Free MCAT-style practice, 3A
MCAT Endocrine System, Hormone Axes and Feedback Practice Questions
Eight free MCAT-style practice questions on hormone receptors and second messengers, the hypothalamic-pituitary axes, thyroid labs, calcium regulation, pancreatic hormones, the adrenal gland and diabetes insipidus, with explanations.
Quick concept primer
Hormones fall into three chemical classes. Peptide hormones (insulin, glucagon, ADH) bind surface receptors and act quickly through second messengers such as cAMP or IP3 and Ca2+. Steroid hormones (cortisol, aldosterone, sex steroids) cross the membrane, bind intracellular receptors and change gene expression more slowly, traveling in blood bound to carrier proteins. Thyroid hormones are amino acid-derived but behave like steroids with nuclear receptors.
The hypothalamus controls the anterior pituitary through releasing and inhibiting hormones carried in the portal system, while ADH and oxytocin are made in the hypothalamus and released from the posterior pituitary. Most axes are governed by negative feedback: the end hormone suppresses the hypothalamus and pituitary, so a failing gland produces a high trophic hormone while a failing pituitary produces a low one.
Traps: a hormone's effect depends on the receptor on the target cell, and C-peptide, not insulin, tells you about endogenous production in someone taking insulin.
8 practice questions
Question 1
Which of the following hormones acts mainly through an intracellular receptor and alters gene transcription?
- Epinephrine
- Glucagon
- Insulin
- Cortisol
Show answer and explanation
Answer: D. Cortisol
Cortisol is a steroid hormone; it is lipid soluble, crosses the plasma membrane and binds a cytoplasmic receptor that moves to the nucleus to regulate transcription. Insulin, glucagon and epinephrine bind receptors on the cell surface and act through second messengers or receptor kinases, producing faster effects.
Question 2
Cholera toxin permanently activates the alpha subunit of Gs in intestinal epithelial cells. Which sequence best explains the resulting watery diarrhea?
- Activation of phospholipase C and release of IP3 only
- Increased adenylyl cyclase activity, increased cAMP, activation of PKA, and opening of chloride channels that drives secretion of Cl- and water into the lumen
- Blockade of the Na+/K+ ATPase
- Decreased cAMP and reduced secretion
Show answer and explanation
Answer: B. Increased adenylyl cyclase activity, increased cAMP, activation of PKA, and opening of chloride channels that drives secretion of Cl- and water into the lumen
Gs stimulates adenylyl cyclase to make cAMP. Locked in the active state, Gs keeps cAMP elevated, PKA phosphorylates the CFTR chloride channel, and chloride secretion draws sodium and water into the lumen. The result is massive fluid loss. Gq, not Gs, activates phospholipase C.
Question 3
Which two hormones are made in hypothalamic cell bodies but secreted into the blood from axon terminals in the neurohypophysis?
- FSH and LH
- ADH (vasopressin) and oxytocin
- TSH and ACTH
- Growth hormone and prolactin
Show answer and explanation
Answer: B. ADH (vasopressin) and oxytocin
The posterior pituitary (neurohypophysis) is an extension of the hypothalamus. Neurons in the supraoptic and paraventricular nuclei make ADH and oxytocin and transport them down their axons for release into the blood. The anterior pituitary, by contrast, synthesizes its own hormones (GH, prolactin, TSH, ACTH, FSH, LH) under control of hypothalamic releasing hormones.
Question 4
Thyroid function tests were obtained from three patients.
| Patient | TSH | Free T4 |
|---|---|---|
| P1 | high | low |
| P2 | low | low |
| P3 | low | high |
Which patient most likely has a failing pituitary (secondary hypothyroidism)?
- P3
- None of them
- P2
- P1
Show answer and explanation
Answer: C. P2
In secondary hypothyroidism the pituitary fails to make TSH, so the thyroid is under-stimulated: both TSH and T4 are low. P1 has primary hypothyroidism, where the thyroid fails and the loss of negative feedback causes TSH to rise. P3 has the picture of primary hyperthyroidism (such as Graves disease), in which excess T4 suppresses TSH.
Question 5
A patient has her parathyroid glands accidentally removed during thyroid surgery. Which finding is most expected?
- Hypercalcemia from increased bone resorption
- Hypercalcemia with high urinary phosphate
- Increased vitamin D activation
- Hypocalcemia with neuromuscular excitability, such as muscle spasm or tetany
Show answer and explanation
Answer: D. Hypocalcemia with neuromuscular excitability, such as muscle spasm or tetany
PTH raises blood calcium by stimulating bone resorption, increasing renal calcium reabsorption and stimulating activation of vitamin D in the kidney, which increases intestinal calcium absorption. Without PTH, calcium falls. Low extracellular calcium increases neuronal excitability, which leads to tetany. Phosphate would rise, since PTH normally promotes renal phosphate excretion.
Question 6
A patient with diabetes who takes insulin injections has a low blood C-peptide level, while a different patient with newly diagnosed hyperglycemia has a high C-peptide. What is C-peptide?
- A hormone made by the adrenal cortex
- A glucagon precursor
- A form of insulin that is injected
- A fragment released in equimolar amounts with insulin when proinsulin is cleaved, so it reflects endogenous insulin production
Show answer and explanation
Answer: D. A fragment released in equimolar amounts with insulin when proinsulin is cleaved, so it reflects endogenous insulin production
Proinsulin is cleaved in beta cells into insulin and C-peptide, which are secreted together. Injected insulin contains no C-peptide, so a low C-peptide in a patient on insulin indicates little endogenous production, consistent with type 1 diabetes. A high C-peptide with hyperglycemia suggests insulin resistance with ongoing secretion, as in type 2 diabetes.
Question 7
Which statement about aldosterone is correct?
- It is released from the adrenal medulla in response to sympathetic stimulation
- It decreases blood volume
- It is released from the adrenal cortex in response to angiotensin II and high plasma K+, and it increases Na+ reabsorption and K+ secretion in the distal nephron
- It is a peptide hormone released from the posterior pituitary
Show answer and explanation
Answer: C. It is released from the adrenal cortex in response to angiotensin II and high plasma K+, and it increases Na+ reabsorption and K+ secretion in the distal nephron
Aldosterone is a steroid mineralocorticoid made in the zona glomerulosa of the adrenal cortex. It upregulates ENaC channels and the Na+/K+ ATPase in principal cells of the collecting duct, which retains Na+ (and water, raising blood volume) and excretes K+. The adrenal medulla secretes epinephrine and norepinephrine.
Question 8
A patient produces 8 liters of very dilute urine per day (urine osmolality 90 mOsm/kg) and has a high plasma sodium. After a dose of desmopressin (a synthetic ADH analog), urine osmolality rises to 600 mOsm/kg. What is the most likely diagnosis?
- Primary polydipsia with normal ADH
- Central diabetes insipidus, from deficient ADH secretion
- Nephrogenic diabetes insipidus
- SIADH
Show answer and explanation
Answer: B. Central diabetes insipidus, from deficient ADH secretion
The patient makes large volumes of dilute urine, so ADH action is lacking. Because exogenous ADH corrects the defect, the kidney can respond, which means the problem is a lack of hormone (central diabetes insipidus). In nephrogenic diabetes insipidus the kidney does not respond to ADH, so desmopressin would have no effect. SIADH produces the opposite pattern, with concentrated urine and a low plasma sodium.