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DiBart 2021 > Chapter 3: Sodium and Water > Flashcards

Chapter 3: Sodium and Water Flashcards

1
Q

What is the normal osmolality (range) for a dog? What is the normal osmolality (range) for a cat?

A

Dogs: 290-310 mOsm/kg Cats: 290-330 mOsm/kg

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2
Q

What is the definition of specific gravity?

A

The ratio of weight of a volume of liquid to the weight of equal volume of distilled water.

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3
Q

Which of the following does specific gravity not depend on? A. Number of particles B. Size of particles C. Weight of particles D. How well your refractometer is calibrated.

A

C. Size of particles (depends on # of particles and molecular weight)

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4
Q

What is the definition of solute, or osmotic diuresis? What is the specific gravity of urine in this state?

A

Increased urine flow due to excess non-reabsorbable solutes. USG = approaches plasma osmolality

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5
Q

What is the definition of water diuresis? What is the specific gravity of urine in this state?

A

Increased urine flow due to decreased reabsorption of (solute-free) water. USG = less than plasma osmolality

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6
Q

Fill in the blanks:

A
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7
Q

Where are the high pressure baroreceptors?

A

Aortic arch

Carotid Sinus

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8
Q

Where is renin released in the kidney?

This is released in response to what?

A

Renin is released in the juxtaglomerular apparatus in response to changes in perfusion (blood flow)

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9
Q

What is glomerulotubular balance?

A

Mechanism incompletely understood.

Describes how kidneys take into account small changes in GFR and maintain static FF.

Spontaneous increase in GFR increases filtered load of all sultues and their increased concentration in the proximal tubules enhances Na+ reabsorption.

Change in peritubular hydrostatic and oncotic pressure proabbly play a role

Autoregulation plays a role.

However…this does not occur as a secondary increase in GFR tue to increased ECF [Na+]; only works as primary mechanism

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10
Q

Approximately 67% of filtered sodium is reabsorbed isosmotically with water where?

A

Proximal tubules

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11
Q

Where are the volume receptors (low pressure mechanoreceptors)

A

Cardiac atria

Pulmonary vessels

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12
Q

In the early proximal tubule, sodium crosses luminal membrane by cotransport with __________? In exchange for what?

A

Sodium crosses early proximal tubule with glucose, amino acids, phosphate.

In exchange for H+ ions (via Na-H antiporter). HCO3- is reabsorbed during this process.

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13
Q

25% of filtered load of sodium is reabsorbed where?

A

Loop of Henle

Primarily in thick ascending limb

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14
Q

5% of the filtered load of sodium is reabsorbed where?

A

Distal convoluted tubule and connecting segment. Sodium enters passively.

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15
Q

3% of filtered load of sodium is reabsorbed where?

A

Collecting ducts

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16
Q

What are thiazide diuretics MOA?

A

Inhibit Na+-Cl- cotransporter in early distal tubule

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17
Q

In the late proximal tubule, Na+ is reabsorbed primarily with what?

A

Chloride

Here the luminal Na+-H+ antiporter works in parallel with a luminal Cl--anion- antiporter

Net effect = NaCl reabsorption

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18
Q

Sodium is reabsorbed in the thin descending and ascending limbs of LOH by what mechanism?

A

passively reabsorbed

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19
Q

Sodium is reabsorbed in the thick ascending LOH by what mechanism?

A

Na+-H+ antiporter and Na+-K+-2Cl- cotransporter

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20
Q

Aldosterone alters sodium reabsorption how?

A

In response to dietary sodium intake, aldosterone increases the number of open luminal Na+ channels in the cortical collecting ducts.

This increases sodium reabsorption.

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21
Q

Aldosterone is produced and released in response to what?

A

Angiotensin II, hyperkalemia, and ACTH

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22
Q

Aldosterone is inhibited by what?

A

Dopamine

Atrial natriuretic peptide

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23
Q

Catecholamines stimulate proximal tubule reabsorption of Na+ through what effect?

A

directly stimulate alpha 1 adrenergic effect

stimulates renin release from granular cells of JGA via beta 1 adrenergic effect

This mechanism is important, as there is typically an increase in systemic BP and this offsets pressure natriuresis

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24
Q

Angiotensin II directly stimulates what in the proximal tubules, facilitating Na+ reabsorption and stimulating secretion of aldosterone from adrenals.

A
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25
Q

Renin release leads to production of what?

