac.
problems. Her mother is alive a:td we!L :No pill1i1ary aJe210:nas arc present in he:· n:other's s.:de of :be family.
The patient has 2 d:1iL:ire::. (9-yea:-ol<l boy and 7-ycar• oid gir:), anC she asks w.hetherthey are at ris~ for pituitary
adenomas.

A pathogenic variant in which of the following genes is the most likely culprit underlying this
syndrome?
A. ]l,1£NJ (nwnln 1)
D. RET(ret proto oncogene)
C. AJP (a:;'1 hydrocarbon receptor i:1teract:ng ;,rotein;
D, PRKAR1A (prntcin kioose cAMP-depec;dent type [ ,egubtm-y sub"nie "[ph,)
E, GNAS (GNAS cmoplex locus)

46 A 67-year-old man presen:s for ongoing ::ardiovascuiar ri.sk n:rnagc:nent and genetic dyslipidemia.
He has known cardiovascular d;se,:se :md hiid a 1~1yornrdial infarction and ?,-vessel coronary ane:y
bypass grafting at ilg<' 47 years. Since then, he has reqvire<l 2 more percutaneous coronary ir.terventi.ons, the most
rccc:it being 8 months ago, while on therapy. He llas t:·ealed hypertension, as well as type 2 diabeles treated with
metfonnin, Mbred-pattern dyslipidemia has been lreated for many years with rosuvastatin, 40 mg Jally; e:r.etimibe,
lO mg daily; and fenofibrate, 145 mg daily. As he i.s at ve:ry '.1.igh cardiovascular risk, lherapy is initiated -.,vith
evolocumab, a PCSK9 inhibitor. E:r.etlmibe is stopped after initiation of injecwble therapy. He returns for a follnw-
up visil1 and he has no concerns and feels well.
On physical ex:aminatio:1, his heighl is 68 in (173 cm), and wei~hl is 182.5 lb (83 kg) (13Ml = 27,7 kg/m1 ), His
blood pressure is ; 18/6,f 1:un Hg,
Laboratory test resu1ls are prescntcJ in the "."able.
Previous (on rosuvostatin, Present (on rosuvastatin.
40 mg doily, ezetimibe, 40 mg daily, fe11ofibmte,
10 mg daily, and fe11ofibmte 145 mg daily, and evolocumab,
Measurement 145 mg daily) 140 mg every 2 weeks) Reference ranges
:"ot::;: cho:estero· :: 09 mgicl (S" 4.38 mn,ol/'...J 59 rig/:i;_ (SI: 1.53 m~ol/L.) <200 r1g!dl (o,.;!irnol) IS·· 5.18 mmol/l/
7riglycerides 295 -ng/dl 1s: 4..:16 mrr.ol/LI 114 mgjdl. {SI: 1.29 r:1molil) <15:) 'l"lg/dl {optirrmi) (Si: <1.70 11mol/L)
HDL cho:estero· 2E 11g/d:.. (S:: J.67 rnrr.ol/U 33 mgiciL IS·. 0.85 mrml/L) >60 rng/dl (onc:irnal) (>1.55 mrrol/L)
LC:L c:10 1es:e•ol 04 mgial IS·: 1.66 rrimol/l.l 3 f'lg/cic. (S·. 0.78 mrml/L) <l()'.) 1n;i/r:i (optimal) {SI: 2.59 mrrol/:..)
Noi--'0L cho·es1c~r:-;I 143 rrgtdl {SI: 3.70 P1r:10l/l.i ?6 mgidl {51: C.67 r:1mol/L) <DO mqk'! \cptiMal) {SI: 337 mmol/L)
Herro(/obin A1, E.2% (44 rr.:ncl/r:10:) 6.4% ('16 11.;n•ol/r:io·) 4.'.l~":- 5.f:i% (20 38 rnmolimo:)
l-ost::19 plui;nw ;;:dcosc 113 ITg/dL {SI: 6.27 mr:10:Il.) '.09 ~g/dl :s1: 6.0S m1~0·/L) 70-99 rr:q/dl {SI: 3.0-!';.5 rnmol/:..)
Creati-1irie 1.1,: mg/dL \SI: 2.00.8 µ11101/L.i 1.18 rng/dL \SI: .'..0'1.3 µr10:ILi 0./-!.3 P19/:!L (SI: GL0 ":.:4.9 ;11rnl/L)

36 ESAP 2021-QUESTIONS
 Which of the following is the best next step in this patient's ongoing management?
A, Stop evo!ocG.mab
R, Stop :osuvastatin
C. Stop fc:10flbrate
D, A<ld sc;-iuglu:i.:ie
E, Recommend no chrngc ot ,his time

47 A 50 ·yeat-rn,m is reS.o:-:·ed for evaluation ()f new!y identified hypercakemia after presenting to his priBary
care physicinn with sy:11:ptoms of fatigue and polyuria over the last6 months, He is otherwise healthy
and '.i.as no history cf :1.otahle r:iedkal problercs. Specifically, he has no history of fractures,, nephrolithiasis, or
::raniocervical ra<liat~orL He does not take medications or over the-coun~er supplements. Family history is negarive
for osteor.-orosis, ncp'.1.ro:ithiasis, endocrine tumors, or head anC. neck malignancies.
On physi::al exambacion, he appe:irs we:1. V:ral signs ate 1.mrcmarkab:e, includi:i.g a B.Ml of 27 kg/m1 . Findings
on exan:inalio:1 ofchc eyes, cars, i;ose, an<l throat (ir:c:ucing oral exam) are norn:al. There i3 a fu:Jness appreciated
over the right ~ower antcri,)r nc6:. withovt associated pre::e:rvical or supraciavicufar adenopathy. The rest of the
examination Endings are normal.

;..atio.rJtory !est :esdts (serum):

Calc:\;m = 12.9 :,,g/C.L (il.2- lG.2 mg/d,) (SJ: 3.2 1r_GJ0'./L [2.1-2.6 rr.mv)L;)
Ph0:;pia1e., l'J lag/di.. (2.3-".7 n:g/dl.) '.SI: 1..IJ mrnoliL [0.7-1.5 mmol/Lj)
C~catir_ir,r = OJ\ mg/ dL (0.7-1.3 mg/ d,) (Sl: 7'J.7 y.mol/L [61.9-114.9 1.n:1.ol/L; j
Albuni:'l. = 4), g/dL (15-5.0 g/::iL) (SI: 42 g/L :3.S-50g.lLJ)
AlhEnc p.ho,~1h;l:a~e = : 25 U/L (50-120 ~; IL! (SI: 2.09 pJct/L [0.lA-2.J0 ,.i.;.,;_:dLJ)
::uac: PTH = ~;so ps/m:, {10-65 pg/mL) (SJ: 350 ng/L l I0- 65 ng/1.]]
25-Hydrm..y,-i:amin fl = ; S ng/C.L (3C-8G r:ghiL :oplir:10:1]) (SI: 37A um::il/L '.7 4.9-199,7 nmol/L])

Techne:ium 99T c parathyroid scan shows delayed t:pt.;kc ir: the rig.ht lower :tcck.

Which of the following is the best next step in this patient's management?
A, Refer '."o endocrine surg,e:-y for minimally invasive parathyroidectomy
B. S:an cholccalciforol and n~easure intact PTH agai.n in 6 weeks
C. Start cinacaket
D. Perform neck ultrasonogmplly
E. Pe,fonn renal ultrason0graphy

48 A :\5-year--olci r.ian presents for evaluation of suspected hypogonadisnL He .:'.'equested that his primary care
r,hysician measu:·e his '."cstosteroue because he did ll()t react with anger when his girlfriend broke up with
:'lim_, wllich his family thought was unusual.

Laboratory test results:

Serum total tcw1slernr.e (sample drawn a: 4 P:V[) - 181 nghL (3(}'.)-900 ng/dL) (SI: 6.3 r:mo]/L [IOA JU l'.r;wl/L:'J
Rc<peat [c'.:al t<:stos'.:<'nme (snmple drawn at 8 AM wbilc fasting) = 268 J:.g/ dL (300--900 ng/ dL) (SI: 9.3 nmo:/L
[ 10.4-3 1.2 nmol/f.])
Ul.,. 4.0 mJU/□ L (1.0 9Jl mllJi1::1L) (Sl: 4.0 ?..:/L [:.0-9.0 JU/L])

He underwent normal pubeny at age 12 yea:·s and de:1ies sexual <lysftnction. He plays bad:ninton on a regufor hasis
and has no~ noticed recc:.11 fatigu" o:- mi.:sde loss. He is cur:-ently not in a rebionship and is not planr:ing a fami:y.
On physical examination, his heir;ht is 68 in (173 ::m) an<l wcigb.t ~s 207 lh (94 kg) (BMl - 32 kg/m 2). His blood
prem:re is 134i9~ mr.1 Hg, a,cd resting pulse rate is 67 beacs/mir.. His waist circumference .:s 40 it. (101.6 cm). Neck
in;;pection reveals acanthosi~ nigrica::.s. lhere is :10 di:1ical visua'. fic!J. dcif:li, anci be has full range of ey-.., movements, He
has rr:ildly enlarged l:ireasl~ b.tt no palp2blc breast tissue, i\-ksc'.c bulk appea:;ss norn:al, and tes~es are 25 n:L bila~era.lly,

E
I
L
Which of the following is the best test to order now to further evaluate his gonadal axis?
A. SHBG measurement and free testosterone estimation
B. Pituitary-directed MRI
C. Prolactin measurement
D. Iron studies
E. Estra<liol measurement

A 26-year-old woman presents with a 3-month

history of intermittent headaches. Her neurologist
thinks she most likely has a variant of migraine but arranges
for brain MRI to exclude an underlying structural cause. This
reveals a possible pituitary abnormality that is confirmed
on further dedicated imaging. MRI of the sella is shown (Tl
contrast) (see image). The patient is referred to endocrinology.
On questioning, she has no features of pituitary
dysfunction. In childhood, she was diagnosed with attention-
deficit/hyperactivity disorder and had recurrent middle ear
infections. She has no other relevant medical history and is not
taking any medications.
On physical examination, her height is 65 in (165 cm)
and weight is 159 lb (72 kg) (BM!= 26 kg/m 2). Her resting
pulse rate is 88 beats/min and regular, and blood pressure is
105/75 mm Hg. She has a symmetric, smooth goiter (30 g).
Visual acuity is 20/20 (6/6) in both eyes and visual fields are
full to confrontation. The rest of the physical examination
findings are normal.

Initial laboratory test results:

TSH = 2.4 m!U/L (0.5-5.0 m!U/L)
Free T 4 = 2.5 ng/ dL (0.8-1.8 ng/ dL) (SI: 32.18 pmol/L [10.30-23.17 pmol/L])
Free T 3 = 5.9 pg/mL (2.3-4.2 pg/mL) (SI: 9.06 pmol/L [3.53-6.45 pmol/L])
Cortisol (8 AM)= 14.0 µg/dL (5-25 µg/dL) (SI: 386.2 nmol/L [137.9-689.7 nmol/L])
Prolactin = 28 ng/mL (4-30 ng/mL) (SI: 1.22 nmol/L [0.17-1.30 nmol/L])
IGF-1 = 160 ng/mL (117-321 ng/mL) (SI: 21.0 nmol/L [14.8-38.9 nmol/L])
FSH = 6.2 mIU/mL (2.0-12.0 mlU/mL [follicular]) (SI: 6.2 IU/L [2.0-12.0 IU/L])
LH = 5.0 mIU/mL (1.0-18.0 mIU/mL [follicular]) (SI: 5.0 IU/L [1.0-18.0 (IU/L])
Estradiol = 60 pg/mL (10-180 pg/mL [follicular]) (SI: 220.3 pmol/L (36.7-660.8 pmol/L])

Follow-up laboratory test results:

TSH = 2.5 mlU/L (0.S-5.0 mlU/L)
Free T 4 = 2.4 ng/dL (0.8-1.8 ng/dL) (SI: 30.89 pmol/L [10.30-23.17 pmol/L])
Free T3 = 5.7 pg/mL (2.3-4.2 pg/mL) (SI: 8.76 pmal/L [3.53-6.45 pmol/L])
TRAb = 0.1 IU/L (:s;J .75 IU/L)
SHBG = 6.9 µ.g/mL (2.2-14.6 ~.g/mL) (SI: 61.4 nmol/L [20-130 nmol/1]}
rt-Subunit of pituitary glycoproteiu hormones= 0.6 ng/mL (<1.2 ng/mL) (SL 0.6 µg/L [<1.2 µg/L]}

There is no evidence oflaboratory assay interference in the free thyroid hormone and TSH assays.

