Adrenal Disorder

Adrenal Gland 
2 adrenal gland, attached to upper portion of kidney  2 areas: medulla and cortex  Medulla ± catecholamines  Cortex ± steroid hormones  Regulated by hypothalamic-pituitaryhypothalamic-pituitaryadrenal axis (negative feedback mech.)  CRH ± ACTH ± Glucocortecoid hormone (cortisol)

Adrenal Function  Adrenal Medulla  Part of ANS  Catecholamines promote catabolism of stored fuels  Flight ± or ± fight response  SNS response .

mineralocorticoids.   Adrenal Cortex Adrenocortical secretions make it possible for the body to adapt to stress Produces: glucocorticoids. H) Stimulated by ACTH ± minimal Angiotensin II ± main stimulus Also stimulated by hyperkalemia C. ADRENAL SEX HORMONES (Androgen) ± ± Similar effects as male sex hormones In normal amount have little effect. sex hormones GLUCOCORTICOIDS ± ± ± ± Glucose metabolism Hydrocortisone (prototype) Corticosteroid: Inhibit inflammatory response and suppress allergic manifestations S/E: DM. K. B. osteoporosis. and redistribution of body fat A.I. MASCULINIZATION (adrenogenital syndrome) . peptic ulcer. epithelium (Na. in excess. MINERALOCORTICOIDS ± ± ± ± ± Electrolye metabolism Renal tubular and G. increased protein breakdown leading to muscle wasting and poor wound healing.

PHEOCHROMOCYTOMA  Tumor of the chromaffin cells of the adrenal medulla  May be extra adrenal (near aorta. spleen and other organs)  Peak incidence is at 40 ± 50 y. ovaries.  Strong familial involvement or predisposition ± implication?  Causes HPN that is curable by surgery .o.

feeling of impending doom  Postural Hypotension if untreated . headache. nausea. air hunger and dyspnea  Polyuria. vomiting. flushing. tinnitus. and anxiety  Hyperglycemia ± implication?  Triad:  Headache  Diaphoresis  Palpitations  Vertigo. blurring of vision. diarrhea.Manifestation of Pheochromocytoma  Depends on the amount of catecholamines secreted ± implications?  HPN (250/ 150) and CV disturbances  Tremor. abdominal pain.

aspirin) Urine: 2 ± 3 hour after attack of HPN Epi. catecholamines is < 40 % from baseline  Imaging studies  131I-metaiodobenzylguanidine MIBG ± specific isotope targeting catecholamine producing tissue .Assessment and Diagnostics  Increase sympathetic activity with marked elevation of BP  Five Hs : HPN. Headache. hypermetabolism. > 400 pg/ mL or norepi. hyperhidrosis. scalp vbein needle or venous catheter ± 30 mins  Clonidine (Catapress) suppression test  Normal if: after 2 ± 3 hrs.000 pg/mL Patient supine and at rest for 30 minutes Use butterfly needle. hyperglycemia  Urine and plasma catecholamines ± most direct and conclusive Dx (3x normal)      Avoid meds and food (stimulants. > 2..

after surgery  Nipride and alpha-blockers during and after surgery alpha- .Management  Bed rest and elevate HOB ± during attack  Alpha-adrenergic blocking agents (phentolamine Alpha[regitine])  Smooth muscle relaxants (Sodium nitroprusside [Nipride]) ± quick  Phenoxybenzamine (Dibenzyline) ± long-acting longalphaalpha-blocker  Beta-adrenergic Blocker Beta Catecholamine synthesis inhibitors ± alphaalphamethylmethyl-p-tyrosine (metyrosine)  Surgery ± ADRENALECTOMY  Provide hydration before.during.

 Emphasize need for follow-up check up followand monitoring of BP  Emphasize the need for family member to undergo screening .Nursing Management  Teach client that need for corticosteroid use after surgery ± provide info.

ADDISON·S DISEASE  ADRENOCORTICAL INSUFFICIENCY Etiology: 1. Adrenalectomy d. Neoplasm e. Tuberculosis 2. hemorrhage into the gland c. Inadequate cortisol replacement. Suppression of the H-P axis from exogenous steroid use Hb. Pituitary destruction or removal c. Fungal infection d. esp. during time of stress . Addison¶s disease: a. Secondary adrenal insufficiency a. autoimmune or idiopathic b.

Hypoglycemia .Pathophysiology: Deficiencies of adrenocortical hormones.Increased WBC .Hyperkalemia . and metabolic disturbances. . Results to fluid. electrolyte.Hyponatremia .

nausea. and possible increased pigmentation with ACTH stimulation . and arthralgias . decreased body hair.GI complaints. Clinical manifestation a. abdominal pain. Addison¶s disease .Dry skin.Decrease alertness and confusion .Fatigue. anorexia. and diarrhea . vomiting. muscle weakness.Assessment Findings 1.weight loss .

ACTH and Metyrapone . Definitive findings: .Serum potassium level is increased .Hypotension (dehydration & SNS) . weak pulse .Serum blood glucose is decreased .Serum cortisol & ACTH .Pallor and extreme weakness .b. Laboratory and Diagnostic Findings a.Hyperthermia 2.Rapid respiratory rate .White blood cell count is increased b.Serum sodium level is decreased . Addison¶s Crisis ± precipitated by cold. infection or in general stress .Stimulation and Suppression tests ex.Rapid. Suggestive finding .

