adrenal physiology and hypofunctioning states heidi chamberlain shea, md endocrine associates of...

Adrenal Physiology Adrenal Physiology and Hypofunctioning and Hypofunctioning

StatesStates

Heidi Chamberlain Shea, MDHeidi Chamberlain Shea, MD

Endocrine Associates of Endocrine Associates of DallasDallas

Goals of DiscussionGoals of Discussion

Review Adrenal PhysiologyReview Adrenal Physiology Identify the clinical features of Identify the clinical features of

Adrenal InsufficiencyAdrenal Insufficiency Etiologies of Adrenal InsufficiencyEtiologies of Adrenal Insufficiency Understand testing of adrenal Understand testing of adrenal

functionfunction Treatment of Adrenal InsufficiencyTreatment of Adrenal Insufficiency

Adrenal DevelopmentAdrenal Development Derived Derived

– Neuroectodermal cells Neuroectodermal cells (medulla)(medulla)

– Mesenchymal cells Mesenchymal cells (cortex)(cortex)

Fetal adrenal is present Fetal adrenal is present by 2 months gestationby 2 months gestation– Mostly cortexMostly cortex– Glomerulosa and Glomerulosa and

fasiculata are present at fasiculata are present at birthbirth

– Reticularis develops Reticularis develops during first year of lifeduring first year of life

Adrenal AnatomyAdrenal Anatomy

Adult adrenalAdult adrenal– 2-3cm wide2-3cm wide– 1cm thick1cm thick– 4-6 grams 4-6 grams

LocatedLocated– Upper pole of Upper pole of

kidneyskidneys Vascular supplyVascular supply

– 12 small arteries 12 small arteries from aortafrom aorta

Adrenal PhysiologyAdrenal Physiology GlomerulosaGlomerulosa

– 15% of cortex15% of cortex– AldosteroneAldosterone

Renin-AngiotensinRenin-Angiotensin

FasciulataFasciulata– 75% of cortex75% of cortex– CortisolCortisol– DHEADHEA

ACTHACTH

ReticularisReticularis– Androgens and estrogensAndrogens and estrogens

ACTHACTH

MedullaMedulla– CatecholaminesCatecholamines

Congenital Adrenal Congenital Adrenal Hyperplasia Hyperplasia

Most adrenal Most adrenal biosynthetic defects biosynthetic defects result inresult in– Virilized femaleVirilized female– Normally virilized Normally virilized

malemale– DeficienciesDeficiencies

Mineralocorticoid Mineralocorticoid Glucocorticoid Glucocorticoid

– 21-OH deficiency21-OH deficiency– 11-OH deficiency11-OH deficiency

Congenital Adrenal HyperplasiaCongenital Adrenal Hyperplasia Deficiency of CYP 17Deficiency of CYP 17

– 1717αα- hydroxylase and - hydroxylase and 17-20 lyase deficiency17-20 lyase deficiency

– Rare causeRare cause– Diagnosed due to Diagnosed due to

delayed pubertal delayed pubertal developmentdevelopment

– 46xx46xx HypertensiveHypertensive +/- Hypokalemic+/- Hypokalemic Primary amenorrheaPrimary amenorrhea Absent secondary sex Absent secondary sex

characteristicscharacteristics

Congenital Adrenal HyperplasiaCongenital Adrenal Hyperplasia Deficiency of CYP 17Deficiency of CYP 17

– 46XY46XY Complete male Complete male

pseudohermaphroditispseudohermaphroditismm

Female external Female external genitaliagenitalia

Blind-ended vaginaBlind-ended vagina No mullerian No mullerian

structuresstructures Testes intra-abdominalTestes intra-abdominal

– Leydig cell Leydig cell hyperplasiahyperplasia

HypertensiveHypertensive +/- Hypokalemic+/- Hypokalemic

Cortisol sufficientCortisol sufficient– Tolerates general Tolerates general

anesthesia and anesthesia and surgerysurgery

TreatmentTreatment– Steroids to Steroids to

suppress excesssuppress excess– Gonadal Gonadal

replacementreplacement

Congenital Adrenal HyperplasiaCongenital Adrenal Hyperplasia

3 3 ββ-Hydroxysteroid -Hydroxysteroid DehydrogenaseDehydrogenase– Presents early infancyPresents early infancy– Adrenal insufficiencyAdrenal insufficiency– Females can be Females can be

virilized due to DHEAvirilized due to DHEA– Males Males

Normal genital Normal genital developmentdevelopment

HypospadiasHypospadias PseudohermaphroditisPseudohermaphroditis

mm

Can present in Can present in pubertypuberty– HyperandrogenemiHyperandrogenemi

aa HirsuitismHirsuitism OligomenorrheaOligomenorrhea

TreatmentTreatment– Cortisol Cortisol

replacementreplacement

Congenital Adrenal HyperplasiaCongenital Adrenal Hyperplasia Congenital Lipoid Congenital Lipoid