38 ESAP 2021-QUESTIONS
 Which of the following is the most appropriate next step in this patient's management?
A. ArrangE' frir ;1nother ~>itui:;q-' M Rl in 3 r.10r.t'.1s
B. Initiate ;nethim2zole
C. hitiate uctreotide LAR
[)_ ~cfor i·or genf!tic testng
E. Refer for minsspbe:-ioidal surgery

f'\ A 54-ycar· olJ woman p:-ese:1ts with :ciausea, a few episodes of ernesls, fatigue, and general malaisP over
5\J tl-:e past frw days. She h,1$ J S-yed: bisto:;, ofrype 2 cia:>c:.es rcel:itus that is rnrrer.tly mar.ageJ with
1

met'.Ornin, S00 mg twice daily: canag:iGozin, 100 mg daEy; insulin aspa:.t, l0 mi.bat each :neal; and insulin
degludec, 42 units daily at bcdtirr.e. This 11:gimen has been stable for 6e past 6 r::iont.hs.
Afrer 2_ ::lrief trial of ord therapy at the t~me oh-liagnosis 8 years ago (hemoglobin A,,,"' 8.6% [70 mmol/mo!J,
i nsdin was initialed tc contra: glyce:nia. Her most rece:~t he:noglobir: 1\, measurement is 7.2% (55 mrr:cl/mol).
Si1e chf!cks ber blood iucose before each meal and at bedtime, She reports tha: her blood 13lucose va:ues have
been i1~ d1f! lt,cd :-;mge ,,f 80 ~o 150 mg/dL (4.4-8.3 mmol/U with occ2sio.r:al highe1 readings ( i 80--250 mg/dL
[:C.0 13.9 rnmol/L)~.
S:1c contacted :1er ;,rirr,,ary care physician earEer Lhis \Yeek, rnd she was given a prescriptio::. fo: onda:1se: rm:,
4 mg ora: Jissolving t,,h:et, to help with the nausea, w;,.::d1 w,ls prcsulYleC to be secondary cu gastroenteritis.
Althm:gh on<lar,,etro:\ has ameliorated her ;iausca, she ~ell: <lops no: foe] better over~ll. She repo~ts thJ! she has
increased '.1er flaiJ int,tkf' ever the ~ast few weeks but has noc :w~iced any increase '.n the frC(jUi.!:ity 0f u:ination.

Which of the following is the best step in this patlent's management?

A. Urdet 2. basic metaboEc p,:ne: a:;d measure scnr:n ketones
8, _:lerfom: urin<-' ai:.alysis
C. l'ecfc.cm, gcstcic enptyin3 study
D. Perform esophagogaslro<leodenoscopy
E. Stup rnetformir:

51 A 51-year-old womar with ischerr:ic congestive he::irt failure, hypertension, obstructive sleep apnea,
se:zme disorder, dcp:-ession, glattrnma, and Crol:n disease is referred for assistance with weight loss. The
_patient reports that weight gain 1:as been a problem since she was in elementary school Her weight gain has been
gz·adirnl; howevff, every time she initiates ste;-oids for Crohn disec.se, she gains mo.re weight than usual. Sht has
followeC commercial 1.Veig~1t-:oss pwgrams but has been unable to keep the weigh\. off. !he patient ears -1 meals
a Jay and describes her portions as large. She snacks on coo's.ies, chips, cake, an<l ice cream. She cannot c11rrcntly
cxerche bei..·ai:se of decondi:ioning,
Her ho:ne medic:tions include duloxctine, metoprnlol, eluxadoline, f:uticasmll'/saimete;o], aspirin, ;,otassii.:m
~hlori<l0 1 li.!vetiracetarn, a:td esomeprazole.
On physical e,,;:amin;i~i.on, her height is 66 in (168 cm) and weigh: is 278 lb (126.4 kg) (B!,Al = 45 kgfr:il).
Her blood prcssu:-e is I ?.1/R0 rr.m Hg, and pulse rate is 78 beats/min. findings on pulrr.cnary atJ<l cardiovasrnlar
exambati.on are no;.-ma.L
Bariatri.c si.:rgery is no:: an option give1: her history of Ctnlm di.seas<:'. A low-caloric meal µla:1 ( l S00 calories
daily) is recommc:ided. Six weeks after staning her new plan, slw has lost 6 ;b {2.7 kg). However, sl~e ls st:-"Jggli:tg
·with hm:ger, The paticn~ Lielieves hi.:nger is a barrier that will i:npair further weigh: loss, Starting a weight-:oss
rr::edication is di.scLL~scd.

Which of the following medications should be recommended for this patient?

A. Naltrcxo:1e/hu::-ropior:
B. ;jragh,t:de
C. Orlista:
D. Phen:er:nine
f Phenrcmindtovrnnuk

:
L
5 A 25-year-old man with a 15-year history of type 1 diabetes mellitus presents for routine follow-up. He
has microvascular complications, including background retinopathy and microalbuminuria. His treatment
consists of a basal-bolus insulin regimen (insulin aspart, 4 to 6 units with meals; insulin detemir, 6 units in the
morning with 4 units at bedtime) and ramipril, 5 mg daily. He has recently been feeling more tired than usual,
which he attributes to waking up at night with an increased frequency of nocturnal hypoglycemic episodes.
On physical examination, his height is 72 in (182.9 cm) and weight is 160 lb (72.7 kg) (BMI = 22 kg/m2) . His
blood pressure is 110/70 mm Hg, and pulse rate 88 beats/min and regular. The rest of the examination findings are
normal.

Laboratory test results:

Hemoglobin A = 6.1 % (4.0%-5.6%) (43.2 mmol/mol [20-38 mmol/mol])
1,

Serum sodium= 133 mEq/L (136-142 mEq/L) (Sl: 133 mmol/L [136-142 mmoi/L])
Serum potassium= 5.3 mEq/L (3.5-5.0 mEq/L) (SI: 5.3 mmol/L (3.5-5.0 mmol/L])
Serum creatinine = I J mg/dL (0.7-1.3 mg/ dL) (SI: 114.9 mmol/L [61.9-114.9 mmol/L])
Serum urea nitrogen= 24.3 mg/dL (8-23 mg/dL) (Sl: 8.7 mmol/L (2.9-8.2 mmol/L])

Which of the following is the most appropriate next step in management?

A. Reduce the insulin detemir dosage
B. Reduce the insulin-to-carbohydrate ratio
C. Measure serum tissue transglutaminase antibodies
D. Measure serum TSH
E. Perform a 250-mcg cosyntropin-stimulation test

~
5 A 65-year-old woman presents for evaluation of a nodule in the thyroid isthmus that was detected
on examination at her annual preventative visit with her primary care provider. The patient has no
symptoms and has no personal history of head or neck radiation and no family history of thyroid cancer.
On physical examination, her blood pressure is 120/82 mm Hg and pulse rate is 80 beats/min. Her height is
65 in {165.1 cm), and weight is 160 lb (72.7 kg) (BMl == 26.6 kg/m2). Examination is notable for a soft, mobile,
1.5-cm nodule in the thyroid isthmus. The rest of the findings, including palpation of the right and left thyroid
lobes and cervical lymph nodes, are normal.
The TSH concentration is 3.0 mIU/L (0.5-5.0 mIU/L).
Neck ultrasonography demonstrates a 1.8 x 1.4 x 1.0-cm nodule in the thyroid isthmus (see image, arrow).
No abnormal cervical lymph nodes or additional thyroid nodules are observed.

Which of the following is the most appropriate diagnostic

test to perform next?
A. Neck ultrasonography in 24 months
B. NeckCT
C. Radioactive iodine uptake and scan
D. Serum calcitonin measurement
E. Ultrasound-guided FNA biopsy

54 A 52-year-old man seeks consultation regarding type 2

diabetes mellitus. Diabetes was diagnosed 6 years ago on the
basis of routine laboratory tests that documented a hemoglobin A10 value of 8.2% (66 mmol/mo]). His current regimen
consists of metformin, 500 mg twice daily, and glimepiride, 4 mg once daily. He has no acute concerns today, and
there is no history of hypoglycemia.
On physical examination, his blood pressure is 168/102 mm Hg and pulse rate is 78 beats/ min. His height is
71 in (180.3 cm), and weight is 202 lb (91.8 kg) (BMI = 28.2 kg/m2). On foot examination, he has normal pulses and
there are no wounds. On neurologic examination, both vibratory sensation and 10-g microfilamen t testing are normal.
Review of records indicates that blood pressure was similarly elevated at a previous primary care visit.

40 ESAP 2021-QUESTIONS
 ~aLoracory Les: :-esults:
Senrr: u:·(;'a ifrrogen - 16 mg/dL (8. 23 mg/r'.Lj ;SJ: S,'/ rarno:/;, [2.9-3.2 mrr:ol/Lj;
Cmtlni:H· - O.S r.1g/ d~ (J.7- '. .3 mg/ d:....) (SI: 79,6 r.,rnol/I '.6; 9 1; 1.9 µJ-:-ic'./L;)
HemogloU:n A:, - t-5'.t (i,0%-5.6%) (52 mmol/mo'. [J0-38 :r;rnol/;rol])
Uri1e albu:nln-to<rc2.tini:Je ra;:io"' 14 ng/g (dO mE/f. c·e~t)

In addition to lifestyle management, which of the following options for p:harmacologic

management is the best next step for this patient?
A. Lisino;;,dl
3. Amlodip:ne
C. Lis:nopr:l and valsartan
:). Am'.o<lipine and cltlo:"lblidone
,, Am;odpb.e and :cneloprolol

55, .A :s-year-old wo~:~n is ;eforred ~Or.r.:an~gerr.ent ofhr~e~th_Y\oi~ism.' Fm;r mu:1lb ag:~, she s,1w her
;.inmary ca;·f' ;ihys:c1an because of ;n~p1tat10ns and a 10-b (4.::,- e:gJ wcc&ht loss, At :ha1 tnnE', faborn:o;y
testins revealed st;pµress<Cd TSH ~1:d elevated free T 4• Her primary co.re ?hys'.c;an &agnose<l tlcyrnidicis a_;~d
prcscribnl atenolol, 100 mg d,1,ily. However, she continues lo experience palpitat'.ons and '.::..as devdopeJ diatrhea
anJ trcnors. She also has irregular 1:12nses and mild '.eft lower a:Odnminal pai:1. She h2.s r.o kEow1c J.rug a]e1gies ,1,nd
tc,kcs 2 daily :1.m'.Livilamin. Her fam~ily his~rwy is rerr:arkable for hypothyrnidsm in be: rr:o:-.hc:.
On physical examination, her blood pressure is t 10/60 mrr: H~ and p:1lse rate :s 90 beats/min. Her height
is 64 ir. ('.62.6 em), an<l wcigill is :36 lb '.61.8 k8) (BM]= 23.3 kg/m1), He:· :hym.d gland is not~Jalpab1e. She has
no nee..< pain. Her hear~ :a:'-' b regular, a:1d bngs are deJT to auscdtation. There is no Jower-cxtremity cdcna. He1
abdomen is ~ender in the left lower (.;_uadraut wit ho at a palpable mass. The re~t of the exami.nation findings are ,10,maL

Laboratory test results:

B2.sic m'..'tabolic panel. 1:orma;
Complete blood ce;] count, normal
TSll'"' d.l.O: m!U/L (0,5-5.S m!V/L_l
Free T1 - 3.2 ngldL (0.3-1,8 ng!dL) (Si: 41.2 pmoliL [!(}30·J3.l'/ pnrol/J.:)
ThY:"og;ohEn - 56 ng/mL (3-<l ng/mL) (S1: 56 f,g/L U "2 vg/L])
Pregnancy tes:, negative

She also ur:dergoes a pi:tl10le thyroid scan, whkh demor:slrales decreased tracer uptake i:1 bo:h thyroid lobes,

Which of the following is the best next step in this patient's management?
A, Order :byrOiC. ultrasonography
B. :;,itiate r,iethimazole
C Me11.snre thyroid-stimulating immunoglobulin
D. Order 1• 31who:e-hody s~an with SPECT-CT
E. lr:iliale µrednisone

A 23-ycar,ol<l w01:1an p~t>se:::ts with i;;egu:ar and \eavy menses. :Vk:1an::he was at age 12 years,
56 adrcnarc:1.e oc:..:uned a1 ,1ge 10 years, and thela:-che ocn:rreC about a year later. The imerval be1weea her
:nenstruaJ pc-:iods is typically 45 lO 60 <lays,
On physical examination, her L:~ood pressun' is [ l0/74 rr:m Hg. He, heigh: is 65 in\ 165.1 cm), a~d weight is 14G fo
(63.5 kg) (BMl - 23.3 kg/m'). She has nu 1en~linal hai:- grovvth or acanthosis, Sexaal developmcnc is Tinr.er slage S.

