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MNE > Posterior Pituitary > Flashcards

Posterior Pituitary Flashcards

1
Q

Posterior Pituitary Peptide structure

A
  1. Both are 9AA (differ only at 2AA)

ADH: Phe, Arg// Oxy: Ile, Leu

  1. Internal disulfide bond
  2. Possible progenitor gene: vasotocin (expressed in pineal gland)
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2
Q

Function & physiological advantages of modifications to posterior pituitary peptide hormones

A
  1. amidated glycine at carboxy end protects peptide from degradation
  2. amino terminal end is protected by a disulfide bond
  3. Prolongs half-life
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3
Q

Vasopressin receptors (3)

A
  1. V2: Gαs –> adenylyl cyclase
    * distal and collecting tubules
  2. V1a: Gαq –> phospholipase C
    * smooth muscle; vasoconstriction
  3. V1b: Gαq –> phospholipase C
    * anterior pituitary; +ACTH
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4
Q

Circumventricular organs (6)

A
  1. OVLT: organum vasculosum laminae terminalis

SFO: subfornical organ

  1. Location of cerebral osmoreceptors
  2. Responds to changes in blood osmolality (less than 1%)
  3. Windows through the blood brain barrier; sample salt and solute concentrations in blood
  4. Rich in osmoreceptors
  5. Send positive signals to magnocellular neurons
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5
Q

Non-osmotic receptor afferents (3)

A

Baroreceptors (cardiovascular input)

  1. Mainly inhibitory, negative signals
  2. As blood pressure increases, secretion of ADH decreases
  3. Senses changes in volume
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6
Q

Osmotic threshold

A

280 mOsm/kg

Minimum osmolality in which vasopressin secretion will occur

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7
Q

Regulation of vasopressin secretion

A
  1. Linear relationship with osmolality
  2. Maximal antidiuresis: 5pg/ml plasma ADH
    - above this, can no longer concentrate urine further
    - Signals thirst
  1. Linear relationship with uring osmolality
  2. Maximal/normal concentrated urine:

800-1000 mOsm/kg

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8
Q

Osmoreceptor-vasopressin-renal reflex (4)

  1. 1% Increase TBW
  2. 2% Increase TBW
  3. 2% Decrease TBW
  4. Increase in plasma osmolality
A
  1. 1% increase TBW: 1/2 decrease plasma ADH & 1/2 urine osmolality
  2. 2% increase TBW- Maximal ADH suppression:

low plasma ADH & low urine osmolality (max dilute)

  1. 2% decrease TBW- Maximal concentration of urine:

2x increase plasma ADH & high urine osmolality

  1. Increase Uos: slight increase in ADH & urine osmolality

1/3 increase in ADh = 1/2 amount of urine

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9
Q

Antiduresis & Thirst

A
  1. Above maximal diuresis, additional ADH secreted, but no increase in urine concentration
  2. Avoid dehydration by stimulating osmoreceptors (5-10 mOsm/kg) FOR THIRST
  3. Cold-sensitive Oropharyngeal receptors inhibit ADH secretion
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10
Q

Baroreceptor activation

A
  1. Sources: left atrium, caroic sinus, aortic arch
  2. Activated when hypervolemic and hypertensive:

INHIBITS ADH secretion

  1. At a given BP, relationship remains linear
  2. As BP rises, osmotic threshold increases = more changes in plasma osm to secrete ADH
  3. Hypovolemic and hypotensive - steep linear
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11
Q

Vasopressin action

A
  1. ADH binds to V2 receptors
  2. Activate adenylate cyclase: ATP –> cAMP
  3. Protein kinase A
  4. Fusion of aquaporins (AQP2) to apical membrane

Facilitated diffusion

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12
Q

Excretion of sodium in kidney

A
  1. Low blood volume –> increase renin
  2. Angiotensinogen –> angiotensin I
  3. ACE converts to angiotensin II
  4. increase ALDOSTERONE
  5. Na reabsorption; increase serum tonicity K excretion
  1. Can stimulate ADH secretion
  2. Angiotensin II stimulates vasoconstriction of smooth muscle
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13
Q

Atrial Natriuretic protein (ANP) (4)

A
  1. Activated by stress receptors in the heart
  2. Negative feedback on Renin secretion from kidney
  3. Causes increased GFR to ultimately decrease ADH secretion and decrease blood volume
  4. Vasorelaxation on vascular smooth muscle to decrease blood pressure
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14
Q

Central diabetes insipidus

&

Etiologies (4)

A
  1. Mutation in secreting biologically active ADH
    - gene mutation
    - improper processing
  2. Exretion of large volume of dilute urine that can’t be reduced by fluid intake; kidney can not concentrate urine

Etiologies: hypothalamic/pituitary tumor*(before/after surgery), idiopathic (spontaneous), histiocytosis, trauma*

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15
Q

Nephrogenic diabetes insipidus

(peripheral)

A
  1. Dysfunction at the level of the kidney
    - mutation in V2 receptor
    - mutation in aquaporin 2
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16
Q

Dipsogenic diabetes insipidus

&

Gestational diabetes insipidus

A
  1. chronic water drinkers; decrease in ADH secretion
  2. enzymes from placenta/uterus degrade ADH
    - transient: typically resolves at birth
17
Q

Oxytocin: secretion of milk

A
  1. Stimulated by sucking reflex
  2. Responds to olfactory, visual, and auditory stimuli
  3. Regulated by number of receptors present in tissue (myoepithelial cells)
  4. Ejection in mammary glands (vasoconstriction)

(prolactin stimulates milk production)

18
Q

Oxytocin: uterine contraction

A
  1. Occurs during parturition (child birth)
  2. progesterone levels fall at term of pregnancy
  3. Increase in estrogen + # OT receptors (myometrium)
  4. stimulates uterine contractions
19
Q

Oxytocin action

A
  1. Oxytocin binding stimluates:

Gαq –> PLC –> IP3 –> increase Ca –> contraction

uterus: +PLA2 –> free arachidonic acid –> prostaglandins –> soften, stretch cervix

20
Q

Oxytocin receptor antagonists

A
  1. Tocolysis goal: delaying or inhibiton of labor during the birth process
  2. Ex: Atosiban

*reviews show no more effective than placebo

MNE (16 decks)

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