ADRENAL GLANDS Zelne Zamora, DNP, RN

LAUGHTER IS THE BEST MEDICINE

PHYSIOLOGY Adrenal medulla secretes catecholamines Adrenal cortex secretes steroid hormones

ADRENAL MEDULLA ANS Epinephrine, Norepinephrine Regulate metabolic pathways Release free fatty acids ↑ basal metabolic rate ↑ blood glucose level

HYPOTHALAMIC PITUITARY ADRENAL AXIS Hypothalamus secretes corticotropin-releasing hormone (CRH) Pituitary gland stimulated, secretes adrenocortiotropic hormone (ACTH)

HYPOTHALAMIC PITUITARY ADRENAL AXIS Stimulates adrenal cortex to secrete glucocorticoids Increased levels of adrenal hormone inhibit production or secretion of CRH and ACTH

NEGATIVE FEEDBACK

ADRENAL CORTEX Glucocorticoids Mineralocorticoids Sex hormones (Sugar hormone) Hydrocortisone Mineralocorticoids (Salt hormone) Aldosterone Sex hormones Androgens

GLUCOCORTICOIDS Affect glucose metabolism ↑ hydrocortisone causes ↑ blood glucose levels Secreted in response to the release of ACTH Negative feedback Glucocorticoids in the blood inhibit the release of CRH from the hypothalamus and also inhibits ACTH secretion from the pituitary resulting in decrease ACTH secretion and decrease release of glucocorticoids from the adrenal cortex

GLUCOCORTICOIDS Corticosteroids Exogenous glucocorticoids Inhibit the inflammatory response Suppress allergic reactions Side effects Diabetes mellitus Osteoporosis Peptic ulcer Increased protein breakdown Muscle wasting Poor wound healing Redistribution of body fat

GLUCOCORTIOIDS Exogenous glucocorticoids Large amounts inhibit release of ACTH and endogenous glucocorticoids Adrenal cortex atrophy Adrenal insufficiency

MINERALOCORTICOIDS Electrolyte metabolism Renal tubular and GI epithelium Increased sodium absorption, excretion of potassium or hydrogen Secreted in response to angiotensin II

MINEARLOCORTICOIDS Increase aldosterone promotes sodium reabsorption Increased by hyperkalemia Primary hormone for long-term regulation of sodium balance

ANDROGENS (Sex hormones) Effects similar to male sex hormone Secrete small amount of estrogen Controlled by ACTH

ADRENOCORTICAL INSUFFICIENCY Primary Autoimmune Idiopathic Surgical Removal Infection Tuberculosis Histoplasmosis Cancer Secondary Inadequate secretion of ACTH from pituitary gland Hypothalamic dysfunction

ADDISON’S DISEASE Chronic primary adrenocortical insufficiency Deficiency of all 3 hormones Glucocorticoids Mineralocorticoids: Aldosterone Sex hormones: Androgens

CLINICAL MANIFESTATIONS Onset is insidious Progresses over weeks to months Hyponatremia Dehydration Hypotension Hyperkalemia

CLINICAL MANIFESTATIONS Hypoglycemia Weakness Fatigue Weight loss Dark pigmentation of oral mucosa and skin Decreased axillary and pubic hair

CLINICAL MANIFESTATIONS Depression Emotionally labile Apathy Confusion

ASSESSMENT AND DIAGNOSTIC FINDINGS Primary insufficiency ↓ Aldosterone level ↓ Cortisol level Hypoglycemia Hyponatremia Hyperkalemia ↑ BUN ↑ Hematocrit ACTH Stimulation Test Primary ↑ ACTH ↓ Cortisol Secondary ↓ or normal ACTH Gradual ↑ in Cortisol Early morning serum cortisol and plasma ACTH are performed to differentiate primary adrenal insufficiency from secondary adrenal insufficiency from normal adrenal function

MEDICAL MANAGEMENT Mineralocorticoid Fludrocortisone acetate (Florinef) Correct fluid and electrolyte imbalance Glucocorticoids Corticosteroids Hydrocortisone (Solu-Cortef) IV Check blood glucose

SIDE EFFECTS ↑ Blood glucose Delayed wound healing Infection Ulcers or gastritis Weight gain Hypertension Insomnia Avoid abrupt withdrawal

ADDISONIAN CRISIS Most common cause Sudden cessation or withdrawal of corticosteroids Infection Surgery Trauma

CLINICAL MANIFESTATIONS Cyanosis Pallor Apprehension Rapid and weak pulse Rapid respirations Hypotension Disease progression and acute hypotension Circulatory shock Overexertion can put a patient into addisonian crisis: exposure to cold, acute infection, decrease in salt intake

ADDISONIAN CRISIS Headache Nausea Abdominal pain Diarrhea Confusion Restlessness

MEDICAL MANAGEMENT Steroids Fluid replacement Vasopressors Antibiotics Hydrocortisone IV then Prednisone PO Fluid replacement NS or plasma Vasopressors Antibiotics Oxygen Monitor BP Electrolytes Blood glucose EKG I & O

PREVENTION Do not stop steroids abruptly Take medication as prescribed Notify physician if anticipating stressful situation Cortisone IM Medic-alert bracelet

CUSHING’S SYNDROME Hyperfunction Primary Secondary Iatrogenic Glucocorticoid oversecretion Primary Cortisol-secreting adrenal tumors Benign or malignant Secondary ACTH secreting tumor Pituitary or hypothalamus Iatrogenic Overdosage of glucocorticoids

CLINICAL MANIFESTATIONS Hyperglycemia Protein tissue wasting Muscle weakness and wasting Thin extremities Bruising Osteoporosis Delayed wound healing

