Endocrinology Combined Practice Questions

*Adrenal Cortex Pathophys* Increased adrenocorticotropic hormone (ACTH) secretion would be expected in patients A. with chronic adrenocortical insufficiency (Addison's disease) B. with primary adrenocortical hyperplasia C. who are receiving glucocorticoid for immunosuppression after a renal transplant D. with elevated levels of angiotensin II

A. with chronic adrenocortical insufficiency (Addison's disease) [NOTE: It says "secretion". This means there would be an increase of production at the anterior pituitary by either negative feedback or a tumor here.] [Addison Disease (Chronic Adrenal Insufficiency): - *↑ ACTH --> Low cortisol levels stimulate ACTH secretion by negative feedback.* - ↓ adrenal glucocorticoids, androgen, and mineralocorticoid - Weight loss, weakness, nausea, and vomiting - hypoglycemia - ↓ pubic and axillary hair in women - ECF volume contraction - hypotension - hyperkalemia - metabolic acidosis - hyperpigmentation (ADD SOME CORTISOL, SONNNN = Addison's Disease lol)] [Primary adrenocortical hyperplasia = Congenital adrenal hyperplasia: - individuals lack an enzyme (11β-hydroxylase) needed to make cortisol and aldosterone. - Excess androgen is produced - Causes male characteristics to appear early (or inappropriately)] [Cushing's Syndrome is an increase in blood cortisol level due to: - adrenal cortex tumor - ACTH-secreting tumor in the anterior pituitary, - pharmacological use of cortisol - ↓ ACTH if caused by primary adrenal hyperplasia or pharmacological doses of glucocorticosteroids] [Increased ACTH eventually causes increased ADH which increases renin which increases angiotensin II production. While they are related, there is no direct feedback mechanism with angiotensin II that affects ACTH secretion.]

Which of the following hormones acts on its target tissues by increasing gene expression? A: Cortisol B: Parathyroid hormone (PTH) C: Antidiuretic hormone (ADH) D: beta adrenergic agonists E: Glucagon

A: Cortisol [CORTISOL IS A STEROID Steroids use intracellular receptors, meaning that they pass through the membrane without using a 2nd messenger system. Steroids then bind with a receptor protein inside the cell cytoplasm to create a complex Complex goes to the nucleus to stimulate mRNA Transcription from DNA --> creates more proteins from those specific genes One purpose of creating proteins are to carry out reactions for a specific response (in this case, This is known as "GENE EXPRESSION" This is different from hormones that use a 2nd messenger system --> they use a messenger in the cytoplasm to activate proteins that have already been made.] [Steroid Hormones: "VETTT CAP" The VET on STEROIDS is wearing a baseball CAP V Vitamin D3 E Estrogen T Testosterone T T3 (Triiodothyronine) T T4 (Thyroxine) C Cortisol ***** A Aldosterone P Progesterone]

*Adrenal Cortex Pathophys* A 46-year-old woman has hirsutism, hyperglycemia, obesity, muscle wasting, and *decreased* circulating levels of adrenocorticotropic hormone (ACTH). The most likely cause of her symptoms is A. primary adrenocortical insufficiency (Addison's disease) B. pheochrromocytoma C. primary overproduction of ACTH (Cushing's disease) D. treatment with exogenous glucocorticoids E. Cushing's syndrome

E. Cushing's syndrome [Addison Disease (Chronic Adrenal Insufficiency): - ↑ ACTH --> Low cortisol levels stimulate ACTH secretion by negative feedback. - ↓ adrenal glucocorticoids, androgen, and mineralocorticoid - Weight loss, weakness, nausea, and vomiting - ↓ pubic and axillary hair in women - ECF volume contraction - hypotension - hyperkalemia - metabolic acidosis - hyperpigmentation (ADD SOME CORTISOL, SONNNN = Addison's Disease lol)] [Pheochromocytoma (Medullary Suprarenal Adenoma): tumor of the adrenal medulla (Chromaffin cells) that secrets excessive amounts of catecholamines and increased excretion of VMA] [Cushing's Disease is an increase in blood cortisol level due to: - ACTH-secreting tumor - ↑ ACTH (if caused by overproduction of ACTH) - ↑ cortisol and androgen levels - Hyperglycemina (caused by elevated cortisol level) - ↑ protein catabolism and muscle wasting - Central obesity - Virilization of women = "Hirsutism" - Hyperpigmentation (disease only)] [With exogenous glucocorticoids, you get Cushing's Syndrome --> you don't get the Hirsutism!!!!] [Cushing's Syndrome is an increase in blood cortisol level due to: - adrenal cortex tumor - ACTH-secreting tumor in the anterior pituitary, - pharmacological use of glucocorticoids/glucocorticosteroids -*↓ ACTH* - ↑ cortisol and androgen levels - *Hyperglycemia* (caused by elevated cortisol level) - ↑ protein catabolism and *muscle wasting* - *Central obesity* - Virilization of women = "*Hirsutism*"]

Testes are the target for which of the following hormones (choose best answer): A. TSH B. Testosterone C. Prolactin D. Thyroxin E. FSH

E. FSH [FSH or LH - See picture]

*Pancreas* The pancreatic hormone that *decreases* blood glucose levels is: A. Glucagon B. Cortisol C. Erythropoietin D. Somatotropin E. Insulin

E. Insulin [Insulin is secreted by the pancreatic beta cells in response to an increase in blood glucose. Insulin works to decreases blood glucose levels.]

One treatment for erectile dysfunction requires the injection of a substance into the corpos cavernosa of the penis. The injection of which of the following causes an erection? A. Norepinephrine B. A substance that inhibits formation of nitric oxide C. Thromboxane A2, which is a vasoconstrictor prostaglandin D. Angiotensin H E. None of the above

E. None of the above

*Pancreas* Which of the following symptoms would you expect to observe in a person suffering from type I Diabetes Mellitus? A. Glucosuria B. Hyperglycemia C. acidosis D. Increased thirst E. all of the above

E. all of the above ***ASK DR. GIBLIN ABOUT ACIDOSIS*** BOTH DIABETES MELLITUS: Results from either hyposecretion or hypoactivity of insulin The three cardinal signs of DM are: - Polyuria - huge urine output - Polydipsia - excessive thirst - Polyphagia - excessive hunger and food consumption [Type I- Diabetes mellitus: Insulin deficiency Insulin-Dependent Diabetes Usually first seen in youth Due to destruction of β cells in pancreatic islets (THINK: "B. M. I. " --> Beta Makes Insulin") Genetic or environmental factors lead to attack on β cells by the immune system Poor uptake of glucose, body responds as if no glucose present weight loss despite eating normally Treatment - Diet: Low carbohydrates (to slow increase in serum glucose) & Low fats (to decrease heart disease) - Insulin injections: Blood monitoring of glucose & Insulin pumps (newer technology)]

*Female Development* Development of the fallopian tubes in a female fetus depends upon: A. hormonal stimulation of Mullerian ducts B. hormonal stimulation of Wolffian ducts C. estrogens D. FSH E. none of the above

E. none of the above [Female genitalia are the default regardless]

*Male Development* The development of testes in an XY embryo is due to: A. adrenal androgens B. FSH C. a lack of estrogens D. testosterone E. none of the above

E. none of the above [It is the Y-chromosome that carries testis-determining factor (TDF), which promotes the development of testes. Do not confused Testosterone: this hormone is produced by the already established gonads.]

Which of the following is inconsistent with the diagnosis of Graves' disease? A: Increased heart rate B: Exophthalmos C: Increased plasma levels of triiodothyronine (T3). D: Increased plasma levels of thyroxine (T4). E: Increased plasma levels of thyroid-stimulating hormone

E: Increased plasma levels of thyroid-stimulating hormone [*FALSE*] [Autoimmune disease (Grave's Disease): Antibodies act like TSH Stimulate thyroid gland to grow and oversecrete T3 + T4 = *hyperthyroidism* (excessive thyroxine secretion which leads to goiter) Too much T3 + T4 in blood sends negative feedback to anterior pituitary Because the antibodies are replacing function of TSH and over stimulating the production of T3 + T4, that means there is more negative feedback to both the hypothalamus for TRH and A.P. for TSH, which now does not create TSH in the first place --> *This decreases plasma levels of thyroid-stimulating hormone*.]

The pititutary hormone that controls the release of corticosteroids from the adrenal gland is: A: TSH B: ACTH C: CRH D: LH E: GH

B: ACTH [ACTH = Adrenocorticotropic Hormone --> Stimulates Corticosteroids (cortisol) produced in the Zona Fasiculata in the Adrenal Cortex]

The proliferative phase of the menstrual cycle is stimulated by A: progesterone B: FSH C: Inhibin D: adrenal steroid hormones

B: FSH [Proliferative Phase: *- Stimulated by FSH* - Occurs while ovary is in the follicular phase - Increasing levels of estrogen stimulate the growth of the stratum functionale of the endometrium. - The endometrium also becomes more vascular and develops LH receptors. - A new *functional layer of endometrium* is formed in the uterus] {THINK: *F*unctional Layer = *F*SH = Proli*F*erative Phase]

In order to make thyroid hormone, follicular cells uptake A: Iodide via facilitated transport B: Iodide via sodium coupled transport C: Iodine via facilitated transport D: Iodine via sodium coupled transport

B: Iodide via sodium coupled transport [See picture - "sodium-iodide symporter" Iodide comes through a plasma membrane (from blood) along with a sodium --> aka "coupled transport"]

A major action of oxytocin is to cause: A. Increased blood exygenization B. Uterine contractions C. Milk ejection D. Both B and C

D. Both B and C [Oxytocin causes: - Contraction of lactiferous ducts = "milk letdown" or "milk ejection" -Uterine contractions]

Parathyroid hormone directly A. Controls the rate of glycogen formation B. Inhibits the rate of calcium transport in the mucosa of the small intestine C. Decreases the rate of formation of calcium binding protein D. Controls the rate of formation of 1,25-dihydroxycholicalciferol E. Stimulates renal tubular phosphate reabsorption

D. Controls the rate of formation of 1,25-dihydroxycholicalciferol

*Pancreas* Which of the following symptoms would you *NOT* expect to observe in a person suffering from type I Diabetes Mellitus? A. Glucosuria B. Hyperglycemia C. Ketoacidosis D. Decreased appetite E. Increased thirst

D. Decreased appetite [The three cardinal signs of DM are: • Polyuria - huge urine output • Polydipsia - excessive thirst • Polyphagia - excessive hunger and food consumption Hyperinsulinism - excessive insulin secretion, resulting in hypoglycemia Poor uptake of glucose due to insufficient insulin --> polyphagia *(excessive hunger and food consumption)* --> weight loss in TYPE 1 despite eating normally Ketoacidosis = DM Type 1 Excess glucose in renal tube filtrate with water since it can't reabsorb it ("too many seats on the bus") --> Glucosuria --> excess glucose in urine --> causes polyuria (huge urine output)]

*Male Development* In males, A. FSH in not secreted by the pituitary gland B. FSH receptors are located on the Leydig cells C. FSH receptors are located on the spematogonia D. FSH receptors are located on the Sertoli cells