Adrenal HyperplasiaAdrenal Hyperplasia StAR DeficiencyStAR Deficiency

– Transports cholesterol Transports cholesterol to inner mitochondrial to inner mitochondrial membranemembrane

Rarest formRarest form Autosomal recessiveAutosomal recessive All adrenal steroids All adrenal steroids

are deficientare deficient Present with adrenal Present with adrenal

insufficiencyinsufficiency Typically fatal infancyTypically fatal infancy MalesMales

– Female external Female external genitaliagenitalia

Renin and AldosteroneRenin and Aldosterone ReninRenin

– Enzyme released from the Enzyme released from the kidneys (macula densa)kidneys (macula densa)

– Activates Angiotensinogen Activates Angiotensinogen Angiotensin 1 Angiotensin 1 Angiotensin 2Angiotensin 2

– Increased secretionIncreased secretion Low blood pressureLow blood pressure Low sodiumLow sodium High potassiumHigh potassium Upright postureUpright posture

AldosteroneAldosterone– Sodium homeostasisSodium homeostasis– Regulates arterial Regulates arterial

pressurepressure– RegulatedRegulated

Angiotensin 2Angiotensin 2

– Increases Increases Renal sodium retentionRenal sodium retention Renal potassium Renal potassium

excretionexcretion

– Low AldosteroneLow Aldosterone Adrenal insufficiencyAdrenal insufficiency

– High reninHigh renin HyperkalemiaHyperkalemia

Renin and AldosteroneRenin and Aldosterone

Mineralocorticoid DeficiencyMineralocorticoid Deficiency Hyporeninemic Hyporeninemic

HypoaldosteronismHypoaldosteronism– Impaired renin Impaired renin

releaserelease– 50-70 years50-70 years– Chronic Chronic

assymptomatic assymptomatic hyperkalemiahyperkalemia

– Mild-moderate renal Mild-moderate renal insufficiencyinsufficiency

– Muscle weaknessMuscle weakness– Cardiac arrhythmiasCardiac arrhythmias

Mineralocorticoid DeficiencyMineralocorticoid Deficiency

50% of patients with 50% of patients with Diabetes Diabetes

Type IV RTAType IV RTA– Metabolic acidosisMetabolic acidosis– Decreased renal Decreased renal

ammoniagenesisammoniagenesis– Decreased H ion Decreased H ion

secretionsecretion– Decreased bicarbonate Decreased bicarbonate

resorbtionresorbtion

Other diseasesOther diseases– SLESLE– Multiple myelomaMultiple myeloma– Renal amyloidosisRenal amyloidosis– CirrhosisCirrhosis– Sickle CellSickle Cell– AIDSAIDS– POEMSPOEMS

Transient with drugsTransient with drugs– NSAIDNSAID– Cyclosporin ACyclosporin A– Mitomycin CMitomycin C– CosyntropinCosyntropin

Mineralocorticoid DeficiencyMineralocorticoid DeficiencyPrimary HypoaldosteronismPrimary Hypoaldosteronism

Aldosterone synthase Aldosterone synthase deficiency (CYP11B2)deficiency (CYP11B2)– Autosomal recessiveAutosomal recessive– Diagnosed in infancyDiagnosed in infancy

Recurrent dehydrationRecurrent dehydration Failure to thriveFailure to thrive Salt wastingSalt wasting

TreatmentTreatment– FlorinefFlorinef

AcquiredAcquired– Heparin Heparin

Suppresses Suppresses aldosteronealdosterone

Increase in reninIncrease in renin Healthy person, Healthy person,

asymptomaticasymptomatic Critically ill, can be Critically ill, can be

symptomaticsymptomatic

Mineralocorticoid DeficiencyMineralocorticoid DeficiencyPrimary HypoaldosteronismPrimary Hypoaldosteronism

