1. Regulation of Body Fluid Osmolality – Regulation of Water Balance (DSA)

Question 1

What can cause SIADH/SIAD?

Answer 1

Infections and neoplasms of the brain.

Some drugs.

Pulmonary diseases.

Carcinoma of the lung.

Question 2

Where does ADH increase the permeability of urea?

Answer 2

The terminal portion of the inner medullary collecting ducts

(The VERY end of the nephron)

Question 3

To what do low-pressure baroreceptors respond, causing them to encourage secretion of ADH?

Answer 3

Low-pressure baroreceptors respond to blood volume.

Question 4

What is arginine vasopressin?

Answer 4

Antidiuretic hormone

Question 5

What are the effects of nausea, atrial natriuretic peptide, and angiotensin II on ADH secretion?

Answer 5

Nausea stimulates ADH secretion (might lose water in vomiting)

Atrial natriuretic peptide inhibits ADH secretion (increase in preload – need to get rid of water)

Angiotensin II stimulates ADH secretion (blood pressure is low, need to retain water)

Question 6

What is the osmolality of the intertubular fluid in the presence and absence of ADH within the inner medullary collecting duct?

Answer 6

With ADH: 1200 mOsm / kg H20

Without ADH: 50 mOsm / kg H20

(It makes sense that this would be where the most significant difference is)

Question 7

What are the two primary physiologic regulators of ADH secretion?

Answer 7

Osmolality of the bodily fluids, and the volume/pressure of the vascular system

Question 8

Where does ADH stimulate sodium chloride reabsorption?

Answer 8

Thick ascending loop of Henle, distal tubule, and collecting duct.

Question 9

How does ADH increase permeability of urea?

Answer 9

By increasing the abundance of UT-1 and UT-3.

Question 10

What is responsible for the negative feedback of ADH production?

Answer 10

ADH is short-lived, so when the baroreceptors or osmoreceptors are no longer firing, ADH stops being produced and it clears from the bloodstream.

Question 11

Why might osmoreceptors not respond to high urea concentration in the blood?

Answer 11

Urea is an ineffective osmole, and does not affect AVP secretion

Question 12

What is the equation for osmolar clearance?

Answer 12

C(osm) = (urine osmolality x urine flow rate) / plasma osmolality

Question 13

What is the basic pathology of central diabetes insipidus, what would be the expected plasma ADH level, and the response to ADH injection?

Answer 13

Central diabetes insipidus is due to an inability to produce ADH. We would see low plasma ADH levels, which can be corrected by ADH injection.

Question 14

How would decrease in blood volume increase our sensation of thirst?

Answer 14

Angiotensin II acts on the subfornical organ in the brain.

Question 15

What sort of urine will be produced by an individual producing little / no ADH?

Will their free water clearance (C(H20)) be positive or negative?

Answer 15

They will have dilute urine.

Their free water clearance will be positive.

Question 16

Do changes in sodium balance usually alter the volume of the ECF, or the osmolality of the ECF?

Answer 16

Changes in sodium balance usually alter the volume of the ECF, not the osmolality

Question 17

What is the osmolality at the distal end of the descending loop of Henle with and without the presence of ADH?

Answer 17

With ADH: 1200 mOsm / kg H20

Without ADH: 600 mOsm / kg H20

Question 18

What is the osmolality of the tubular fluid at the distal end of the cortical collecting duct with and without the presence of ADH?

Answer 18

With ADH: 290 mOsm / kg H20

Without ADH 100 mOsm / kg H20

Question 19

What is the osmolality of the tubular fluid at the distal end of the ascending loop of Henle?

Answer 19

140 mOsm / kg H20 with and without ADH

(the Na/K/2 Cl channels bring the osmolality down to 140 despite the amount of solute in the initial concentration, and there are few aquaporins to act on)

Question 20

How do signals from the high and low pressure baroreceptors encourage ADH secretion?

Answer 20

The signal travels via the vagus and glossopharyngeal nerve to the solitary tract nucleus of the medulla oblongata, and from there to the supraoptic and paraventricular hypothalmic nuclei.

Question 21

What is the osmolality of the proximal convoluted tubule with and without the presence of ADH?

Answer 21

290 mOsm / kg H20

Question 22

What sort of urine will be produced by an individual producing large amounts of ADH?

Will their free water clearance (C(H20)) be positive or negative?

Answer 22

They will have concentrated urine.

They will have negative free water clearance.

Question 23

What is the basic pathology involved in SIADH?

Answer 23

Increased plasma ADH levels. The plasma becomes hypotonic, and the urine becomes hypertonic.

Question 24

What three sodium transporters (and their locations) are responsible for sodium chloride reabsorption as a function of aldosterone?

Answer 24

Na/K/Cl in the thick ascending loop of Henle

Na-Cl symporter in the distal tubule

Epithelial sodium channels (ENaC) in the very end of the distal tubule and in the collecting duct

Question 25

How does ADH increase water retention?

Answer 25

Increases the permeability of the collecting duct to water. Increases the abundance of aquaporin 2 and aquaporin 3 channels. Increases reabsorption of urea and sodium chloride by the thick ascending loop of Henle, the distal tubule, and the collecting duct.

Question 26

What is the equation for free water clearance?

Answer 26

Free water clearance = urine flow rate - osmolar clearance OR Free water clearance = urine flow rate - (urine flow rate x urine osmolality / plasma osmolality)

Question 27

To what do the high-pressure baroreceptors respond, causing them to then encourage secretion of ADH?

Answer 27

High-pressure baroreceptors respond to low arterial pressure

Question 28

What is the basic pathology of **nephrogenic** diabetes insipidus, what would be the expected plasma ADH levels, and the expected response to an injection of ADH?

Answer 28

Nephrogenic diabetes insipidus is due to an inability of the kidneys to respond to ADH (often due to decreased aquaporin 2 channels in the collecting duct). We would expect normal or high plasma ADH levels, and an injection of ADH would not be as useful. (Note that nephrogenic diabetes insipidus can also be caused by an inability of the nephron to establish an osmotic gradient in the medullary interstitium)

Question 29

Where is AVP (ADH) synthesized?

Answer 29

In neuroendocrine cells located within the **supraoptic** and **para-ventricular** nucleus of the hypothalamus.

Question 30

What causes the clinical symptoms of an increase in plasma osmolality?

Answer 30

Shrinking of the brain cells, primarily. (Lethargy, weakness, seizures, coma, death)