Difference between revisions of "Endocrinology Quiz"
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|linktext = WikiQuiz | |linktext = WikiQuiz | ||
|pagetype=Quiz | |pagetype=Quiz | ||
− | |Review= David Gardner BSc (Hons) PhD Associate Professor in developmental physiology <br> Alison Mostyn BSc (Hons) PhD Lecturer in Comparative Cellular Physiology | + | |Review=''' David Gardner''' BSc (Hons) PhD Associate Professor in developmental physiology <br> '''Alison Mostyn''' BSc (Hons) PhD Lecturer in Comparative Cellular Physiology}}<br> |
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choice2="Glucocorticoids, insulin and thyroxine (T4)" | choice2="Glucocorticoids, insulin and thyroxine (T4)" | ||
correctchoice="5" | correctchoice="5" | ||
− | feedback5="'''Correct!''' Growth hormone is the main regulator of IGF-I production in the liver. Insulin and oestradiol are stimulatory in other tissues. [[IGF-1 - Anatomy & Physiology|WikiVet Article: Insulin-like growth factor]] | + | feedback5="'''Correct!''' Growth hormone is the main regulator of IGF-I production in the liver. Insulin and oestradiol are stimulatory in other tissues. [[IGF-1 - Anatomy & Physiology|WikiVet Article: Insulin-like growth factor]]" |
− | feedback4="'''Incorrect.''' Thyroxine (T4) does not directly affect IGF-I production. However growth hormone is the main regulator of IGF-I production in the liver and insulin is stimulatory in other tissues. The missing hormone is oestradiol which is also stimulatory in other tissues. [[IGF-1 - Anatomy & Physiology|WikiVet Article: Insulin-like growth factor]] | + | feedback4="'''Incorrect.''' Thyroxine (T4) does not directly affect IGF-I production. However growth hormone is the main regulator of IGF-I production in the liver and insulin is stimulatory in other tissues. The missing hormone is oestradiol which is also stimulatory in other tissues. [[IGF-1 - Anatomy & Physiology|WikiVet Article: Insulin-like growth factor]]" |
− | feedback3="'''Incorrect.''' Growth hormone is the main regulator of IGF-I production in the liver and insulin is stimulatory in other tissues. Glucocorticoids are inhibitory in other tissues. The missing hormone is oestradiol which is also stimulatory in other tissues. [[IGF-1 - Anatomy & Physiology|WikiVet Article: Insulin-like growth factor]] | + | feedback3="'''Incorrect.''' Growth hormone is the main regulator of IGF-I production in the liver and insulin is stimulatory in other tissues. Glucocorticoids are inhibitory in other tissues. The missing hormone is oestradiol which is also stimulatory in other tissues. [[IGF-1 - Anatomy & Physiology|WikiVet Article: Insulin-like growth factor]]" |
− | feedback1="'''Incorrect.''' Growth hormone is the main regulator of IGF-I production in the liver and oestradiol is stimulatory in other tissues. Glucocorticoids are inhibitory in other tissues. The missing hormone is insulin which is also stimulatory in other tissues. [[IGF-1 - Anatomy & Physiology|WikiVet Article: Insulin-like growth factor]] | + | feedback1="'''Incorrect.''' Growth hormone is the main regulator of IGF-I production in the liver and oestradiol is stimulatory in other tissues. Glucocorticoids are inhibitory in other tissues. The missing hormone is insulin which is also stimulatory in other tissues. [[IGF-1 - Anatomy & Physiology|WikiVet Article: Insulin-like growth factor]]" |
− | feedback2="'''Incorrect.''' Insulin is stimulatory in many tissues and glucocorticoids are inhibitory in several tissues. Thyroxine (T4) does not directly affect IGF-I production.The missing hormones are growth hormone which is the main regulator of IGF-I production in the liver and oestradiol which is also stimulatory in other tissues. [[IGF-1 - Anatomy & Physiology|WikiVet Article: Insulin-like growth factor]] | + | feedback2="'''Incorrect.''' Insulin is stimulatory in many tissues and glucocorticoids are inhibitory in several tissues. Thyroxine (T4) does not directly affect IGF-I production.The missing hormones are growth hormone which is the main regulator of IGF-I production in the liver and oestradiol which is also stimulatory in other tissues. [[IGF-1 - Anatomy & Physiology|WikiVet Article: Insulin-like growth factor]]" |
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</WikiQuiz> | </WikiQuiz> | ||
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choice2="Kidney" | choice2="Kidney" | ||
correctchoice="4" | correctchoice="4" | ||
− | feedback4="'''Correct!''' Vitamin D3 is absorbed from the intestine or formed in the skin by the action of UV light on 7-dehydrocholesterol. It is then converted to 25-OH D3 in the liver by 25-hydroxylase. Next it is converted to its active form, calcitriol in the kidney. Calcitriol stimulates resorption of calcium and phosphate from bone and an increase in the amount of calcium and phosphate absorbed from the intestine. [[Calcium | + | feedback4="'''Correct!''' Vitamin D3 is absorbed from the intestine or formed in the skin by the action of UV light on 7-dehydrocholesterol. It is then converted to 25-OH D3 in the liver by 25-hydroxylase. Next it is converted to its active form, calcitriol in the kidney. Calcitriol stimulates resorption of calcium and phosphate from bone and an increase in the amount of calcium and phosphate absorbed from the intestine. [[Calcium#Active Vitamin D Synthesis|WikiVet Article: Active vitamin D synthesis]]" |
− | feedback5="'''Incorrect.''' Vitamin D3 is absorbed from the intestine or formed in the skin by the action of UV light on 7-dehydrocholesterol. It is then converted to 25-OH D3 in the liver by 25-hydroxylase. Next it is converted to its active form, calcitriol in the kidney. Calcitriol stimulates resorption of calcium and phosphate from bone and an increase in the amount of calcium and phosphate absorbed from the intestine. [[Calcium | + | feedback5="'''Incorrect.''' Vitamin D3 is absorbed from the intestine or formed in the skin by the action of UV light on 7-dehydrocholesterol. It is then converted to 25-OH D3 in the liver by 25-hydroxylase. Next it is converted to its active form, calcitriol in the kidney. Calcitriol stimulates resorption of calcium and phosphate from bone and an increase in the amount of calcium and phosphate absorbed from the intestine. [[Calcium#Active Vitamin D Synthesis|WikiVet Article: Active vitamin D synthesis]]" |
− | feedback3="'''Incorrect.''' Vitamin D3 is absorbed from the intestine or formed in the skin by the action of UV light on 7-dehydrocholesterol. It is then converted to 25-OH D3 in the liver by 25-hydroxylase. Next it is converted to its active form, calcitriol in the kidney. Calcitriol stimulates resorption of calcium and phosphate from bone and an increase in the amount of calcium and phosphate absorbed from the intestine. [[Calcium | + | feedback3="'''Incorrect.''' Vitamin D3 is absorbed from the intestine or formed in the skin by the action of UV light on 7-dehydrocholesterol. It is then converted to 25-OH D3 in the liver by 25-hydroxylase. Next it is converted to its active form, calcitriol in the kidney. Calcitriol stimulates resorption of calcium and phosphate from bone and an increase in the amount of calcium and phosphate absorbed from the intestine. [[Calcium#Active Vitamin D Synthesis|WikiVet Article: Active vitamin D synthesis]]" |