PseudohypoaldosteronisPseudohypoaldosteronismm– Salt wasting syndromeSalt wasting syndrome– InfancyInfancy– Renal tubular insensitivity Renal tubular insensitivity

to mineralocorticoidsto mineralocorticoids– Autosomal DominantAutosomal Dominant

Resistance to aldosterone Resistance to aldosterone at the renal tubuleat the renal tubule

– Autosomal RecessiveAutosomal Recessive SevereSevere Also affects sweat and Also affects sweat and

salivary glandssalivary glands ColonColon

Features of Features of hypoaldosteronismhypoaldosteronism– HyopnatremiaHyopnatremia– HyperkalemiaHyperkalemia– Hyper-reninemiaHyper-reninemia– Increased aldosterone Increased aldosterone

levelslevels Many kindreds Many kindreds

– Homozygous mutation Homozygous mutation in amiloride-sensitive in amiloride-sensitive epithelial sodium epithelial sodium channelchannel

TreatmentTreatment– NaClNaCl– KK++ binding resins binding resins

(+) POSTERIORPITUITARYANTERIOR

PITUITARY

(-)

CRH

HYPOTHALAMUS

HYPOTHALAMIC-PITUITARY

PORTAL SYSTEM

ACTH

CORTISOLAdrenal Fasiculata

(-)

Adrenal PhysiologyAdrenal Physiology

ACTH and cortisolACTH and cortisol– Pulsatile secretionPulsatile secretion– Highest in AM at Highest in AM at

wakeningwakening– Lowest late afternoon Lowest late afternoon

and eveningand evening– Nadir is 1-2 hrs after the Nadir is 1-2 hrs after the

start of sleepstart of sleep– CircadianCircadian

Blind patientBlind patient Reverts to a 24.5-25hrReverts to a 24.5-25hr

– DHEA and DHEA and Androstenedione Androstenedione regulated by ACTHregulated by ACTH

Increase in response Increase in response to stressto stress– HypoglycemiaHypoglycemia– SurgerySurgery– IllnessIllness– HypotensionHypotension– SmokingSmoking– Cold exposureCold exposure

Blunted responseBlunted response– Chronic illnessChronic illness

Circulation of Cortisol and Circulation of Cortisol and Adrenal AndrogensAdrenal Androgens

Secreted unboundSecreted unbound In circulation bind In circulation bind

to plasma proteinsto plasma proteins Unbound is activeUnbound is active CortisolCortisol

– Free (10%)Free (10%)– Corticosteroid-Corticosteroid-

binding globulin binding globulin (CBG) (75%)(CBG) (75%)

– AlbuminAlbumin

AndrogensAndrogens– AlbuminAlbumin– TestosteroneTestosterone

Sex Hormone Sex Hormone binding (SHBG)binding (SHBG)

Cortisol EffectsCortisol Effects

Connective TissueConnective Tissue– Inhibit fibroblastsInhibit fibroblasts– Loss of collagenLoss of collagen– Thinning of skinThinning of skin

BoneBone– Inhibit bone Inhibit bone

formationformation– Stimulate bone Stimulate bone

resorptionresorption– Potentiate actions of Potentiate actions of

PTHPTH Increased resorptionIncreased resorption

Calcium Calcium metabolismmetabolism– Decrease intestinal Decrease intestinal

calcium absorptioncalcium absorption– Stimulates renal 1Stimulates renal 1αα--

hydroxylasehydroxylase Increases 1,25 OH Increases 1,25 OH

vitamin D synthesisvitamin D synthesis

– Increased calciuriaIncreased calciuria– Increased Increased

phosphaturiaphosphaturia


GrowthGrowth– Accelerate development Accelerate development

of fetal tissuesof fetal tissues Lung maturityLung maturity

– Inhibit linear growthInhibit linear growth Decreased growth Decreased growth

hormonehormone ErythrocytesErythrocytes

– Minimal effectMinimal effect LeukocytesLeukocytes

– Increase PMN by Increase PMN by increasing release from increasing release from bone marrowbone marrow

– Decreases lymphocytes, Decreases lymphocytes, monocytes and monocytes and eosinophilseosinophils

