HTH SCI 2H03

Alana M., Larissa G., Diana Z., Jahziel T.

1) Identify and describe the pathophysiology and risk factors

associated with Addisons disease

2) Examine the clinical manifestations of Addisons disease 3) Discuss the diagnostic findings of Addisons disease 4) Describe the purpose of the prescribed orders 5) Identify the most common adverse reactions associated

with the prescribed medications

6) Discuss the management of hyponatremia and hyperkalemia found in Addisons disease

 Clinical Manifestations (signs and symptoms): -weakness, fatigue, anorexia, nausea, vomiting, and weight loss during the past month. -dizziness and weakness when getting out of bed in the morning or when standing from a sitting position for an extended period of time Past health history: Tuberculosis Respirations: 14 Vital signs: Blood pressure: 90/64 Temperature: 37.2 C Pulse: 126 ACTH: 24 pmol/L Lab results: Serum cortisol: 331 nmol/L CT scan: beginning atrophy of the Potassium: 6 mmol/L adrenal gland Sodium: 128 mmol/L MRI: negative for tumors or infections Medication Hydrocortisone (Cortisol) 30 mg IV three times per day Fludrocortisone acetate (Florinef) 0.1 mg PO daily

 Addison's disease is a

disorder that occurs when the adrenal glands do not produce enough of their hormones.(hypo-secretion of the hormones)

(Jenkins, N.,2010).

The adrenal glands are hormonesecreting organs anterior toeach kidney. Adrenal cortex Adrenal medulla Addison's disease results from the damage to the adrenal cortex. The damage causes the cortex to produce less of its hormones

The adrenal cortex produces three types of hormones: The glucocorticoid hormones (such as cortisol) Maintain glucose control Decrease immune response Respond to stress. The mineralocorticoid hormones (such as aldosterone) Regulate sodium and potassium balance. The sex hormones, androgens and estrogens affect sexual development and sex drive.

This damage may be caused by the following: The immune system mistakenly attacking the gland (autoimmune disease) Infections such as tuberculosis, HIV, or fungal infections Hemorrhage, blood loss Tumors Use of blood-thinning drugs (anticoagulants)

 Having the following autoimmune diseases can put you at risk for

an associated autoimmune-based Addisons disease: Hypopituitarism Type I diabetes Hyperthyroidism (Graves Pernicious anemia disease) or hypothyroidism Hypoparathyroidism (Hashimotos disease) Stress Myasthenia gravis Anticoagulant medications Abdominal injury Family members with autoimmune-caused Addison's disease Long-term steroid medication treatment, followed by: Surgery Severe stress Trauma Infection Previous surgery on adrenal glands

 Hyperpigmentation: skin (bronze tone), body creases, nipples, and mucous membranes Hypoglycemia, poor tolerance to stress, fatigue, muscle weakness

Weight loss: emaciation, anorexia, vomiting and diarrhea

Cardiac insufficiency; hypotension

Adrenal atrophy/destruction
Urinary losses: sodium, water

Retention of potassium

(Hannon et al., 2010)

Blood Test measures your blood levels of sodium, potassium, cortisol and ACTH ACTH Stimulation Test measures the level of cortisol in your blood before and after an injection of synthetic ACTH Insulin-Induced Hypoglycemia Test checks your blood glucose and cortisol levels at various intervals after an injection of insulin Imaging Tests (CT) scan of your abdomen to check the size of your adrenal glands MRI scan of your pituitary gland if testing indicates you might have secondary adrenal insufficiency (Mayo Clinic,2011)

Hydrocortisone (Cortisol) 30 mg IV three times per day

Indications: used for the management of adrenocortical insufficiency (Addisons Disease) Action: suppresses inflammation and the normal immune response, replaces endogenous cortisol in deficiency states, have potent mineralocorticoid (sodium-retaining) activity

Adverse Reactions/Side Effects: CNS: depression, headache, personality changes, restlessness CV: hypertension GI: peptic ulceration, anorexia, nausea, vomiting Derm: acne, decreased wound healing Endo: adrenal suppression, hyperglycemia MSK: muscle wasting, osteoporosis, avascular necrosis of joints, muscle pain (Davis, 2011)

