Endocrine System: Comprehensive Study Notes

Endocrine System – Scope & Purpose

• Acts as the body’s second major communication and control network (the nervous system is the first).

• Consists of endocrine glands and diffuse endocrine tissues that secrete hormones directly into the bloodstream.

• Works hand-in-hand with the nervous system to coordinate and integrate the activity of virtually every cell.

• Hormones, although released in tiny concentrations (often picogram–nanogram ranges), regulate growth, metabolism, reproduction, stress responses, fluid balance, and more.

Key Terminology

• Hormone – chemical messenger secreted ("squirted") into blood, travelling to distant target cells to elicit characteristic responses.

• Endocrine gland – ductless structure that releases hormones into interstitial fluid → blood.

• Exocrine gland – possesses ducts; releases non-hormonal products onto epithelial surfaces (e.g., sweat into skin ducts, digestive enzymes into the duodenum).

• Target cell – cell bearing specific hormone receptors; only these cells respond.

• Half-life (t{1/2}) – time required for 50 % of a circulating hormone to be degraded (e.g., cortisol t{1/2} \approx 1\,\text{h}).

Learning Objectives Addressed

• Define hormone & endocrine system ✔️

• Contrast endocrine vs exocrine glands ✔️

• Locate major endocrine organs ✔️

• Compare endocrine & nervous systems ✔️

• Classify other chemical messengers ✔️

• Classify hormones chemically; explain transport & receptor mechanisms ✔️

• Explain target-cell sensitivity, feedback loops, and three secretion stimuli ✔️

Endocrine vs Exocrine Glands

Major Endocrine Organs & Representative Hormones

• Hypothalamus – releasing/inhibiting hormones (e.g., CRH, TRH, GnRH)

• Pituitary

  • Anterior (GH, ACTH, TSH, LH, FSH, PRL)

  • Posterior (ADH, oxytocin – synthesized in hypothalamus, stored/released here)

• Pineal – melatonin

• Thyroid – T3, T4, calcitonin

• Parathyroids – PTH

• Adrenal cortex – glucocorticoids (cortisol), mineralocorticoids (aldosterone), androgens

• Adrenal medulla – adrenaline (epinephrine), noradrenaline (norepinephrine)

• Pancreatic islets – insulin, glucagon, somatostatin

• Gonads – testes (testosterone); ovaries (estrogens, progesterone)

Endocrine vs Nervous System: Similarities & Differences

Shared Features

• Both provide long-distance communication.

• Both use brain structures (hypothalamus links the two).

• Certain chemicals act as both neurotransmitters & hormones (e.g., noradrenaline).

• Both require receptors; may generate similar end-organ effects.

Distinguishing Features

Other Classes of Chemical Messengers

1. Autocrine – acts on the same cell that secreted it (e.g., interleukin-1 in inflammation).

2. Paracrine – affects neighboring cells locally (e.g., histamine causing local vasodilation).

3. Neurotransmitters – released into synaptic clefts by neurons; bind postsynaptic receptors.

4. Hormones – systemic messengers via blood.

Chemical Classes of Hormones

Solubility determines transport mode, receptor location, signal transduction, and speed.

Hormone Transport in Blood

• Water-soluble hormones are polar ➜ dissolve freely in plasma.

• Lipid-soluble hormones are non-polar ➜ require carrier proteins (e.g., albumin, globulins).

  • Only the free fraction can exit capillaries & bind receptors.

  • Carriers extend t_{1/2} by shielding from enzymatic degradation/renal excretion.

Receptor Locations & Mechanisms

1. Intracellular (Cytosolic/Nuclear) Receptors – Lipid-Soluble Hormones

1. Hormone diffuses through plasma membrane.

2. Binds cytosolic or nuclear receptor → hormone–receptor complex.

3. Complex binds DNA hormone-response element (HRE).

4. Initiates transcription → mRNA → new proteins.

5. Response latency: minutes–hours (gene expression + translation).

2. Plasma-Membrane Receptors – Water-Soluble Hormones

1. Hormone (1st messenger) binds G-protein-coupled receptor (GPCR).

2. G-protein activates adenylyl cyclase.

3. ATP → cyclic AMP (cAMP, 2nd messenger).

4. cAMP activates protein kinase A ➜ protein phosphorylation cascade.

5. Rapid amplification; responses in milliseconds–minutes (enzyme activation, ion channel opening, secretion, etc.).

Other 2nd messengers = \text{IP}_3, \text{Ca^{2+}}, DAG.

Modulating Target-Cell Sensitivity

• Down-regulation – high hormone levels → fewer receptors, ↓ sensitivity (e.g., chronic hyperinsulinemia in type 2 diabetes).

• Up-regulation – low hormone levels → more receptors, ↑ sensitivity (e.g., LH receptor surge at ovulation).

Hormone–Hormone Interactions

1. Permissive – one hormone enables effect of another (thyroid hormones for normal reproductive function).

2. Synergistic – hormones add or multiply effects (FSH + estrogen for follicle maturation).

3. Antagonistic – hormones exert opposite effects (insulin ↓ vs glucagon ↑ blood glucose).

Feedback Loops Controlling Hormone Levels

Negative Feedback (Most Common)

Hypothalamus \xrightarrow{CRH} Pituitary \xrightarrow{ACTH} Adrenal cortex \xrightarrow{cortisol} → rising cortisol inhibits CRH & ACTH – maintains narrow plasma range.

Stages:

1. Homeostasis

2. Imbalance (↓ cortisol)

3. Hormone cascade (↑ CRH/ACTH)

4. Correction (↑ cortisol)

5. Negative feedback restores balance.

Positive Feedback (Rare)

• Oxytocin in childbirth

  • Initial uterine stretch → oxytocin release → stronger contractions → more stretch → more oxytocin … until birth & placental delivery remove the stimulus.

Stimuli Initiating Hormone Release

1. Humoral – blood levels of non-hormone substances.

   • Example: ↑ blood glucose → insulin; ↓ glucose → glucagon.

   • Changes in plasma osmolality → ADH release.

2. Hormonal – hormone triggers another endocrine gland.

   • CRH → ACTH → cortisol; TRH → TSH → thyroid hormones.

3. Neural – neuronal input triggers secretion.

   • Sympathetic nerves → adrenal medulla releases adrenaline & noradrenaline in fight-or-flight ("bear chase" analogy).

   • Rapidly increases heart rate, respiratory rate, redirects blood to muscles/brain.

Practical & Clinical Connections

• Pancreatic dual function illustrates coordination of digestive (exocrine) and metabolic (endocrine) roles.

• Understanding half-life and carrier proteins is critical for pharmacological hormone replacement or blockade.

• Mis-regulation (e.g., receptor down-regulation) underlies disorders such as type 2 diabetes mellitus.

• Feedback failures can cause endocrine pathologies (e.g., Cushing’s disease – excess cortisol).

• Neural–endocrine overlap (neuroendocrinology) is central to stress, growth, reproduction, and homeostasis research.