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Addison's Disease, Subjective data, Synacthacen stimulation test,…
Addison's Disease
Clinical Manifestations
salt craving
muscle or joint pain
lightheadedness
Hypoglycemia (low blood glucose)
Gastrointestional problems including nausea, vomiting, and abdominal pain
sexual dysfunction in females
Unintentional weight loss
Irritability
Severe fatigue
Depression or other behavioral symptoms
Hyperpigmentation (darkening areas of the skin)
Pathogenesis
During the initial stages of disease development inflammation is established and there is and immune response against the adrenal cortex.
Untreated Addison's Disease can lead to an addisonian crisis due to physical injury like illness, infection, or injury. An addisonian crisis is life threatening and a person with one will need immediate medical care.
In autoimmune Addison's disease, the adrenal cortex is gradually destroyed and replaced by fibrous tissue. This negatively impacts the ability of the adrenal glands to produce hormones. This can cause the adrenal glands to produce insufficient amounts of certain hormones that they would otherwise produce grater amounts of.
Parenchymal cells are exposed to microbial products and cytokines during infections. This can impact their status with the immune system. It is thought that this is important to autoimmune disease development and progression such as that of Autoimmune Addison's Disease.
Adrenal cortex antibodies target 21OH which is an enzyme that is involved in the production of steroid hormones produced by the the adrenal cortex. This may negatively impact the production of these hormones from the adrenal cortex.
It is thought that primary adrenocortical zona fascicular cells and adrenocortical carcinoma cells may contribute to self-reactive lymphocytes being recruited to the adrenal cortex.
Diagnostics
Physical examination
Upon seeing this, lab work may be requested to help determine if an individual has Addison's disease. This is because while hyperpigmentation in the areas mentioned previously are not sufficient evidence to diagnose Addison's disease, they may lead the health care provider to suspect that an individual has Addison's disease. Blood work may be able to be used to detect Addison's disease.
A skin examination may show hyperpigmentation in areas including lips, scars, elbow crease, and creases of palms.
Blood tests: A blood test of an individual with Addison's disease may reveal low levels of sodium, glucose, potassium, cortisol, and aldosterone.
A patient may be asked about their family history. Genetics can influence risk factors for Addison's disease such as autoimmune diseases.
A blood test of an individual with Addison's disease may reveal high levels of adrenotropic hormone (ACTH). It may also reveal the presence of adrenal antibodies. Adrenal antibodies are designed to attack the adrenal gland.
If the blood test reveals that an individual has abnormally low levels of cortisol in their blood and/or their symptoms very strongly suggest that they have Addison's disease, the individual may have a synacthacen stimulation test.
A synacthen stimulation test involves synacthen which is a synthetic form of adrenocorticotropic hormone. (Normally, this test would cause an increase in cortisol and other steroid hormones in the blood due to the adrenal glands releasing them.) If blood samples taken after this show a high adrenocorticotropin hormone level but low cortisone and aldosterone levels, this is generally excepted as enough proof to diagnose an individual as having Addison's disease.
Computed Tomography (CT) scan: A CT scan of a patient who has autoimmune Addison's disease will show the glands as small or normal size. If the patient has Addison's disease as a result of infection or cancer cells in the adrenal glands, the adrenal glands can appear enlarged.
Incidence/prevalence
Addison's Disease is considered
to be a rare disease and affects males and female equally.
Approximately 1 in 100,000 people in the United States have Addison's Disease.
Undiagnosed cases of Addison's Disease make it difficult to know the true prevalence of Addison's Disease. It is suspected that the true number of individuals who have Addison's disease is greater than the number of individuals who have been diagnosed with Addison's Disease.
Addison's disease most usually happens in people who are between thirty and fifty years old.
When Addison's disease was first described by Thomas Addison, its most common cause was related to Tuberculosis.
The most common cause of Addison's disease today is autoimmune disease. Autoimmune disease today accounts for 70-90% of cases while Tuberculosis is estimated to count for 7-20% of cases.
Risk factors
Taking anticoagulants (also known as blood thinners)
Chronic infections like Tuberculosis: Tuberculosis can cause Addison's Disease.
Cancer: Cancer cells in the adrenal glands can cause them to not function properly.
Autoimmune disease such as Graves' disease
Treatment
Hormones to mimic those normally produced by adrenal gland (ex: Hydrocortisone pills, Prednisone, or Methylprednisolone to replace cortisol)
Fludrocortisone can help individuals that don't have enough aldosterone. Individuals taking Fludrocortisone may be advised to increase their salt intake.
Individuals with Addison's Disease may obtain a glucocorticoid injection kit so that they have an injectable form of corticosteroids in the case of an emergency.
Sources
Macon, Brindles Lee. “Addison's Disease.” Healthline, Healthline Media, 19 July 2019, www.healthline.com/health/addisons-disease.
“Addison's Disease.” NORD (National Organization for Rare Disorders), 17 Jan. 2018, rarediseases.org/rare-diseases/addisons-disease/.
“Addison's Disease.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 9 Oct. 2019, www.mayoclinic.org/diseases-conditions/addisons-disease/symptoms-causes/syc-20350293.
“Addison's Disease Management and Treatment.” Cleveland Clinic, 2019, my.clevelandclinic.org/health/diseases/15095-addisons-disease/management-and-treatment.
“Addison's Disease.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 9 Oct. 2019, www.mayoclinic.org/diseases-conditions/addisons-disease/diagnosis-treatment/drc-20350296.
“Addison's Disease.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 9 Oct. 2019, www.mayoclinic.org/diseases-conditions/addisons-disease/diagnosis-treatment/drc-20350296.
“Addison's Disease.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 9 Oct. 2019, www.mayoclinic.org/diseases-conditions/addisons-disease/symptoms-causes/syc-20350293.
“Addison's Disease.” NORD (National Organization for Rare Disorders), 17 Jan. 2018, rarediseases.org/rare-diseases/addisons-disease/.
“Diagnosis of Adrenal Insufficiency & Addison's Disease.” National Institute of Diabetes and Digestive and Kidney Diseases, U.S. Department of Health and Human Services, 1 Sept. 2018, www.niddk.nih.gov/health-information/endocrine-diseases/adrenal-insufficiency-addisons-disease/diagnosis.
Hellesen, Alexander, et al. “Autoimmune Addison's Disease – An Update on Pathogenesis.” Annales D'Endocrinologie, vol. 79, no. 3, 2018, pp. 157–163., doi:10.1016/j.ando.2018.03.008.
NHS Choices, NHS, www.nhs.uk/conditions/addisons-disease/diagnosis/.
UpToDate, www.uptodate.com/contents/causes-of-primary-adrenal-insufficiency-addisons-disease.
A Project Made by Gina Bodette
Subjective data
Synacthacen stimulation test
Blood tests