Hormone Classes, Receptors and Feedback Axes
Core endocrine principles: chemical class, transport, receptor type, half-life and axis testing logic.
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Questions Covered in This Set
10 cards to master
What are the three chemical classes of hormones?
Peptides/proteins, steroids, and amines (tyrosine-derived: catecholamines and thyroid hormone).
Where are peptide hormone receptors located, and why?
On the cell surface — peptides are water-soluble and cannot cross the plasma membrane. They act via second messengers, so effects occur in seconds to minutes.
Why are steroid hormones not stored in the cell?
They are lipophilic and diffuse straight out, so synthesis equals secretion. The rate-limiting step is StAR-mediated cholesterol transport into mitochondria, then CYP11A1 cleavage to pregnenolone.
Compare half-lives: peptides vs steroids vs thyroid hormone.
Peptides = minutes (free in plasma, rapid renal/hepatic clearance); steroids = hours (carrier-protein bound); T4 ≈ 7 days (TBG-bound) — hence recheck thyroid dose at 6 weeks but titrate insulin hourly.
Which amine hormone behaves like a steroid?
Thyroid hormone — lipophilic, carried on TBG, nuclear receptor, very long half-life. Catecholamines instead behave like peptides (surface receptors, seconds-long half-life).
Why does pregnancy or oral estrogen raise total T4 without causing hyperthyroidism?
Estrogen raises hepatic TBG; total T4 rises, free T4 briefly dips, TSH nudges up, and a new steady state gives high total T4 with normal free T4 — the patient is euthyroid. Measure free hormone or TSH.
Which hormones signal via JAK–STAT?
GH, prolactin and leptin — STAT dimers alter transcription, latency minutes to hours.
Which hormones use GPCR–Gs (↑cAMP → PKA)?
ACTH, TSH, glucagon and PTH; latency in seconds.
Why does continuous GnRH agonist suppress gonadotropins?
Chronic high hormone levels cause receptor down-regulation; only pulsatile GnRH stimulates. This is the basis of leuprolide therapy in prostate cancer.
Define permissiveness with a clinical example.
One hormone is required for another to act — cortisol permits catecholamine vasoconstriction, so adrenal insufficiency causes vasopressor-refractory shock.
