This is an extract of our Hpa Axis document, which we sell as part of our Endocrinology and Integument 1 Notes collection written by the top tier of University Of Nottingham students.
The following is a more accessble plain text extract of the PDF sample above, taken from our Endocrinology and Integument 1 Notes. Due to the challenges of extracting text from PDFs, it will have odd formatting:
1. The HPA axis The HPA (hypothalamic-pituitary-adrenal) axis controls the release of glucocorticoids. The PVN of the hypothalamus produced corticotropin releasing hormone (CRH), which stimulates the secretion of adrenocorticotrophic hormone (ACTH) from the pituitary gland. ACTH is formed from POMC in the pars distalis. ACTH then stimulates the adrenal cortex to produce glucocorticoids, predominantly cortisol. The entire pathway is controlled by negative feedback of cortisol on the pituitary gland and hypothalamus. This can be by a short or long loop. The short loop is where cortisol feeds back directly on the hypothalamus, whereas the long loop is where it feeds back on the pituitary first.
The negative feedback system of the HPA axis keeps glucocorticoid concentration within a normal range.
2. Hyperadrenocorticism Hyperadrenocorticism (HAC) is a dysfunction of the HPA axis causing excess glucocorticoid (cortisol) levels. There are four possible causes of HAC:
A tumour of the pars distalis of the pituitary gland resulting in excessive ACTH production, and so excessive cortisol levels.
A tumour of the pars intermediate resulting in excessive ACTH production and so excessive cortisol levels (pituitary dependent HAC).
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