Type of hormonal and Metabolic Dysfunction - Coggle Diagram
Type of hormonal and Metabolic Dysfunction
Syndrome of Inappropriate Antidiuretic Hormone Secretion
Clinical Manifestations: Decrease and concentrated unrine output. Symptoms usually do not manifest until serum sodium is less than 115 to 120 mEq/L. Related to hypotonic and hyponatremia. More rapid onset hyponatremina symptoms include muscle cramps, anorexia, nausea, ad weakness.
Diagnostic Criteria: Hyponatremia (Less then 135mEq/L) Hypotonicity ( Less than 280mOsm/kg) Decreased urine volume, Highly concentrated urine with a high sodium content, and Absence of renal, adrenal, or thyroid abnormalities.
Treatments: Focusing on removing the cause of SIADH, Medications are administered to block the effects of ADH or to increase urine output is removing the cause is not feasible.
Diagnostic Criteria: Made through a very careful look through patient history and physical examination. Patient history may show recent surgeries to remove the tumor in the brain, or other cranial surgeries. The physical Examinations can detected dehydration, or possible enlargement of the bladder.
Treatments: Most patients can drink enough water to replace the urine loss. Hydration is very important in order to be treated, done through IV's or drinking. Pharmacologic treatments use desmopresions.
Clinical Manifestations: Depending on the severity of DI. Loss of ADH or inadequate kidney response to ADH results in polyuria. Loss of fluids leads to serum hyperosomolality and severe dehydration. shock and death may occur if not treated.
Treatments: Measured on the based on the reducing thyroid hormone level often through gland destruction via radio active iodine. medications that block thyroid hormone production or less commonly, surgical removal of all parts.
Diagnostic Criteria Base on patient History and physical examination. History may be significant for a family history of autoimmune disease, thyroid disease or emigration. Physical examination reveal the enlargement and firm thyroid gland and protrusion of the eyes.
Clinical Manifestations: Related to enlargement of the thyriod gland and the excessive metabolic rate of the body. Weight loss, agitation, restless, sweating, heat tolerance.
Clinical Manifestations: Excesses of gluccorticiods can result in metabolic alterations, excessive circulating glucose and subsequent glucose intolerance, suppression of the inflammatory and immune responses, behavioral changes and an impaired stress response.
Diagnostic Criteria: Based off a 24 hour urine collection during which elevations in cortisol excretion are noted. There is a possibility of false positive testing for those with obesity, alcoholism and chronic renal failure.
Treatment: Focused on the removing that cause the excess hormone production. Corticosteroids medications may be prescribed.
Clinical Manifestations; They are gradual and include fatigue, cold tolerance, weakness, weight gain adn dry skin Goiter may also be present as the gland enlarges in an effort to increase function. Dietary iodine deficiency, exces, or the use of medications that suppress thyroid hormone can stimulate the development of hypothyroid goiter.
Diagnostic Criteria: Based on patients medical history and physical examination, Laboratory studies include the sensitive TSH assay, free T4, total T4 and T3 uptake, thyroid autoantibodies and antithyrioglobulin test to confirm the diagnose and provide evidence.
Treatments Focuses on replacing the deficient hormone with the goals of normalization of TSH, T4, and T3 levels along with alleviation of the clinical signs and symptoms.
Clinical Manifestations: Based on insufficient levels of the steroid hormones. Elevation in ACTH levels stimulate skin melanocytes, resulting in characteristics hyperpigmentation or darkening.
Treatments: Isotonic IV fluid replacement is infused along with hydrocortisone sodium succinate or phosphate.
Diagnostic Criteria: Based on clinical presentation and lab results. Serum corsteriods level can also be measured, adn results will show corticosteroids levels that remain depressed after administration of ACTH.