Lecture 36: Adrenal glands, adrenaline, cortisol and stress

The adrenal cortex and adrenal medulla derive from ❌ embryonic tissue. The cortex is ❌, while the medulla is ❌.

Cortisol is a ❌ hormone which can permeate the membrane. Within the ❌, it binds to a mobile ❌, and forms a hormone-receptor complex that migrates to the ❌ and binds to DNA at ❌ sites. Specific genes are activated to up-regulate ❌ of mRNA. In the cytoplasm, mRNA ❌ and synthesizes a new protein.

Either stress or non-stress neural inputs (e.g. circadian rhythm or ❌ blood glucose level) can stimulate the ❌ to release ❌ releasing hormone (CRH). CRH travels via capillaries to the ❌ pituitary gland and ❌ of adrenocorticotropic hormone (ACTH). ACTH travels via the bloodstream and reaches the kidney's ❌ where it stimulates release of cortisol.

The metabolic effects of cortisol ❌ glucose uptake by cells in muscle and fat. In skeletal muscle, there is also stimulation of protein ❌, and in fat, there is also stimulation of ❌ breakdown. In the ❌, gluconeogenesis is ❌.
The other effects of cortisol are that it aids in coping with stress in the ❌ term and that it ❌ the immune system in the ❌ term.

Addison's disease results from adrenal ❌ dysfunction: low cortisol and aldosterone levels. Low cortisol levels mean that cortisol will not properly feed back negatively to the ❌, meaning more ACTH (adrenocorticotropic hormone) is released into the blood. ACTH stimulates melanin synthesis and bronzing of the ❌ is observed. Other symptoms include ❌ blood glucose level, low blood pressure, fatigue, weakness, and unexplained ❌ loss.

Cushing syndrome is a result of ❌ cortisol. Symptoms include ❌ blood pressure and glucose levels, weakness, fat deposition in the face, neck and trunk (particularly ❌), edema (swelling), muscular ❌, and ❌ of bone mass.