D. FSH receptors are located on the Sertoli cells [F*S*H = *S*ertoli = *S*perm] [Sperm is simillar to *Follicle* --> Associate Sperm with *Follicle* Stimulating Hormone]

*Calcium Hormones* Which of the following conditions would you expect to decrease the normal synthesis of the vitamin D3 metabolite, 1, 25 -dihydroxycholecalciferol (the most physiologically active metabolite of D3)? A. Diet low in Ca2+ B. adrenal insufficiency C. Hyperparathyroidism D. Hypercalcemia

D. Hypercalcemia [The production of 1,25-dihydroxycholecalciferol in the kidney is catalyzed by the enzyme 1α-hydroxylase. (In the kidneys) 1α-hydroxylase activity is increased by the following: ↓ serum [Ca2+] ↑ PTH levels ↓ serum [phosphate] PTH normally increases intestinal [Ca2+] and [phosphate] absorption indirectly by stimulating the production of 1,25-dihydroxycholecalciferol in the kidney. *SO* if the serum Ca2+ is HIGH, then it negatively feedsback to parathyroids, PTH will stop being produced, so *Vitamin D3 production is also decreased.*]

Pathophysiology of the Adrenal Cortex table in course notes: Glucocorticoids (Cortisol)

Glucocorticoids (cortisol) Adrenal cortex - Zona Fasiculata Stimulates glucogenesis; anti-inflammatory; immunosuppression

Review of Conn's Syndrome

Hyperaldosteronism (Conn's Syndrome) - is caused by an aldosterone-secreting tumor in the zona glomerulosa. Symptoms: - Hypertension (because aldosterone increase Na+ reabsorption, which leads to increases in ECF volume and blood volume. - Hypokalemia (because aldosterone increase K+ secretion) - Metabolic alkalosis (because aldosterone increases H+ secretion) - ↓ renin secretion (because increased ECF volume and blood pressure inhibit rennin secretion by negative feedback)

xxxxxxxxxxxxxxxxx (EXTRA OLD ENDO Q's I HAVEN'T SORTED YET SORRY) xxxxxxxxxxxxxxxxx

wow okay lazy

Match the following hormones (numbered 3 - 6 below) with the primary agent (a - e) that stimulates its release: a. TSH b. ACTH c. Growth hormone d. Sympathetic nerves e. CRH 1. Epinephrine ___ 2. Thyroxine ___ 3. Corticosteroids ___ 4. ACTH ___

1. Epinephrine *D* <-- Sympathetic nerves 2. Thyroxine *A* <-- TSH [Thyroid Stimulating Hormone] 3. Corticosteroids *B* <-- ACTH [Adrenocorticotropic Hormone] 4. ACTH *E* <-- CRH [Cortico-tropin releasing Hormone]

Match the following intracellular signaling mechanism with the hormones listed below: A. cAMP B. DAG-IP3 C. Steroid D. Activation of tyrosine kinase E. Can be A or B above, depending on target cell and receptor 1. Insulin - ___ 2. Parathyroid hormone - ___ 3. Epinephrine - ___

1. Insulin - D 2. Parathyroid hormone - A 3. Epinephrine - E

Starting day 1 with the menstrual cycle, the endometrial phases of the uterus occur in the following order:

1. Menstrual 2. Proliferative 3. Secretory

Match the following intracellular signaling mechanism with the hormones listed below: a. cAMP b. DAG-IP3 c. Steroid d. Activation of Tyrosine kinase e. Can be a or b above, depending on target cell and receptor 1. Oxytoxcin ___ 2. ADH ___ 3. Insulin ___ 4. Testosterone ___

1. Oxytoxcin *B* <-- DAG-IP3 2. ADH *E* <--cAMP or DAG-IP3 depending on target cell 3. Insulin *D* <--Tyrosine kinase 4. Testosterone *C* <--Steroid

Review for 17a hydroxylase deficiency:

17α-Hydroxylase deficiency Symptoms: - ↓ androgen and glucocorticoids levels (because the enzyme block prevents the production of 17-hydroxypregnenolone and 17-hydroxyprogesterone) - ↑ aldosterone levels (because intermediates accumulate to the left of the enzyme block and are shunted toward the production of mineralocorticoids) - Lack of pubic and axillary hair (which depends on adrenal androgens) in women - Hypoglycemia (because of decreased glucocorticoids) - Metabolic alkalosis, hypokalemia, and hypertension (because of increased aldosterone) - ↑ ACTH (because decreased cortisol levels stimulate ACTH secretion by negative feedback) - Hyperpigmentation and hyperplasia of zona fasciculata and reticularis.

Review of 21 α -Hydroxylase deficiency

21 α -Hydroxylase deficiency - is the most common biochemical abnormality of the steroidogenic pathway Symptoms: - ↓ cortisol and aldosterone levels (because the enzyme block prevents the production of 11-deoxycorticosterone and 11-deoxycortisol, the precursors for cortisol and aldosterone) - ↑ 17-hydroxyprogesterone and progesterone levels (because of accumulation of intermediates above the enzyme block) - ↑ ACTH (because of decreased feedback inhibition by cortisol) - Hyperpigmentation - Hyperplasia of zona fasciculata and zona reticularis (because of high levels of ACTH) - ↑ adrenal androgens (because 17-hydroxyprogesterone is their major precursor) - Virilization in women - Early acceleration of linear growth and early appearance of pubic and axillary hair - Suppression of gonadal function in both men and women

*Male Development* A 24 year old male with an untreated deficiency in testicular production of testosterone since early childhood will likely exhibit which of the following signs? A. Be somewhat taller than average B. Have a deep voice C. Have abundant chest hair D. Have large testicles E. Lack pubic hair

A. Be somewhat taller than average [What affects the fusion of the growth plates? TESTOSTERONE] [GH continues to stimulate the height.] [Pubic hair is controlled by Adrenal Androgens]

*Adrenal Cortex* The adrenal hormone that causes blood glucose levels to rise is: A. Cortisol B. Erythropoietin C. Somatotropin D. Insulin

A. Cortisol [Cortisol (from adrenal cortex - zona fasiculata) provokes: •Gluconeogenesis (formation of glucose from noncarbohydrates) •*Rises in blood glucose*, fatty acids, and amino acids •Enhances effects of sympathetic vasoconstriction •Inhibits inflammatory response (depresses immune system NOTE: Glucagon from the pancreas can also cause an increase in blood glucose levels]

*Adrenal Cortex* Selective destruction of the zona fasciculata of the adrenal cortex would produce a deficiency of which hormone? A. Cortisol B. Androstenedione C. Aldosterone D. Dehydroepiandrosterone E. Testosterone

A. Cortisol [Layers of Adrenal Cortex: GFR 1. Zona Glomerulosa = Aldosterone (mineralcorticoid) --> stimulates kidneys to reabsorb Na+ and secrete K+ 2. *Zona Fasiculata* = *Cortisol* (glucocorticoid) --> which inhibits glucose breakdown for energy and stimulates gluconeogenesis (i.e. formation of glucose from noncarbohydrates) 3. Zona Reticularis = Sex steroids (gonadocorticoids) --> mostly androgens (male sex hormones)]

*Adrenal Cortex* Which of the following causes *increased* aldosterone secretion? A. Decreased blood volume B. Administration of an inhibitor of angiotensin-converting enzyme (ACE) C. Hyperosmolarity D. Hypokalemia

A. Decreased blood volume [*Aldosterone secretion is stimulated by:* Rising blood levels of K+ = Hyperkalemia Low blood Na+ = Hyponatremia *Decreasing blood volume or pressure*] [Hyperosmolarity = Hyperosmolar blood (high solutes to low water ratio) stimulates synthesis and release of ADH (NOT aldosterone)] [Renin-angiotensin mechanism: kidneys release renin, which results in the production of angiotensin II that in turn stimulates aldosterone release. Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE). So normally ACE increases Aldosterone, but answer choice B says administration of an INHIBITOR to ACE, so that would in turn decrease aldosterone.]

The parasympathetic nervous system activity causes ______________, while activity in the sympathetic nervous system causes ______________. A. Erection; ejaculation B. Ejaculation; emission C. Emission; ejaculation D. Ejaculation; erection

A. Erection; ejaculation

Which of the following hormones initiates the follicular phase of the menstrual cycle? A. FSH B. LH C. Epinephrine D. T cell

A. FSH

*Pancreas* The pancreatic hormone that causes blood sugar levels to rise is: A. Glucagon B. Cortisol C. Erthyrpoietin D. Somatotropin E. Insulin

A. Glucagon [Blood "Sugar" = Blood "Glucose"] [Glucagon increases blood glucose (breaks down glycogen): glycogenolysis (decreased by Insulin)]

*Pancreas* The pancreatic hormone that increases blood glucose levels is: A. Glucagon B. Cortisol C. Erythropoietin D. Somatotropin E. Insulin

A. Glucagon [Glucagon increases blood glucose:(breaks down glucagon): glycogenolysis (decreased by Insulin)]

*Adrenal Cortex* Which of the following causes *increased* aldosterone secretion? A. Hyperkalemia B. Administration of an inhibitor of angiotensin-converting enzyme (ACE) C. Hyperosmolarity D. Increased blood volume

A. Hyperkalemia [*Aldosterone secretion is stimulated by:* *Rising blood levels of K+* = *HYPERKALEMIA* (aldosterone gets rid of potassium) Low blood Na+ (aldosterone works to increase sodium) Decreasing blood volume or pressure] [Hyperosmolarity = Hyperosmolar blood (high solutes) stimulates synthesis and release of ADH (NOT aldosterone)] [Renin-angiotensin mechanism: kidneys release renin, which results in the production of angiotensin II that in turn stimulates aldosterone release. Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE). So normally ACE increases Aldosterone, but answer choice B says administration of an INHIBITOR to ACE, so that would in turn decrease aldosterone.]