i..:
L::.boratory te~t H'Sll~h un ;.;yc:e day 3:
·;'.:3H = 1: r:1HJ/T, (0.5 5.0 rr:IU/L)
F:ol.icin = U Pg/;r I (4. :!C ng/ rn :, ;:wnlactat;nh fenl2lc 1; (SI: 0 ..)6 rr;wl/_;_ [0 ; 7 '. ..1C r:n:w;/:, :)
LI!= 15.Smlll:':1,:,'.l.0- !8.0:n'.~;/:nL l!0Eic;1;df;j (S'.: 15 iU/J, :1.0 18,0, ')
~·sH = S.fl ;r;\;/;rL [2./J.-12.0 mil/id. [fol!in1far]) (SI: 5,6 ;;,;/;, f:;_,r) '.'.1..0 !L:IL:)
'.Ostradiol ~ l~ pghr:L iW-180 ;Jg/:n'., lfoEku'.ad '..SI: 128.S prno:/L '..l67.'.-66C 8 pmol/L1:
lot:1l tes1i:~l c:ror::: "' 68 □ g/d. (8-6fl 1:g/ dL) (Sl: 2.4 :imol/J, '.C.3 2. 1 nmo;/L 1;
Fr1c~ re~I o;;Le::onc '--- ;:'i,43 :1g/ dL '.Ci}--'. .9 nb/ ciL) \SL D.'JJ ;m,ol fl. \G.O l-iJ.07 nmol/L])
DHFA-S = 257 f'.g/dL (t+-332 i.tg!dl.) (S'.: 6.'.~6 f,n;o]/;, [;,: 9 'i.00 ;.:rr.'.)1/L])
Andrn$':C'nedione - 13 7 ng/dL '. 30- 200 ng/ ail) '.Sl: •l.'/i-: '"1'.l>ol!L : 1.05-6.% nmol/Lj)
1'/ Hy:hoxyprogccoteror:e - 45 ng/JL (dO :1g/d. [follicub.rl) (S[: ;J6 nt:1t '.ii~ [<2.,;2 1:1110]/J.])
Hc::noglobin A;, "' S. I'.Yi (4,0/2--4.67:,) (32 ;nu:o]/:r;ol [20-38 rr:m0lhnc::1)

Which of the following is the best next step in this patient's evaluation?
A. Pelvic :11tnso,:ograpl:y
B. Measurement of :mtim;1]]prh_;~ hunEonc
C. Measu:·emem chfay 21 proge~teronc
~). Cosy:1trcp;n-~tiPrnlatio:1 tes( wit:'1 mc;;smement of co:cLiso: 2:Hl 17- hydmxyvroses:cronc
"· 2--IIo·Jr 7:."1-c ora'. gltccose ',o'.era-:icc ,est

57 '
A 31-year-oJJ pregnant woma1: ,ct 28 weeks' 15e~tatim; seel-o eva;ua.Lion of hypercake:nia. She was frmnd
to he mil&y hypercakemic on routine blooC wor~ pr:fom.ed Jnr;:,g her pre:1atal care. Sl:e has a l:istory
of Hodgkin lyriplwma trl'atcd with c'.1errto:he:·apy at 2.ge 2: yf':1xs, Slte is lakir:g 2 prenatal nn:ltivitam:n d,dy hut no
othG svpple,nents. She reports no nausea, vomi:ing, or c:uPges in he: bowel moven:e □ ts. She has :10 fractures o:
kiCT1wy stones, She has n•) ;.;:nown fam:ly history of .::a:rfon~ or p,c.-at.hyrdd <liscase.
On phy~ica: exarr:in<'tion, !ier we.ight is 149 lh '.117.7 kg) ani.i ~he has a gravid <.bdome:1. ?indings a:e othe!·wise
unrrncarkaLle.

l ,abo:-a(ory le\: results:

Scrum ca:ci:lm - 10,6 mg/dL (8.2-lU.2 mg/<ll.) (SI: 'J..7 rr::mol/L !2.1-2.6 mr:wl/l:j
Senn, ?hosp.Cla1e "' 2.t> mg/ dL (2.J-4.7 mg/dl.i (ST: O..S m:1101/L :G.7-1.5 nm:o]/ LJ;
Senm cmtlni:ie - 0.6 rr:g/dL (0.6-1.J mg/d.) '.SJ: 53.0 1.m,ol/;, [53.D-97,2 ctmo;/LJ}
Serum '.ntacl?TIT - 35 pg/mL (l0-65 Pliml.} (SI: 35 ng/L :10-6.J :1g/'.,;J
Se:·mr. 25-hydrnxyviuJ:J.i:J. D "" 30 ag/;r:L (JO 80 :ig/:-nL rop1i:na\:) (S~: 7L.9 m101/L [74. 0- 199.'/ n:r,ol/LJ
Serum ; 125-dihydro:xyvita:1:in D "' i l'/ j)g/mL (16-65 pg/m~,; (ST: .':\04,2 ?'1:ol/L '. ,j 1.6- J69. l pr;10JL;)
Se:·um ;1fo:imi":1 - 3.il y'::IL (3.5-S.O g/dL; (SI·. 38 giL 1.35-50 r/Ll_:
Urin::ry cakicEl"' 338 mg/2,1 h ( [00· :100 mg/24 h) (SJ: 8.5 nmt:)l/d '.2.5-7.5 m:no;/J;)

Which of the following is the most appropriate next step in the management of this patient's
hyperca!cemla?
A. Ini::.i.1te cina;.a'.cd thetaµy
B. T r<:'at with i:Jtnrver.01.:s pamid:onate
C Refn for paradcyroi<l surgery
!). Rt'fer to or.rnlogy for cvalua:ion of possible ly:nphom,1 rrcarrence
E. ;l;T O.'.J.itor labor<'tory values for the remainder of her r,regJ~ancy

58 A 30 yea:--old wom<en pn;sents fo: ongoi:1[; :nJaagrment of polycystic 0V<17 sv:1drome after recently
nwvir.g to the .;rea. She was diagnosed a\ ai:;e ·17 ye,ir~ \1.·he,1 s'.1e dcveJoped irregular Bense, anJ incre8se,i
terr1ii~al ha:r growth 0:1 :'lcr face, chin, and be:ow the u:nhib::1.:~. Menses :iavc beer. i:-reg:ilar for sever a: yeJrs.
She is nol sexva'.ly active. Her paren:~ are alive and we:[ in thtir 6:)s, ar,<l r:1erc is □ o fo.mily h.:story of prs;:11atvre
c-;:\liovs\sn:k,· <liseasc.

42 C:S/\P 2021.-QUEST!ONS
 1
On physical examination, her height is 63.5 in '.161 cm) and wcighl is 200 lb (91 kg) (BM] - 34,9 kg/m ), Her
blood pressure is l 04/iO mm Hg, She has evider.ce of rw-eezed hairs on her chin, Central adi;:,osity is present, but
she has no purple striae or bruising. Examination findings are otherwise unremarkable.

'Laboratory studies con:lrr.:t milG hyperandrogenism withoat evidence of Cushing synd;--ome or o:her
hyper.androgenic states, Additional lahorntory test results:
~01,1! dwleslerol = 257 mg/dL (dtll) mg/dJ, [optimal;) '.Sf: 6.66 mmoliL [ <5,18 ;nrr:ol/L:)
Triglycerides "" 236 mg/ GL ; d 50 mg/ t!L [optimalJ; (SI: 2.67 mmol/L >:::L70 r.:nno!iL])
HDL cholesterol'" 49 ng/dL (>60 rng/dL '.op:i:naC) (Sl: 1.27 mmol/L l>l.55 :nmol/L]l
LD;:. cholesterol'--- 16! mg/dL (<100 mg/dL '.optimal;) (SI: 4.17 mmol/L [<2,59 m;:nol/L])
Non-HDL cbo'.esterol = 208 mg/d1. (<130 mg/dL [optimal]) (SI: 5.39 :nmol/L [d.37 m:nol/L])
Apolipoprotei.u B - 175 ng/dL (.'i0-: 10 mg/dLj (SI: LS g/L [0,5-1.l g/L])
Fasti.-1.g ?lasma g'.ucosc"" 99 mgldL ;7()-99 mg/dL) (SI: 5.5 mmol/L [3.9-5.5 :nmoLIL])
llenoglo:lin A1,"" 5.6% (4.0%-5.6%_1 (:'IR rr:.mo:/mol [20-38 mmol/rr:oJ];
TSH "'2.7 mIC/L (0.5-5.0 mlU/L)
AST"" 59 U/L \20-48 U/L) (SI: 0.99 y.kat/L [0,3il-0,80 f-.kat/L:)
ALT"" 66 U/L (10-40 U/L) (Sl: LlC µkat/L l0,17-0,67 pJrn1/Ll)
Creat:nine"' 0.6 mg/dL (0.6- L1 mg/dL) (SI: 53.0 y.nol/L ;sl0-97.2 rmol/L])

Which of the following is the best next step in the mcmagement of this patient's lipids?
A. Refer to a dletiti:;.n for li:estyie modification
B. Start a si:atin
C. Start fibrate
n Start omega-3 fish oil
E. Start rr.ctform.in

A 59-year-o1d man is adrr.ltte<l to the hospital with severe hypoglycemia. His wiCe called p~ramedics after
59 finding him unconscious, The initial point-of-care glucose value was 34 mg/dL (1.9 mmoVJ .), He was
treated with glucagon and 2 ampules ofDS0 and transported to the emergency department. The inidal pfasm,,
glucose vah:e at the hospital wa~ 54 ;.ng/dL '..~.O mmol/L). He was treated aga'.n with glu.cagon and staned on a
D5 infusion.
He ts now alert and able to answer s.;:uestions. He last ate food about 18 hours ago, He repo:ts that he vomited
twke in the last day. He has stage 4 chronic kidney disease due to hypertension. .Yledications include losarlan,
diltiaz.em, doxazosin_, foroserr.ide, c:opidogrel, and a statin. He started metoprotol 4 weeks ago, Giprofloxacin was
iniliated ,1 days ago for treatment of a urinary trn.i. infection, He l'tas no history of Giabe:es.
In the iast 4 years, he has gone through treatment twice for alcohol dependency. He stopped drinking alcohol
for 14 months, but he relapsed and has been drinking <laily for the last 2 months (sometimes up to three-quarters of
a liter of vodka pe:r day). He does not smoke cigarettes.
2
On physici examination1 his height is iO in (177.8 cmi, and weight is J 46 lb (66.4 kg) (B.MI - 21 kg/m ). H:s
blood pressure is 158/83 mm Ilg, a!l.d pulse race is 82 beat~/min, He does not ,,ppear inebriated. The epigaslric area
is slightly tender. The liver P<lge is palpable and non tender. There is+ 1 pedal edema, Distal pulses are good.

Initial laboratory test resulls:

Hemoglobin A,,, - 4.9% (4.0%· 5.6%) (30 n:mol/mol [20-38 mmol/mol])
Creatinine "" 2.4 mg/ dL (0.7-1.3 rr.g/;11.) '.SI: 212.2 µmol/L [61.9-114.9 11:mol/L])
Serum -,ma r;itrogen - 36 mg/dL (g,.z3 mg/dL) [Sl: 12.S mr:wl/L [2.9-8,2 mmol/1.1)
Plasma glucose"" 79 mg/dL (70-99 n:g/dL) :sr: 4A mn,ol/L '.3.9-5.5 mr.10:/L])
Ethanol :eve! - 2GL mg/ dL

The D5 infusion is stopped a:id his glucose concentrat'.on is monitored. Nir.ety minutes later, his point-of-rnre
glucose value is 48 mg/dL (2.7 mmol/L;,
Laboratory test results (sample collected at the time of hypoglycemia):
Plasma glucose~ 51 mg/dL (70-99 mg/dL) {SI: 2.8 mrnol/L [3.9-5.5 mmol/L])
Insulin= 3.0 !-(IU/mL (1.4-14.0 !-(lU/mL) (SI: 20.8 pmol/L [9.7-97.2 pmol/L])
C-peptide = 1.0 ng/mL (0.9-4.3 ng/mL) (SI: 0.33 nmol/L [0.30-1.42 nmol/L])
Proinsulin = 42.3 pg/mL (26.5-176.4 pg/mL) (SI: 4.8 nmol/L [3.0-20.0 nmol/L])
Sulfonylurea/hypoglycemia agent screen, negative

Which of the following is the most likely etiology of this patient's hypoglycemia?
A, Insulin-secreting neuroendocrine tumor
B. Ethanol
C. Stage 4 chronic kidney disease
D. Metoprolol
E. Ciprofloxacin

A 20-year-old woman presents for follow-up of papillary thyroid carcinoma, which was diagnosed after
thyroid nodules were detected on neck examination 2 months ago. Neck ultrasonography revealed a
well-circumscribed, 2.1-cm, isoechoic, mixed cystic and solid nodule in the right thyroid lobe. A similar-appearing,
2.5-cm nodule was also observed in the left lobe. There were no abnormal lymph nodes. The patient underwent
ultrasound-guided FNA biopsy of both nodules 1 week ago. The left thyroid nodule was benign, but the right
nodule demonstrated findings consistent with the cribriform-morular variant of papillary thyroid cancer.
A photograph of the cytopathology smear is shown (see image).
The patient presents to discuss the next management steps. She reports chronic diarrhea and intermittent rectal
bleeding over the past year, but no other symptoms. Family history is notable for both thyroid and colon cancer in
her father. Her paternal grandfather died of metastatic colon cancer.
Her 25-year-old brother has a history of multiple adenomatous
colon polyps and underwent resection of an abdominal desmoid
tumor earlier this year. Her mother and younger sister are healthy.
On physical examination, her blood pressure is 110/70 mm Hg
and pulse rate is 72 beats/min. Her height is 66 in (167.6 cm), and
weight is 145 lb (65.9 kg) (BMI"' 23 kg/m2). She has bilateral
thyroid nodules and no cervical lymphadenopathy. Examination
of the skin is notable for multiple epidermoid cysts on her arms
and trunk, but no other cutaneous findings. The rest of the
find ings are normal.
The TSH concentration is 1.2 mIU/L (0.5-5.0 mIU/L).

