case conference hyperthyroidism april2008
TRANSCRIPT
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14 yr old Male With Altered14 yr old Male With Altered
Mental StatusMental Status
David Josey Jr. M.D.David Josey Jr. M.D.
April 1, 2008April 1, 2008
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HPIHPI
14 yr old male presented to the RWJ ED with a14 yr old male presented to the RWJ ED with a1 day history of headache, slurred speech,1 day history of headache, slurred speech,
confusion, problems walking, and dizziness.confusion, problems walking, and dizziness. Patient was in Gym class and experienced aPatient was in Gym class and experienced a
sudden onset of these symptoms.sudden onset of these symptoms.
Headache-B/L temporal area, pounding in nature (-)Headache-B/L temporal area, pounding in nature (-)
photophobia/phonophibiaphotophobia/phonophibia Speech-inability of school nurse to understand himSpeech-inability of school nurse to understand him
Walking- unable to walk in a straight lineWalking- unable to walk in a straight line
Symptoms continued at his PMDs office.Symptoms continued at his PMDs office.
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Review of SystemsReview of Systems
(+) 10 lb weight loss over an 8 month(+) 10 lb weight loss over an 8 monthperiod despite increased appetiteperiod despite increased appetite
(+) increased thirst(+) increased thirst (-) increased urine output(-) increased urine output
(+) easy fatigability(+) easy fatigability
(+) tremors(+) tremors
(+) increased watery stools(+) increased watery stools
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ROS cont.ROS cont.
(-) chest pain/palpitations(-) chest pain/palpitations
(-) preceding behavioral changes(-) preceding behavioral changes
(-) history of ingestion of any over the counter or(-) history of ingestion of any over the counter orprescription drugs or medicationsprescription drugs or medications
(-) exposure to carbon monoxide(-) exposure to carbon monoxide
(-) trauma(-) trauma
(-) fever(-) fever
(-) neck stiffness(-) neck stiffness
(-) night sweats(-) night sweats
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PMHPMH
Born full term by normal deliveryBorn full term by normal delivery Diagnosed with ADHD as a childDiagnosed with ADHD as a child
Not treated with medications as patient ableNot treated with medications as patient ableto function well in school without it.to function well in school without it.
Normal baseline functionNormal baseline function
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History cont.History cont.
Allergic to Penicillin : rashAllergic to Penicillin : rash Immunizations: UTDImmunizations: UTD Meds: MVIsMeds: MVIs
Diet: RegularDiet: Regular Family HX:Family HX:
Mom GERDMom GERD
16 yr old brother with eczema and ADHD16 yr old brother with eczema and ADHD
(-) family hx of medical problems(-) family hx of medical problems Soc hx: lives with parents and brother, (+) parakeet,Soc hx: lives with parents and brother, (+) parakeet,
plays basketball and baseball, attends 9plays basketball and baseball, attends 9thth grade, (-)grade, (-)alcohol, illicit drug use, tobacco, denies sexual activityalcohol, illicit drug use, tobacco, denies sexual activity
Development: appropriateDevelopment: appropriate
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In the EDIn the ED Initial vitals:Initial vitals:
T 99.2T 99.2 HR 160HR 160
BP 145/84BP 145/84
RR 22RR 22
Sats 99% RASats 99% RA
Awake, alert, anxious appearing, diaphoretic but speechAwake, alert, anxious appearing, diaphoretic but speechnormal, headache decreased, dizziness resolvednormal, headache decreased, dizziness resolved
Eyes: PERRL, EOM intact, fundi not observedEyes: PERRL, EOM intact, fundi not observed Ears: TM clear B/LEars: TM clear B/L
Throat: MMM, orapharynx clearThroat: MMM, orapharynx clear Neck:Neck:
supplesupple
thyroid which was diffusely enlarged and firm to palpation,thyroid which was diffusely enlarged and firm to palpation,
(-) bruit(-) bruit CV: NL S1 S2 tach cardic -I-II/VI SEM LLSB
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Physical Exam cont.
