Appendix F · Hormone Reference Table

How to use this appendix

There are roughly fifty hormones in this book, and students routinely try to learn them as fifty independent facts. That approach fails, and it fails predictably: fifty unlinked items exceed what anyone can hold, and the exam does not ask you to recite them anyway. It asks you what happens to a variable when a gland fails.

Learn hormones on three axes instead. Each one collapses a large amount of memorization into a small amount of reasoning.

1 · Chemical class predicts the physical behavior of the molecule. A hormone is either water-soluble (peptides, proteins, glycoproteins, and the catecholamines) or lipid-soluble (steroids and thyroid hormone). That single fact predicts four others: how it travels in plasma, how long it survives there, where its receptor sits, and how fast it acts (§16.2). Water-soluble hormones dissolve free in plasma, are cleared in seconds to minutes, bind surface receptors, and act through second messengers within seconds. Lipid-soluble hormones ride on carrier proteins, persist for hours to days, bind intracellular receptors, and act by changing gene transcription over hours. If you know the class, you have already answered half the questions that can be asked.

2 · The axis tells you where a lesion can hide. Most of the classic endocrine hormones sit in a three-tier chain: hypothalamus releases a trophic factor into the portal blood, anterior pituitary releases a tropic hormone into the systemic blood, target gland releases the effector hormone, and the effector hormone feeds back on both tiers above it. Once you can draw that chain, the diagnostic logic in §F.5 follows mechanically — and it is the same logic for the thyroid, the adrenal cortex, and the gonads.

3 · The defended variable tells you the point of the whole thing. Every hormone exists to hold some variable inside a range. Glucose. Plasma calcium. Extracellular fluid volume. Plasma osmolality. Core metabolic rate. Plasma sodium. Oxygen-carrying capacity. When you meet a hormone you cannot recall, ask what it is defending; the actions usually fall out of the answer. Aldosterone defends extracellular fluid volume, therefore it retains sodium, therefore it retains water, therefore it raises blood pressure, therefore it excretes potassium and hydrogen ion in the exchange. That is one fact expanded into five.

F.1 Chemical class at a glance

Two consequences worth memorizing because they are asked constantly. First, steroid hormones cannot be stored, so a gland that must raise steroid output must raise synthesis, which is why steroid responses take at least half an hour and why chronic stimulation causes gland hypertrophy rather than just faster release. Second, only free hormone is active; protein-bound hormone is a circulating reservoir. This is why pregnancy, which raises thyroxine-binding globulin, raises total T₄ while leaving free T₄ and the patient euthyroid — and why total hormone assays mislead and free assays do not.

F.2 Master table

Chapter numbers in the final column give the chapter where the hormone is developed, not merely mentioned.

Hypothalamic releasing and inhibiting hormones

All are peptides, all travel the short hypophyseal portal system to the anterior pituitary in high concentration, and all are secreted in pulses — a fact that matters clinically, because continuous administration of GnRH paradoxically shuts the axis down.

Anterior pituitary

Six hormones from five cell types. Three are tropic (they command other endocrine glands) and three act directly on non-endocrine tissue.

Posterior pituitary

Not a gland. The posterior pituitary is the axon terminals of hypothalamic neurons whose cell bodies sit in the supraoptic and paraventricular nuclei; the hormones are made in the hypothalamus and stored downstream. This is neurosecretion, and it explains why the posterior lobe has no portal system and no releasing hormones.

Thyroid and parathyroid

Adrenal cortex and medulla

The cortex is three zones, and the mnemonic that matters is that they run outside-in with their products: salt, sugar, sex — glomerulosa/aldosterone, fasciculata/cortisol, reticularis/androgens. The medulla is not cortex at all; it is a modified sympathetic ganglion whose postganglionic neurons lost their axons and secrete into blood.

Pancreatic islets

Roughly one to two million islets, about 1–2% of pancreatic mass, with an internal blood supply arranged so that beta cell products bathe the alpha cells downstream — an anatomical detail with a physiological point: insulin directly restrains glucagon.

Gonadal

Placental

The placenta is a temporary endocrine organ that outproduces every other gland in the body, and its hormones explain most of the physiology of pregnancy.

Pineal and thymic

Hormones from organs that are not glands

This is the section students underestimate, and it is where the integration questions come from. Every organ below has a day job and a hormone on the side, and the hormone almost always defends the variable the day job is about.

F.3 The three-tier axes

Four of the endocrine system's control loops share one architecture. Learn the architecture once and you have learned four systems, plus the diagnostic method in §F.5.

