Nursing Field Notes / Endocrine · Hormone Hall of Fame 1 of 3 · Med-Surg: Endocrine

🩸 ENDOCRINE SET NG-278 Hormones I NG-279 Hormones II NG-280 Hormones III NG-281 Pituitary Disorders NG-282 SIADH vs DI (1) NG-283 SIADH vs DI (2)

Hormone Hall of Fame I 🧠

The hypothalamus, the anterior pituitary’s six, and the sugar pair

NG-278 ENDOCRINE · PART 1 OF 3 ADHD-friendly visual edition

Endocrine looks like a list of 20 random hormones. It is not. It is one chain of command: hypothalamus → pituitary → target gland → hormone → and the hormone circles back and shuts the chain off. Learn the chain on this page and every disorder for the rest of the unit becomes the same question — which link broke, and which way did the numbers move? Part 1 covers the hypothalamus, the anterior pituitary’s six, and the pancreas pair.

🧠 One chainHypothalamus → pituitary → gland → hormone → feedback shuts it off.

⭐ FLAT PEGFSH · LH · ACTH · TSH · Prolactin · Endorphins · GH — all anterior.

🧪 Low hormone + HIGH tropic= the gland is broken (primary). Both low = the pituitary is broken.

🍬 Insulin is the only onethat lowers glucose. Four different hormones raise it.

🧠

THE CHAIN OF COMMAND

STEP 1 · FOUNDATION

Master this one drawing and you have already learned half of the endocrine unit.

🔬 Master diagram — the hypothalamic–pituitary axis

The hypothalamus sits directly above the pituitary and talks to its two lobes in two completely different languages: a chemical message down the portal veins to the anterior lobe, and an electrical message down actual nerve axons to the posterior lobe.

hypothalamus anterior lobe (glandular) posterior lobe (neural) stalk / infundibulum

🧠 "Front makes, back stores." The anterior lobe is a real gland that manufactures six hormones. The posterior lobe manufactures nothing — it is a loading dock for two hormones the hypothalamus already made.

🧬 What a hormone actually is

A chemical messenger made by a gland, poured into the blood, that travels everywhere but only changes cells carrying the matching receptor.

No duct. Endocrine glands dump straight into capillaries.
Whole-body delivery, selective effect. TSH bathes your toe too — your toe has no TSH receptor, so nothing happens.
Tiny amounts. Hormones work at concentrations measured in pg/mL. Small changes in a lab value are a big deal.

🧠 Lock and key. The hormone is the key; the receptor is the lock. No lock, no effect — which is exactly what goes wrong in nephrogenic DI and in type 2 diabetes.

🔁 Endocrine vs exocrine — one gland can be both

Endocrine = ductless, secretes into blood, acts far away.
Exocrine = has a duct, secretes onto a surface, acts locally.

The pancreas is both: its acinar cells send digestive enzymes down a duct into the duodenum (exocrine), while its islets drop insulin and glucagon straight into the blood (endocrine).

🧠 "EXo = EXit through a tube." ENdo = stays IN the blood.

🔬 Two hormone classes — why some act in seconds and some take days

This single difference explains a huge amount of pharmacology: IV insulin drops glucose in minutes, while a steroid like hydrocortisone needs hours to show its full anti-inflammatory effect, and stopping a long-term steroid abruptly is dangerous because the gene-level changes take days to reverse.

🧠 "Steroids are Sneaky and Slow — they walk right in. Peptides Knock and are Prompt."

📣 What actually makes a gland fire — three triggers, drawn

📣 Three things that trigger a hormone release

Humoral — a level in the blood changes. Glucose rises → insulin. Calcium falls → PTH.
Neural — a nerve fires. Sympathetic nerves fire → adrenal medulla dumps epinephrine.
Hormonal — another hormone orders it. TSH → thyroid releases T3/T4.

🧠 "H-N-H: blood, nerve, boss." Every "stimulus for release" column on your hormone chart is one of these three.

🎯 Tropic vs direct — a hormone with a day job

Tropic hormones boss another gland: TSH, ACTH, FSH, LH. Their name usually ends in -tropin or -tropic.

Direct-acting hormones act on ordinary tissue themselves: GH on bone and muscle, prolactin on breast tissue, insulin on every cell.

🧠 "-TROPIC = TRAFFIC cop." It doesn't do the work, it directs somebody else who does.

♻️ Negative feedback — the thermostat that runs the whole system

Almost every endocrine lab you will ever read is a feedback question. Ask two things: is the end hormone high or low? and is the stimulating hormone above it high or low? The pattern tells you where the break is.