*Gonadotropins* Inhibin exerts feedback: A. In males, inhibiting the secretion of follicle-stimulating hormone by the anterior pituitary B. In males, stimulating secretion of gonadotropin-releasing hormone by the hypothalamus C. In females, greatly decreasing the release of luteinizing hormone from the anterior pituitary D. On none of the above

A. In males, inhibiting the secretion of follicle-stimulating hormone by the anterior pituitary

*Male Development* A 16 -year-old, seemingly normal, girl has never had a menstrual cycle. She has a blind end vagina, NO uterus, cervix, fallopian tubes or ovaries, a 46 XY genotype and intra-abdominal testes. Her serum testosterone is elevated. Her lack of a uterus is due to: A. MIF (Mullerian Inhibitory Factor) B. testosterone C. insufficient estrogens D. TDF E. all of the above

A. MIF (Mullerian Inhibitory Factor) [Because she has an XY genotype so she develops testes, but she has a female phenotype. She is classified as a hermaphrodite. It is the Y-chromosome that carries testes-determining factor (TDF) (protein made from the SRY gene), which promotes the development of testes (even though she looks like a girl) Here, since she is a hermaphodite, the patient should have been a boy genotypically but must have had an excess sex hormone during fetal development. *Wolffian duct* = male internal genital tract and external genitalia *Mullerian duct* = female internal genital tract and external genitalia Testes are made from the SRY gene (on y chromosome) and developed from the TDF protein. Testes secrete BOTH *Testosterone* and *Mullerian Inhibitory Factor (MIF).* Testosterone normally stimulates the growth and differentiation of the wolffian ducts --> develops the male internal genital tract (Leydig cells from the Testes) Müllerian duct is normally developed into female internal genital tract and external genitalia. Controlled by *Mullerian Inhibitory Factor (MIF)* --> Inhibits Mullerian duct development ("female genitalia") to create male genetalia. (Sertoli cells from the testes secrete MIF) THUS Without antimüllerian (*Mullerian Inhibitory Factor (MIF))* hormone, *the müllerian ducts are NOT suppressed* and therefore develop into the female internal genital tract even though they have the Y chromosome --> *development of both male and female genitalia*] CONCLUSION: androgen insensitivity disorder (male pseudo hermaphroditism) -- (if it was alpha-5 reductase syndrome, it would result in a penis developing around puberty at age 12). [NOTE: It says her testosterone levels are elevated. This is due to her intrabdominal testes also being present --> SINCE SHE IS 16 this means she has already gone thru puberty so we can differeniate between AIS vs 5 alpha reductase] [Extra side note on AIS vs 5-apha reductase def.: similarities: XY chromosome, undescended testes, male pseudohermaphroditism. Differences AIS: no internal genitals at all Appears female thru out LIFE HIGH Testosterone levels male internal genitals develops penis @ puberty (due to test) normal testosterone levels]

*Calcium Hormones* The hormone that *increases* renal phosphate excretion: A. Parathyroid hormones B. calcitonin C. aldosterone D. thyroxine

A. Parathyroid hormones [PTH action increases ionized Ca2+ in serum by: -increasing bone resorption - increasing renal Ca2+ reabsorption - increasing intestinal Ca2+absorption - decreasing renal phosphate reabsorption --> (*i.e. INCREASES RENAL PHOSPHATE EXCRETION*) - Hyperparathryoidism causes hypercalemia and hypophosphatemia]

Hormones released from the anterior pituitary are: A. Trophic B. Steroid C. Neuroendocrine D. Amine

A. Trophic [Trophic hormones stimulate the activity of another endocrine gland.] [*Hormones released by A.P.*: FLAT PIG" FSH LH ACTH TSH PRL (I - Ignore) GH]

*Female Development* The female pattern of pubic hair is due to A. adrenal androgens B. estrogens C. progesterone D. aromatase E. none of the above

A. adrenal androgens [Virilization of women (development of male sex characteristic in a female) = elevated levels of adrenal androgens Conversely: ↓ pubic and axillary hair in women = deficiency of adrenal androgens]

Hormones secreted from the posterior pituitary: A. Are produced by neurosecretory cells in the hypothalamus B. Are transported in the hypothalmohyophysial portal system C. Include GH and ACTH D. Are classified as pheromones

A. are produced by neurosecretory cells in the hypothalamus [Neurosecretory cells synthesize and secrete hormones into: *Capillary plexus of posterior pituitary* (neurohypophysis) --> ADH, oxytocin AND *Primary Capillary plexus of the median eminence* --> hypothalamic-releasing (& inhibiting) hormones that act on *anterior pituitary* (adenohypohysis)]

*Adrenal Cortex* Which of the following would *decrease* aldosterone secretion? A. increased blood volume B. increased angiotensin-converting enzyme (ACE) C. decreased blood volume D. Hyperkalemia

A. increased blood volume [NOTICE: it says what decreases, so the opposite of what normally stimulates it! *Aldosterone secretion is decrease by:* Decreasing blood levels of K+ = Hypokalemia High blood Na+ = Hypernatremia *Increasing blood volume or pressure*] [Renin-angiotensin mechanism: Kidneys release renin, which results in the production of angiotensin II that in turn stimulates aldosterone release. Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE). So normally ACE increases Aldosterone, but answer choice B says administration of ACE would would increase, NOT decrease aldosterone.]

*Female Cycle* Oral contraceptives: A. inhibit of gonadotropin secretion B. stimulate the corpus luteum C. stimulate Graafian follicles D. are androgens E. none of the above

A. inhibit of gonadotropin secretion [Gonadotropin-releasing hormone (GnRH) causes release of FSH and LH Contraceptive Pill: Includes synthetic estrogen and progesterone Acts like a prolonged luteal phase *Produces negative-feedback inhibition of GnRH, so ovulation never occurs* The endometrium still proliferates. Placebo pills are taken for 1 week to allow menstruation.]

*Gonadotropins* Inhibin: A. inhibits the secretion of follicle-stimulating hormone by the anterior pituitary B. inhibits the secretion of FSH by the hypothalamus C. inhibits the release of luteinizing hormone from the anterior pituitary D. none of the above

A. inhibits the secretion of follicle-stimulating hormone by the anterior pituitary [FSH acts on the Sertoli cells to maintain spermatogenesis. Sertoli cells also secrete inhibin, which is involved in negative feedback of FSH secretion. Too much FSH --> Sertoli cells secrete Inhibin --> Inhibin inhibits more creation of FSH from the Anterior Pituitary]

*Female Cycle* Starting with day one of the menstrual cycle, the endometrial phases of the uterus occur in the following order: A. menstrual, proliferative, secretory B. secretory, proliferative, menstrual C. proliferative, secretory, menstrual D. proliferative, menstrual, secretory

A. menstrual, proliferative, secretory [REMEMBER: The menstrual cycle begins with menstruation at the end of the previous ovarian cycle. *End of Previous menstruation* --> Proliferative --> Secretory --> Menstruation]

*Female Cycle* The surge in luteinizing hormone (LH) that occurs during the middle of the ovarian cycle triggers: A. ovulation B. menstruation C. follicle maturation D. atresia E. menopause

A. ovulation [LH surge begins ~24 hours before ovulation]

*Male Development* The fetal development of a male phenotype depends upon stimulating hormone production by the: A: Leydig cells B: Sertoli cells C: Wolffian duct D: Mullerian duct

A: Leydig cells [*L*eydig = *L*H LH creates Testosterone Testosterone creates male phenotype (physical appearance / characteristics)]

Which of the following statements is TRUE? A: Progesterone is secreted by the corpus luteum B: Progesterone is secreted by the pituitary gland C: Progesterone decreases basal temperature D: Progesterone secretion stimulates menstruation

A: Progesterone is secreted by the corpus luteum [Progesterone: *Secreted by the Corpus Luteum* ACTIONS: -Has negative feedback effects on FSH and LH secretion during luteal phase. - Maintains secretory activity of the uterus during the luteal phases. - Maintains pregnancy. - Participates in the development of the breasts. - Highest between day 14 (ovulation) and day 21 (menstruation) - INCREASES Basal Body Temperature]

Which of the following statements about hypothalamic releasing hormones is true? A: They are secreted into capillaries in the median eminence B: They are transported by portal veins to the posterior pituitary C: They stimulate the secretion of specific hormones from the posterior pituitary D: all of the above(a-c) are true E: none of the above (a-c) are true

A: They are secreted into capillaries in the median eminence [Hypothalamic Releasing Hormones: Releasing hormones are secreted in the capillaries of the median eminence to go to the *anterior* pituitary. (Neurosecretory cells in the hypothalamus are what send them to the posterior pituitary!) They are transported by portal veins to the *anterior* pituitary (not the posterior - neurosecretory cells send them to the posterior pituitary). They stimulate the secretion of specific hormones from the *anterior* pituitary (Hypothalamus sends them to the posterior pituitary which sends them directly into the blood, no other secretion is made there).]

Which of the following increases the gene expression? A: Thyroid hormone B: Vitamin B12 C: Antidiuretic hormone (ADH) D: Beta adrenergic agonists E: Glucagon

A: Thyroid hormone [Thyroid Hormone = T3 + T4 THYROID HORMONES ARE STEROIDS Steroids use intracellular receptors, meaning that they pass through the membrane without using a 2nd messenger system. Steroids then bind with a receptor protein inside the cell cytoplasm to create a complex Complex goes to the nucleus to stimulate mRNA Transcription from DNA --> creates more proteins from those specific genes One purpose of creating proteins are to carry out reactions for a specific response (in this case, This is known as "GENE EXPRESSION" This is different from hormones that use a 2nd messenger system --> they use a messenger in the cytoplasm to activate proteins that have already been made.] [Steroid Hormones: INTRACELLULAR RECEPTORS "VETTT CAP" The VET on STEROIDS is wearing a baseball CAP V Vitamin D3 E Estrogen T Testosterone T T3 (Triiodothyronine) ***** T T4 (Thyroxine) ***** C Cortisol A Aldosterone P Progesterone]

A goiter is due to A: activation of TSH receptors B: hyperthyroidism C: hypothyroidism D: activation of TRH receptors

A: activation of TSH receptors [Goiter --> Activation of the TSH receptors]

Oocytes fully complete meiosis A: after fertilization B: during gestation C: in primary follicles D: in secondary follicles E: in Graafian follicles

A: after fertilization [Ovum is stuck in meiosis II Miosis occurs when it is fertilized by a sperm cell]

Hormones secreted from the posterior pituitary: A: are produced by neurosecretory cells in the hypothalamus B: are transported in the hypothalmohyophysial portal system C: include GH and ACTH D: are classified as pheromones

A: are produced by neurosecretory cells in the hypothalamus [*Neurosecretory cells in the hypothalamus* synthesize hormones to send to posterior pituitary which goes directlyinto the blood, there are no cells that create/secrete any hormones in the posterior pituitary. They come straight from the hypothalamus! Neurosecretory cells secrete hormones into: *Capillary plexus of posterior pituitary* (neurohypophysis) --> ADH, oxytocin Hypophyseal portal system: The system of blood vessels that link the hypothalamus and the anterior pituitary in the brain --> NOT the posterior pituitary GH and ACTH are from A.P. ADH & oxytocin are both steroids, not pheremones.]

Which of the following increases with elevated thyroid hormone? A: basal metabolic rate B: fat stores C: body weight D: skin dryness

A: basal metabolic rate [Thyroid Hormone is known as both T3 + T4 T3 + T4 stimulate the basal metabolic rate (BMR). Therefore, elevated thyroid hormone increases BMR.] [Elevated Thryoid Hormone = *HYPER*thyroidism inc. basal metabolic rate = *hyper*thyroidism inc. fat stores = hypothyroidism inc. body weight = hypothyroidism inc. skin dryness = hypothryoidism]

Insufficient ADH (antidiuretic hormone) production results in: A: increased urine volume B: decreased blood osmolality C: increased blood volume D: decreased urine volume

A: increased urine volume [Insufficient ADH = Increased Urine Volume + Increased Blood Osmolality] [ADH stimulates the reabsorption of water in the kidney If there is not enough ADH, there is little to no reabsorption of water (in the kidney) to send to the blood. More water in kidneys --> More water in urine = *Increased Urine Volume* *Insufficient ADH:* Increased urine volume Increased blood osmolality (less water means a higher concentration of solutes in the blood)]

*Female Cycle* Oral contraceptives: A: inhibit of FSH secretion B: stimulate the corpus luteum C: stimulate Graafian folicules D: are androgens E: none of the above

A: inhibit of FSH secretion [*Gonadotropin-releasing hormone (GnRH) causes release of FSH* and LH Contraceptive Pill: Includes synthetic estrogen and progesterone Acts like a prolonged luteal phase *Produces negative-feedback inhibition of GnRH, so ovulation never occurs* The endometrium still proliferates. Placebo pills are taken for 1 week to allow menstruation.]

