Addison’sdisease is a potentially life-threatening disorder. Thomas Addisonidentified the disease in 1855, and it is commonly referred to asprimary adrenal insufficiency. It is associated with the failure ofadrenal glands to produce sufficient steroid hormones. The illnessdevelops from the progressive damage of adrenal cortex, the body’simmune system, and the adrenal glands. The destruction of the cortexfurther contributes to adrenal insufficiency due to low levels ofcortisol as well as aldosterone. The current study aims at diagnosingthe existence of Addison’s disease as the only possible cause ofunexplained hyperglycaemia in patients with diabetes one Mellitususing Synacthen tests (Ross & Levit, 2013).
Addisondisease is associated with the insufficient production of cortisoland aldosterone. The lack of sufficient cortisol and aldosterone mayoccur from either primary or secondary adrenal insufficiency. Theprimary adrenal shortage is caused by a disorder in the adrenalglands. Cortisol is created by adrenal glands situated above thekidney. The hormone is linked to a group of hormones namedglucocorticoids that affect most of the body organs and tissues.According to Betterle and Morlin (2011), cortisol has a myriadeffect on the body, and its most significant use is assisting thebody in responding to stress. It also aids in maintaining bodypressure and slows the immune response to inflammation. Itfacilitates breaking down insulin and balances the levels of energyby regulating the metabolism of carbohydrates, sugars, and fats(Betterle&Morlin, 2011).
Dueto its importance in the body, the production of cortisol isbalanced. Its production is controlled by the hypothalamus andpituitary glands of the brain. The hypothalamus sends hormones torelease cortisol to the pituitary glands that further secreteschemicals that regulate the development of adrenal and thyroidfunctions as well as the manufacture of sexual elements such astestosterone and estrogen (Puttanna et al., 2013).
Secondaryadrenal insufficiency occurs from inadequate production of ACTH bythe pituitary glands. The key function of the pituitary gland issecretion of adrenocorticotropic (ACTH) to stimulate the adrenalglands. Upon the receipt of pituitary’s signal, the adrenal glandsproduce cortisol, which later signals the pituitary to reduce thesecretion of ACTH (Lewis, 2011).
Aldosteronebelongs to the mineralocorticoids group of hormones produced by theadrenal glands. The key function is to control blood pressure andmaintain the salt and water balance. Specifically, it helps thekidneys to excrete potassium and retain sodium. When the productionof aldosterone is low, kidneys fail to adjust the amount of salt andwater balance that results in lower blood volume and pressure. Consequently, the disease is either referred to as hypocortisolism orthe chronic adrenal insufficiency condition, based on the cause (Ross& Levit, 2013).
Addison’sdisease has an equal prevalence in both male and female sexes. It isestimated that one out of a hundred thousand people in the UnitedStates of America have the infection. The overall prevalence in theworld is valued at a range between 40 and 60 million. The disease hasa tendency to go unnoticed and consequently, it is hard to determineits actual prevalence. It has the potential of affecting individualsaged between 35-55 years (Passanisi et al., 2014).
Thekey symptoms of Addison’s disease emanate from adrenalinsufficiency and begin gradually. They include chronic muscleweakness that creates a worsening fatigue. The patients lack appetiteand lose a lot of weight. A majority, 50%, of the cases includediarrhea, vomiting, and nausea. The patients experience low bloodpressure that deteriorates when the victim stands. Low blood pressureresults in dizziness and possible fainting. The patient encountersskin changes and hyperpigmentation on exposed and non-exposed bodyparts (Ross &Levit, 2013).
Thechange of the skin is heavily evident on scars, pressure joints suchas the knees, elbows, knuckles, toes, mucous membranes, and skinfolds. The disease is also associated with depression andirritability. Due to lack of salt, the patient craves for saltyfoods. Blood pressure or hyperglycemia associated with the diseaseis more common in children than adults. Women menstrual periods mayeither stop or become irregular. Due to the slow progress of theAddison’ disease symptoms, they are most of the times ignored untilwhen an illness incident makes them evidently worse. Such incidencesare referred to as the Addisonian crisis (Lewis, 2011).
Adrenalinsufficiency associated with Addison’s disease is rare, but a lifethreatening illness when it progresses to the adrenal crisis stage.Addison’s disease can occur with recurrent hypoglycemia in patientswith type 1 diabetes mellitus. The following is a two monthsretrospective study on the frequency of Addison’s disease as areason for recurrent hypoglycemia in diabetes one Mellitus patients(Puttanna et al., 2013).