Chest: NL breathing easilyChest: NL breathing easily ABD: NLABD: NL Genitalia: Tanner IV pubic hair, L gynecomastiaGenitalia: Tanner IV pubic hair, L gynecomastia Extremities: WWP, FROM, (-) C/C/EExtremities: WWP, FROM, (-) C/C/E Neuro: CN II-XII grossly intact,Neuro: CN II-XII grossly intact, fine peripheral tremorfine peripheral tremor
of fingersof fingers, 5/5 muscle strength U/L,, 5/5 muscle strength U/L, 2-3/4 DTR2-3/4 DTRpatellar tendonpatellar tendon, (+), (+) clonus at Achilles tendon,clonus at Achilles tendon, fingerfingerto nose NL, gait nl, toe walk nl, heel walk nl,to nose NL, gait nl, toe walk nl, heel walk nl, somesomedifficulty with toe to heel walking.difficulty with toe to heel walking.
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SummarySummary
14 yr old male without significant past medical14 yr old male without significant past medicalhistory who presents with sudden onset ofhistory who presents with sudden onset of
headache, slurred speech, confusion, problemsheadache, slurred speech, confusion, problemswalking, and dizziness,walking, and dizziness,
Symptoms are associated clinically withSymptoms are associated clinically withtachycardia and hypertension on thetachycardia and hypertension on the
background of an 8background of an 8thth month history of weightmonth history of weightloss despite polyphagia, fatigue, and polydyspia.loss despite polyphagia, fatigue, and polydyspia.
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Physical exam.on the floorPhysical exam.on the floor
All the same except the following:All the same except the following: HRHR 132132 withwith BP now 119/61BP now 119/61
Neuro: (-) Romberg, (-) dysmetria (-)Neuro: (-) Romberg, (-) dysmetria (-)ataxia nl muscle toneataxia nl muscle tone
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DifferentialDifferential
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DifferentialDifferential
PsychePsyche Anxiety/panic attackAnxiety/panic attack ADHDADHD
NeoplasmNeoplasm Brain tumorBrain tumor LymphomaLymphoma
NeurologicNeurologic TIA/StrokeTIA/Stroke Intracranial hemorrhageIntracranial hemorrhage Meningitis/encephalitisMeningitis/encephalitis PorphyriaPorphyria Concussion/increased ICPConcussion/increased ICP
EndocrineEndocrine HyperthyroidismHyperthyroidism DIABETESDIABETES PheochromocytomaPheochromocytoma HypercalcemiaHypercalcemia
HypoglycemiaHypoglycemia
Drug ingestionDrug ingestion CocaineCocaine AmphetaminesAmphetamines SteroidsSteroids
PhenylepherinePhenylepherine EphedrineEphedrine MAO InhibitersMAO Inhibiters PCPPCP MushroomsMushrooms Lead poisoningLead poisoning Carbon monoxide poisoningCarbon monoxide poisoning
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Diagnostic testing
Blood/urine:Blood/urine: CBCCBC CMPCMP
ESRESR UAUA Urine Drug ScreenUrine Drug Screen Thyroid function studies (TFTs)Thyroid function studies (TFTs)
Radiology:Radiology: Head CTHead CT EKGEKG
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Diagnostic Test ResultsDiagnostic Test Results
13.3
39.2
347
60 N0 B
26 L
11 M
137
4.2
102
27.2
11
0.5
103
10.0
Prot: 6.1 Tbili 1.0 AST: 27
Albumin 4 Allk Phos: 224 ALT:32
UDS: (-) barbiturates, Benzodiazepines, Cocaine , opiates, PCP, THC
UA: 1.018, trace protein, (-) blood, nitrite, bilirubin, ketonesESR: 12
10.7
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TFTs: pending
EKG: sinus tachycardia, incomplete
RBBB, LVH, normal axis deviation
Head CT: normal
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DifferentialDifferential
PsychePsyche Anxiety/panic attackAnxiety/panic attack ADHDADHD
CardiacCardiac Coarctation of the AortaCoarctation of the Aorta
ArrhythmiaArrhythmia RenalRenal Renal Artery StenosisRenal Artery Stenosis Polycystic kidney diseasePolycystic kidney disease GlomerulonephritisGlomerulonephritis
TraumaTrauma Concussion/increased ICPConcussion/increased ICP
