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

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Flashcards in 1. Regulation of Body Fluid Osmolality – Regulation of Water Balance (DSA) Deck (30)
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1
Q

What can cause SIADH/SIAD?

A

Infections and neoplasms of the brain.

Some drugs.

Pulmonary diseases.

Carcinoma of the lung.

2
Q

Where does ADH increase the permeability of urea?

A

The terminal portion of the inner medullary collecting ducts

(The VERY end of the nephron)

3
Q

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

A

Low-pressure baroreceptors respond to blood volume.

4
Q

What is arginine vasopressin?

A

Antidiuretic hormone

5
Q

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

A

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)

6
Q

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

A

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)

7
Q

What are the two primary physiologic regulators of ADH secretion?

A

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

8
Q

Where does ADH stimulate sodium chloride reabsorption?

A

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

9
Q

How does ADH increase permeability of urea?

A

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

10
Q

What is responsible for the negative feedback of ADH production?

A

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

11
Q

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

A

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

12
Q

What is the equation for osmolar clearance?

A

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

13
Q

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

A

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.

14
Q

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

A

Angiotensin II acts on the subfornical organ in the brain.

15
Q

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?

A

They will have dilute urine.

Their free water clearance will be positive.

16
Q

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

A

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

17
Q

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

A

With ADH: 1200 mOsm / kg H20

Without ADH: 600 mOsm / kg H20

18
Q

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

A

With ADH: 290 mOsm / kg H20

Without ADH 100 mOsm / kg H20

19
Q

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

A

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)

20
Q

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

A

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.

21
Q

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

A

290 mOsm / kg H20

22
Q

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?

A

They will have concentrated urine.

They will have negative free water clearance.

23
Q

What is the basic pathology involved in SIADH?

A

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

24
Q

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

A

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

25
Q

How does ADH increase water retention?

A

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.

26
Q

What is the equation for free water clearance?

A

Free water clearance = urine flow rate - osmolar clearance

OR

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

27
Q

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

A

High-pressure baroreceptors respond to low arterial pressure

28
Q

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?

A

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)

29
Q

Where is AVP (ADH) synthesized?

A

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

30
Q

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

A

Shrinking of the brain cells, primarily.

(Lethargy, weakness, seizures, coma, death)