- a control centre in 🧠 (hypothalamus & pituitary) which integrate feedback & send signals (⬇️⬆️) to the
- primary endocrine glands (e.g. thyroid) re. how much “effector hormone” to make
"Tropic" hormones (e.g. corticotropin aka ACTH) signal to another endo gland.
"Effector" hormones have widespread targets throughout the body & usually affect processes e.g. growth, metabolism 👶👧👩🦰
They also ‘feed back’ on the control centre 🔄
Tropic hormones include ACTH, TSH, FSH, LH and GH (anterior pituitary) 🧠.
Their respective effector hormones are cortisol, thyroid hormones (T3/T4), oestradiol/testosterone & IGF-1.
The “primary” gland is the one which makes the effector hormone – problems in this gland cause PRIMARY hyper/hypo function (-ism).
The “secondary” gland is the control centre so problems with this gland cause SECONDARY hypo/hyper function (-ism).
Example:
1ry hypothyroidism: the thyroid gland doesn’t make enough T3/4 (effector) hormone.
2ry hypothyroidism: the pituitary doesn’t send enough TSH (tropic hormone) to the thyroid, so in turn it doesn’t make enough T3/4.
Outcome is the same; cause is v different! 💡
• • •
Missing some Tweet in this thread? You can try to
force a refresh
Diabetes insipidus (DI) is the inability to hold onto water due to lack of /resistance to ADH.
Remember ADH is released as serum osmolality ⬆️ to ⬆️ renal water reabsorption, but in patients with DI this doesn’t occur and so they pass large vol watery urine - can be >10L/day!🛁
Note diabetes insipidus has nothing to do with glucose/sugar like diabetes mellitus! ⛔️❌⛔️
Misunderstandings are so common (even with HCPs) that there is a campaign to change the name to "pituitary insipidus"