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VM602 Q2/Final PHYSI
VM 602 Q2/Finals PHYSIO
| Question | Answer |
|---|---|
| What is the definition of a hormone and how does it differ from a neurotransmitter? | A hormone is a chemical messenger secreted into blood by ductless glands that acts on distant target cells. |
| How do endocrine, paracrine, and autocrine signals differ in where they act? | Endocrine acts on distant targets, paracrine acts locally on neighbors, autocrine acts back on same cell. |
| What are the three classes of hormones and give one example of each class? | Steroids (cortisol), protein/peptide (insulin), amino acid derivatives (thyroxine). |
| What organs secrete steroid hormones and what examples come from them? | Ovaries, testes, adrenal cortex; produce estrogen, testosterone, cortisol, aldosterone. |
| What organs secrete peptide hormones and what examples come from them? | Pituitary, thyroid, pancreas; produce insulin, oxytocin, prolactin, ADH. |
| What organs secrete amino acid derivative hormones and what examples come from them? | Thyroid and adrenal medulla; produce thyroxine, epinephrine, norepinephrine. |
| What are the two major mechanisms of hormone action and how do they differ? | Surface receptor with 2nd messengers vs intracellular/nuclear receptor altering transcription. |
| What external and internal factors regulate hormone release in the body? | External: light, stress, temperature. Internal: blood sugar, other hormones, ions. |
| What is negative feedback and what is positive feedback in endocrine control? | Negative feedback: hormone inhibits further release. Positive feedback: hormone enhances release. |
| What are the three structural arrangements of endocrine cells in the body? | Discrete glands, endocrine portions of organs, scattered cells in other tissues. |
| What are the three principal functions of the endocrine system in animals? | Maintain homeostasis, regulate growth/development, control reproduction. |
| What is the main endocrine role of the hypothalamus and how does it act? | Produces releasing and inhibiting hormones to control pituitary, and oxytocin/ADH. |
| Which hypothalamic hormones stimulate the anterior pituitary to release hormones? | CRH, GnRH, GHRH, TRH, PRH. |
| Which hypothalamic hormones inhibit anterior pituitary release of hormones? | GHIH (somatostatin) and dopamine (PIH). |
| Which hypothalamic hormone stimulates ACTH release and what is its target? | CRH stimulates corticotrophs to secrete ACTH. |
| Which hypothalamic hormone stimulates FSH and LH release and from which cells? | GnRH stimulates anterior pituitary gonadotropes to release FSH and LH. |
| Which hypothalamic hormone stimulates GH release and which cells does it act on? | GHRH stimulates somatotrophs to produce GH. |
| Which hypothalamic hormone inhibits GH release and what is its other name? | GHIH, also called somatostatin, inhibits GH from somatotrophs. |
| Which hypothalamic hormone stimulates TSH release and what is its size? | TRH stimulates thyrotrophs; it is a tripeptide of 3 amino acids. |
| Which hypothalamic hormones regulate prolactin and how do they act? | PRH stimulates PRL; dopamine inhibits PRL release. |
| Which two hormones are released by the posterior pituitary and what are their functions? | Oxytocin (milk let-down, uterine contraction), ADH (water retention, vasoconstriction). |
| Where are oxytocin and ADH synthesized before being released in the posterior pituitary? | In hypothalamic nuclei (paraventricular and supraoptic). |
| How are oxytocin and ADH transported to the posterior pituitary? | Packaged with carrier proteins, sent down axons, stored in Herring bodies. |
| What is the main function of oxytocin in females and what hormones regulate it? | Stimulates uterine contraction and milk let-down; enhanced by estrogen, inhibited by progesterone. |
| What veterinary drug mimics oxytocin and what clinical uses does it have? | Pitocin; used for inducing parturition and aiding milk let-down. |
| What role does oxytocin play in males? | Released during ejaculation, contracts ductus deferens, may aid prostate function. |
| What is the primary role of ADH and what are its three main targets? | Decreases urine output (kidneys), decreases sweating (glands), increases blood pressure (arterioles). |
| What stimuli increase ADH secretion and what stimuli decrease it? | Stimulated by fear, thirst, anesthesia, opioids. Inhibited by water intake. |
| What receptors mediate ADH actions and where are they located? | V1 (vessels), V2 (renal collecting ducts), V3 (pituitary corticotrophs). |
| How does ADH act on the kidney to promote water reabsorption? | Binds V2 receptors → cAMP → aquaporins inserted into collecting duct membrane. |
| What are aquaporins and how are they regulated by ADH? | Water channels; inserted into membranes with ADH, removed by endocytosis without ADH. |
| What is diabetes insipidus and what are its two main forms? | Disorder of ADH deficiency (central) or renal insensitivity (nephrogenic). |
| What causes central diabetes insipidus and what are its signs? | Tumors, idiopathic neuron loss; causes polyuria, polydipsia, dilute urine. |
| How is central diabetes insipidus diagnosed and treated? | Measure ADH, give desmopressin; response indicates central DI. |
| What causes nephrogenic diabetes insipidus in dogs? | Congenital V2 receptor defects (huskies) or acquired downregulation of aquaporins. |
| How is nephrogenic diabetes insipidus treated? | Use drugs that increase water permeability, not desmopressin. |
| What is primary polydipsia and how does it differ from diabetes insipidus? | Behavioral over-drinking in dogs; ADH system is normal. |
| What is ADH excess called and what are the main consequences? | Syndrome of Inappropriate Antidiuresis; causes hyponatremia, cerebral edema. |
| What are clinical signs of ADH excess in dogs? | Weakness, lethargy, tremors, seizures, coma. |
| How is ADH excess treated? | Restrict water, give V2 antagonists. |
| Multiple Choice: Which of the following are synthesized in the hypothalamus? A. CRH B. Thyroid hormone C. GnRH D. Dopamine E. A, C, and D | E. A (CRH), C (GnRH), and D (Dopamine). |
| Multiple Choice: Which hormone is NOT released by the posterior pituitary? A. Oxytocin B. Anti-diuretic hormone C. Vasopressin D. Dopamine | D. Dopamine. |
| Multiple Choice: ADH is involved in which process? A. Parturition B. Milk-let down C. Social attachment D. All of the above E. None of the above | E. None of the above. |
| Multiple Choice: The posterior pituitary is composed of neural tissue. A. True B. False | A. True. |
| Multiple Choice: Which of the following is NOT a peptide hormone? A. Somatostatin B. Thyroid-stimulating hormone C. Dopamine D. Growth hormone releasing hormone E. All of the above | C. Dopamine. |
| Multiple Choice: Diabetes insipidus is caused by which condition? A. Too little ADH B. Too much ADH C. Too little oxytocin D. Too much oxytocin | Too little ADH. |
| Multiple Choice: Syndrome of Inappropriate Diuresis is characterized by which features? A. Elevated/normal ADH with low osmolality B. Water retention C. Cellular overhydration D. All of the above | D. All of the above. |
| Which five cell types in the anterior pituitary secrete distinct hormones? | Lactotrophs (PRL), Gonadotrophs (FSH/LH), Thyrotrophs (TSH), Corticotrophs (ACTH), Somatotrophs (GH) |