− | feedback1="'''Incorrect.''' Vitamin D3 is absorbed from the intestine or formed in the skin by the action of UV light on 7-dehydrocholesterol. It is then converted to 25-OH D3 in the liver by 25-hydroxylase. Next it is converted to its active form, calcitriol in the kidney. Calcitriol stimulates resorption of calcium and phosphate from bone and an increase in the amount of calcium and phosphate absorbed from the intestine. [[Calcium | + | feedback1="'''Incorrect.''' Vitamin D3 is absorbed from the intestine or formed in the skin by the action of UV light on 7-dehydrocholesterol. It is then converted to 25-OH D3 in the liver by 25-hydroxylase. Next it is converted to its active form, calcitriol in the kidney. Calcitriol stimulates resorption of calcium and phosphate from bone and an increase in the amount of calcium and phosphate absorbed from the intestine. [[Calcium#Active Vitamin D Synthesis|WikiVet Article: Active vitamin D synthesis]]" |
− | feedback2="'''Incorrect.''' Vitamin D3 is absorbed from the intestine or formed in the skin by the action of UV light on 7-dehydrocholesterol. It is then converted to 25-OH D3 in the liver by 25-hydroxylase. Next it is converted to its active form, calcitriol in the kidney. Calcitriol stimulates resorption of calcium and phosphate from bone and an increase in the amount of calcium and phosphate absorbed from the intestine. [[Calcium | + | feedback2="'''Incorrect.''' Vitamin D3 is absorbed from the intestine or formed in the skin by the action of UV light on 7-dehydrocholesterol. It is then converted to 25-OH D3 in the liver by 25-hydroxylase. Next it is converted to its active form, calcitriol in the kidney. Calcitriol stimulates resorption of calcium and phosphate from bone and an increase in the amount of calcium and phosphate absorbed from the intestine. [[Calcium#Active Vitamin D Synthesis|WikiVet Article: Active vitamin D synthesis]]" |
image= ""> | image= ""> | ||
</WikiQuiz> | </WikiQuiz> | ||
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choice1="Insulin" | choice1="Insulin" | ||
correctchoice="2" | correctchoice="2" | ||
− | feedback2="'''Correct!''' Parathyroid hormone stimulates the formation of active vitamin D3 (calcitriol) and inhibits the formation of inactive vitamin D3, (24,25 (OH)2 D3). The release of parathyroid hormone is inhibited by an increase in calcitriol and blood calcium levels (an example of negative feedback). [[Calcium | + | feedback2="'''Correct!''' Parathyroid hormone stimulates the formation of active vitamin D3 (calcitriol) and inhibits the formation of inactive vitamin D3, (24,25 (OH)2 D3). The release of parathyroid hormone is inhibited by an increase in calcitriol and blood calcium levels (an example of negative feedback). [[Calcium#Active Vitamin D Synthesis|WikiVet Article: Active vitamin D synthesis]]." |
− | feedback4="'''Incorrect.''' Thyroxine is not related to the regulation of the amount of active vitamin D3 in the body. Parathyroid hormone stimulates the formation of active vitamin D3 (calcitriol) and inhibits the formation of inactive vitamin D3, (24,25 (OH)2 D3). The release of parathyroid hormone is inhibited by an increase in calcitriol and blood calcium levels (an example of negative feedback). [[Calcium | + | feedback4="'''Incorrect.''' Thyroxine is not related to the regulation of the amount of active vitamin D3 in the body. Parathyroid hormone stimulates the formation of active vitamin D3 (calcitriol) and inhibits the formation of inactive vitamin D3, (24,25 (OH)2 D3). The release of parathyroid hormone is inhibited by an increase in calcitriol and blood calcium levels (an example of negative feedback). [[Calcium#Active Vitamin D Synthesis|WikiVet Article: Active vitamin D synthesis]]" |
− | feedback3="'''Incorrect.''' Triiodothyronine is not related to the regulation of the amount of active vitamin D3 in the body. Parathyroid hormone stimulates the formation of active vitamin D3 (calcitriol) and inhibits the formation of inactive vitamin D3, (24,25 (OH)2 D3). The release of parathyroid hormone is inhibited by an increase in calcitriol and blood calcium levels (an example of negative feedback). [[Calcium | + | feedback3="'''Incorrect.''' Triiodothyronine is not related to the regulation of the amount of active vitamin D3 in the body. Parathyroid hormone stimulates the formation of active vitamin D3 (calcitriol) and inhibits the formation of inactive vitamin D3, (24,25 (OH)2 D3). The release of parathyroid hormone is inhibited by an increase in calcitriol and blood calcium levels (an example of negative feedback). [[Calcium#Active Vitamin D Synthesis|WikiVet Article: Active vitamin D synthesis]]" |
− | feedback5="'''Incorrect.''' Epinephrine is not related to the regulation of the amount of active vitamin D3 in the body. Parathyroid hormone stimulates the formation of active vitamin D3 (calcitriol) and inhibits the formation of inactive vitamin D3, (24,25 (OH)2 D3). The release of parathyroid hormone is inhibited by an increase in calcitriol and blood calcium levels (an example of negative feedback). [[Calcium | + | feedback5="'''Incorrect.''' Epinephrine is not related to the regulation of the amount of active vitamin D3 in the body. Parathyroid hormone stimulates the formation of active vitamin D3 (calcitriol) and inhibits the formation of inactive vitamin D3, (24,25 (OH)2 D3). The release of parathyroid hormone is inhibited by an increase in calcitriol and blood calcium levels (an example of negative feedback). [[Calcium#Active Vitamin D Synthesis|WikiVet Article: Active vitamin D synthesis]]" |
− | feedback1="'''Incorrect.''' Insulin is not related to the regulation of the amount of active vitamin D3 in the body. Parathyroid hormone stimulates the formation of active vitamin D3 (calcitriol) and inhibits the formation of inactive vitamin D3, (24,25 (OH)2 D3). The release of parathyroid hormone is inhibited by an increase in calcitriol and blood calcium levels (an example of negative feedback). [[Calcium | + | feedback1="'''Incorrect.''' Insulin is not related to the regulation of the amount of active vitamin D3 in the body. Parathyroid hormone stimulates the formation of active vitamin D3 (calcitriol) and inhibits the formation of inactive vitamin D3, (24,25 (OH)2 D3). The release of parathyroid hormone is inhibited by an increase in calcitriol and blood calcium levels (an example of negative feedback). [[Calcium#Active Vitamin D Synthesis|WikiVet Article: Active vitamin D synthesis]]" |
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</WikiQuiz> | </WikiQuiz> | ||