🧠 Thermostat. Room cold → furnace ON. Room warm → furnace OFF. If the room is freezing and the furnace is roaring, the furnace is broken, not the thermostat.

⭐ Positive feedback — the two exceptions

Positive feedback amplifies instead of shutting off, and it always ends with an event that stops it.

Oxytocin in labor — contractions stretch the cervix → more oxytocin → stronger contractions. Ends at delivery.
The LH surge — rising estrogen briefly flips to stimulating LH, producing the surge that causes ovulation.

🧠 "Positive feedback = a snowball." Only labor and ovulation get to roll downhill.

🗺️

WHERE EVERY GLAND LIVES

STEP 1b · ORIENTATION

Nine glands, skull to pelvis — you will meet each one across Parts 1, 2 and 3.

🗺️ The endocrine map — anatomical positions

SERIES Part 1 (here) = hypothalamus, anterior pituitary, pancreas. Part 2 = posterior pituitary, thyroid, parathyroid, pineal, thymus. Part 3 = adrenals and gonads.

⭐

THE ANTERIOR SIX (PLUS ENDORPHINS)

STEP 2 · THE LIST

Source · target · effect · what makes it fire. Learn all four columns for each one.

🧠 FLAT PEG — the only mnemonic you need for the front lobe

FFSH — follicle stimulating hormone

LLH — luteinizing hormone

AACTH — adrenocorticotropic hormone

TTSH — thyroid stimulating hormone

PProlactin

EEndorphins

GGrowth hormone

🧠 If it is not in FLAT PEG, it is not anterior pituitary. Only ADH and oxytocin come out of the back — and the hypothalamus made those two.

🧪 TSH — thyroid stimulating hormone (thyrotropin)

Source: Anterior pituitary
Target: Thyroid gland
Effect: Tells the thyroid to make and release T3 and T4 — the metabolic rate hormones
Trigger: TRH from the hypothalamus; cold and stress raise it

Why nurses care: TSH is the single most sensitive screening test for thyroid disease, because the pituitary reacts to a tiny drop in thyroid hormone by shouting louder.

🧠 TSH moves OPPOSITE to the thyroid. Lazy thyroid (hypo) → TSH climbs. Overactive thyroid (hyper) → TSH gets suppressed to almost nothing.

🧪 ACTH — adrenocorticotropic hormone

Source: Anterior pituitary
Target: Adrenal cortex (the outer rind only)
Effect: Drives release of cortisol, adrenal androgens, and to a much smaller degree aldosterone
Trigger: CRH from the hypothalamus · physical or emotional stress · the early-morning peak of the body clock

ACTH does not control the adrenal medulla — the medulla answers to sympathetic nerves, not to the pituitary.

🧠 "ACTH knocks on the CORTEX, nerves shock the MEDULLA."

📈 GH — growth hormone (somatotropin)

Source: Anterior pituitary
Target: Bone, cartilage, muscle, liver, fat — almost everything
Effect: Anabolic: protein synthesis, cartilage and long-bone growth, organ growth. Catabolic on fat: breaks fat down for fuel. Raises blood glucose (anti-insulin). Enhances the effect of T3/T4.
Trigger: GHRH from the hypothalamus · low blood glucose · exercise · deep sleep · protein meals. Blocked by GHIH / somatostatin.

GH does most of its growth work indirectly, by making the liver release IGF-1 (somatomedin C) — which is why IGF-1 is the blood test used to screen for acromegaly.

🧠 "GH builds you up and burns fat down — and it fights insulin." That last part is why acromegaly so often comes with glucose intolerance or frank diabetes.

🤱 PRL — prolactin

Source: Anterior pituitary
Target: Breast (mammary alveolar cells)
Effect: Makes the milk. Also suppresses FSH/LH, which is why heavy breastfeeding often delays the return of menses
Trigger: Pregnancy · high estrogen · infant suckling. Uniquely, it is held switched off by dopamine from the hypothalamus

Prolactin is the one anterior hormone under tonic inhibition — the hypothalamus keeps a foot on the brake with dopamine. Cut the stalk, and prolactin is the only hormone that goes up.

🧠 "PRolactin PRoduces, oxytocin PUSHES." Prolactin makes the milk; oxytocin ejects it. Two different hormones, two different lobes.

🧪 FSH — follicle stimulating hormone

Source: Anterior pituitary
Target: Ovaries · testes
Effect: Female: grows the ovarian follicle that holds the egg, and drives estrogen production. Male: drives sperm production in the seminiferous tubules
Trigger: GnRH released in pulses from the hypothalamus

🧠 "FSH = Follicles & Sperm Helper."