| Which six main hormones are secreted from the anterior pituitary? | Prolactin, FSH, LH, TSH, ACTH, GH |
| Which hypothalamic hormone stimulates prolactin release and which inhibits it? | TRH/PRH stimulate; dopamine inhibits |
| What are the two main functions of prolactin in females? | Mammary gland development and milk production |
| How is prolactin secretion controlled by feedback during lactation? | Suckling decreases dopamine inhibition, increasing prolactin |
| What is the difference between prolactin and oxytocin in lactation? | Prolactin stimulates milk formation; oxytocin triggers milk ejection |
| What role does prolactin play in males? | Low levels, may support testosterone production; function unclear |
| What is hyperprolactinemia and its common consequences? | High PRL, infertility via GnRH inhibition, pseudopregnancy in dogs |
| What drug is used to treat hyperprolactinemia? | Dopamine agonist bromocriptine |
| What causes pseudopregnancy in dogs? | High PRL after rapid progesterone drop in nonpregnant cycles |
| What structural feature makes glycoprotein hormones FSH, LH, and TSH unique? | Common alpha subunit; unique beta subunit gives specificity |
| What is the role of LH in females? | Triggers ovulation, maintains corpus luteum, stimulates progesterone |
| What is the role of FSH in females? | Stimulates follicle growth and estrogen production |
| What is the role of LH in males? | Stimulates Leydig cells to produce testosterone |
| What is the role of FSH in males? | Stimulates Sertoli cells to support spermatogenesis |
| What is the difference between primary and secondary hypogonadism? | Primary: gonadal failure, high FSH/LH. Secondary: hypothalamic/pituitary problem, low/normal FSH/LH |
| What is a common cause of secondary hypogonadism via pituitary dysfunction? | Hyperprolactinemia or hypopituitarism |
| Which hypothalamic hormone stimulates ACTH release and what does ACTH target? | CRH stimulates ACTH; ACTH targets adrenal cortex |
| Which hypothalamic hormones regulate growth hormone secretion? | GHRH stimulates, somatostatin (GHIH) inhibits |
| What are the major actions of growth hormone? | Promotes growth, protein synthesis, metabolism via liver IGF-1 |
| Which hypothalamic hormone stimulates TSH release and what is TSH’s target? | TRH stimulates TSH; TSH targets thyroid gland |
| What is the primary function of thyroid-stimulating hormone (TSH)? | Stimulates thyroid hormone secretion (T3, T4) |
| Which of the following is NOT secreted by the anterior pituitary: A. FSH and LH B. Prolactin C. TSH D. GnRH | D. GnRH |
| Which of the following statements about prolactin is wrong: A. Peptide hormone B. Milk-ejection reflex C. Inhibited by dopamine D. Increased in pregnancy | B. Milk-ejection reflex (that’s oxytocin) |
| Which hypothalamic hormones regulate GH secretion and what are their effects? | GHRH stimulates; GHIH (somatostatin) inhibits |
| Which stomach hormone also stimulates GH secretion? | Ghrelin |
| What are the main anabolic effects of GH on protein metabolism? | ↑ amino acid uptake, ↑ protein synthesis, ↑ muscle mass |
| What are the main effects of GH on carbohydrate metabolism? | ↑ blood glucose, ↑ hepatic glucose output, ↓ glucose uptake, insulin resistance |
| What are the main effects of GH on lipid metabolism? | ↑ lipolysis, ↓ fat synthesis, ↓ adipose mass |
| How does GH act through IGF-1 to promote growth? | GH stimulates systemic and local IGF-1 production, which acts on bone, muscle, and organs for growth |
| Where is most IGF-1 produced and what stimulates its production? | Liver produces systemic IGF-1; GH stimulates IGF-1 production |
| What is the structural similarity between IGF-1 and insulin? | IGF-1 structurally resembles insulin but has different functions |
| Does IGF-1 function like insulin? | No, IGF-1 is structurally similar but functionally different from insulin |
| How do systemic IGF-1 and local IGF-1 differ in action? | Systemic IGF-1 circulates as a hormone; local IGF-1 acts paracrine/autocrine in tissues |
| How does GH secretion vary with age and time of day? | Highest during youth and sleep; secretion decreases with age |
| What are the clinical consequences of excess GH in juveniles vs adults? | Juveniles: gigantism; Adults: acromegaly with abnormal proportions |
| What are the clinical consequences of GH deficiency or resistance? | Dwarfism, slow growth, alopecia, abnormal body proportions |
| What dog breed is predisposed to pituitary dwarfism from GH deficiency? | German Shepherds |
| What diseases result from adult GH deficiency? | Adult-onset GH responsive dermatosis, alopecia, thin skin |
| Why is excess GH often linked to diabetes mellitus? | GH antagonizes insulin, increases blood glucose, induces insulin resistance |
| What is bovine somatotropin (BST) used for and how is it administered? | Injected to dairy cows to ↑ milk production (every 14 days post-calving) |
| What are the economic effects of BST on milk yield? | Up to 40% increase in milk production, large financial benefit |
| What are potential animal health issues associated with BST use? | ↑ mastitis, ↑ lameness, ↑ antibiotic use, resistance concerns |
| Does BST have direct biological effects in humans consuming milk? | No, BST is degraded in GI tract and does not bind human GH receptors |
| What is the concern about IGF-1 levels in milk from BST-treated cows? | IGF-1 survives digestion/pasteurization; long-term human effects unknown |
| What is porcine somatotropin (PST) and what is its purpose? | Pig pituitary hormone; ↑ muscle growth, ↓ fat, ↑ feed efficiency |
| How does PST improve pork production economically? | ↑ feed efficiency, ↑ muscle gain, ↓ fat deposition |
| Diseases of GH hypersecretion include which main conditions? | Gigantism (juvenile), acromegaly (adult) |
| Diseases of GH hyposecretion or resistance include which conditions? | Pituitary dwarfism, Laron dwarfism, GH-responsive dermatosis |
| Which of the following does GH do: A. Increases amino acid uptake B. Decreases glucose uptake C. Decreases fat synthesis D. All of the above | D. All of the above |
| Growth hormone is NOT affected by age or time of day? A. True B. False | B. False |
| Excess growth hormone causes: A. Acromegaly B. Dermatosis C. Dermatitis D. All of the above E. None of the above | A. Acromegaly |
| IGF-1 has a similar structure to insulin: A. True B. False | A. True |
| IGF-1 has a similar function to insulin: A. True B. False | B. False |
| BST does which of the following: A. Increases milk production B. Decreases milk production C. Increases IGF-1 levels in milk D. Decreases IGF-1 levels in milk E. A and C | E. A and C |
| What are the six sequential steps of hormone signaling from synthesis to termination of response? | Synthesis→release→transport→recognition by receptor→signal transduction→removal/termination. |
| What are the two major classes of hormones by structure, and give an example of each? | Peptide/protein (GH, FSH); Steroid (estrogen, testosterone). |
| How are peptide/protein hormones synthesized, stored, and released compared to steroid hormones? | Peptides synthesized, stored in vesicles, released by exocytosis; steroids made on demand, diffuse out. |
| What is the difference in transport of peptide/protein hormones versus steroid hormones in blood? | Peptides travel free in plasma; steroids bind carrier proteins. |