        THE THREE-TIER ENDOCRINE AXIS — one pattern, four instances

  TIER 1     ┌────────────────────────────────────────┐
  HYPO-      │  HYPOTHALAMUS                          │◄──────────────┐
  THALAMUS   │  releasing hormone · PULSATILE · tiny  │               │
             │  amounts · never reaches systemic blood│               │
             └──────────────────┬─────────────────────┘               │
                                │  hypophyseal PORTAL veins           │
                                ▼  (short trip, very high [ ])        │
  TIER 2     ┌────────────────────────────────────────┐          LONG │
  ANTERIOR   │  ANTERIOR PITUITARY                    │◄────────┐LOOP │
  PITUITARY  │  TROPIC hormone → systemic circulation │         │ (−) │
             └──────────────────┬─────────────────────┘   SHORT │     │
                                │                          LOOP │     │
                                ▼                           (−) │     │
  TIER 3     ┌────────────────────────────────────────┐         │     │
  TARGET     │  TARGET GLAND                          │─────────┘     │
  GLAND      │  EFFECTOR hormone → every tissue       │───────────────┘
             └──────────────────┬─────────────────────┘
                                ▼
                    TISSUE EFFECT = the DEFENDED VARIABLE
                    (also the thing the patient feels)

  ══════════════════════════════════════════════════════════════════════

   AXIS       TIER 1         TIER 2        TIER 3            DEFENDS
   ──────────────────────────────────────────────────────────────────────
   HPT        TRH        →   TSH       →   T₄ → T₃           metabolic rate,
                                                             heat production
   HPA        CRH        →   ACTH      →   CORTISOL          plasma glucose,
                                                             stress response
   HPG ♂      GnRH       →   LH        →   TESTOSTERONE      spermatogenesis
              (pulses)   →   FSH       →   (inhibin B)       gamete number
   HPG ♀      GnRH       →   FSH → LH  →   ESTRADIOL →       ovulation, the
              (pulses)       surge         PROGESTERONE      endometrial cycle
   GH axis    GHRH  (+)  →   GH        →   IGF-1 (liver)     linear growth,
              SST   (−)                                      fuel partitioning
   ──────────────────────────────────────────────────────────────────────

   THE ONE PLACE THIS BREAKS:  ovulation.  Sustained HIGH estradiol for
   ~36 h flips the pituitary from negative to POSITIVE feedback, producing
   the LH surge.  Same hormone, same receptor, opposite sign — because the
   variable being defended has changed from "steady state" to "fire once."

What each loop actually controls

HPA. Cortisol feeds back on both CRH and ACTH. Because the axis has a strong circadian drive peaking just before waking, a single random cortisol value is nearly uninterpretable; timing is everything. Exogenous glucocorticoids suppress the whole axis, which is why steroids are tapered rather than stopped — the atrophied adrenal cortex needs weeks to recover.

HPT. T₃ and T₄ feed back on both tiers, and TSH is exquisitely sensitive: a small fall in free T₄ produces a large, logarithmic rise in TSH. That amplification is what makes TSH the best single screening test in all of endocrinology, and it is why TSH moves before free T₄ does in early disease (the "subclinical" state).

HPG. Two hormones, two feedback signals. Sex steroids restrain LH; inhibin selectively restrains FSH. This division exists because the gonad has two jobs — making steroids and making gametes — and the body needs to regulate them independently. It is also why a man with damaged seminiferous tubules but intact Leydig cells has a high FSH with a normal LH and normal testosterone.

GH axis. The only axis with a dedicated inhibitory hypothalamic hormone as well as a stimulatory one, and the only one whose effector hormone (IGF-1) is made by the liver rather than an endocrine gland. GH is secreted in large pulses, mostly during slow-wave sleep, so random GH levels are useless; IGF-1, which is stable across the day, is the practical measure.

F.4 Excess and deficiency: what each hormone looks like when it goes wrong

The fastest way to consolidate a hormone's actions is to read them in both directions. Every row below is the same physiology stated twice.

F.5 Localizing an endocrine lesion

Here is the single most useful diagnostic rule in endocrinology, and it follows directly from the loop diagram in §F.1:

Never measure a hormone alone. Measure the hormone and its tropic hormone together, and read the pair. In primary disease (the target gland is at fault) the two move in opposite directions, because feedback is intact and the pituitary is reacting correctly to a broken gland. In secondary disease (the pituitary is at fault) they move in the same direction, because the pituitary is the thing that is broken.

Terminology, so the labels stay straight:

Worked decision table · Thyroid axis (measure TSH + free T₄)

Worked decision table · Adrenal axis (measure 08:00 cortisol + ACTH)

Worked decision table · Gonadal axis (measure testosterone or estradiol + LH and FSH)

F.6 Second-messenger systems by hormone class

Water-soluble hormones cannot enter the cell, so every one of them works by converting an extracellular binding event into an intracellular chemical signal. There are only a handful of mechanisms, and knowing which one a hormone uses predicts both its speed and its drug interactions.

Two patterns are worth extracting. First, amplification is a property of the cascade, not the hormone: one molecule of glucagon can, through Gs, adenylate cyclase, cAMP, and PKA, liberate on the order of 10⁶ to 10⁸ glucose molecules from hepatic glycogen. That is why picomolar hormone concentrations produce millimolar metabolic effects. Second, the pathway predicts the latency: G-protein and kinase cascades act in seconds because they modify proteins that already exist, whereas intracellular receptors act in 30 minutes to days because they must build proteins that do not.

See also: Appendix B · Normal Laboratory Reference Values for reference intervals on the hormone assays named here, Appendix H · Units, Measures, and Physiological Constants for the unit conversions, and Chapter 16 · The Endocrine System for the mechanisms these tables compress.