Which of the following is this patient's most likely diagnosis?

A. Carney complex
B. PTENhamartoma tumor syndrome (Cowden syndrome)
C. Familial adenomatous polyposis
D. Hereditary nonpolyposis colorectal cancer (Lynch syndrome)
E. Multiple endocrine neoplasia type 2B

6 A 40-year-old man presents with new-onset hot flashes, sweats, worsening fatigue, and low libido.
He fir.st noted these symptoms about 4 weeks ago.

Laboratory test results:

Serum testosterone 2 weeks ago (sample drawn at 8 AM while fasting) = 66 ng/dL (300-900 ng/dL)
(SI: 2.3 nmol/L [10.4-31.2 nmol/L])
Serum testosterone 6 months ago "' 400 ng/ dL (SI: 13.9 mnol/L)

44 ESAP 2021--QUESTIONS
 ~-.'.e has s:age JV adreTicconical carcinonn. ?oc1r ernrths 2.go, i:.e commei:c<:<l con:,.bb:atio:1 i:::.11m:ne cbeckpo'.nt
id1ibitor therapy wifr:. i;:;ili:numa [l plus 7'.ivolcnn,lh fa: progressive di5case. Two 1,1onths ago, he was tospi'." alize<l
\1-•ery i:nwrll) with gnde 4 im m:.in..:-,cl~Jcd hep,111ti~ t:eated with high-dosage glucoc:::i~tico;d the:·apy and
my~·ophenobt<:' rr.ofotil. He iso smtained an al:ov,c-bee deep veno:.1s thrombosis. Ac r::a~ tirr.e, endocrine testing
was consL'>tent wit!1 il!:.nn:ne-re'.accd ti-1yrci<li~is and a<lre11,lliris. Immunmherapy was stoppf'd, -::,1.:.t renark~b:y,
a c,,r:.·enc f:uo:-oc\eo:rygluco~e-PET scan sh0ws no evide;;cr of disease anivity. He also has ,1 r:r.icrcp;_·olact'.n0:na
treate:J wit!: cahergoline. Currer.t medic?.tions incltide 1:1ycophe1:.olate mofot:C 500 rng twice (hiiy; prednisolonc,
2:'J mg daily (wra1:ing Jose); t1uCroco:·tisone, '. SO ,neg ciai'.y; metiJdor:e, 10 r.1g :wic:.:- JJi~y; utbergoline, 0,25 mg
twice weekly; ,1 _protcn-p1ir:1p inhibito:·; ;1nd ~ non vitflmin K antagonis~ ora'. a.ntirnag,tlan1,
On physical exami:1~ci0:1, his heihht is 70 in (178 en:) ~nd weigf:.t is 209 lb (95 kg) (BM] ec. Y) kg/rn"). His b'.ood
pressu:c is 134/39 nnn Eg with::i:it a posrnral drop. He has fl :nildly cushinfoid ippca;-ance J;~d 11:ik: pnximal
mycpathy. There is 21c goirer- Ile has normal body haiL The:e is no gynecomastia. T eslcs are 15 r:il, bJ;a:eraEy anC
soft, v.,-jthoutpaipab~e 1n1sses.

Curren: labo:atory tcsl results (s;,:mr,le Crawi: al 8 AM while fa~ting):

Total tt:s:osterout - 55 ng/dL (:100-90'.) ug/2Li (SJ: l.9 n:nol/L :10.'" ·_; : ..\ n:uol!L];
l.J--i =73.0mIU/mL \1.0-9.0 mlU/ml.) (Sl: 73.0 lU/L '.1.0-?.Q 1L:1::..,;)
FSrt = 71.6 ni:L'./:nl. (LO- 13.0 rdV/inL) (Sl: 71.6 IU/L l ;.O-B.O ::_:/:..,;)
Henwglobi:1 - 12,6 g/ c:1. ( 118-17 .2 gl dL) (Sl: : 26 g/;_, [ 138- : 72 g/'.,;)
Pr()[ac:m = 52. ng/m'., (4-23 ng/mL) '.SJ; ?.,L:i Pmd'.... l0.17-1.08 nmo]/L:)
TSH"' 2.9 :n'.U/'..., (0,5,S.0 mJU/U
Fn,c T. 1.: ng/ dL (0.8- : ,8 ng/ dL) (SI: 14. l:i pnrn;/t, [ '. QJQ. 23.17 pmo:/L)
1
"'

Free T.1 = 2.S _;-ig/mL :2.}-4,l pg/mU (Sl: 3.8'" ~:mot/!. ;3.5)-6.45 ;miol!L])

Which of the following ls the most likely explanation for his low testosterone?
A Treat;ne:1t with glucocoitic:iid~-
B. Innmmr ,heckpoin: fr1hibitor therapy aSsodJted or:hifa
C. Inadeqt1ar2ly t~eated prol.actino:na
D. Thyrniditis-,·el.<ted ci,nges in SHBG
E. Recovery phJse from severe illness

A 58-year-old wmun returns for consultation regarding type 2 diabetes mellitus, She w~.nts to mow if
62 there is a diet that rnu'.d help her avoid increasing brr medication burden. 0iabetes- \vas diagnosed 7 yems
<>go :Jased on routine s~reening blood tests that docuT'.lcnced a hemoglobin A1, level of 7.8% (62 mmoUmol). She was
p:escribed metfo::nin and engaged in lifestyle modification chat mostly involved increasing her physical activi:y.
bltially, she had a good respmse, with hemoglo'.)ln A1, values in the :ange of 6.7% to 7.0% {50-53 mmoi/mol).
However, ove:· the l~st year, bf!::- hemoglobin A,, has increasc<l to 7.6W, (60 mrr!.ol/mol). Current 2nedk,:tions include
nie::forrr.in, :000 mg twice daily, and s:tagliptin 1 100 mg daily. She bns no micro vascular :::ompE.cations of diabetes.
On physical examination, her blood pressure is 132/78 mm Hg and pulse ra:e is 78 beats/min. Her bf!igl1t is
6-1 ii: (162.5 c,n), and weight is 158.S lb {72 kg) (3Ml - 27.2 kg/ni2), There is no t'viCence of pcriphera.i neu:-opathy.
The rest of the examina~ion findings arr unremarkable.

Laborntory test resu_;lJ, indud:ng a b,1.sic :ne:-aholic pane'., hepatic function panel, and mine abumin cx:.:relion,
are r_ormaL

Regarding diet, which of the following eating patterns should be recommended for this patient to
improve her glycemic control?
/\_Lvw-carhohydrate (less tha:i 40% o!' ~alories from c:H·-:,ohyCrn:es)
B. Paleo
C. Low •fa1 '.less tha:, 30% of ~alor'.cs from fat)
U. DASH (D1f'tary Approc1cbes to Stop .I-Iyper1ension;
E. bte:-:11i1trnt fasting

45
63 1:_ ~-l--yea~-.ok ;l"la::. is referrcJ. for :n2nilg:me:1t of hypg?:::adi~n'., Fi~e years ago, :1c noticed reCuced
lu:ndo anc ,aboratory tes: results at '."kt time doc:nnentec the ~ol:ow1q;:

S~ru:n :.2,tosternne ~ 91 rig/:IL (3JC-SOO ng/UL) '.S'.: 12 .r:EJo;/L r:cA-.~U :1mol/LJ_;

r:SH - 2-3 m'.UhrL (1.0-13.0 ;r_!Li/mL) '.S:: 2.3 JU!T. '.1.0-L3.0 JU/L]J
~J'. - 4.5 1:1JU/ml, (l.!i-4.tJ rnilJ/mLl (SI:.+ ..) '.U!L [l.0-4.0 JU/L]j
T'ro:acti:r. = 10.0 ng/mL (<1 '/,3 ::1.g/mL) 1:SJ: 0.43 ::i.mol/L '.O. 17- LOO n:r;ol/L])

[li:uitary MRI reveale<l ,1 piluctary macroadeno.:na, and l1e u:1derwe11l si;cgical rc11:cya'.. Current MRI shows .:.n
enb.:·ged, mos:ly e:nply sella. There :s t:o evide:ccce of residual a(fa'.10r:1a.
I le is alrrady ,rsing a tcstos'."erone gel, He :ee'.s overnll '"'f'll nnd has no concerns exce;:;t for constipat'.o:::. an<l fatigi!e,
Phys:~,ll examination f.ndi.ngs are normal, wich the excepcion of scnat tcstca (approxin:ately 6-8 mL in volumic).

Curre:lt laboratory test resu:ts:

Testos;:crone - .+25 ng/ dL (300-:lOO og/ JJ,) (S'.: 1t1.7 nmol/L (10.4-3;.2 nn:ol/Lj)
Free''.', - 0.6 ng/ dL (0.8 -1.8 1:.g/ d;,) (S[: '/, 'i pmol/L [ 10.30-23.17 pmo):__.;j
TSH - 2.t;; m~l!/L (0.S-5.0 m!U/L)
Cortis::,\ (8 A.M; - 18.5 µg/dL (5-'.'.S 1,g/dL) (SI: 5;0..1 imdL ll37.9-689.7 1:mol/;j
'.GF-1 - 120 :'1.g/rr.L \S 1f-2.B ng/mL) (S~: l:>,7 nn:ol/L: 1; .0--3D.'.J nrn:,J/:,;)

Which of the foUowing best describes the chance that he has GH deficiency?
A. Very bw, as his lGF-1 level is no:":nal
B. Very high, as hie has o~her impaired pit1:itary a..a::es
C. Very hieh, as he ~las an empty sella on imaging
D. Very low, as he ha~ no sympto:os
E. Trrelf'VJ:11, ,is he is an aduh:

64 A 67-!~ar old woman wit£: ?steoporosis presencs for _eva:uation ofhyperparat.1:yroidism. S~e bas a history
of an LL vertebral compress:on fracture ,,nd was me lmµhosphonate therapy b1.:t sto:?ped tlm l 2 months
ago lwca,:se ~he sustabcd a right atypica~ fen11.::: fracture. Recrr.t DXA sen reveals declining bone mil:eral de1~sity
in the forearr:1 compared with 2 years prl::i:, with a ·;·-score o£'-2.4 ir: che spine, -3.0 in the left femorJl neck, and
-.l2 in the left one-third radius. She is on calci t!nl and vitamin D sup?lementatior:.

Laboratory test results:

Se run calcium = I 0.1 mg/ dL '.S.2-10.2 :r;g/dL) (Si: 2.5 mm'.:ll/'., [2.; -2,6 :nmol/L:)
Se:um phosphate - J.O mg(dL (2J-1,7 mg/dL: (SI: -:_,n mmo;/L [0,7 · J..5 mr.:io'./L])
Serum creat:nine. 0.6 l":lg/dL '.0.0- Ll n.g/dL) (SJ: 53.0 µmol/L '.53.0-97.2 ~.mol/J.:)
Glomerular filtratio:i rate (es1itra1 ed) = >90 mL/ mi[] per 1.73 m2 (>W :11i.../in;n per 1.'/.-1 rn")
Serum btactPTH"' 10.1 pt;/rnl (10-65 pgh:r.L) (SI: 103 ng/L ll:J-65 i:g/LI)
Senrn 2:':,-'.'lydroxyv:itwnll: :") = 32 ng/mL (30-80 ng/n:L loptima'.]) '.SL 79.9 ;uno:/L [74.9· 119.7 :imol/Ll)
Ser-.in: albumi1: = ,i,fi g/dL LtS-5.0 g/dL) (SI: 46 g/L '.JS-50 g/L:)
Sernrrc :nagnes:um = 1.9 a:g/dL (1.5-2.3 :ng/dL) (SI: 0.8 2:moU:, [0.6-0.9 ;nm(;J/Lj
~r:r.ary ca:d<.m: = 180 mg/24 h (!00-.)00 mg/24 hj \SJ: 4.5 m;1:ol/d [L'i 7,5 n.r:10:/dj
\.Jrinar1 creaLlrinc = 0.7 g/24 h (LQ-2.0 g/z.'- h) (SI: 6.2 mmol/d [8,H 17] nmol/d:)
Fraction;tl exnctioE of calcium - O.C1S

Which of the following ·1s the most likely diagnosis?