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choice3="Sodium, chloride, potassium and water excretion." | choice3="Sodium, chloride, potassium and water excretion." | ||
correctchoice="2" | correctchoice="2" | ||
− | feedback2="'''Correct!''' Renin increases aldosterone secretion from the zona glomerulosa. Aldosterone acts to increase the reabsorption of sodium by cells in the collecting ducts of the kidney. Sodium ions are exchanged for hydrogen and potassium ions, leading to decreased sodium and increased potassium excretion. Water follows sodium, blood volume increases, and this increases blood pressure and glomerular filtration rate. [[ | + | feedback2="'''Correct!''' Renin increases aldosterone secretion from the zona glomerulosa. Aldosterone acts to increase the reabsorption of sodium by cells in the collecting ducts of the kidney. Sodium ions are exchanged for hydrogen and potassium ions, leading to decreased sodium and increased potassium excretion. Water follows sodium, blood volume increases, and this increases blood pressure and glomerular filtration rate. [[Renin Angiotensin Aldosterone System|WikiVet Article: RAAS. ]]" |
− | feedback1="'''Incorrect.''' Renin increases aldosterone secretion from the zona glomerulosa. Aldosterone acts to increase the reabsorption of sodium by cells in the collecting ducts of the kidney. Sodium ions are exchanged for hydrogen and potassium ions, leading to decreased sodium and increased potassium excretion. Water follows sodium, blood volume increases, and this increases blood pressure and glomerular filtration rate. [[ | + | feedback1="'''Incorrect.''' Renin increases aldosterone secretion from the zona glomerulosa. Aldosterone acts to increase the reabsorption of sodium by cells in the collecting ducts of the kidney. Sodium ions are exchanged for hydrogen and potassium ions, leading to decreased sodium and increased potassium excretion. Water follows sodium, blood volume increases, and this increases blood pressure and glomerular filtration rate. [[Renin Angiotensin Aldosterone System|WikiVet Article: RAAS]]." |
− | feedback4="'''Incorrect.''' Renin increases aldosterone secretion from the zona glomerulosa. Aldosterone acts to increase the reabsorption of sodium by cells in the collecting ducts of the kidney. Sodium ions are exchanged for hydrogen and potassium ions, leading to decreased sodium and increased potassium excretion. Water follows sodium, blood volume increases, and this increases blood pressure and glomerular filtration rate. [[ | + | feedback4="'''Incorrect.''' Renin increases aldosterone secretion from the zona glomerulosa. Aldosterone acts to increase the reabsorption of sodium by cells in the collecting ducts of the kidney. Sodium ions are exchanged for hydrogen and potassium ions, leading to decreased sodium and increased potassium excretion. Water follows sodium, blood volume increases, and this increases blood pressure and glomerular filtration rate. [[Renin Angiotensin Aldosterone System|WikiVet Article: RAAS]]." |
− | feedback5="'''Incorrect.''' Renin increases aldosterone secretion from the zona glomerulosa. Aldosterone acts to increase the reabsorption of sodium by cells in the collecting ducts of the kidney. Sodium ions are exchanged for hydrogen and potassium ions, leading to decreased sodium and increased potassium excretion. Water follows sodium, blood volume increases, and this increases blood pressure and glomerular filtration rate. [[ | + | feedback5="'''Incorrect.''' Renin increases aldosterone secretion from the zona glomerulosa. Aldosterone acts to increase the reabsorption of sodium by cells in the collecting ducts of the kidney. Sodium ions are exchanged for hydrogen and potassium ions, leading to decreased sodium and increased potassium excretion. Water follows sodium, blood volume increases, and this increases blood pressure and glomerular filtration rate. [[Renin Angiotensin Aldosterone System|WikiVet Article: RAAS]]." |
− | feedback3="'''Incorrect.''' Renin increases aldosterone secretion from the zona glomerulosa. Aldosterone acts to increase the reabsorption of sodium by cells in the collecting ducts of the kidney. Sodium ions are exchanged for hydrogen and potassium ions, leading to decreased sodium and increased potassium excretion. Water follows sodium, blood volume increases, and this increases blood pressure and glomerular filtration rate. [[ | + | feedback3="'''Incorrect.''' Renin increases aldosterone secretion from the zona glomerulosa. Aldosterone acts to increase the reabsorption of sodium by cells in the collecting ducts of the kidney. Sodium ions are exchanged for hydrogen and potassium ions, leading to decreased sodium and increased potassium excretion. Water follows sodium, blood volume increases, and this increases blood pressure and glomerular filtration rate. [[Renin Angiotensin Aldosterone System|WikiVet Article: RAAS]]." |
image= ""> | image= ""> | ||
</WikiQuiz> | </WikiQuiz> | ||
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choice2="Thyroid Stimulating Hormone (TSH) / Somatostatin" | choice2="Thyroid Stimulating Hormone (TSH) / Somatostatin" | ||
correctchoice="5" | correctchoice="5" | ||
− | feedback5="'''Correct!''' Thyrotrophin releasing hormone (TRH) from the hypothalamus stimulates the release of thyroid stimulating hormone (TSH) from the anterior pituitary which in turn stimulates the release of thyroid hormone form the thyroid gland. Somatostatin inhibits the release of TSH. [[ | + | feedback5="'''Correct!''' Thyrotrophin releasing hormone (TRH) from the hypothalamus stimulates the release of thyroid stimulating hormone (TSH) from the anterior pituitary which in turn stimulates the release of thyroid hormone form the thyroid gland. Somatostatin inhibits the release of TSH. [[Thyroid_Gland_- Anatomy & Physiology#Regulationn|WikiVet Article: Thyroid physiology]]" |
− | feedback4="'''Incorrect.''' Be careful not to confuse thyroid stimulating hormone(TSH) (secreted from the anterior pituitary to target the thyroid gland) with TRH (secreted from the hypothalamus to target the anterior pituitary's thyrotrophic cells). Also Growth Hormone does not inhibit TSH secretion. The correct stimulatory/inhibitory combination is Thyrotrophin Releasing Hormone / Somatostatin. [[ | + | feedback4="'''Incorrect.''' Be careful not to confuse thyroid stimulating hormone(TSH) (secreted from the anterior pituitary to target the thyroid gland) with TRH (secreted from the hypothalamus to target the anterior pituitary's thyrotrophic cells). Also Growth Hormone does not inhibit TSH secretion. The correct stimulatory/inhibitory combination is Thyrotrophin Releasing Hormone / Somatostatin. [[Thyroid_Gland_- Anatomy & Physiology#Regulation|WikiVet Article: Thyroid physiology]]" |
