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51 Cards in this Set
- Front
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This is when there is elevated serum prolactin.
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Hyperprolactinemia
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This is the most common pituitary hypersecretion syndrome in both men and women.
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Hyperprolactinemia
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What are 9 causes of Hyperprolactinemia?
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1. Decreased dopaminergic inhibition
2. Hypothyroidism 3. Lacotroph adenoma (Prolactinoma) 4. Estrogen 5. Stress 6. Nipple Stimulation 7. Idiopathic 8. Macroprolactinemia 9. Chronic renal failure |
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The following are responsible for what kind of cause of hyperprolactinemia?
Hypothalamic or pituitary disease or trauma Drugs: antipsychotics, antidepressants, opiates, cimetidine, certain antihypertensives |
Decreased dopaminergic inhibition
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Correction of this cause of hyperprolactinemia can result in prolactin levels normalizing.
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Hypothyroidism
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This accounts for 30-40% of pituitary adenomas, and about 10% co-secrete growth hormone.
May be micro- (slight elevation of PRL) or macroadenomas (significant elevation of PRL) |
Lactotroph Adenoma (Prolactinoma)
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This is when hyperprolactinemia is caused by pregnancy of OCP, women have greater PRL response to stress than men, may directly affect transcription in lactotroph.
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Estrogen
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This can be either physical or psychological and it is a cause of hyperprolactinemia.
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Stress
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This can cause hyperporlactinemia and can be from sucking, injury, shingles, trauma etc.
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Nipple Stimulation
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This is a cause of hyperprolactinemia that may be associated with non-visible microadenomas.
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Idiopathic
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This is when there is big PRL leading to decreased clearance of PRL causing hyperprolactinemia.
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Macroprolactinemia
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This is when there is decreased clearance of prolactin as the cause of hyperprolactinemia.
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Chronic Renal Failure
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What are the manifestations of excess prolactin?
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Hypogonadotropic Hypogonadism
Mammary Gland Effects |
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When you have enlargement of the pituitary associated with hyperprolactinemia, this can manifest as what?
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Headache and visual changes, ie. bitemporal hemianopsia
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Abnormal prolactin levels associated with hyperprolactinemia can manifest as what in pregnancy?
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Cardiomyopathy
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The excess prolactin in hyperprolactinemia that manifest as hypogonadotropic hypogonadism can do what in men?
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Decreaed libido, erectile dysfunction, infertility, decreased muscle mass, osteoporosis
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The excess prolactin in hyperprolactinemia that manifest as hypogonadotropic hypogonadism can do what in pre-menopausal women?
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Amenorrhea, infertility, osteoporosis
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The excess prolactin in hyperprolactinemia that manifest as hypogonadotropic hypogonadism can do what in post-menopausal women?
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Already hypogonadal, so wouldn't notice it.
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With the manifestations of hyperprolactinemia, what are the mammary gland effects in men?
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Gynecomastia or galactorrhea (rarely)
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With the manifestations of hyperprolactinemia, what are the mammary gland effects in pre-menopausal women?
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May get galactorrhea
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With the manifestations of hyperprolactinemia, what are the mammary gland effects in post menopausal women?
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most do not get galactorrhea because also hypoestrogenic.
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When you are measuring serum prolactin this can happen if there is a macroprolactinoma, ultimately resulting in test disruption, but visual field defects will still usually show up.
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Hook effect with extreme elevations of prolactin
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When you do an MRI in the presence of hyperprolactinemia, what are the two options you are looking for?
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1. If mass is present - check levels of all other pituitary hormones
2. If no mass and no other apparent cause then make diagnosis of idiopathic hyperprolactinemia. |
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What is the first line tx of hyperprolactinemia?
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Dopamine agonist - ex. carbergolide
Always try this first Adenoma may shrink Prolactic levels often come down Fertility may return - let patient know pregnancy may occur |
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If there is no effect from using a dopamine agonist to tx hyperprolactinemia what is the next step?
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Trans-sphenoidal surgery.
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What are the three main metabolic actions of growth hormone?
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1. Increase fat breakdown
2. Decrease glucose uptake by skeletal muscles, resulting in glucose for the brain. 3. Increased gluconeogenesis by the liver. |
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What are the three growth promoting actions of IGF-1?
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1. Increased cell division
2. Increased protein synthesis 3. Increased bone growth (thickness and length) |
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What are three main causes of growth hormone deficiency?
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1. Hypothalamic dysfunction (lack of GHRH, so GH low)
2. Pituitary defect (lack of GH, so GH low) 3. Unresponsiveness to GH (GH high) |
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What are the effects of growth hormone deficiency?
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Dwarfism if prior to growth plate fusion
May be symptomatic in an adult. |
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If this is congenital it will show up as low birth size, hypoglycemia, prolonged jaundice, length 3-4 standard deviations below mean at 6-12 months.
In Adults, this is seen as increased fat, decreased lean body mass, decreased bone minteral density and possibly cardiovascular disease, impaired psychological function. |
Effects of GH deficiency
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How do you evaluate for GH deficiency?