*Female Cycle* Oral contraceptives: A: inhibit of LH secretion B: stimulate the corpus luteum C: stimulate Graafian folicules D: are androgens E: none of the above

A: inhibit of LH secretion [*Gonadotropin-releasing hormone (GnRH) causes release of* FSH and *LH* Contraceptive Pill: Includes synthetic estrogen and progesterone Acts like a prolonged luteal phase *Produces negative-feedback inhibition of GnRH, so ovulation never occurs* The endometrium still proliferates. Placebo pills are taken for 1 week to allow menstruation.]

Inhibin A: is produced by granulosa cells of ovarian follicles B: is produced by cytotrophoblast cells C: is produced by primary oocytes D: is produced by secondary oocytes E: none of the above

A: is produced by granulosa cells of ovarian follicles [There may also be inhibin production (within granulosa cells of ovarian follicles), which helps inhibit FSH.]

The secretory phase of the menstrual cycle is stimulated by A: progesterone B: FSH C: Inhibin D: adrenal steroid hormones

A: progesterone [DRAFT]

The enzyme that is activated by cAMP is: A: protein kinase A B: Phosphodiesterase C: adenylate cyclase D: phospholipase C

A: protein kinase A [Think: Cyclic *A*MP = *A* in Protein Kinase *A* G*s* linked receptor = *s*timulatory Ligand stimulates *Gs receptor* Alpha-subunit from G-protein then goes to adenylate cyclase Adenylate cyclase changes ATP to cAMP *cAMP activates Protein Kinase A* Protein Kinase A phosphorylates a protein to illicit a specific cellular response] [See "DAG and IP3 mechanisms"]

Increased adrenocorticotropic hormone (ACTH) secretion would be expected in patients A: with chronic adrenocortical insufficiency (Addison's disease) B: with primary adrenocortical hyperplasia C: who are receiving glucocorticoid for immunosuppression after a renal transplant D: with elevated levels of angiotensin II

A: with chronic adrenocortical insufficiency (Addison's disease) [CRH Stimulates adrenal cortex Adrenocortical hyperplasia --> puts out more cortisol, creates negative feedback, which leads to less produced by the anterior pituitary because the hyperplastic cells are producing too much for them.]

Pathophysiology of the Adrenal Cortex table in course notes: Aldosterone

Aldosterone Adrenal cortex ↑ renal Na+ reabsorption ↑ renal K+ secretion ↑ renal H+ secretion

Some cells secrete chemicals into the extracellular fluid that act on cells in neighboring tissue. Which of the following terms best refers to this type of regulation? A) Endocrine B) Paracrine C) Neuroendocrine D) Autocrine

B) Paracrine [Endocrine: releases hormone into blood Paracrine: releases hormone to neighboring cells Neuroendocrine cells: are cells that receive neuronal input and, as a consequence of this input, release message molecules (hormones) to the blood Autocrines: affects same cells that secreted them]

During the 12-hr period preceding ovulation, which of the following is true? A. The plasma concentration of estrogen is rising B. A surge of LH is secreted from the pituitary C. The surge occurs immediately after the formation of the corpus luteum D. The surge followed immediately by a fall in the plasma concentration of progesterone E. The number of developing follicles is increasing

B. A surge of LH is secreted from the pituitary

*Glucocorticoid Axis* The pituitary hormone that controls the release of glucocorticoids from the adrenal gland is: A. TSH B. ACTH C. FSH D. LH E. GH

B. ACTH [Corticotropin-releasing (aka CRH) is released from the Hypothalamus --> Anterior Pituitary --> stimulates secretion of ACTH --> Stimulates the adrenal cortex to release glucocorticoids (i.e. Cortisol) --> Increases blood glucose levels by gluconeogenesis] [Side note: ACTH = cAMP mechanism]

Which of the following is most likely to produce the greatest increase in insulin secretion (choose best answer)? A. Amino acids B. Amino acids and glucose C. Amino acids and somatostatin D. Glucose and somatostatin

B. Amino acids and glucose

*Calcium Hormones* Which of the following conditions would you expect to decrease the normal synthesis of the vitamin D3 metabolite, 1, 25 -dihydroxycholecalciferol (the most physiologically active metabolite of D3)? A. Diet low in Ca2+ B. Chronic renal failure C. Hyperparathyroidism D. Hypocalcemia

B. Chronic renal failure (ALSO: HYPERCALCEMIA but it is not an answer choice here) [Effects of *Chronic Renal Failure* on Calcium Balance: - Decreased filtration by kidneys leads to phosphate retention and increased serum phosphate - Increased serum phosphate complexes with unbound calcium, reducing serum ionized calcium levels - *Decreased metabolism of Vitamin D3 (1,25 -dihydroxycholecalciferol)* - Decreases calcium levels in serum - Decreased calcium causes secondary hyperparathyroidism - Decreased Vitamin D3 (1,25 dihydroxycholecalciferol) and increased PTH produces renal osteodystrophy --> increased bone reabsorption and osteomalacia]

A patient has a goiter associated with high plasma levels of both thryotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH). Her heart rate is elevated. This patient most likely has which of the following? A. Endemic goiter B. Hypothalamic tumor secreting large amounts of TRH C. Pituitary tumor secreting large amounts of TSH D. Graves' Disease

B. Hypothalamic tumor secreting large amounts of TRH

*Gonadotropins* In males, A. LH in not secreted by the pituitary gland B. LH receptors are located on the Leydig cells C. LH receptors are located on the spematogonia D. LH receptors are located on the Sertoli cells

B. LH receptors are located on the Leydig cells [*L*eydig = *L*H]

Secretion of parathyroid hormone occurs mainly in response to: A. Low serum glucose B. Low serum calcium C. Low serum calcitonin D. Elevated serum potassium

B. Low serum calcium

A baby is born with a penis, a scrotum with no testes, no vagina, and XX chromosomes. This condition is referred to as hermaphroditism. Which of the following could cause this abnormality? A. Abnormally high levels of human chorionic gonadotropin production by the trophoblast cells B. The presence of a testosterone-secreting tumor in the mother's right adrenal gland C. Abnormally high levels of LH in the maternal blood D. Abnormally low levels of testosterone in the maternal blood E. Abnormally low rates of estrogen production by the placenta

B. The presence of a testosterone-secreting tumor in the mother's right adrenal gland

The major active (potent) form of thyroid hormone is: A. Tetraiodothryonine (T4) B. Triiodothyronine (T3) C. Thyroglobulin D. Tyrosine

B. Triiodothyronine (T3)

*Calcium Hormones* Which of the following increases the expression of calcium transport mechanisms in the intestine? A. Thyroid hormone B. Vitamin D C. Antidiuretic hormone (ADH) D. beta adrenergic agonists E. Glucagon

B. Vitamin D [Actions of 1,25-dihydroxycholecalciferol: - Coordinated to increase both [Ca2+] and [phosphate] in ECF to mineralize new bone. - *Increases intestinal calcium absorption; cellular calcium transport* - Increases intestinal phosphate absorption *[Vitamin D3 Increases calbindin, a calcium binding protein in intestinal located in brush border (apical) membrane - binding protein is induced by 1,25-dihydroxycholecalciferol. --> Transports calcium into intestinal cells]*

*Male Development* The development of a male fetus depends on stimulating the development of the ___________and suppressing development of the ____________. A. Leydig cells; Sertoli cells B. Wolffian ducts; Mullerian ducts C. urogenital folds, labioscrotal folds D. genital tubercle, clitoris

B. Wolffian ducts; Mullerian ducts [Wolffian duct = male internal genital tract and external genitalia (*TIP:* Wolf = Manly) Mullerian duct = female internal genital tract and external genitalia]

Melatonin is a(n) A. peptide hormones B. amine hormones C. steroid hormones D. glycoprotein hormones

B. amine hormones ["The pineal gland •secretes melatonin *(amine hormone)* in response to activity of suprachiasmatic nucleus (SCN) of hypothalamus.] [AMINE HORMONES: Melatonin Epinephrine Norepinephrine Thyroid Hormone (T3+T4)]

*Male Development* A 16 -year-old, seemingly normal, girl has never had a menstrual cycle. She has a blind end vagina, NO uterus, cervix or ovaries, a 46 XY genotype and intra-abdominal testes. Her serum testosterone is elevated. The most likely diagnosis is: A. primary hyperparathyroidism B. androgen insensitivity disorder (male pseudo hermaphroditism) C. female pseudo hermaphroditism D. delayed puberty

B. androgen insensitivity disorder (male pseudo hermaphroditism) [Because she has an XY genotype she develops testes, but she has a female phenotype. She is classified as a hermaphrodite. It is the Y-chromosome that carries testes-determining factor (TDF) (protein made from the SRY gene), which promotes the development of testes (even though she looks like a girl) Here, since she is a hermaphodite, the patient should have been a boy genotypically but must have had an excess sex hormone during fetal development.] [Androgen insensitivity syndrome (AIS) is when a person who is genetically male (who has one X and one Y chromosome) is resistant to male hormones (called androgens). As a result, the person has some or all of the physical traits of a woman, but the genetic makeup of a man] [Androgen insensitivity is a lack of response to all androgens from fetal period despite high circulating androgen levels. Thus the child is chromosomally XY but due to lack of androgenic effects the wolffian ducts degenerate, the external genitalia is feminized. AIS can be Complete, partial or mild. the above description is for complete and is the tested subtype.]

*Calcium Hormones* The actions of parathyroid hormone are antagonized by the actions of: A. vitamin D B. calcitonin C. Lutenizing hormone D. insulin

B. calcitonin [Calcitonin: - *Antagonist to parathyroid hormone (PTH)* - acts primarily to inhibit bone resorption] [Remember that PTH causes bone resorption to increase the calcium blood level] [Calcitonin targets the skeleton, where it: - Inhibits osteoclast activity (and thus bone resorption) and release of calcium from the bone matrix]

*Calcium Hormones* The hormone released from the thyroid gland in response to elevated calcium ions in blood plasma: A. vitamin D B. calcitonin C. thyroxine D. triiodothyronine

B. calcitonin [Calcitonin: secretion is mainly stimulated by an increase in serum [Ca2+].]

*Male Development* Before sperm are able to fertilize an egg, they must undergo a process called _________, which normally requires that sperm be present for about seven hours in the female reproductive tract A. spermatogenesis B. capacitation C. implantation D. LH surge

B. capacitation [Over 300 million sperm enter the female at ejaculation (this number has gotten lower over the years). Only about 100 of these live to enter the fallopian tube. In order to fertilize the ovum, a sperm must become capacitated. *Sperm capacitation* refers to the physiological changes spermatozoa must undergo in order to have the *ability to penetrate and fertilize an egg*. This takes *at least 7 hours* after ejaculation.]