NeurologicNeurologic TIA/StrokeTIA/Stroke Sub-dural hemorrhageSub-dural hemorrhage Brain tumorBrain tumor MeningitisMeningitis
EndocrineEndocrine HyperthyroidismHyperthyroidism DiabetesDiabetes PheochromocytomaPheochromocytoma Pituitary TumorPituitary Tumor HypoglycemiaHypoglycemia HypercalcemiaHypercalcemia
NeoplasmNeoplasm NeuroblastomaNeuroblastoma
Drug ingestionDrug ingestion CocaineCocaine AmphetaminesAmphetamines SteroidsSteroids
PhenylepherinePhenylepherine EpherdrineEpherdrine MAO InhibitersMAO Inhibiters PCPPCP
OtherOther Lead poisoningLead poisoning Carbon monoxide poisoningCarbon monoxide poisoning
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Hospital Course: Day #1Hospital Course: Day #1
Admitted to the PICU for CR monitoringAdmitted to the PICU for CR monitoring
Initially tachycardic to the 130sInitially tachycardic to the 130s
Echo ordered 2 to LVH on EKGEcho ordered 2 to LVH on EKG
TFTs reordered with thyroid antibodies forTFTs reordered with thyroid antibodies forboth Hashimotos Thyroditis and Gravesboth Hashimotos Thyroditis and Graves
DiseaseDisease
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Hospital Course: Day #2Hospital Course: Day #2 Patient remained tachycardic but mostly normotensivePatient remained tachycardic but mostly normotensive Echo:Echo:
normal studynormal study
Results of initial TFTs:Results of initial TFTs: TSH 0.08 [0.35-5.5 miu/L] T4 21.8 [5.0/12.0 mcg/dl]
F T4 7.22 [0.90-1.80 ng/dl] T3 >800 [60-181 ng/dl]
Results of repeat TFTS:Results of repeat TFTS: TSH
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Hospital Course: Day #2 cont.Hospital Course: Day #2 cont.
Pediatric Endocrinology consultedPediatric Endocrinology consulted Diagnosis of hyperthyroidism presenting withDiagnosis of hyperthyroidism presenting with
thyrotoxicosis madethyrotoxicosis made
Thought to be secondary to Graves Disease untilThought to be secondary to Graves Disease until
proven otherwiseproven otherwise
Confirmatory antibodies pendingConfirmatory antibodies pending
Therapy initiatedTherapy initiated Methimazole 10 mg bidMethimazole 10 mg bid
Propanalol 10mg bidPropanalol 10mg bid
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Hospital Course: Day #3Hospital Course: Day #3
HR decreased to
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HyperthyroidismHyperthyroidism
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Thyroid anatomyThyroid anatomy
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HyperthyroidismHyperthyroidism
Hyperthyroidism and thyrotoxicosis are usedHyperthyroidism and thyrotoxicosis are usedsynonymouslysynonymously
However they refer to different aspects of the sameHowever they refer to different aspects of the samecondition as follows:condition as follows:
Hyperthyroidism- BIOCHEMICALLY over activity ofHyperthyroidism- BIOCHEMICALLY over activity ofthyroid gland leading to excessive synthesis of thyroidthyroid gland leading to excessive synthesis of thyroid
hormones and accelerated metabolism in the peripheralhormones and accelerated metabolism in the peripheral
tissuestissues Thyrotoxicosis- CLINICALLY Clinical effects of unboundThyrotoxicosis- CLINICALLY Clinical effects of unbound
thyroid hormone whether to not the thyroid gland is thethyroid hormone whether to not the thyroid gland is the
primary sourceprimary source
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PathophysiologyPathophysiology
Controlled by a complex feed backControlled by a complex feed backmechanismmechanism
The release of TSH from the anteriorThe release of TSH from the anteriorpituitary gland is stimulated by lowpituitary gland is stimulated by low
circulating levels of thyroid hormonescirculating levels of thyroid hormones
TSH is under the influence ofTSH is under the influence ofthyrotropin-releasing hormone (TRH),thyrotropin-releasing hormone (TRH),
somatostatin, or dopamine.somatostatin, or dopamine.