A

Angiotensin II

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26
Q

Atrial natriuretic peptide (ANP) is released in response to what?

A

atrial distension caused by volume expansion

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27
Q

Atrial natriuretic peptide facilitates excretion of Na+ how?

A

Causes dilation of afferent arterioles.

Constriction efferent arterioles

= increase in GFR

Relaxes mesangial cells ⇒ increase in surface area

Inhibits sodium reabsorption in cortical/inner medullary collecting ducts

Inhibits renin secretion

Inhibits aldosterone secretion by zona glomerulosa

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28
Q

True or false:

Pressure natriuresis is entirely intrarenal (it could occur in the isolated denervated kidney)

A

True

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29
Q

Osmoreceptors live where?

What is released in response to plasma hyperosmolality?

Osmoreceptors shrink =

Osmoreceptors swell =

A

Hypothalamus

Vasopressin

vasopressin is released

vasopressin release is inhibited

30
Q

Vasopressin is synthesized where (specifically?)

Released specifically where?

A

Neurons of supraoptic and paraventricular nuclei in the hypothalamus.

Vasopressin travels down axons of these neurons and released at the level of the neurohypophysis.

31
Q

Vasopressin increases reabsorption of water how?

A

Increases reabsorption of water in collecting ducts

Increases permeability of medullary collecting ducts to urea

32
Q

Why may vasopressin not be as effective in chronic PU/PD cases?

A

In these cases, there can be medullary washout ⇒

depletion of urea from medullary interstitium ⇒

impaired urea reabsorption in medullary collecting ducts

33
Q

Changes in plasma osmolality of ____% can lead to maximal vasopressin release

A

1-2%

34
Q

In addition to plasma osmolality, vasopressin is also released in response to:

A

Volume depletion

Left atrium, aortic sinus, carotid sinuses

35
Q
A
36
Q

A decrease of _____% of volume (actual or perceived) lowers the threshold for vasopressin release.

A

5-10%

37
Q

Other than hyperosmolality and decrease in volume status, what are three other stimuli for vasopressin release?

A

Nausea

Pain

Emotional anxiety

38
Q

What three disease states cause hyponatremia secondary to perceived hypovolemia

(yet there is hypervolemia)

A

Nephrotic syndrome

Heart failure

Liver failure

39
Q

What three conditions must be met for the kidneys to excrete a water load normally?

A
  1. Adequate delivery of tubular fluid to distal diluting sites (ascending LOH), where Na+ is removed without water.
  2. Ascending LOH must function normally
  3. In the absence of vasopressin, the collecting ducts must remain impermeable to water
40
Q

How does the brain defend itself from a drop in tonicity?

A

Immediately forces Na+ containing water into CSF (minutes)

Movement of K+ out of cells (24 hours)

Reduction in cellular content of organic solutes/osmolytes (>24→48 hours)

41
Q

List some organic osmolytes (idiogenic osmoles)

A

TIGGS =

Taurine

Inosine

Glutamate

Glutamine

Sorbitol

Others: myoinositol, phosphocreatine

42
Q

Which is more common in veterinary medicine?

Hypernatremia or hyponatremia

A

Hyponatremia

Increased thirst normally protects against hypernatremia (unless water not available or thirst mechanism not intact)

43
Q

What are three mechanisms to hypernatremia?

A

Pure water deficit

Hypotonic fluid loss

Impermeant solute gain

44
Q

What are some mechanisms of pure water deficit?

A

Primary hypodipsia

Diabetes insipidus (central & nephrogenic)

High environmental temp

Fever

Inadequate access to water

45
Q

What are some mechanisms to hypotonic fluid loss?

A

Extrarenal & renal (many in both)

46
Q

What are some causes of impermeant solute gain?

A

Salt poisoning

Hypertonic fluid administration

Hyperaldosteronism

Hyperadrenocorticism

47
Q

Which typically takes precedence - response to changes in osmolality or changes in volume?

A

Usually response to osmolality.

This response is not typically seen with diabetes insipidus when administered HTS

48
Q

How can one differentiate between renal or non-renal sodium losses?

A

Fractional excretion of sodium

FeNa <1% (non-renal losses)

FeNa >1% (renal losses)

49
Q

What is the definition of CDI?

What are some causes of CDI?

A

CDI is a partial or complete lack of vasopressin production and release from the neurohypophysis

Causes: trauma, neoplasia, idiopathic, visceral larval migrans, congenital (rare)

50
Q

What is the USG typically with CDI?

