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  • Overview
  • Hormone classes and receptors
  • Hypothalamic–pituitary axes (survey)
  • Thyroid and calcium homeostasis
  • Pancreas and metabolism (survey)
  • Lab patterns (qualitative recognition)
  • Worked micro‑examples
  • Pitfalls
  • Practice prompts
  • References

Anatomy and Physiology - Endocrine System

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Type: Study
Divisions: B, C
Participants: Up to 2
Approx. Time: 50 minutes
Allowed Resources: Binders/notes allowed per rules; non‑programmable calculator as permitted.

Overview

Endocrinology examines hormone synthesis, secretion, transport, receptor signaling, and feedback across major axes. Exam questions favor axis diagrams, lab pattern interpretation, and receptor mechanisms.

Hormone classes and receptors

  • Peptide/amine hormones: membrane receptors (GPCR/RTK); fast signaling via second messengers (cAMP, IP₃/DAG, Ca²⁺).
  • Steroid/thyroid hormones: intracellular/nuclear receptors; transcriptional modulation; slower onset, longer duration; require carriers in blood.

Hypothalamic–pituitary axes (survey)

  • HPT: TRH → TSH → T₄/T₃; negative feedback on pituitary/hypothalamus.
  • HPA: CRH → ACTH → cortisol; diurnal rhythm, stress response; feedback suppresses CRH/ACTH.
  • HPG: GnRH (pulsatile) → LH/FSH → sex steroids (testosterone, estrogen/progesterone); feedback with sex‑specific nuances.
  • Posterior pituitary: ADH (V₂ renal water reabsorption; V₁ vasoconstriction) and oxytocin (milk let‑down, uterine contraction) released from hypothalamic neurons.

Thyroid and calcium homeostasis

  • Thyroid: iodide uptake, thyroglobulin iodination, TPO activity, T₄→T₃ conversion peripherally.
  • Calcium–phosphate: PTH increases serum Ca²⁺ (bone resorption, kidney reabsorption, ↑1,25‑(OH)₂‑D synthesis); calcitonin opposes resorption; vitamin D increases Ca/PO₄ absorption.

Pancreas and metabolism (survey)

  • Insulin (β cells): promotes glucose uptake (GLUT4 translocation), glycogen/lipid synthesis, protein synthesis; lowers blood glucose.
  • Glucagon (α cells): raises blood glucose via glycogenolysis and gluconeogenesis; lipolysis.

Lab patterns (qualitative recognition)

  • Primary vs secondary/tertiary: primary target gland failure → hormone low with tropic high (e.g., primary hypothyroid: low T₄/T₃, high TSH); secondary (pituitary) or tertiary (hypothalamus) deficiencies → low both.
  • Hyperfunction: e.g., Cushing patterns (ACTH‑dependent vs independent) at concept level; Graves (TSI stimulating TSH receptor) vs toxic nodules.

Worked micro‑examples

  1. Axis defect
  • Low free T₄ with high TSH → primary hypothyroidism; symptoms (fatigue, weight gain, cold intolerance) discussed qualitatively.
  1. Receptor mechanism
  • Epinephrine binding β‑adrenergic GPCR → ↑cAMP → PKA activation → glycogen phosphorylase activation → ↑glucose release.
  1. Ca²⁺ homeostasis
  • Low dietary Ca²⁺ elevates PTH → ↑1,25‑(OH)₂‑D; increases intestinal absorption and renal reabsorption; prolonged elevation increases bone resorption.

Pitfalls

  • Confusing hormone class with receptor location and signaling speed.
  • Misreading primary vs secondary lab patterns; forgetting negative feedback logic.
  • Ignoring binding proteins’ effect on total vs free hormone levels.

Practice prompts

  • Draw the HPA axis and predict cortisol/ACTH changes after exogenous glucocorticoids.
  • Explain why TSH can be low‑normal in central hypothyroidism despite low T₄.
  • Describe insulin vs glucagon effects on liver, muscle, and adipose tissues.

References

  • SciOly Wiki – Anatomy & Physiology (Endocrine system)
  • OpenStax Anatomy & Physiology (Endocrine system)