glucocorticoids Flashcards
Q: What are glucocorticoids, and how do they function in the body?
A: Glucocorticoids are steroid hormones secreted by the adrenal cortex. These hormones have powerful anti-inflammatory and metabolic effects. They work by binding to glucocorticoid receptors within target cells, inducing structural changes that allow them to enter the nucleus and bind with glucocorticoid response elements (GRE) on chromatin. This triggers the transcription of specific mRNA, leading to the synthesis of proteins that modify various cell functions and metabolic effects in the body.
Q: Describe the negative feedback mechanism involved in the regulation of glucocorticoids.
A: The release of glucocorticoids is regulated by the hypothalamic-pituitary-adrenal (HPA) axis. The hypothalamus secretes corticotropin-releasing hormone (CRH), stimulating the anterior pituitary gland to release adrenocorticotropic hormone (ACTH). ACTH travels to the adrenal glands, prompting the release of glucocorticoids. Excess glucocorticoids suppress the release of both CRH and ACTH, maintaining a negative feedback loop that regulates their secretion.
These flashcards provide a clear understanding of the function of glucocorticoids in the body and the negative feedback mechanism that regulates their release.
Q: What are glucocorticoids, and how do they function in the body?
A: Glucocorticoids are steroid hormones secreted by the adrenal cortex. These hormones have powerful anti-inflammatory and metabolic effects. They work by binding to glucocorticoid receptors within target cells, inducing structural changes that allow them to enter the nucleus and bind with glucocorticoid response elements (GRE) on chromatin. This triggers the transcription of specific mRNA, leading to the synthesis of proteins that modify various cell functions and metabolic effects in the body.
Q: Describe the negative feedback mechanism involved in the regulation of glucocorticoids.
A: The release of glucocorticoids is regulated by the hypothalamic-pituitary-adrenal (HPA) axis. The hypothalamus secretes corticotropin-releasing hormone (CRH), stimulating the anterior pituitary gland to release adrenocorticotropic hormone (ACTH). ACTH travels to the adrenal glands, prompting the release of glucocorticoids. Excess glucocorticoids suppress the release of both CRH and ACTH, maintaining a negative feedback loop that regulates their secretion.
These flashcards provide a clear understanding of the function of glucocorticoids in the body and the negative feedback mechanism that regulates their release.
Q: What is the primary function of cortisol in the body?
A: Cortisol regulates immune responses and cellular metabolism during times of stress or illness.
Q: How does cortisol affect the immune response?
A: Cortisol promotes an anti-inflammatory state by inhibiting prostaglandins, leukotrienes, and interleukin-2 production by white blood cells.
Q: What metabolic effects does cortisol have?
A: Cortisol triggers lipolysis in adipose tissue, proteolysis in muscles, and stimulates gluconeogenesis in the liver.
Q: What is the diabetogenic effect of cortisol?
A: High cortisol levels increase insulin resistance, leading to elevated blood glucose levels, similar to the effects seen in diabetes.
Q: How does cortisol affect blood pressure?
A: Cortisol up-regulates alpha1 adrenergic receptors in blood vessels, causing vasoconstriction, and contributing to maintaining blood pressure levels.
Q: What is the primary function of cortisol in the body?
A: Cortisol regulates immune responses and cellular metabolism during times of stress or illness.
Q: How does cortisol affect the immune response?
A: Cortisol promotes an anti-inflammatory state by inhibiting prostaglandins, leukotrienes, and interleukin-2 production by white blood cells.
Q: What metabolic effects does cortisol have?
A: Cortisol triggers lipolysis in adipose tissue, proteolysis in muscles, and stimulates gluconeogenesis in the liver.
Q: What is the diabetogenic effect of cortisol?
A: High cortisol levels increase insulin resistance, leading to elevated blood glucose levels, similar to the effects seen in diabetes.
Q: How does cortisol affect blood pressure?
A: Cortisol up-regulates alpha1 adrenergic receptors in blood vessels, causing vasoconstriction, and contributing to maintaining blood pressure levels.
Q: What effect do synthetic glucocorticoids have on neutrophils?
A: Synthetic glucocorticoids increase the number of neutrophils in the blood by decreasing their attachment to the endothelial lining, allowing them to enter circulation.
