Password recovery. Recover your password. Wednesday, July 15, Related Posts: You can search for other related posts. OnlineMedEd Whiteboard Snapshot Connect with. Barbara Hansen etc. ZAlerts allow you to be notified by email about the availability of new books according to your search query. A search query can be a title of the book, a name of the author, ISBN or anything else.
Read more about ZAlerts. Free ebooks since Europe Part of Z-Library project. Language: english File: PDF, Hello everyone, so below you will find what resources I have used, how I have utilized those resources, and how Upload a file! Share your ebooks and files. Macroadenomas can obstruct the pituitary stalk, increasing prolactin release by blocking dopamine transport from hypothalamus stalk effect. Other examples are tumors such as craniopharyngioma, meningioma, and dysgerminoma; empty sella; and trauma.
Hyperprolactinemia can also occur with decreased inhibitory action of dopamine. Tricyclic antidepressants, narcotics, cocaine, SSRIs, and risperidone can also cause increased prolactin. Stimuli that overcome the normal dopamine inhibition can also lead to hyperprolactinemia. An example of this is primary hypothyroidism resulting in an increase in thyrotropin-releasing hormone [TRH] and subsequently an increase in prolactin release.
Clinical Presentation. Men typically do not develop galactorrhea. Women are detected earlier because of menstrual symptoms. Hence, microadenomas are more common in women. Always exclude states such as pregnancy, lactation, hypothyroidism and medications before starting the work-up of hyperprolactinemia. Prolactinomas may co-secrete growth hormone GH. Treat initially with cabergoline or bromocriptine a dopamine-agonist , which will reduce prolactin level in hyperprolactinemia.
Dopamine normally inhibits prolactin release. Use radiation therapy if drug therapy and surgery are ineffective at reducing tumor size and prolactin level.
Which of the following therapeutic options is most appropriate in the management of prolactinoma? Acromegaly called gigantism in children is a syndrome of excessive secretion of growth hormone GH. Rarely ectopic tumors can produce growth hormone-releasing hormone GHRH and cause this syndrome. Clinical Findings. GH excess occurs most frequently around decades The following findings may be seen.
Enlargement of the hands and feet, coarsening of facial features, and thickened skin folds; increase in shoe, hat, glove, and ring size. Enlarged nose and mandible prognathism and separation of teeth , sometimes causing underbite. Interstitial edema, osteoarthritis, and entrapment neuropathy carpal tunnel syndrome.
Menstrual problems common due to co-secretion of prolactin by GH-producing tumor. Metabolic changes, i. The best initial test is IGF-1 level, which is significantly elevated. Normally, glucose load should completely suppress levels of GH. Measurement of insulin-like growth factor IGF or somatomedin correlates with disease activity.
Radiologic studies such as MTI and CT are used to localize the tumor but should be done only after GH excess is documented biochemically. The objectives are to decrease GH levels to normal, stabilize or decrease tumor size, and preserve normal pituitary function.
Transsphenoidal surgery provides a rapid response. Primary treatment is surgery. Somatostatin analogues are the drugs of choice. Octreotide is the best medical therapy for acromegaly. The main side effect of concern with somatostatin analogues is cholestasis, leading to cholecystitis.
Pegvisomant is a growth hormone analogue which antagonizes endogenic GH by blocking peripheral GH binding to its receptor in the liver. Important to note, pegvisomant is a second-line agent. Complications of acromegaly can arise from pressure of the tumor on the surrounding structures or invasion of the tumor into the brain or sinuses.
Other complications include cardiac failure most common cause of death in acromegaly , diabetes mellitus, cord compression, and visual field defects. Hypopituitarism is partial or complete loss of anterior function that results from any lesion which destroys the pituitary or hypothalamus or which interferes with the delivery of releasing and inhibiting factors to the anterior hypothalamus.
Large pituitary tumors, or cysts, as well as hypothalamic tumors craniopharyngiomas, meningiomas, gliomas can lead to hypopituitarism. Pituitary adenomas are the most common cause of panhypopituitarism; the mass compresses the gland, causing pressure, trauma, and necrosis.
Pituitary apoplexy is a syndrome associated with acute hemorrhagic infarction of a preexisting pituitary adenoma, and manifests as severe headache, nausea or vomiting, and depression of consciousness. It is a medical and neurosurgical emergency. Inflammatory diseases can lead to hypopituitarism: granulomatous diseases sarcoidosis, tuberculosis [TB], syphilis , eosinophilic granuloma, and autoimmune lymphocytic hypophysitis usually associated with other autoimmune diseases such as Hashimoto thyroiditis and gastric atrophy.
Trauma, radiation, surgery, infections, and hypoxia may also damage both the pituitary and hypothalamus. Vascular diseases such as Sheehan postpartum necrosis initial sign being the inability to lactate and infiltrative diseases including hemochromatosis and amyloidosis may induce this state as well. Stroke can also damage these cells. The following hormones appear in the order in which they are lost in hypopituitarism. Gonadotropin deficiency LH and FSH can occur in women and lead to amenorrhea, genital atrophy, infertility, decreased libido, and loss of axillary and pubic hair.
In men, decreased LH and FSH results in impotence, testicular atrophy, infertility, decreased libido, and loss of axillary and pubic hair. GH deficiency occurs next and is not clinically detectable in adults, though it may manifest as fine wrinkles and increased sensitivity to insulin hypoglycemia.
GH deficiency gives an asymptomatic increase in lipid levels and a decrease in muscle, bone, and heart mass. It also may accelerate atherosclerosis, and it increases visceral obesity. Thyrotropin TSH deficiency results in hypothyroidism with fatigue, weakness, hyperlipidemia, cold intolerance, and puffy skin without goiter.
Adrenocorticotropin ACTH deficiency occurs last, and results in secondary adrenal insufficiency caused by pituitary disease. There is decreased cortisol, which results in fatigue, decreased appetite, weight loss, decreased skin and nipple pigment, and decreased response to stress as well as fever, hypotension, and hyponatremia.
Electrolyte changes like hyperkalemia and salt loss are minimal in secondary adrenal insufficiency because aldosterone production is mainly dependent on the renin-angiotensin system.
ACTH deficiency does not result in the salt wasting, hyperkalemia, and death that are associated with aldosterone deficiency. The most reliable stimulus for GH secretion is insulin-induced hypoglycemia. After injecting 0. This is why a provocative test is used. Arginine infusion can also stimulate growth hormone release. Measure GH levels after infusing arginine.
This is less dangerous because it does not lead to hypoglycemia. To diagnose ACTH deficiency, basal cortisol levels may be preserved the problem could be only in response to stress. Insulin tolerance test is diagnostic and involves giving 0.
Metyrapone tests for decreased ACTH production. Metyrapone blocks cortisol production, which should increase ACTH levels. A failure of ACTH levels to rise after giving metyrapone would indicate pituitary insufficiency. Cosyntropin ACTH stimulation may give abnormally low cortisol output if pituitary insufficiency has led to adrenal atrophy. Management of hypopituitarism involves treating the underlying causes. Multiple hormones must be replaced, but the most important is cortisol.
ESS is in the differential diagnosis of enlarged sella caused by pituitary tumors. In ESS, the sella has no bony erosion. It is caused by herniation of the suprasellar subarachnoid space through an incomplete diaphragma sellae.
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