A. !\"0rrnocaicemic primry hyperparathy:oidisr:i
B. Seco:1:lary hypcrpaathyroicism
C Te,ci"Y hypcrparnthyrnidi,m
[\ Familial hypocakiuric hr:Jerca:cemia
E. PseudolcypoparathyToidism ly;:;e la

46 ESAP 2021-QUESTIONS
 A 67-year~old wornw was diar,rnhe<l with derm~.tomyositis i year ago. }.s part of surveillance for
65 <lermatomyositis-associate<l malir,n,;:nc.ies, 2bdo:r1inal CT was ;:ierformed, wh'.d". revealed a 11:1ilater.;.l
adrenal reass. N"nncontrast CT of clw ah<lonwn : rnon:h later showed a ~,6 x 1,5-cm '.eft adre;.cal .re.ass th.1t wa.s
round and ;,;i<l an ;rnf'ahaacf'd actPnaation valve cf-), H:::i;rnsfield u:1.its. Sie now ;,resents for fucher evaka~k,n
1 year after her hist CT.
On physical examination, .i'.er b:ood pc:essure is 121 /78 mm Hr ar.d pulse rate is 66 ::>cats/mi,1, Hf!:· height is
64 i11 (162.6 en), anJ weight is 140 '.b (63.6 kg) (Brv11 _,. , 7.1 kg/n: 1-). .She does Ttot have rr:co:1 facies, dorsocervicai ,_.r
sl'.praclavicular fat p~.ds. :1.irsutisrr., acne, acar:lhosis nigrica:is, hyperpigme;,tat:cn, or striae.
Results of a basic :nct2boli-.: panel show rw,.-cna: elec1:·olyt<'s and kidney function. Her morning scn;m coFisol
concentration iollowing ovcrr:ight 1 mg t'.e.li.amelh,1som' is '. A :.lr,fdL (SI: 3r.6 nrr_ol/L).

Which of the following is the best next step in this patient's management?
A. Measurerr:ent of aldcster:.me and 1enh
B. Measurement ofDHEA-S
C. Measu;·err.ent of plasna metan,?h,ines
D. Abdomin<1.l c·1· now'.'. year after the lase CTi
E. Reassurance anC r.c fo:rtl:er tcstc:1g

A J2-year-,•ld woman presents fo: follow-up ,.)f papillary thyroid card:~on:a. Slie has a history of stage
66 l (T 2N1bM0) p2.piilary thyroid carcinor:u tha:-was diagnosc<l 6 months ago, She anderwent r:ea:·--wtal
~hyroidectnmy a-:-id central a:;d r:ght lateral neck d'.ssectim:s. Pa:-bologic examir.atio1;. Cen:nnstnted a 2.5-cm
primary U;mor in the :ight thyroid lobe an<l nc vascular ir:vasion or cxtra('lyroidal extension. The si.;rgka'.1:iargir:s
were negatiw, A total of;:; of .;.0 lymph node, were posicive for mcustasis. Scvc;1 days ago, slw w~s treJted with
radioactive i.ocfow ther,1py (75 :nCi ' 1 '1) ·wilh reco:nbinar:t hu:nar. TSE. Her posttheraµy who:e-0ody scar: shows
uplaKe in the thyroi<l he<l and pbysio:ogic uptake in the salivary glands, but n::i cvi<lcrxc of metastJsis,
To<lay, lhe pa~ient n:·pnrts ~hJt for the p;=.st week she :ias been experiencing mil<l discomforl, fo1[nf!ss, «nd
i:1tc:"millcnt swellkg in the :ight ar.d le~ uppe:- neck. just i.nforior to the lower jaw. The swelling is usually
associated with ealing. She bas :10 othe:- sy::nptoms. She is taking levothyroxir:c daily an<l no ocher 1~1edkatiom,
On pl:ysical c.li.amirwtion, 1w: ~Joo<l pressure is 95/50 mm Hg, pulse rate is 55 bcits/min, an<l te2nperntnre is
98.2°F U6.8 1'C). Her height is 6?. in (1 .17.5 u:1), 2.nd weight is 120 lb (54.5 kg) (BMI = 22 kg/m 2). Exan~ination i.s
:iotab'.e for a pa'.pable cnass in rlghc w:1e ; B, which correlates wilh the patient's area of clinical concern, and it is
mildly te:1der to the touch. The ff!S! of her examination findings are normal.

Laboratory test results:

1 rr,ontb afrer rnrgery before rad'.:::ra.ctiw iodi:ce ::1.~rnpy ):
TSll ~ 0,5 mJU/L
Thy:-o~o:Julin = 0.8 ug/:m:::., (SJ: 0-8 r,.g/L)
Thyrng'.ob·J!in an1ibodies ~ <!. :::-;;/mL (SI: <4 kIU/L)
7 days ago (at the time o:" radioactive iodine therapy):
TSH =' 65 mlU/L
Slimulateii tl,y:'ogl,1bulin ~ 0.8 ng/rd. (SI: 0.8 f,g/L)
Thy:rnglot:ulb ar.tibodies = "1, JU/:nL (SI:<"- '...IU/L)

Which of the following is the most appropriate initial treatment of the patient's right neck mass?
A. lniti;,te ,m1oxld:Hn-clavdanate tw:ce dai'.y
B. Increase the levothy:-oxine dosage to achieve a serum TSH value <0.1 m[U/L
C. Ret:0mG1end :nassar;e, warm com;:iresses, oral hydrncion, and nor:stcroi<lal a11tiinl1,1:nn:atory drugs :css
;1ce<led for pain
D. Perform FNA biopsy
E. AJminister radioactive iodine thera?Y agai:ci with a hig'.1er aCministcrc<.'. activil y of Dl[

ESAP 2021, -QUESTIONS 47

ft...'"J A 47-year··o:d rl'.an prese:1.ts to your o:1ice wi~h <-;ucstioT'.S regarding a recent diagl'.osis or' preCiabe:es.
\~) His most recent heTTtoglo~i1: A1c va:ue~ were 5.9% (41 :mno:/mo:) a:1d 6.2% (44 1rm101/:noll. He a:s::i
rcpcrts that his fasfr:g blood glutosi.' values ha\'e '.:em in Lile range of '.GO to: 15 mgidL (5.6--6.4 r:unol/L) owr the
la~t yea:-.
He has obstructive sleep apnea bi:t s:ntes lie cannot :olcratc concirn:o:1s positive airway pressure '.CPAP).
p.._, has :mt t:sed CPAP for fr1e past faw years. He expcri,::1ccs fat'.glle that affects his quali:y of life. He has s1-:101'e<l
l pack of cign-ettes C.aily fer the p,1.s1 30 ;cars. He has been employed in the rubber manm:l.ctt:ring bdustry for thf'
past 25 years. Second;;.;y hypogona<lism was recently diagnosed, :nost likely due to obesity. Two recent seru:n total
~estosterone rr:e2.surenwnts were 255 arni 228 ngfrL (8.3 and 7.9 nmo:/L) (borh d:-awn between Rand '. 0 AM),
He ~1as :10t ye~ initiated tes: oslerone therapy, but he is intere~ted in exploring this option.
He has bd difficulty :nai:1tainir.g a healthy weight mosl of his aduh: life. \'XlhHe he cur..tin,tes to lly ~o exercise
and reduce Gtlcrk :01ake, he always relapses to '.1is old d:etary and seden:2.ry l-ia~its, He is co:'.'l.cernc<l about
developi:1g type 2 diabetes an<l asks about starLng a therapy tc reduce !":is risk.
On rhysica: examin;;,tion, his blood pressure is 122/76 r:m1 Hg and pll:se ra~e is 88 beo.tsimln. His height
i~ 70 :n (177.8 cm), and wc'.ght i~ 225 ~b (102.3 kg) (BMJ = 32 kgin:/J He has +1 _pitting dcma in bo6 '.ewer
extremit~es. Thr res: of t'."le examinatio:i '.i1:dir.gs are no:-:n;;l,

~aboratory tcsc resdts:

Cmt:n'.ne - L l r.igldL (0.7-IJ rng/:ll.) (S:: 97,/, r,mol/;.... l6L9-! 14.9 ftno'./1..1;
Eernatocr:t - 54% (4'. %-5'.:i%) (Si: O .):. :0,,1; 0.50;i

Which of the following interventions ls the best choice to reduce this patient's risk of progression
to type 2 diabetes?
A, Vitamir: D,
B. Pioglitazone
C. Testostero:1.e therapy
D. Liras'.11:i<le
E. :\1~giotrnsin-;:eceµtor l.::lcckcr

68 A 61-year ok. womai1 with a history of hypertension, type 2 diahetes meLit,1s, aad hyperlipidemia is
diagnosed with a J.6-cm right thyro:d 110dule. She reports ihat ,1:1 FNA biopsy of this nodule 8 months
ago had benign results. Recent follow-1lp thyroid u'.trasonography shows a.a increase i11 ~he nodule's size i,vith a
more l1e-~erngc:1cous appearance and microca:cifications. A sernn<l FNA biopsy Jocumcnts follicular neoplasr:.L
She 1"n<lecgocs total thyroidenomy, which con~rl:ls the diagnosis of diffo1e:.1tiate<l widely invasive follicular thyroid
carcinoma. She then develo;:,s hematuria 4 weeks latec Ab<lomi.J:al CT demonstrates a 2.6-cm, her.erogeneous
right adrenal :nass. The unenhanceC. CT attenuation is ?0 Houmfieid units, and 10 r:rinutes afre:- cormast
ir:jection tlie absolute contras: medium washout is nn:y 30%, No kidney stone is vis';lalized. An eval1Jation for
phcochromocy:oma, primary akloste:onism, an<l Cushi:1g syndrome is negative.
Her fare.Uy bstcry is not2bie for type 2 diabetes, i.1yµertens'.on, and kld:1ey stones. Cuc·ent medcatlons .;re
atorv.astatin, losartan, and NPH insulin/regu:ar i.nsdin 70/30.
On physical examination, her blood pressure is 120/80 mm Hg: and pulse rate is 74 beats/min. The:e is ,1 wf'll-
healed scar at the base of her neck. There is no cervical :.denopathy. Her lungs are dear to auscultation hifate:ally.
Her abdomen ls soft- an<l no11lewJer. She ii.as no :ower-€xtremlty edema.

In addition to measuring serum thyroglobulin, which of the following Is the best next step In this
patient's management?
A. FNA biopsy of l:le right adrenal mass
B. Neck :J.krasunograpl-:y
C. D,J who:e--bu<lyscar. witl: S?ECT-CT
n, :.Zigh~ a<lre~wlectomy
K Chest CT

48 ESAP 2021-QUESTIONS
Another Random Scribd Document
with Unrelated Content
and permanent. Moreover, it is the settled policy of most enlightened
governments to appropriate or to prevent all notable increases in the
value of monopolistic goods, either through special taxation or
through regulation of prices and charges. Taking the increment
values of land is, therefore, not so discriminative as it appears at
first glance.[94]
Another objection is that the proposal would violate the canons of
just taxation, since it would impose a specially heavy burden upon
one form of property. The general doctrine of justice in taxation
which is held by substantially all economists to-day, and which has
been taught by Catholic moralists for centuries, is that known as the
"faculty" theory.[95] Men should be taxed in proportion to their ability
to pay, not in accordance with the benefits that they may be
assumed to receive from the State. And it is universally recognised
that the proper measure of "ability" is not a man's total possessions,
productive and unproductive, but his income, his annual revenue.
Now, the increment tax does seem to violate the rule of taxation
according to ability, inasmuch as it would take all of one species of
revenue, while all other incomes and properties pay only a certain
percentage.
All the adherents of the faculty theory maintain, however, that it is
subject to certain modifications. Incomes from interest, rent, and
socially occasioned increases in the value of property should be
taxed at a higher rate than incomes that represent expenditures of
labour; for to give up a certain per cent. of the former involves less
sacrifice than to give up the same per cent. of the latter. Therefore,
increments of land-value may be fairly taxed at a higher rate than
salaries, personal property, or even rent and interest. When,
however, the law absorbs the whole of the value increments, it
seems to be something more than a tax. The essential nature of a
tax is to take only a portion of the particular class of income or
property upon which it is imposed. The nearest approach to the plan
of taking all future increases in land value is to be found in the
special assessments that are levied in many American cities. Thus,
the owners of urban lots are frequently compelled to defray the
entire cost of street improvements on the theory that their land is
thereby and to that extent increased in value. In such cases the
contribution is levied not on the basis of the faculty theory, but on
that of the benefit theory; that is, the owners are required to pay in
proportion to benefits received. All adherents of the faculty theory
admit that the benefit theory is justifiably applied in situations of this
kind. It might be argued that the latter theory can also be fairly
applied to increments of land value that are to arise in the future. In
both cases the owner returns to the State the equivalent of benefits
which have cost him nothing. There is, however, a difference. In the
former case the value increases are specifically due to expenditures
made by the State, while in the latter they are indirectly brought
about by the general activities of the community. We do not admit
with the Single Taxers that this "social production" of value
increments creates a right thereto on the part of either the
community or the civil body; but even if we did we should be
compelled to admit that the two situations are not exactly parallel;
for the social production of increases in the value of land involves no
special expenditure of labour or money. Hence it is very questionable
whether the appropriation of the whole of the future value
increments can be harmonised with the received conceptions and
applications of the canons of taxation.

