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Adrenal Disorders
Adrenal Disorders
aldosterone
cortisol
Sex hormones
1. Mineralocorticoids, mainly aldosterone 2. Glucocorticoids, primarily cortisol 3. Sex hormones, mainly dehydroepiandrosterone, a male sex hormone
Aldosterone
Aldosterone Effects
Site of aldosterone action is on the distal and collecting tubules of the kidney
i.
Promotes Na+ retention osmotic H2O retention increased ECF volumes increased blood pressure
Increase Plasma K+
Renin
Angiotensin II
Aldosterone
Cortisol
Cortisol Effects
i. Metabolic effects
stimulates hepatic gluconeogenesis inhibits glucose uptake and use by many tissues stimulates protein degradation in many tissues, especially muscle facilitates lipolysis
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Cortisol Effects
ii. Permissive actions
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Cortisol Effects
iii. Adaptation to stress
Stress is one of the major stimuli for increased cortisol secretion Increased pool of glucose, amino acids, and fatty acids is available for use in stressful situations
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Cortisol Effects
iv. Anti-inflammatory and immunosuppressive effects
o Pharmacological effect (at higher than normal concentrations) o Suppresses the bodys response to the disease o Useful in allergic disorders and organ transplant rejections o Precautions:
suppression of the normal inflammatory and immune responses negative-feedback effect (decreased ACTH adrenal atrophy) other side effects (high blood pressure, atherosclerosis)
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i.
i.
1. Mineralocorticoid Deficiency
Loss of sodium ions, chloride ions, and water in urine hyponatremia, decreased ECF volume shock Decreased renal secretion of K+ & H+ hyperkalemia, and mild acidosis
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i.
2. Glucocorticoid Deficiency
Disturbance of normal blood glucose concentration between meals Reduces mobilization of both proteins and fats from tissues depressing many other metabolic functions of the body Susceptibility to the deteriorating effects of different types of stresses (like infection)
Addisonian crisis: critical need for extra glucocorticoids and the associated severe debility in times of stress
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i.
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MSH; Melanocyte Stimulating Hormone
i.
Treatment
Small quantities of mineralocorticoids and glucocorticoids are administered daily.
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ii.
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ii.
Causes:
1. Adenomas of the anterior pituitary that secrete large amounts of ACTH, which then causes adrenal hyperplasia and excess cortisol secretion, (most common cause). 2. Abnormal function of the hypothalamus that causes high levels of corticotropin-releasing hormone (CRH), which stimulates excess ACTH release. 3. Ectopic secretion" of ACTH by a tumor elsewhere in the body, such as an abdominal carcinoma
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ii.
Causes:
4. Primary overproduction of cortisol by the adrenal glands (e.g., adenoma) o 25% of cases o Associated with reduced ACTH levels (cortisol feedback inhibition of ACTH secretion)
The dexamethasone test (synthetic glucocorticoid): large doses of dexamethasone leads to inhibition of ACTH in primary hyperadrenalism but not in pituitary adenomas
5.
When large amounts of glucocorticoids are administered over prolonged periods for therapeutic purposes
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ii.
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ii.
ii.
Treatment:
o Surgical removal/ radiation of pituitary o Drugs that block steroidogenesis o Drugs that inhibit ACTH secretion o Bilateral partial (or even total) adrenalectomy, followed by administration of adrenal steroids to make up for any insufficiency that develops
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Diagnosis:
Decreased plasma renin concentration
Na+ deprivation
Treatment:
Surgery Drugs against mineralocorticoid receptor
Renin
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The END
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