| What are the two broad categories of hormone receptors and what type of hormone binds each? | Steroid receptors=intracellular; membrane receptors=peptide/protein, catecholamines. |
| How do steroid receptors transduce signals once hormone binds? | Hormone-receptor complex enters nucleus, binds DNA, alters gene transcription. |
| What are the two main types of membrane receptors for peptide/protein hormones? | GPCRs and tyrosine kinase receptors. |
| What is the adenylate cyclase mechanism of GPCR signaling and which hormones use it? | Hormone→GPCR→Gs protein→adenylate cyclase→cAMP→PKA; used by LH, FSH, TSH, ACTH. |
| What is the phospholipase C mechanism of GPCR signaling and which hormones use it? | Hormone→GPCR→Gq protein→PLC→IP3+DAG→Ca²⁺+PKC; used by GnRH, TRH, ADH. |
| How does the tyrosine kinase receptor pathway work and which hormone uses it? | Hormone binds receptor dimer→autophosphorylation→cascade; used by insulin, IGF-1. |
| What is the main difference between short-lasting and long-lasting hormone signals? | Short=peptides, quick via kinases, degraded fast; Long=steroids, slow via gene expression, long duration. |
| What is desensitization/adaptation of receptors and provide an example? | Prolonged activation reduces receptor activity or removes it; FSH receptor. |
| What is receptor up-regulation and provide an example? | Increased receptor number or affinity after activation; PRL, GH, estrogen. |
| How does negative feedback regulate hormone signaling? | Hormone output inhibits upstream gland to maintain homeostasis. |
| How does positive feedback regulate hormone signaling? | Hormone output amplifies further release, e.g., oxytocin in labor. |
| What is the definition of a hormone agonist and how does it act? | Binds receptor, mimics natural hormone, causes same conformational change. |
| What is the definition of a hormone antagonist and how does it act? | Binds receptor, blocks or alters conformation, prevents hormone action. |
| What is hormone therapy and how is it clinically applied? | Use of hormone analogs (agonists/antagonists) to treat disease. |
| How do GnRH agonists act initially versus after prolonged exposure, and what clinical uses do they have? | Initially ↑FSH/LH, later pituitary desensitization ↓FSH/LH; reversible sterilization, prostate/mammary therapy. |
| How do ADH antagonists act clinically and what effects do they produce? | Block ADH, ↑urine output, ↓water reabsorption in kidney. |
| Which of the following statements about peptide or protein hormones is NOT true: A. Utilize second messengers B. Receptors on cell membrane C. Faster onset than steroids D. Direct gene expression changes | D. Direct gene expression changes. |
| Which of the following statements is NOT true for hormone signaling: A. Negative feedback maintains homeostasis B. cAMP is a GPCR 2nd messenger C. GPCR is a tyrosine kinase D. Agonists/antagonists can provide clinical benefit | C. GPCR is a tyrosine kinase. |
| What are the two major thyroid hormones produced by the thyroid gland? | Thyroxine (T4) and Triiodothyronine (T3) |
| Which thyroid hormone is secreted in larger amounts and which is more biologically active? | T4 is secreted more; T3 is more active (3–5× more potent) |
| Where are thyroid hormone receptors located and what are the three main types? | Nucleus; TRα1, TRβ1 (ubiquitous), TRβ2 (nervous system) |
| How does thyroid hormone act once inside a target cell? | T3/T4 binds nuclear receptor → hormone-receptor complex binds DNA → ↑ or ↓ gene expression |
| How is iodine used in thyroid hormone synthesis? | Iodide absorbed from blood, transported to thyroid, converted to iodine, added to tyrosine on thyroglobulin to form T3/T4 |
| Where are thyroid hormones stored before release? | Stored as colloid in follicle lumen |
| What percent of thyroid hormones are bound to proteins in blood and which proteins bind them? | >99% bound; TBG (high affinity), prealbumin, albumin |
| Which form of thyroid hormone is biologically active: free or bound? | Free T3/T4 |
| What hormones regulate thyroid secretion and from where? | TRH (hypothalamus) → TSH (anterior pituitary) → T3/T4 (thyroid) |
| What type of feedback controls thyroid hormone secretion? | Negative feedback from circulating T3/T4 on hypothalamus and pituitary |
| What are the major effects of thyroid hormone on metabolism? | ↑ metabolic rate, ↑ O₂ use, ↑ protein synthesis, ↑ mitochondria, ↑ Na⁺/K⁺ pump activity, affects carbohydrate & fat metabolism |
| Why is thyroid hormone essential for young animals? | Needed for growth, GH secretion, bone development, CNS maturation |
| What neurodevelopmental processes depend on thyroid hormone? | Axon/dendrite growth, neuron size, migration, differentiation, myelination |
| What are the three categories of hypothyroidism based on site of dysfunction? | Primary (thyroid, common), Secondary (pituitary), Tertiary (hypothalamus) |
| What is the most common form of hypothyroidism in dogs? | Primary hypothyroidism (95%) |
| What are common causes of primary hypothyroidism? | Idiopathic atrophy, lymphocytic thyroiditis, rare neoplasia |
| What are hallmark clinical signs of canine hypothyroidism? | Weight gain, lethargy, alopecia/rat tail, dry coat, heat seeking, ↓ immunity, infertility, tragic facial expression |
| What diagnostic test is most often used for hypothyroidism? | Total T4 assay (first-line) |
| What is the treatment for hypothyroidism? | L-thyroxine (T4) replacement |
| In which species is hyperthyroidism most common? | Cats (esp. >10 yrs) |
| What are common causes of feline hyperthyroidism? | Multinodular adenomatous goiter (common), thyroid carcinoma (rare) |
| List common clinical signs of feline hyperthyroidism. | Weight loss, polyphagia, vomiting, PU/PD, diarrhea, ↑ activity, panting, aggression, tremors, heat intolerance |
| What is the best screening test for hyperthyroidism? | Total T4 assay |
| What are treatment options for feline hyperthyroidism? | Radioactive iodine (I-131), methimazole/carbimazole, surgery, transdermal methimazole |
| What is the mechanism of methimazole? | Inhibits thyroid peroxidase (TPO) → blocks T3/T4 synthesis |
| What is the gold standard treatment for hyperthyroidism in cats? | Radioactive iodine (I-131) |
| Cats have a higher incidence of hyperthyroidism than dogs: A. True B. False | A. True |
| Hyperthyroidism is characterized by: A. Weight gain B. Weight loss C. Slow activity D. None of the above | B. Weight loss |
| Which thyroid hormone is most biologically active: A. T3 B. T4 C. TRH D. TSH | A. T3 |
| Which test is first-line for diagnosing hypothyroidism: A. Total T4 B. Free T4 C. T3 assay D. TSH stimulation | A. Total T4 |
| Treatment of canine hypothyroidism usually involves: A. L-thyroxine B. Methimazole C. I-131 therapy D. Carbimazole | A. L-thyroxine |
| Methimazole acts by: A. Blocking TPO B. Blocking deiodinase C. Stimulating TSH D. Blocking TSH receptors | A. Blocking TPO |
| Radioactive iodine treatment works by: A. Destroying thyroid tissue B. Stimulating TSH C. Blocking TRH D. Binding TBG | A. Destroying thyroid tissue |
| What is not a primary function of the endocrine system: homeostasis, vasodilation, growth, or fertility? | Vasodilation and vasoconstriction. |
| How do endocrine, autocrine, and paracrine signals differ? | Endocrine = bloodstream to distant cells, autocrine = self, paracrine = local neighbors. |