TSH then binds to TSH receptors onTSH then binds to TSH receptors onthe thyroid gland to release mostly t4the thyroid gland to release mostly t4
and some T3and some T3
Elevated levels of these T4 and T3 actElevated levels of these T4 and T3 acton the hypothalamus and anterioron the hypothalamus and anterior
pituitary decreasing synthesis of TSH.pituitary decreasing synthesis of TSH.
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TSH receptorTSH receptor
G-proteincoupled receptors.G-proteincoupled receptors.
Large protein embedded inLarge protein embedded inthe cell membrane.the cell membrane.
Contains an extracellularContains an extracellulardomain binds TSH anddomain binds TSH and
intracellular domain that actsintracellular domain that acts
via a G-protein secondvia a G-protein second
messenger system to activatemessenger system to activatethyroid adenyl cyclase,thyroid adenyl cyclase,
yielding cyclic adenosineyielding cyclic adenosine
monophosphate (cAMP).monophosphate (cAMP).
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Synthesis of thyroid hormone is dependentSynthesis of thyroid hormone is dependenton an adequate supply of iodine.on an adequate supply of iodine.
Dietary inorganic iodide is transported intoDietary inorganic iodide is transported intothe gland by an iodide transporterthe gland by an iodide transporter
Iodide is then converted to iodine and boundIodide is then converted to iodine and boundto tyrosine residues on thyroglobulin by theto tyrosine residues on thyroglobulin by the
enzyme thyroid peroxidase in a processenzyme thyroid peroxidase in a processcalled organification.called organification.
Thyroid Hormone SynthesisThyroid Hormone Synthesis
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Synthesis cont.Synthesis cont.
The result is the formation of monoiodotyrosineThe result is the formation of monoiodotyrosine(MIT) and diiodotyrosine (DIT).(MIT) and diiodotyrosine (DIT).
Coupling of MIT and DIT results in the formationCoupling of MIT and DIT results in the formationof T3 and T4, which are then stored within theof T3 and T4, which are then stored within thethyroglobulin in the extracellular thyroid follicularthyroglobulin in the extracellular thyroid follicular
lumen.lumen.
Unlike other endocrine glands, the thyroid has aUnlike other endocrine glands, the thyroid has alarge supply of stored preformed hormone.large supply of stored preformed hormone.
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Causes of ThyrotoxicosisCauses of Thyrotoxicosis
Graves DiseaseGraves Disease
Chronic Lymphocytic Thyroditis (HashimotosChronic Lymphocytic Thyroditis (Hashimotos
Thyroditis)Thyroditis) Toxic AdenomaToxic Adenoma
McCune Albright SyndromeMcCune Albright Syndrome
Subacute Viral ThyroditisSubacute Viral Thyroditis
TSH Secreting Pituitary AdenomaTSH Secreting Pituitary Adenoma
Exogenous Thyroid HormoneExogenous Thyroid Hormone
hCG Secreting TumorhCG Secreting Tumor
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Chronic Lymphocytic ThyroditisChronic Lymphocytic Thyroditis
Autoimmune disorder characterized by thyroglobulinAutoimmune disorder characterized by thyroglobulinand thyroid peroxidase antibodiesand thyroid peroxidase antibodies
Most common cause of acquired thyroid diseaseMost common cause of acquired thyroid disease
Typically results in hypothyroidismTypically results in hypothyroidism However, hyperthyroid phase (Hashitoxicosis) mayHowever, hyperthyroid phase (Hashitoxicosis) may
occuroccur
self limited phase although may last up to 6self limited phase although may last up to 6
monthsmonths
recent study showed 11.5% of pts withrecent study showed 11.5% of pts with
Hashimotos Thyroditis present withHashimotos Thyroditis present with
thyrotoxicosisthyrotoxicosis
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Toxic AdenomaToxic Adenoma
Autonomously functioning thyroid noduleAutonomously functioning thyroid nodulehypersecreting T3 and/or T4 resulting inhypersecreting T3 and/or T4 resulting in
thyrotoxicosisthyrotoxicosis Aka Plummers diseaseAka Plummers disease
Very rare in childrenVery rare in children
Almost never malignantAlmost never malignant
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McCune Albright SyndromeMcCune Albright Syndrome
Clinical syndrome that is classically characterized byClinical syndrome that is classically characterized bypolyostotic fibrous dysplasia, cafau-lait hyperpolyostotic fibrous dysplasia, cafau-lait hyper
pigmentation, and endocrinopathies.pigmentation, and endocrinopathies.
