case conference hyperthyroidism april2008

7/29/2019 Case Conference Hyperthyroidism April2008

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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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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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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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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

www.endotext.comwww.endotext.com


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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

case conference hyperthyroidism april2008

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