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31 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Where is the adrenal located
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Above the kidney
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where are the adrenal cortex produce
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Normal adrenal function produces and modulates
•metabolism and immune responses (glucocorticoids) •blood pressure and volume, and electrolytes (mineralocorticoids) •secondary sexual characteristics (in females) (DHEA) |
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How is the adrenal cortex stimulated
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Glucocorticoids function
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•Predominant action is on intermediary metabolism (enhance production of glucose, reduce all other metabolic activity not directly involved in that process)
•Regulate protein, carbohydrate, lipid, and nucleic acid metabolism •Also have anti-inflammatory properties |
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Mineralocorticoids function
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•Major regulators of ECFV and potassium metabolism
•Aldosteronecauses sodium and water retention with potassium loss |
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Cushing’s Syndrome- definition, types and syndrome
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A syndrome caused by prolonged exposure to elevated levels of either endogenous glucocorticoidsor exogenous glucocorticoids
•Endogenous -due to increased cortisolproduction by the adrenals. May be either –ACTH-dependent, resulting from •Hypersecretionof ACTH by the pituitary gland (egCushing’s disease) •Secretion of ACTH by a nonpituitarytumor, such as small cell carcinoma of the lung or a carcinoidtumor(ectopic ACTH syndrome) •Administration of exogenous ACTH (corticosteroids) –Or ACTH-independent •Usually due to an adrenocorticalneoplasm (adenoma or carcinoma), may also occur with adrenal hyperplasia |
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Diagnosis of Cushing’s Syndrome (Laboratory)
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•Dexamethasonesuppression test
–Lack of suppression of ACTH by a dose of dexamethasoneindicates resistance to feedback •Urinary free cortisol –Detects high levels of cortisolin serum •ACTH levels –Undetectable levels, both basally and particularly in response to corticotropin-releasing hormone (CRH), suggest a primary adrenal cause. –High levels suggest a pituitary cause |
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diagnosis of cushing syndrome cause
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•Most cases of Cushing's syndrome are caused by iatrogenic administration of glucocorticoids.
•Other causes of Cushing's syndrome are rare, but are important to identify because many are curable. |
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Signs indication cushings
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Signs and symptoms of Cushing's syndrome are nonspecific and usually insidious in onset.
23 |
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Treatment of Cushing’s Syndrome and goal of treatment
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•Related to cause
–Steroid Use •Reduction of systemic steroids (if possible) Nonpharmacologictherapy for Cushing's syndrome includes surgery for resectabletumorsand pituitary irradiation for Cushing's disease not cured by surgery –Pharmacological management –Tumours •Surgery or radiation •Regardless of Cause –Manage consequences •Potassium •Glucose •Hypertension •Calcium •Infections In some cases of pituitary-dependent Cushing’s syndrome or ectopic ACTH/CRH production, adrenal corticosteroid production is blocked pharmacologically –Ketoconazole –Aminoglutethimide –Metyrapone –Mitotane The goal of therapy is to restore HPA hormonal balance by eliminating excess glucocorticoidsand mineralocorticoids. |
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detailed drug treatment of cushings syndrome
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steroidogenicinhibitors, neuromodulatorsof ACTH release, and glucocorticoidreceptor antagonists.
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What is Primary hyperaldosteronism and two frequent causes
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A syndrome characterised by increased secretion of aldosteronefrom the adrenal glands, resulting in
–Hypertension –Hypokalaemia –Suppression of plasma reninactivity The most common cause of secondary hypertension (0.05-2% of hypertensive patients) Two most frequent causes –Aldosteroneproducing adenoma (Conn’s syndrome) •50-60% of cases –Bilateral adrenal hyperplasia (idiopathic hyperaldosteronismor IHA) •40-50% of cases 26 |
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what is normal regulation of Aldosterone
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Primary hyperaldosteronism
Treatment |
–Conn’s syndrome
•unilateral adrenalectomyis curative –Hypertension resolves slowly over 3 to 6 months in a majority of patients –Some have persistent hypertension –Bilateral adrenal hyperplasia •surgery often not an option –Aldosteroneantagonists (spironolactone12.5-200mg daily) will usually control blood pressure, and correct hypokalaemiaand alkalosis –Amiloridemay be used if spironolactonenot tolerated |
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What is Addison’s Disease
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•Addison's disease is an insidious, usually progressive hypofunctioningof the adrenal cortex. It produces various symptoms, including hypotension and hyperpigmentation, and can lead to adrenal crisis with cardiovascular collapse.
29 Addison’s Disease Diagnosis is clinical and by finding elevated plasma ACTH with low plasma cortisol. Treatment depends on the cause but generally includes hydrocortisone and sometimes other hormones. |
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Aetiology addisons disease
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About 70% of cases are due to idiopathic atrophy of the adrenal cortex, probably caused by autoimmune processes.
