Three-level axes: hypothalamus→anterior pituitary→target gland with the end hormone feeding back negatively on both upper levels. Lab patterns localize disease: low target hormone with high tropic hormone means primary gland failure; both low means pituitary failure; both high means a tropic-hormone tumor.
Peptide hormones (insulin, ADH) bind surface receptors and act fast via second messengers; steroids and thyroid hormone enter the nucleus and change transcription — slow but durable.
Antagonistic pairs: insulin stores glucose while glucagon mobilizes it (the ratio matters); PTH raises serum calcium via bone resorption, renal reabsorption, and vitamin D activation, while calcitonin lowers it.
Neurons and Synapses
Resting potential (about mV) is set by leak channels and the ATPase; threshold near mV opens voltage-gated channels for the all-or-none spike, then efflux repolarizes. Refractory periods enforce one-way, frequency-coded signaling; myelin enables saltatory conduction (lost in MS).
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At synapses, Ca2+ influx triggers vesicle release; glutamate EPSPs and GABA IPSPs summate at the axon hillock. Sympathetic (norepinephrine) drives fight-or-flight; parasympathetic (ACh) rest-and-digest.
Key Takeaways
Use tropic-vs-target hormone patterns to localize endocrine lesions.
Receptor location explains why peptides act in seconds and steroids in hours.
The action potential is all-or-none; intensity is coded by firing frequency.
Neurotransmitter identity plus receptor type determines excitation or inhibition.