Sodium Disorders Flashcards

1
Q

define osmolality

A

particles per kg

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2
Q

define osmolarity

A

particles per litre

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3
Q

what is the normal osmolality in canine and feline plasma

A

dog: 290 to 310
mOsm/kg in dogs

cat: from290 to 330mOsm/kg in cats

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4
Q

what is the equation for osmolality?

A

osm =2Na +BUN/2.8 + glucose/18

2.8 and 18 are conversion factors to SI units

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5
Q

What does the specific gravity depend on?

A

number of particles present in the solution and also on their molecular weight

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6
Q

What does tonicity refer to?

A

Tonicity
refers to the ability of a solution to initiate water movement and is dependent on the presence of
impermeant solutes in the solution.
may be thought of as effective osmolality

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7
Q

What is the normal sodium for a dog and cat

A

Dog 140-155
Cat 149-162

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8
Q

Why may hyponatreamia occur

A

when the patient is unable to excrete ingested
water
or when urinary and insensible fluid losses have a
combined osmolality greater than that of ingested or parenterally administered fluids.

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9
Q

Why may hypernatraemia develop?

A

when water intake has been inadequate,
when the lost fluid is hypotonic to ECF,
or when an excessive amount of
sodium has been ingested or administered parenterally

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10
Q

renal handling of sodium

A
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11
Q

What is the main effect of aldosterone in relation to Sodium handling?

A

Increase the number of open luminal Na changes in the collecting duct

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12
Q

What are the two main control points for renal sodium balance?

A

glomerular filtration and tubular reabsorption

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13
Q

What is glomerulotubular balance

A

A mechanism in which the kidneys keep the fraction of filtered load resorbed constant regardless of GFR - this mains that filtered load will change appropriately with GFR

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14
Q

What stimulates aldosterone release?

A

stimulated by angiotensin
II, hyperkalemia, and adrenocorticotropic hormone
(ACTH). Its release is inhibited by dopamine and atrial
natriuretic peptide.

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15
Q

Which arteriole is usually more affected by catecholamine induced vasoconstriction? Afferent or efferent

A

Efferent

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16
Q

WHat vessel does angiotensin II preferentially constrict

A

Efferent

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17
Q

What are the effects of Atrial Natriuretic Peptide

A

Released in response to atrial stretch
dilation of the afferent
arterioles and constriction of the efferent arterioles
inhibits sodium reabsorption in collecting ducts
Inhibits renin release, and inhibits aldosterone secretion

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18
Q

Water handling

A
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19
Q

How does ADH work

A

Increases absorption of water in collecting duct - binds to V2 receptors –> cAMP –> results in Aquaporin 2 fusing to cell membrane and opening for water movement

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20
Q

What is the main stimuli for vasopressin release?

A

hypertonicity of plasma
changes in plasma osmolality as small
as 1% to 2% above normal lead to maximal vasopressin
release.

21
Q

What is a secondary stimuli for vasopressin release?

A

decrease in blood volume of 5-10% lowers threshold for vasopressin release
Other stimuli for vasopressin release include nausea,
pain, and emotional anxiety.

22
Q

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

A
  1. Adequate delivery of tubular flow to distal tubules were NaCl is removed without water
  2. Ascending limb of Henle must function normally.
  3. in absence of vasopressin collecting duct is impermeable to water
23
Q

How does the brain protect itself from hypotonicity?

A

Movement of CSF into the spinal canal
movement of potassium out of the cells
In 24-48hrs organic osmoles begin to be broken down to reduce cellular osmolality

24
Q

Clinical Approach to Hypernatramia

A
25
Q

What are the three broad causes of hypernatraemia?

A

Pure water deficit - fever, nil water access, diabetes insipidus
Hypotonic fluid loss - GI, third spacing, burns, osmotic diuresis, CKD, post-obstructive diuresis
Solute gain - salt ingestion, hypertonic fluid admin, Hyperaldosteronism, cushings

26
Q

Why is volume depletion usually not associated with pure water loss

A

As plasma volume is only 1/4 of the ECF and 1/3 of the loss comes from the ECF (2/3 from ICF)
Results in only 1/12 of the loss from the intravascular space, and plasma proteins may cause even less loss than this

27
Q

What is central diabetes insipidus?

