Posterior pituitary Flashcards

1
Q

Source and targets of the post pituitary hormones

A

ADH: from supraoptic nucleus, target kidney and blood vessels; Oxytocin: paraventricular nucleus, target uterus and mammary glands

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2
Q

Fn of ADH

A

Kidney: increase permeability of collecting duct (bind G protein R, cAMP/PKA, (P)’s vesicles and release more aquaporins), Vasoconstriction reduces GFR; Pressor Action: Contraction of blood vessel smooth muscle (Only occurs at high concentrations (hemorrhage))

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3
Q

List the three stimuli for ADH release

A

Thirst Centre, Osmoreceptor (Dehydration -> shrinkage of the osmoreceptor neurons, more ADH, more thirst - much less ADH needed here), Baroreceptor (lower BP or BV, postural hypotension)

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4
Q

Describe the clinical manifestations of diabetes insipidus

A

Too little ADH (central diabetes insipidus) or abnormal ADHr in kidney (nephrogenic DI).

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5
Q

Causes of Central and nephrogenic diabetes insipidus

A

Central: Post-hypophysectomy, Post-trauma, Idiopathic, Suprasellar tumor, Infiltration, eg. sarcoidosis, histiocytosis, Familial. Nephrogenic: Congenital, Acquired (interstitial disease, lithium), Hypercalcemia

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6
Q

Differentiate between central diabetes insipidus, nephrogenic diabetes insipidus and primary polydipsia

A

Water deprivation test. Central DI: Uosm remains low after 8h but ↑ with vasopressin. Nephrogenic DI: Uosm remains low after 8h and no increase with vasopressin. Primary polydipsia: Uosm ↑ after 8 h of dehydration (>800 mOsm/l, urine output < 30 cc/hour). Graph.

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7
Q

Identify the diagnostic tests that may aid in diagnosis of diabetes insipidus

A

Serum Na, Serum and urine osmolality, Blood urea nitrogen and creatinine, Calcium and glucose, Water deprivation test (need close supervision), ADH measurement (expensive, not required to make the diagnosis), MRI (after confirmation)

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8
Q

Tx of Central DI

A

Desmopressin (DDAVP, nasal, oral or SC), Chlorpropamide (partial DI)

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9
Q

List the diagnostic criteria of SIADH

A

Syndrome of inappropriate ADH. Water retention. Common in the elderly and patients on anticonvulsants. Euvolemic hyponatremia. Mild hyponatremia, asymptomatic. Severe or rapid onset hyponatremia, confusion, lethargy, weakness, seizure, coma

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10
Q

Identify the common causes of SIADH

A

Increase hypothalamic production of ADH. CNS infection; CNS neoplasm; CNS trauma; CNS vascular events (stroke, hemorrhage); Drugs (antidepressant, narcotics); Pulmonary disease (pneumonia, TB); Ectopic production of ADH (Carcinoma (lung, pancreas)); Potentiation of ADH effect: Psychosis, Drugs (oral hypoglycemic agent, carbamazepine)

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11
Q

Classification of SIADH

A

Type A, erratic, unregulated release of ADH (no relation to plasma osmolality). Type B, modest and constant leak of ADH. Type C, downward resetting of osmostat (sodium 125 - 135 mmol/L). Type D, urine is concentrated even if ADH release is suppressed

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12
Q

Identify the medications that may be involved in SIADH

A

Water restriction (800 to 1200 cc depending on degree of hyponatremia). Hypertonic saline if severe (done with caution, aggressive treatment can lead to central pontine myelinolysis). Demeclocycline or lithium in chronic cases. Vasopressin antagonist

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13
Q

Fn of oxytocin

A

Uterus: Parturition, Clamping ruptured blood vessels, Restoration of uterine size. Mammary glands: Milk let-down. Bonding Behavior: Maternalism, Orgasm

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14
Q

Regulation of oxyctocin

A

Increase oxytocin from distention of the cervix at term of pregnancy and by uterine contraction during parturition. Positive feedback to PVN and SON for further oxytocin release

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