Posterior Pituitary

Question 1

What are the only hormones released from the posterior pituitary?

Answer 1

arginine vasopressin (ADH)
oxytocin

Question 2

Where are the cell bodies for the production of ADH and oxytocin located?

Answer 2

in the supraoptic nucleus and paraventricular nucleus of the hypothalamus

Question 3

What hormones can stimulate the release of ADH?

Answer 3

CRH and Ang II

Question 4

What is the main target tissue for ADH?

Answer 4

1. V2 receptors of the collecting duct
2. V1 receptors where they are able to contract vascular smooth muscle

Question 5

ECF osmolality is kept close to what number?

Answer 5

285 mOsm/kg

Question 6

What are some environmental factors that can suppress ADH?

Answer 6

ingesting ethyl alcohol or being in a weightless environment can suppress ADH

Question 7

What are levels of BNP sometimes used as a marker for and why?

Answer 7

circulating levels of BNP correlate well with degree of dilation in heart failure

Question 8

Where is ANP mainly found?

Answer 8

in the right atrium

Question 9

What are 2 stimuli for the release of ANP?

Answer 9

stretch, an action independent of nervous involvement

CHF and all fluid overload states

Question 10

MOA ANP?

Answer 10

increases sodium loss (natriuresis) and water loss by the kidney because of, in part, an increase in glomerular filtration rate due to the following:

• ANP mediated dilation of afferent arteriole
• ANP-mediated constriction of the efferent arteriole

Also increases sodium loss and water loss by kidney by inhibiting RAAS as well as reabsorption of sodium and water in collecting duct

Question 11

A normal ANP level is used to exclude what condition as a cause of dyspnea?

Answer 11

CHF

Question 12

What enzyme metabolizes ANP and BNP?

Answer 12

neprilysin

Question 13

S/E of neprilysin inhibitors.

Answer 13

Neprilysin is not selective for ANP and BNP and therefore can lead to lack of breakdown of bradykinin and Ang II

Question 14

What is central DI?

Answer 14

When sufficient ADH is not available to affect the renal collecting ducts

Question 15

What are some causes of central DI?

Answer 15

familial, tumors (craniopharyngioma), autoimmune, trauma

Question 16

Can pituitary trauma lead to transient DI?

Answer 16

yes

Question 17

How is CDI treated?

Answer 17

with DDAVP (desmopressin) or vasopressin

Question 18

What are the three ways hyponatremia can be classified?

Answer 18

hypovolemic, hypervolemic, clinically euvolemic

Question 19

What is hypovolemic hyponatremia? What are some conditions it is seen in?

Answer 19

decrease in sodium and water in the body but proportionately more sodium being lost than water.

indicates solute depletion (e.g. mineralocorticoid deficiency, diruetic abuse, renal disease, diarrhea, hemorrhage)

Question 20

What is hypervolemic hyponatremia? (What are associated conditions)

Answer 20

increase in total body sodium with an even greater increase in total body water. in (e.g, CHF, cirrhosis)

Question 21

What conditions is euvolemic hyponatremia associated with?

Answer 21

includes SIADH and primary (psychogenic) polydipsia; a clinically equivalent presentation may occur in glucocorticoid deficiency or hypothyroidism

Question 22

What is the MOA of sacubitril?

Answer 22

inhibits neprilysin

by inhibiting neprilysin, ANP and BN P levels remain elevated for longer periods of time > natriuresis, vasodilation, and reduced cardiac fibrosis and hypertrophy

Question 23

Why is sacubitril used in combination with valsartan?

Answer 23

because blocking neprilysin also increases Ang II, and valsartan helps to counteract the deleterious effects of high levels of Ang II. Although ANP/BNP can inhibit renin (and thus Ang II) in the setting of dilated hearts, their ability to inhibit renin is reduced and/ or absent (precise mechanism unknown)

Question 24

What are the side effects of sacubitril/valsartan?

Answer 24

angioedema and cough ( as indicated above, neprilysin breaks down bradykinin)

Question 25

Indications for sacubitril/valsartan?

Answer 25

improves mortality in patients with systolic heart failure compared to ACE inhibitors alone