🧪 LH — luteinizing hormone

Source: Anterior pituitary
Target: Ovaries · testes
Effect: Female: the mid-cycle LH surge triggers ovulation and then converts the leftover follicle into the corpus luteum, which makes progesterone. Male: tells Leydig cells to make testosterone
Trigger: GnRH; the surge is triggered by peak estrogen (positive feedback)

🧠 "LH = Lets the egg Hatch." Home ovulation predictor kits test for exactly this surge.

💊 Endorphins — the body's own opioid

Source: Anterior pituitary (cut from the same parent molecule as ACTH)
Target: Opioid receptors in the brain and spinal cord
Effect: Blunts pain transmission, produces euphoria and calm
Trigger: Pain · sustained exercise · stress · laughter

🧠 "ENDOgenous morPHINE." The "runner's high" and part of why non-drug pain measures (heat, distraction, massage, breathing) genuinely work.

📋 The releasing hormones — the hypothalamus's memo pad

Hypothalamus sends…	…which makes the pituitary release	…which lands on
TRH thyrotropin-releasing hormone	TSH	Thyroid → T3/T4
CRH corticotropin-releasing hormone	ACTH	Adrenal cortex → cortisol
GnRH gonadotropin-releasing hormone	FSH and LH	Ovary / testis
GHRH growth hormone-releasing hormone	GH	Bone, muscle, liver
GHIH / somatostatin (inhibiting)	turns GH off	—
Dopamine / PIH (inhibiting)	holds prolactin off	—

Notice the naming logic: hypothalamic hormones are -releasing; pituitary hormones are -tropic / -tropin. If a name has "releasing" in it, it came from the hypothalamus.

🧠 Same word, one letter apart: TRH is the memo, TSH is the order. The memo (Releasing) always comes from the brain above.

📋 Anterior pituitary quick chart — the exam version

Hormone	Target	Effect	Stimulus for release
ACTH	Adrenal cortex	Cortisol (and adrenal androgens); small aldosterone effect	CRH · stress · morning peak
FSH	Ovary / testis	Follicle growth & estrogen; sperm production	GnRH
LH	Ovary / testis	Ovulation, corpus luteum, testosterone	GnRH · estrogen surge
GH	Bone, muscle, liver, fat	Growth, protein building, fat breakdown, raises glucose	GHRH · low glucose · sleep · exercise
PRL	Breast	Milk production	Estrogen · pregnancy · suckling; blocked by dopamine
TSH	Thyroid	Release of T3 & T4	TRH · cold · stress
Endorphins	CNS opioid receptors	Pain relief, euphoria	Pain · exercise · stress

🍬

THE SUGAR PAIR — PANCREAS

STEP 3 · FUEL

Two hormones from two cell types in the same tiny island, pulling in opposite directions all day.

🔬 The glucose see-saw

beta cell / insulin alpha cell / glucagon glucose molecule liver glycogen store

🔬 Where the islets live — pancreas anatomy

The pancreas lies across the back of the upper abdomen: head tucked inside the C of the duodenum, body crossing the midline, tail touching the spleen. Damage the exocrine part (pancreatitis) and you get pain and malabsorption; damage enough islets and you get diabetes.

💉 Insulin — the only hormone that lowers glucose

Source: Pancreatic islet beta cells
Effect: Lowers blood glucose. Opens the door for glucose to enter muscle and fat, tells the liver to store glucose as glycogen, builds protein and fat, and drives potassium into cells with the glucose
Trigger: High blood glucose — chiefly after a meal

That potassium effect is why IV insulin plus dextrose is a standard emergency treatment for hyperkalemia, and why treating DKA drops the potassium fast enough to need replacement.

🧠 "Insulin is the KEY that lets sugar IN — and it drags potassium in with it."

🍬 Glucagon — the emergency crowbar

Source: Pancreatic islet alpha cells
Effect: Raises blood glucose. Breaks liver glycogen back down into glucose (glycogenolysis) and builds new glucose from protein and fat (gluconeogenesis)
Trigger: Low blood glucose — fasting, exercise, too much insulin

Nursing use: injectable or intranasal glucagon is the rescue for severe hypoglycemia in a patient who is unconscious or unable to swallow. It is useless if the liver has no glycogen left (starvation, advanced liver disease, alcohol use disorder). Turn the patient on their side — vomiting is common on waking.

