Hypothalamic pituitary adrenal axis suppression and inhaled corticosteroid therapy

The circadian pattern of cortisol release is controlled by the suprachiasmatic nucleus (SCN) of the hypothalamus, also known as the body clock. Nerve signals from the SCN cause the paraventricular nucleus (PVN) of the hypothalamus to release pulses of CRH roughly once per hour, resulting in HPA axis activation and cortisol release. There are also direct links between the SCN and the adrenal gland itself (bypassing the HPA axis) through sympathetic nerve fibres, causing the adrenal gland to become more sensitive to ACTH stimulation during the morning, further adding to the circadian pattern of cortisol release throughout the day.

FSH and LH are secreted by the anterior pituitary in response to gonadotropin-releasing hormone (GNRH) secreted by the hypothalamus. In both males and females, FSH and LH secretion is regulated by a balance of positive and negative feedback mechanisms involving the hypothalamic-pituitary axis, the reproductive organs, and the pituitary and sex steroid hormones. FSH and LH play a critical role in maintaining the normal function of the male and female reproductive systems. Abnormal FSH levels with corresponding increased or decreased levels of LH, estrogens, progesterone, and testosterone are associated with a number of pathological conditions. Increased FSH levels are associated with menopause and primary ovarian hypofunction in females and primary hypogonadism in males. Decreased levels of FSH are associated with primary ovarian hyper-function in females and primary hypergonadism in males. Normal or decreased levels of FSH are associated with polycystic ovary disease in females. In males, LH is also called interstitial cell-stimulating hormone (ICSH). Abnormal LH levels with corresponding increased or decreased levels of FSH, estrogens, progesterone, and testosterone are associated with a number of pathological conditions. Increased LH levels are associated with menopause, primary ovarian hypofunction, and polycystic ovary disease in females and primary hypo-gonadism in males. Decreased LH levels are associated with primary ovarian hyperfunction in females and primary hyper-gonadism in males.

The hypothalamus senses low circulating levels of thyroid hormone (Triiodothyronine (T3) and Thyroxine (T4)) and responds by releasing thyrotropin-releasing hormone (TRH). The TRH stimulates the pituitary to produce thyroid-stimulating hormone (TSH). The TSH, in turn, stimulates the thyroid to produce thyroid hormone until levels in the blood return to normal. Thyroid hormone exerts negative feedback control over the hypothalamus as well as anterior pituitary, thus controlling the release of both TRH from hypothalamus and TSH from anterior pituitary gland. [2]

Hypothalamic pituitary adrenal axis suppression and inhaled corticosteroid therapy

hypothalamic pituitary adrenal axis suppression and inhaled corticosteroid therapy

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hypothalamic pituitary adrenal axis suppression and inhaled corticosteroid therapyhypothalamic pituitary adrenal axis suppression and inhaled corticosteroid therapyhypothalamic pituitary adrenal axis suppression and inhaled corticosteroid therapyhypothalamic pituitary adrenal axis suppression and inhaled corticosteroid therapyhypothalamic pituitary adrenal axis suppression and inhaled corticosteroid therapy

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