Endocrine Deficiency: Case Study - Essay Example

 Endocrine Deficiency: Case Study A woman in her late fifties was found unconscious and admitted to hospital. On investigation, it transpired that she had felt unwell for some time, and had felt dizzy and occasionally had episodes of vomiting. Over the past few days, she had been feeling rather tired and sleepy. On testing, her urine was negative for glucose and ketones. Her blood count was normal, and there was no evidence or history of trauma to the head. The following tests were performed:  Plasma value Recorded value Reference value  Na 118 mmol/L 135-145 mmol/L  K 5.90 mmol/L 3.6-5.0 mmol/L  Cl 85 mmol/L 98-106 mmol/L  CO2 20 mmol/L 23-30 mmol/L  Urea 24.5 mmol/L 3.0-8.0 mmol/L  Creatinine 168 µmol/L 50-140 µmol/L  Questions to address in your answer  1. What endocrine deficiency could result in these findings?  2. The blood glucose was not tested, but might be expected to be lower than normal. Why might this be the case?  3. What test could be used to assist in confirming the diagnosis? The patient is suffering from primary adrenal insufficiency in which the normal functioning capability of the adrenal gland is lost. The adrenal gland mainly functions in the secretion of aldosterone and cortisol which are hormones essential to the normal functioning of the human body. Aldosterone is responsible for the regulation and maintenance of the ions in the body. It is mainly involved in the re-absorption of sodium in the kidney tubules and at the same time excretion of potassium and hydrogen ions. Cortisol functions towards the regulation of the blood glucose levels. This hormone is a steroid and performs the role of lowering the effects of inflammation. The adrenal gland also leads to the secretion of androgens which are important for the normal sexual development in a person along with the proper hair distribution (GANONG, 2005). The presentation of the patient clearly shows that the disease has progressed in an acute form because the patient explained her symptoms had been appearing since a few days. The chronic form of the disease is ruled out since it takes a very long time in development (Robbins et al 2005). In primary adrenal insufficiency the hormone that is initially and mainly affected is aldosterone. It is then that cortisol and the androgens follow. The laboratory findings indicate the ionic imbalance led to by aldosterone deficiency. The decreased levels of sodium arise because the ions cannot be reabsorbed due to the absence of aldosterone and hence they are lost in urine which results in low levels of the sodium ions in the blood. At the same time potassium ions which are exchanged for sodium in the kidney tubules with the assistance of this hormone do not get excreted and this results in high levels of potassium in the blood and hence the condition hyperkalemia. The retention of hydrogen ions also occurs because aldosterone plays a role in the excretion of hydrogen ions. Thus this results in increased levels of hydrogen ions and resultant acidosis. Retention of chloride cannot occur due to decreased aldosterone as well which results in low levels of chloride ions in the blood. Another reason for low chloride level is that there is an exchange of chloride with the bicarbonate in the cells. This is because bicarbonate is required for the compensation of the acidosis which has resulted and hence the chloride ions enter the cell and the bicarbonate ions are ejected in the extracellular compartment. The loss of chloride ions can also be associated with the vomiting episodes that the patient had. This is because the gastric juices contain a high content of chloride and prolonged vomiting can lead to a reduction in the level of the chloride ions. The low level of carbon dioxide is also because of the compensatory hyperventilation which results to overcome the metabolic acidosis. This occurs in the form of deep breaths and is referred to as Kussmaul breathing. This results in loss of carbon dioxide and hence the patient presents with lower than normal carbon dioxide levels. (Robbins et al 2005, Greenspan et al 1994, Dorin et al 2003 and FALORNI et al 2002) The laboratory tests show very high levels of urea and creatinine. These levels have resulted due to the loss of fluids from the body because of the vomiting as well as the improper balance of the ions which leads to fluid loss. This results in an increased concentration of these substances. On the other hand there is disruption in kidney function as well which can also account for these high levels (Greenspan 1994). The test for glucose and ketones in the urine is performed to rule out the presence of diabetes. The gastrointestinal system is also affected by the primary adrenal insufficiency which accounts for the vomiting that the patient has been experiencing. The patient’s blood pressure should also be investigated as due to the low levels of sodium and the loss of fluid due to the improper kidney function can lead to hypotension in this case. This hypotension can be a reason for the unconsciousness that the patient presents with. Another reason is that the high levels of urea and creatinine are indicative of the fact that the ammonia levels in the blood are high. Ammonia is toxic to the brain as it is capable of crossing the blood brain barrier and can be a cause of coma. The patient felt dizzy and tired in these days because of the electrolytic imbalance, low blood pressure as well as the vomiting that she was experiencing. Another cause is that primary adrenal insufficiency can affect the diet of a person and patient presents with loss of appetite and weight which can also be considered in this case. The normal blood count is indicative of the fact that the patient is not suffering from anemia since hemolytic anemia can also be one of the reasons for the imbalance in ionic concentration in the blood. The history that there is no evidence of the fact of trauma and injury to the head is to prove that hypothalamic injury can be excluded from the diagnosis. The normal blood count also indicates the fact that the white blood cell level in the blood is normal. This assists in ruling out the diagnosis of the presence of antibodies that might