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There is no gold standard
Rule out other causes of growth failure (ex. hypothyroidism) Obtain IGF-1 level (decreased) Perform GH stimulation test MRI |
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How do you TX GH deficiency in children?
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Once diagnosis is confirmed begin treatment with growth hormone replacement and continue until linear growth ceases.
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How do you treat GH deficiency in adults?
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Growth hormone replacement is usually reserved for patients with severe symptoms.
GH repalcement leads to decreased fat, increased lean body mass, and increased bone mineral density in men (but not in women) |
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What are four causes of growth hormone excess?
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1. Pituitary adenoma (macroadenoma in acromegaly)
2. GHRH excess (gigantism) 3. Ectopic GH or GHRH 4. Disruption of neuroendocrine control of GH |
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What are the effects of GH excess?
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Pituitary gigantism if prior to growth plat closure.
Acromegaly if after growth plate closure. |
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This may occur at any age, rare, typically sporadic. Growth in height typically preceded by weight gain. Height exceeds +3 to +4 standard deviations from mean, and may grow taller than 8ft. May also see thickening of bones in face or extremities (but more common in acromegaly). Rule out other causes of rapid growth (ex. hyperthyroidism).
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Pituitary gigantism.
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How do you diagnose pituitary gigantism?
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1. Screen with IGF-1 (will be increased)
2. Gold standard for making diagnosis is GH suppression test - measure GH response to oral glucose load. 3. Confirm with MRI 4. Trans-sphenoidal surgery is tx of choice. 5. Meds include somatostatin analogs (octreotide), dopamine agonists (bromocriptine), and GH receptor antagonist (pegvisomant) |
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What is the major cause of mortality in acromegaly?
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Hypertension, Cardiomegaly, CHF
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How do you diagnose acromegaly?
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Screen with IGF-1:
IGF-1 normal then active acromegaly is ruled out. IGF-1 elevated then move to GH suppression test. GH suppression test (oral glucose) -GH suppressed lead to active acromegaly ruled out. -GH inadequately suppressed leads to a move to MRI. Pituitary MRI Adenoma leads to treat Normal, small, or hyperplastic leads to check for extrapituitary acromegaly lead to CT of chest and abdomen and measure GHRH levels. |
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How do you TX acromegaly?
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1. Transphenoidal surgery is tx of choice.
2. Meds alone or with surgery - somatostatin analogs work best: Octreotide, lanreotide. Dopamine agonists: Cabergoline, bromocriptine. GH receptor antagoinst (Pegvisomant) - For inadequate response to drug intolerance. Repeat surgery or radiotherapy if still inadequate response. |
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What is involved with the long term monitoring of acromegaly?
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Every 3-4 months following initial tx - clinical exam, IGF-1, GH suppression test.
MRI - yearly for several years Visual field assessment Colonoscopy every 3-4 years for patients over 50 or patients with over 3 skin tags. |
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This is a partial or complete deficiency of or resistance to antidiuretic hormone - ADH - Vasopressin
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Diabetes insipidus
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This is when you have polyuria with large volume of dilute urine. Nocturia may be noticed first, and then new onset nocturia in absence of another cause could be the first clue to this.
Polydipsia If fluid intake is inadequate leads to hypernatremia. Hyperuricemia (due to decreased clearance) |
Diabetes insipidus (DI)
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This is when there is complete or partial absence of ADH - it is idipathic (autoimmune - accounts for 30% of cases), Familial DI, Wolfram syndrome, Anorexia nervosa, post Supra ventricular tachycardia, and damage to hypothalamus from neurosurgery, other trauma, tumor, hypoxia, or infiltrative disease.
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Central Diabetes insipidus
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This is when you have vasopressinase being secreted by the placenta during pregnancy, breaks down ADH.
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Vasopressinase induced DI
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This can be hereditary - mutation in gene for the vasopressin receptor or the vasopressin sensitive aquaporin.
This can be acquired - Chronic lithium therapy, persistant hypercalcemia or hypokalemia, post op craniopharyngeoma, drugs-demeclocycline, cidofovir, foscarnet, kidney disease - obstruction, infection, sickle cell disease/trait, amyloidosis, myeloma, Sjogren's syndrome. |
Nephrogenic DI
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How do you diagnose central DI?
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Water restriction leads to increase in plasma osomolarity but there is no ADH, so uring osmolarity is inappropriately low. DdAVP leads to complete or partial improvement.
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How do you diagnose Nephrogenic DI?
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Water restriction leads to increase in plasma osmolarity, plasma ADH is high but urine osmolarity is inappropriately low. DdAVP lead to either no improvement or only partial improvement.
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What is the TX for central DI?
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Desmopressin is most effective
IV Fluids - must give desmopressin before giving IV fluids |
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What is TX for vasopressinase induced DI?
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dDAVP
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What is TX for nephrogenic DI?
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Correct underlying cause if identified.
Low solute diet - decrease solute excretion - in adults low Na-low protein diet, in kids, low Na diet. Prevention of urinary tract dilation Children with complex congenital syndrome start with NSAIDS All other children and adults start with a thiazide. |