Provide immediate treatment for an addisonian crisis .5 % dextrose in normal saline ± 2 function .Medical & Nursing Management PRIORITY : SHOCK 1.Initiate oral intake as soon as tolerated .Hydrocortisone (Solu-cortef) IV (Solu.Antibiotics .Other treatment for shock . Administer prescribed medications .Vasopressor amine ± if hypotension persist .May include synthetic glucocorticosteroids (prednisone) and mineralocorticosteroids (Florinef) 2.

maximal suppression of the gland)  4pm ± 6am ± serum levels are normally low (mnimizing cushingoid effect)  Up to 1 year or more after use of corticosteroid the patient is still at risk for adrenal insufficiency in times of stress. a once a day or every-other-day may be every-otherimplemented  Best time for total corticosteroid is early in the morning from 7 to 8 AM  Large dose therapy at 8 am (gland is most active. .Therapeutic uses of Cortecosteriods  2 weeks of corticosteroid therapy may suppress the adrenal gland for up to a year  Gradually reduced and tapered  When symptoms have been controlled on a 6-hour or 8 ± 6hour program.

3.Teach signs of under-dosing and over dosing under- . single-injection syringes of singlecorticosteroid .) .Supplementary intake of additional salt in times of GI disturbance and very hot weather 4.Preloaded. procedures.Medical alert bracelet .Discuss hormone therapy . Help prevent adrenal crisis . Provide client and family teaching .Need for lifelong hormone therapy . ect.Additional corticosteroid therapy in times of stressful events (illness.

Ectopic ACTH production from other organs 4. Glucocorticoid therapy   . but also androgen and mineralocorticoids  Women > Men Etiology: 1.CUSHING·S SYNDROME Results from excessive adrenocortical activity Primarily cortisol. The most common cause of adrenal insufficiency is bilateral adrenal hyperplasia 2. Adrenal neoplasm 3.

Pathophysiology  The normal feedback mechanism that control the function of the adrenal cortex become ineffective. and the usual diurnal pattern of cortisol is lost .

Mental status changes and mood swings f. proximal muscle wasting.Assessment Findings 1. Moon face b. Clinical manifestation a. Weight gain and altered fat metabolism/ redistribution of fat (GH on adipose) a. Symptoms of hyperglycemia e. Muscle weakness. Central obesity/ truncal obesity b. Menstrual disturbances such amenorrhea . Frequent infections and poor wound healing d. Buffalo hump c. and fatigue c.

bruises. Susceptibility to compression fractures f. Sleep pattern disturbance ± altered diurnal secretion of cortisol . Diminished libido b. Skin changes. acne. edema g. bruises. and thinning of scalp HPN c. such as striae. Visual disturbance (ptuitary) h. hair d. Hirsutism ( VIrilization) e.a.

Serum potassium level is decreased -./ b. Serum glucose level is elevated ± DM c.2. Diurnal variation plasma levels reveal elevated plasma cortisol and 24 hour urine cortisol result e. Dexamethasone suppression test ± administration of 1 mg dexa. Laboratory and Diagnostic study findings a. d.normal < 5mg/ dL coortisol f. WBC reveals depressed eosinophils and lymphocyte counts. Plasma ACTH (determine if 1o or 2o) . The night before (11pm ± 8am test) .

Adrenal enzyme inhibitors ± ectopic ACTH secretion for signs of adrenal insufficiency 12 ± 48 hrs p op .alternate ± day dose . Adrenalectomy ± tx of choice for primary adrenal hypertrophy .why not stop? . aminoglutethimide. Metyrapone.may warrant temporary replacement 3. ketoconazole 4.Medical Management PRIORITY: HPN & HF 1. Reduce or taper dose if cause by administration of corticosteroid --. mitotane. Transphenoidal hypophysectomy/ Radiations ± pros & con pituitary tumors 2.

protect patient from falls. insomnia ± why????  Avoid using adhesive tape ± Why???  Provide meticulous skin care--. fractures. wasting. fatigue.assess skin and bony prominences care--and change position  Give info about Corticosteroid therapy --.but this is Cushings????  Advice patient in wearing Medical alert bracelet . low sodium and low calories  Watch for subtle signs of infection. during and after)  Encourage moderate activity in spite of difficulty from weakness.Why?  Assist patient with ambulation if very weak  Provide foods high in CHON. OCCULT (before.why? Give 2  ANTI-ULCER MEDS ---. ± Fever?  Avoid unnecessary exposure to others with infection  Prepare patient for surgery  INSULIN THERAPY ---.Nursing Management  Reduce safety hazards. and other injures to bones and soft tissue ---. calcium and Vit D.why? ANTI CBG.

PRIMARY ALDOSTERONISM  Excessive production of aldosterone that occurs in some patient with functioning tumors of the adrenal gland. .

and fatigue Inability of the kidney to acidify or concentrate the urine Polyuria ---. secondary increase in blood volume  Decrease serum Ca ± due to hypokalemic alkalosis  Glucose intolerance ± due to hypokalemic alkalosis action on pancreas .Clinical Manifestation  Profound Hypokalemia and decrease in H+      Muscle weakness.contradictory question anyone? Polydipsia due increase osmolality Increase pH and bicarbonate  Sodium may be normal or elevated ± depends on amount of water reabsorbed with sodium  Hypertension ± most prominent and universal sign. cramping.

1o .Assessment and Diagnostics     High or normal Sodium level Low serum Potassium High serum Aldosterone Low serum Renin  Aldosterone excretion rate after salt loading --.

Management  Surgery ± removal of the tumor(Adrenalectomy)  Will address the problem of Hypokalemia  Spironolactone ± for HPN .

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