6.28.10 Barnes Adrenal Insufficiency

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Transcript of 6.28.10 Barnes Adrenal Insufficiency

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    Adrenal Insufficiency

    UNC Internal Medicine Morning ReportJune 28, 2010

    Edward L. Barnes, MD

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    Adrenal Insufficiency

    Primary Adrenal Insufficiency is also known

    as Addisons Disease in honor of Dr. Thomas

    Addison

    Born in April 1793, at Long Benton,

    Newcastle-upon-Tyne and died on June 29

    1860, at 15 Wellington Villas, Brighton Dr. Addison is also credited with the discovery

    of Pernicious Anemia

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    Introduction

    Adrenocorticotropic Hormone (ACTH) is the

    major factor in the secretion of cortisol and

    androgenic steroids by the adrenal cortex

    ACTH secretion is regulated as a balance

    between the stimulatory effects of CRH

    (mediated by the CNS) and the negativefeedback mediated by circulating levels of

    glucocorticoids

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    Adrenal Insufficiency

    Arises when cortisol levels are not sufficient to

    meet the needs of the body

    Cortisol aids in maintaining vascular tone,

    hepatic gluconeogenesis, and in maintaining

    glycogen

    Inadequate cortisol in times of stress can leadto hypotension, shock, and hypoglycemia

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    Adrenal Insufficiency

    Mineralocorticoid deficiency typically leads to

    renal wasting of sodium, retention of

    potassium, and reduced intravascular volume

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    Primary Adrenal Insufficiency

    Most commonly is of an autoimmune etiology,resulting from chronic destruction of the adrenalcortex

    Typical histologic feature is lymphocytic infiltration

    Antibodies to adrenal cortical antigens are presentearly in the disease process

    Patients with autoimmune adrenal disease are morelikely to have polyglandular autoimmune systemscausing deficiency of other endocrine glands

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    Primary Adrenal Insufficiency

    Several Other Mechanisms Exist:

    Bilateral adrenal hemorrhage

    Infection: Tuberculosis, CMV, Histoplasmosis Metastatic Disease

    Deposition Diseases: Hemochromatosis, Amyloidosis,

    Sarcoidosis

    Drug Induced: Ketoconazole, Etomidate, Rifampin,Anticonvulsants

    Congenital Adrenal Hyperplasias

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    Secondary Adrenal Insufficiency

    Caused by pituitary failure of ACTH secretion

    Etiologies include:

    any cause of primary or secondary

    hypopituitarism

    Exogenous Glucocorticoid Therapy

    Megestrol, which has some glucocorticoid therapy

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    Clinical Presentation

    Acute adrenal insufficiency (Adrenal Crisis)

    should be expected in any patient acute,

    unexplained volume depletion and shock

    Hyperkalemia, acidosis, and hypoglycemia

    may also be accompanying

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    Clinical Presentation

    Chronic insufficiency typicallydevelops more insidiously

    Symptoms may include weakness,weight loss, nausea, vomiting,

    anorexia, and posturalhypotension

    Increased skin pigmentation canbe seen with primary adrenalinsufficiency secondary tomelanocyte stimulating activityassociated with ACTH

    Hyponatremia and Hyperkalemiamay develop secondary to a lackof aldosterone

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    Clinical Presentation

    Secondary Adrenal Insufficiency may present

    with evidence of adrenal insufficiency as well

    as other evidence of hypopituitarism

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    Differential Diagnosis

    Acute Adrenal insufficiency

    Various conditions can cause hypotension and or shock

    Chronic Adrenal Insufficiency Chronic Starvation (anorexia nervosa)

    Gastrointestinal Disease secondary to inflammation or

    malignancy

    Other causes of hyperpigmentation including drugexposures

    Other causes of fatigue and malaise

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    Diagnostic Workup

    Baseline Cortisol and ACTH levels should be

    obtained in the early morning

    A morning cortisol level of

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    Diagnostic Workup

    Cosyntropin Stimulation Test Measure morning cortisol level (pre-test level)

    Administer 1 mg dose Cosyntropin

    Measure a second cortisol level 1 hour after Cosyntropinadministration

    Normal response demonstrates a level of greater than 20 mg/dLafter cosyntropin

    Patients with both primary and secondary adrenal insufficiency willnot demonstrate appropriate response

    Patients with primary insufficiency will fail to respond torepeated administrations, however patients with secondaryinsufficiency may show an increased response to repeatedtesting/stimulation

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    Diagnostic Workup

    Further determination of primary vs. secondary

    adrenal insufficiency will be based upon ACTH

    level High ACTH level expected in primary

    insufficiency

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    Treatment: Acute Adrenal

    Insufficiency Treat Acute Adrenal Insufficiency with

    Hydrocortisone 50-100 mg IV q8 hrs

    In addition, volume resuscitate with Normal Saline

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    Treatment: Chronic Adrenal Insufficiency

    Hydrocortisone 20-30 mg po daily

    Typically divide dose 2/3 in am, 1/3 in pm

    May use Prednisone 5 mg po daily instead Fludrocortisone 0.05-0.1 mg po qam

    Not necessary in patients with secondary adrenal

    insufficiency

    Provide instruction for periods of acute illness or

    increased stress

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    The End

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    References:

    1. Pearce, JMS. Thomas Addison. J R Soc Med. 2004 June; 97(6): 297300.

    2. Ontjes, DA. Disorders of the Adrenal Cortex. Netters Internal Medicine, 2nd ed. 2009; 321-4.

    3. Adrenal Insufficiency. Little: Dental Management of the Medically Compromised Patient, 7th

    ed. 2007.

    4. Oelkers, W. Adrenal Insufficiency. N Engl J Med. 1996 Oct 17;335(16):1206-12.