Q: What is the term for the process where neutrophils detach from the endothelial lining?
A: This process is known as “demargination.”
Q: Besides neutrophils, which other immune cells are affected by synthetic glucocorticoids?
A: Synthetic glucocorticoids decrease counts of lymphocytes, monocytes, basophils, and eosinophils in the blood.
Q: What effect do synthetic glucocorticoids have on neutrophils?
A: Synthetic glucocorticoids increase the number of neutrophils in the blood by decreasing their attachment to the endothelial lining, allowing them to enter circulation.
Q: What is the term for the process where neutrophils detach from the endothelial lining?
A: This process is known as “demargination.”
Q: Besides neutrophils, which other immune cells are affected by synthetic glucocorticoids?
A: Synthetic glucocorticoids decrease counts of lymphocytes, monocytes, basophils, and eosinophils in the blood.
Q: What is the duration of action for short-acting glucocorticoids?
A: Short-acting glucocorticoids typically have a duration of action of 8 to 12 hours.
Q: Name two short-acting glucocorticoids and their properties.
A: Cortisone and hydrocortisone are short-acting glucocorticoids. Cortisone requires conversion to hydrocortisone in the liver and isn’t active in topical forms. Hydrocortisone, identical to cortisol, acts rapidly but briefly and is often used in acute adrenal insufficiency.
Q: How is hydrocortisone administered, and why is it preferred in certain conditions?
A: Hydrocortisone can be taken orally, intravenously, or intramuscularly. It’s the drug of choice in acute adrenal insufficiency due to its rapid action.
Q: What is the duration of action for short-acting glucocorticoids?
A: Short-acting glucocorticoids typically have a duration of action of 8 to 12 hours.
Q: Name two short-acting glucocorticoids and their properties.
A: Cortisone and hydrocortisone are short-acting glucocorticoids. Cortisone requires conversion to hydrocortisone in the liver and isn’t active in topical forms. Hydrocortisone, identical to cortisol, acts rapidly but briefly and is often used in acute adrenal insufficiency.
Q: How is hydrocortisone administered, and why is it preferred in certain conditions?
A: Hydrocortisone can be taken orally, intravenously, or intramuscularly. It’s the drug of choice in acute adrenal insufficiency due to its rapid action.
Q: What is the duration of action for intermediate-acting glucocorticoids?
A: Intermediate-acting glucocorticoids typically have a duration of action of 12 to 36 hours.
Q: Name some intermediate-acting glucocorticoids and their routes of administration.
A: Prednisone, prednisolone, methylprednisolone, and triamcinolone are intermediate-acting glucocorticoids. Prednisone is taken orally, prednisolone has oral, intravenous, and topical use, methylprednisolone can be taken orally, intravenously, intramuscularly, or intra-articularly, and triamcinolone has oral, intramuscular, topical, and intra-articular use.
Q: How do intermediate-acting glucocorticoids compare to short-acting ones in terms of potency?
A: Intermediate-acting glucocorticoids are approximately 4 to 5 times more potent than short-acting ones, meaning a lower dose is needed to achieve the desired response.
Q: What is the duration of action for intermediate-acting glucocorticoids?
A: Intermediate-acting glucocorticoids typically have a duration of action of 12 to 36 hours.
Q: Name some intermediate-acting glucocorticoids and their routes of administration.
A: Prednisone, prednisolone, methylprednisolone, and triamcinolone are intermediate-acting glucocorticoids. Prednisone is taken orally, prednisolone has oral, intravenous, and topical use, methylprednisolone can be taken orally, intravenously, intramuscularly, or intra-articularly, and triamcinolone has oral, intramuscular, topical, and intra-articular use.
Q: How do intermediate-acting glucocorticoids compare to short-acting ones in terms of potency?
A: Intermediate-acting glucocorticoids are approximately 4 to 5 times more potent than short-acting ones, meaning a lower dose is needed to achieve the desired response.
Q: What is the duration of action for long-acting glucocorticoids?
A: Long-acting glucocorticoids typically have a duration of action of 36 to 72 hours.
Q: Name some long-acting glucocorticoids and their routes of administration.
A: Betamethasone and dexamethasone are long-acting glucocorticoids. They can be taken orally, injected into a vein, muscle, or joint. Dexamethasone can also be used topically.
