Endocrinology: physiology and mechanisms

15 ASCP MLS practice questions on Endocrinology: physiology and mechanisms, part of Chemistry. The first 15 are below; the first 5 with answers and explanations (tap Show answer after you have chosen), the rest in Learn with a free account.

1. Question 1 · Hard

   A 16-year-old raised as a girl is seen for primary amenorrhea. She has normal breast development but sparse pubic and axillary hair. Examination finds a short, blind-ending vagina, and ultrasound shows no uterus and two gonads in the inguinal canals. Results: testosterone 640 ng/dL [22.2 nmol/L] (adult male reference 264-916 ng/dL [9.2-31.8 nmol/L]); LH 28 IU/L (female follicular reference 2-12 IU/L); estradiol 45 pg/mL [165 pmol/L]; karyotype 46,XY. Which mechanism best explains this pattern of hormones and development?

   1. AAbsent Müllerian duct development
   2. BDeficient 5-alpha-reductase activity
   3. CA testosterone-secreting gonadal tumor
   4. DAndrogen receptors unable to respond

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   Answer: D · Androgen receptors unable to respond

   Testosterone in the male range with a high LH means the hypothalamus and pituitary are not sensing the testosterone, which happens when androgen receptors do not work. Without androgen feedback, LH stays high and drives the testes, and the extra testosterone is aromatized to estradiol, which develops the breasts. Sparse pubic and axillary hair shows that the tissues ignore androgen, while anti-Müllerian hormone from the testes has prevented a uterus from forming. A testosterone-secreting tumor would suppress LH, 5-alpha-reductase deficiency causes virilization at puberty with little breast growth, and Müllerian agenesis occurs in 46,XX females with female testosterone levels. The diagnosis is complete androgen insensitivity syndrome.

   • A: Müllerian agenesis occurs in 46,XX females, with female testosterone levels and normal pubic hair.
   • B: 5-alpha-reductase deficiency causes virilization at puberty, with normal pubic hair and little breast growth.
   • C: A tumor making testosterone would suppress LH through negative feedback.

2. Question 2 · Easy

   Thyroid hormones act on target cells mainly by binding to:

   1. AG protein-coupled receptors on the cell surface
   2. BTyrosine kinase receptors on the cell surface
   3. CIon channels in the plasma membrane
   4. DNuclear receptors that regulate gene transcription

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   Answer: D · Nuclear receptors that regulate gene transcription

   T4 and T3 enter cells through membrane transporters, and T4 is converted to T3 inside the cell. T3 binds thyroid hormone receptors in the nucleus, which bind DNA and change the transcription of target genes. Steroid hormones act in a similar way through intracellular receptors. Because they work through gene expression, their effects take hours to days to appear.

   • A: G protein-coupled surface receptors serve peptide hormones such as TSH and ACTH.
   • B: Tyrosine kinase receptors serve insulin and growth factors.
   • C: Ion channels are not the main target of thyroid hormones.

3. Question 3 · Medium

   How does long-term high-dose prednisone cause atrophy of the adrenal cortex?

   1. ALoss of renin and angiotensin stimulation
   2. BFeedback suppression of CRH and ACTH
   3. CA direct toxic effect of the drug on adrenal cells
   4. DAutoimmune destruction of the adrenal cortex

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   Answer: B · Feedback suppression of CRH and ACTH

   Prednisone is a synthetic glucocorticoid, and the hypothalamus and pituitary sense it just as they sense cortisol. Long-term use suppresses CRH and ACTH, and without ACTH the zona fasciculata and zona reticularis shrink. If the drug is stopped suddenly, the atrophied glands cannot make enough cortisol, so doses are tapered. Aldosterone is usually preserved because the zona glomerulosa is controlled mainly by the renin-angiotensin system.

   • A: Renin and angiotensin control the zona glomerulosa, which is usually spared.
   • C: Prednisone does not damage adrenal cells directly; it removes ACTH support.
   • D: Autoimmune destruction causes Addison disease, not drug-induced atrophy.

4. Question 4 · Hard

   A 32-year-old woman has amenorrhea and galactorrhea. Prolactin 58 ng/mL [58 µg/L] (reference < 25), TSH 62 mIU/L (0.4-4.0), free T4 0.4 ng/dL [5 pmol/L] (0.8-1.8 [10-23]). The raised prolactin is best explained by:

   1. AHigh TRH stimulating the lactotrophs
   2. BMacroprolactin in the sample
   3. CExcess dopamine from the hypothalamus
   4. DA prolactin-secreting pituitary adenoma

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   Answer: A · High TRH stimulating the lactotrophs

   In primary hypothyroidism, low thyroid hormone removes negative feedback on the hypothalamus, so TRH rises along with TSH. TRH also stimulates prolactin release from lactotrophs, giving a mild hyperprolactinemia that can cause galactorrhea and menstrual changes. Long-standing TRH drive can even enlarge the pituitary and mimic an adenoma. Prolactin falls to normal with levothyroxine, so TSH should be checked before a prolactinoma is investigated.