Thepatients experienced recurrent hyperglycemia that was unrelated tothe treatment of insulin, exercise, alcohol consumption, meal plans,and concurrent medication. The study eliminated patients with ahistory of steroid prescriptions. It also excluded patients with ahistory of liver, renal, asthma, and pituitary malignant disease(Lewis, 2011).
Theresearchers performed short Synacthen tests on 95 patients diagnosedwith type 1 diabetes mellitus. The studies were carried out atspecific times of the afternoon. Intravenous cannulas were insertedin the patients’ antecubital veins to collect a baseline bloodsample between 2.00 and 2.30 pm. The patients were later injectedwith a dose of 250 micrograms tetracosactide. Afterward, theresearchers obtained additional blood samples after intervals of 30to 60 minutes (Ross & Levit, 2013).
Theblood samples were separated, and the amount of serum cortisol wasmeasured through electrochemiluminescence immunoassay using the RocheModular Analytics E 170 immunoassay analyzer. The test is usedbecause it has a detection limit of 2nmol/1. The inter-assaycoefficient of variation for the cortisol assay was found to be 1.7%at 410nmol/1. The analysis maintained satisfactory internal qualitycontrol and external quality evaluation for cortisol throughout thestudy process. The researchers defined an average cortisol reactionto synacthen at a post-stimulation peak cortisol value of less orequal to 500nmol at both 30 and 60 minutes. They also defined anincremental cortisol level of less or equal to 200 nmol/1 (Puttannaet al., 2013).
ProblemsAssociated With the Nursing Diagnosis
Addisondisease co-occurs in patients diagnosed with type1 diabetes mellitus.It mostly occurs as part of the autoimmune polyendocrine syndrome. The diagnosis of the disease is most of the times delayed since theonset of diabetes one Mellitus occurs before the diagnosis ofAddison’s disease. The deficiency of cortisol in diabetic patientsincreases their sensitivity to insulin. Consequently, the patient’sbody increases the utilization of peripheral glucose and reducesglucogenesis as well as the body’s hepatic glucose output.Therefore, it is expected that hyperglycemia is a common feature inpatients diagnosed with diabetes one Mellitus and receivinghypoglycemic treatment (Betterle&Morlin, 2011).
Theresults revealed that one patient, a 39-year-old man with type 1diabetes mellitus, had an autoimmune Addison’s disease. The peakcortisol for the patient was 111nmol/1. He also had adrenalantibodies and lacked thyroid microsomal antibodies. The results ofthe study revealed that Addison’s disease leads to the occurrenceof hypoglycemia in diabetic patients. Addison’s disease should beconsidered in cases that involve typical clinical and biochemicalfeatures in addition to organ-specific autoimmune diseases such asthe thyroid disease (Betterle & Morlin, 2011).
Thefirst intervention to meet the outcome was the use of Synacthentests. The tests enable the investigation of adrenocorticalinsufficiency. The process is time-consuming as it involves theadministration of ACTH. Besides, it requires a patient to be admittedfor a day. The tests enhanced the determination of specific diabeticpatients with recurring hyperglycemia and unlikely to have theAddison’s disease as a strategy to reduce the number of Synacthentests (Puttanna et al., 2013).
Thesecond intervention was eliminating patients with thyroid disease.The patients in the study did not have any characteristics of thyroiddisease other than recurrent hyperglycemia. The feature of thepatients indicates that hyperglycemia was the only early presentingsymptom of adrenal failure. The study shows that Addison’s diseaseshould be considered as the cause of frequent hypoglycemia in allpatients diagnosed with type 1 diabetes mellitus (Lewis, 2011).
Thethird intervention entailed the use of 9.00 serum cortisol. The aimwas to reduce the number of synacthen costs by 21%. Besides, theintervention controlled for abnormal responses to ACTH by usingsynthetic tetracosactide. ACTH was injected intramuscularly for theperiod of 48 to 72 hours. The blood’s cortisol levels were measuredbefore and after injection to differentiate between secondary andprimary adrenal insufficiency. Patients diagnosed with primaryadrenal insufficiency fail to produce cortisol during the 42 and72-hour period. In contrast, patients with secondary adrenalinsufficiency produce adequate cortisol on the second day. The timefor the study provided room for the elimination of secondary adrenalinsufficiency (Ross & Levit, 2013).