Q: How do long-acting glucocorticoids compare to short-acting ones in terms of potency?
A: Long-acting glucocorticoids are approximately 25 times more potent than short-acting ones.
Q: In what medical conditions are glucocorticoids used for treatment?
A: Glucocorticoids are used to treat adrenal conditions characterized by low corticosteroid levels in the body, such as primary adrenal insufficiency (Addison’s disease) and congenital adrenal hyperplasia caused by genetic enzyme deficiencies.
Q: What is the duration of action for long-acting glucocorticoids?
A: Long-acting glucocorticoids typically have a duration of action of 36 to 72 hours.
Q: Name some long-acting glucocorticoids and their routes of administration.
A: Betamethasone and dexamethasone are long-acting glucocorticoids. They can be taken orally, injected into a vein, muscle, or joint. Dexamethasone can also be used topically.
Q: How do long-acting glucocorticoids compare to short-acting ones in terms of potency?
A: Long-acting glucocorticoids are approximately 25 times more potent than short-acting ones.
Q: In what medical conditions are glucocorticoids used for treatment?
A: Glucocorticoids are used to treat adrenal conditions characterized by low corticosteroid levels in the body, such as primary adrenal insufficiency (Addison’s disease) and congenital adrenal hyperplasia caused by genetic enzyme deficiencies.
Q: How are short-acting glucocorticoids utilized in treating adrenal conditions?
A: Short-acting glucocorticoids are employed in physiologic replacement therapy to manage conditions like primary adrenal insufficiency (Addison’s disease) and congenital adrenal hyperplasia. These medications aim to mimic the body’s normal diurnal cortisol pattern, with higher doses in the morning and lower doses later in the day.
Q: What is the treatment for a life-threatening adrenal crisis or acute adrenal insufficiency?
A: An adrenal crisis is a medical emergency, and hydrocortisone is administered due to its rapid onset of action in managing this critical condition.
Q: How are short-acting glucocorticoids utilized in treating adrenal conditions?
A: Short-acting glucocorticoids are employed in physiologic replacement therapy to manage conditions like primary adrenal insufficiency (Addison’s disease) and congenital adrenal hyperplasia. These medications aim to mimic the body’s normal diurnal cortisol pattern, with higher doses in the morning and lower doses later in the day.
Q: What is the treatment for a life-threatening adrenal crisis or acute adrenal insufficiency?
A: An adrenal crisis is a medical emergency, and hydrocortisone is administered due to its rapid onset of action in managing this critical condition.
Q: What are the therapeutic uses of glucocorticoids as anti-inflammatory/immunosuppressive agents?
A: Glucocorticoids are used to manage asthma, autoimmune disorders like rheumatoid arthritis, Crohn’s disease, and ulcerative colitis, acute exacerbations of multiple sclerosis, idiopathic thrombocytopenic purpura, inflammatory skin, eye, ear, or nasal conditions (eczema, allergic conjunctivitis, rhinitis), severe allergic reactions, and to prevent graft-versus-host disease.
Q: What are some miscellaneous conditions where glucocorticoids are utilized?
A: Glucocorticoids are used for chemotherapy-induced vomiting, hypercalcemia, and in cases of mountain sickness. Additionally, betamethasone is administered to pregnant women before birth to accelerate fetal lung maturation.
Q: What are the therapeutic uses of glucocorticoids as anti-inflammatory/immunosuppressive agents?
A: Glucocorticoids are used to manage asthma, autoimmune disorders like rheumatoid arthritis, Crohn’s disease, and ulcerative colitis, acute exacerbations of multiple sclerosis, idiopathic thrombocytopenic purpura, inflammatory skin, eye, ear, or nasal conditions (eczema, allergic conjunctivitis, rhinitis), severe allergic reactions, and to prevent graft-versus-host disease.
Q: What are some miscellaneous conditions where glucocorticoids are utilized?
A: Glucocorticoids are used for chemotherapy-induced vomiting, hypercalcemia, and in cases of mountain sickness. Additionally, betamethasone is administered to pregnant women before birth to accelerate fetal lung maturation.
Q: How are glucocorticoids utilized in neoplastic conditions?
