Addisons Disease

Question: Give a discussion on identification of problem and underlining pathophysiology ? Answer: Abstract Addisons disease is a rare kind of endocrine disease. Serum cortisol and aldosterol levels are reduced. The symptoms may be ignored initially but it gets worsen with time if not treated. Identification of problem and underlining Pathophysiology Addisons disease is an endocrine disease. Patients suffering in Addisons disease have very low secretion of aldosterone and cortisol as a result of adrenal insufficiency. The Pathophysiology of Addisons disease includes nausea, anorexia, hypotension, early fatigability, dizziness, blurred vision and weight loss, Hyperpigmentation in skin and in the high lips. Ms. Beth has 5.4 mEq/L serum potassium levels; therefore she is identified with hyperkalemia (Pearce, 2014). She has the serum sodium concentration of about 129 mEq/L, therefore hyponatremia is occured. Ms. Beth has the blood glucose level of 61 mg/dl; therefore she is in hypoglycemic condition. Patient may suffer in GI disorder with frequent diarrhea and constipation. The BUN level is about 34ml/dl which is really high and it is an indication of kidney damage (Lewis Bendre, 2011). Generally, the symptoms of Addisons disease are ignored but it gets worsen with time. Sudden piercing pain in the abdomen and lower back region is c onsidered as a secondary symptom of the disease. Along with this, she also had the tuberculosis in her case history. Case Synopsis Thomas Addison first identified the clinical features of primary adrenal insufficiency as a potential cause of Addisons disease. In this particular case, a 42 year old woman is identified with various kinds of symptoms which are hyperpigmentation in lips and skin, dizziness, early fatigability, and nausea with recurrent vomiting, constipation and diarrhea, underweight since eight months. Pathophysiology Addisons disease is the caused by primary or chronic adrenal insufficiency. The two main hormonal deficiencies are involved in Addisons disease. Mineralocorticoid deficiency Mineralocorticoids mainly aldosterone stimulates Na+ reabsoption and K+ excretion. The decreased secretion of mineralocorticoid is presented as increased excretion of sodium and decreased excretion of potassium principally in urine and additionally in saliva, sweat and GI tract. Low serum concentration of sodium along with high concentration of potassium is identified in Addisons disease. Urinary salt and water loss is also observed in patients affected in Addisons disease. As a consequence, severe dehydatrion is occurred as diagnosed in this particular case. Plasma hypertonicity, acidosis, reduced circulatory volume, hypotension and in due course circulatory collapse may be occurred. Though, adrenal insufficiency is caused by inadequate ACTH secretion in secondary adrenal insufficiency which leads to Addisons disease in some extent. Glucocorticoid Deficiency Hypotension is happened due to glucocortocid (cortsol) deficiency and as a consequence, insulin sensitivity is occurred and this leads to turbulence in fat, carbohydrate and protein metabolism. Because of that, carbohydrate production from the protein in reduced and this leads to hypoglycemia as observed in Ms. Beths Case. Severe muscular weakness and vertigo is observed in patients suffering in Addisons disease due to the impairment of neuromuscular function. In addition to that myocardial insufficiency and dehydration decreases the cardiac output and as a consequence to that circulatory failure is occurred. Low serum cortisol stimulates pituitary ACTH production. This results in melanocyte stimulating activity which is the principal reason of hyperpigmentation in the skin and lips. Autoimmune disorder The Addisons disease in 80% cases is caused by autoimmune disorder. This is most frequently observed in the females of middle ages. In autoimmune issues, the immune system destroys the adrenal glands and due to that primary adrenal insufficiency is happened (Napier Pearce, 2012). Tuberculosis infection Tuberculosis infection can cause severe adrenocortical cell damage which leads to primary adrenal insufficiency. Dr. Thomas Addison in 1984 first identified the tuberculosis as the most familiar cause of the Addisons disease. As reported in this case, the history of tuberculosis is a potential cause behind the Addisons disease. Diagnosis and Treatment Diagnosis After suspecting the Addisons disease from the initial signs and symptoms, hormonal blood and urine tests are performed (Nascimento, Rodrigues, Espada Fonseca, 2012). These are the following- ACTH stimulation test CRH stimulation test Ultrasound of the abdomen Tuberculin skin test Antibody blood tests Computerized tomography (CT) scan Magnetic resonance imaging (MRI) Treatment As , Addisons disease is occurred due to reduced secretion of seum cortisol and aldosterone produced by adrenal glands, the disorder can be treated by external ingestion. Tablets containing synthetic steroid namely Fludrocortisone acetate is taken orally once a day. The dosage should be increased during times of infection, stress, injury or surgery. In Addisonian crisis, injections of salt, fluids, and glucocorticoid hormones should be taken instantly as advised by GP (Pearce, 2014). Nursing action Nursing action includes, the assessment of mucous membranes and skin to detect dehydration and hyperpigmentation, assessment of vital signs like heart rate and blood pressure, weight loss. Blood tests for Na+ and K+ should be done to check the hyponatraemia and hyperkalemia. The nurse should also concern about the diet of patient as because the presence of GI tract functional impairment (Kundu, Bryk Alam, 2014) Routine tests of blood sugar should also done during the treatment period. References list Kundu, S., Bryk, J., Alam, A. (2014). Resolution of Suicidal Ideation With Corticosteroids in a Patient With Concurrent Addisons Disease and Depression. The Primary Care Companion For CNS Disorders. Lewis, K., Bendre, S. (2011). An 18-Year-Old Male Newly Diagnosed With Addison's Disease That Masked Type 1 Diabetes Mellitus. Journal Of Pediatric Nursing, 26(3), 276-277. Pearce, S. (2014). Curing Addison's disease. EJEA. Napier, C., Pearce, S. (2012). Autoimmune Addison's disease. La Presse Mdicale, 41(12), e626-e635. Nascimento, M., Rodrigues, N., Espada, F., Fonseca, M. (2012). Adrenoleukodystrophy: a forgotten diagnosis in children with primary Addison's disease. Case Reports, 2012(aug21 1), bcr2012006308-bcr2012006308. Napier, C., Pearce, S. (2012). Autoimmune Addison's disease. La Presse Mdicale, 41(12), e626-e635. Nascimento, M., Rodrigues, N., Espada, F., Fonseca, M. (2012). Adrenoleukodystrophy: a forgotten diagnosis in children with primary Addison's disease. Case Reports, 2012(aug21 1), bcr2012006308-bcr2012006308. Pearce, S. (2014). Curing Addison's disease. EJEA. doi:10.1530/endoabs.36.s2.2