ImmunologicImmunologic– Inhibit Inhibit

prostaglandin prostaglandin synthesissynthesis Phospholipase APhospholipase A22

– Decreases IL-1Decreases IL-1 IL-1 stimulates CRH IL-1 stimulates CRH

and ACTHand ACTH

– Impairs AB Impairs AB production and production and clearanceclearance


CardiovascularCardiovascular– Increase COIncrease CO– Increase peripheral Increase peripheral

vascular tonevascular tone– HypertensionHypertension

Renal functionRenal function– Mineralocorticoid Mineralocorticoid

receptorsreceptors Na retentionNa retention Hypokalemia Hypokalemia HTNHTN

– Glucocorticoid receptorsGlucocorticoid receptors Increased GFRIncreased GFR

Nervous systemNervous system– Enters the brainEnters the brain– EuphoriaEuphoria– Irritability, depression Irritability, depression

and emotional labilityand emotional lability– Hyperkinetic or manic Hyperkinetic or manic

behaviorbehavior– Overt psychosisOvert psychosis– Increased appetiteIncreased appetite– Impaired memory or Impaired memory or

concentrationconcentration– Decreased libidoDecreased libido– InsomniaInsomnia

Decreased REM and Decreased REM and increased Stage II increased Stage II sleepsleep

Cortisol EffectsCortisol EffectsMetabolismMetabolism

GlycogenGlycogen– Activates glycogen Activates glycogen

production\production\– Deactivates Deactivates

glycogen glycogen breakdownbreakdown

GlucoseGlucose– Increase hepatic Increase hepatic

glucose productionglucose production– Inhibits peripheral Inhibits peripheral

tissue utilization of tissue utilization of glucoseglucose

LipidsLipids– Activate lipolysis in Activate lipolysis in

adipose tissueadipose tissue– Redistributes body Redistributes body

fat fat Sparing of the Sparing of the

extremitiesextremities

Adrenal InsufficiencyAdrenal Insufficiency

IncidenceIncidence– 6 cases per 1 million 6 cases per 1 million

adults/yearadults/year PrevalencePrevalence

– 40-110 cases per 1 40-110 cases per 1 million adultsmillion adults

More common in More common in femalesfemales– 2.6:12.6:1

Diagnosed in the 3-5Diagnosed in the 3-5thth decadesdecades

Adrenal InsufficiencyAdrenal InsufficiencyPresentationPresentation

Signs and Signs and symptomssymptoms– Rate and degree of Rate and degree of

loss of adrenal loss of adrenal functionfunction

– Degree of Degree of physiologic stressphysiologic stress

– PrimaryPrimary Mineralocorticoid Mineralocorticoid

deficiencydeficiency

– Secondary/TertiarySecondary/Tertiary Mineralocorticoid Mineralocorticoid

sufficientsufficient

Adrenal InsufficiencyAdrenal InsufficiencyPresentationPresentation

DehydrationDehydration Hypotension/shockHypotension/shock

– SyncopeSyncope Abdominal painAbdominal pain

– Recurrent and unexplainedRecurrent and unexplained Mental status changesMental status changes Nausea and vomitingNausea and vomiting Weight lossWeight loss FatigueFatigue HyperpigmentationHyperpigmentation VitiligoVitiligo

Adrenal CrisisAdrenal CrisisPresentationPresentation

Unexplained Unexplained hypoglycemiahypoglycemia

HyponatremiaHyponatremia HyperkalemiaHyperkalemia HypercalcemiaHypercalcemia EosinophiliaEosinophilia Other autoimmune Other autoimmune

deficienciesdeficiencies– HypothyroidHypothyroid– HypogonadalHypogonadal

Adrenal CrisisAdrenal CrisisPopulations at RiskPopulations at Risk

Secondary adrenal Secondary adrenal insufficiencyinsufficiency– Exogenous steroid Exogenous steroid

useuse Joint injections Joint injections Herbals from MexicoHerbals from Mexico High dose inhaled High dose inhaled

steroidssteroids

Congenital Adrenal Congenital Adrenal HyperplasiaHyperplasia

Primary Adrenal InsufficiencyPrimary Adrenal InsufficiencyEtiologyEtiology

Autoimmune adrenalitisAutoimmune adrenalitis– 70% of cases70% of cases– Polyendocrinopathy-candidiasis-Polyendocrinopathy-candidiasis-

ectodermal dystrophy (APECED)- PGA Iectodermal dystrophy (APECED)- PGA I Autosomal recessive disorderAutosomal recessive disorder Mutation in zinc finger proteinMutation in zinc finger protein Adrenal failure, hypoparathyroidism, Adrenal failure, hypoparathyroidism,

mucocutaneous candidiasis, dental enamel mucocutaneous candidiasis, dental enamel hypoplasia, dystrophy of the nailshypoplasia, dystrophy of the nails


