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endocrine system practice test for A&P 2: Exam 1

Quick, free hormone quiz with endocrine practice questions. Instant results.

Editorial: Review CompletedCreated By: Nimit GalaUpdated Aug 27, 2025
Difficulty: Moderate
2-5mins
Learning OutcomesCheat Sheet
Paper art illustration for Anatomy and Physiology 2 Exam 1 quiz on endocrine system hormone mechanisms on coral background.

This quiz helps you review the endocrine system for A&P 2 Exam 1, including hormone actions, feedback loops, and receptors. Work through clear questions with concise explanations to spot weak areas fast. For more practice, try our a&p exam 1 practice test, build broader skills with a physiology quiz, or check another system with a lymphatic system quiz.

Which second messenger is directly increased by activation of a Gs protein-coupled receptor?
Diacylglycerol (DAG)
Cyclic GMP (cGMP)
Inositol 1,4,5-trisphosphate (IP3)
Cyclic AMP (cAMP) - Explanation: Gs activates adenylyl cyclase, raising cAMP.
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Steroid hormones typically exert their primary effects by binding to receptors located where?
On the apical membrane of epithelial cells
In the cytoplasm or nucleus - Explanation: Steroids are lipophilic and bind intracellular receptors that regulate gene transcription.
In the plasma membrane caveolae
Within lysosomes
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Peptide hormones are most often stored and released by which mechanism?
Transport through nuclear pores
Carrier-mediated antiport
Simple diffusion across the plasma membrane
Exocytosis from secretory vesicles - Explanation: Peptide hormones are synthesized, packaged, and released via Ca2+-dependent exocytosis.
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The enzyme that degrades cAMP to AMP, thereby attenuating PKA signaling, is:
Adenylyl cyclase
Phosphodiesterase - Explanation: PDE hydrolyzes cAMP to 5'-AMP, reducing PKA activation.
Protein kinase C
Phospholipase C
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Which term describes increased number of hormone receptors on a target cell after prolonged low hormone levels?
Internalization
Downregulation
Desensitization
Upregulation - Explanation: Low ligand often induces receptor upregulation, enhancing sensitivity.
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Activation of phospholipase C directly generates which two second messengers?
Ca2+ and ATP
cGMP and nitric oxide
cAMP and AMP
IP3 and DAG - Explanation: PLC cleaves PIP2 to form IP3 and DAG.
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Insulin receptor signaling primarily involves which receptor class?
Serine-threonine kinase receptor for SMADs
GPCR (Gs)
Receptor tyrosine kinase - Explanation: Insulin receptor autophosphorylates and activates IRS pathways.
Ligand-gated ion channel
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Which best explains why steroid hormones have longer plasma half-lives than peptide hormones?
They are stored in vesicles before release
They are broken down by peptidases
They bind extensively to carrier proteins - Explanation: Protein binding reduces renal clearance and degradation.
They cannot be metabolized by the liver
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A patient with nephrogenic diabetes insipidus most likely has a defect in which signaling route?
Insulin receptor tyrosine kinase in muscle
Oxytocin Gq pathway in myometrium
ADH V2 receptor Gs-cAMP pathway in collecting duct - Explanation: Impaired V2 or downstream signaling blocks aquaporin-2 insertion.
Aldosterone MR genomic pathway in distal nephron
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Which situation exemplifies hormone antagonism?
Insulin lowering blood glucose while glucagon raises it - Explanation: Opposite effects on the same variable represent antagonism.
Epinephrine and glucagon increasing blood glucose together
Thyroid hormone permitting catecholamine effects
LH and FSH stimulating gonadal function together
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Which best describes the effect of phospholamban phosphorylation by PKA in endocrine-stimulated cardiomyocytes?
Opening of L-type Ca2+ channels
Reduced SERCA activity
Activation of Na+/K+ ATPase
Increased SERCA Ca2+ uptake - Explanation: PKA phosphorylation relieves inhibition of SERCA, enhancing relaxation and contractility.
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Which change shifts a hormone dose-response curve leftward without changing maximal efficacy?
Decreased receptor affinity
Reduced signal amplification
Increased receptor number with spare receptors - Explanation: More receptors or coupling efficiency increases apparent potency (lower EC50).
Irreversible receptor antagonism
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Which is a distinguishing feature of Gq versus Gi signaling?
Opening of cAMP-gated channels
Reduction of cAMP
Activation of adenylyl cyclase
Activation of phospholipase C and IP3/DAG production - Explanation: Gq stimulates PLC; Gi inhibits adenylyl cyclase.
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A mutation causing constitutive activation of the TSH receptor would most likely lead to:
Hyperthyroidism with diffuse goiter - Explanation: Constitutive Gs-cAMP signaling increases thyroid hormone synthesis and growth.
Hypothyroidism with low T3/T4
Euthyroid state
Isolated hypothalamic dysfunction
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Which endocrine pattern best defines circadian regulation?
Random secretion throughout the day
Ultrashort pulses every minute
Weekly cycles only
Approximately 24-hour rhythmic variation - Explanation: Many hormones (e.g., cortisol) follow circadian cycles.
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Which dynamic endocrine test exploits negative feedback to assess cortisol regulation?
Water deprivation test
Cosyntropin stimulation test
Dexamethasone suppression test - Explanation: Dexamethasone should suppress ACTH and cortisol in normal physiology.
Oral glucose tolerance test
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A G protein mutation prevents GTP hydrolysis on Gs. The most likely signaling consequence is:
Persistent adenylyl cyclase activation - Explanation: Without GTPase activity, Gs remains active, prolonging cAMP production.
Activation of PLC
Enhanced phosphodiesterase activity
Shortened cAMP signal
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Which molecular event follows T3 binding to thyroid hormone receptor on DNA?
Displacement of co-repressors and recruitment of co-activators - Explanation: T3-TR-RXR complex recruits co-activators to upregulate transcription.
Recruitment of co-repressors to TREs
Activation of guanylyl cyclase
Opening of voltage-gated Na+ channels
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Which mechanism explains reduced effect of a full agonist in the presence of a competitive antagonist?
Increase in spare receptors
Rightward shift in dose-response that can be overcome by higher agonist dose - Explanation: Competitive antagonism decreases apparent potency (raises EC50) without changing Emax.
Irreversible receptor internalization
Lower maximal efficacy that cannot be overcome
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Which signaling outcome is expected from receptor serine phosphorylation by GRKs?
Increased ligand affinity
Beta-arrestin binding and reduced G protein signaling - Explanation: GRK phosphorylation promotes arrestin binding, desensitizing GPCRs.
Enhanced G protein coupling
Activation of adenylyl cyclase
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Study Outcomes