The Morality of the Proposal

However, it is neither necessary nor desirable to justify the proposal

on the mere ground of taxation. Only in form and administration is it
a tax; primarily and in essence it is a method of distribution. It
resembles the action by which the State takes possession of a newly
discovered territory by the title of first occupancy. The future
increases of land value may be regarded as a sort of no man's
property which the State appropriates for the benefit of the
community. And the morality of this proceeding must be determined
by the same criterion that is applied to every other method or rule of
distribution; namely, social and individual consequences. No
principle, title, or practice of ownership, nor any canon of taxation,
has intrinsic or metaphysical value. All are to be evaluated with
reference to human welfare. Since the right of property is not an end
in itself, but only a means of human welfare, its just prerogatives
and limitations are determined by their conduciveness to the welfare
of human beings. By human welfare is meant not merely the good of
society as a whole, but the good of all individuals and classes of
individuals. For society is made up of individuals, all of whom are of
equal worth and importance, and have equal claims to consideration
in the matter of livelihood, material goods, and property. In general,
then, any method of distribution, any modification of property rights,
any form of taxation, is morally lawful which promotes the interests
of the whole community, without causing undue inconvenience to
any individual. Whether a given rule of ownership or method of
distribution which is evidently conducive to the public good is,
nevertheless, unduly severe on a certain class of individuals, is a
question that is not always easily answered. Some of the methods
and practices appearing in history were clearly fair and just, others
clearly unfair and unjust, and still others of doubtful morality.
Frequently the State has compelled private persons to give up their
land at a lower price than they paid for it; in more than one country
freebooters and kingly favourites robbed the people of the land, yet
their heirs and successors are recognised by both moralists and
statesmen as the legitimate owners of that land; in Ireland stubborn
landlords are to-day compelled by the British government to sell
their holdings to the tenants at an appraised valuation; in many
countries men may become owners of their neighbours' lands by the
title of prescription, without the payment of a cent of compensation.
All these practices and titles inflict considerable hardship upon
individuals, but most of them are held to be justified on grounds of
social welfare.
Now the public appropriation of all future increments of land value
would evidently be beneficial to the community as a whole. It would
enable all the people to profit by gains that now go to a minority,
and it would enable the landless majority to acquire land more easily
and more cheaply. We have in mind, of course, only those value
increases that are not due to improvements in or on the land, and
we assume that these could be distinguished in practice from the
increments of value that represent improvements. Would the
measure in question inflict undue hardship upon individuals? Here
we must make a distinction between those persons who own land at
the time that, and those who buy land after, the law is enacted.
The only inconvenience falling upon the latter class would be
deprivation of the power to obtain future increases in value. The law
would not cause the value of the land to decline below their
purchase price. Other forces might, indeed, bring about such a
result; but, as a rule, such depreciation would be relatively
insignificant, for the simple reason that it would already have been
"discounted" in the reduction of value which followed the law at the
outset. The very knowledge that they could not hope to profit by
future increases in the value of the land would impel purchasers to
lower their price accordingly. While taking away the possibility of
gaining, the law enables the buyers to take the ordinary precautions
against losing. Therefore, it does not, as sometimes objected, lessen
the so called "gambler's chances." On the other hand, the tax does
not deprive the owners of any value that they may add to the land
through the expenditure of labour or money, nor in any way
discourage productive effort. Now it is, as a rule, better for
individuals as well as for society that men's incomes should
represent labour, expenditure, and saving instead of being the result
of "windfalls," or other fortuitous and conjunctural circumstances.
And the power to take future value increments is not an intrinsically
essential element of private property in land. Like every other
condition of ownership, its morality is determined by its effects upon
human welfare. But we have seen in the last paragraph that human
welfare in the sense of the social good is better promoted by a
system of landownership which does not include this element; and
we have just shown that such a system causes no undue hardship to
the individual who buys land after its establishment. Such is the
answer to the contention, noticed a few pages back, that the
landowner has a right to future increments of value because they
are a kind of fruit of his property. It is more reasonable that he
should not enjoy this particular and peculiar "fruit." Were the
increment tax introduced into a new community before any one had
purchased land, it would clearly be a fair and valid limitation on the
right of ownership. Those who should become owners after the
regulation went into effect in an old community would be in exactly
the same moral and economic position. Finally, there exists some
kind of legal precedent for the proposal in the present policy of
efficient governments with regard to the only important increases
that occur in the value of goods other than land; namely, increases
due to the possession of monopoly power. By various devices these
are either prevented or appropriated by the State.
Those persons who are landowners when the increment tax goes
into effect are in a very different situation from those that we have
just been considering. Many of them would undoubtedly suffer injury
through the operation of the measure, inasmuch as their land would
reach and maintain a level of value below the price that they had
paid for it. The immediate effect of the increment tax would be a
decline in the value of all land, caused by men's increased desire to
sell and decreased desire to buy. In all growing communities a part
of the present value of land is speculative; that is, it is due to
demand for the land by persons who want it mainly to sell at an
expected rise, and also to the disinclination of present owners to sell
until this expectation is realised. The practical result of the attitude
of these two classes of persons is that the demand for, and therefore
the value of land is considerably enhanced. Let a law be enacted
depriving them of all hope of securing the anticipated increases in
value, and the one group will cease to buy, while the other will
hasten to sell, thus causing a decline in demand relatively to supply,
and therefore a decline in value and price.
All persons who had paid more for their land than the value which it
came to have as a result of the increment tax law, would lose the
difference. For, no matter how much the land might rise in value
subsequently, the increase would all be taken by the State. And all
owners of vacant land the value of which after the law was passed
did not remain sufficiently high to provide accumulated interest on
the purchase price, would also lose accordingly. To be sure, both
these kinds of losses would exist even if the law should cause no
decline in the value of land, but they would not be so great either in
number or in volume.
Landowners who should suffer either of these sorts of losses would
have a valid moral claim against the State for compensation.
Through its silence on the subject of increment-tax legislation, the
State virtually promised them at the time of their purchases that it
would not thus interfere with the ordinary course of values. Had it
given any intimation that it would enact such a law at a future time,
these persons would not have paid as much for their land as they
actually did pay. When the State passes the law, it violates its
implicit promise, and consequently is under obligation to make good
the resulting losses.
Is it not obliged to go further, and pay for the positive gains that
many of the owners would have reaped in the absence of the law?
For example: a piece of land is worth one thousand dollars the day
after the tax goes into effect, and that was exactly the price paid for
it by the present owner; another piece has the same value, but was
bought by the present owner for eight hundred dollars. While neither
of these men suffer any loss on their investments, they are deprived
of possible gains; for had the law not been enacted their holdings
would be worth, say, eleven hundred dollars. Nevertheless, they are
no worse off in this respect than those persons who buy land after
the increment tax goes into effect, and have no greater claim to
compensation for abolished opportunities of positive gain. As we
have seen above, the certain advantages of the measure to the
community, the doubtful advantages to individuals of profiting by
changes in price which do not represent labour, expense, or saving,
show that the owners have no strict right to compensation. And it is
still clearer that no landowner has a valid claim on account of value
increases that would have taken place subsequent to the time that
the measure was enacted. There is no way by which owners who
would have held their land long enough to profit by these
increments can be distinguished from owners who would not have
availed themselves of this conjectural opportunity, nor any method
by which the amount of such gains can be determined.
On the other hand, it might be objected that, in reimbursing all
owners who suffer the positive losses above described, the State is
unduly generous; for if the law had not been enacted many of the
reimbursed persons would have sold their holdings at a price
insufficient to cover their losses. But these cannot be distinguished
from those who would have sold at a remunerative price. Hence the
State must compensate all or none. The former alternative is not
only the more just all round, but in the long run the more expedient.
In view of the social benefits of the increment tax, especially the
removal of many of the inequities of the present taxing system, the
State might sometimes be justified in making good only a part of the
losses that we have been discussing. But this could probably occur
only for administrative reasons, such as the difficulty of determining
the persons entitled to and the amounts of compensation. It would
not be justified merely to enable the State to profit at the expense of
individuals. And, in any case, there seems to be no good reason why
the unpaid losses should amount to more than a small fraction of the
whole.
In the foregoing pages we have been considering a law which would
from the beginning of its operation take all the future increments of
land value. There is, however, no likelihood that any such measure
will soon be enacted in any country, least of all, in the United States.
What we shall probably see is the spread of legislation designed to
take a part, and a gradual growing part, of value increases, after the
example of Germany and Great Britain. Let us glance at the laws in
force in these two countries.
 The German and British Increment Taxes

The first increment tax (Werthzuwachssteuer) was established in the

year 1898 in the German colony of Kiautschou, China. In 1904 the
principle of the tax was adopted by Frankfort-am-Main, and in 1905
by Cologne. By April, 1910, it had already been enacted in 457 cities
and towns of Germany, some twenty of which had a population of
more than 100,000 each, in 652 communes, several districts, one
principality, and one grand duchy. In 1911 it was inserted in the
imperial fiscal system, and thus extended over the whole German
Empire. While these laws are all alike in certain essentials, they vary
greatly in details. They agree in taking only a per cent. of the value
increases, and in imposing a higher rate on the more rapid
increases. The rates of the imperial law vary from ten per cent. on
increases of ten per cent. or less to thirty per cent. on increases of
290 per cent. or over. In Dortmund the scale progresses from one to
12½ per cent. Inasmuch as the highest rate in the imperial law is 30
per cent., and in any municipal law (Cologne and Frankfort) 25 per
cent.; inasmuch as all the laws allow deductions from the tax to
cover the interest that was not obtained while the land was
unproductive; and inasmuch as only those increases are taxed which
are measured from the value that the land had when it came into
the possession of the present owner,—it is clear that landowners are
not obliged to undergo any positive loss, and that they are permitted
to retain the lion's share of the "unearned increment."[96]
It is to be noted that most of the German laws are retroactive, since
they apply not merely to future value increases, but to some of
those that occurred before the law was enacted. Thus, the Hamburg
ordinance measures the increases from the last sale, no matter how
long ago that transaction took place. The imperial law uses the same
starting point, except in cases where the last sale occurred before
1885. Accordingly, a man who had in 1880 paid 2500 marks for a
piece of land which in 1885 was worth only 2000 marks, and who
sold it for 3000 marks after the law went into effect, would pay the
increment tax on 1000 marks,—unless he could prove that his
purchase price was 2500 marks. In all such cases the burden of
proof is on the owner to show that the value of the land in 1885 was
lower than when he had bought it at the earlier date. Obviously this
retroactive feature of the German legislation inflicts no wrong on the
owner, since it does not touch value increases that he has paid for.
Indeed, the value of the land when it came into the present owner's
possession seems to be a fairer and more easily ascertained basis
from which to reckon increases than any date subsequent to the
enactment of the law. On the one hand, persons whose lands had
fallen in value during their ownership would be automatically
excluded from the operation of the law until such time as the
acquisition value was again reached; on the other hand, those
owners whose lands had increased in value before the law went into
effect would be taxed as well as those whose gains began after that
event; thus the law would reach a greater proportion of the existing
beneficiaries of "unearned increment." Moreover, it would bring in a
larger amount of revenue.
The British law formed a part of the famous Lloyd-George budget of
1909. It taxes only those increments that occur after its enactment.
These are subject to a tax of twenty per cent. on the occasion of the
next transfer of the land, by sale, bequest, or otherwise.[97] In some
cases this arrangement will undoubtedly cause hardship. For
example: if land which was bought for 1,000 pounds in 1900 had
fallen to 800 pounds in 1909, and were sold for 1,000 pounds in
1915, the owner would have to pay a tax of twenty per cent. on 200
pounds. This would mean a net loss of forty pounds, to say nothing
of the loss of interest in case the land was unproductive. It would
seem that some compensation ought to be given here; yet the rarity
of such instances, the administrative difficulties, and the general
advantages of this sort of legislation quite conceivably might forbid
the conclusion that the owner was made to suffer certain injustice.
The compensating social advantages of the increment tax as well as
of other special taxes on land, will receive adequate discussion
presently.
 Transferring Other Taxes to Land

