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TAS Nephrology > Fluid And Electrolyte Homeostasis ✅ > Flashcards

Fluid And Electrolyte Homeostasis ✅ Flashcards

1
Q

How is fluidr distributed in the body?

A

Between intracellular fluid and extracellular fluid

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2
Q

How are the fluids in the intracellular and extracellular compartments different?

A

The volume composition differs

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3
Q

What maintains the solute composition of the intracellular and extracellular compartments?

A
  • Cell membrane pump activity

- Solute size and electrical charge

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4
Q

What effect will a 10% decrease in plasma water have on sodium?

A

Will lead to plasma sodium decrease from 140 to 154mmol/l

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5
Q

What effect will dilution of the plasma by 10% have on sodium?

A

Will decrease sodium to 126

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6
Q

What is the most important stimulus for the kidney?

A

Volume preservation (rather than serum sodium concentration )

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7
Q

How can the body detect serum sodium concentration?

A

There are no bodily receptors that can detect serum sodium levels directly, but changes in plasma tonicity can be detected by osmoreceptors in the brain

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8
Q

What do changes in plasma tonicity detected by osmoreceptorsin the brain affect?

A

Renal water handling

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9
Q

How do changes in plasma tonicity cause changes in renal water handling?

A

Via anti-diuretic hormone (vasopressin)

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10
Q

What happens when there is conflicting information regarding volume status and plasma tonicity?

A

The most important principle is preservation or restoration of a normal plasma volume, rather than sodium concentration

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11
Q

What is explained by the concept that plasma volume status is prioritised over plasma sodium concentration?

A
  • Even in the presence of hypernatraemic dehydration, urine sodium may be low
  • Urine sodium is usually elevated in SIADH or in acute water intoxication despite profound hyponatraemia
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12
Q

What can biochemical parameters such as fractional excretion of sodium be useful for?

A

Assisting in determining plasma volume status

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13
Q

What is hyponatraemia defined as?

A

Plasma Na <135mmol/l

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14
Q

When does hyponatraemia occur?

A

When there is either water gain in excess of sodium gain, or sodium loss in excess of water loss

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15
Q

What can cause factitious hyponatraemia?

A

The presence of abnormal solutes in the ECF, eg: mannitol, sorbitol, or excessive glucose

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16
Q

How does the presence of abnormal solutes in the ECF lead to fictitious hyponatraamia?

A

The extra molecules result in a fluid shift which alters the sodium measurement

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17
Q

How can factitious hyponatraemia due to the presence of abnormal solutes in the ECF be detected?

A

High measured osmolality in contrast to calculated osmolality despite low serum Na

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18
Q

How is calculated osmolality determined?

A

2 x (Na + K) + rea + glucose

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19
Q

What are the principles for managing hyponatraemia?

A
  • Rapid correction only if symptomatic, and should stop once symptoms improve
  • Fluid restriction often helpful
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20
Q

What symptoms indicate a need for rapid correction in hyponatraemia?

A
  • Coma

- Seizures

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21
Q

Who can initiate rapid correction of hyponatraemia?

A

Only specialists

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22
Q

How can rapid correction of hyponatraemia be achieved?

A

2-3ml/kg of 3% NaCl

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23
Q

What is the maximum rate of correction of hyponatraemia?

A

8-12mmol/24 hours

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24
Q

Why is fluid restriction often helpful in the management of hyponatraemia?

A

Most cases are due to excess water

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25
Q

What might also be helpful in the management of hyponatraemia caused by excess water?

A

Furosemide

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26
Q

Why might furosemide be helpful in cases of hyponatraemia?

A

It increases free water clearance

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27
Q

In what condition are fluid restriction and furosemide often used in?

A

SIADH

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28
Q

What drug is being explored for use in refractory hyponatraemia?

A

Tolvaptan

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29
Q

What is tolvaptan?

A

A vasopressin receptor 2 antagonist

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30
Q

What is required in the management of hyponatraemia where salt loss is in excess of water loss?

A

Replacement of volume deficit and ongoing losses with normal saline

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31
Q

What is hypernatraemia defined as?

A

Plasma Na >145mmol/L

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32
Q

What can cause hypernatraemia?

