Physiology of adrenal gland Glucocorticoids-Corti of adrenal gland Anatomy ! Weight = 4g ! 2 adrenal…

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  • Phys io logy o f adrena l g land


    Weight = 4g 2 adrenal gland, right and left 2 component inner adrenal medulla and outer adrenal cortex situated near upper poles of kidney in retroperitoneum within Gerotas capsule

    Adrena l hormones

    Glucocorticoids-Cortisol Mineralocorticoids-Aldosterone Androgens-DHEA(S), testosterone, androstenedione Estrogens Catecholamines-Epinephrine, Dopamine

    Cor t iso l Da i ly

    ACTH/Cor t iso l Trends

    ACTH is the principal regulator of Glucocorticoids secretion. Secretion of ACTH and glucocorticoids exhibit a diurnal rhythm, s t imu la ted by stress and inh ib i ted by circulating glucocorticoids. Endogenous production of cortisol averages 20 mg \ day.

    Ac t ions o f G lucocor t ico ids

    Maintains metabo l ic homeostasis Regulates blood glucose levels Raises insulin levels Increases catabolism/decreases anabolism Inh ib i ts reproductive, thyroid and growth hormone

    axes Minera locor t ico id activity of cortisol

    Affects connect ive tissue Causes loss of collagen Loss of connective tissue Inhibits fibroblasts Inhibits bone formation/incr. resorption

    Maintains card iovascu lar function Increases cardiac output Increases vascular tone Permissive effects on pressor hormones Increases sodium retention

    Affects behav ior and cogn i t i ve function Affects immune system

    Decrease # of circulating lymphocytes, monocytes, and eosinophils

    decrease migration of PMNs to sites of injury Regulates about 25% of human genome

    Ren in-Ang io tens in-A ldosterone

    Act ions

    Angiotensin II vasopressor stimulates aldosterone

    Aldosterone Activates sodium/potassium pump Increases plasma sodium Decreases plasma potassium Decreases plasma hydrogen

    *A ldosterone s t imu la ted by RAS, ACTH, Hyperkalemia, hypovolemia, hypotension, CHF, Surgery

  • Adrena l insu f f i c iency

    S tages in Deve lopment o f Pr imary Adrena l

    Insu f f i c iency

    Stage1- renin rises, aldosterone normal Stage 2- ACTH rises, cortisol normal Stage 3- impaired cortisol response to ACTH Stage 4- aldosterone levels drop Stage 5- cortisol levels drop

    E t io logy o f adrena l

    insu f f i c iency

    Primary adrenal insufficiency Secondary adrenal

    insufficiency Chronic adrenal insufficiency Acute adrenal insufficiency

    Usually occurs after a prolonged of non specific complains

    Is more frequently observed in patients with primary adrenal insufficiency

    D i f fe rent Types o f G lucocor t ico id

    Insu f f i c iency

    Primary Adrenal Insufficiency Glucocorticoid and Mineralocorticoid Insufficiency Compensatory Increase in POMC (hyperpigmentation)

    Secondary (Central) Adrenal Insufficiency Glucocorticoid Insufficiency On ly

    Glucocorticoid Withdrawal Glucocorticoid Insufficiency On ly

    Pr imary adrena l insu f f i c iency

    1. Is most commonly caused by autoimmune adrenalitis Isolated autoimmune adrenalitis accounts for 30 40

    % 60 70% develop adrenal insufficiency as part of

    autoimmune polyglandular syndrome (APS) APSH, APS2

    2. Congenital adrenal hyperplasia 3. infection / hemorrhage/ infiltration/ tuberculous adrenalitis /

    adrenal metastases (rarely caused adrenal insufficiency and this occurs only with bilateral bulky metastases)

    Secondary adrena l

    insu f f i c iency

    Is the consequence of dysfunction of hypothalamic pituitary component of the HPA axis Majority of cases are caused by

    Pituitary tumor Pituitary irradiation Pituitary apoplexy/hemorrhage Pituitary infiltration Drug induced Congenital isolated ACTH deficiency

    Glucocorticoid Withdrawal Glucocorticoid Insufficiency On ly

  • C l in ica l presenta t ion

    Pr imary adrena l insu f f i c iency are character ized by the loss o f both g lucocor t ico id and minera locor t ico id secre t ion

    Hyponatremia is a characteristic biochemical feature in primary adrenal insufficiency and is found in 80% of patient at presentation Hyperkalemia is present in 40% of patient at initial diagnosis

    Secondary adrena l insu f f i c iency. On ly g lucocor t ico id de f ic iency is present Due to diminished inhibition of ADH by cortisol, resulting in mild symptoms of inappropriate secretion of antidiuretic hormone (SIADH) Glucocorticoid deficiency increased TSH

    Adrenal androgen secretion is disrupted in both primary and secondary adrenal insufficiency

    Chron ic adrena l insu f f i c iency

    Non specific sign and symptoms such as fatigue and loss of energy A distinguishing feature of primary adrenal insufficiency is hyperpigmentation, which is caused by excess ACTH stimulation of melanocytes.

    Hyperpigmentation is most pronounced in skin areas exposed to increased friction or shear stress and is increased by sunlight Conversely, in secondary adrenal insufficiency then skin has an alabaster like paleness due to lack of ACTH secretion

    Adrena l Cr is is

    Usually in Patients with Primary Adrenal Insufficiency Precipitated by Stress Newly diagnosed vs. established patient

    stopped medicines illness vomiting

    Presentation of Adrenal Crisis (usually primary adrenal insufficiency) Hypotension/shock (90%) Abdominal pain (80%) DD Acute abdomen Fever (65%) Anorexia/nausea/vomiting (60%) Confusion (40%) Hyponatremia/hyperkalemia/acidosis (80%) Hypoglycemia (20%)

    D iagnos is o f Adrena l

    Insu f f i c iency

    Laboratory Findings of Primary Adrenal Insufficiency Hyponatremia Hyperkalemia Hypoglycemia Lymphocytosis Eosinophilia Mild normochromic Anemia

    Cosyntrop in tes t A safe and reliable tool with excellent predictive diagnostic value The cut off for failure is usually defined at cortisol levels of 12 ug/dl

    respectively. 2. Should on ly be done in subjects with signs/symptoms of adrenal insufficiency or history consistent with it. 3. Can be used in those patients with a moderate index of suspicion. 4. Measurement of ACTH levels can differentiate between primary and secondary insufficiency 5. Consistently high ACTH can be a sign of early adrenal insufficiency

    Workup/Treatment for Suspected Adrena l Cr is is

    Establish IV access Draw blood for electrolytes, glucose, cortisol, ACTH,

    aldosterone and plasma renin activity Infuse up to 3 liters of normal saline

    Follow fluid status Give 100 mg of IV hydrocortisone Supportive Measures

    Treatment o f acute adrena l insu f f i c iency

    1. Immediate initiation of rehydration, usually carried out by saline infusion at initial rates of 1L/H 2. Continuous cardiac monitoring 3. Glucocorticoid replacement should be initiated by bolus injection of 100mg hydrocortisone 4. Followed by the administration of 100 200 mg hydrocortisone over 24hours either by continuous infusion or provided by several IV or IM

    injection 5. Mineralocorticoid replacement can be initiated once the daily hydrocortisone dose has been reduced to