Stockham & Scott Chapter 9 Electrolytes AKG

Question 1

H20 followed sodium via osmotic pressure, but which membranes of the nephron are impermeable to water?

Answer 1

Distal nephron tubules (unless you have ADH)

Ascending limb of loop of Henle is impermeable to water

Question 2

How does hypokalemia alter Na? What about hyperkalemia?

Answer 2

Hypokalemia will decrease exchangable (free) potassium, requiring plasma Na concentrations to decrease by allowing Na to enter the cells - this is needed to maintain electroneutrality.

Hyperkalemia does not cause hypernatremia however becuase marked hyperkalemia is life threatening and hypernatremia stimulates thirst centers and intake of water reduces mangitude of change.

Question 3

What are the three factors that alter aldosterone secretion? Which ones are the two main factors?

Answer 3

1. Hyperkalemia
2. Blood volume
3. Hyponatremia

First 2 are main factors

Question 4

Where is ADH formed? Where is it stored?

Answer 4

Formed in the hypothalamus

Stored in the pituitary gland

Question 5

Angiotensin II promotes sodium resorption in the _____ of the kidney, while aldosterone promotes active sodium resorption in the _____ of the kidney.

Answer 5

Angiotensin II –> proximal tubules

Aldosterone –> CTs

Question 6

Plasma sodium concentrations are controlled mainly by 2 main mechanisms:

Answer 6

1. Regulation of blood volume - detected by kidney juxtaglomerular cells and carotid sinus baroreceptors (RAS –> angiotensin II and aldo; ADH)
2. Regulation of osmolality –> detected by hypothalamus –> (thirst centers and ADH secretion)

Question 7

There is an aldosterone-independent Na-Cl cotransporter that will increase NaCl resoprtion when there is increased Na delivery to the ditsal nephron. Which drug binds to Cl receptor and BLOCK the co-transporter.

Answer 7

Thiazide diuretics

Question 8

For measuring sodium:

• serum vs plasma

Answer 8

serum preferred

Question 9

Which is okay to use: NaEDTA or NaHeparin?

Answer 9

Na-Heparin becuase there is not enough sodium to cause a clinically significant change

Question 10

What is “aldosterone escape”?

Answer 10

Although aldosterone increases Na and water retention, patients with hyperaldosteronism will subsequently increase urinary sodium extretion (aka natriuresis) d/t effects of hypervolemia (increased renal perfusion pressure, decreased proximal sodium reabsoprtion and increased Na delivery to the distal nephron) - this increased delivery of sodium overrides the enhanced aldosterone sodium reabsoprtion. Volume expansion increases ANP, which also promotes natriuesis. Together, these events prevent edema formation.

Question 11

What is the difference between direct potentiometry and indirect potentiometry when measuring [Na+]?

Answer 11

Both use an ion selective electrode to measure electrical potential.

Direct potentiometry measures electrical potential in a NONdiluted sample, and Na activity is only measured in the aqueous (H2O) phase.

Indirect potentiometry measures electrical potential in a DILUTED sample.

Lipids and proteins will falsely decrease Na using indirect potentiometry.

Question 12

____ and ____ will falsely ______ sodium measurement using indirect potentiometry.

Answer 12

Lipids; proteins; decrease

Question 13

What can lead to spurious hypernatremia when measuring sodium?

Answer 13

Sample evaporation

Question 14

List the differentials for hypernatremia caused by a water deficit (hypertonic dehydration)?

Answer 14

Think “free water” loss:

1. Insensible loss (panting, hyperventilation, fever)
2. Defective ADH activity (central + nephrogenic DI)

Inadequate water intake:

1. Water deprivation
2. Defective thirst response (brain injury, hypodypsic hypernatremia in miniature schnauzers)

Free water loss >> Na loss

1. Osmotic diuresis (glucosuria from DM or dextrose administration; synthetic colloid administration)
2. Osmotic sequestration in GIT (ruminal acidosis - build up of lactate; paintball toxicosis - glycerol and sorbital; phosphate enemas)

Question 15

Which molecules are responsible for osmotic pull of water in GIT in painball toxicosis?

Answer 15

Glycerol & Sorbitol

Question 16

How does ruminal acidosis lead to osmotic pull into GIT?

Answer 16

Proliferation of lactate producing bacteria - build up of lactate and other molecules - creates hyperosmolar environment/osmotic gradient for water to enter and get sequestered into the GIT

Question 17

List the differentials for hypernatremia caused by an excess of sodium?

