What is the do of "buffalo hump" and " moon face" within patients beside cushing's syndrome?
why is the symptom of "buffalo hump" and "moon face".
ex. buffalo hump = increase androgen levels due to pituitary gland injury
P. S. seperate explanation please for buffalo hump and moon face...tnx
Answer: Cushing's Syndrome (also call hypercortisolism or hyperadrenocorticism) is an endocrine disorder caused by big levels of cortisol contained by the blood from a variety of cause, including a pituitary adenoma (known as Cushing's disease), adrenal hyperplasia or neoplasia, ectopic ACTH production (e.g., from a small cell lung cancer), and iatrogenic (steroid use). Normally, cortisol is released from the adrenal gland in response to ACTH self released from the pituitary gland. Both Cushing's syndrome and Cushing's disease are characterized by elevated levels of cortisol contained by the blood, but the cause of elevated cortisol differs between the two. Cushing's disease specifically refers to a tumour surrounded by the pituitary gland that stimulates excessive release of cortisol from the adrenal gland by releasing large amounts of ACTH. In Cushing's disease, ACTH level do not respond to negative feedback from the glorious levels of cortisol.
Cushing's disease be described by American physician, surgeon and endocrinologist Harvey Cushing (1869-1939) and reported by him in 1932.
Cushing's syndrome--which is also a relatively adjectives condition in domestic dogs and horses--is characterised by atypical fat deposition. (The syndrome within horses leads to weightiness loss, polyuria and polydipsia and may cause laminitis.)
1 Signs and symptoms
1.1 Exogenous Versus Endogenous
6 Hyperadrenocorticism within companion animals
7 See also
9 External links
 Signs and symptoms
Symptoms include rapid mass gain, particularly of the trunk and obverse with sparing of the limb (central obesity), a round face commonly referred to as a "moon face", excess sweating, telangiectasia (dilation of capillaries), thinning of the skin (which causes graceful bruising) and other mucous membranes, purple or red striae (the weight gain within Cushing's stretches the skin, which is thin and feeble, causing it to hemorrhage) on the trunk, buttocks, arms, legs or breasts, proximal muscle fearfulness (hips, shoulders), and hirsutism (facial male-pattern hair growth). A adjectives sign is the growth of fat pad along the collar bone and on the back of the nouns (known as a lipodystrophy). The excess cortisol may also affect other endocrine systems and cause, for example, insomnia, reduced libido, impotence, amenorrhoea and infertility. Patients frequently suffer an assortment of psychological disturbances, ranging from euphoria to psychosis. Depression and anxiety are also adjectives.
Other signs include persistent hypertension (due to cortisol's improvement of epinephrine's vasoconstrictive effect) and insulin resistance (especially common surrounded by ectopic ACTH production), leading to hyperglycemia (high blood sugars) which can head to diabetes mellitus. Untreated Cushing's syndrome can lead to heart disease and increased mortality. Cushing's syndrome due to excess ACTH may also result surrounded by hyperpigmentation. This is due to Melanocyte-Stimulating Hormone production as a byproduct of ACTH synthesis from Proopiomelanocortin (POMC). Cortisol can also exhibit mineralcorticoid activity surrounded by high concentrations, worsening the hypertension and influential to hypokalemia (common in ectopic ACTH secretion). Furthermore, gastrointestinal disturbances, opportunistic infections and impair wound healing (cortisol is a stress hormone, so it depresses the immune and inflammatory responses). Osteoporosis is also problem contained by Cushing's Syndrome, as mentioned before, cortisol evokes a stress-like response. The body's continuation of bone (and other tissues) is therefore no longer one of its foremost priorities, so to speak.
 Exogenous Versus Endogenous
There are two types of Cushing’s syndrome: exogenous and endogenous. In endogenous disease, excess cortisol production within the body is the mete out, whilst in exogenous disease the contributing factor is typically steroid medication (i.e. it originates outside the body) mimicing cortisol's hum. The signs and symptoms are therefore virtually very, aside from those induced by ACTH in pituitary-dependent disease and ectopic ACTH-producing tumours (such as hyperpigmentation). The exogenous route is by far the most commonly taken within Cushing’s syndrome (a fact that adjectives too many give the impression of being to forget). Examples of such exogenous steroid medications are those used to treat inflammatory disorders such as asthma and rheumatoid arthritis, or to suppress the immune system after an organ transplant. This type of Cushing’s is pro tem and goes away after the long-suffering has finished taking the cortisol-like medication. Endogenous Cushing’s syndrome is unusual, it usually comes on slowly and can be difficult to diagnose.
