Secondary adrenal insufficiency due to steroid use

During minor illness (., flu or fever >38° C [° F]) the hydrocortisone dose should be doubled for 2 or 3 days. The inability to ingest hydrocortisone tablets warrants parenteral administration. Most patients can be educated to self administer hydrocortisone, 100 mg IM, and reduce the risk of an emergency room visit. Hydrocortisone, 75 mg/day, provides adequate glucocorticoid coverage for outpatient surgery. Parenteral hydrocortisone, 150 to 200 mg/day (in three or four divided doses), is needed for major surgery, with a rapid taper to normal replacement during the recovery. Patients taking more than 100 mg hydrocortisone/day do not need any additional mineralocorticoid replacement. All patients should wear some form of identification indicating their adrenal insufficiency status.

“The pituitary gland makes a hormone called adrenocorticotropic hormone (ACTH), which stimulates the adrenal cortex to produce its hormones. Inadequate production of ACTH can lead to insufficient production of hormones normally produced by your adrenal glands, even though your adrenal glands aren’t damaged. Doctors call this condition secondary adrenal insufficiency.
Another more common cause of secondary adrenal insufficiency occurs when people who take corticosteroids for treatment of chronic conditions, such as asthma or arthritis, abruptly stop taking the corticosteroids.” http:///diseases-conditions/addisons-disease/symptoms-causes/dxc-20155757

In secondary hyperparathyroidism, a disease outside of the parathyroids causes all of the parathyroid glands to become enlarged and hyperactive. It is usually caused by kidney failure, a problem where the kidney is unable to clean the blood of phosphorus produced by the body and unable to make enough vitamin D (specifically calcitriol, the active form of vitamin D). The build-up of phosphorous leads to low levels of calcium in the blood, which in turn stimulates the parathyroid glands to increase parathyroid hormone (PTH) production which in turn causes them to grow. As the disease progresses, the parathyroid glands no longer respond normally to calcium and Vitamin D. During early secondary hyperparathyroidism, the blood calcium levels are normal or low, but the PTH level is high. As the disease gets worse, some of the treatments for the kidney disease (Vitamin D and calcium-containing phosphate binders) may eventually lead to abnormally high levels of calcium in the blood. High PTH levels can lead to 1) weakening of the bones 2) calciphylaxis (when calcium forms clumps in the skin and leads to ulcers and potentially death of surrounding tissue), 3) cardiovascular complications, 4) abnormal fat and sugar metabolism, 5) itching (pruritis), and 6) low blood counts (anemia).
Figure 7: Calciphylaxis Other less common causes of secondary hyperparathyroidism are long-term lithium therapy, vitamin D deficiency, gastrointestinal malabsorption syndromes (when the intestines do not absorb vitamins and minerals properly), malnutrition, vitamin D-resistant rickets, or hypermagnesemia (abnormally high blood magnesium levels). 87 Calciphylaxis is uncommon. These painful skin lesions begin as small nodules or plaques with a purplish color, mottling, or livedo reticularis in a stellate pattern. The ulcers grow and parts become necrotic (. the tissue dies). They rarely heal with routine wound care measures.

Secondary adrenal insufficiency due to steroid use

secondary adrenal insufficiency due to steroid use


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