MCAT - Organ Systems:: Endocrine System

Endocrine signaling differs fundamentally from neural signaling in that endocrine communication is:

- **A)** Always faster and more localized than neural signaling
- **B)** Mediated by hormones released into the bloodstream, acting on distant target cells that express the appropriate receptor, and generally slower/longer-lasting than neural signaling
- **C)** Only capable of inhibitory effects, never stimulatory
- **D)** Restricted to a single target organ per hormone

Steroid hormones (e.g., cortisol, estrogen, testosterone) typically act on target cells by:

- **A)** Binding cell-surface G-protein-coupled receptors exclusively
- **B)** Opening ligand-gated ion channels directly
- **C)** Diffusing across the lipophilic cell membrane and binding intracellular (cytoplasmic or nuclear) receptors, which then act as transcription factors to alter gene expression
- **D)** Being rapidly degraded before reaching any target cell

Peptide hormones (e.g., insulin, growth hormone, ADH) typically act on target cells by:

- **A)** Binding cell-surface receptors (since they are too large/polar to cross the membrane), triggering intracellular second-messenger cascades
- **B)** Diffusing directly across the plasma membrane like steroid hormones
- **C)** Directly entering the nucleus without any receptor
- **D)** Only functioning within the cell that produced them

Thyroid hormone is unusual among hormones in that it:

- **A)** Is a peptide hormone acting only on cell-surface receptors
- **B)** Cannot cross the cell membrane at all
- **C)** Has effects lasting only seconds to minutes
- **D)** Is a modified amino acid (tyrosine derivative) that, despite not being a classic steroid, is lipid-soluble enough to cross the cell membrane and act on nuclear receptors like a steroid hormone, producing slow, long-lasting effects on metabolism

Negative feedback is the dominant regulatory pattern in most endocrine axes; this means that:

- **A)** Rising hormone levels further stimulate their own release, creating a runaway increase
- **B)** Rising levels of a hormone (or its downstream effect) suppress further release of that hormone or its upstream stimulating hormones, keeping levels within a homeostatic range
- **C)** Hormone levels are entirely random and unregulated
- **D)** Feedback only ever occurs at the level of the target organ, never involving the pituitary or hypothalamus

The hypothalamus controls anterior pituitary hormone release primarily via:

- **A)** Direct neural synapses onto anterior pituitary cells
- **B)** Hormones traveling through the general systemic circulation, like any other endocrine signal
- **C)** Releasing and inhibiting hormones secreted into the hypothalamic-hypophyseal portal system, a specialized local blood supply connecting the hypothalamus directly to the anterior pituitary
- **D)** No connection at all; the anterior pituitary functions autonomously

Unlike the anterior pituitary, the posterior pituitary does not synthesize its own hormones; instead, it:

- **A)** Stores and releases ADH (vasopressin) and oxytocin, which are actually synthesized in hypothalamic neuron cell bodies (supraoptic and paraventricular nuclei) and transported down axons to the posterior pituitary for release
- **B)** Produces cortisol locally
- **C)** Only responds to portal blood-borne releasing hormones, like the anterior pituitary
- **D)** Has no functional role and is vestigial in adult humans

Growth hormone (GH) exerts many of its growth-promoting effects indirectly by stimulating the liver to produce:

- **A)** Thyroid-stimulating hormone (TSH)
- **B)** Insulin-like growth factor 1 (IGF-1), which mediates much of GH's anabolic and growth-promoting action on bone and other tissues
- **C)** Cortisol
- **D)** Erythropoietin