Most common endocrinopathy is peripheralMost common endocrinopathy is peripheralprecocious pubertyprecocious puberty
Caused by activation mutation in GNAS1Caused by activation mutation in GNAS1
Hyperthyroidism can be observedHyperthyroidism can be observed can present with a diffuse goiter in addition to other signscan present with a diffuse goiter in addition to other signs
of hyperthyroidismof hyperthyroidism
associated with mutation in the alpha subunit of the Gassociated with mutation in the alpha subunit of the G
regulatory protein that links TSH receptor with cAMPregulatory protein that links TSH receptor with cAMP
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Subacute Viral ThyroditisSubacute Viral Thyroditis
Generally associated with a viral URIGenerally associated with a viral URI
Classically characterized by tender, warmClassically characterized by tender, warm
thyroid glandthyroid gland Hyperthyroidism caused by inflammationHyperthyroidism caused by inflammation
of the thyroid gland and subsequentof the thyroid gland and subsequent
release of preformed thyroid hormone.release of preformed thyroid hormone.
Once inflammation resolves, symptomsOnce inflammation resolves, symptomsresolveresolve
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TSH Secreting Pituitary AdenomaTSH Secreting Pituitary Adenoma
Can result in thyrotoxicosisCan result in thyrotoxicosis
Biochemically:Biochemically:
elevated TSH levels, leading to elevated T4elevated TSH levels, leading to elevated T4and T3 levelsand T3 levels
Extremely rareExtremely rare
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Exogenous Thyroid IngestionExogenous Thyroid Ingestion
Ingestion of L thyroxin medicationsIngestion of L thyroxin medications
T4 is converted to T3 in the peripheralT4 is converted to T3 in the peripheral
tissues, leading to inhibition of TSHtissues, leading to inhibition of TSH Lab studies:Lab studies:
elevated T4 and T3 levelselevated T4 and T3 levels
suppressed TSH levelsuppressed TSH level
Occasionally T3 is ingested:Occasionally T3 is ingested: similar lab results but T4 is lowsimilar lab results but T4 is low
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hCG Secreting TumorshCG Secreting Tumors
Adolescents with tumors such asAdolescents with tumors such ashydatiform mole and choriocarcinoma canhydatiform mole and choriocarcinoma can
present with thyrotoxicosispresent with thyrotoxicosis hCG binds directly to the TSH receptor,hCG binds directly to the TSH receptor,
leading to excessive thyroid hormoneleading to excessive thyroid hormone
releaserelease Very rareVery rare
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Graves DiseaseGraves Disease
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Graves DiseaseGraves Disease
Most common cause of hyperthyroidism inMost common cause of hyperthyroidism inchildrenchildren
accounts for >95% of childhood cases ofaccounts for >95% of childhood cases ofhyperthyroidismhyperthyroidism
Prevalence approximately 0.02% in childhoodPrevalence approximately 0.02% in childhood
Gets it name from the Irish physician RobertGets it name from the Irish physician RobertGraves who described it in 1835.Graves who described it in 1835.
