Hyponatremia in dogs and cats. Burton and Hopper. 2019. JVECC

Question 1

What percentage of an animal’s lean bodyweight is total body water?

Answer 1

60%

Question 2

What is the equation for osmolarity in serum

Answer 2

mOsm/kg = 2Na + BG/18 + BUN/2.8

Question 3

What are the 2 main mechanisms regulating osmolarity in the body?

Answer 3

thirst (water intake)
kidney water retention or excretion

Question 4

how does the body detect osmolality?

Answer 4

osmoreceptors in the hypothalamus

detects osmolality of all body compartments as water moves freely between compartments and will equillibrate the osmolality
can sense changes in osmolality as little as 1%

Question 5

What are the 2 major stimuli for the sensation of thirst?

Answer 5

• hyperosmolality (direct stimulation)
• decreased effective circulating volume (ECV) (activates RAAS system, which activates angiontensin II, which stimulates ADH release

Question 6

Where is ADH synthesized and stored?

Answer 6

synthesized in the hypothalamus, stored in secretory granules in the posterior pituitary gland

Question 7

Explain the mechanism of action by which ADH leads to water retention

Answer 7

Activates vasopressin 2 (V2) receptors in the luminal membrane of the cortical and medullary collecting tubules
–> insertion of aquaporin 2 (water channels)
–> water will passively move through AQP2 channels down its osmotic gradient

Question 8

What are the 2 major stimuli for vasopressin release?

Answer 8

• increased osmolality
• decreased effective circulating volume

Question 9

where are the baroreceptors located that monitor the effective circulatory volume?

Answer 9

• cardiopulmonary circulation
• carotid sinus
• aortic arch
• afferent glomerular arterioles in the kidney

Question 10

How does decreased effective circulatory volume lead to ADH release?

Answer 10

baroreceptors sense decrease in ECV –> increased sympathetic tone –> RAAS activation –> angiontensin II activation –> ADH release

Question 11

Explain how a patient may have hypoosmolar plasma but increased water retention

Answer 11

decrease in ECV will lead to RAAS and subsequent ADH release despite concurrent hypoosmolality

Question 12

Explain how a patient in systolic heart failure develops hyponatremia

Answer 12

systolic heart failure –> decreased cardiac output –> decreased ECV
* –> RAAS activation (Na and water retention) and ADH release (water retention), thirst –> if water intake+retention exceeds Na retention –> hyponatremia
* decreased tubular flow –> impaired water excretion

Question 13

What is the expected decrease of serum Na concentration for every 100 mg/dL increase in glucose

Answer 13

1.6 to 2.4 mmol/L for every 100 mg/dL

the higher the glucose concentration the greater the reduction in plasma, 2.4 mmol/L likely more reliable as a factor

Question 14

Why does an increase in BUN not lead to hyponatremia?

Answer 14

BUN moves freely in and out of cells –> thus is not an effective osmole –> no water drag into the ECF

Question 15

Explain how you can use urine Na+ cc to assess a patient’s volume status

Answer 15

the urine Na+ cc of a euvolemic patient is expected to be > 30 mmol/L
the urien Na+ cc of a hypovolemic patient is < 30 mmol/L due to decrease in ECV leading to RAAS activation and aldosterone increasing Na retention in the distal nephrone

Question 16

By which 3 mechanisms can hypovolemia lead to increased TBW and hyponatremia?

Answer 16

volume depletion
–> potent nonosmotic stimulus for ADH secretion (through RAAS pathway) –> water retention in kidneys
–> decreased GFR –> increased proximal renal tubular Na+ and water reabsorption –> less fluid delivered to the diluting segments of the tubule –> less free water excreted
–> directly stimulates thirst

Question 17

Explain the theory of cortisol deficiency leading to hyponatremia in Addisonian patients

Answer 17

lack of cortisol –> lack of negative feedback from cortisol on CRH –> uninhibited release of ACTH and ADH –> water retention –> hyponatremia

Question 18

What is the expected urine Na+ cc of dogs with hypoadrenocorticism as opposed to dogs with pseudo-addison’s (i.e., hypovolemic hyponatremia with hyperkalemia from other causes)?

Answer 18

addisons: > 30 mmol/L, reflecting the absence of aldosterone
other: low urine Na+ (low ECV –> aldosterone –> Na retention)

Question 19

How do diuretics lead to hyponatremia?

Answer 19

• increased thirst and ingestion of water
• loss of isotonic fluids from diuretics –> ADH release –> dilutional hyponatremia from water retention
• diminised NaCl reabsorption in the loop of Henle and distal tubule –> less urine dilution
• severe potassium depletion

Question 20

What artifacts can lead to pseudohyponatremia?

Answer 20

*hypoproteinemia
hyperlipidemia

serum Na+ will decreae by ~ 1 mmol/L for every 10 mmol/L increase in total serum lipid cc
high serum protein –> artifactual hyponatremia, low serum protein inverse

Question 21

What is the major organic osmolyte accumulating or decreasing in brain cells in response to Na+ cc changes

Answer 21

Myoinositol

Question 22

What condition is caused by too rapid correction of hyponatremia?

Answer 22

osmotic demyelination syndrome (ODS)

Question 23

What parts of the brain are most prone to ODS?

Answer 23

the midbrain and striatum are the slowest to recover osmolytes and therefore most severely affected by too fact correction of hyponatremia

Question 24

2 mL/kg IV 3% hypertonic saline will raise serum Na+ cc by approximately how much?

Answer 24

2 mmol/L

can be used to alleviate neurologic abnormalities from hyponatremia

Question 25

Hyponatremia is considered to be acute if it has a known duration of < ____ hours

Answer 25

48 hours

Question 26

How do you calculate the Na deficit?

Answer 26

Na deficit = TBW x (normal Na - patient Na)