Principles of Hormone Action

Peptide hormones
Bind to cell surface receptors as they are hydrophilic and cannot cross the lipid membrane.
Signal transduction typically via
second messengers (e.g. cAMP, IP₃/DAG pathways).
Examples:
Insulin, ACTH, ADH, glucagon.


Steroid hormones
Lipophilic: cross the cell membrane and bind to intracellular receptors (cytoplasmic or nuclear).
Hormone–receptor complex acts as a
transcription factor, regulating gene expression.
Onset of action is
delayed but prolonged.
Examples:
Cortisol, aldosterone, oestrogen, testosterone, vitamin D.


Amino acid–derived hormones
Synthesised from tyrosine or tryptophan.
Action varies:
 o
Thyroxine (T₄) and triiodothyronine (T₃) act via nuclear receptors genomic effects.
 o
Adrenaline and noradrenaline act via membrane receptors rapid non-genomic effects.
Other examples:
dopamine, melatonin.


Hormone resistance syndromes
Target tissues are unresponsive to hormone action, despite normal or elevated levels.
Common mechanisms: receptor defects or post-receptor signalling abnormalities.
Examples:
 o
Pseudohypoparathyroidism – resistance to PTH hypocalcaemia, PTH.
 o
Type 2 diabetes mellitus – insulin resistance.
 o
Androgen insensitivity syndrome – resistance to testosterone in XY individuals.


Feedback regulation
Endocrine systems commonly regulated by negative feedback loops.
Hormone secretion is inhibited by the downstream product.
Example:
Cortisol inhibits CRH and ACTH release via feedback on hypothalamus and pituitary.
Some systems use
positive feedback (e.g. oestrogen surge pre-ovulation increasing LH).


Pulsatile and circadian release
Many hormones exhibit pulsatile or diurnal (circadian) secretion patterns.
Maintains receptor sensitivity and physiological rhythm.
Examples:
 o
Growth hormone (GH) – released in pulses, especially during sleep.
 o
Cortisol – peaks in early morning (8 AM), lowest at night circadian rhythm.
 o
LH/FSH – pulsatile secretion is essential for reproductive function.










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Author & Educational Disclaimer


Author:

Dr Phillip Cockrell BM FRCP DipClinEd


Dr Phillip Cockrell is a UK Consultant Physician in Internal Medicine, currently working at Queen Alexandra Hospital, Portsmouth University Hospitals NHS Trust. He has previously worked as a registrar across Intensive Care Medicine, Gastroenterology, Cardiology, Stroke Medicine, Acute Medicine, and Respiratory Medicine.


He has held senior leadership roles including Associate Clinical Director of the Acute Medical Unit, Clinical Director of Internal Medicine, and Chief of Medicine. Dr Cockrell has over 15 years’ experience in postgraduate medical education, having lectured extensively across the MRCP syllabus and contributed to MRCP revision teaching and course development.


Dr Cockrell holds a Bachelor of Medicine (BM), Fellowship of the Royal College of Physicians (FRCP), and a Diploma in Clinical Education (DipClinEd). His teaching approach is based on structured consolidation of complex medical topics to support efficient and effective revision for postgraduate examinations.


Purpose of this content:

The material on this page is intended solely for educational purposes to support revision for the MRCP (UK) Part 1 examination. It reflects examination-relevant principles of internal medicine and is designed to aid learning and pattern recognition.


Medical disclaimer:

This content is designed for postgraduate medical examination revision and does not constitute medical advice, diagnosis, or treatment guidance and must not be used as a substitute for professional clinical judgement, local guidelines, or specialist consultation. Clinical decisions should always be made in the context of individual patient circumstances and current national guidance.