Another taxation plan for reducing the evils of our land system
consists in the imposition of special taxes on the present value of
land. As a rule, these imply, not an addition to the total tax levy, but
a transfer of taxes from other forms of property. The usual practice
is to begin by exempting either partly or wholly buildings and other
kinds of improvements from taxation, and then to apply the same
measure to certain kinds of personal property. In most cases the
transfer of such taxes to land is gradual, extending over a period of
five, ten, or fifteen years. The plan is in operation in Canada and
Australasia, and to a slight extent in the United States.
It has received its greatest development in the western provinces of
Canada; namely, British Columbia, Alberta, Saskatchewan, and
Manitoba. The cities of Edmonton, Medicine Hat, and Red Deer;
Vancouver, Victoria, and thirteen others of the thirty-three cities of
British Columbia; all the towns of Alberta except two; all but one of
the villages of Alberta, and one-fourth of those in Saskatchewan; all
the rural municipalities and local improvements districts in Alberta,
Manitoba, and Saskatchewan, and 24 of the 28 in British Columbia,
—exempt improvements entirely from taxation. The three cities in
Alberta which retain some taxes on improvements; all the cities and
towns and three-fourths of the villages in Saskatchewan; the four
largest cities in Manitoba; and a considerable number of the
municipalities in Ontario (by the device of illegal under-assessment
in this instance),—tax improvements at less than full value, in some
cases as low as fifteen per cent. Land is invariably assessed at its full
value. It is to be observed that these special land taxes provide only
local revenues; they do not contribute anything to the maintenance
of either the provincial or the dominion governments. The reason
why the local jurisdictions have adopted these taxes so much more
extensively in Alberta than in the other provinces is to be found in a
provincial law enacted in 1912, which requires all towns, villages,
and rural areas to establish within seven years the practice of
exempting from taxation personal property and buildings.
Saskatchewan permits cities and towns to tax improvements up to
sixty per cent. of their value, while British Columbia and Manitoba
leave the matter entirely in the hands of the local authorities. The
provincial revenues are derived from many sources, chiefly real
estate, personal property, and incomes; but British Columbia,
Saskatchewan, and Alberta levy a special tax on unimproved and
only slightly improved rural land. The rate of this "wild lands tax" is
in British Columbia four per cent., and in the other two provinces
one per cent. Some of the municipalities of British Columbia and
Saskatchewan also impose a "wild lands tax." By a law passed in
1913 Alberta levies a provincial tax of five per cent. on the value
increases of non-agricultural lands. A movement for the reduction of
the tax on buildings has developed considerable strength in the
eastern provinces of Ontario, Nova Scotia, and New Brunswick.[98]
New Zealand and most of the states of Australia have for several
years levied special taxes on land, consisting mainly of general rates
on estates of moderate size, and a progressive super tax on large
estates. The Commonwealth of Australia also imposes a tax of one
penny in the pound on the value of land. A considerable proportion
of the cities and towns in both New Zealand and Australia derive
practically all their revenues from land, exempting improvements
entirely. In both countries, however, the bulk of the total revenue is
obtained from other sources than land taxes. In New Zealand they
yield less than thirteen per cent. of the national receipts.[99]
Pittsburgh and Scranton were required by a law enacted in 1913 to
reduce the local tax rate on buildings at such a pace that in 1925
and thereafter it would be only one-half the highest rate on other
forms of property. Everett, Wash., and Pueblo, Col., within recent
years adopted by popular vote more sweeping measures of the
same character, but the Everett law has never gone into effect, and
the Pueblo statute was repealed two years after it had been passed.
In many cities of the United States, buildings are undervalued
relatively to land by the informal and illegal action of assessors. The
most pronounced and best known instance of this kind is Houston,
Texas, where in 1914 land was assessed at seventy per cent. of its
value and buildings at only twenty-five per cent. In 1915, however,
the practice was forbidden by the courts as contrary to the Texas
constitution. At more than one recent session of the New York
legislature, bills have been introduced providing for the gradual
reduction of the tax on buildings in New York City to a basis of fifty
per cent. of their value. While none of them has been passed, the
sentiment in favour of some such measure is probably increasing. A
similar movement of opinion is apparent in many other sections of
the country.
On the whole, the special land taxes of Canada and Australasia are
not remarkably high. They seem to be as low or lower than the
average rates imposed on land, as well as on other forms of general
property, in the United States. In the provinces, the special land
taxes provide only a small portion of the total revenues; in the cities
and towns, there are, as a rule, other sources of revenue as well as
land, and the expenses of municipal government are probably not as
high as in this country. Hence the land taxes of Canada have not
reached an abnormally high level, and are probably lower than most
persons who have heard of them would be inclined to expect. The
chief exceptions to the foregoing statements are to be found in the
"wild lands tax" of British Columbia, and in the land taxes of some of
the towns (not the cities) of Alberta. A rate of four per cent. on
unimproved and slightly improved rural land is extraordinary in fiscal
annals, and is scarcely warranted by any received principle of
taxation, although it may possibly be justified by peculiar social and
administrative conditions in the province of British Columbia. Some
of the smaller towns of Alberta which adopted the land tax during
the recent period of depression have been compelled to impose even
higher rates, the maximum being reached by Castor in 1912, with a
rate of 8½ per cent. As a natural consequence, a large proportion of
the land in this town was surrendered by its owners to the
municipality. While this amazing tax rate is probably temporary, and
is likely to be lowered after the return of the average conditions of
prosperity, it inflicts unfair hardship upon those owners whose
circumstances are such that they must give up their land, instead of
awaiting the hoped for decline in the rate of taxation.

The Morality of the Plan

The losses of various kinds that would result from the transfer of
other taxes to land may be thus summarised. Land would depreciate
in value by an amount equal to the capitalised tax. For example; if
the rate of interest were five per cent., an additional tax of one per
cent. would reduce land worth one hundred dollars an acre to eighty
dollars. This decline might, indeed, be partly, wholly, or more than
offset by a simultaneous rise due to economic forces. In any case,
however, the land would be worth twenty dollars less than it would
have been worth had the tax not been imposed. For some owners
this would mean a positive loss; for others it would signify mere
failure to gain. The latter would happen in the case of all those
owners who at any time after the imposition of the tax sold their
land at as high a price as they had paid for it. Not all of the owners
whose land was forced by the tax to a figure below their purchase
price would suffer positive loss; for the land might subsequently rise
in value sufficiently to wipe out the unfavourable difference. In this
respect a special tax on the present value of land has a different
effect from a tax that appropriates all the future value increases.
Only those owners who actually sold their land below their purchase
price could charge the former tax with inflicting upon them positive
losses. In the case of the land exemplified above, the owner who
sold at ninety dollars per acre could properly attribute to the tax a
loss of ten dollars; the owner who sold at eighty dollars would have
a grievance amounting to twenty dollars; and a loss would be
suffered by any owner who sold for less than eighty dollars. In the
second place, all owners of vacant land who sold at a price
insufficient to provide for accumulated interest on the purchase
price, could justly hold the tax responsible, so long as the deficiency
did not exceed the value-depreciation caused by the tax. Thirdly, all
persons whose land had an unusually high value relatively to the
value of their exempted property, would suffer losses as taxpayers.
They would lose more through the heavier land taxes than they
would gain through the lighter taxes, or the absence of taxes, on
their other property.
To compensate all owners who underwent these three kinds of
losses would be practically impossible. The number of persons would
be too large, the difficulty of proving many of the claims would be
too expensive, and the compensation process would be too long
drawn out, since it would have to continue until the death of all
persons who had owned land when the last instalment of the
increased land taxes went into effect. Therefore, the losses in
question must be counterbalanced by other and indirect methods.
These will be found mainly in the following considerations: the
amount of the new taxes; the gradual method of imposing them;
and their socially beneficial results.

Amount of Taxes Practically Transferable

According to Professor King's computations, the total rent of land in

the United States in 1910 was $2,673,900,000, while the total
expenditures of national, state, county and city governments were
$2,591,800,000.[100] In his opinion (p. 162) "the rent would have
been barely sufficient to pay off the various governmental budgets
as at present constituted, and with the growing concentration of
activities in the hands of the government, it appears that rent will
soon be a quantity far too small to meet the required changes. With
increasing pressure on our natural resources, however, it is probable
that the percentage of the total income paid for rent will gradually
increase and, since this is true, the lag behind the growing
governmental expenses will be considerably less than would
otherwise be the case."
A change in our fiscal system providing for the immediate derivation
of all revenues from land taxes would, therefore, involve the
confiscation of all rent, and the destruction of all private land values.
Land would be worth nothing to the owners when its entire annual
return was taken by the State in the guise of taxes. Even if the
process of imposing the new taxes on land were extended over a
long term of years the same result would be reached in the end; for
whatever increase had taken place in the economic value of land
during the process would in all probability have been neutralised by
the increase in governmental expenditures. It is evident, therefore,
that the proposal to put all taxes on land must be rejected on
grounds of both morals and expediency.
Let us suppose that all national revenues continued, as now, to be
raised from other sources than land, and that all state, county, and
city revenues remained as they are, except those derived from the
general property tax. This would mean that all the following taxes
would be unchanged: all federal taxes, the taxes on licenses of all
kinds, all taxes on business, incomes, and inheritances, and all
special property taxes. If, then, the whole of the general property
tax were concentrated on land; that is, if all the taxes on
improvements and on all forms of personal property were legally
shifted to land,—the entire revenue to be raised from land would in
1912 have amounted to $1,349,841,038.[101] This is slightly more
than one-half of Professor King's estimate of the total rent for 1910,
which was $2,673,900,000. But this figure equals four per cent. of
the land values of the country; hence the concentration of the
general property tax on land would mean a tax rate of two per cent.
on the full value of the land.
How much would this change increase the present rate of land
taxes, and decrease existing land values? While no accurate and
definite answer can be given to either of these questions, certain
approximations can be attempted which should be of considerable
service.
In 1912 the average tax rate on the assessed valuation of all goods
subject to the general property tax was .0194, or $19.40 per
thousand dollars.[102] The assessed valuation of taxed real property
and improvements (land, buildings, and other improvements) was
nearly fifty-two billion dollars, while the true value of the same
property was nearly ninety-eight and one-half billions.[103]
Consequently, the actual tax rate of .0194 on the assessed valuation
was exactly one per cent. on the true value of real estate. On the
assumption that both land and improvements were undervalued to
the same extent, the land tax was one per cent. of the full value of
the land. If now we take Thomas G. Shearman's estimate, that land
values form sixty per cent. of the total value of real estate, we find
that the taxes derived from land constituted only forty-four per cent.
of the total revenues raised by the general property tax. To
concentrate the whole of the general property tax on land, by
transferring thereto the taxes on improvements and on personal
property, would, accordingly, cause the land tax to be somewhat
more than doubled. It would be slightly above two per cent. on the
full value of the land. This is the same estimate that we obtained
above by a different process; that is, by comparing Professor King's
estimate of land value and rent with the total revenues derived from
the general property tax.
However, it is not improbable that sixty per cent. is too low an
estimate of the ratio of land values to entire real estate values. In
1900, farm land and improvements, exclusive of buildings, formed
78.6 per cent. of the value of real estate, i.e., land, improvements,
and buildings. In 1910, the per cent. was a little less than 82. Now it
is quite unlikely that the value of non-building improvements on
farms amounted to the difference between sixty per cent. and
seventy-eight per cent. in 1900, or between sixty per cent. and
eighty-two per cent. in 1910. Hence the value of farm land is
something more than sixty per cent. of farm real estate. On the
other hand, the value of factory land in 1900 formed only 41.5 per
cent. of the total value of factory land and buildings, while the value
of city and town lots in five rural states varied from 34 to 62 per
cent. of this species of real estate.[104] In Greater New York land
constitutes 61 per cent. of real estate values.[105] Owing to the lack
of data, the average ratio for all kinds of real estate for the whole
country is impossible of determination. If the estimate of seventy per
cent. be adopted, which is probably the upper limit of the average
proportion between land values and real estate values throughout
the country, the portion of the general property tax now paid by land
amounts to about fifty-two per cent. Consequently the imposition of
the whole general property tax on land would not quite double the
present rate on land. To the first of the two questions raised above
the answer can be given with a fair amount of confidence that the
transfer of improvement and personal property taxes to land would
cause land taxes to be about twice what they are at present.
To the second question, concerning the extent to which land values
would fall in consequence of the heavier taxes, the answer must be
somewhat less definite. The added land taxes would be about one-
half the present general property taxes, or $675,000,000. This is
about one per cent. the total land values of the country. One per
cent. of land values capitalised at five per cent. represents a
depreciation of twenty per cent. in the value of land; capitalised at
four per cent., it represents a depreciation of twenty-five per cent.
For example; if land worth one hundred dollars an acre returns to its
owner a net income of five dollars annually, the appropriation of one
dollar by a new tax will leave a net revenue of only four dollars;
capitalised at the current rate of five per cent., this represents only
eighty dollars of land value, or a depreciation of twenty per cent. If
the land has the same value of one hundred dollars, and still yields
only four dollars revenue, a deduction of one dollar in new taxes will
leave only three dollars net; capitalised at the current rate of four
per cent., this represents only seventy-five dollars of land value, or a
depreciation of twenty-five per cent. Using the other method of
calculation, which estimated the present tax rate on the full value of
land at one per cent., we get exactly the same results; namely, the
new tax is one per cent., which is equivalent to a depreciation of
twenty per cent. or of twenty-five per cent., according as we assume
an interest rate of five per cent. or of four per cent. Suppose,
however, that the assessors do not undervalue land to the extent
that we have been assuming; suppose that the present rate of .0194
on assessed valuation is equivalent to, not merely one per cent., but
one and one-half per cent. of the full value of land. In that
hypothesis the additional tax would likewise be one and one-half per
cent., which capitalised at five per cent, would represent a
depreciation of thirty per cent., and at four per cent. a depreciation
of thirty-seven and one-half per cent. Combining in one
generalisation the various suppositions made in this paragraph, we
estimate the depreciation of land values resulting from the proposed
tax transfer as somewhere between twenty and forty per cent.
We have considered two hypothetical transfers of taxes to land. The
first we found to be out of the question because it would appropriate
the whole of the rent and destroy all private land values. The second
would apparently amount to two per cent. of the value of land, and
cause land values to depreciate from twenty to forty per cent. It is
unnecessary to consider the probable effects of any plan that would
involve heavier land taxes than the second; that is, the scheme of
imposing all the general property tax on land; for it represents the
extreme feasible and fair limit of the movement within, at any rate,
the next fifteen or twenty years.
Even this degree of tax transference would be unjust to the
landowners if it were brought about at once. No social or other
considerations exist that would justify a depreciation in land values
of from twenty to forty per cent. If, however, the process were
extended over a period of, say, twenty years, the decline would be
only one or two per cent. annually, which is considerably less than
the rate at which farm lands and the land in large cities have risen in
value during recent years. Under such an arrangement the great
majority of owners would probably find that the depreciation caused
by the heavier land taxes, had been more than offset by the upward
tendency resulting from the increased demand for land.
Nevertheless, there would still be positive losses of the three kinds
described a few pages back; namely, to owners who sold land below
the price that they had paid for it; to owners who sold vacant land at
a price insufficient to cover accumulated interest on the investment;
and to owners whose aggregate tax burdens were increased. Some
degree of each of these sorts of losses would be due specifically to
the new land taxes. As noted above, public compensation in all such
cases would be impracticable. Consequently the justification of a law
that inflicts such losses must be found, if it exists, in social
considerations.