   • B: Macroprolactin raises results without symptoms and is unrelated to the thyroid failure.
   • C: Dopamine suppresses prolactin, so excess dopamine would lower it.
   • D: A prolactinoma would not explain the very high TSH and low free T4.

5. Question 5 · Medium

   Most of the T3 circulating in a healthy adult comes from:

   1. APeripheral deiodination of T4
   2. BConversion of reverse T3 in liver
   3. CThyroglobulin breakdown in plasma
   4. DDirect thyroid gland secretion

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   Answer: A · Peripheral deiodination of T4

   The thyroid secretes mostly T4, and only about 20% of circulating T3 comes directly from the gland. The other 80% or so is made in the liver, kidney and other tissues by deiodinase enzymes that remove one iodine from the outer ring of T4. Removing an inner-ring iodine instead gives inactive reverse T3. Illness, fasting and some drugs reduce this conversion and lower T3.

   • B: Reverse T3 is inactive and is not converted to T3.
   • C: Thyroglobulin is broken down inside thyroid cells, not in plasma.
   • D: Direct secretion supplies only about one fifth of circulating T3.

6. Question 6 · Hard

   A man with prostate cancer starts continuous leuprolide, a GnRH agonist. Week 1: LH and testosterone above baseline. Week 4: LH low, testosterone at castrate level. What explains the week 4 results?

   1. AContinuous stimulation desensitizes the GnRH receptors
   2. BThe drug destroys pituitary gonadotroph cells
   3. CThe drug blocks androgen receptors in the prostate
   4. DTestosterone feedback is enhanced by the drug

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7. Question 7 · Medium

   Why is serum IGF-1 preferred over a random growth hormone level to assess growth hormone status?

   1. AIGF-1 is secreted directly by the pituitary
   2. BGH is released in pulses, while IGF-1 is stable all day
   3. CIGF-1 is not affected by nutrition or liver disease
   4. DGH is rapidly destroyed in the collection tube

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8. Question 8 · Medium

   Antipsychotic drugs such as risperidone often raise serum prolactin. The mechanism is:

   1. ADirect stimulation of TRH release from the hypothalamus
   2. BReduced renal clearance of prolactin
   3. CBlockade of dopamine D2 receptors on lactotrophs
   4. DIncreased estrogen production by the ovaries

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9. Question 9 · Medium

   Which Sertoli cell product feeds back on the pituitary to lower FSH selectively, with little effect on LH?

   1. AActivin
   2. BAnti-Müllerian hormone
   3. CInhibin B
   4. DTestosterone

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10. Question 10 · Hard

    A 26-year-old man has injected testosterone for bodybuilding for a year. Which result set is expected?

    1. ALH low, FSH high, sperm count normal
    2. BLH high, FSH high, sperm count low
    3. CLH low, FSH low, sperm count low
    4. DLH high, FSH low, sperm count normal

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11. Question 11 · Easy

    Thyroxine and epinephrine are both synthesized from which amino acid?

    1. AHistidine
    2. BArginine
    3. CTyrosine
    4. DTryptophan

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12. Question 12 · Medium

    Compared with peptide hormones, steroid hormones are:

    1. AMostly protein-bound, with longer plasma half-lives
    2. BUnable to cross target cell membranes
    3. CStored in granules until they are released
    4. DMostly free, with half-lives of a few minutes

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13. Question 13 · Easy

    When ACTH binds its receptor on adrenal cortical cells, which second messenger carries the signal?

    1. ACyclic GMP
    2. BInositol trisphosphate
    3. CNitric oxide
    4. DCyclic AMP

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14. Question 14 · Easy

    The first step in the synthesis of adrenal and gonadal steroid hormones converts cholesterol to:

    1. AProgesterone
    2. BPregnenolone
    3. C17-hydroxyprogesterone
    4. DDehydroepiandrosterone

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15. Question 15 · Easy

    Which hormonal event is driven by positive feedback?

    1. AInhibin suppressing FSH release
    2. BFree T4 suppressing TSH release
    3. CEstradiol triggering the LH surge
    4. DHigh cortisol suppressing ACTH release

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