− | feedback3="'''Incorrect.''' Thyrotrophin releasing hormone does stimulate the secretion of thyroid stimulating hormone (TSH), however dopamine does not inhibit TSH secretion. Dopamine inhibits prolactin secretion from the anterior pituitary. The correct stimulatory/inhibitory combination is Thyrotrophin Releasing Hormone / Somatostatin. [[ | + | feedback3="'''Incorrect.''' Thyrotrophin releasing hormone does stimulate the secretion of thyroid stimulating hormone (TSH), however dopamine does not inhibit TSH secretion. Dopamine inhibits prolactin secretion from the anterior pituitary. The correct stimulatory/inhibitory combination is Thyrotrophin Releasing Hormone / Somatostatin. [[Thyroid_Gland_- Anatomy & Physiology#Regulation|WikiVet Article: Thyroid physiology]]" |
− | feedback1="'''Incorrect.''' Adrenocorticotrophic hormone is secreted form the anterior pituitary gland and it stimulates secretion of glucocorticoids from the adrenal cortex, it has no effect on the thyroid gland. Thyrotrophin Releasing Hormone does not inhibit the secretion of Thyroid Stimulating Hormone (TSH), it stimulates it. The correct stimulatory/inhibitory combination is Thyrotrophin Releasing Hormone / Somatostatin. [[ | + | feedback1="'''Incorrect.''' Adrenocorticotrophic hormone is secreted form the anterior pituitary gland and it stimulates secretion of glucocorticoids from the adrenal cortex, it has no effect on the thyroid gland. Thyrotrophin Releasing Hormone does not inhibit the secretion of Thyroid Stimulating Hormone (TSH), it stimulates it. The correct stimulatory/inhibitory combination is Thyrotrophin Releasing Hormone / Somatostatin. [[Thyroid_Gland_- Anatomy & Physiology#Regulation|WikiVet Article: Thyroid physiology]]" |
− | feedback2="'''Incorrect.''' Be careful not to confuse thyroid stimulating hormone (TSH) (secreted from the anterior pituitary to target the thyroid gland) with Thyrotrophin Releasing Hormone (TRH) (secreted from the hypothalamus to target the anterior pituitary's thyrotrophic cells). Somatostatin is inhibitory though. The correct stimulatory/inhibitory combination is Thyrotrophin Releasing Hormone / Somatostatin. [[ | + | feedback2="'''Incorrect.''' Be careful not to confuse thyroid stimulating hormone (TSH) (secreted from the anterior pituitary to target the thyroid gland) with Thyrotrophin Releasing Hormone (TRH) (secreted from the hypothalamus to target the anterior pituitary's thyrotrophic cells). Somatostatin is inhibitory though. The correct stimulatory/inhibitory combination is Thyrotrophin Releasing Hormone / Somatostatin. [[Thyroid_Gland_- Anatomy & Physiology#Regulation|WikiVet Article: Thyroid physiology]]" |
image= ""> | image= ""> | ||
</WikiQuiz> | </WikiQuiz> | ||
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choice5="It decreases blood calcium by increasing renal excretion of calcium." | choice5="It decreases blood calcium by increasing renal excretion of calcium." | ||
correctchoice="4" | correctchoice="4" | ||
− | feedback4="'''Correct!''' Calcitonin decreases blood calcium by decreasing osteolysis and increasing osteogenesis. [[Calcium | + | feedback4="'''Correct!''' Calcitonin decreases blood calcium by decreasing osteolysis and increasing osteogenesis. [[Calcium#Calcitonin |WikiVet Article: Calcium homeostasis]]" |
− | feedback2="'''Incorrect.''' Decreasing osteolysis and increasing osteogenesis will decrease, not increase blood calcium. Calcitonin decreases blood calcium by decreasing osteolysis and increasing osteogenesis. [[Calcium | + | feedback2="'''Incorrect.''' Decreasing osteolysis and increasing osteogenesis will decrease, not increase blood calcium. Calcitonin decreases blood calcium by decreasing osteolysis and increasing osteogenesis. [[Calcium#Calcitonin|WikiVet Article: Calcium homeostasis]]" |
− | feedback1="'''Incorrect.''' Increased osteolysis and decreased osteogenesis will increase blood calcium. Calcitonin decreases blood calcium by decreasing osteolysis and increasing osteogenesis. [[Calcium | + | feedback1="'''Incorrect.''' Increased osteolysis and decreased osteogenesis will increase blood calcium. Calcitonin decreases blood calcium by decreasing osteolysis and increasing osteogenesis. [[Calcium#Calcitonin |WikiVet Article: Calcium homeostasis]]" |
− | feedback3="'''Incorrect.''' Calcitonin decreases blood calcium by decreasing osteolysis and increasing osteogenesis. PTH causes increased blood calcium by increasing osteolysis and decreasing osteogenesis. [[Calcium | + | feedback3="'''Incorrect.''' Calcitonin decreases blood calcium by decreasing osteolysis and increasing osteogenesis. PTH causes increased blood calcium by increasing osteolysis and decreasing osteogenesis. [[Calcium#Calcitonin|WikiVet Article: Calcium homeostasis]]" |
− | feedback5="'''Incorrect.''' Calcitonin has its effects on bone, not the kidney. Calcitonin decreases blood calcium by decreasing osteolysis and increasing osteogenesis. [[Calcium | + | feedback5="'''Incorrect.''' Calcitonin has its effects on bone, not the kidney. Calcitonin decreases blood calcium by decreasing osteolysis and increasing osteogenesis. [[Calcium#Calcitonin |WikiVet Article: Calcium homeostasis]]" |
image= ""> | image= ""> | ||
</WikiQuiz> | </WikiQuiz> | ||
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choice3="Posterior pituitary nuclei" | choice3="Posterior pituitary nuclei" | ||
correctchoice="2" | correctchoice="2" | ||
− | feedback2="'''Correct!''' Prolactin is produced in the lactotrophs of the anterior pituitary and it acts on mammary secretory epithelial cells to stimulate synthesis of milk proteins. [[ | + | feedback2="'''Correct!''' Prolactin is produced in the lactotrophs of the anterior pituitary and it acts on mammary secretory epithelial cells to stimulate synthesis of milk proteins. [[Pituitary_Gland_- Anatomy & Physiology#Hormones_of_the_Anterior_Pituitary_Gland|WikiVet Article: Anterior pituitary hormones]]" |
− | feedback5="'''Incorrect.''' The somatotrophs of the anterior pituitary produce growth hormone. Prolactin is produced in the lactotrophs of the anterior pituitary. [[ | + | feedback5="'''Incorrect.''' The somatotrophs of the anterior pituitary produce growth hormone. Prolactin is produced in the lactotrophs of the anterior pituitary. [[Pituitary_Gland_- Anatomy & Physiology#Hormones_of_the_Anterior_Pituitary_Gland|WikiVet Article: Anterior pituitary hormones]]" |
− | feedback1="'''Incorrect.''' Prolactin acts on mammary secretory epithelial cells to stimulate synthesis of milk proteins. Prolactin is produced in the lactotrophs of the anterior pituitary. [[ | + | feedback1="'''Incorrect.''' Prolactin acts on mammary secretory epithelial cells to stimulate synthesis of milk proteins. Prolactin is produced in the lactotrophs of the anterior pituitary. [[Pituitary_Gland_- Anatomy & Physiology#Hormones_of_the_Anterior_Pituitary_Gland|WikiVet Article: Anterior pituitary hormones]]" |
