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


 

Adrenal Cortex
Adrenocortical secretions make it possible for the body to adapt to stress Produces: glucocorticoids, mineralocorticoids, sex hormones GLUCOCORTICOIDS
Glucose metabolism Hydrocortisone (prototype) Corticosteroid: Inhibit inflammatory response and suppress allergic manifestations S/E: DM, osteoporosis, peptic ulcer, increased protein breakdown leading to muscle wasting and poor wound healing, and redistribution of body fat

A.

B.

MINERALOCORTICOIDS
Electrolye metabolism Renal tubular and G.I. epithelium (Na, K, 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, in excess, MASCULINIZATION (adrenogenital syndrome)

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

Manifestation of Pheochromocytoma
 Depends on the amount of catecholamines secreted implications?  HPN (250/ 150) and CV disturbances  Tremor, headache, flushing, and anxiety  Hyperglycemia implication?  Triad:
 Headache  Diaphoresis  Palpitations

 Vertigo, blurring of vision, tinnitus, air hunger and dyspnea  Polyuria, nausea, vomiting, diarrhea, abdominal pain, feeling of impending doom  Postural Hypotension if untreated

Assessment and Diagnostics

 Increase sympathetic activity with marked elevation of BP  Five Hs : HPN, Headache, hyperhidrosis, hypermetabolism, hyperglycemia  Urine and plasma catecholamines most direct and conclusive Dx (3x normal)
     Avoid meds and food (stimulants; aspirin) Urine: 2 3 hour after attack of HPN Epi. > 400 pg/ mL or norepi. > 2,000 pg/mL Patient supine and at rest for 30 minutes Use butterfly needle, scalp vbein needle or venous catheter 30 mins

 Clonidine (Catapress) suppression test

 Normal if: after 2 3 hrs., catecholamines is < 40 % from baseline

 Imaging studies  131I-metaiodobenzylguanidine MIBG specific isotope targeting catecholamine producing tissue

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, after surgery  Nipride and alpha-blockers during and after surgery alpha-

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

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

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

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

b. Addisons

Crisis precipitated by cold, infection or in general

stress - Hypotension (dehydration & SNS) - Rapid, weak pulse - Rapid respiratory rate - Pallor and extreme weakness - Hyperthermia 2. Laboratory and Diagnostic Findings a. Suggestive finding - Serum blood glucose is decreased - Serum sodium level is decreased - Serum potassium level is increased - White blood cell count is increased b. Definitive findings: - Serum cortisol & ACTH - Stimulation and Suppression tests ex. ACTH and Metyrapone

Medical & Nursing Management

PRIORITY : SHOCK 1. Administer prescribed medications
- May include synthetic glucocorticosteroids (prednisone) and mineralocorticosteroids (Florinef)

2. Provide immediate treatment for an addisonian crisis - Hydrocortisone (Solu-cortef) IV (Solu- 5 % dextrose in normal saline 2 function - Vasopressor amine if hypotension persist - Antibiotics - Initiate oral intake as soon as tolerated - Other treatment for shock

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, 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, 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.

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

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

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

Assessment Findings
1. Clinical manifestation
a. Weight gain and altered fat metabolism/ redistribution of fat (GH on adipose)
a. Central obesity/ truncal obesity b. Buffalo hump c. Moon face

b. Muscle weakness, proximal muscle wasting, and fatigue c. Frequent infections and poor wound healing d. Symptoms of hyperglycemia e. Mental status changes and mood swings f. Menstrual disturbances such amenorrhea

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

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

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

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

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

Clinical Manifestation
 Profound Hypokalemia and decrease in H+
    

Muscle weakness, cramping, and fatigue Inability of the kidney to acidify or concentrate the urine Polyuria ---- 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; secondary increase in blood volume  Decrease serum Ca due to hypokalemic alkalosis  Glucose intolerance due to hypokalemic alkalosis action on pancreas

Assessment and Diagnostics

   
High or normal Sodium level Low serum Potassium High serum Aldosterone Low serum Renin

 Aldosterone excretion rate after salt loading --- 1o

Management
 Surgery removal of the tumor(Adrenalectomy)
 Will address the problem of Hypokalemia

 Spironolactone for HPN