| Match hormones to class: Epinephrine, Insulin, Oxytocin, Testosterone, Glucocorticoids, ADH → Steroid, Protein, Amino acid derived. | Epi = amino acid, Insulin = protein, Oxytocin = protein, Testosterone = steroid, Glucocorticoids = steroid, ADH = protein. |
| What are steroid hormones derived from? | Cholesterol. |
| How does the anterior pituitary connect to the hypothalamus? | Via blood vessels, hypophyseal portal system. |
| How does the posterior pituitary connect to the hypothalamus? | Via nerves, hypothalamic-hypophyseal tract. |
| Which hormones are synthesized by the anterior pituitary? | TSH, ACTH, GH, PRL, FSH, LH. |
| Which hormones are stored and released by the posterior pituitary? | Oxytocin, ADH. |
| Which hypothalamic hormone stimulates ACTH release? | CRH acting on corticotrophs. |
| Which hypothalamic hormone stimulates FSH and LH release? | GnRH acting on gonadotrophs. |
| Which hypothalamic hormones regulate GH release? | GHRH stimulates; GHIH inhibits. |
| Which hypothalamic hormone stimulates TSH release? | TRH acting on thyrotrophs. |
| Which hypothalamic hormones regulate prolactin? | PRH stimulates; dopamine (PIH) inhibits. |
| What stimulates oxytocin release and what inhibits it? | Stim: suckling, cervix dilation, infant cues. Inhib: opioids. |
| What stimulates ADH release and what inhibits it? | Stim: ↑osmolarity, ↓ECF, Ang II, stress/pain. Inhib: ↓osmolarity. |
| How does ADH act on kidney tubules? | Binds V2 receptors → inserts AQPs → ↑water reabsorption. |
| What hormone is deficient or ineffective in diabetes insipidus? | ADH (low or ineffective). |
| What are 3 signs of central diabetes insipidus? | Polyuria, polydipsia, large dilute urine volumes. |
| What is nephrogenic diabetes insipidus? | Kidneys don’t respond to ADH; no response to desmopressin. |
| What happens in syndrome of inappropriate ADH secretion (SIADH)? | Too much ADH → water retention, hyponatremia, brain edema. |
| Which anterior pituitary cell secretes prolactin? | Lactotrophs. |
| What does prolactin do and how is it controlled? | Stimulates milk production; inhibited by dopamine/progesterone, stimulated by estrogen, suckling. |
| What is pseudopregnancy in dogs? | High prolactin after progesterone drop → pregnancy-like behavior. |
| What do LH and FSH do in ovaries? | FSH: follicle growth, estrogen. LH: ovulation, corpus luteum, progesterone. |
| What do LH and FSH do in testes? | Stimulate spermatogenesis, testosterone, inhibin. |
| What is primary hypogonadism? | Gonad problem → high LH/FSH, low sex steroids. |
| What is secondary hypogonadism? | Brain problem → low GnRH/LH/FSH, low sex steroids. |
| What are the 3 major effects of GH? | ↑Protein synthesis, ↑Blood glucose/insulin resistance, ↑Lipolysis. |
| What hormone is released from the liver in response to GH? | IGF-1. |
| What is the role of IGF-1? | Stimulates bone/muscle growth, ↑protein synthesis, ↑glucose uptake. |
| What condition results from GH excess in juveniles? | Gigantism (before growth plate closure). |
| What condition results from GH excess in adults? | Acromegaly (after growth plate closure). |
| What condition results from GH deficiency? | Pituitary dwarfism (small size, alopecia). |
| How does chronic GH excess contribute to diabetes mellitus? | Causes insulin resistance and ↑blood glucose. |
| Which hormone signal lasts longer, steroid or peptide? | Steroid hormones. |
| Why are peptide hormone effects short-lived? | Stored premade, released quickly, rapidly degraded. |
| Why are steroid hormone effects long-lasting? | Synthesized on demand, regulate gene expression, slow degradation. |
| What is receptor desensitization? | Target cell reduces response by removing or shutting off receptors. |
| What is receptor up-regulation? | Target cell increases receptors or affinity to increase sensitivity. |
| What is a hormone agonist? | Mimics natural hormone by binding same receptor and activating. |
| What is a hormone antagonist? | Binds same receptor but blocks natural hormone action. |
| What is a clinical use of GnRH agonists? | Initially ↑FSH/LH, then desensitize pituitary → ↓FSH/LH. |
| What is a clinical use of ADH antagonists? | Block ADH → ↑urine output, treat SIADH. |
| Which class of hormones comes from cholesterol? | Steroids. |
| What is the composition of the posterior pituitary? | Neural tissue. |
| Which two hormones are synthesized in hypothalamus but released from posterior pituitary? | Oxytocin, ADH. |
| ADH acts on kidney tubules to cause what effect? | ↓Urine output via ↑water reabsorption. |
| What is the role of oxytocin in mammary glands? | Milk let-down. |
| SIADH is characterized by what finding? | High ADH despite low plasma osmolarity. |
| Which is NOT a sign of central diabetes insipidus: polydipsia, thirst, hunger, or polyuria? | Excessive hunger. |
| Which hypothalamic factor inhibits prolactin secretion? | Dopamine. |
| What is the main stimulator of prolactin after birth? | Suckling. |
| Which condition in dogs is due to high prolactin and mimics pregnancy? | Pseudopregnancy. |
| Which pituitary cells secrete GH? | Somatotrophs. |
| What is one effect of GH on protein metabolism? | ↑Protein synthesis. |
| What is GH’s action on carbohydrate metabolism? | ↑Blood glucose and insulin resistance. |
| Hypersecretion of GH in adults causes which condition? | Acromegaly. |
| What is the economic effect of bovine somatotropin (BST) use? | ↑Milk yield in cows. |
| Which disease is associated with chronic GH excess due to insulin resistance? | Diabetes mellitus. |
| Where are peptide hormone receptors located? | Cell membrane. |
| Which class of hormones binds DNA directly to regulate gene expression? | Steroid hormones. |
| What are the three cardinal signs of diabetes mellitus? | Polydipsia, polyuria, polyphagia. |
| What additional clinical sign is common in untreated diabetes? | Weight loss. |
| What life-threatening complication results from untreated diabetes? | Diabetic ketoacidosis (DKA). |
| What systemic signs are seen in diabetic ketoacidosis? | Vomiting, weakness, listlessness. |
| In cats, what clinical signs may indicate diabetic neuropathy? | Hindlimb weakness, plantigrade stance, decreased jumping. |
| Which species shows higher risk of cataracts with diabetes? | Dogs (females > males, 5–15 yrs). |
| Which cells of the pancreas produce insulin? | Beta cells in the islets of Langerhans. |
| Which cells of the pancreas produce glucagon? | Alpha cells. |
| Which cells of the pancreas produce somatostatin? | Delta cells. |
| What are the exocrine functions of the pancreas? | Secretes digestive enzymes and bicarbonate into intestine. |
| What are the endocrine functions of the pancreas? | Secretes insulin, glucagon, somatostatin, GLP-1 into blood. |
| How is insulin synthesized? | Preproinsulin → proinsulin → insulin + C-peptide. |
| What marker parallels insulin secretion 1:1? | C-peptide. |
| What nutrients stimulate insulin secretion? | Glucose, amino acids, free fatty acids, ketones. |
| How does sympathetic activity affect insulin release? | Inhibits secretion. |
| How does parasympathetic activity affect insulin release? | Stimulates secretion. |
| What hormone from alpha cells regulates insulin secretion? | Glucagon (stimulates). |