− | feedback4="'''Incorrect.''' The placenta produces many hormones including prostaglandin F2α, progesterone, oestrogen and placental lactogen. Prolactin is produced in the lactotrophs of the anterior pituitary. [[ | + | feedback4="'''Incorrect.''' The placenta produces many hormones including prostaglandin F2α, progesterone, oestrogen and placental lactogen. Prolactin is produced in the lactotrophs of the anterior pituitary. [[Pituitary_Gland_- Anatomy & Physiology#Hormones_of_the_Anterior_Pituitary_Gland|WikiVet Article: Anterior pituitary hormones]]" |
− | feedback3="'''Incorrect.''' The posterior pituitary produces antidiuretic hormone (ADH) and oxytocin. Prolactin is produced in the lactotrophs of the anterior pituitary. [[ | + | feedback3="'''Incorrect.''' The posterior pituitary produces antidiuretic hormone (ADH) and oxytocin. Prolactin is produced in the lactotrophs of the anterior pituitary. [[Pituitary_Gland_- Anatomy & Physiology#Hormones_of_the_Anterior_Pituitary_Gland|WikiVet Article: Anterior pituitary hormones]]" |
image= ""> | image= ""> | ||
</WikiQuiz> | </WikiQuiz> | ||
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choice4="GLUT 4" | choice4="GLUT 4" | ||
correctchoice="5" | correctchoice="5" | ||
− | feedback5="'''Correct!''' GLUT 5 transporters are responsible for uptake of glucose from intestinal cells into the blood. [[Small Intestine - Anatomy & Physiology#Carbohydrate Digestion and Absorption|WikiVet Article: | + | feedback5="'''Correct!''' GLUT 5 transporters are responsible for uptake of glucose from intestinal cells into the blood. [[Small Intestine Overview - Anatomy & Physiology#Carbohydrate Digestion and Absorption|WikiVet Article: Carbohydrate digestion and absorption]]" |
− | feedback3="'''Incorrect.''' The glucose/Na+ symport is responsible for the uptake of glucose from the intestinal lumen into intestinal cells. GLUT 5 transporters are responsible for uptake of glucose from intestinal cells into the blood. [[Small Intestine - Anatomy & Physiology#Carbohydrate Digestion and Absorption|WikiVet Article: | + | feedback3="'''Incorrect.''' The glucose/Na+ symport is responsible for the uptake of glucose from the intestinal lumen into intestinal cells. GLUT 5 transporters are responsible for uptake of glucose from intestinal cells into the blood. [[Small Intestine Overview - Anatomy & Physiology#Carbohydrate Digestion and Absorption|WikiVet Article: Carbohydrate digestion and absorption]]" |
− | feedback2="'''Incorrect.''' The Na+/K+ ATPase is responsible for pumping sodium ions into the blood in order to maintain a low concentration of sodium inside the intestinal cells. This is important as the action of the glucose/Na+ symport depends upon their being a lower concentration of sodium inside the intestinal cells than in the gut lumen. GLUT 5 transporters are responsible for uptake of glucose from intestinal cells into the blood. [[Small Intestine - Anatomy & Physiology#Carbohydrate Digestion and Absorption|WikiVet Article: | + | feedback2="'''Incorrect.''' The Na+/K+ ATPase is responsible for pumping sodium ions into the blood in order to maintain a low concentration of sodium inside the intestinal cells. This is important as the action of the glucose/Na+ symport depends upon their being a lower concentration of sodium inside the intestinal cells than in the gut lumen. GLUT 5 transporters are responsible for uptake of glucose from intestinal cells into the blood. [[Small Intestine Overview - Anatomy & Physiology#Carbohydrate Digestion and Absorption|WikiVet Article: Carbohydrate digestion and absorption]]" |
− | feedback1="'''Incorrect.''' γ Glutamyl transferase spans the enterocyte membrane and combines glutathione from the inside of the cell with a di-,tri- or oligo-peptide from the intestinal lumen forming a γ-glu-aa complex which is transported into the cell. GLUT 5 transporters are responsible for uptake of glucose from intestinal cells into the blood. [[Small Intestine - Anatomy & Physiology#Carbohydrate Digestion and Absorption |WikiVet Article: | + | feedback1="'''Incorrect.''' γ Glutamyl transferase spans the enterocyte membrane and combines glutathione from the inside of the cell with a di-,tri- or oligo-peptide from the intestinal lumen forming a γ-glu-aa complex which is transported into the cell. GLUT 5 transporters are responsible for uptake of glucose from intestinal cells into the blood. [[Small Intestine Overview - Anatomy & Physiology#Carbohydrate Digestion and Absorption |WikiVet Article: Carbohydrate digestion and absorption]]" |
− | feedback4="'''Incorrect.''' GLUT 4 transporters are used for uptake of glucose into muscle and adipose tissue cells. GLUT 5 transporters are responsible for uptake of glucose from intestinal cells into the blood. [[Small Intestine - Anatomy & Physiology#Carbohydrate Digestion and AbsorptionPancreas - Anatomy & Physiology|WikiVet Article: | + | feedback4="'''Incorrect.''' GLUT 4 transporters are used for uptake of glucose into muscle and adipose tissue cells. GLUT 5 transporters are responsible for uptake of glucose from intestinal cells into the blood. [[Small Intestine Overview - Anatomy & Physiology#Carbohydrate Digestion and AbsorptionPancreas - Anatomy & Physiology|WikiVet Article: Carbohydrate digestion and absorption]]" |
image= ""> | image= ""> | ||
</WikiQuiz> | </WikiQuiz> | ||
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choice5="Somatostatin, Dopamine and Oxytocin" | choice5="Somatostatin, Dopamine and Oxytocin" | ||
correctchoice="4" | correctchoice="4" | ||
− | feedback4="'''Correct!''' Oxytocin and ADH are produced by cell bodies in the paraventricular and supraoptic nuclei of the hypothalamus. They are then transported down axons into the posterior pituitary for storage, prior to release. [[ | + | feedback4="'''Correct!''' Oxytocin and ADH are produced by cell bodies in the paraventricular and supraoptic nuclei of the hypothalamus. They are then transported down axons into the posterior pituitary for storage, prior to release. [[Pituitary_Gland_- Anatomy & Physiology#Posterior_Pituitary_Gland|WikiVet Article: Pituitary gland]]" |
− | feedback1="'''Incorrect.''' Prolactin is secreted by the anterior pituitary and dopamine is secreted by the hypothalamus. Oxytocin and ADH are produced by cell bodies in the paraventricular and supraoptic nuclei of the hypothalamus. They are then transported down axons into the posterior pituitary for storage, prior to release. [[ | + | feedback1="'''Incorrect.''' Prolactin is secreted by the anterior pituitary and dopamine is secreted by the hypothalamus. Oxytocin and ADH are produced by cell bodies in the paraventricular and supraoptic nuclei of the hypothalamus. They are then transported down axons into the posterior pituitary for storage, prior to release. [[Pituitary_Gland_- Anatomy & Physiology#Posterior_Pituitary_Gland|WikiVet Article: Pituitary gland]]" |
