# Hormones > Endocrine physiology for FMGE: hormone classes and mechanisms, pituitary-thyroid-adrenal axes, insulin, calcium regulation and feedback logic. - Canonical URL: https://prepelephant.com/topics/fmge/physiology/hormones-fmge - Exam / course: FMGE · Subject: Physiology - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Hormones", PrepElephant, https://prepelephant.com/topics/fmge/physiology/hormones-fmge ## Direct answer Hormones signal through three broad mechanisms: water-soluble peptides and catecholamines bind membrane receptors and act within minutes through second messengers such as cAMP and IP3, while steroid hormones and thyroid hormone slip into cells and change gene transcription over hours, and insulin-type receptors carry their own kinase activity. Most endocrine glands sit in hypothalamus-pituitary-target axis loops in which the target hormone feeds back negatively on the pituitary and hypothalamus. Any endocrine question becomes systematic once you classify the hormone, draw its loop and ask which step the pathology breaks — and where the feedback signature points. ## What you must remember - Classes: peptide hormones stored in vesicles, water-soluble, short plasma half-life, membrane receptors (insulin, PTH, ACTH); steroids synthesised on demand from cholesterol, carried bound, nuclear receptors (cortisol, aldosterone, vitamin D); amines split — catecholamines act at membranes, thyroid hormone at nuclei. - Second-messenger map: Gs raises cAMP (TSH, ACTH, LH, glucagon, PTH); Gq raises IP3-calcium (GnRH, TRH, angiotensin II, V1 ADH); insulin works through a receptor tyrosine kinase moving GLUT4. - Anterior pituitary acidophils secrete growth hormone and prolactin, basophils the rest; prolactin alone is under tonic dopamine inhibition, so any stalk lesion raises it while every other anterior hormone falls. - Growth hormone — the most abundant anterior pituitary hormone — acts mainly through IGF-1 from the liver; excess before epiphyseal fusion gives gigantism, after fusion acromegaly. - Thyroid: iodide trapped by the NIS symporter, thyroglobulin processed to mostly T4 with peripheral conversion to the more potent T3; TSH remains the single best thyroid-function test paired with free T4. - Adrenal cortex in zones: glomerulosa makes aldosterone under renin, fasciculata cortisol under ACTH with a strong early-morning peak, reticularis androgens; cortisol is permissive, anti-inflammatory and gluconeogenic. - Calcium trio: PTH raises calcium fast (bone resorption, renal reabsorption, vitamin D activation), vitamin D raises it slowly through the gut, calcitonin opposes weakly; corrected calcium adds 0.8 mg/dL per 1 g/dL of albumin below 4. ## How to solve any endocrine stem Put the patient on the axis before touching the diagnosis. If the target gland fails primarily, its hormone falls while the trophic hormone rises — primary hypothyroidism shows high TSH with low free T4 and a goitre from constant stimulation; Addison disease shows low cortisol with high ACTH and, because POMC splits to MSH, the hyperpigmentation of the skin creases and mouth. If the pituitary fails secondarily, both hormones are low and the creases stay pale — secondary hypothyroidism and Sheehan syndrome follow that grammar. If a gland secretes autonomously, the target hormone rises while the trophic hormone is suppressed — a cortisol story with ACTH crushed suggests an adrenal adenoma, and the same logic catches a prolactinoma except that prolactin itself is the exception with no meaningful target-gland feedback. Two worked examples carry the whole method. A woman with weight gain and cold intolerance: test TSH first; high TSH with low free T4 settles primary hypothyroidism, most often Hashimoto thyroiditis, and starting levothyroxine follows. A man with moon face and striae: measure overnight dexamethasone suppression, then ACTH to separate pituitary Cushing disease (ACTH high-normal, bilateral hyperplasia) from adrenal tumour (ACTH suppressed); the physiology of feedback — suppressed ACTH means the tumour is autonomous — is the examinable reasoning, not the drug doses. ## Where students slip The recurring slips are conceptual. Steroid hormones are not stored — they are synthesised on demand, which is why stimulation tests read synthesis capacity, not release. Total hormone levels mislead when binding proteins shift: pregnancy raises thyroxine-binding globulin and total T4 while free T4 stays normal, and only the free fraction is bioactive. Prolactin's unique inhibitory control is forgotten, so stalk-compression patterns are misread. The hyperpigmentation of primary adrenal failure is attributed to cortisol rather than to ACTH-MSH overproduction, missing why secondary failure looks pale. ## Frequently asked questions ### Why does prolactin rise after pituitary stalk damage? It is the only anterior pituitary hormone under dominant inhibitory control by hypothalamic dopamine; cutting the stalk removes the brake while every other trophic hormone falls. ### Which second messengers do Gs and Gq systems use? Gs raises cAMP (TSH, ACTH, LH, glucagon, PTH); Gq raises IP3 and calcium (GnRH, TRH, angiotensin II, V1 ADH) — insulin stands apart with receptor tyrosine kinase. ### How do primary and secondary adrenal insufficiency differ? Primary (Addison) shows low cortisol with high ACTH, hyperpigmentation and salt craving; secondary pituitary failure shows low ACTH, pallor and normal pigment. ### Why is T3 more potent than T4 though less is secreted? T4 is the main secretory product and circulating prohormone, but T3 binds the nuclear receptor with several-fold higher affinity and mediates most tissue action. ### What is the corrected calcium formula and why? Add 0.8 mg/dL to measured calcium for each 1 g/dL of albumin below 4 g/dL, because hypoalbuminaemia lowers total but not physiologically active calcium. ### How does insulin lower serum potassium? It stimulates the Na-K ATPase and drives potassium into cells, which is why insulin with glucose is first-line temporising therapy in hyperkalaemia.