| What hormone from delta cells regulates insulin secretion? | Somatostatin (inhibits). |
| What is the main function of insulin? | Anabolic: promotes glucose storage, protein/fat synthesis. |
| Which insulin-dependent transporter mediates glucose uptake in muscle/adipose? | GLUT-4. |
| What happens to lipolysis under insulin action? | Inhibited. |
| What happens to glycogen synthesis under insulin action? | Stimulated. |
| What happens to protein synthesis under insulin action? | Stimulated. |
| What receptor type initiates insulin signaling? | Tyrosine kinase receptor. |
| What are the two main defects in Type 2 diabetes mellitus? | Insulin resistance + beta-cell dysfunction. |
| What species most commonly develops Type 1 diabetes? | Dogs. |
| What species most commonly develops Type 2 diabetes? | Cats. |
| What risk factors predispose cats to Type 2 diabetes? | Obesity, inactivity, male sex, age, genetics, steroids. |
| What is the main defect in Type 1 diabetes? | Absolute insulin deficiency from beta-cell loss. |
| What is the main defect in Type 2 diabetes? | Relative insulin deficiency + insulin resistance. |
| What hormone predominates after feeding? | Insulin (also incretins GLP-1, GIP). |
| What pathways are activated in the liver after feeding? | Glycogenesis, glycolysis, lipogenesis. |
| What pathway is not active in muscle after feeding? | Glycogenolysis. |
| What hormone predominates after short-term fasting? | Glucagon. |
| What pathways are activated in the liver after fasting? | Glycogenolysis, gluconeogenesis, ketogenesis. |
| What pathway predominates in adipose during short fasting? | Lipolysis (fatty acid release). |
| How do animals maintain glucose homeostasis? | Insulin lowers glucose, glucagon raises glucose. |
| What happens when blood glucose rises? | Insulin + GLP-1 released → glycogenesis, glycolysis, lipogenesis. |
| What happens when blood glucose falls? | Glucagon released → glycogenolysis, gluconeogenesis, ketogenesis. |
| What are incretins and their role? | GI hormones (GLP-1, GIP); enhance insulin secretion, inhibit glucagon. |
| Where is GLP-1 secreted from? | L-cells of ileum/colon. |
| Where is GIP secreted from? | K-cells of duodenum. |
| What additional effects does GLP-1 have? | Delays gastric emptying, reduces food intake, weight loss. |
| What enzyme rapidly inactivates incretins? | DPP-4 enzyme. |
| What new therapy uses GLP-1 analogs in cats? | Long-acting GLP-1 injections replace insulin injections. |
| How is DKA defined? | Hyperglycemia >250 mg/dL, ketosis, acidosis (pH <7.3). |
| What hormones drive DKA pathophysiology? | Insulin deficiency + glucagon excess. |
| What are the metabolic consequences of DKA? | Hyperglycemia, lipolysis, ketogenesis, acidosis, dehydration. |
| In liver of a Type I diabetic, what pathway is NOT active? | Glycogenesis. |
| In muscle of a Type I diabetic, what pathway predominates? | Protein degradation. |
| What are the three cardinal signs of diabetes mellitus? | Polydipsia, polyuria, polyphagia. |
| Could you describe the structural organization of the islet of Langerhans? | Clusters of alpha (glucagon), beta (insulin), delta (somatostatin) cells with rich blood supply. |
| What do alpha cells secrete? | Glucagon. |
| What do beta cells secrete? | Insulin. |
| What do delta cells secrete? | Somatostatin. |
| How is insulin synthesized and released? | Preproinsulin → proinsulin → insulin + C-peptide; secreted in response to glucose, AA, FFA. |
| Which hormone is produced by beta cells, what regulates it, and what are its target actions? | Insulin; stimulated by glucose, AA, parasympathetic input, GLP-1; inhibits by stress, somatostatin; promotes glucose uptake/storage in liver, muscle, fat. |
| Which hormone is produced by alpha cells, what regulates it, and what are its target actions? | Glucagon; stimulated by low glucose, amino acids, sympathetic activity; inhibited by insulin, GLP-1; increases glycogenolysis, gluconeogenesis, lipolysis. |
| Which hormone is produced by intestinal L-cells, what regulates it, and what are its target actions? | GLP-1; secreted after nutrient intake; enhances insulin secretion, inhibits glucagon, slows gastric emptying. |
| Which hormone is produced by delta cells, what regulates it, and what are its target actions? | Somatostatin; regulates islet communication; inhibits insulin, glucagon, GI hormones. |
| After short-term fasting, what hormone is released from the pancreas? | Glucagon. |
| After short-term fasting, what pathways are activated? | Glycogenolysis, gluconeogenesis, ketone body formation, lipolysis. |
| After short-term fasting, what pathways are not active? | Glycogenesis, glycolysis, lipogenesis. |
| After feeding, what hormones are released from the pancreas and intestine? | Insulin, GLP-1, GIP. |
| After feeding, what pathways are activated? | Glycolysis, glycogenesis, lipogenesis, protein synthesis. |
| After feeding, what pathways are not active? | Glycogenolysis, gluconeogenesis, ketogenesis, lipolysis. |
| How do animals keep the homeostasis of blood glucose levels? | Insulin lowers glucose (storage), glucagon raises glucose (mobilization), incretins fine-tune balance. |
| When blood glucose levels fall, what hormone is released from the pancreas? | Glucagon. |
| When blood glucose levels go up, what hormones are released from pancreas and intestine? | Insulin, GLP-1, GIP. |
| In Type I diabetic patients, what pathways are activated? | Glycogenolysis, gluconeogenesis, lipolysis, ketogenesis, proteolysis. |
| In Type I diabetic patients, what pathways are not active? | Glycogenesis, glycolysis, lipogenesis, protein synthesis. |
| The action of insulin is initiated by stimulation of what kind of receptor? | Tyrosine kinase receptor. |
| What are the two major categories of diabetes in dogs and cats? | Type 1 (insulin deficiency, dogs), Type 2 (insulin resistance, cats). |
| What are the two major defects of Type 2 Diabetes Mellitus? | Insulin resistance (muscle/liver) + beta-cell dysfunction/deficiency. |
| What is the function of GLP-1? | Enhances insulin secretion, inhibits glucagon, delays gastric emptying, reduces appetite. |
| Can you describe the pathophysiology of diabetic ketoacidosis (DKA)? | Insulin deficiency + glucagon excess → lipolysis, ketogenesis, hyperglycemia → acidosis, dehydration. |
| What is the definition of diabetes mellitus in veterinary medicine and how is it diagnosed? | It is an absolute or relative insulin deficiency diagnosed by documenting persistent hyperglycemia while ruling out stress hyperglycemia. |
| How do dogs and cats differ in insulin deficiency and resistance? | Dogs almost always have absolute insulin deficiency, cats may have relative deficiency and commonly insulin resistance. |
| Do dogs and cats both require insulin therapy for diabetes management? | Dogs always require insulin, cats may be managed with insulin, SGLT-2 inhibitors, and diet, sometimes achieving remission. |
| What is diabetic remission in cats and how common is it in dogs? | In cats, remission means no therapy is required to maintain normal glucose, often transient; in dogs it is unlikely. |
| What are the main goals of diabetic therapy in small animals? | Provide good quality of life, control clinical signs, prevent hypoglycemia and DKA, normalize body condition, and achieve remission in cats. |