The Social Benefits of the Plan

These may be summed up under three heads: making land easier to

acquire; cheapening the products and rent of land; and reducing the
burdens of taxation borne by the poorer and middle classes. An
increase in the tax on land would reduce its value and price, or at
least cause the price to be lower than it would have been in the
absence of the tax. This does not mean that land would be more
profitable to the purchaser, since he is enabled to buy it at a lower
price only because it yields him less net revenue, or because it is
less likely to increase in value. The value of land is always
determined by its revenue-producing power, and by its probabilities
of price-appreciation. Consequently, what the purchasers would gain
by the lower price resulting from the new tax, they would lose when
they came to pay the tax itself, and when they found the chances of
value increases diminished. If a piece of land which brings a return
of five dollars a year costs one hundred dollars before the new tax of
one per cent. is imposed, and can be bought for eighty dollars
afterward, the net interest on the purchase price has not changed. It
is still five per cent. Hence the only advantage to the prospective
purchaser of land in getting it cheaper consists in the fact that he
can obtain it with a smaller outlay of capital. For persons in
moderate circumstances this is a very important consideration.
In the second place, higher taxes would cause many existing owners
either to improve their land, in order to have the means of meeting
the added fiscal charges, or to sell it to persons who would be willing
to make improvements. And the desire to erect buildings and other
forms of improvements would be reinforced by the reduction or
abolition of taxes on those kinds of personal property which consist
of building materials. An increase in the rapidity of improvements on
land would mean an increase in the rate at which land was brought
into use, and therefore an unusual increase in the volume of
products. This virtual increase in the supply of land, and actual
increase in the supply of products, would cause a fall in three kinds
of prices: the price of products, the rent of land, and the price of
land. The last named reduction would be distinct from the reduction
of land value caused in the first instance by the imposition of the
tax.
In the third place, the reduction, and finally the abolition, of taxes on
improvements and personal property would be especially beneficial
to the poorer and middle classes because they now pay a
disproportionate share of these charges. Lower taxes on dwellings
would mean lower rents for all persons who did not own their
homes, and lower taxes for all owners whose residence values were
unusually large relatively to their land values. And the tendency to
lower rents on dwellings would be reinforced by the lower cost of
building materials resulting, as noted above, from the increased
supply and the lower tax on this form of personal property. Lower
taxes on that species of personal property which consists of
consumers' goods, such as household furniture and wearing apparel,
would lessen the present inequity of taxation because this class of
goods is reached to a much greater extent in the case of the poor
than in the case of the rich. It is not easy to conceal or to
undervalue a relatively small number of simple and standard articles;
but diamonds, costly furniture, and luxurious wardrobes can be
either hidden, or certified to the assessor at a low valuation. As for
those forms of personal property which are of the nature of capital
and other profit producing goods, such as machinery and tools of all
kinds, productive animals, money, mortgages, securities, the stocks
of goods held by manufacturers and merchants, and likewise
buildings which are used for productive purposes,—the taxes on all
these kinds of property are for the most part shifted to the
consumer. The latter ultimately pays the tax in the form of higher
prices for food, clothing, shelter, and the other necessaries and
comforts of life.[106] Now a tax on consumption is notoriously unfair
to the poorer and middle classes because it affects a greater portion
of their total expenditures, and takes a larger per cent. of their
income than in the case of the rich. Hence the removal of the taxes
specified in this paragraph would be at once the abolition of a fiscal
injustice, and a considerable assistance to the less fortunate classes.
All those landowners who occupied rented dwellings would benefit
by the reduction in house rent, and all landowners without exception
would reap some advantage from the reduction or abolition of the
taxes on consumers' goods and on the various forms of producers'
goods. It is not improbable that a considerable proportion of them
would gain as much in these respects as they would lose in the
capacity of landowners.
Would the social benefits summarily described in the foregoing
paragraphs be sufficient to justify the increased land taxes in the
face of the losses that would be undergone by some landowners in
the three ways already specified? In view of our ignorance
concerning the probable amount of benefits on the one hand and
losses on the other, it is impossible to give a dogmatic answer.
However, when we reflect on the manifold social evils that are
threatened by a rapid and continuous increase in land values, and
the resulting decrease in the proportion of the population that can
hope to participate in the ownership of land, we are forced to
conclude that some means of checking both tendencies is urgently
necessary for the sake of social justice and social peace. The project
that we have been considering; namely, the transfer of taxes on
improvements and on personal property to land by a process
extending over twenty years, seems to involve a sufficiently large
amount of advantage and a sufficiently small amount of
disadvantage to justify systematic and careful experiment.

A Supertax on Large Holdings

Every estate containing more than a maximum number of acres, say,

ten thousand, whether composed of a single tract or of several
tracts, could be compelled to pay a special tax in addition to the
ordinary tax levied on land of the same value. The rate of this
supertax should increase with the size of the estate above the fixed
maximum. Through this device large holdings could be broken up,
and divided among many owners and occupiers. For several years it
has been successfully applied for this purpose in New Zealand and
Australia.[107] Inasmuch as this tax exemplifies the principle of
progression, it is in accord with the principles of justice; for relative
ability to pay is closely connected with relative sacrifice. Other things
being equal, the less the sacrifice involved, the greater is the ability
of the individual to pay the tax. Thus, the man with an income of ten
thousand dollars a year makes a smaller sacrifice in giving up two
per cent. of it than the man whose income is only one thousand
dollars; for the latter case the twenty dollars surrendered represent
a privation of the necessaries or the elementary comforts of life,
while the two hundred dollars taken from the rich man would have
been expended for luxuries or converted into capital. While the
incomes of both are reduced in the same proportion, their
satisfactions are not diminished to the same degree. The wants that
are deprived of satisfaction are much less important in the case of
the richer than in that of the poorer man. Hence the only way to
bring about anything like equality of sacrifice between them is to
increase the proportion of income taken from the former. This means
that the rate of taxation would be progressive.[108]
It is in order to object that the principle of progression should not be
applied to the taxation of great landed estates, since a considerable
part of them is unproductive, and consequently does not directly
affect sacrifice. But the same objection can be urged against any
taxation of unoccupied land. The obvious reply is that the equal
taxation of unproductive with productive land is justified by social
reasons, chiefly, the unwisdom of permitting land to be held out of
use. The same social reasons apply to the question of levying an
exceptionally high tax on large estates, even though they may at
present produce no revenue.
While the tax is sound in principle, it is probably not much needed in
America in connection with agricultural or urban land. Its main
sphere of usefulness would seem to be certain great holdings of
mineral, timber, and water power lands. "There are many great
combinations in other industries whose formation is complete. In the
lumber industry, on the other hand, the Bureau now finds in the
making a combination caused, fundamentally, by a long standing
public policy. The concentration already existing is sufficiently
impressive. Still more impressive are the possibilities for the future.
In the last forty years concentration has so proceeded that 195
holders, many interrelated, now have practically one-half of the
privately owned timber in the investigation area (which contains
eighty per cent. of the whole). This formidable process of
concentration, in timber and in land, clearly involves grave future
possibilities of impregnable monopolistic conditions, whose far
reaching consequences to society it is now difficult to anticipate fully
or to overestimate."[109] In January, 1916, the Secretary of
Agriculture called the attention of Congress to the fact that a small
number of corporations closely associated in a policy of community
of interest were threatening to secure and exercise a monopoly over
the developed water power of the country. Ninety per cent. of the
anthracite coal lands of Pennsylvania are owned or controlled by
some nine railroads acting as a unit in all important matters. For
situations of this kind a supertax on large estates would seem to
hold the promise of a large measure of relief.
To sum up the main conclusions of this very long chapter:
Exceptionally valuable lands, as those containing timber, minerals,
oil, gas, phosphate, and water power, which are still under public
ownership should remain there. Through a judicious system of loans,
deserving and efficient persons should be assisted to get possession
of some land. Municipalities should lease rather than sell their lands,
and should strive to increase their holdings. To take all the future
increases in the value of land would be morally lawful, provided that
compensation were given to owners who thereby suffered positive
losses of interest or principal. To take a small part of the increase,
and to transfer very gradually the taxes on improvements and on
personal property to land, would probably be just, owing to the
beneficial effects upon public welfare. A supertax on large holdings
of exceptionally valuable and scarce land would likewise be
beneficial and legitimate.[110]

REFERENCES ON SECTION I

Ashley: The Origin of Property in Land. London; 1892.

Laveleye: Primitive Property. London; 1878.
Whittaker: The Taxation, Tenure, and Ownership of Land.
London; 1914.
Preuss: The Fundamental Fallacy of Socialism. St. Louis; 1908.
George: Progress and Poverty; and A Perplexed Philosopher.
Marsh: Land Value Taxation in American Cities. N. Y.; 1911.
Fillebrown: A Single Tax Handbook for 1913. Boston; 1912.
Young: The Single Tax Movement in the United States.
Princeton; 1916.
Shearman: Natural Taxation. N. Y.; 1898.
 Mathews: Taxation and the Distribution of Wealth. N. Y.; 1914.
Cathrein: Das Privatgrundeigenthum und seine Gegner. Freiburg;
1909.
Fallon: Les Plus-Values et l'Impot. Paris; 1914.
Nearing: Anthracite. Philadelphia; 1916.
Haig: Final Report of the Committee on Taxation of the City of
New York; 1916.
The exemption of Improvements from Taxation in Canada and
U. S.; 1915.
Some Probable Effects of Exemption in City of New York; 1915.
Kelleher: Private Ownership. Dublin; 1911.
Proceedings of the 1913 Meeting of the American Economic
Association.
U. S. Commissioner of Corporations: Reports on the Lumber,
Petroleum, Steel, and Water Power of the United States.
Seligman: Essays in Taxation; Shifting and Incidence of Taxation;
and Progressive Taxation in Theory and Practice.
Also the works of Taussig, Devas, Carver, Pesch, King,
Vermeersch, Willoughby, and the Commission on Industrial
Relations, all of which are cited at the end of the introductory
chapter.

SECTION II

THE MORALITY OF PRIVATE CAPITAL AND INTEREST

 CHAPTER IX
THE NATURE AND THE RATE OF INTEREST

Interest denotes that part of the product of industry which goes to

the capitalist. As the ownership of land commands rent, so the
ownership of capital commands interest; as rent is a price paid for
the use of land, so interest is a price paid for the use of capital.
However, the term capital is less definite and unambiguous, both in
popular and in economic usage, than the word land. The farmer, the
merchant, and the manufacturer often speak of their land, buildings,
and chattels as their capital, and reckon the returns from all these
sources as equivalent to a certain per cent. of interest or profit. This
is not technically correct; when we use the terms capital and interest
we should exclude the notions of land and rent.

Meaning of Capital and Capitalist

Capital is ordinarily defined as, wealth employed directly for the

production of new wealth. According as it is considered in the
abstract or the concrete, it is capital-value or capital-instruments. For
example, the owner of a wagon factory may describe his capital as
having a value of 100,000 dollars, or as consisting of certain
buildings, machines, tools, office furniture, etc. In the former case
he thinks of his capital as so much abstract value which, through a
sale, he could take out of the factory, and put into other concrete
capital forms, such as a railroad or a jobbing house. In the latter
case he has in mind the particular instruments in which his capital is
at present embodied. The capital-value concept is the more
convenient, and is usually intended when the word capital is used
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