Problem 1 In the case study of your instructor’s sister, corticosteroid drug, ad

Question

Problem 1 In the case study of your instructor’s sister, corticosteroid drug, administered therapeutically as an anti-inflammatory, resulted in the onset of signs/symptoms of Cushing’s syndrome. Because the severity of these side effects increased as her corticosteroid therapy continued, the doctor decided to try taking her off the corticosteroid and moving her to other drugs. She was told to taper off the corticosteroid drug by gradually reducing her dosage over a period of time. Suddenly stopping her corticosteroid drugs and not tapering off would be problematic because of “feedback suppression”. Why would corticosteroid drug result in feedback suppression? (What is being suppressed by feedback?) How and why would administration of high-dosage corticosteroid drug change the activity of the organs in the control pathway regulating natural cortisol secretion? What would happen if she suddenly stopped taking her corticosteroid drug without tapering off?

Problem 2 Pathologies (disease states) of a hypothalamic-anterior pituitary-endocrine gland control pathway may involve hypersecretion or hyposecretion of the terminal hormone from the last endocrine gland in the pathway. When the last endocrine gland itself is responsible for the abnormal hormone level, the problem is considered a primary pathology (i.e. primary hypersecretion or primary hyposecretion). Similar to primary pathologies, secondary pathologies still result in abnormal secretion of the terminal hormone by the last endocrine gland, but the etiology (cause) is instead a problem with the secretion activity of the hypothalamus or the anterior pituitary.

a) The majority (two-thirds) of cortisol hypersecretion pathologies are due to anteriorpituitary tumors that uncontrollably secrete trophic hormone (anterior-pituitary hypersecretion). Is this a case of primary or secondary hypersecretion? What trophic hormone is secreted by the tumor? If anterior pituitary secretion is uncontrolled, what normal control must not be effective? What is the expected effect on hypothalamic trophic-hormone secretion? Explain.

b) You have a patient who you suspect has a cortisol imbalance and decide to order a blood test. Hormone Blood concentration (relative to normal) CRH Slightly elevated ACTH Elevated Cortisol Low Is this a case of primary or secondary pathology? Justify your conclusion.

Explanation / Answer

1.Why would corticosteroid drug result in feedback suppression? (What is being suppressed by feedback?) How and why would administration of high-dosage corticosteroid drug change the activity of the organs in the control pathway regulating natural cortisol secretion? What would happen if she suddenly stopped taking her corticosteroid drug without tapering off?

answer ; glucocorticosteriod are helpful in immunosupression and anti inflamattory effects in natural immune response . they involve in mobilisation of substrates for the gluconeogensis and maintanace of normal bood sugar ,by gluconeogenesis in liver, mobilising the aminoacids to ectra hepatic tissue ,reducing glucose usage by inhibhiting uptake in muscle and fat and stimulating fats .adrenal shrinkage occurs . there are severe adverse effects if you withdraw the corticosteriods it will effect all organs include cardiovascular -hypertension , nervous system - pyschosis , endocrine - aderenal; supression , leukocytosis ,myopathy ,catarct ,turnacal obesity .

withdrawal of glucocorticostriods;

usage of high dose of steriods for more than week causes the supression of the adrenal gland because the exogenous supplement causes the supression of the hypothlamic corticotropin release hormone and pitutary adrenocorticotropic hormone . the patient is vulnarable to adrenal insufficiency which the adrenal gland do not produce the suffiecient amount of steriod hormones primarily cortisol which may include the impaired secretion of the aldosterone which regulates sodium conservation ,potassium secretion and water retension . the longterm usage of the steriods causes the hibirenation of HPAA axis .

2. The majority (two-thirds) of cortisol hypersecretion pathologies are due to anteriorpituitary tumors that uncontrollably secrete trophic hormone (anterior-pituitary hypersecretion). Is this a case of primary or secondary hypersecretion? What trophic hormone is secreted by the tumor? If anterior pituitary secretion is uncontrolled, what normal control must not be effective? What is the expected effect on hypothalamic trophic-hormone secretion? Explain

the tropic hormone involved is the adrenocortoctropin hormone ACTH ,excess of hormone produced , this causes the adenomas beacuse of excess of corticostrone hormone .which causes the excess of weight gain , rashes on the body cotisol exhibhit the negative feedback mechanism , cushing syndrome is becaus eof the hypersecretion of the cortisol .decreased secretion f the cortiosol this inturn causes the decreased secretion of the ACTH feed back mechanism ,this leads to the production of the tumours .

You have a patient who you suspect has a cortisol imbalance and decide to order a blood test. Hormone Blood concentration (relative to normal) CRH Slightly elevated ACTH Elevated Cortisol Low Is this a case of primary or secondary pathology? Justify your conclusion.

This condition is caused due to the impoper function of the adrenal gland .this is considered as the primary pathology as because of the adrenal insufficency there is less hormone secretion hormones

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