| Is achieving exact blood glucose targets the primary goal of therapy? | No, the focus is on clinical signs and safety, not strict numerical BG targets. |
| What is the role of endogenous insulin compared to pharmaceutical insulin? | Endogenous insulin secretion matches the body’s needs based on portal glucose and other signals, while pharmaceutical insulin tries to mimic this with subcutaneous dosing. |
| What factors influence selection of a pharmaceutical insulin in dogs and cats? | Species differences, pharmacokinetics (onset, peak, duration), trial and error, and clinical response. |
| Which insulins are short, intermediate, and long acting used in veterinary medicine? | Regular is short, NPH and Vetsulin are intermediate, ProZinc, glargine, and degludec are long acting. |
| Why is regular insulin not suitable for long-term home therapy? | Its duration is only a few hours, so it is used only in hospital settings such as DKA. |
| What is unique about Vetsulin compared to other insulins? | It is porcine zinc insulin identical to dog insulin structure, reducing risk of anti-insulin antibodies. |
| What is ProZinc and how does it act? | It is protamine zinc human insulin, long-acting due to delayed absorption from protamine and zinc. |
| What is glargine and how does U100 differ from U300 formulations? | Glargine is modified human insulin that forms depots at physiologic pH; U300 is more concentrated, slower absorbing, and longer lasting. |
| Which insulin can be used once daily and is often used in dogs? | Degludec (Tresiba). |
| What is the importance of U-40 vs U-100 syringes in veterinary insulin use? | Using the wrong syringe concentration can cause dangerous overdosing or underdosing. |
| Besides insulin, what non-insulin antidiabetic drugs are relevant in cats? | SGLT-2 inhibitors are now approved for cats, improving signs by increasing glucosuria. |
| What are the limitations of SGLT-2 inhibitors in diabetic cats? | They reduce glucose but do not address ketogenesis or hepatic gluconeogenesis, so not for use after DKA. |
| What type of diet is best for diabetic cats and why? | High-protein, low-carbohydrate diets because cats are obligate carnivores poorly adapted to carbs, improving remission rates. |
| Why is meal feeding often recommended for diabetic cats? | It coordinates with insulin dosing and reduces post-prandial glucose spikes, improving remission chances. |
| How does dietary therapy differ for diabetic dogs compared to cats? | Dogs benefit from balanced diets, sometimes high-fiber/complex carb to slow absorption; cats require high protein/low carb. |
| What are common causes of insulin resistance in dogs and cats? | Obesity, drugs (steroids, cyclosporine, etc.), co-morbid endocrinopathies (Cushing’s, hypothyroidism, acromegaly), and infections. |
| What is the most important part of diabetic monitoring? | Monitoring clinical signs such as PU/PD, polyphagia, and weight change. |
| What laboratory tests can assess long-term glucose control in diabetics? | Fructosamine (2–3 weeks average) and HbA1C (reflects RBC lifespan: ~110 days dogs, ~70 days cats). |
| How does a glucose curve help evaluate diabetic control? | It shows glucose levels over 12 hours to assess onset, peak, nadir, and duration of insulin effect. |
| What is the role of continuous glucose monitors in diabetic animals? | They measure interstitial glucose frequently, provide up to 14 days of data, and detect hypoglycemia, though costly. |
| Why is a spot blood glucose not reliable for adjusting insulin dose? | It represents only one time point, could be nadir or not, and must never be used to increase dose. |
| What complications can arise if diabetes is not well managed? | DKA, secondary infections, cataracts in dogs, diabetic neuropathy, and hypoglycemia. |
| What is the overall prognosis for small animals with diabetes mellitus? | Generally good with committed owners and veterinarians, though management is intensive and complications are possible. |
| What is the structure and role of the adrenal medulla, where is it located relative to the cortex, what is its embryologic origin, and what cells predominate in this region? | Medulla, neural crest, chromaffin cells, secrete catecholamines. |
| What is the function of chromaffin cells, what do they look like histologically, how are they connected, and how do they release catecholamines in basal versus stress conditions? | Dark stain, gap junctions, basal low release, stress large surge. |
| What are the two main catecholamines secreted by the adrenal medulla, what is their chemical structure, and which is the dominant secretion? | Norepinephrine and epinephrine, catechol ring+amine side chain, epinephrine main. |
| How does the adrenal medulla serve as the neuroendocrine arm of the sympathetic nervous system compared to direct sympathetic nerve release of norepinephrine? | Sym nerves release NE locally, medulla releases Epi/NE into blood. |
| What are the key steps in catecholamine biosynthesis starting from tyrosine, and what enzyme catalyzes each step? | Tyrosine→L-DOPA TH, →Dopamine DOPA decarb, →NE DBH, →Epi PNMT. |
| Which enzyme in catecholamine biosynthesis is the rate-limiting step and why is it important for regulation? | Tyrosine hydroxylase, controls synthesis rate. |
| Where does dopamine become norepinephrine, what enzyme performs this conversion, and in what cellular compartment does it occur? | In vesicles, dopamine β-hydroxylase converts dopamine→NE. |
| How is norepinephrine converted into epinephrine, what enzyme is required, and what hormone from the adrenal cortex enhances this process? | PNMT in cytosol, cortisol boosts PNMT. |
| How are catecholamines stored inside chromaffin cells, what transporter is used, and what triggers their release into the bloodstream? | Stored in vesicles via VMAT, released by ACh→Ca2+ influx exocytosis. |
| What additional molecules besides catecholamines are found in chromaffin vesicles, and what is their role? | Chromogranin peptides, modulate release. |
| How is catecholamine synthesis regulated by feedback from norepinephrine, by PACAP, and by cortisol? | NE inhibits TH, PACAP ↑TH/PNMT, cortisol ↑PNMT. |
| How does blood supply from adrenal cortex versus direct arterial supply affect NE versus Epi production in chromaffin cells? | Cortex venous blood→↑cortisol→↑PNMT→more Epi; arterial supply less cortisol→more NE. |
| What is the half-life of circulating catecholamines, how are they metabolized, and what enzymes are primarily responsible? | 1–2 min, degraded by COMT and MAO. |
| What are the main physiological stimuli that cause adrenal medulla catecholamine release? | Stress, trauma, pain, cold, hypoglycemia. |
| What cardiovascular changes are caused by catecholamines during acute stress and through which receptors? | ↑HR, ↑contractility, ↑BP via β1 and α1. |
| What respiratory changes are caused by catecholamines during acute stress and which receptor mediates them? | ↑rate, bronchodilation via β2. |
| What metabolic effects do catecholamines exert during acute stress on glucose and fat stores? | ↑glycogenolysis, ↑lipolysis, ↑glucagon. |
| What smooth muscle effects are mediated by catecholamines in GI tract, bladder, and blood vessels? | GI/bladder relax, most vessels constrict, skel muscle vessels dilate. |
| What are the five main adrenergic receptor subtypes, what type of signaling do they use, and how do their affinities for Epi versus NE differ? | α1 α2 β1 β2 β3, GPCRs, α1/α2/β1 Epi=NE, β2 Epi≫NE, β3 NE≫Epi. |