*Male Development* Sperm is stored in the: A. rete testes B. epididymis C. seminiferous tubules D. seminal vesicles E. prostate gland

B. epididymis [Spermatids move from the seminiferous tubules → rete testis → efferent ductules → epididymis. The *epididymis* is the *site of sperm maturation and storage*.]

*Fetal Development and Parturition* Maintenance of the corpus luteum during the first 8 weeks of pregnancy is dependent upon which of the following hormones? A. Estrogen B. hCG (human chorionic gonadotropin) C. DHEA-S (Dehydroepiandrosterone sulphate) D. Insulin

B. hCG (human chorionic gonadotropin) [*Corpus Luteum* - After ovulation, the remaining follicle becomes a corpus luteum. - Development Stimulated by LH - This secretes both estrogen and progesterone. - These hormones play a role in the menstrual cycle. - *Maintained by Human Chorionic Gonadotropin (hCG) during the 1st 8 weeks of pregnancy*]

Blockage of the hypothalamo-hypophyseal portal system between the hypothalamus and the anterior pituitary would result in A. increased ACTH secretion B. increased prolactin secretion C. increased FSH secretion D. increased growth hormone secretion

B. increased prolactin secretion [Anterior pituitary is blocked. Hormones normally secreted by hypothalamus Corticotropin RH ("GRH")--> stimulates ACTH secretion Gonadotrophin RG ("GnRH") --> stimulates FSH (& LH) secretion Two for Growth hormone: GHRH and SRIF --> stimulates GH and the other inhibits GH. *But prolactin is also secreted by the Anterior pituitary. So why is it increased?* This is because the hypothalamus secretes *prolactin-inhibiting factor* (dopamine), which *inhibits the secretion of the prolactin* by the A.P. Note this difference because the majority of the hypothalamus hormones are *RELEASING* factors. *This means that prolactin will continue to be produced if there is no input from the blocked hypothalamus to stop it being produced*.]

*Female Cycle* The rise in progesterone during the *OVARIAN* cycle: A. triggers ovulation B. inhibits ovulation C. triggers menstruation D. inhibits menstruation

B. inhibits ovulation D. inhibits menstruation DRAFT: (Ask Dr. Giblin diff between asking "ovarian" vs. "menstrual") [High levels of estrogen and progesterone have *NEGATIVE FEEDBACK* on the pituitary gland and *inhibit* FSH and LH secretion = *OVULATION* Decreasing levels of estrogen and progesterone *stimulate* the sloughing of the endometrium and *menstruation* --> Inversely: *THE RISE WOULD PREVENT MENSTRUATION*] [Think of BC pills or day after pills - they are made (mostly) of progesterone. These pills prevent Ovulation but you also have to take the placebo pills (with no progesterone) to have the actual period itself.]

*Female Cycle* A rapid increase in LH stimulates: A. the menstrual phase of the endometrium B. ovulation C. spermatogenesis D. lactation

B. ovulation [LH surge begins ~24 hours before ovulation]

*Fetal Development and Parturition* Uterine contractions are stimulated by: A. Oxygen B. prostaglandins C. prolactin D. progesterone E. none of the above

B. prostaglandins [*Oxytocin and prostaglandins* stimulate the release of Ca2+, which stimulates muscle contraction.]

What is the role of IP3 in hormonal action on cells? A: Activate adeylyl cyclase B: Stimulate the release of calcium from the ER C: Directly activate a protein kinase D: All of the above

B: Stimulate the release of calcium from the ER [IP3 diffuses through cytosol and binds to a gated IP3-gated calcium channel in the ER membrane, causing it to open and release calcium.] [Protein Kinase A is activated by cAMP Protein Kinase C is activated by DAG IP3 is created by Phospholipase C, but it does not activate any protein kinase or adenyl cyclase --> it goes straight to ER membrane by itself to a membrane receptor for IP3]

*Male Development* The development of testes in an XY embryo is due to: A: adrenal androgens B: TDF C: a lack of estrogens D: testosterone E: none of the above

B: TDF [It is the Y-chromosome that carries testes-determining factor (TDF), which promotes the development of testes. Do not confused Testosterone: this hormone is produced by the already established gonads.]

The most physiologically active (i.e., most potent) form of thyroid hormone is: A: Tetraiodothyronine (T4) B: Triiodothyronine (T3) C: Thyroglobulin D: thyroxine

B: Triiodothyronine (T3) [Triiodothryonine = T3 T3 is 4x more potent (aka reactive) than T4 Thyroxine = T4 (not the first choice) T4 is produced more (80%) than T3 (20%), but in the cells it must be cleaved to T3 to be used since it is not very potent. Thyrogloblin is what cleaves T4 into T3]

Overproduction of somatotropin (growth hormone) in an adult (i.e., an individual with closed skeletal physes) will result in: A: achondroplasia B: acromegaly C: giantism D: osteogenesis imperfecta tarda

B: acromegaly [Acromegaly is a disorder that results from excess growth hormone (GH) after the growth plates have closed. Acromegaly is typically due to the pituitary gland producing too much growth hormone. In more than 95% of cases the excess production is due to a benign tumor, known as a pituitary adenoma.]

A major action of oxytocin is to cause: A: increased blood oxygenization B: contraction of lactiferous ducts (milk letdown) C: ovulation D: oxygen retention

B: contraction of lactiferous ducts (milk letdown) [Oxytocin causes: - Contraction of lactiferous ducts = "milk letdown" or "milk ejection" -Uterine contractions]

One effect of ADH (antidiuretic hormone) is to: A: increase urine volume B: decrease blood osmolality (i.e. decrease the concentration of blood solutes) C: decrease blood volume D: none of the above [NOTE: typo on old test about "increased concentration" --> correct format is here saying "decreased concentration"]

B: decrease blood osmolality (i.e. decrease the concentration of blood solutes) [Sufficient ADH = Decreased Urine Volume + Decreased Blood Osmolality] [ADH stimulates the reabsorption of water in the kidney to send to extracellular water volume. More water in extracellular water --> More water in blood = *Decreased Blood Osmolality* (Sufficient) ADH decreased urine volume and decreases blood osmolality (more water means a lower concentration of solutes in the blood)]

Which hormone activates a tyrosine kinase linked receptor mechanism? A: testosterone B: insulin C: epinephrine D: prolactin

B: insulin [Tyrosine Kinase Linked Receptor: "I - I" Aye-Aye, Captain Tyrone! I = Insulin I = IGF-1 (insulin like growth factor)]

Vitamin D3: A: must be obtained in the diet (i.e. a true vitamin) B: is a steroid hormone C: is the most active form of Vitamin D D: activates G protein linked receptors

B: is a steroid hormone [Vitamin D3 is named "cholecalciferol". It is a fat-soluble vitamin (acts as a steroid) that helps your body absorb calcium and phosphorus --> passes through the membrane easily so it does *not* need a secondary messenger (g-protein linked receptor) Steroids are lipids derived from cholesterol] [Vit. D3 can be from sun or diet] [NOTE: The active form of vitamin D is 1,25-dihydroxycholecalciferol.--> NOT VITAMIN D3] [Steroid Hormones: INTRACELLULAR RECEPTORS "VETTT CAP" The VET on STEROIDS is wearing a baseball CAP V *Vitamin D3* E Estrogen T Testosterone T T3 (Triiodothyronine) T T4 (Thyroxine) C Cortisol A Aldosterone P Progesterone]

An ovulated ovum A: is in meiosis I B: is in meiosis II C: is in mitosis D: is a polar body

B: is in meiosis II [Ovum is stuck in meiosis II Meiosis II occurs when it is fertilized by a sperm cell]

Inhibin A: is produced by the hypothalamus B: is produced by Sertoli cells C: is produced by Leydig cells D: none of the above

B: is produced by Sertoli cells [Sertoli cells also secrete inhibin, which is involved in negative feedback of FSH secretion.]

The pulsatile secretion of hormones: A) describes how all hormones are released B) prevents the up-regulation of secretory cells C) prevents the down-regulation of target cell receptors D) prolongs the half-life of hormones

C) prevents the down-regulation of target cell receptors [*Regulation of receptors:* the responsiveness of the target cells is regulated by the number or sensitivity of receptors *Down-regulation of receptors:* A decrease in the number or affinity of receptors for a hormone. Prolonged exposure to high concentrations of hormone *Desensitization avoided by the pulsatile secretion (Pulsatile secretion prevents down-regulation of target cell receptors)* *Up-regulation of receptors:* An increase in the number or affinity (sensitivity) of receptors for a hormone. (For example, in the ovary, estrogen up-regulates its own receptor and the receptor for LH, leading to ovulation.)]

*Adrenal Cortex* A hormone that helps to regulate the *potassium* concentration of the blood is: A. PTH B. Cortisol C. Aldosterone D. Calcitonin E. Insulin

C. Aldosterone [Aldosterone increase renal K+ secretion (gets rid of K+ from blood to excrete in urine), restoring blood K+ to normal]

*Adrenal Cortex* A hormone that helps to regulate the *sodium* concentration of the blood is: A. PTH B. Cortisol C. Aldosterone D. Calcitonin E. Insulin

C. Aldosterone [Aldosterone increases renal Na+ reabsorption (reabsorbs Na+ from renal tube to save from being excreted in urine), thereby restoring extracellular fluid (ECF) volume and blood volume to normal.]

*Adrenal Cortex* Selective destruction of the zona glomerulosa of the adrenal cortex would produce a deficiency of which hormone? A. Cortisol B. Androstenedione C. Aldosterone D. Dehydroepiandrosterone E. Testosterone

C. Aldosterone [Layers of Adrenal Cortex: GFR 1. *Zona Glomerulosa* = *Aldosterone* (mineralcorticoid) --> stimulates kidneys to reabsorb Na+ and secrete K+ 2. Zona Fasiculata = Cortisol (glucocorticoid) --> which inhibits glucose breakdown for energy and stimulates gluconeogenesis (i.e. formation of glucose from noncarbohydrates) 3. Zona Reticularis = Sex steroids (gonadocorticoids) --> mostly androgens (male sex hormones)]

Steroid hormones: A. Are polar molecules B. Include the prostaglandins and the sex hormone testosterone C. Are derived from cholesterol molecules D. Bind mostly to receptors in the cell surface membranes

C. Are derived from cholesterol molecules

*Glucocorticoid Axis* The hypothalamic hormone that controls the release of corticosteroids from the adrenal gland is: A. TSH B. ACTH C. CRH D. LH E. GH

C. CRH [Corticotropin-releasing hormone (CRH) causes release of ACTH *READ THE QUESTION:* It says "Hypothalamic hormone"! This means its CRH not ACTH (that comes from the anterior pituitary)]

Selective destruction of the zona fasciculata of the adrenal cortex would produce a deficiency of which hormone? A. Aldosterone B. Androstenedione C. Cortisol D. Dehydroepiandrosterone E. Testosterone

C. Cortisol

The adrenal medulla produces the following two hormones: A. Cortisol and epinephrine B. Androgens and progesterone C. Epinephrine and norepinephrine D. Cortisol and androgen

