Endocrine & Nervous Systems

Hormone Axes and Feedback

• Three-level axes: $\text{hypothalamus} \to \text{anterior pituitary} \to \text{target gland}$ 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 $-70$ mV) is set by $K^+$ leak channels and the $Na^+/K^+$ ATPase; threshold near $-55$ mV opens voltage-gated $Na^+$ channels for the all-or-none spike, then $K^+$ efflux repolarizes. Refractory periods enforce one-way, frequency-coded signaling; myelin enables saltatory conduction (lost in MS).
• At synapses, $Ca^{2+}$ 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.