•The remainder result from destruction of the adrenal gland by granuloma(eg, TB), tumor, amyloidosis, hemorrhage, or inflammatory necrosis. •Hypoadrenocorticismcan also result from administration of drugs that block corticosteroid synthesis –(eg, ketoconazole). •Addison's disease may coexist with diabetes mellitus or hypothyroidism in polyglandulardeficiency syndrome |
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Addison’s Disease-Signs & Symptoms
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Diagnosis –Laboratory Findings34
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Biochemistry
•Serum Na < 135 mEq/L •Serum K > 5 mEq/L •Ratio of serum Na:K < 30:1 •Plasma glucose, fasting < 50 mg/dL(< 2.78 mmol/L) •Plasma HCO3 < 15–20 mEq/L •BUN > 20 mg/dL (> 7.1 mmol/L) Haematology •Hct Elevated •WBC count Low •Lymphocytes Relative lymphocytosis •Eosinophils Increased •Imaging Evidence of Calcification in adrenal areas Renal TB Pulmonary TB |
•ACTH stimulation test (Synacthentest)
–Stimulation of cortisolrelease indicates adequate adrenal function –Undetectable levels, both basally and particularly in response to corticotropin-releasing hormone (CRH), suggest a primary adrenal cause. –High levels suggest a pituitary cause |
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Adrenal crisis:what is it
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•Adrenal crisis is characterized by profound asthenia; severe pain in the abdomen, lower back, or legs; peripheral vascular collapse; and, finally, renal shutdown with azotemia.
•Body temperature may be low, although severe fever often occurs, particularly when crisis is precipitated by acute infection. •A significant number of patients with partial loss of adrenal function (limited adrenocorticalreserve) appear well but experience adrenal crisis when under physiologic stress (eg, surgery, infection, burns, critical illness). •Shock and fever may be the only signs. 36 |
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Cause of adrenal crisis
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treatment of adrenal crisis
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addisons diesease management
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Hydrocortisone or cortisone acetate, are usually used in treating Addison’s disease. Although both these drugs have shortplasmahalf-lives, biological action is prolonged, so that twice daily therapy is generally satisfactory. To reflect normal diurnal variation, two-thirds of the total glucocorticoiddose is generally given in the morning and one-third in the afternoon.
•For a standard upper limit regimen for routine maintenance therapy, use •cortisone acetate OR hydrocortisone 20 to 30 mg orally, per day in divided doses (2/3 morning, 1/3 afternoon) •Even at these doses, glucocorticoidtherapy may be excessive and can occasionally cause Cushingoidfeatures, osteoporosis and glucose intolerance. |
•Glucocorticoids with minimal mineralocorticoidactivity (egprednisolone, dexamethasone) are not recommended for routine replacement. However, if a longer-acting glucocorticoidis preferred, the afternoon dose of cortisone acetate or hydrocortisone may then be substituted with oral dexamethasone 125 micrograms. Even this dose, combined with the recommended morning glucocorticoiddoses may cause Cushingoidfeatures. Dexamethasone is best avoided in children as its prolonged action may impair growth.
•Most patients are better controlled with daily / alternate day therapy with fludrocortisone. The dose may vary considerably from 100 micrograms weekly to 300 micrograms daily, depending on salt intake, activity, climate and renal function. Acute adjustments of mineralocorticoidtherapy are generally not required for stress or intercurrentillness. Adequate mineralocorticoidreplacement generally allows good control at lower glucocorticoiddosage, thus minimising the long-term adverse effects of glucocorticoidexcess. |
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addisons diesease management
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Hydrocortisone or cortisone acetate, are usually used in treating Addison’s disease. Although both these drugs have shortplasmahalf-lives, biological action is prolonged, so that twice daily therapy is generally satisfactory. To reflect normal diurnal variation, two-thirds of the total glucocorticoiddose is generally given in the morning and one-third in the afternoon.
•For a standard upper limit regimen for routine maintenance therapy, use •cortisone acetate OR hydrocortisone 20 to 30 mg orally, per day in divided doses (2/3 morning, 1/3 afternoon) •Even at these doses, glucocorticoidtherapy may be excessive and can occasionally cause Cushingoidfeatures, osteoporosis and glucose intolerance. |
•Glucocorticoids with minimal mineralocorticoidactivity (egprednisolone, dexamethasone) are not recommended for routine replacement. However, if a longer-acting glucocorticoidis preferred, the afternoon dose of cortisone acetate or hydrocortisone may then be substituted with oral dexamethasone 125 micrograms. Even this dose, combined with the recommended morning glucocorticoiddoses may cause Cushingoidfeatures. Dexamethasone is best avoided in children as its prolonged action may impair growth.
•Most patients are better controlled with daily / alternate day therapy with fludrocortisone. The dose may vary considerably from 100 micrograms weekly to 300 micrograms daily, depending on salt intake, activity, climate and renal function. Acute adjustments of mineralocorticoidtherapy are generally not required for stress or intercurrentillness. Adequate mineralocorticoidreplacement generally allows good control at lower glucocorticoiddosage, thus minimising the long-term adverse effects of glucocorticoidexcess. |
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addisons disease- when to increase treatment
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•During significant intercurrentillness, glucocorticoiddosage should be doubled, and if necessary given parenterally. The dose can be doubled for 2 to 3 days without adverse effect. An increased dose is also appropriate after physical trauma, and may be required after emotional stress.
