Posterior Pituitary Flashcards

1
Q

where is ADH produced?

A

supraoptic* and paraventricular nuclei of the anterior hypothalamus

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2
Q

where is ADH released?

A

posterior pituitary

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3
Q

to what kind of receptor does ADH bind to regulate serum osmolarity?

A

V2 receptors

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4
Q

where does ADH cause aquaporin channels to be inserted into?

A

principal cells of the renal collecting duct

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5
Q

primary and secondary regulation of ADH

A

primary: osmoreceptors in hypothalamus
secondary: hypovolemia

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6
Q

SIADH: pathogenesis

A

excessive release of ADH from the posterior pituitary causing excessive free water retention –> hyponatremia, urine osmolality > serum osmolality

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7
Q

SIADH: consequences of severe hyponatremia

A

cerebral edema, seizures

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8
Q

what drug can cause SIADH?

A

cyclophosphamide (chemo)

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9
Q

what cancer can cause ectopic ADH to be released, causing SIADH?

A

small cell lung cancer

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10
Q

cardinal feature of SIADH

A

euvolemic hyponatremia

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11
Q

what measurements are low in SIADH?

A

serum sodium and serum osmolality

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12
Q

treatment for SIADH (4)

A

fluid restriction, IV hypertonic saline, conivaptan and tolvaptan (ADH receptor (V2) antagonists), demeclocyline (tetracycline antibiotic used as ADH antagonist)

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13
Q

why is it important to correct SIADH slowly?

A

osmotic demyelination syndrome: rapid resolution of sodium levels can cause water to leave brain cells too quickly, leading to osmotic shrinkage that results in severe damage to the myelin sheath of axons

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14
Q

diabetes insipidus: pathogenesis

A

characterized by intense thirst and polyuria with inability to concentrate urine due to lack of ADH (central) or renal resistance to ADH activity (nephrogenic)

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15
Q

what is central (neurogenic) diabetes insipidus and what are some etiologies?

A

deficient production/release of ADH; autoimmune, trauma, surgery, ischemic encephalopathy, pituitary tumors

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16
Q

what is nephrogenic diabetes insipidus and what are some etiologies?

A

renal resistance to ADH; hereditary (ADH receptor mutation), hypercalcemia, demeclocycline (ADH antagonist), lithium

17
Q

describe the water deprivation test and distinguish the findings between central and nephrogenic diabetes insipidus

A

no water intake for 2-3 hours followed by hourly measurements of urine volume and osmolarity and plasma Na+ concentration and osmolarity. ADH analog (desmopressin) is administered if normal values are not clearly reached.

central: >50% increase in urine osmolality only after administration of desmopressin
nephrogenic: minimal change in urine osmolality, even after administration of desmopressin

18
Q

treatment for diabetes insipidus: central vs. nephrogenic

A

central: hydration, intranasal desmopressin
nephrogenic: hydration, HCTZ, indomethacin (NSAID), amiloride