C. Epinephrine and norepinephrine

Overproduction of somatotrophin (GH) in a child i.e., an individual with open skeletal physes will result in: A. Achondroplasia B. Acromegaly C. Gigantism D. Osteogenesis imperfect tarda

C. Gigantism [*Gigantism is caused by excessive GH production in a child or adolescent* Hypersecretion of growth hormone causes acromegaly after closure of epiphyseal plates at puberty. Before puberty, excess growth hormone causes increased linear growth (gigantism). ]

Releasing hormones and inhibiting hormones: A. Are secreted from the posterior pituitary B. Are all neurohormones C. Influence the release of hormones from the anterior pituitary D. Affect target cells throughout the body

C. Influence the release of hormones from the anterior pituitary

Propylthiouracil can be used to reduce the synthesis of thyroid hormones in hyperthyroidism because it inhibits oxidation of: A. Triiodothryonine (T3) B. Thyroxine (T4) C. Iodide (I-) D. Thyroid-stimulating hormone E. Diiodotyrosine (DIT)

C. Iodide (I-) [See picture: I^-1 to I^0 conversion means oxidation - loss of an election (LEO says GER)] [Propythiouracil inhibits oxidation of Iodide = "T4 cleaved into T3] [Used in Hyperthyroidism treatment to decrease high T3 levels (because T3 is more potent than T4)]

*Female Cycle* Which of the following statements is FALSE? A. Progesterone is secreted by the corpus luteum B. Progesterone is secreted by the placenta C. Progesterone decreases body basal temperature D. Progesterone secretion drops near the end of the non-fertile luteal phase

C. Progesterone decreases body basal temperature [Progesterone: Secreted by the Corpus Luteum ACTIONS: -Has negative feedback effects on FSH and LH secretion during luteal phase. - Maintains secretory activity of the uterus during the luteal phases. - Maintains pregnancy. - Participates in the development of the breasts. - Highest between day 14 (ovulation) and day 21 (menstruation) - *INCREASES Basal Body Temperature*]

Which of the following anterior pituitary hormones plays a major role in the regulation of a nonendocrine target gland? A. Adrenocorticotropic hormone B. Thyroid-stimulating hormone C. Prolactin D. Follicle-stimulating hormone E. Luteinizing hormone

C. Prolactin

Which of the following statements are true about GH? A. Secretion is stimulated by hypoglycemia B. Secretion decreased by sleep C. Secretion regulated by GHRH and somatostatin D. Causes inhibition of somatomedins in target cells

C. Secretion regulated by GHRH and somatostatin

*Female Development* An embryo with the genotype of XX develops into the female reproductive phenotype because of A. androgens B. estrogens C. a lack of androgens D. a lack of estrogens

C. a lack of androgens [Female Phenotype: - The ovaries of gonadal females secrete estrogen, but not antimüllerian hormone or testosterone. - *Without testosterone, the wolffian ducts do not differentiate.* - Without antimüllerian hormone, the müllerian ducts are not suppressed and therefore develop into the female internal genital tract.] [- Wolffian duct is developed into male internal genital tract and external genitalia. - Müllerian duct is developed into female internal genital tract and external genitalia.]

*Female Cycle* During the proliferative phase of the menstrual cycle, A. the corpus luteum is formed B. ovulation occurs C. a new functional layer of endometrium is formed in the uterus D. the old endometrial lining is sloughed off

C. a new functional layer of endometrium is formed in the uterus [Proliferative Phase: - Stimulated by FSH - Occurs while ovary is in the follicular phase - Increasing levels of estrogen stimulate the growth of the stratum functionale of the endometrium. - The endometrium also becomes more vascular and develops LH receptors. - *A new functional layer of endometrium is formed in the uterus*]

Experiments with a novel chemical find that it elicits a decrease in cellular Protein Kinase A activity. The chemical is probably: A. a steroid B. activating a tyrosine kinase linked receptor C. activating a Gi linked receptor D. activating a Gq linked receptor E. epinephrine

C. activating a Gi linked receptor [Think: Cyclic *A*MP = *A* in Protein Kinase *A* G*i* linked receptor = *i*hibitory INHIBITS cAMP PATHWAY = DECREASE PROTEIN KINASE A [*NORMAL cAMP pathway* (Gi Linked would INHIBIT this process): Ligand stimulates *Gs receptor* (stimulatory) Alpha-subunit from G-protein then goes to adenylate cyclase Adenylate cyclase changes ATP to cAMP cAMP activates *Protein Kinase A* Protein Kinase A phosphorylates a protein to illicit a specific cellular response] [See "DAG and IP3 mechanisms"]

*Male Development* A 24 year old male with an untreated deficiency in testicular production of testosterone since early childhood will likely exhibit which of the following? A. shorter than average B. abundant chest hair C. higher pitched voice D. lack of pubic hair

C. higher pitched voice [Voice pitch is determined by testosterone] [Deep voice = normal testosterone High voice = deficiency in testosterone] [NOTE: Pubic hair is caused by testosterone from ADRENAL androgens (not from testes)]

*Calcium Hormones* A 41-year-old woman has hypocalcemia, hyperphosphatemia, and decreased urinary phosphate excretion. Serum PTH levels are low but injection of parathyroid hormone (PTH) causes an increase in urinary cAMP. The most likely diagnosis is A. primary hyperparathyroidism B. vitamin D deficiency C. hypoparathyroidism after thyroid surgery D. pseudohypoparathyroidism E. Grave's syndrome

C. hypoparathyroidism after thyroid surgery [*Hypoparathyroidism*: Commonly caused by *thyroid surgery* or is congenital Symptoms: - ↓ serum PTH - ↓ serum calcium (*hypocalcemia*) --> causes tetany - ↑ serum phosphate (*hyperposphatemia*) - *↓ urinary phosphate excretion*]

*Calcium Hormones* Parathyroid hormone: A. Is released from the thyroid gland B. promotes calcium and phosphate incorporation into bone C. is released in response to low serum calcium D. deficiency causes osteoporosis E. inhibits osteoclast differientation and activation

C. is released in response to low serum calcium [Decreased serum Ca2+ increases PTH secretion]

Most hormones are A. amines B. steroids C. peptides D. none of the above

C. peptides [see picture]

*Adrenal Cortex Pathophys* A 46-year-old woman has hirsutism, hyperglycemia, obesity, muscle wasting, and increased circulating levels of adrenocorticotropic hormone (ACTH). The most likely cause of her symptoms is A. primary adrenocortical insufficiency (Addison's disease) B. pheochromocytoma C. primary overproduction of ACTH (Cushing's disease) D. treatment with exogenous glucocorticoids E. hypophysectomy

C. primary overproduction of ACTH (Cushing's disease) [Addison Disease (Chronic Adrenal Insufficiency): - ↑ ACTH --> Low cortisol levels stimulate ACTH secretion by negative feedback. - ↓ adrenal glucocorticoids, androgen, and mineralocorticoid - Weight loss, weakness, nausea, and vomiting - hypoglycemia - ↓ pubic and axillary hair in women - ECF volume contraction - hypotension - hyperkalemia - metabolic acidosis - hyperpigmentation (ADD SOME CORTISOL, SONNNN = Addison's Disease lol)] [Pheochromocytoma (Medullary Suprarenal Adenoma): tumor of the adrenal medulla (Chromaffin cells) that secrets excessive amounts of catecholamines and increased excretion of VMA] [Cushing's Disease is an increase in blood cortisol level due to: - ACTH-secreting tumor - *↑ ACTH (if caused by overproduction of ACTH)* - ↑ cortisol and androgen levels - *Hyperglycemina* (caused by elevated cortisol level) - ↑ protein catabolism and muscle wasting - *Central obesity* - Virilization of women = "*Hirsutism*" - Hyperpigmentation (disease only)] [Cushing's Syndrome is an increase in blood cortisol level due to: - adrenal cortex tumor - ACTH-secreting tumor in the anterior pituitary, - pharmacological use of cortisol - ↓ ACTH - ↑ cortisol and androgen levels - Hyperglycemina (caused by elevated cortisol level) - ↑ protein catabolism and muscle wasting - Central obesity - Virilization of women = "Hirsutism"] [Hypophysectomy = removal of hypophysis --> would cause decrease in like... almost every hormone lol.]

*Calcium Hormones* Hypocalcemia, hyperphosphatemia, and decreased urinary phosphate excretion is most consistent with: A. primary hyperparathyroidism B. vitamin D deficiency C. thyroid surgery D. Grave's syndrome

C. thyroid surgery [*Hypoparathyroidism*: Commonly caused by *thyroid surgery* or is congenital Symptoms: - ↓ serum PTH - ↓ serum calcium (*hypocalcemia*) --> causes tetany - ↑ serum phosphate (*hyperposphatemia*) - *↓ urinary phosphate excretion*]

*Female Cycle* The decrease in progesterone during the *MENSTRUAL* cycle: A. triggers ovulation B. inhibits ovulation C. triggers menstruation D. inhibits menstruation

C. triggers menstruation [Menstrual Phase Occurs as a result of the *fall in estrogen and progesterone* when the corpus luteum degenerates --> layers sloughs off (i.e. bleeding occurs)]

The hypothalamic hormone that controls the release of corticosteroids from the adrenal gland is: A: TSH B: ACTH C: CRH D: LH E: GH

C: CRH [CRH (Cortico-tropin releasing Hormone) is released from the hypothalamus --> controls the release of ACTH (Adrenocorticotropic Hormone) in the anterior pituitary --> stimulates the adrenal cortex to produce Aldosterone, Cortisol, and Precursor Sex Hormones (androgens in both sexes).]

A hypothalamic hormone that regulates the release of growth hormone is: A: TSH B: ACTH C: GHIH D: LH E: GH

C: GHIH [*GHIH* = Growth Hormone Inhibiting Hormone (aka "Somatostatin" GHIH comes from the hypothalamus --> inhibits the release of Growth hormone in the Anterior Pituitary] [*REMEMBER*: Growth hormone is regulated by *TWO* hormones from the hypothalamus: GHRH = Growth Hormone Releasing Hormone *GHIH* = Growth Hormone Inhibiting Hormone *ALSO KNOWN AS Somatostatin*] [If GHIH or GRH are options, either of them are the answer]

The pituitary hormone that regulates the production of gonadal hormones is: A: GnRH B: ACTH C: FH D: LH E: GH

C: LH [FSH and luteinizing hormone (LH) work together in the reproductive system. *LH:* In both sexes, LH stimulates secretion of sex steroids from the gonads. MALES: LH binds to receptors on Leydig cells, stimulating synthesis and secretion of *testosterone*. FEMALES: a large preovulatory LH surge induces ovulation of mature follicles on the ovary. Residual cells within ovulated follicles proliferate to form corpora lutea, which *secrete the steroid hormones progesterone and estradiol*. *FH:* stimulates maturation of of sex cells in both sexes FEMALES: stimulates the maturation of ovarian follicles. MALES: critical for sperm production. It supports the function of Sertoli cells, which in turn support many aspects of sperm cell maturation. REMEMBER: FSH helps in the maturing of the egg inside the follicle. LH or luteinizing hormone comes into play once the egg is mature inside the follicle by creating gonadal hormones. Do not mix up the two.]

