Clinical Biochemistry- Case Study - Essay Example

EXAMINATION OF THE PATIENT Findings: Patient complains of repeated vomiting, nausea, and generalised tiredness for two weeks. Patient is found to be hypotensive, tachypnic, with normal temperature and pulse rate. She also suffers from hyponatremia and hyperkalemia. Because no other abnormalities were revealed upon abdominal, cardiovascular, respiratory, and neurological examinations, an endocrinal abnormality lead is followed. Laboratory tests reveal that the patient has high serum urea, creatinine and adrenocorticotropic hormone (ACTH) levels.

High ACTH levels may indicate a non-responsiveness of its target organ, the adrenal glands. The result of short ACTH stimulation test and random serum cortisol levels confirm this suspicion. Upon doing a CT scan, adrenal glands are small, atrophic, and calcified. The damage may have been caused by an autoimmune disease or secondary to diseases such as Histoplasma, Coccidiodes, Tuberculosis infections, metastases, lymphomas, hemorrhage, amyloid, sarcoid, and hemochromatosis, to which the patient is currently suffering or has already been freed from.

To see whether the adrenal gland disorder is autogenic, presence of adrenocortical autoantibodies is assayed. None were detected. When thorax of the patient underwent CT scan, both lungs are fibrous, and the right apex has calcifications. The fibrotic scars and the calcified right apex cavity are indications of a previous Tuberculosis infection. Because no respiratory problems were identified, the infection has already been resolved. Because Tuberculosis is common in Third World countries, and was still one of the leading causes of mortality during the 1950s, the patient may have been infected during her stay at Kenya when she worked as a missionary.

Four months prior to consult, the patient felt similar symptoms, and was then found to be hyponatremic, hyperkalemic and hypoglycaemic. No further tests were reported to have been performed at that time.Assessment: The patient is suffering from Addison’s disease, secondary to a resolved Tuberculosis infection.Plan: Therapy involves hormonal replacement. Oral corticosteroids such as Fludrocortisones (Florinef) to replace aldosterone, and Hydrocortisone (Cortef), prednisone, and cortisone acetate to replace cortisol may be provided.

Corticosteroid injections may also be an option, especially during Addisonian crisis, when blood pressure drops together with a decrease in blood sugar and an increase in serum potassium levels.ADDISON’S DISEASEUnlike Cushing’s syndrome, which involves an increase in the levels of adrenal gland hormones, Addison’s disease is an illness in which the adrenal glands are damages, thereby decreasing the levels of glucocorticoids such as cortisol and mineralocorticoids such as aldosterone. Low levels of glucocorticoids signal for gluconeogenesis, and without this process blood sugar levels decrease and protein biproducts such as urea increase.

Because the body cannot use food for energy efficiently, patient suffers from vomiting and nausea, possibly including diarrhea. In addition, since energy provided by glucose is low, the body will recruit other forms of energy such as creatine phosphate, as manifested by high levels of creatinine. On the other hand, low levels of glucocorticoids prevent reabsorption of sodium and exretion of potassium, thus resulting to hyponatremia and hyperkalemia, respectively. REFERENCESMayo Foundation for Medical Education and Research 2010, Addison’s Disease, viewed November 20, 2010, < http://www.

mayoclinic.com/health/addisons-disease/DS00361>.