When Cushing's is suspected, either a dexamethasone suppression oral exam (administration of dexamethasone and frequent determination of cortisol and ACTH level), or a 24-hour urinary measurement for cortisol propose equal detection rates. Dexamethasone is a glucocorticoid and simulates the effects of cortisol, including negative feedback on the pituitary gland. When dexamethasone is administered and a blood indication is tested, high cortisol would be indicative of Cushing's syndrome because at hand is an ectopic source of cortisol or ACTH (eg: adrenal adenoma) that is not inhibited by the dexamethasone. A original approach, recently cleared by the US FDA, is sampling cortisol surrounded by saliva over 24 hours, which may be equally sensitive, as late dark levels of salivary cortisol are elevated in Cushingoid patients. Other pituitary hormone level may need to be ascertained. Performing a physical nouns to determine any visual grazing land defect may be important if a pituitary lesion is suspected, which may compress the optic chiasm causing typical bitemporal hemianopia.
When any of these test are positive, CT scanning of the adrenal gland and MRI of the pituitary gland are perform to detect the presence of any adrenal or pituitary adenomas or incidentalomas (the incidental discovery of harmless lesions). Scintigraphy of the adrenal gland next to iodocholesterol scan is occasionally necessary. Very once in a while, determining the cortisol levels contained by various vein in the body by venous catheterisation, working towards the pituitary (petrosal sinus sampling) is compulsory.
Both the hypothalamus and the pituitary gland are in the brain. The hypothalamus releases corticotropin-releasing hormone (CRH), which stimulates the pituitary gland to release corticotropin (ACTH). ACTH travels via the blood to the adrenal gland, where on earth it stimulates the release of cortisol. Cortisol is secreted by the cortex of the adrenal gland from a region called the zona fasciculata surrounded by response to ACTH. Elevated levels of cortisol exert cynical feedback on the pituitary, which decreases the amount of ACTH released from the pituitary gland. Strictly, Cushing's syndrome refers to excess cortisol of any etiology. One of the cause of Cushing's syndrome is a cortisol secreting adenoma within the cortex of the adrenal gland. The adenoma causes cortisol level in the blood to be extraordinarily high, and gloomy feedback on the pituitary from the high cortisol level causes ACTH level to be very low. Cushing's disease refers merely to hypercortisolism secondary to excess production of ACTH from a corticotrophic pituitary adenoma. This cause the blood ACTH levels to be elevated along near cortisol from the adrenal gland. The ACTH levels remain big because a tumor causes the pituitary to be unresponsive to refusal feedback from high cortisol level.
The main point to remember is that the beyond measure majority of cases of Cushing's syndrome are caused by steroid medication (such causes are described as iatrogenic) so healthcare workers must other remember to check patients' medications first, as stopping or reducing the dose will usually resolve the problem.
If an adrenal adenoma is identified it may be removed by surgery. An ACTH-secreting corticotrophic pituitary adenoma should be removed after diagnosis. Regardless of the adenoma's location, most patients will require steroid replacement postoperatively at least possible in the interim as long-term suppression of pituitary ACTH and typical adrenal tissue does not recover on the double. Clearly, if both adrenals are removed, replacement with hydrocortisone or prednisolone is imperative.
In those patients not suitable for or unwilling to put up with surgery, several drugs have be found to inhibit cortisol synthesis (e.g. ketoconazole, metyrapone) but they are of limited efficacy.
Removal of the adrenals within the absence of a prearranged tumor is occasionally performed to wipe out the production of excess cortisol. In some occasions, this removes distrustful feedback from a previously occult pituitary adenoma, which starts growing rapidly and produces extreme level of ACTH, leading to hyperpigmentation. This clinical situation is certain as Nelson's syndrome.
Iatrogenic Cushing's (caused by treatment with corticosteroids) is the most adjectives form of Cushing's syndrome. The incidence of pituitary tumors may be relatively high, as much as one within five people,  but just a minute fraction are active and produce excessive hormones
It be set to coole. It's caused by too much cortisol person released --that's what Cushing's syndrome is about.
People who own to take cortisol for amalgamated problems or sometimes for other diseases that go along next to AIDS for instance, can develop both the buffalo hump and moonface.
Almost everyone who either take Cortisol for a while or makes too much of it smoothly, also gains substance.