Autoimmune adrenalitisAutoimmune adrenalitis– Polyglandular autoimmune IIPolyglandular autoimmune II

Primary adrenal insufficiency, Autoimmune Primary adrenal insufficiency, Autoimmune thyroid disease (hypo and hyper), Type I thyroid disease (hypo and hyper), Type I Diabetes, hypogonadismDiabetes, hypogonadism

InfectiousInfectious– TuberculosisTuberculosis

5% of cases5% of cases Rifampin will increase cortisol metabolism-Rifampin will increase cortisol metabolism-

higher dose neededhigher dose needed

– HistoplasmosisHistoplasmosis Ketoconazole inhibits steroid synthesisKetoconazole inhibits steroid synthesis


Bilateral adrenal hemorrhageBilateral adrenal hemorrhage– Ill patients on anticoagulantsIll patients on anticoagulants– CoagulopathiesCoagulopathies– HeparinHeparin

Thrombosis and thrombocytopeniaThrombosis and thrombocytopenia

– Primary antiphospholipid antibody Primary antiphospholipid antibody syndromesyndrome


Adrenoleukodystrophy and Adrenoleukodystrophy and adrenomyeloneuropathyadrenomyeloneuropathy– X-linkedX-linked– Defect in Defect in ββ-oxidation-oxidation– Mutations in gene encoding a peroxisomal Mutations in gene encoding a peroxisomal

membrane protein of the ABC superfamily of membrane protein of the ABC superfamily of membrane transportersmembrane transporters

– Demyelination of central and peripheral Demyelination of central and peripheral nervous systemnervous system

– High levels of High levels of very long chain fatty acidsvery long chain fatty acids (VLCFA)(VLCFA)


Familial glucocorticoid Familial glucocorticoid DeficiencyDeficiency– Autosomal recessiveAutosomal recessive– ACTH resistanceACTH resistance

High plasma ACTH High plasma ACTH concentrationsconcentrations

– Cortisol and androgen Cortisol and androgen deficiencydeficiency

– Aldosterone is normalAldosterone is normal– Presents in childhoodPresents in childhood

HyperpigmentationHyperpigmentation Muscle weaknessMuscle weakness Hypoglycemia and seizuresHypoglycemia and seizures Low epinephrineLow epinephrine


HIV/AIDSHIV/AIDS– Adrenal necrosisAdrenal necrosis

Infiltrative etiologiesInfiltrative etiologies– CMV or TBCMV or TB

Bilateral metastatic infiltrationBilateral metastatic infiltration– Breast cancer Breast cancer – Bronchogenic carcinomaBronchogenic carcinoma– Renal malignanciesRenal malignancies


Drugs that inhibit Drugs that inhibit cortisol synthesiscortisol synthesis– AminoglutethimideAminoglutethimide– EtomidateEtomidate– KetoconazoleKetoconazole– MetyraponeMetyrapone– SuraminSuramin– MitotaneMitotane

Accelerate cortisol Accelerate cortisol metabolismmetabolism– PhenytoinPhenytoin– BarbituatesBarbituates– RifampinRifampin

Secondary Adrenal Secondary Adrenal InsufficiencyInsufficiency

EtiologyEtiology Glucocorticoid useGlucocorticoid use PituitaryPituitary

– TumorsTumors– HemorrhageHemorrhage

Pituitary necrosis Pituitary necrosis (Sheehan Syndrome)(Sheehan Syndrome)

– Metastatic Metastatic malignanciesmalignancies

– Lymphocytic Lymphocytic hypophysitishypophysitis

– SarcoidosisSarcoidosis– Histiocytosis XHistiocytosis X

Developmental Developmental abnormalitiesabnormalities– Pit-1Pit-1– Prop-1Prop-1– Septo-optic Septo-optic

dysplasiadysplasia

Adrenal InsufficiencyAdrenal InsufficiencyDiagnosisDiagnosis

Always test for thyroid Always test for thyroid sufficiencysufficiency

Insulin Hypoglycemia Insulin Hypoglycemia testtest– Tests anterior pituitary Tests anterior pituitary

functionfunction– Insulin 0.15U/kg/bodyInsulin 0.15U/kg/body– Cortisol and growth Cortisol and growth

hormone drawn at hormone drawn at baselinebaseline

– Repeat when glucose Repeat when glucose <35 mg/dl<35 mg/dl

ContraindicatedContraindicated– Elderly, CAD, seizuresElderly, CAD, seizures


Overnight Metyrapone Overnight Metyrapone testingtesting– Tests for secondary or Tests for secondary or

tertiary abnormalitiestertiary abnormalities– Blocks 11Blocks 11ββ--

deoxycortisol to cortisoldeoxycortisol to cortisol– Can initiate adrenal Can initiate adrenal

crisiscrisis– Useful in determining Useful in determining

return of function from return of function from steroid suppressionsteroid suppression