− | feedback3="'''Incorrect.''' Prolactin is secreted by the anterior pituitary and somatostatin is secreted by the hypothalamus. Oxytocin and ADH are produced by cell bodies in the paraventricular and supraoptic nuclei of the hypothalamus. They are then transported down axons into the posterior pituitary for storage, prior to release. [[ | + | feedback3="'''Incorrect.''' Prolactin is secreted by the anterior pituitary and somatostatin is secreted by the hypothalamus. Oxytocin and ADH are produced by cell bodies in the paraventricular and supraoptic nuclei of the hypothalamus. They are then transported down axons into the posterior pituitary for storage, prior to release. [[Pituitary_Gland_- Anatomy & Physiology#Posterior_Pituitary_Gland|WikiVet Article: Pituitary gland]]" |
− | feedback2="'''Incorrect.''' Oxytocin and ADH are produced by cell bodies in the paraventricular and supraoptic nuclei of the hypothalamus. They are then transported down axons into the posterior pituitary for storage, prior to release. Dopamine is synthesised in several areas of the brain, including the hypothalamus but is not secreted by the posterior pituitary. [[ | + | feedback2="'''Incorrect.''' Oxytocin and ADH are produced by cell bodies in the paraventricular and supraoptic nuclei of the hypothalamus. They are then transported down axons into the posterior pituitary for storage, prior to release. Dopamine is synthesised in several areas of the brain, including the hypothalamus but is not secreted by the posterior pituitary. [[Pituitary_Gland_- Anatomy & Physiology#Posterior_Pituitary_Gland|WikiVet Article: Pituitary gland]]" |
− | feedback5="'''Incorrect.''' Somatostatin is secreted by the hypothalamus, dopamine is synthesised in several areas of the brain, including the hypothalamus but is not secreted by the posterior pituitary. Oxytocin and ADH are produced by cell bodies in the paraventricular and supraoptic nuclei of the hypothalamus. They are then transported down axons into the posterior pituitary for storage, prior to release. [[ | + | feedback5="'''Incorrect.''' Somatostatin is secreted by the hypothalamus, dopamine is synthesised in several areas of the brain, including the hypothalamus but is not secreted by the posterior pituitary. Oxytocin and ADH are produced by cell bodies in the paraventricular and supraoptic nuclei of the hypothalamus. They are then transported down axons into the posterior pituitary for storage, prior to release. [[Pituitary_Gland_- Anatomy & Physiology#Posterior_Pituitary_Gland|WikiVet Article: Pituitary gland]]" |
image= ""> | image= ""> | ||
</WikiQuiz> | </WikiQuiz> | ||
Line 160: | Line 160: | ||
choice1="The ascending limb of the loop of Henle." | choice1="The ascending limb of the loop of Henle." | ||
correctchoice="2" | correctchoice="2" | ||
− | feedback2="'''Correct!''' All major hormonal controls of reabsorption are exerted on these parts of the nephron. [[Aldosterone#Aldosterone |WikiVet Article: | + | feedback2="'''Correct!''' All major hormonal controls of reabsorption are exerted on these parts of the nephron. [[Aldosterone#Aldosterone |WikiVet Article: Aldosterone]]" |
− | feedback5="'''Incorrect.''' All major hormonal controls of reabsorption are exerted on the late distal convoluted tubule and the collecting ducts. [[Aldosterone#Aldosterone|WikiVet Article: | + | feedback5="'''Incorrect.''' All major hormonal controls of reabsorption are exerted on the late distal convoluted tubule and the collecting ducts. [[Aldosterone#Aldosterone|WikiVet Article: Aldosterone]]" |
− | feedback4="'''Incorrect.''' All major hormonal controls of reabsorption are exerted on the collecting ducts. [[Aldosterone#Aldosterone|WikiVet Article: | + | feedback4="'''Incorrect.''' All major hormonal controls of reabsorption are exerted on the collecting ducts. [[Aldosterone#Aldosterone|WikiVet Article: Aldosterone]]" |
− | feedback3="'''Incorrect.''' All major hormonal controls of reabsorption are exerted on the late distal convoluted tubule and the collecting ducts. [[Aldosterone#Aldosterone |WikiVet Article: | + | feedback3="'''Incorrect.''' All major hormonal controls of reabsorption are exerted on the late distal convoluted tubule and the collecting ducts. [[Aldosterone#Aldosterone |WikiVet Article: Aldosterone]]" |
− | feedback1="'''Incorrect.''' All major hormonal controls of reabsorption are exerted on the late distal convoluted tubule and the collecting ducts. [[Aldosterone#Aldosterone|WikiVet Article: | + | feedback1="'''Incorrect.''' All major hormonal controls of reabsorption are exerted on the late distal convoluted tubule and the collecting ducts. [[Aldosterone#Aldosterone|WikiVet Article: Aldosterone]]" |
image= ""> | image= ""> | ||
</WikiQuiz> | </WikiQuiz> | ||
Line 176: | Line 176: | ||
choice1="Glycogenolysis and glycolysis" | choice1="Glycogenolysis and glycolysis" | ||
correctchoice="5" | correctchoice="5" | ||
− | feedback5="'''Correct!''' The function of insulin is to reduce blood sugar levels when they rise too high. Therefore glycolysis (glucose breakdown) is stimulated as this process uses glucose to make ATP, NADH and pyruvate. And glycogenesis (glycogen synthesis) is stimulated, as in this pathway glucose is used to make the storage product, glycogen. [[Pancreas - Anatomy & Physiology#Insulin|WikiVet Article: | + | feedback5="'''Correct!''' The function of insulin is to reduce blood sugar levels when they rise too high. Therefore glycolysis (glucose breakdown) is stimulated as this process uses glucose to make ATP, NADH and pyruvate. And glycogenesis (glycogen synthesis) is stimulated, as in this pathway glucose is used to make the storage product, glycogen. [[Pancreas - Anatomy & Physiology#Insulin|WikiVet Article: Pancreas]]" |
− | feedback4="'''Incorrect.''' The function of insulin is to reduce blood sugar levels when they rise too high. The process of gluconeogenesis (glucose synthesis) would further increase glucose levels and is therefore not stimulated by high blood glucose. Glycolysis (glucose breakdown) is stimulated as this process uses glucose to make ATP, NADH and pyruvate. Glycogenesis (glycogen synthesis) is also stimulated, as in this pathway glucose is used to make the storage product, glycogen. [[Pancreas - Anatomy & Physiology#Insulin|WikiVet Article: | + | feedback4="'''Incorrect.''' The function of insulin is to reduce blood sugar levels when they rise too high. The process of gluconeogenesis (glucose synthesis) would further increase glucose levels and is therefore not stimulated by high blood glucose. Glycolysis (glucose breakdown) is stimulated as this process uses glucose to make ATP, NADH and pyruvate. Glycogenesis (glycogen synthesis) is also stimulated, as in this pathway glucose is used to make the storage product, glycogen. [[Pancreas - Anatomy & Physiology#Insulin|WikiVet Article: Pancreas]]" |