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PathophysiologyPathophysiology
Associated with HLA-B8 and HLA-DR3 haplotypesAssociated with HLA-B8 and HLA-DR3 haplotypes
Polygenic inheritancePolygenic inheritance
The reasons for the development of Graves Disease areThe reasons for the development of Graves Disease arepresently unknown. Some postulated causes include:presently unknown. Some postulated causes include: Environmental Factors-Environmental Factors- damage to the thyroid, by radiation or ethanol injection,
with liberation of antigens, has been noted, smoking also increases the risk
Thymic Selection of Lymphocytes- pre-T lymphocytes may be educated in the
thymus to recognize thyroid-related epitopes, and thus to generate self-tolerance
against these thyroid-related antigens.
Molecular Mimicry-exposure to a particular peptide epitope in an environmental
antigen might develop immune reactivity to an amino acid sequence identical tothat present in an human endogenous antigen such as TSH receptor, TPO, or
TG.
Thyroid Injury and Antigen Release- certain types of injury to the thyroid are
followed by the development of thyroid autoimmunity, including Graves' disease.
i.e. radiation
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Pathophysiology cont.
Patients likely have defective immune tolerance, leading toPatients likely have defective immune tolerance, leading tothe development of specific auto antibodies directed againstthe development of specific auto antibodies directed against
various thyroid antigensvarious thyroid antigens
The TSH receptor is the most significant thyroid auto antigenThe TSH receptor is the most significant thyroid auto antigenin this disorder.in this disorder.
However, children with Graves disease also produceHowever, children with Graves disease also produceimmunoglobulin's directed against thyroperoxidase (anti-TPO)immunoglobulin's directed against thyroperoxidase (anti-TPO)
and thyroglobulin, as well as TSH receptorblockingand thyroglobulin, as well as TSH receptorblocking
antibodiesantibodies
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Morbidity and MortalityMorbidity and Mortality
Potentially life threateningPotentially life threatening
Most severe manifestation is thyroid stormMost severe manifestation is thyroid storm
Rare in childrenRare in children Can also see signs of CHFCan also see signs of CHF
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DemographicsDemographics
Females affected more often than malesFemales affected more often than males3-6:1 ratio3-6:1 ratio
Incidence increases throughout childhoodIncidence increases throughout childhoodwith peak incidence in children 10-15 yrswith peak incidence in children 10-15 yrs
No racial predilection seems to existNo racial predilection seems to exist
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ClinicalClinical
Children are usually identified because ofChildren are usually identified because ofenlarged thyroid, weight loss or behavioralenlarged thyroid, weight loss or behavioral
changeschanges Exophthalmos less commonly observed inExophthalmos less commonly observed in
childrenchildren
Enlarged thyroid may cause dysphasiaEnlarged thyroid may cause dysphasia Symptoms may mimic ADHDSymptoms may mimic ADHD
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SymptomsSymptoms
DysphasiaDysphasia
Irritability and emotionalIrritability and emotional
liabilityliability
Sleeplessness andSleeplessness andrestlessnessrestlessness
Inability to concentrateInability to concentrate
Deterioration ofDeterioration of
handwriting and schoolhandwriting and schoolperformanceperformance
Frequent stools orFrequent stools or
diarrheadiarrhea
PalpitationsPalpitations
PruritusPruritus
Weight lossWeight loss
Increased appetiteIncreased appetite
Nocturia, increase inNocturia, increase in
urination and thirsturination and thirst
Infrequent or lightInfrequent or light
mensesmenses Weakness and tirednessWeakness and tiredness
Exercise intoleranceExercise intolerance
Heat intoleranceHeat intolerance
Frequency of signs andFrequency of signs and
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Frequency of signs andFrequency of signs and
symptomssymptoms
The frequency ofThe frequency ofsymptoms :symptoms : Increased appetite (60%)Increased appetite (60%)
Weight loss (50%)Weight loss (50%)
Increased sweating (49%)Increased sweating (49%)
Hyperactivity (44%)Hyperactivity (44%)
Heat intolerance (33%)Heat intolerance (33%)
Palpitations (30%)Palpitations (30%) Fatigue (16%)Fatigue (16%)
Diarrhea (13%)Diarrhea (13%)
The frequency ofThe frequency ofsigns :signs :
Goiter (99%)Goiter (99%)
Tachycardia (82%)Tachycardia (82%)
Exophthalmos (47%)Exophthalmos (47%)
Tremor (61%)Tremor (61%)
Thyroid bruit (53%)Thyroid bruit (53%) Increased pulseIncreased pulse
pressure (50%)pressure (50%)
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PhysicalPhysical
Patients can be thinPatients can be thinwith a fixed stare andwith a fixed stare and
fidgety behaviorfidgety behavior
Can see multipleCan see multipleophthalmological,ophthalmological,
thyroidal,thyroidal,
cardiopulmonary,cardiopulmonary,neuromuscular andneuromuscular and
dermal findings.dermal findings.