have developed in the body against the adrenal gland and provide a cause for the autoimmunity ( Ganong 2005, Greenspan et al 1994, Dorin et al 2003 and FALORNI et al 2002) The patient might also be suffering from high levels of thyroid hormones. This is because hyperthyroidism is associated with high metabolic rates. The high metabolic rate can also be the reason for the increased utilization of glucose and low levels of glucose in the blood. This increased functioning of the body systems can be the reason for fatigue which the patient is experiencing because there is increased utilization of energy associated with the levels of the thyroid hormones. The patient also has gastrointestinal tract disturbances with increased motility leading to regurgitation and vomiting. This can also be associated with the high levels of thyroid hormones which can increase these functions. The thyroid hormone also increases the metabolism of hormones which include aldosterone and cortisol and this can also lead to decreased levels of these hormones in the blood due to the impaired functioning of the adrenal gland and hence be associated with the primary adrenal insufficiency. Thus it is important that the levels of the thyroxine and triiodothryonine should be checked (SOFFER1963). The levels of blood glucose are checked to confirm that the patient is suffering from the deficiency of cortisol as well. This is because cortisol functions to maintain the blood glucose levels in a normal limit when required. Thus if cortisol is deficient the blood glucose levels would be low and this would indicate that the adrenal cortex has also been affected. With the destruction of the adrenal gland, though the deficiency of aldosterone is evident but if the destruction has increased a lot, the corticosteroid secretion might also be disrupted. Another reason can be that loss of fluids and persistent vomiting can also be a cause of it. This is also essential for the protocol of treatment because if the patient is suffering from hypoglycemia she would need immediate intravenous administration of glucose along with sodium to maintain the normal balance of blood glucose and ions within the body (Robbins et al 2005). To confirm that the pathology exists in the adrenal gland, the patient should be given an ACTH stimulation. In this test the patient is injected with ACTH and the levels of the ions are checked. If changes are observed in the level, that is if they improve, it is indicative of the fact that the defect lies in the pituitary gland and not in the adrenals (Greenspan 1994). In the case of primary adrenal insufficiency, the levels of ACTH are high in the blood and this patient should be properly checked for pigmentation which results due to increased production of melanin as a result of the high ACTH levels. This is because proopiomelanocortin which is the hormone which leads to production of ACTH is secreted in increased amounts. This leads to increased levels of ACTH and melanocortin which can both lead to the formation of pigments and hence pigmentation (Lang et al 2000). The hair distribution should also be observed and this should be checked for some time since the adrenal gland is also responsible for the secretion of androgens and this eventually results in loss of hair in females (Mohan 2005, Robbins et al 2005). Calcium levels should also be checked because there is a rise in the levels of these ions. The radiograph of the abdomen should also be done. Calcium deposition on the adrenals is indicative of the fact that the adrenal gland has been subjected to tuberculous destruction. A radiograph of the abdomen is performed to see for the calcium deposition on adrenals to find out the underlying cause. A CT scan is also performed to confirm the cause of the adrenal insufficiency which might include bleeding within the adrenal glands. Changes in the ECG should also be checked because the loss of ions results in abnormalities in the ST waves (Greenspan 1994). The plasma levels of rennin should also be checked and this should be compared with the blood hormonal levels of aldosterone. If the activity of plasma rennin is high, it would clearly suggest that the patient has primary adrenal insufficiency and low levels of aldosterone are present. Also cortisol levels should be monitored to confirm if the hormone is deficient as well and these levels should be mainly checked in the morning. The patients should also be checked for chronic renal failure which is also associated with ionic imbalance. In this condition the proper functioning of the kidneys is lost because of which the proper exchange of ions cannot occur. Thus the patients Renal Function Test should be done to rule out this condition. This is also important because the high levels of urea and creatinine in the blood can also be because of this (Dorin 2003). References: Top of Form Top of Form DORIN RI, QUALLS CR, & CRAPO LM. (2003). Diagnosis of adrenal insufficiency. Annals of Internal Medicine. 139, 194-204. Bottom of Form Bottom of Form Top of Form GANONG, W. F. (2005). Review of medical physiology. New York, McGraw-Hill Medical. Top of Form GREENSPAN, F. S., & BAXTER, J. D. (1994). Basic & clinical endocrinology. Norwalk, Conn, Appleton & Lange. Bottom of Form Top of Form HUSEBYE E, & LØVÅS K. (2009). Pathogenesis of primary adrenal insufficiency. Best Practice & Research. Clinical Endocrinology & Metabolism. 23, 147-57. Bottom of Form Top of Form KOWAL J, & SOFFER LJ. (1963). "PITUITARY RESERVE" IN MYXEDEMA AND THYROTOXICOSIS.Annals of Internal Medicine. 59, 79-83. Bottom of Form Top of Form KUMAR, V., ABBAS, A. K., FAUSTO, N., ROBBINS, S. L., & COTRAN, R. S. (2005). Robbins and Cotran pathologic basis of disease. Philadelphia, Elsevier Saunders. Top of Form LAURETI, S., SANTEUSANIO, F., & FALORNI, A. (2002). Recent Advances in the Diagnosis and Therapy of Primary Adrenal Insufficiency. CURRENT MEDICINAL CHEMISTRY IMMUNOLOGY ENDOCRINE AND METABOLIC AGENTS. 2, 251-272. Bottom of Form Top of Form MOHAN, H. (2005). Textbook of pathology. New Delhi, Jaypee Bros. Top of Form SILBERNAGL, S., & LANG, F. (2000). Color atlas of pathophysiology. Stuttgart, Thieme. Bottom of Form Bottom of Form Bottom of Form Bottom of Form Read More