Normal resultNormal result– Increased ACTHIncreased ACTH– Increased 11Increased 11ββ--

deoxycortisoldeoxycortisol Metyrapone is difficult Metyrapone is difficult

to obtainto obtain


Secondary causeSecondary cause– Normal renin-Normal renin-

angiotensin systemangiotensin system Normal kalemiaNormal kalemia No hyperpigmentation No hyperpigmentation

Baseline critical Baseline critical samplessamples– Hypoglycemia or Hypoglycemia or

hypotensionhypotension– Metabolic panel, CBC, Metabolic panel, CBC,

Cortisol, ACTHCortisol, ACTH– Thyroid function studiesThyroid function studies

High dose- High dose- – 250 mcg ACTH250 mcg ACTH– Evaluates primary Evaluates primary

diseasedisease– Critically ill Critically ill – Inpatient settingInpatient setting

Low doseLow dose– 1 mcg ACTH1 mcg ACTH– Evaluates primary Evaluates primary

Secondary if long Secondary if long standingstanding

Outpatient settingOutpatient setting Evaluating for return of Evaluating for return of

adrenal functionadrenal function

SteroidsSteroidsPotencyPotency

SteroidSteroid Anti-Anti-InflammatorInflammator

y Actiony Action

HPA HPA SuppressioSuppressio

nn

Salt Salt RetentioRetentio

nn

CortisolCortisol 11 11 11

PrednisolonePrednisolone 33 44 0.740.74

MethylprednisoloMethylprednisolonene

6.26.2 44 0.50.5

DexamethasoneDexamethasone 2626 1717 00

FludrocortisoneFludrocortisone 1212 1212 125125

Adrenal CrisisAdrenal CrisisInpatient TreatmentInpatient Treatment

Fluid resuscitationFluid resuscitation– Saline and dextroseSaline and dextrose

Hydrocortisone Hydrocortisone (Solucortef)(Solucortef)– 100 mg IV bolus 100 mg IV bolus

then 100mg IV then 100mg IV Q6hrsQ6hrs

Once stableOnce stable Wean hydrocortisoneWean hydrocortisone

– 50 mg IV Q6-8hrs50 mg IV Q6-8hrs– Taper and transition Taper and transition

to oral therapyto oral therapy If primaryIf primary

– Once saline Once saline heplockedheplocked

– Start Florinef Start Florinef (fludrocortisone 0.1 (fludrocortisone 0.1 mg PO QD)mg PO QD)

Outpatient TreatmentOutpatient Treatment CortisolCortisol

– HydrocortisoneHydrocortisone 10mg AM and 5 mg PM10mg AM and 5 mg PM 6-8 mg/m6-8 mg/m22/day/day Stress dosingStress dosing

– Fever, illness, surgeryFever, illness, surgery– 20 mg/m20 mg/m22/day/day– Double or triple daily Double or triple daily

dosedose– 100 mg x1 then 25-50 100 mg x1 then 25-50

mg Q6-8hrsmg Q6-8hrs

All adrenal insufficient All adrenal insufficient patients need a patients need a medic alert braceletmedic alert bracelet

Outpatient TreatmentOutpatient Treatment

Alternative glucocorticoid Alternative glucocorticoid replacementreplacement– Dexamethasone 0.5 mg (0.25-0.75) per Dexamethasone 0.5 mg (0.25-0.75) per

dayday– Prednisone 5 mg (2.5-7.5) per dayPrednisone 5 mg (2.5-7.5) per day

Florinef dosingFlorinef dosing– Usual production 100mcg per dayUsual production 100mcg per day– 0.05-0.2 mg (50-200mcg) per day0.05-0.2 mg (50-200mcg) per day

Questions?Questions?

adrenal physiology and hypofunctioning states heidi chamberlain shea, md endocrine associates of...

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