Answer 17

1. Excess sodium with H2O restriction (salt poisoning, hypertonic saline, sodium-bicarbonate administration)
2. Decreased renal excretion of sodium (hyperaldosteronism - rare since aldosterone escape will mitigate hypernatremia if you have normal ADH activity and normal water intake + ANP which promotes natriuesis)
3. Spurious hypernatremia due to sample evaporation (in vitro)
4. Unknown mechanisms:
   
   1. Severe exercise in greyhounds

Question 18

List disorders that lead to net retention of isotonic fluids to hypotnic fluids (usually normonatremic, sometimes mildly hyponatremic) leading to edema or transudate formation

Answer 18

1. CHF
2. Hepatic cirrhosis
3. Nephrotic syndrome

Question 19

Explain the mechanism of edema/transudate formation in CHF:

Answer 19

↓ CO → ↓ BV → RAS + SNS activation → Na & Cl resorption → plasma hyperosmolality → ADH + thirst response → hypervolemia → increased venous hydrolic pressure → edema/trasnudative effusion

Question 20

Hypoalbuminemia plays a primary role in causing edema/transudative effusions in patients with hepatic cirrhosis. T/F

Answer 20

False - hypertension/increased hydraulic pressure in the liver (‘underfilling theory’) plays a primary roll in the formation of edema and transudative effusions; hypoalbuminemia (decreased oncotic pressure) only plays a secondary role

Question 21

Nephrotic syndrome develops secondary to damage of what part of the kidney? Give differentials that could cause it.

Answer 21

Glomerular damage

Ddx:

Secondary glomerulopathies (e.g., sequelae of systemic of glomerular hypertension in animals with late stage CKD; venous thrombuss formation)

Primary glomerulopathies (e.g., immune-mediated complex deposition incited by neoplasia, rickettsial diseases, SLE, HWD, adenovirus, or idiopathic; chronic infection - FeLV, FIV; amyloidosis)

Question 22

What is nephrotic syndrome?

Answer 22

A protein-losing nephropathy that leads to abdominal transudation. Other characteristics of nephrotic syndrome include: hypoalbuminemia, proteinuria, hypercholesterolemia, and edema/transudative effusion

Question 23

List the differentials for hyponatremia caused by expanded ECF volume without edema:

Answer 23

1. Inappropriate ADH secretion (SIADH) - secondary to drugs, and neuro, pulmonary and thyroid disease
2. Excessive Na+ poor fluids (dextrose, hypotonic saline)
3. Primary polydypsia - uncommon b/c normal renal function would regulate and excrete excess water

Question 24

List the differentials for hyponatremia that are caused by net sodium loss (‘dilutional hyponatremia’)

Answer 24

1. Hypoadrenocorticism
2. Ketonuria (pulls sodium into renal tubules to maintain electroneutrality)
3. Na-wasting npehrapties (most common in horses)
4. Third-space loss with repeated removal of effusions and drinking water

These ddx may be result in net isotonic fluid loss and cause normonatremic dehydration, or may cause dilutional hyponatremia if followed by unrestricted access to water:

1. GI loss (vomiting, diarrhea, salivation, sequestration, canine whipworm, bovine hemorrhagic diarrhea)
2. Renal loss (defective tubular function, osmotic diuresis, diuretic agents)
3. Skin loss (sweating in horses)

Question 25

List the differentials that cause hyponatremia due to fluid or Na shifts between ICF and ECF, and from intravascular to extravascular spaces

Answer 25

1. Shifting of water from ICF → ECF
   
   1. Occurs during increased plasma osmolality (hyperglycemia or mannitol administration) → H2O shift to ECF → dilutes Na
2. Shifting of Na from ECF → ICF
   
   1. Acute damage to cell membranes (muscle trauma) allowed Na to follow concentration gradient INTO the cells. Other expected changes: hypovolemia, ↓ Ca2+, ↑K+, ↑ Ph
   2. Potassium depletion (results in Na to enter cells to maintain electroneutrality; K depletion also causes Cl to leave cell and decrease intracellular osmolality, moving water out of cells and diluting circulating Na)
3. Shifting of Na from IV to EV space
   
   1. Uroperitoneum (urine is NaCl poor → NaCl diffuses into abdominal cavity from circulation; see decreases in Na and Cl wihtin 1-2 days of onset, and see marked changes after 4 days of onset

Question 26

What are the clinico-pathologic changes that occur after acute damage to cell membranes/muscle trauma?

Answer 26

1. Hypovolemia
2. Hyponatremia
3. Hypocalcemia
4. Hyperkalemia
5. Hyperphosphatemia