| What are the main actions of α1 receptors, where are they found, and what is their net physiological effect? | Vasoconstriction, sphincters contract, pupils dilate, ↑BP. |
| What are the main actions of α2 receptors, what feedback do they provide, and what are their metabolic effects? | Inhibit NE release, GI relax, ↓insulin ↑glucagon. |
| What are the main actions of β1 receptors, where are they found, and what is their overall effect on circulation? | Heart ↑HR/contractility, kidney ↑renin, ↑CO BP. |
| What are the main actions of β2 receptors, what tissues are affected, and why is epinephrine more potent here? | Bronchioles dilate, vessels to muscle dilate, GI/bladder relax, Epi≫NE. |
| What are the main actions of β3 receptors, what tissue do they affect, and what metabolic process do they stimulate? | Bladder relax, ↑lipolysis, NE≫Epi. |
| What is a pheochromocytoma, what cell type does it originate from, what clinical signs does it cause, and how is it treated? | Chromaffin tumor, excess catecholamines, HT/panting/tachy/weight loss, treat surgery+BP control. |
| Which enzyme is the rate-limiting step in catecholamine biosynthesis: DOPA decarboxylase, Dopamine β-hydroxylase, Tyrosine hydroxylase, or PNMT? | Tyrosine hydroxylase. |
| Which adrenergic receptor subtype is most responsive to epinephrine compared to norepinephrine: α1, α2, β1, or β2? | β2. |
| Which of the following is a well-recognized trigger for adrenal medulla catecholamine release: low blood glucose, high plasma calcium, increased stomach acid, or low thyroid hormone? | Low blood glucose. |
| What are the major physiological roles of calcium in the body, including its functions in enzymes, signaling, and structure? | Enzymatic activation, signal transduction, neurotransmission, muscle contraction, coagulation, exocytosis, and bone/teeth structure. |
| What are the key physiological roles of phosphate in metabolism, signaling, and structure? | Energy (ATP), nucleic acids, phospholipids, signal transduction, bone/teeth structure, and buffering. |
| How is calcium distributed among plasma compartments and which form is physiologically active? | Ionized calcium (iCa) is active; others are protein-bound or complexed to anions. |
| What effect does plasma pH have on ionized calcium levels and why? | Alkalosis increases protein binding → ↓ iCa; acidosis reduces binding → ↑ iCa. |
| Where is intracellular calcium mainly stored and why is its regulation so tight? | Stored in mitochondria and ER; excess cytosolic iCa is cytotoxic. |
| How are phosphate forms distributed in the ECF compared to the ICF? | ECF: HPO₄²⁻ > H₂PO₄⁻; ICF: H₂PO₄⁻ > HPO₄²⁻ due to lower pH. |
| What proportions of total body calcium and phosphate are found in bone? | ~99% of Ca²⁺ and ~85% of phosphate. |
| What crystal form stores calcium and phosphate in bone and which cells manage its turnover? | Hydroxyapatite; osteoblasts deposit, osteoclasts resorb. |
| Which three hormones regulate calcium and phosphate balance and what organs do they target? | Calcitriol, PTH, calcitonin; target intestine, kidney, and bone. |
| What are the two major sources of vitamin D in animals and which species rely mainly on diet? | Dermal synthesis and diet; dogs and cats rely on diet. |
| What are the sequential steps converting cholecalciferol to calcitriol, including organs and key enzymes? | Skin/liver/kidney pathway via 25-hydroxylase (liver) and 1α-hydroxylase (kidney). |
| How does calcitriol act at the cellular level to change calcium and phosphate handling? | Binds VDR → gene transcription for Ca²⁺ transport proteins. |
| What mechanisms does calcitriol use to enhance intestinal calcium absorption? | Upregulates TRPV6 channels, calbindin-D, and Ca²⁺ ATPase for transcellular transport. |
| How does calcitriol influence intestinal phosphate absorption? | Increases active phosphate transport through hormone-dependent mechanisms. |
| What are calcitriol’s effects on renal calcium and phosphate reabsorption? | ↑ iCa reabsorption (TRPV5/6, calbindin); minimal effect on phosphate reabsorption. |
| How does calcitriol act on bone to modify calcium and phosphate levels? | Stimulates osteoblast RANKL → activates osteoclasts → ↑ Ca²⁺, ↑ phosphate. |
| What is the overall effect of calcitriol on plasma calcium and phosphate levels? | Increases both iCa and phosphate. |
| Where is parathyroid hormone secreted, what triggers its release, and how long does it act? | From chief cells; secreted when iCa decreases; short-term regulator. |
| How does PTH act on bone, kidneys, and intestine to restore plasma calcium levels? | Bone resorption ↑ iCa; kidneys ↑ iCa reabsorption and calcitriol; intestines indirectly ↑ iCa. |
| How does PTH regulate phosphate levels in plasma? | Decreases renal phosphate reabsorption → ↑ excretion. |
| What is the relationship between PTH and calcitriol activation in the kidney? | PTH ↑ CYP27B1 activity → ↑ calcitriol synthesis. |
| What is PTHrP, when is it physiologically important, and what disease can it cause if overproduced? | PTH-like fetal hormone; excess causes humoral hypercalcemia of malignancy. |
| Where is calcitonin produced and when is it released? | From thyroid C cells; released when plasma iCa is high. |
| What are calcitonin’s effects on bone, kidneys, and intestines? | Inhibits bone resorption, decreases renal and intestinal Ca²⁺/phosphate reabsorption. |
| What is the overall effect of calcitonin on plasma calcium and phosphate levels? | Lowers both iCa and phosphate. |
| How does the calcium-sensing receptor (CaSR) regulate PTH secretion? | Low iCa → CaSR inactive → ↑ PTH; high iCa → CaSR active → ↓ PTH. |
| How does CaSR activation affect calcitonin release and renal calcium handling? | ↑ iCa activates CaSR → ↑ calcitonin, ↓ PTH, ↑ urinary Ca²⁺ excretion. |
| How do PTH and calcitonin together control renal calcitriol activation via CYP27B1? | PTH ↑, calcitonin ↑, and low PTH ↓ renal CYP27B1 activity. |
| What feedback does calcitriol exert on PTH secretion? | Calcitriol suppresses PTH synthesis and secretion. |
| Summarize how PTH, calcitonin, and calcitriol coordinate calcium and phosphate homeostasis. | PTH/calcitonin handle short-term iCa shifts; calcitriol mediates long-term balance. |
| What disease results from insufficient vitamin D or phosphorus, and what are its effects on bone? | Rickets; soft, poorly mineralized bones. |
| What condition arises from plant toxicity or mineral imbalance causing soft tissue calcification? | Enzootic calcinosis. |
| How does hypocalcemia affect neuromuscular excitability? | Increases excitability → muscle spasms, tetany. |
| How does hypercalcemia affect nerve and muscle function? | Decreases excitability → muscle weakness, lethargy. |
| What is metastatic calcification and when does it occur? | Soft tissue calcium phosphate deposition during hypercalcemia and hyperphosphatemia. |
| Which cortical zone of the adrenal gland synthesizes mineralocorticoids, and what is their primary physiological role in the body, especially regarding electrolyte balance and blood pressure? | Zona glomerulosa; maintains Na⁺, K⁺, and water balance to regulate blood pressure. |
| Which cortical zone produces glucocorticoids and what is their main function in metabolism and stress response? | Zona fasciculata; regulates metabolism and stress response through cortisol. |