🧠 "GLUCAGON = GLUCOSE GONE — go get it." Awake and able to swallow → give 15 g fast carbohydrate instead.

🧪 The other two islet cells

Delta cells → somatostatin. The islet's brake pedal — it damps down both insulin and glucagon and slows GI absorption, keeping the swings smooth.

PP / F cells → pancreatic polypeptide. Fine-tunes appetite and pancreatic exocrine secretion. Rarely tested, but it is why an islet is not just two cell types.

🧠 Alpha = Away with low sugar. Beta = Bring sugar in. Delta = Damp it all Down.

🚨 The four hormones that RAISE glucose

Glucagon — from the alpha cell, the fastest responder.
Cortisol — the stress steroid, sustains glucose for hours.
Growth hormone — anti-insulin, worst overnight.
Epinephrine — the fight-or-flight surge, plus the sweaty/shaky warning signs.

One hormone lowers glucose; four raise it. The body is far more afraid of hypoglycemia than of hyperglycemia — because the brain runs on glucose alone.

🧠 "GCGE — Get Cortisol, Growth, Epi." These four are also why any acutely stressed, infected or steroid-treated patient runs a higher glucose.

📋 Insulin vs glucagon — side by side

💉 INSULIN	🍬 GLUCAGON
Beta cells	Alpha cells
Released when glucose is HIGH	Released when glucose is LOW
Lowers blood glucose	Raises blood glucose
Storage hormone — "fed state"	Mobilizing hormone — "fasted state"
Pushes K⁺ into cells (lowers serum K⁺)	No meaningful potassium effect
Given for hyperglycemia and hyperkalemia	Given for severe hypoglycemia when the patient cannot swallow

🧠 "BIG": Beta = Insulin, Glucagon = the other one (alpha). If you can only remember one letter pairing, remember β → insulin.

🩺

THE NURSING LENS

STEP 4 · APPLY IT

How these six-plus-two hormones actually show up on a shift and in a question stem.

⭐ Read any endocrine lab in two moves

Move 1 — the end hormone. Is the actual working hormone (T4, cortisol, testosterone) high or low? That tells you the patient's symptoms.
Move 2 — the tropic hormone above it. High tropic = the gland failed and the pituitary is shouting. Low tropic = the pituitary itself failed.

🧠 "Symptoms come from the bottom, the diagnosis comes from the top."

🚨 Stress changes every one of these numbers

Surgery, trauma, infection, pain and even fear all fire the CRH → ACTH → cortisol axis and the sympathetic nerves at the same time. Predictable consequences on your patient:

Blood glucose rises — even in a patient with no diabetes.
Sodium and water are held on to — urine output falls, weight rises.
Potassium is dumped in the urine.
Immune response is blunted — a stressed patient may not mount a fever.

🧠 "Stress = sugar up, salt in, potassium out, immunity down."

✅ How specimens are actually collected

Cortisol is drawn with the time written on the tube — it peaks around 06:00–08:00 and troughs near midnight. A "high" cortisol is meaningless without the clock time.
GH is released in pulses, mostly during deep sleep, so a single random level is not diagnostic — IGF-1 or a suppression test is used instead.
Prolactin rises with stress, nipple stimulation, sleep and even venipuncture — repeat before acting on a borderline value.
Glucose — a fasting sample means 8 h with no calories; water is allowed.

🧠 "Hormones watch the clock." Timing is part of the specimen.

❌ Never stop a long-term steroid abruptly

Exogenous steroids feed back and shut down CRH and ACTH. The adrenal cortex, unstimulated for weeks, atrophies. Stop the drug suddenly and the patient has no cortisol at all — an adrenal crisis with hypotension, hypoglycemia, vomiting and shock.

Steroids are tapered, and doses are often increased during illness or surgery ("stress dosing") on the prescriber's order.

🧠 "You cannot fire the boss and expect the workers to show up." Feedback suppression is the reason tapers exist.

🧪 Reference ranges to carry in your head ADULT

Fasting glucose 70–99 mg/dL; a random <70 is hypoglycemia and needs treating now.
HbA1c <5.7% normal · 5.7–6.4% prediabetes · ≥6.5% diabetes.
TSH roughly 0.4–4.0 mIU/L (assay ranges vary between labs — always read the range printed on the report).
Serum sodium 135–145 mEq/L; serum osmolality 275–295 mOsm/kg.

🧠 Ranges differ slightly by lab and by assay. On an exam, use the range the question gives you.