A

partial or complete lack of vasopressin production
and release from the neurohypophysis
Caused by trauma, neoplasia or idiopathic

28
Q

What may the USG of CDI animals be

A

hypothenuric however may also be isosthenuric if partial CDI is present and the animal is dehydrated

29
Q

Why may trestment with vasopressin in dogs with CDI result in less of an increase in USG than expected?

A

because
of renal medullary washout of solute. In one study, USG
values increased to 1.018 to 1.022 after vasopressin
administration in dogs with complete CDI and to
1.018 to 1.036 in dogs with partial CDI.

30
Q

What is nephrogenic diabetes insipidus?

A

a diverse group
of disorders in which structural or functional
abnormalities interfere with the ability of the kidneys to
concentrate urine
May be congenital or acquired

31
Q

What are the clinical signs of hypernatraemia ?

A

Result from rapid movement of water out of the brain. CSx neuro and often observed above 170mEq/L
anorexia,
lethargy, vomiting, muscular weakness, behavioral
change, disorientation, ataxia, seizures, coma, and
death

32
Q

What is the calculation of water deficit

A

Free water def equals = BW x ((current Na/normal Na)-1)

33
Q

At what rate should hypernatraemia be corrected

A

Rapidly if quick. At 10-12mEq/L/day if unknown or chronic

34
Q

Clinical Approach to Hyponatraemia

A
35
Q

If indirect measures are used for Na, what abnormalities may result in a falsely low sodium

A

Hyperlipidaemia and hyperproteinaemia.
Doesn’t affect blood gas measures

36
Q

WHat may cause hyponatraemia with elevated osmolality

A

admin of impermeable solutes - mannitol, hyperglycaemia due to translocation of water

37
Q

What is the likely cause of hypovolaemic hyponatraemia ?

A

Hypotonic fluid loss then resulting in decreased vascular volume consequently resulting in thirst, AHD release and decreased GFR (which results in increased water resorption proximally)

38
Q

In what conditions may you see hypervolaemic hyponatraemia?

A

congestive heart failure, severe liver disease, and
nephrotic syndrome

39
Q

Why does hypervolaemic hyponatraemia occur?

A

Body perceived decrease in circulating volume
RAAS activation, decreased GFR resulting in less flow reaching distal sites and ADH release

40
Q

When may normovolaemic hyponatraemia occur

A

psychogenic polydipsia, Syndromes of inappropriate antidiuretic hormone
secretion
Antidiuretic drugs (see Fig. 3-6)
Myxedema coma of hypothyroidism
Hypotonic fluid infusion

41
Q

What does SIADH stand for

A

Syndrome of inappropriate release of adh
refers to vasopressin release in the absence of
normal osmotic or nonosmotic stimuli.
may be drug induced or
associated with various types of malignancies, pulmonary
diseases, and central nervous system disorders

42
Q

How is SIADH diagnosed?

A
  1. Exclude all other causes
  2. hyponatraema with plasma hypoosmolality
  3. inappropriately high urine osmolality
  4. normal adrenal, renal and thyroid function
  5. presence of natriuresis despite hyponatraemia
  6. nil hypovolemia
  7. Nil third spacing
  8. Correction of hyponatraemia by fluid admin
43
Q

Clnical Signs of Hyponatreamia

A
44
Q

What are the CSx of acute hyponatremia

A

Seizures, incoordination, weakness, coma

45
Q

Over what period of time should chronic hyponatremia be corrected?

A

they recommend less than 8mEq/l/day

or 10-12mEq/L per 24hrs

46
Q

WHere may demyelenolysis occur

A

cerebellum, pons, thalamus, white matter

47
Q

PU/PD

A
48
Q

When in CKD does urinary concentrating ability become impaired

A

2/3 nephron loss

49
Q

In what animals is a water deprivation test contraindicated

A

Isothenuric and already dehydrated
animals that are azotaemic