TRH is the abbreviation for A: Thyroxine Releasing Hormone B: Thyroid Releasing Hormone C: Thyrotropin Releasing Hormone D: Thyroid Regenerating Hormones

C: Thyrotropin Releasing Hormone [Tropin hormones are hormones that induces the release of other hormones. (As in all "releasing" hormones are considered tropin hormones) A tropic hormone is a hormone that stimulates an endocrine gland to grow and secrete it's hormones.]

The hormone primarily responsible for setting the basal metabolic rate and for promoting the maturation of the brain is A: cortisol B: ACTH C: Thyroxine D: TSH

C: Thyroxine [*Thyroxine is known at T4*, and Triiodothyronine is known as T3 Thyroxine is primarily responsible for setting BMR. Thyroxine regulates basal metabolic rate, blood pressure, glucose metabolism, heat production, growth and development.]

Ovulation is the release of an ovum from A: a primary follicle B: a secondary follicle C: a Graafian follicle D: an atretic follicle E: none of the above

C: a Graafian follicle

Experiments with a novel chemical find that it elicits an increase in cellular protein kinase A activity. The chemical is probably: A: a steroid B: activating a tyrosine kinase linked receptor C: activating a Gs linked receptor D: activating a Gq linked receptor E: epinephrine

C: activating a Gs linked receptor [Think: Cyclic *A*MP = *A* in Protein Kinase *A* G*s* linked receptor = *s*timulatory Ligand stimulates *Gs receptor* Alpha-subunit from G-protein then goes to adenylate cyclase Adenylate cyclase changes ATP to cAMP cAMP activates *Protein Kinase A* Protein Kinase A phosphorylates a protein to illicit a specific cellular response] [See "DAG and IP3 mechanisms"]

Steroid hormones: A: are polar molecules B: include the prostaglandins and the sex hormone testosterone C: are all derived from cholesterol molecules D: bind mostly to receptors in the cell surface membrane

C: are all derived from cholesterol molecules [All steroids are derived from the 4 carbon rings from cholesterol Lipids are hydrophobic Cholesterol is a lipid Since steroids are a derivative of cholesterol, this means they are also hydrophobic and insoluble in water = the reason why steroids can pass through the polar lipid bilayer of plasma membranes to reach an intracellular receptor (inside the cell, not the cell surface). This is also why other hormones must use some type of secondary messenger, because they are not derived from cholesterol and are therefore water-soluble (hence the name "water-soluble hormones") --> cannot pass through the polar bilipid membrane --> all other hormones besides steroids must use a receptor on the cell surface]

Oxytocin causes: A: increased gene expression B: increased Protein Kinase A activity C: increased Phospo Lipase C activity D: all of the above

C: increased Phospo Lipase C activity [G-protein activates phospholipase C in the following secondary messengers: IP3 DAG Ca2+] [*Hormones that use IP3 2nd Messenger (IP3/DAG/CA2+): * "GOA(1)T GA(1)A(2)" The Goat (says) Gaa G GnRH (Gonadotropin Releasing Hormone O *Oxytocin* A(1) ADH (Antidiuretic Hormone: V1 Receptor for blood vessels ONLY) T TRH (Thyrotropin Releasing Hormone) G GHRH (Growth Hormone Releasing Hormone) A(1) Alpha-1 Adrenergic Receptor A(2) Angiotensin II]

Hypothalamic releasing and inhibiting hormones: A: are secreted from the posterior pituitary B: are all neurohormones C: influence the release of hormones from the anterior pituitary D: affect target cells throughout the body

C: influence the release of hormones from the anterior pituitary [Hypothalamic releasing and inhibiting hormones are secreted from the hypothalamus Carried by hypothalamo-hypophyseal portal system directly to another capillary bed in anterior pituitary. Diffuse into anterior pituitary and regulate secretion of its hormones]

Which of the following statements are true about growth hormone? A: secretion stimulated by hypogylcemia B: secretion decreased by sleep C: secretion is regulated by GHRH and somatostatin D: causes inhibition of somatomedins in target cells

C: secretion is regulated by GHRH and somatostatin [Remember: Growth hormone is regulated by TWO hormones from the hypothalamus: GHRH = Growth Hormone Releasing Hormone *GHIH* = Growth Hormone Inhibiting Hormone *ALSO KNOWN AS Somatostatin*]

*Adrenal Cortex* Which of the following causes *increased* aldosterone secretion? A. Hypokalemia B. Administration of an inhibitor of angiotensin-converting enzyme (ACE) C. Hyperosmolarity D. Hypornatremia

D. Hypornatremia [*Aldosterone secretion is stimulated by:* Rising blood levels of K+ = Hyperkalemia *Low blood Na+* = *HYPONATREMIA* Decreasing blood volume or pressure] [Hyperosmolarity = Hyperosmolar blood (high solutes) stimulates synthesis and release of ADH (NOT aldosterone)] [Renin-angiotensin mechanism: kidneys release renin, which results in the production of angiotensin II that in turn stimulates aldosterone release. Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE). So normally ACE increases Aldosterone, but answer choice B says administration of an INHIBITOR to ACE, so that would in turn decrease aldosterone.]

Which of the following statements about ADH is true? A. It is synthesized in the posterior pituitary gland B. In increases salt and water reabsorption in the collecting tubules and ducts C. It stimulates thirst D. It has opposite effects on urine and plasma osmolality

D. It has opposite effects on urine and plasma osmolality

*Gonadotropins* Luteinizing hormone (LH) stimulates: A. Sertoli cells B. menstruation C. follicle maturation D. Leydig cells

D. Leydig cells [*L*eydig = *L*H]

*Calcium Hormones* Increased serum levels of the hormone _____ results in increased absorption of _____ by the intestines and increased excretion of _____ by the kidneys. A. Calcitonin, Ca2+, Pi B. PTH, Pi, Ca2+ C. Vitamin D, Pi, Ca2+ D. PTH, Ca2+, Pi

D. PTH, Ca2+, Pi [Parathyroid hormone: - Most important hormone for control of blood Ca2+ levels- acting on the bones, kidneys, and intestines *to increase calcium blood levels.* In order to increase blood Ca2+ levels PTH acts on: - bones (bone reabsorption) - kidney (decrease excretion of calcium) - intestines (increased absorption)] [Parathyroid hormone (PTH) ALSO *inhibits phosphate (Pi) reabsorption* *(i.e. "increases excretion")* in the proximal tubule by activating adenylate cyclase, generating cyclic AMP (cAMP), and inhibiting Na+-phosphate cotransport.]

Some cells secrete chemicals into the extracellular fluid that act on cells in neighboring tissue, which of the following terms best refers to this type of regulation? A. Neural B. Endocrine C. Neuroendocrine D. Paracrine E. Autocrine

D. Paracrine

The responses of target cells to hormones can result in A. altered enzyme activity within the cell B. altered protein production C. the insertion of transport proteins into the cell membrane D. all of the above

D. all of the above

Peptide hormones A. are made as inactive preprohormones and processed to prohormones in the endoplasmic reticulum B. are transported freely in blood plasma C. have a relatively short half life D. all of the above

D. all of the above [*Protein and peptide hormone synthesis:* - *preprohormone (INACTIVE)* synthesis occurs on the *rough endoplasmic reticulum* and is directed by a specific mRNA. - *signal peptides are cleaved from the preprohormone, producing a prohormone* (no biological activity), which is transported to Golgi apparatus for packing into secretory vesicles. - additional peptide sequences are cleaved inside vesicles to form the biologically active peptide hormone and inactive fragment, which are released together into the *blood circulation* upon stimulations. - this class of hormones are water-soluble and are released by exocytosis *The half-life of hormones circulating in the blood ranges from minutes to hours*: o Most hormones are removed from the blood by the liver.]

*Female Cycle* The endometrial phases of the uterus include: A. secretory B. menstrual C. proliferative D. all of the above

D. all of the above [Three phases of Endometrial Buildup (28-Cycle): - Menstrual - Proliferative - Secretory]

Receptor upregulation can occur due to: A. increased number of receptors B. increased responsiveness of receptors C. increased plasma concentration of hormone D. all of the above (a-c) E. none of the above (a-c)

D. all of the above (a-c) [*Regulation of receptors:* the responsiveness of the target cells is regulated by the number or sensitivity of receptors *Down-regulation of receptors:* A decrease in the number or affinity of receptors for a hormone. Prolonged exposure to high concentrations of hormone *Desensitization avoided by the pulsatile secretion (Pulsatile secretion prevents down-regulation of target cell receptors)* *Up-regulation of receptors:* An increase in the number or affinity (sensitivity) of receptors for a hormone. (For example, in the ovary, estrogen up-regulates its own receptor and the receptor for LH, leading to ovulation.)]

*Fetal Development and Parturition* Uterine contractions are stimulated by: A. Oxytocin B. prostaglandins C. prolactin D. both a and b E. both a and c

D. both a and b [*Corpus Luteum* - After ovulation, the remaining follicle becomes a corpus luteum. - Development Stimulated by LH - This secretes both estrogen and progesterone. - These hormones play a role in the menstrual cycle. - Maintained by Human Chorionic Gonadotropin (hCG) during the 1st 8 weeks of pregnancy]

*Pancreas* *Elevated* concentrations of *glucagon* would result in: A. decreased lipolysis B. decreased gluconeogenesis C. decreased ketoacid production D. decreased glycogen synthesis

D. decreased glycogen synthesis [Glucagon INCREASES blood glucose -glycogenolysis (decreased by Insulin) Glucagon INCREASES blood fatty acid & ketoacid production (decreased by Insulin) Glucagon INCREASES gluconeogenesis (decreased by insulin) SO Since glucagon increases glycogenolysis (breakdown of glycogen to glucose) = *decreased glycogen synthesis*(which is done by insulin)

*Pancreas* *Elevated* concentrations of *insulin* would result in: A. increased lipolysis B. increased gluconeogenesis C. increased ketoacid production D. increased glycogen synthesis

D. increased glycogen synthesis [Insulin changes GLUCOSE --> GLYCOGEN for storage (aka Glygocen Synthesis) (takes glucose monomer from blood to make polymer glycogen in the liver for storage) Cortisol provokes gluconeogenesis = the formation of glucose from noncarbohydrates (insulin decreases gluconeogenesis by decreasing glucose concentration in blood) Glucagon provokes ketogenesis = formation of ketone bodies from free fatty acids by the liver for energy (Insulin inhibits ketoacid formation in the liver) Glucagon stimulates lipolysis = breakdown of lipids (but Insulin stimulates lipogenesis)]

*Adrenal Medulla pathophys* A medullary suprarenal adenoma (pheochromocytosis) exhibits constant, uncontrolled epinephrine secretion. Based on this expected change, which of the following symptoms would you expect? A. thin, shiny skin (tropic changes) B. warm skin C. anhydrosis (lack of sweating) D. pallor (pale skin)