  1. Understand hormone secretion mechanisms -

    Describe the main classes of hormones and their release processes, preparing you for the anatomy and physiology 2 exam 1 quiz.

  2. Identify endocrine cell origins -

    Locate and trace the cellular lineages of major endocrine glands in the context of A&P 2 exam 1 content.

  3. Differentiate signal transduction pathways -

    Contrast membrane-bound receptor cascades with intracellular receptor actions to explain hormone effects.

  4. Analyze feedback regulation loops -

    Examine negative and positive feedback mechanisms to understand hormone homeostasis for anatomy and physiology ii exam 1.

  5. Apply quiz insights -

    Use instant-feedback results to pinpoint knowledge gaps and reinforce critical endocrine system concepts.

  6. Evaluate your proficiency -

    Assess your readiness for the anatomy and physiology 2 test 1 by interpreting quiz outcomes and planning targeted study.

Cheat Sheet

  1. Hormone Chemical Classes & Solubility -

    Review the four major chemical classes: amino acid derivatives, peptides, steroids, and eicosanoids, noting that water-soluble hormones (peptides and catecholamines) circulate freely while lipid-soluble ones (steroids and thyroid hormones) require carrier proteins. For example, cortisol (a steroid) binds transcortin, whereas insulin (a peptide) diffuses in plasma. Remember "SALP" (Steroids, Amino, Lipid, Peptides) to keep classes straight when tackling anatomy and physiology 2 exam 1.

  2. Membrane vs Intracellular Receptors -

    Water-soluble hormones activate second-messenger systems (e.g., cAMP, IP₃/DAG) via membrane receptors, while lipid-soluble hormones cross membranes to bind intracellular receptors and directly modulate gene transcription. A classic example is epinephrine using cAMP to trigger PKA, versus thyroid hormone binding nuclear receptors to regulate mRNA. Use the phrase "Surface for speed, nucleus for notes" to recall which hormones use which pathway.

  3. Hypothalamic - Pituitary Axis & FLAT PiG -

    The hypothalamus controls the anterior pituitary via the hypophyseal portal system, releasing TRH, CRH, GnRH, and GHRH to regulate tropic hormones. Memorize the anterior pituitary hormones with FLAT PiG (FSH, LH, ACTH, TSH = tropic; Prolactin, GH = direct). Don't forget the posterior pituitary stores oxytocin and ADH produced by the hypothalamus - essential for a and p 2 exam 1 success.

  4. Feedback Mechanisms in Endocrine Regulation -

    Negative feedback keeps most axes in check: high cortisol levels inhibit CRH and ACTH release, stabilizing the HPA axis. Positive feedback is rarer but crucial in processes like oxytocin-driven uterine contractions during labor. Recall "negate to regulate" for negative loops and link positive loops to a "push to the peak" scenario for anatomy and physiology 2 test 1.

  5. Endocrine Gland Cell Origins & Zones -

    Differentiate cell types and zones: adrenal cortex zones "GFR - salt, sugar, sex" (zona glomerulosa, fasciculata, reticularis) and adrenal medulla from neural crest. In the thyroid, follicular cells synthesize T₃/T₄ while parafollicular (C) cells produce calcitonin. These cellular origins form the backbone for mastering a&p 2 exam 1 content.

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