| Which adrenal cortical zone primarily produces androgens, and what is their general physiological significance? | Zona reticularis; contributes to secondary sex characteristics and reproductive function. |
| How does adrenal cortical histology differ among species such as equine, pigs, ruminants, and primates? | Equine/pigs: zona arcuata; ruminants/primates: zona glomerulosa; similar functions. |
| What is the universal precursor molecule for all adrenocortical steroids, and which enzyme catalyzes the rate-limiting step in their synthesis? | Cholesterol; enzyme CYP11A1 catalyzes the rate-limiting step. |
| How do the enzyme profiles of adrenal cortical zones determine the hormone produced, and why is this pharmacologically relevant? | Each zone expresses unique enzymes; allows selective inhibition of cortisol or aldosterone synthesis. |
| How do corticosteroids primarily exert their effects at the cellular level, and what type of receptor do they act on? | Genomic action via intracellular receptors—mineralocorticoid or glucocorticoid receptors. |
| What is the difference between genomic and non-genomic effects of corticosteroids in terms of speed and duration of action? | Genomic: slow, long-term; non-genomic: fast, short-term. |
| Why are corticosteroids bound to plasma proteins, and which are the two main binding proteins involved? | Improve solubility and stability; main proteins are CBG and albumin. |
| Which adrenal steroid is more tightly bound in plasma, cortisol or aldosterone, and what does that mean for their bioactive fractions? | Cortisol is more bound; aldosterone has a higher free fraction and shorter half-life. |
| Where are corticosteroids metabolized, and through which routes are they excreted from the body? | Metabolized in liver; excreted via kidney (urine) and bile (feces). |
| Why can liver disease alter corticosteroid effects, and how are urinary corticoids used clinically? | Reduced clearance exaggerates effects; urinary corticoids assess cortisol for Cushing’s. |
| What are the main physiological effects of aldosterone in the kidney and on overall fluid balance? | ↑ Na⁺/water retention, ↑ K⁺/H⁺ excretion → maintains volume and pressure. |
| Why does cortisol require inactivation by 11β-HSD2 in mineralocorticoid target tissues such as the kidney? | To prevent cortisol from overstimulating MR; converts cortisol to inactive cortisone. |
| What happens in apparent mineralocorticoid excess and how can licorice consumption trigger it? | Licorice inhibits 11β-HSD2 → cortisol activates MR → hypertension, hypokalemia. |
| Which factors stimulate aldosterone release and which inhibit it? | Stimulated by renin-angiotensin, K⁺; inhibited by ANP and high Na⁺. |
| What are the main physiological actions of glucocorticoids on carbohydrate, protein, and lipid metabolism? | ↑ Gluconeogenesis, lipolysis, and protein catabolism for glucose sparing. |
| Why are glucocorticoids considered “stress hormones” and what role do they play in energy balance? | Mobilize energy substrates and suppress nonessential functions during stress. |
| What are the key anti-inflammatory mechanisms of glucocorticoids involving phospholipase A2 and lipocortin? | Stimulate lipocortin → inhibit PLA2 → ↓ arachidonic acid → ↓ prostaglandins/leukotrienes. |
| How do glucocorticoids suppress the immune system and what hematologic effect is commonly observed? | Inhibit T-cells and antibody production; cause stress leukocytosis. |
| What are the cardiovascular effects of glucocorticoids and how do they interact with adrenergic receptors? | ↑ α₁/β₁ receptors → ↑ contractility, HR, BP; ↓ vascular permeability. |
| How do glucocorticoids alter water balance and why can excessive levels cause PU/PD? | Interfere with ADH signaling; cause Na⁺ retention and increased urine output. |
| What are the effects of glucocorticoids on bone, collagen, and calcium absorption? | ↓ Collagen, ↓ osteoblasts, ↓ intestinal Ca²⁺ absorption → weak bones. |
| Which hypothalamic and pituitary hormones regulate adrenal glucocorticoid secretion, and what is the feedback mechanism? | CRH → ACTH → cortisol; cortisol exerts negative feedback on both. |
| Which adrenal zones are most responsive to ACTH and which rely more on renin-angiotensin control? | Zona fasciculata (glucocorticoids) responsive to ACTH; zona glomerulosa (mineralocorticoids) mainly renin-controlled. |
| What are the three main causes of adrenal cortical dysfunction and what distinguishes them? | Primary (gland), secondary (pituitary/hypothalamic), iatrogenic (drug-induced). |
| What causes primary hypercortisolism and how does it affect ACTH and CRH levels? | Adrenal tumor → ↑ cortisol → ↓ ACTH/CRH via feedback. |
| What causes secondary hypercortisolism and what is its most common etiology in dogs and horses? | Pituitary tumor → ↑ ACTH → ↑ cortisol. |
| How does an ACTH-secreting non-pituitary tumor cause hypercortisolism? | Ectopic ACTH ↑ cortisol; pituitary ACTH suppressed. |
| How does chronic glucocorticoid therapy induce iatrogenic hypercortisolism? | Excessive external GC → mimic cortisol effects → suppress HPA axis. |
| List the hallmark clinical signs of Cushing’s disease (“6 Ps”) in dogs. | Polyuria, polydipsia, polyphagia, pot-belly, panting, proteinuria. |
| What skin and hair abnormalities are seen in canine and equine hypercortisolism? | Dogs: alopecia, thin skin; horses: hirsutism (hypertrichosis). |
| How does an adrenal tumor in ferrets differ in hormone secretion from that in dogs? | Ferrets: ↑ sex hormones; dogs: ↑ cortisol. |
| What is the primary cause of Addison’s disease in dogs and what ions are altered? | Immune-mediated adrenal destruction; ↓ Na⁺, ↑ K⁺. |
| What are clinical signs of Addisonian crisis due to adrenal failure? | Hypovolemia, dehydration, hypotension, bradycardia, shock. |
| How can abrupt withdrawal of glucocorticoid therapy lead to iatrogenic hypocortisolism? | Atrophic adrenal cortex cannot resume cortisol production quickly. |
| What test evaluates adrenal responsiveness to ACTH, and what are expected results in normal vs Addisonian animals? | ACTH stimulation test; normal ↑ cortisol, Addison’s minimal or no response. |
| What diagnostic test differentiates healthy vs hypercortisolemic animals based on feedback suppression? | Low-dose dexamethasone suppression test (LDDST). |
| How does dexamethasone affect cortisol levels in normal vs hypercortisolemic animals? | Normal ↓ cortisol (feedback); hypercortisolemic no suppression. |
| Which tests can help identify whether hypercortisolism originates from pituitary or adrenal causes? | LDDST plus ACTH measurement; pituitary: ACTH high, adrenal: ACTH low. |
| Summarize the physiological and regulatory differences among mineralocorticoids, glucocorticoids, and androgens. | Mineralocorticoids regulate electrolytes; glucocorticoids metabolism/stress; androgens reproductive effects. |
| Summarize how HPA axis feedback maintains homeostasis and how dysfunction causes disease. | Cortisol feedback limits CRH/ACTH; over/underactivity → Cushing’s/Addison’s. |
| Which diagnostic test evaluates hyperfunction and which assesses hypofunction of the adrenal cortex? | LDDST for hyperfunction; ACTH stimulation test for hypofunction. |
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Hoofin'it