D. pallor (pale skin) [Pheochromocytoma: Tumor of the adrenal medulla (Chromaffin cells) that secrets excessive amounts of catecholamines and is associated with increased excretion of 3-methoxy-4-hydroxymandelic acid (VMA). The catecholamines secreted include: norepinephrine epinephrine dopamine dopa Causes persistent or paroxysmal hypertension, cool skin, anhydrosis, & *pallor*]

A medullary suprarenal adenoma (pheochromocytosis) exhibits which of the following symptoms? A. thin, shiny skin (tropic changes) B. warm skin C. anhydrosis (lack of sweating) D. tachycardia

D. tachycardia [Tachycardia is due to excess epinephrine being produced by the pheochromocytoma] [Pheochromocytoma: Tumor of the adrenal medulla (Chromaffin cells) that secrets excessive amounts of catecholamines and is associated with increased excretion of 3-methoxy-4-hydroxymandelic acid (VMA). The catecholamines secreted include: norepinephrine epinephrine dopamine dopa Causes persistent or paroxysmal hypertension, cool skin (not warm - incorrect in class notes), anhydrosis, & pallor]

The pituitary hormone that increases blood glucose levels is: A: Glucagon B: Cortisol C: Erthyrpoietin D: ACTH E: Insulin

D: ACTH [Adrenocorticotrophic Hormone (ACTH) stimulates the adrenal cortex to release corticosteroids --> Increases blood glucose levels]

Which of the following is consistent with hyperthyroidism? A: Hypotension B: Bradycardia C: Decreased plasma levels of triiodothyronine (T3) D: Increased TSH

D: Increased TSH [*hyperthyroidism results in excessive thyroxine secretion*] [Autoimmune disease (Grave's Disease) where antibodies act like TSH --> stimulate thyroid gland to grow and oversecrete T3 + T4 or Adenoma of the Anterior pituitary (oversecretion of TRH --> oversecretion of TSH --> oversecretion of T3 + T4)]

Which of the following symptoms would you expect to observe in a person suffering from Diabetes Insipidus? A: Glucosuria B: Hyperglycemia C: Metabolic acidosis D: Increased thirst E: all of the above

D: Increased thirst [Diabetes Insipidus: disorder of salt and water metabolism marked by *intense thirst* and *heavy urination*. Not producing enough ADH --> no retention of water from kindeys --> creates "thirst" due to lack of water in blood volume]

If communication between the hypothalamus and anterior pituitary is disrupted, which of the following will increase A: ACTH B: FSH C: TSH D: Prolactin

D: Prolactin [PIH also known as Dopamine] [Anterior pituitary is blocked. Hormones normally secreted by hypothalamus: Corticotropin RH ("GRH")--> stimulates ACTH secretion Gonadotrophin RG ("GnRH") --> stimulates FSH (& LH) secretion Two for Growth hormone: GHRH and SRIF --> stimulates GH and the other inhibits GH. *But prolactin is also secreted by the Anterior pituitary. So why is it increased?* This is because the hypothalamus secretes *prolactin-inhibiting factor* (dopamine), which *inhibits the secretion of the prolactin* by the A.P. Note this difference because the majority of the hypothalamus hormones are *RELEASING* factors. *This means that prolactin will continue to be produced if there is no input from the blocked hypothalamus to stop it being produced*.]

Which of the following inhibits the secretion of growth hormone (choose best answer)? A: Sleep B: GHRH C: Puberty D: Somatomedins E: none of the above

D: Somatomedins [*Negative feedback control by somatomedins:* Somatomedins are produced when growth hormone acts on target tissues. Somatomedins inhibit the secretion of growth hormone by acting directly on the anterior pituitary and by stimulating the secretion of somatostatin (aka SRIF = "somatropin release-inhibiting hormone* SRIF) from the hypothalamus. SRIF from the hypothalamus then inhibitis the secretion of growth hormone in the anterior pituitary.] [KNOW DIFFERENCE BETWEEN Somatostatin vs Somatomedin]

Experiments with a novel chemical find that it elicits an increase in cellular protein kinase C activity. The chemical is probably A: a steroid B: activating a tyrosine kinase linked receptor C: activating a Gs linked receptor D: activating a Gq linked receptor E: epinephrine

D: activating a Gq linked receptor [Dr Giblin said: Think: *C*alcium = *C* in Protein Kinase *C* --> Calcium sounds like = "*q*oalcium!!!" (instead of Gc for calcium, it's G*q*) Gq linked receptor --> activates phospholipase c (aka PLC) Phospholipase C cleaves PIP2 into IP3 and DAG DAG activates the enzyme protein kinase C.] [See "DAG and IP3 mechanisms"]

Suckling activates a neuroendocrine reflex that stimulates A: oxytocin release B: lactation C: mother child bonding D: all of the above

D: all of the above

Which of the following adrenal hormones activates an intracellular receptor? A: Aldosterone B: Cortisol C: androgens D: all of the above E: none of the above

D: all of the above [Steroid Hormones: INTRACELLULAR RECEPTORS "VETTT CAP" The VET on STEROIDS is wearing a baseball CAP V Vitamin D3 E Estrogen T *Testosterone* = *ANDROGENS* T T3 (Triiodothyronine) T T4 (Thyroxine) C *Cortisol* A *Aldosterone* P Progesterone]

Hormones secreted from the anterior pituitary: A: are produced by neurosecretory cells in the hypothalamus B: are transported in the hypothalmohyophysial portal system C: include GnRH and ADH D: are classified as trophic hormones

D: are classified as trophic hormones [Trophic hormones stimulate the activity of another endocrine gland.] [*Hormones released by A.P.*: FLAT PIG" FSH LH ACTH TSH PRL (I - Ignore) GH]

*Fetal Development and Parturition* Uterine contractions are stimulated by A: inhibin B: prolactin C: sympathetic innervaton D: oxytocin

D: oxytocin [*Oxytocin and prostaglandins* stimulate the release of Ca2+, which stimulates muscle contraction.]

Female pseudohermaphroditism (XX) can A: result from congenital adrenal hyperplasia B: have Mullerian duct derivatives C: have Wolffian duct derivatives D: have male external genitalia E: all of the above

E: all of the above [Female pseudohermaphroditism: may be due to excessive secretion of adrenal androgens in a female = congenital adrenal hyperplasia. Both Mullerian and Wolffian duct derivatives and male external genitalia]

A dietary iodine deficiency causes: A: decreased TSH production B: increased T3 and T4 production C: decreased TRH production D: all of the above E: none of the above

E: none of the above [Dietary iodine deficiency: Iodine is used to create T3 + T4 (the thyroid hormones) No iodine = No negative feedback inhibition of both TRH and TSH *TRH production increases* (since there is no inhibition) There is an *increased TSH production* (because there's no inhibition from T3+T4) (This leads to Goiter aka "thyroid enlargment" from too much TSH being produced) But since there's no iodine --> *decreased production of T3 + T4*]

What is a medicine treatment for hypothyroidism?

Levothyroxine It replaces or provides more thyroid hormone, which is normally produced by the thyroid gland.

Match the following: A. High estrogen and progesterone; low FSH and LH B. Low estrogen and progesterone C. LH surge D. increasing estrogen; low LH and low progesterone Menstrual phase ___ Luteal phase ___ Follicular Phase ___ Ovulation ___

Menstrual phase *B* Luteal phase *A* Follicular Phase *D* Ovulation *C* [Menstual Phase = Low estrogen and progesterone Luteal Phase = High estrogen and progesterone, low FSH and LH Follicular Phase = Increasing estrogen; low LH and low progesterone Ovulation Phase = LH surge]

*Fetal Development and Parturition* Match the following hormones to the numbered functions below. A. Inhibin B. LH C. TDF D. MIF Promotes the development of the testes in XY embryos: ____ Female accessory organs develop in the absence of: ____

Promotes the development of the testes in XY embryos: *C* Female accessory organs develop in the absence of: *D*

Pathophysiology of the Adrenal Cortex table in course notes: Steroids

Steroid hormones are synthesized from cholesterol in the adrenal cortex, testes, ovaries and placenta. Steroids are lipids derived from cholesterol. Examples: testosterone, estradiol, progesterone, cortisol

*Female Cycle* When do progesterone levels rise to their highest point during the female hormonal cycle? a. Between ovulation and the beginning of menstruation b. Immediately before ovulation c. When the blood concentration of luteinizing hormone is at its highest point d. When medullary androgens are highest

a. Between ovulation and the beginning of menstruation [Progesterone is highest between day 14 (ovulation) and day 21 (menstruation)]

*Male Development* The development of a male fetus depends upon stimulating ___________hormone production. a. Leydig cell b. Sertoli cell c. Wolffian duct d. Mullerian duct

a. Leydig cell [Sertoli cells with FSH input make the sperm, *but* the Leydig cells with LH input create testostorone *which then goes on to develop a male fetus* (view flow-cart)]

*Female Cycle* After ovulation, ______________ stimulates development of the corpus luteum. a. Estrogen b. LH c. DHEA-S (Dehydroepiandrosterone sulphate) d. FSH

b. LH [Corpus Luteum: After ovulation, the remaining follicle becomes a corpus luteum. *Development Stimulated by LH* - This secretes both estrogen and progesterone. - These hormones play a role in the menstrual cycle. - Maintained by Human Chorionic Gonadotropin (hCG) during the 1st 8 weeks of pregnancy]

Which describes the role of inositol triphosphate in hormone action? a. Activates adenylate cyclase b. Stimulates the release of calcium from endoplasmic reticulum c. Activates protein kinase d. All of the above

b. Stimulates the release of calcium from endoplasmic reticulum [*THINK:* IP*3* looks like *E* for Endoplasmic Reticulum] [IP3 is one of the 3 major hormone signaling mechanism] [Hormones that use IP3: GnRH TRH GHRH Angiotensin II]

*Female Cycle* Which of the following statements is true? a. Progesterone is secreted by the corpus albicans b. Progesterone is secreted by the pituitary gland c. Progesterone increases basal temperature d. Progesterone secretion stimulates menstruation

c. Progesterone increases basal temperature [Progesterone: Secreted by the Corpus Luteum ACTIONS: -Has negative feedback effects on FSH and LH secretion during luteal phase. - Maintains secretory activity of the uterus during the luteal phases. - Maintains pregnancy. - Participates in the development of the breasts. - Highest between day 14 (ovulation) and day 21 (menstruation) - INCREASES Basal Body Temperature] Menstrual Phase: *Occurs as a result of the fall in estrogen and progesterone when the corpus luteum degenerates* Arteries in the endometrium constrict, cells in the stratum functionale die, and this region is sloughed.]

Which of the following statements about hypothalamic releasing hormones is true? a. They are secreted into capillaries in the median eminence b. They are transported by portal veins to the anterior pituitary c. They stimulate the secretion of specific hormones from the anterior pituitary d. all of the above (a-c) are true e. none of the above are true

d. all of the above (a-c) are true [Releasing and inhibiting hormones from hypothalamus are released from axon endings into capillary bed in median eminence Carried by hypothalamo-hypophyseal portal system directly to another capillary bed in anterior pituitary. Diffuse into anterior pituitary and regulate secretion of its hormones] [NOT related to posterior pituitary cause they just go straight into blood]

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oh hey you made it this far???? how do u have time for this ?????? go take a nap !!!