CLINICAL MANIFESTATIONS Abnormal fat distribution Truncal obesity Striae Cervical fat pad Moon face

CLINICAL MANIFESTATIONS Hypokalemia Cardiac arrhythmias Muscle weakness Edema Weight gain Increased susceptibility to infection

ASSESSMENT AND DIAGNOSTIC FINDINGS Laboratory Values ↑ plasma cortisol and urinary cortisol excretion ↑ blood glucose ↑ Sodium ↓ Potassium Plasma ACTH ACTH Suppression Test Administer dexamethasone Check cortisol levels Positive for Cushing’s syndrome if cortisol levels rise

MEDICAL MANAGEMENT Adrenalectomy Medications Mitotane (Lysodren) Aminogluethimide (Cytadren) Metyrapone (Metopirone)

NURSING MANAGEMENT Pre-operative Administer glucocorticoid Operative Hydrocortisone or cortisol continuous IV Post-operative Bleeding Addisonian Crisis Prevent infection NPO Replacement hormones

HYPERALDOSTERONISM Primary Conn’s syndrome Adrenal tumor Typically benign Secondary Alteration in RAAS Renal artery disease Cardiac failure

ASSESSMENT AND DIAGNOSTIC FINDINGS ↑ sodium and water ↓ potassium Polyuria Polydipsia Metabolic alkalosis No overt edema ↑ plasma and urine aldosterone level Plasma renin level CT Scan: Adrenal gland Variable causes Increased salt intake ACE-inhibitor ingestion

MEDICAL MANAGEMENT Surgical Adrenalectomy Medical Potassium Sparing Diuretic Spironolactone (Aldactone) Amiloride (Amiloride) ACE-inhibitor Enalapril (Vasotec)

CONGENITAL ADRENAL HYPERPLASIA Adrenogential syndrome Excessive androgen secretion Defective negative feedback mechanism Adrenal tumor that secretes androgens

CLINICAL MANIFESTATION Adult females Hirsutism Balding Breast atrophy Masculine body build Female infants Masculinization of external genitalia

CLINICAL MANIFESTATIONS Adult males Not so dramatic Boys may develop secondary sex characteristics early

MEDICAL MANAGEMENT Tumor Congenital Medications to restore negative feedback mechanism Decrease ACTH Reverse overproduction of androgens

ADRENAL MEDULLA Controlled by sympathetic nervous system Secretes catecholamines Increase of vitals Increase BMR Increase blood sugar Epinephrine and norepinephrine

MEDULLA HYPOFUNCTION Rarely causes problems Sympathetic nervous system produces similar effects

MEDULLA HYPERFUNCTION Caused by a pheochromocytoma Benign tumor Chromaffin cells of the adrenal medulla 40-50 years old Cause of high blood pressure in 0.1% of patients with HTN

CLINICAL MANIFESTATIONS Triad of Symptoms Headache Diaphoresis Palpitations Other Symptoms Tremor Flushing Anxiety Polyuria Nausea and vomiting Diarrhea Abdominal pain Impending doom

PAROXYSMAL PHEOCHROMOCYTOMA Characteristics Acute, unpredictable Seconds to hours Symptoms are abrupt and subside slowly Signs & Symptoms Extremely anxious Tremulous Weakness Vertigo Blurring of vision Tinnitus Air hunger Dyspnea

COMPLICATIONS Cardiac dysrhythmias Dissecting aneurysm Stroke Acute renal failure

ASSESSMENT Marked elevation of blood pressure Hypertension Headache Hyperhidrosis Hypermetabolism Hyperglycemia

DIAGNOSTIC FINDINGS Plasma and urine catecholamine and metanephrine 24-hour urine sample Free catecholamines Metanephrine Vanillymandelic acid Clonidine suppression test CT, MRI, and ultrasonography Most direct and conclusive tests for overactivity of the adrenal medulla Test results can be altered by medications, food (coffee, tea, chocolate) Total plasma catecholamine concentration is measured with the patient supine and at rest for 30 minutes Factors that elevate catecholamine concentration: tobacco use, emotional and physical stress, amphetamines, nose drops or sprays, decongestants, bronchodilators Clonidine suppression test: clonidine is a centrally acting antiadrenergic medication that suppresses the release of neurogenically mediated catecholamines. Pheochromocytoma, increased catecholamine levels result from the diffusion of excess catecholamines into the circulation, bypassing normal storage and release mechanism. Patients with pheochromocytoma, clonidine does not suppress the release of catecholamines. Imaging studies localize the pheochromocytoma and determine whether more than one tumor is present

PHARMACOLOGIC MANAGEMENT Alpha-adrenergic blockers Phentolamine (Regitinel) Smooth muscle relaxants Nitroprusside (Nipride) Long acting alpha-adrenergic blockers Phenoxybenzamine (Dibenzyline) Calcium channel blockers Nifedipine (Procardia) Beta blockers Propanolol (Inderal) Lower the blood pressure quickly

SURGICAL MANAGEMENT Adrenalectomy Surgical removal of the tumor Definitive treatment for pheochromocytoma

NURSING MANAGEMENT Pre-operative Stabilize blood pressure Nifedipine (Procardia) Nicardipine (Cardene) IV corticosteroids Methylprednisolone (Solu-Medrol) Post-operative IV corticosteroid replacement Methylprednisolone (Solu-Medrol) Oral corticosteriod replacement Prednisone

NURSING MANAGEMENT Blood pressure Blood glucose ECG changes Fluid and electrolyte balance

QUESTIONS