− | feedback3="'''Incorrect.''' The function of insulin is to reduce blood sugar levels when they rise too high.The process of gluconeogenesis (glucose synthesis) would further increase glucose levels and is therefore not stimulated by high blood glucose. Glycolysis (glucose breakdown) is stimulated as this process uses glucose to make ATP, NADH and pyruvate. Glycogenesis (glycogen synthesis) is also stimulated, as in this pathway glucose is used to make the storage product, glycogen. [[Pancreas - Anatomy & Physiology#Insulin|WikiVet Article: | + | feedback3="'''Incorrect.''' The function of insulin is to reduce blood sugar levels when they rise too high.The process of gluconeogenesis (glucose synthesis) would further increase glucose levels and is therefore not stimulated by high blood glucose. Glycolysis (glucose breakdown) is stimulated as this process uses glucose to make ATP, NADH and pyruvate. Glycogenesis (glycogen synthesis) is also stimulated, as in this pathway glucose is used to make the storage product, glycogen. [[Pancreas - Anatomy & Physiology#Insulin|WikiVet Article: Pancreas]]" |
− | feedback2="'''Incorrect.''' The function of insulin is to reduce blood sugar levels when they rise too high. Glycogenesis (glycogen synthesis) is stimulated, as in this pathway glucose is used to make the storage product, glycogen. Glycolysis (glucose breakdown) is stimulated as this process uses glucose to make ATP, NADH and pyruvate. Glycogenolysis is the breakdown of glycogen stimulated by glucagon. [[Pancreas - Anatomy & Physiology#Insulin|WikiVet Article: | + | feedback2="'''Incorrect.''' The function of insulin is to reduce blood sugar levels when they rise too high. Glycogenesis (glycogen synthesis) is stimulated, as in this pathway glucose is used to make the storage product, glycogen. Glycolysis (glucose breakdown) is stimulated as this process uses glucose to make ATP, NADH and pyruvate. Glycogenolysis is the breakdown of glycogen stimulated by glucagon. [[Pancreas - Anatomy & Physiology#Insulin|WikiVet Article: Pancreas]]" |
− | feedback1="'''Incorrect.''' The function of insulin is to reduce blood sugar levels when they rise too high. Glycogenolysis is not stimulated as this would produce more glucose through glycogen breakdown.This processwould stimulated by glucago. Glycogenesis is stimulated, as in this pathway glucose is used to make the storage product, glycogen. Glycolysis is stimulated as this process uses glucose to make ATP, NADH and pyruvate. [[Pancreas - Anatomy & Physiology#Insulin|WikiVet Article: | + | feedback1="'''Incorrect.''' The function of insulin is to reduce blood sugar levels when they rise too high. Glycogenolysis is not stimulated as this would produce more glucose through glycogen breakdown.This processwould stimulated by glucago. Glycogenesis is stimulated, as in this pathway glucose is used to make the storage product, glycogen. Glycolysis is stimulated as this process uses glucose to make ATP, NADH and pyruvate. [[Pancreas - Anatomy & Physiology#Insulin|WikiVet Article: Pancreas]]" |
image= ""> | image= ""> | ||
</WikiQuiz> | </WikiQuiz> | ||
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choice5="Stimulates glycolysis and and inhibits glycogenesis" | choice5="Stimulates glycolysis and and inhibits glycogenesis" | ||
correctchoice="4" | correctchoice="4" | ||
− | feedback4="'''Correct!''' Glucagon is released in response to low blood sugar levels in order to stimulate processes that will raise blood glucose concentrations. Therefore glucagon stimulates gluconeogenesis which produces glucose from non-carbohydrate sources and also stimulates glycogenolysis, which is the breakdown of stored glycogen to glucose. [[Pancreas - Anatomy & Physiology#Glucagon|WikiVet Article: | + | feedback4="'''Correct!''' Glucagon is released in response to low blood sugar levels in order to stimulate processes that will raise blood glucose concentrations. Therefore glucagon stimulates gluconeogenesis which produces glucose from non-carbohydrate sources and also stimulates glycogenolysis, which is the breakdown of stored glycogen to glucose. [[Pancreas - Anatomy & Physiology#Glucagon|WikiVet Article: Pancreas]]" |
− | feedback2="'''Incorrect.''' Glucagon is released in response to low blood sugar levels in order to stimulate processes that will raise serum glucose concentrations. Therefore glucagon stimulates gluconeogenesis which produces glucose from non-carbohydrate sources and also stimulates glycogenolysis, which is the breakdown of stored glycogen to glucose. Glycolysis (glucose breakdown) is not stimulated, this would lead to the breakdown of glucose, further reducing blood levels. [[Pancreas - Anatomy & Physiology#Glucagon|WikiVet Article: | + | feedback2="'''Incorrect.''' Glucagon is released in response to low blood sugar levels in order to stimulate processes that will raise serum glucose concentrations. Therefore glucagon stimulates gluconeogenesis which produces glucose from non-carbohydrate sources and also stimulates glycogenolysis, which is the breakdown of stored glycogen to glucose. Glycolysis (glucose breakdown) is not stimulated, this would lead to the breakdown of glucose, further reducing blood levels. [[Pancreas - Anatomy & Physiology#Glucagon|WikiVet Article: Pancreas]]" |
− | feedback1="'''Incorrect.''' Glucagon is released in response to low blood sugar levels in order to stimulate processes that will raise serum glucose concentrations. Therefore glucagon stimulates gluconeogenesis which produces glucose from non-carbohydrate sources and also stimulates glycogenolysis, which is the breakdown of stored glycogen to glucose. [[Pancreas - Anatomy & Physiology#Glucagon|WikiVet Article: | + | feedback1="'''Incorrect.''' Glucagon is released in response to low blood sugar levels in order to stimulate processes that will raise serum glucose concentrations. Therefore glucagon stimulates gluconeogenesis which produces glucose from non-carbohydrate sources and also stimulates glycogenolysis, which is the breakdown of stored glycogen to glucose. [[Pancreas - Anatomy & Physiology#Glucagon|WikiVet Article: Pancreas]]" |
− | feedback3="'''Incorrect.''' Glucagon is released in response to low blood sugar levels in order to stimulate processes that will raise serum glucose concentrations. Therefore you are correct that glucagon stimulates gluconeogenesis (glucose synthesis) which produces glucose from non-carbohydrate sources, but glucagon also stimulates glycogenolysis, which is the breakdown of stored glycogen to glucose. [[Pancreas - Anatomy & Physiology#Glucagon|WikiVet Article: | + | feedback3="'''Incorrect.''' Glucagon is released in response to low blood sugar levels in order to stimulate processes that will raise serum glucose concentrations. Therefore you are correct that glucagon stimulates gluconeogenesis (glucose synthesis) which produces glucose from non-carbohydrate sources, but glucagon also stimulates glycogenolysis, which is the breakdown of stored glycogen to glucose. [[Pancreas - Anatomy & Physiology#Glucagon|WikiVet Article: Pancreas]]" |
