Editing Adrenal gland (section)

===Adrenal insufficiency===
Adrenal insufficiency (the deficiency of [[glucocorticoid]]s) occurs in about 5 in 10,000 in the general population.<ref name="harrison's" /> Diseases classified as ''primary adrenal insufficiency'' (including [[Addison's disease]] and genetic causes) directly affect the adrenal cortex. If a problem that affects the [[hypothalamic–pituitary–adrenal axis]] arises outside the gland, it is a ''secondary adrenal insufficiency''.<ref>{{cite web | url=https://www.ncbi.nlm.nih.gov/books/NBK279083/ | pmid=25905309 | date=2000 | last1=Feingold | first1=K. R. | last2=Ahmed | first2=S. F. | last3=Anawalt | first3=B. | last4=Blackman | first4=M. R. | last5=Boyce | first5=A. | last6=Chrousos | first6=G. | last7=Corpas | first7=E. | last8=De Herder | first8=W. W. | last9=Dhatariya | first9=K. | last10=Dungan | first10=K. | last11=Hofland | first11=J. | last12=Kalra | first12=S. | last13=Kaltsas | first13=G. | last14=Kapoor | first14=N. | last15=Koch | first15=C. | last16=Kopp | first16=P. | last17=Korbonits | first17=M. | last18=Kovacs | first18=C. S. | last19=Kuohung | first19=W. | last20=Laferrère | first20=B. | last21=Levy | first21=M. | last22=McGee | first22=E. A. | last23=McLachlan | first23=R. | last24=Muzumdar | first24=R. | last25=Purnell | first25=J. | last26=Rey | first26=R. | last27=Sahay | first27=R. | last28=Shah | first28=A. S. | last29=Singer | first29=F. | last30=Sperling | first30=M. A. | title=Adrenal Insufficiency | publisher=MDText.com | display-authors=1 }}</ref>

====Addison's disease====
[[File:T. Addison; On...supra-renal capsules Wellcome L0018484.jpg|thumb|right|Characteristic skin [[hyperpigmentation]] in [[Addison's disease]]]]
Addison's disease refers to primary hypoadrenalism, which is a deficiency in glucocorticoid and mineralocorticoid production by the adrenal gland. In the Western world, Addison's disease is most commonly an [[autoimmunity|autoimmune]] condition, in which the body produces [[Antibody|antibodies]] against cells of the adrenal cortex. Worldwide, the disease is more frequently caused by infection, especially from [[tuberculosis]]. A distinctive feature of Addison's disease is [[hyperpigmentation]] of the skin, which presents with other nonspecific symptoms such as fatigue.<ref name=williams />

A complication seen in untreated Addison's disease and other types of primary adrenal insufficiency is the [[adrenal crisis]], a [[medical emergency]] in which low glucocorticoid and mineralocorticoid levels result in [[hypovolemic shock]] and symptoms such as vomiting and fever. An adrenal crisis can progressively lead to [[stupor]] and [[coma]].<ref name=williams /> The management of adrenal crises includes the application of [[hydrocortisone]] injections.<ref>[http://www.pituitary.org.uk/media/134894/Factsheet-for-Ambulance-Personnel.pdf Hydrocortisone Emergency Factsheet for Ambulance Personnel] {{Webarchive|url=https://web.archive.org/web/20150924073703/http://www.pituitary.org.uk/media/134894/Factsheet-for-Ambulance-Personnel.pdf |date=24 September 2015 }} The Pituitary Foundation</ref>

====Secondary adrenal insufficiency====
In secondary adrenal insufficiency, a dysfunction of the [[hypothalamic–pituitary–adrenal axis]] leads to decreased stimulation of the adrenal cortex. Apart from suppression of the axis by glucocorticoid therapy, the most common cause of secondary adrenal insufficiency are tumors that affect the production of [[adrenocorticotropic hormone]] (ACTH) by the [[pituitary gland]].<ref name="harrison's" /> This type of adrenal insufficiency usually does not affect the production of [[mineralocorticoid]]s, which are under regulation of the [[renin–angiotensin system]] instead.<ref name=williams />

====Congenital adrenal hyperplasia====
[[Congenital adrenal hyperplasia]] is a family of [[congenital diseases]] in which [[mutation]]s of enzymes that produce steroid hormones result in a [[glucocorticoid deficiency]] and malfunction of the negative feedback loop of the [[HPA axis]]. In the HPA axis, cortisol (a glucocorticoid) inhibits the release of [[corticotropin-releasing hormone|CRH]] and [[Adrenocorticotropic hormone|ACTH]], hormones that in turn stimulate corticosteroid synthesis. As cortisol cannot be synthesized, these hormones are released in high quantities and stimulate production of other adrenal steroids instead. The most common form of congenital adrenal hyperplasia is due to [[21-hydroxylase]] deficiency. 21-hydroxylase is necessary for production of both mineralocorticoids and glucocorticoids, but not [[androgen]]s. Therefore, ACTH stimulation of the adrenal cortex induces the release of excessive amounts of [[adrenal androgen]]s, which can lead to the development of ambiguous [[genitalia]] and [[secondary sex characteristic]]s.<ref name=charmandari />