Theuse of ACTH was to control further to avoid the use of otherinefficient alternatives such as the antibodies to test for Addison’sdisease. The antibody test criterion is associated withinefficiencies whereby only a minor 15% of diabetic patients thatindicate signs of adrenal antibodies test positive to Addison’sdisease. Besides, negative antibody results associated with the trialare not a complete proof of the absence of Addison’s disease(Lewis, 2011).
Synacthentests are used to verify whether a patient’s adrenal glands producea chemical called cortisol. During the trials, the adrenal glands arestimulated by injecting tetracosactide to evaluate their response.Synacthen is synonymous to tetracosactide (ACTH) used during thechemical test. ACTH is the chemical hormone produced by the body’spituitary gland. It stimulates the adrenal glands to emit cortisol.In a case where the adrenal glands function properly, they areexpected to produce cortisol as a response to tetracosactide. Duringthe test, the levels of cortisol are checked before and after theinjection of tetracosactide. When the levels of Cortisol remain lowirrespective of the amount of tetracosactide injected, it indicatesthere is a hitch with the operation of the adrenal glands (Ross &Levit, 2013).
Inthe above case, the study controlled for diabetes-specific symptomsin the patients that could lead to severe hypoglycemia or lack ofsugar in the blood. The study included all patients who experiencedrecurrent hypoglycemic incidences that were unrelated to thepatient’s meals, exercise, alcohol consumption, co-morbidity andpatient’s concurrent medication. It also excluded patients who hadexperienced recent steroid treatments as well as those withidentified liver, pituitary, renal and asthmatic diseases (Passanisiet al., 2014).
Subsequently,the study was able to diagnose that Addison’s disease is the onlypossible cause of unexplained hyperglycaemia in patients withdiabetes one Mellitus using Synacthen tests. The patient experiencesa decrease in insulin requirement and a simultaneous butunexplainable improvement in glaecamic control that is foreshowed bythe change in the patient’s endocrine status. The results from thestudy highlights that patients diagnosed with diabetes one Mellitusare at risk of developing other endocrinopathies like the Addison’sdisease (Betterle&Morlin, 2011).
Thetreatment of Addison’s disease varies depending on the symptomsdepicted by a patient. Some treatments may call for the coordinatedefforts of various specialists. Patients are treated by replacing theundersupplied steroid hormones (aldosterone and cortisol). Thehydrocortisone drug is used to replace cortisol while fludrocortisoneis used to change the aldosterone hormone. The appropriate dosagesfor each hormone also vary from one patient to the other. Occurrencessuch as trauma, infections, stressful situations or surgery maydemand an increase in the dosage. The patients are also encouraged toincrease the amount of salt in their diets (Puttanna et al., 2013).
Theoccurrence of an adrenal crisis requires immediate hormonalinvestigations. It also requires the administration of a high dose ofhydrocortisone fluid that is made of salt and water and anelectrolyte replacement. It also requires the use of vasopressors inthe short term to maintain the patient’s blood pressure. As aprecaution, patients that have experienced the adrenal crisis arerequired to carry a tag signifying that they have the Addison’sdisease (Passanisi et al., 2014).
Betterle, C.& Morlin, L. (2011). Autoimmune Addison’s disease. Journalof Endocrinology Devevelopment,20(6),161-172. Retrieved from http://www.karger.com/Article/Abstract/321239
Lewis, K.(2011). Autoimmune diseases associated with type 1 diabetes. Journalof Pediatric Nursing, 26(2): 174-175. Retrieved fromhttp://www.pediatricnursing.org/article/S0882-5963(10)00383-0/pdf
Passanisi,S., Timpanaro, T., Presti, D., & Caruso, M. (2014). Recurrenthypoglycaemia in type-1 diabetes mellitus may unravel the associationwith Addison’s disease: A case report. BiomedicalCentral.Retrieved on 09August 2016 fromhttp://bmcresnotes.biomedcentral.com/articles/10.1186/1756-0500-7-634
Puttanna, A.,Cunningham A., & Dainty, P. (2013). Addison’s disease and itsassociations. BiomedicalJournal Case Reports,26(4),56-93. Retrieved fromhttp://casereports.bmj.com/content/2013/bcr-2013-010473.abstract
Ross, I. L.,& Levitt, N. S. (2013). Addison’s disease symptoms – A crosssectional study in urban South Africa. PLoSONE, 8(1),e53526. http://doi.org/10.1371/journal.pone.0053526