•Any features of impending adrenocorticalcrisis (egnausea, vomiting, abdominal pain) suggest the need for parenteral hydrocortisone therapy. |
when pregant keep taking doses which may need to be increased in third semester.
When hospitalised - UV hydrocortisone usually inidicated - doses 50 to 100mg twice daily or every 8 hours depending on 'stress' involved |
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addisons disease- when to increase treatment
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•During significant intercurrentillness, glucocorticoiddosage should be doubled, and if necessary given parenterally. The dose can be doubled for 2 to 3 days without adverse effect. An increased dose is also appropriate after physical trauma, and may be required after emotional stress.
•Any features of impending adrenocorticalcrisis (egnausea, vomiting, abdominal pain) suggest the need for parenteral hydrocortisone therapy. |
when pregant keep taking doses which may need to be increased in third semester.
When hospitalised - UV hydrocortisone usually inidicated - doses 50 to 100mg twice daily or every 8 hours depending on 'stress' involved |
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Corticosteroids
Adrenal suppression |
•chronic use of corticosteroids can cause adrenal suppression; consider need for withdrawing treatment gradually as abrupt withdrawal can result in adrenal crisis
•risk of adrenal suppression depends on many factors and is difficult to predict; doses <7.5 mg daily of prednisolone or equivalent or treatment for <3 weeks are unlikely to cause adrenal suppression; if unsure seek specialist endocrinology advice before stopping corticosteroids •minimise the risk of adrenal suppression by giving corticosteroid doses in the morning •adrenal response may be depressed for >1 year after corticosteroids are stopped; corticosteroids may be needed during periods of stress |
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Corticosteroids
Adrenal suppression |
•chronic use of corticosteroids can cause adrenal suppression; consider need for withdrawing treatment gradually as abrupt withdrawal can result in adrenal crisis
•risk of adrenal suppression depends on many factors and is difficult to predict; doses <7.5 mg daily of prednisolone or equivalent or treatment for <3 weeks are unlikely to cause adrenal suppression; if unsure seek specialist endocrinology advice before stopping corticosteroids •minimise the risk of adrenal suppression by giving corticosteroid doses in the morning •adrenal response may be depressed for >1 year after corticosteroids are stopped; corticosteroids may be needed during periods of stress |
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addisons diesease management
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Hydrocortisone or cortisone acetate, are usually used in treating Addison’s disease. Although both these drugs have shortplasmahalf-lives, biological action is prolonged, so that twice daily therapy is generally satisfactory. To reflect normal diurnal variation, two-thirds of the total glucocorticoiddose is generally given in the morning and one-third in the afternoon.
•For a standard upper limit regimen for routine maintenance therapy, use •cortisone acetate OR hydrocortisone 20 to 30 mg orally, per day in divided doses (2/3 morning, 1/3 afternoon) •Even at these doses, glucocorticoidtherapy may be excessive and can occasionally cause Cushingoidfeatures, osteoporosis and glucose intolerance. |
•Glucocorticoids with minimal mineralocorticoidactivity (egprednisolone, dexamethasone) are not recommended for routine replacement. However, if a longer-acting glucocorticoidis preferred, the afternoon dose of cortisone acetate or hydrocortisone may then be substituted with oral dexamethasone 125 micrograms. Even this dose, combined with the recommended morning glucocorticoiddoses may cause Cushingoidfeatures. Dexamethasone is best avoided in children as its prolonged action may impair growth.
•Most patients are better controlled with daily / alternate day therapy with fludrocortisone. The dose may vary considerably from 100 micrograms weekly to 300 micrograms daily, depending on salt intake, activity, climate and renal function. Acute adjustments of mineralocorticoidtherapy are generally not required for stress or intercurrentillness. Adequate mineralocorticoidreplacement generally allows good control at lower glucocorticoiddosage, thus minimising the long-term adverse effects of glucocorticoidexcess. |
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addisons disease- when to increase treatment
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•During significant intercurrentillness, glucocorticoiddosage should be doubled, and if necessary given parenterally. The dose can be doubled for 2 to 3 days without adverse effect. An increased dose is also appropriate after physical trauma, and may be required after emotional stress.
•Any features of impending adrenocorticalcrisis (egnausea, vomiting, abdominal pain) suggest the need for parenteral hydrocortisone therapy. |
when pregant keep taking doses which may need to be increased in third semester.
When hospitalised - UV hydrocortisone usually inidicated - doses 50 to 100mg twice daily or every 8 hours depending on 'stress' involved |
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Corticosteroids
Adrenal suppression |
•chronic use of corticosteroids can cause adrenal suppression; consider need for withdrawing treatment gradually as abrupt withdrawal can result in adrenal crisis
•risk of adrenal suppression depends on many factors and is difficult to predict; doses <7.5 mg daily of prednisolone or equivalent or treatment for <3 weeks are unlikely to cause adrenal suppression; if unsure seek specialist endocrinology advice before stopping corticosteroids •minimise the risk of adrenal suppression by giving corticosteroid doses in the morning •adrenal response may be depressed for >1 year after corticosteroids are stopped; corticosteroids may be needed during periods of stress |
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drugs that interact with steroids
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