Fludrocortisone acetate (Florinef) 0.1 mg PO daily

Indications: used for sodium loss and hypotension associated with adrenocortical insufficiency (co-administered with hydrocortisone). Action: causes sodium reabsorption, hydrogen and potassium excretion, and water retention by its effects on the distal tubule. Therapeutic Effects: maintenance of sodium balance and blood pressure in patients with adrenocortical insufficiency (Addisons Disease) Adverse Reactions/ Side Effects: CNS(Central Nervous System): dizziness, headache CV (Cardiovascular System): CHF(chronic heart failure), arrhythmias, edema, hypertension GI: anorexia, nausea Endo: adrenal suppression, weight gain F and E: hypokalemia, hypokalemic alkalosis

Management of hyponatremia and hyperkalemia (Diederich, 2003) found in Addisons disease

What is hyponatremia - A condition that occurs when the level of sodium in the blood is abnormally lowplasma sodium level of less than 135 mmol per L. (Lewis, 2010)
- Mediated by mineralocorticoid deficiency and the inadequate secretion of antidiuretic hormone (ADH or vasopressin), which inhibits the renal reabsorption of sodium; thereby, disrupting sodium homeostasis as a whole (Hannon, 2010)

 Collaborative care: (Lewis,2010) 1) Management initially starts with fluid 2) Replacing losses with commercially available oral rehydration fluids containing electrolytes instead of pure water
(Diederich, 2003)

3) Pharmacological interventions Loop Diuretics or water pills (i.e. Furosemide) Sodium retaining medicines (i.e. Samsca) If severe symptoms (seizures) develop, small amounts of IV hypertonic saline solution (3% NacL) are given to restore the serum sodium level while the body is returning to a normal water balance

 What is hyperkalemia

- A high level of potassium in the blood is referred to as hyperkalemia. (Zelissen,1995)

-It occurs when the blood potassium concentration rises above 5.0 mmol/L of blood (Hannon, 2010) - In adrenal insufficiency, potassium is retained in the serum due to aldosterone deficiency along with the inhibition of the active excretion of potassium in the distal tubule and the collecting duct of the kidneys (Zelissen,1995)

(Diederich, 2003)

 Collaborative care: (Lewis,2010) 1) Eliminate oral and parenteral potassium intake 2) Increase elimination of potassium -Accomplished via diuretics, dialysis -and use of ion-exchange resins, -such as Kayexelate.
(Oelkers, 1992)

3) Reverse the membrane effects of elevated ECF potassium by administering calcium gluconate intravenously.
-Note that normally, potassium is stored in higher levels inside the cells (ICF) than outside the cells (ECF)which significant in the maintenance of cardiac conduction or your Electrocardiogram (ECG) PQRST wave

4) Avoid caffeine and alcohol, as these can cause an individual to have electrolyte disturbances.

Deglin. J. (2011). Davis Drug Guide for Nurses. 12th ed. Philadelphia: F.A. Davis. Diederich, S., Franzen, N., Bhr, V., & Oelkers, W. (2003). Severe hyponatremia due to hypopituitarism with adrenal insufficiency: Report on 28 cases. European Journal of Endocrinology, 148(6), 609-17. Hannon, R.A., Pooler, C., & Porth, C.M. (2010). Porth Pathophysiology: Concepts of altered health states (5th ed.). Philadelphia: Wolters Kluwer Health. Lewis, S.M., Heitkemper, M.M., & Dirksen, S.R. (2010). Medical-surgical nursing in Canada: Assessment and management of professional practice problems (2nd Can. Ed.). Toronto, Canada: Elsevier Can.

Mayo Clinic. (2010). Addisons disease. Mayo Clinic. Retrieved from http://www.mayoclinic.com/health/addisons-disease/DS00361
Oelkers, W., Diederich S., & Bhr, V. (1992). Diagnosis and therapy surveillance in Addison's disease: Rapid adrenocorticotropin (ACTH) test and measurement of plasma ACTH, renin activity, and aldosterone. The Journal of Clinical Endocrinology & Metabolism, 75 (1), 259.