Posterior Pituitary Flashcards

1
Q

all the names for ADH

A
  • arginine vasopressin (AVP)
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2
Q

posterior pituitary is formed by downward growth of axons and neurons from which nuclei

A
  • supraoptic

- paraventricular

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3
Q

precursors for vasopressin and oxytocin

A
  • V: propressophysin (cleaved to form vasopressin and neurophysin)
  • O: proopressophysin (cleaved to form oxytocin and neurophysin)
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4
Q

vasopressin and oxytocin are bonded to ______ prior to storage and release

A
  • neurophysin
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5
Q

action of oxytocin

A
  • stimulates contraction of uterine smooth muscle

- stimulates myoepithelial cells of mammary alveoli (milk ejection)

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6
Q

what stimulates release of oxytocin in the vagina and uterus

in the breast

A
  • distention

- suckling of breast (tactile stimulation)

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7
Q

action of ADH/AVP

A
  • holds onto water in DCT and collecting duct via cAMP and PKA
  • binds to V2 receptors to bring in AQP2
  • excretion of hypertonic urine
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8
Q

how does ADH/AVP regulate ACTH

A
  • increases CRH release which increases ACTH
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9
Q

tonicity of plasma/sodium concentration that stimulates release of ADH

A
  • increased tonicity or plasma concentration

- even a small rise in tonicity will increase ADH a lot!

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10
Q

hemodynamics that stimulates release of ADH

A
  • low pressure
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11
Q

hormones that stimulate release of ADH

horomones that inhibit release of ADH

A
  • beta adrenergic
  • AG II
  • prostaglandlins
  • ANP
  • alpha adrenergic
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12
Q

secretion of ADH is regulated by what receptors

A
  • osmoreceptors in the hypothalamus
  • volume receptors in the atrium of the heart
  • carotid baroreceptors in the neck
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13
Q

what is the most effective regulator of plasma ADH

A
  • osmolality
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14
Q

patients with ADH/AVP deficiency/insufficiency, have what symptoms

A
  • thirst
  • polydipsia
  • polyuria > 3L
  • nocturia
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15
Q

central DI causes

A
  • trauma
  • infiltrative disease
  • post surgery
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16
Q

nephrogenic DI causes

A
  • genetic - AVPR2 or AQP mutations
  • hypercalcemia
  • hypokalemia
  • drugs
  • renal disease
17
Q

difference in serum sodium and osmolality in central/nephrogenic DI versus primary polydipsia

A
  • high in DI

- normal/low in primary polydipsia

18
Q

what test do you use to distinguish DI from primary polydipsia

A
  • water deprivation test
19
Q

what test differentiates nephrogenic DI from central DI

how

A
  • DDAVP
  • in central DI, urine osmolality rises after given DDAVP
  • in nephrogenic DI, there is no response to DDAVNP because the kidneys are resistant to it
20
Q

ADH/AVP level in nephrogenic DI

A
  • high
21
Q

ADH/AVP level in central DI

A
  • low
22
Q

ADH/AVP level in primary polydipsia

A
  • low
23
Q

treatments for central DI

how do they work

A
  • DDAVP - analog of vasopressin with longer half life than vasopressin
  • synthetic AVP
  • chlorpropamide - potentiates effects of endogenous vasopressin. for patients with partial vasopressin deficiency
24
Q

treatments for nephrogenic DI

how do they work

A
  • HCTZ - decreases Na reabsorption so water and sodium will be excreted more equally
  • aimiloride - blocks lithium uptake in kidney (good for patients with lithium induced DI)
25
Q

SIADH is associated with which broad categories of disease

A
  • CNS disease
  • ectopic AVP/ADH production - small cell lung cancer
  • drugs
  • diseases of lung and mediastinum - PNA, TB
26
Q

diagnostic criteria for SIADH

A
  • hyponatremia with low plasma osmolality (too much water absorption)
  • urine osmolality > plasma osmolality
  • urine sodium > 20 mmol/L
  • euvolemic
27
Q

treatment of hyponatremia with no neurologic symptoms

A
  • fluid restriction
28
Q

treatment of hyponatremia with neurologic symptoms

danger of this

hyponatremia should be corrected by how many mEq/L per day

A
  • hypertonic saline
  • osmotic demyelination syndrome
  • over-rapid correction of sodium will cause swelling and necrosis of myelin sheaths around CNS neurons
  • 4-6 mEq/L per day
29
Q

why don’t we use isotonic saline to treat SIADH

A
  • will decrease sodium even further
30
Q

use of vaptans in SIADH

how long can you use them

A
  • block vasopressin receptors
  • excrete free water and improves serum sodium
  • short term use