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LabsLabs
HyperthyroidismHyperthyroidism confirmed simply and quickly withconfirmed simply and quickly with
measurements of FT4 and TSHmeasurements of FT4 and TSH Graves DiseaseGraves Disease
confirmed by measurement ofconfirmed by measurement of TSH receptor
stimulating immunoglobulins, i.e. TSIgs
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ImagingImaging
Diagnostic radioiodine IDiagnostic radioiodine I131 uptake is rarely131 uptake is rarely
performedperformed
Either technetium TcEither technetium Tc99m or99m or123123I scan may beI scan may be
useful if the gland doesuseful if the gland does
not have a uniformnot have a uniform
consistencyconsistency Ultrasound may also beUltrasound may also be
used to image the glandused to image the gland
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TreatmentTreatment
3 main treatments3 main treatments Medical therapyMedical therapy
Radio-iodine Ablation of the thyroid glandRadio-iodine Ablation of the thyroid gland SurgerySurgery
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Antithyroid drugsAntithyroid drugs
2 main medications are used in the U.S.2 main medications are used in the U.S.Propylthiouracil and MethimazolePropylthiouracil and Methimazole
Inhibit thyroid biosynthesis decreasing theInhibit thyroid biosynthesis decreasing theoxidation of iodine and iodination of tyrosine.oxidation of iodine and iodination of tyrosine.
PTU diminishes the peripheral conversion of T4PTU diminishes the peripheral conversion of T4to T3to T3
PTU is required TID because of shorter half lifePTU is required TID because of shorter half life Methimazole can be administered BIDMethimazole can be administered BID
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Therapy cont.
Glucocorticoids Decrease peripheral T 4to T 3conversion, and may have a more
prolonged suppressive effect on thyrotoxicosis Prednisone has been reported to induce remission of Graves' disease,
but at the expense of causing Cushing's syndrome
Potassium Iodide potassium iodide acts promptly to inhibit thyroid hormone secretion from
the Graves' disease thyroid gland. Used more in congenital Gravesdisease.
Adjunctive Therapy: blockers- alleviate many of the signs and symptoms of Graves
Disease However have little effect on the fundamental disease process Palpitations, excessive sweating, and nervousness improve, and tremor
and tachycardia are controlled
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Radio-Iodine AblationRadio-Iodine Ablation
Ablation of the thyroid gland with radio-iodine is theAblation of the thyroid gland with radio-iodine is thetreatment of choice for most adults.treatment of choice for most adults.
After more than 50 years of widespread use, noAfter more than 50 years of widespread use, noevidence of an increased risk of malignancy or geneticevidence of an increased risk of malignancy or genetic
damage exists.damage exists.
Nonetheless, because of the theoretical risk, frequencyNonetheless, because of the theoretical risk, frequencyof radioiodine therapy is much lower in pediatric patients.of radioiodine therapy is much lower in pediatric patients.
131131I is administered orally in 1-2 doses. Ablation may takeI is administered orally in 1-2 doses. Ablation may takeseveral weeks to months, and hyperthyroid symptomsseveral weeks to months, and hyperthyroid symptomsmay continue until that time.may continue until that time.
Propanalol may be used to ameliorate these symptoms.Propanalol may be used to ameliorate these symptoms.
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SurgerySurgery
Surgery is the oldest treatment for Graves DiseaseSurgery is the oldest treatment for Graves Disease
Generally, patients are initially treated with antithyroidGenerally, patients are initially treated with antithyroidmedications.medications.