A: Glucocorticoids serve as adjuvant therapy due to their anti-lymphocytic effect, particularly in hematopoietic cancers like acute lymphocytic leukemia, Hodgkin lymphoma, and non-Hodgkin lymphomas. Additionally, dexamethasone is used to relieve cerebral edema in individuals with brain tumors.
Q: What is an important consideration regarding dexamethasone’s impact on the hypothalamic-pituitary-adrenal axis?
A: Dexamethasone, even in low doses, significantly suppresses the hypothalamic-pituitary-adrenal axis, leading to reduced secretion of adrenocorticotropic hormone (ACTH) by providing negative feedback to the pituitary gland, resulting in decreased natural cortisol production.
Q: How are glucocorticoids utilized in neoplastic conditions?
A: Glucocorticoids serve as adjuvant therapy due to their anti-lymphocytic effect, particularly in hematopoietic cancers like acute lymphocytic leukemia, Hodgkin lymphoma, and non-Hodgkin lymphomas. Additionally, dexamethasone is used to relieve cerebral edema in individuals with brain tumors.
Q: What is an important consideration regarding dexamethasone’s impact on the hypothalamic-pituitary-adrenal axis?
A: Dexamethasone, even in low doses, significantly suppresses the hypothalamic-pituitary-adrenal axis, leading to reduced secretion of adrenocorticotropic hormone (ACTH) by providing negative feedback to the pituitary gland, resulting in decreased natural cortisol production.
How is dexamethasone utilized in diagnosing Cushing syndrome, and what are its symptoms?
A: Dexamethasone is used in the overnight dexamethasone suppression test to diagnose Cushing syndrome, characterized by excessive cortisol production. Symptoms include obesity with a buffalo hump, truncal obesity, and moon facies. Hyperglycemia, muscle weakness, skin stretch marks, hypertension, osteoporosis, and increased infection risk are also common.
How is dexamethasone utilized in diagnosing Cushing syndrome, and what are its symptoms?
A: Dexamethasone is used in the overnight dexamethasone suppression test to diagnose Cushing syndrome, characterized by excessive cortisol production. Symptoms include obesity with a buffalo hump, truncal obesity, and moon facies. Hyperglycemia, muscle weakness, skin stretch marks, hypertension, osteoporosis, and increased infection risk are also common.
Q: How is the overnight dexamethasone suppression test used to diagnose Cushing syndrome?
A: A low dose of dexamethasone is given, aiming to suppress ACTH production in the pituitary gland. Normally, this would lower serum cortisol levels. If the cortisol level remains high, it indicates endogenous cortisol production, confirming the presence of Cushing syndrome.
Q: How is the overnight dexamethasone suppression test used to diagnose Cushing syndrome?
A: A low dose of dexamethasone is given, aiming to suppress ACTH production in the pituitary gland. Normally, this would lower serum cortisol levels. If the cortisol level remains high, it indicates endogenous cortisol production, confirming the presence of Cushing syndrome.
What are some common side effects associated with prolonged use of synthetic glucocorticoids?
A: Side effects of prolonged synthetic glucocorticoid use include Cushing-like symptoms (iatrogenic Cushing syndrome), fluid retention, hypertension, hypokalemia, hyperglycemia, diabetes, adrenal suppression, increased infection risk, impaired wound healing, musculoskeletal issues like osteoporosis and fractures, psychiatric disturbances, peptic ulcers, cataracts, and growth inhibition in children. “Stress doses” may be needed during surgeries or severe illnesses. Alternating daily doses (alternate-day therapy) can help prevent HPA axis suppression and adrenocortical atrophy.
What are some common side effects associated with prolonged use of synthetic glucocorticoids?
A: Side effects of prolonged synthetic glucocorticoid use include Cushing-like symptoms (iatrogenic Cushing syndrome), fluid retention, hypertension, hypokalemia, hyperglycemia, diabetes, adrenal suppression, increased infection risk, impaired wound healing, musculoskeletal issues like osteoporosis and fractures, psychiatric disturbances, peptic ulcers, cataracts, and growth inhibition in children. “Stress doses” may be needed during surgeries or severe illnesses. Alternating daily doses (alternate-day therapy) can help prevent HPA axis suppression and adrenocortical atrophy.