👶 Across the lifespan

Child — GH matters most; the thymus is large and busy training T-cells.
Puberty — GnRH pulses restart, FSH/LH climb, growth plates finally close.
Pregnancy — prolactin climbs all pregnancy but high estrogen blocks milk until the placenta delivers and estrogen falls.
Older adult — GH and sex hormones fall, the thymus is mostly fat, and glucose tolerance drifts down. Blunted stress response means a sick older adult may look flat rather than febrile.

🧠 "Grow it, breed it, keep it." The endocrine priority shifts with age.

⚡

QUICK RECALL

SAY IT OUT LOUD

🧠 Front makes, back storesAnterior = 6+ hormones it built. Posterior = 2 the hypothalamus built.

⭐ FLAT PEGFSH · LH · ACTH · TSH · Prolactin · Endorphins · GH.

♻️ FeedbackHormone low + tropic HIGH = gland broken. Both low = pituitary broken.

🍬 1 down, 4 upInsulin lowers. Glucagon · cortisol · GH · epinephrine raise.

⚠️ Five traps this page exists to prevent

ADH and oxytocin are not made in the pituitary. The hypothalamus makes them; the posterior lobe only stores and releases them.
ACTH does not run the adrenal medulla. Nerves do.
Prolactin makes milk; oxytocin ejects it. Two hormones, two lobes, two jobs.
GH raises glucose. It is not just a "growth" hormone.
Dopamine inhibits prolactin. So dopamine blockers (many antipsychotics, metoclopramide) can cause galactorrhoea, and dopamine agonists are used to treat a prolactinoma.

🔗 Where this goes next

NG-279 · Hall of Fame II — posterior pituitary (ADH, oxytocin), thyroid, parathyroid, pineal, thymus.
NG-280 · Hall of Fame III — adrenal cortex and medulla, ovaries, testes.
NG-281 · Pituitary Disorders — what happens when the anterior lobe makes too much or too little.
NG-282 · SIADH vs DI (1) and NG-283 · SIADH vs DI (2) — the two posterior-lobe water disorders.

🎯 Cover & check — 10 rapid-fire questions

Q1: Name the seven anterior pituitary hormones.

FLAT PEG — FSH, LH, ACTH, TSH, Prolactin, Endorphins, Growth hormone.

Q2: A patient has a low free T4 and a TSH of 42. Where is the problem?

In the thyroid gland itself — primary hypothyroidism. The pituitary is working perfectly; it is shouting TSH at a gland that cannot respond.

Q3: Which hormone class acts in seconds, and why?

Water-soluble peptides and amines (insulin, ADH, epinephrine). They cannot cross the fatty membrane, so they bind a surface receptor and switch on enzymes that already exist — no waiting for new protein to be made.

Q4: Why does cutting the pituitary stalk raise prolactin while every other anterior hormone falls?

Because prolactin is the only one held under constant inhibition. The hypothalamus sends dopamine down the stalk as a brake. Cut the stalk and you cut the brake, so prolactin rises while all the stimulating signals are lost.

Q5: Your patient's blood glucose is 44 mg/dL and she is unresponsive with no IV access. What do you give?

Glucagon by the ordered route (IM/SUBQ or intranasal), then position her on her side because vomiting is common as she wakes. Recheck the glucose and give a complex carbohydrate plus protein once she can swallow safely. Never put oral glucose in the mouth of an unresponsive patient.

Q6: Which three stimuli can trigger hormone release? Give an example of each.

Humoral (rising glucose → insulin), neural (sympathetic firing → epinephrine from the adrenal medulla), and hormonal (TSH → T3/T4 from the thyroid).

Q7: Why must a cortisol level have the collection time on it?

Cortisol follows a daily rhythm — highest around 06:00–08:00, lowest near midnight. A value of "high" at 07:00 may be entirely normal, while the same value at midnight is abnormal.

Q8: A patient on 3 months of prednisone stops it suddenly. What are you watching for?

Adrenal crisis — hypotension that does not respond well to fluids, hypoglycemia, nausea and vomiting, abdominal pain, weakness, hyperkalemia and hyponatremia. It is a medical emergency. Steroids must be tapered, not stopped.

Q9: Which hormone triggers ovulation, and by what unusual mechanism?

LH. It is one of the body's only two positive feedback loops — rising estrogen from the mature follicle flips from inhibiting LH to stimulating it, producing the LH surge that ruptures the follicle.

Q10: Why does giving IV insulin lower serum potassium?

Insulin drives potassium into the cell along with glucose. That is the therapeutic effect in hyperkalemia — but it also means you must monitor potassium closely whenever you run an insulin infusion, especially in DKA.