Iodide then is added before surgery to decrease theIodide then is added before surgery to decrease thevascularity of the thyroid gland.vascularity of the thyroid gland.
To minimize risk of recurrence, most of the gland isTo minimize risk of recurrence, most of the gland isremoved.removed.
Surgical complications can include hypoparathyroidismSurgical complications can include hypoparathyroidismand damage to the recurrent laryngeal nerveand damage to the recurrent laryngeal nerve
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SummarySummary
Graves disease is the most commonGraves disease is the most commoncause of hyperthyroidism is children butcause of hyperthyroidism is children but
with proper treatment can be successfullywith proper treatment can be successfullymanaged.managed.
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Follow up
Microsomal Antibody 1:400 [
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The EndThe End
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ReferencesReferences
Dallas J, Foley T. Hyperthyroidism. In: Pediatric Endocrinology.Dallas J, Foley T. Hyperthyroidism. In: Pediatric Endocrinology. 3rd ed3rd ed. 1996:401-415. 1996:401-415 Sugino K, Ito K, Mimura T, et al. Surgical treatment of Graves' disease inSugino K, Ito K, Mimura T, et al. Surgical treatment of Graves' disease in
children.children. ThyroidThyroid. 2004;14:447-452. 2004;14:447-452
Zimmerman D, Lteif AN. Thyrotoxicosis in children.Zimmerman D, Lteif AN. Thyrotoxicosis in children. Endocrinol Metab Clin NorthEndocrinol Metab Clin NorthAmAm. Mar 1998;27(1):109-26. Mar 1998;27(1):109-26
Bahadada S, Bhansali A, et. Al. Juvemile Hyperthyrodism: an Experience .Bahadada S, Bhansali A, et. Al. Juvemile Hyperthyrodism: an Experience . Indian PediatricsIndian Pediatrics2006 43: 301-3172006 43: 301-317
Ferry RJ, et al. Graves disease Published onlineFerry RJ, et al. Graves disease Published online Rivkees, SA, Sklar C, Freemark M, The Management of Graves Disease in Children withRivkees, SA, Sklar C, Freemark M, The Management of Graves Disease in Children with
Special Emphasis on Radioiodine TreatmentSpecial Emphasis on Radioiodine Treatment. The Journal of Clincical Endocrinology and. The Journal of Clincical Endocrinology andMetabolismMetabolism 1998 83: 3767-37761998 83: 3767-3776
Stalberg P, Svensson A, et al. Surgical Treatment of Graves Disease: Evidence-Based ApproachStalberg P, Svensson A, et al. Surgical Treatment of Graves Disease: Evidence-Based ApproachWorld Journal of SurgeryWorld Journal of Surgery2008 Published online2008 Published online
Glaser NS, Styne DM. Predicting the Likilihood of Remission in Children with Graves Disease: AGlaser NS, Styne DM. Predicting the Likilihood of Remission in Children with Graves Disease: AProspective, Multicenter StudyProspective, Multicenter Study. Pediatrics. Pediatrics 2008 121: 481-4882008 121: 481-488
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Objectives
To present an interesting case of alteredmental status
Discuss the differential diagnosis ofhyperthyroidism
Review the Pathophysiology and
treatment of Graves Disease.
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QuestionsQuestions
1. Are patients with Graves disease who1. Are patients with Graves disease whodo not have their thyroid removed atdo not have their thyroid removed at
greater risk for thyroid cancer later on ingreater risk for thyroid cancer later on inlife?life?
2. What determines which of the anti-2. What determines which of the anti-
thyroid medications are used in a patient.thyroid medications are used in a patient.
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ThanksThanks
Dr. MarshallDr. Marshall
Dr. KellyDr. Kelly
Monica and ArchanaMonica and Archana
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Differential
Acute/Chronic IDDM with DKA
Brain tumor with
seizure/increased ICP
Hypertension with
hypertensive
encephalopathy
Acute Ingestion
Infection
Seizure
Aneursym
Stroke