A

Hyposthenuric

51
Q

With CDI, plasma osmolality is typically ______.

With psychogenic PU/PD, plasma osmolality is typically ______.

A

CDI–>higher

psychogenic PU/PD–>lower

52
Q

What is the MOA of chlorpropramide and how may it be useful in management of patients with partial CDI?

A

Sulfonylurea hypoglycemic agent that can potentiate the renal tubular effects of small amounts of vasopressin

53
Q

How do thiazide diuretics potentially help treat animals with CDI and NDI?

A

Results in mild dehydration, enhanced proximal tubular reabsorption of sodium, decreased delivery of tubular fluid to distal nephron and reduced UOP.

54
Q

List some causes of acquired nephrogenic diabetes insipidus

A

Drugs (glucocorticoids, lithium, E. coli endotoxin, diuretics)

Electrolyte disturbances (hypokalemia, hypercalcemia)

Altered medullary hypertonicity (hypoadrenocorticism)

Hepatic insufficiency, hyperthyroidism, hyperadrenocortism

Post-obstructive diuresis

Acromegaly

Structural- medullary interstitial amyloidosis, polycystic kidneys, pyelonephritis, chronic interstitial nephritis

55
Q

In which conditions can pseudohyponatremia occur?

A

Hyperlipidemia and hyperproteinemia.

56
Q

What should be your suspicion if you have an abnormal osmolal gap with normal measured osmolality?

A

Pseudohyponatremia. (Measured osmolality will be normal, but calculated osmolality will be low)

57
Q

What is the change in sodium for every change in glucose concentration?

A

There is a 2.4 mEq/L decrease in sodium for each 100 mg/dL increase in glucose.

58
Q

What 3 physiologic events need to happen in order to have a hypovolemic hyponatremic patient?

A
  1. Decreased GFR: volume depletion decreases GFR, enhances isosmotic reabsorption of sodium and water in the proximal tubules, and decreases delivery of tubular fluid to distal diluting sites. These events impair excretion of water.
  2. Vasopressin release: volume depletion is a strong nonosmotic stimulus for vasopressin release, and the increased plasma vasopressin concentration further impairs water excretion.
  3. Thirst
59
Q

Why patients with atypical hypoadrenocorticism may have hyponatremia without hyperkalemia?

A

Because glucocorticoids are necessary for complete suppression of vasopressin release, and in their absence impaired water excretion and hyponatremia can occur.

60
Q

In what 3 clinical conditions can you have hypervolemic hyponatremia?

A

Congestive heart failure, severe liver disease, and nephrotic syndrome.

61
Q

What type of water shift between ECF/ICF does hypotonic fluid loss cause?

A

hypotonic fluid loss –> increases osmolality of ECF –> osmotic stimulus driving water from the ICF to ECF compartment

62
Q

Which patient will show more severe cardiovascular compromise: the patient with free water loss of the patient with hypotonic fluid loss? Explain your answer

A
  • Patient with hypotonic fluid loss
  • free water loss from ECF causes a more significant osmotic drift because of higher ECF osmolality –> more water moves from ICF to ECF and replenishes intravascular losses
63
Q

What type of fluid loss does postobstructive diuresis cause?

A

hypotonic fluid loss

64
Q

What type of fluid loss do vomiting, diarrhea, SI obstruction, peritonitis, glucosuria or postobstructive diuresis cause?

A

hypotonic fluid loss

65
Q

Does the gain of an impermeable solute cause Hypo- or Hypernatremia?

A
  • initially hyponatremia: gain of solute draws water from ICF to ECF –> dilutional effect on [Na]
  • then: hypernatremia: the solute takes over Na’s place in tubular excretion and more Na is retained in ECF
66
Q

What has to be absent/dysfunctional for an animal with increased NaCl intake to actually develop hypernatremia?

A

hypernatremia unlikely from increased NaCl intake if thirst mechanism intact and access to water

67
Q

what is the pathophysiologic mechanism of neurologic damage from hypernatremia

A

increased ECF hypertonicity –> draws fluid from ICF to ECF –> shrinkage of brain cells from loss of water

68
Q

clinical signs of hypernatremia

A
  • anorexia
  • vomiting
  • muscular weakness
  • behavioral changes
  • ataxia
  • seizures
  • death
69
Q

equation for Water Deficit

A

Water deficit = total body water (0.6xbw) x [(Napresent/Nadesired)-1]

70
Q
A

DiBart 2021 (9 decks)

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