− | feedback5="'''Incorrect.''' Glucagon is released in response to low blood sugar levels in order to stimulate processes that will raise serum glucose concentrations. Therefore glucagon stimulates gluconeogenesis (glucose synthesis) which produces glucose from non-carbohydrate sources and also stimulates glycogenolysis, which is the breakdown of stored glycogen to glucose. [[Pancreas - Anatomy & Physiology#Glucagon|WikiVet Article: | + | feedback5="'''Incorrect.''' Glucagon is released in response to low blood sugar levels in order to stimulate processes that will raise serum glucose concentrations. Therefore glucagon stimulates gluconeogenesis (glucose synthesis) which produces glucose from non-carbohydrate sources and also stimulates glycogenolysis, which is the breakdown of stored glycogen to glucose. [[Pancreas - Anatomy & Physiology#Glucagon|WikiVet Article: Pancreas]]" |
image= ""> | image= ""> | ||
</WikiQuiz> | </WikiQuiz> | ||
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choice4="PTH increases renal excretion of calcitriol." | choice4="PTH increases renal excretion of calcitriol." | ||
correctchoice="3" | correctchoice="3" | ||
− | feedback3="'''Correct!''' PTH increases the synthesis of calcitriol by enhancing the 1alpha- hydroxylation reaction in the kidney. [[Calcium | + | feedback3="'''Correct!''' PTH increases the synthesis of calcitriol by enhancing the 1alpha- hydroxylation reaction in the kidney. [[Calcium|WikiVet Article: Calcium homeostasis]]" |
− | feedback5="'''Incorrect.''' The 25- hydroxylation reaction in the liver is the unregulated step that produces calcidiol. PTH increases the synthesis of calcitriol by enhancing the 1alpha- hydroxylation reaction in the kidney. [[Calcium | + | feedback5="'''Incorrect.''' The 25- hydroxylation reaction in the liver is the unregulated step that produces calcidiol. PTH increases the synthesis of calcitriol by enhancing the 1alpha- hydroxylation reaction in the kidney. [[Calcium|WikiVet Article: Calcium homeostasis]]" |
− | feedback2="'''Incorrect.''' PTH increases the synthesis of calcitriol by enhancing the 1alpha- hydroxylation reaction in the kidney. [[Calcium | + | feedback2="'''Incorrect.''' PTH increases the synthesis of calcitriol by enhancing the 1alpha- hydroxylation reaction in the kidney. [[Calcium|WikiVet Article: Calcium homeostasis]]" |
− | feedback1="'''Incorrect.''' PTH increases the synthesis of calcitriol by enhancing the 1alpha- hydroxylation reaction in the kidney. [[Calcium | + | feedback1="'''Incorrect.''' PTH increases the synthesis of calcitriol by enhancing the 1alpha- hydroxylation reaction in the kidney. [[Calcium|WikiVet Article: Calcium homeostasis]]" |
− | feedback4="'''Incorrect.''' PTH increases the synthesis of calcitriol by enhancing the 1alpha- hydroxylation reaction in the kidney. [[Calcium | + | feedback4="'''Incorrect.''' PTH increases the synthesis of calcitriol by enhancing the 1alpha- hydroxylation reaction in the kidney. [[Calcium|WikiVet Article: Calcium homeostasis]]" |
image= ""> | image= ""> | ||
</WikiQuiz> | </WikiQuiz> | ||
Line 224: | Line 224: | ||
choice5="Zona reticularis of cortex" | choice5="Zona reticularis of cortex" | ||
correctchoice="3" | correctchoice="3" | ||
− | feedback3="'''Correct!''' The adrenal medulla produces catecholamines including epinephrine and norepinephrine. [[Adrenal Glands - Anatomy & Physiology|WikiVet Article: | + | feedback3="'''Correct!''' The adrenal medulla produces catecholamines including epinephrine and norepinephrine. [[Adrenal Glands - Anatomy & Physiology|WikiVet Article: Adrenal glands]]" |
− | feedback4="'''Incorrect.''' The capsule has no endocrine function. The adrenal medulla produces catecholamines including epinephrine and norepinephrine. [[Adrenal Glands - Anatomy & Physiology|WikiVet Article: | + | feedback4="'''Incorrect.''' The capsule has no endocrine function. The adrenal medulla produces catecholamines including epinephrine and norepinephrine. [[Adrenal Glands - Anatomy & Physiology|WikiVet Article: Adrenal glands]]" |
− | feedback1="'''Incorrect.''' The zona glomerulosa in the adrenal cortex produces mineralocorticoids e.g. aldosterone. The adrenal medulla produces catecholamines including epinephrine and norepinephrine. [[Adrenal Glands - Anatomy & Physiology|WikiVet Article: | + | feedback1="'''Incorrect.''' The zona glomerulosa in the adrenal cortex produces mineralocorticoids e.g. aldosterone. The adrenal medulla produces catecholamines including epinephrine and norepinephrine. [[Adrenal Glands - Anatomy & Physiology|WikiVet Article: Adrenal glands]]" |
− | feedback2="'''Incorrect.''' The zona fasciculata in the adrenal cortex produces glucocorticoids e.g. cortisol. The adrenal medulla produces catecholamines including epinephrine and norepinephrine. [[Adrenal Glands - Anatomy & Physiology|WikiVet Article: | + | feedback2="'''Incorrect.''' The zona fasciculata in the adrenal cortex produces glucocorticoids e.g. cortisol. The adrenal medulla produces catecholamines including epinephrine and norepinephrine. [[Adrenal Glands - Anatomy & Physiology|WikiVet Article: Adrenal glands]]" |
− | feedback5="'''Incorrect.''' The zona reticularis in the adrenal cortex produces adrenal androgens. The adrenal medulla produces catecholamines including epinephrine and norepinephrine. [[Adrenal Glands - Anatomy & Physiology|WikiVet Article: | + | feedback5="'''Incorrect.''' The zona reticularis in the adrenal cortex produces adrenal androgens. The adrenal medulla produces catecholamines including epinephrine and norepinephrine. [[Adrenal Glands - Anatomy & Physiology|WikiVet Article: Adrenal glands]]" |
image= ""> | image= ""> | ||
</WikiQuiz> | </WikiQuiz> | ||
+ | |||
+ | [[Category:Endocrine System Anatomy & Physiology Quizzes]] |
Latest revision as of 11:01, 26 June 2011
|
Questions reviewed by: | David Gardner BSc (Hons) PhD Associate Professor in developmental physiology Alison Mostyn BSc (Hons) PhD Lecturer in Comparative Cellular Physiology |
1 |
Which three hormones directly stimulate Insulin-like growth factor-I (IGF-I)? |
2 |
Vitamin D3 is converted to 25-hydroxycholecalciferol (25-OH D3) in which part of the body? |
3 |
The amount of active vitamin D3 (calcitriol) in the body is regulated by which hormone? |
4 |
What are the final physiological effects of the renin-angiotensin-aldosterone system (RAAS) on the kidney? |
5 |
Thyroid Stimulating Hormone (TSH) secretion is stimulated / inhibited by which two hypothalamic hormones respectively? |
6 |
What are the effects of calcitonin? |
7 |
Where is prolactin synthesised and secreted? |
8 |
Glucose uptake into the blood from intestinal cells is mediated via which type of transporter? |
9 |
Which hormones are secreted by the posterior pituitary gland? |
10 |
On which section of the nephron does aldosterone act to stimulate sodium reabsorption? |
11 |
When glucose levels in the blood are high, which processes does insulin stimulate? |
12 |
When blood glucose levels are low, what role does glucagon perform? |
13 |
What effect does parathyroid hormone (PTH) have on calcitriol (1,25-dihydroxy D3), and how does it exert this effect? |
14 |
Catecholamines are produced in which part of the adrenal gland? |