A
  • Sodium gain in excess of water gain

- Water loss in excess of sodium loss

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33
Q

Why can the assessment of the degree of dehydration in hypernatraemic dehydration be difficult?

A

As sodium is the principle ECF osmole, the ECF volume is relatively well maintained and signs of dehydration/hypovolaemia are less apparent

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34
Q

What can severe hypernatraemia be associated with?

A

Brain damage

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35
Q

Why might severe hypernatraemia be associated with brain damage?

A

Brain tissue shrinks as a result of intracellular dehydration and blood becomes hypercoaguable

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36
Q

What brain pathologies can result from hypernatraemia?

A
  • Encephalopathy
  • Cerebral haemorrhage
  • Thrombosis
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37
Q

What does the management of hypernatraemic dehydration include?

A
  • Avoidance of rapid correction

- Sodium chloride 0.45% or 0.9%

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38
Q

Why should rapid correction be avoided in hypernatraemia?

A

Can result in cerebral oedema

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39
Q

Are boluses of normal saline given in hypernatraemic dehydration?

A

Only if there is shock

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40
Q

How quickly can acute hypernatraemia be corrected?

A

Over 24-48 hours

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41
Q

How does the speed of correction of chronic hypernatraemia compare to acute?

A

It should be slower in chronic

42
Q

How can cerebral oedema result from rapid correction of hypernatraemia?

A

Fluid can pass rapidly into cells

43
Q

At what rate can serum sodium be reduced in hypernatraemia?

A

No more than 0.5mmol/hour

44
Q

How quickly should normal hydration be achieved in hypernatraemia?

A

36-48 hours

45
Q

When might you want to delay normal hydration to over 72 hours in hypernatraemia?

A

If serum sodium >170

46
Q

What % of potassium is intracellular?

A

98%

47
Q

What is the result of potassium being primarily intracellular?

A

Plasma K is a poor representation of total body K

48
Q

Why are acute changes in potassium life threatening?

A

The ratio of intra- and extracellular K is a major determinant for the membrane potential of excitable cells, e.g. in the heart and nervous system

49
Q

What is the relationship between potassium and ECGs?

A

The pattern of the T wave on ECG reflects K concentration

50
Q

What is found on ECG in hypokalaemia?

A
  • ST depression
  • Flat T wave
  • Emergence of U wave
51
Q

What is found on ECG in hyperkalaemia?

A

Peaked T waves

52
Q

What effect does acidosis have on potassium?

A

It causes hyperkalaemia

53
Q

Why does acidosis cause hyperkalaemia?

A

As hydrogen ions displace potassium as the intracellular cation, and potassium shifts from the intracellular to extracellular compartment

54
Q

What controls the distribution of potassium between ICF and ECF?

A

Na/K-ATPase channels

55
Q

What is the result of the Na/K-ATPase channel controlling the distribution of potassium?

A

Compounds that enhance the activity of this pump can be used for the treatment of hyperkalaemia

56
Q

What drugs enhance the activity of the Na/K-ATPase channel?

A
  • Insulin

- Adrenergics (salbutamol)

57
Q

Where is most important K regulation done?

A

At the collecting duct

58
Q

What happens to K at the collecting duct?

A

It is exchanged for Na

59
Q

What controls the exchange of K for Na?

A

Aldosterone

60
Q

What will impair K excretion at the collecting duct?

A
  • Absence of aldosterone activity

- Insufficient sodium delivery

61
Q

What can be used to assess aldosterone activity?

A

The transtubular potassium gradient (TTKG)

62
Q

How is TTKG calculated?

A

(K in urine x serum osmolality) / (K in blood x urine osmolality)

63
Q

What will the TTKG be in the presence of normal aldosterone activity?

A

> 5

64
Q

What will the TTKG be in the absence of aldosterone?

A

<3

65
Q

What is required to be able to interpret TTKG?

A
  • Urinary Na is >20mmol/L

- Urine osmolality is equal to or greater than plasma

66
Q

Why do you need to ensure urinary Na is >20mmol/L when interpreting TTKG?

A

Confirms sodium delivery

67
Q

What is hyperkalaemia defined as?

A

K >5.5mmol/L

68
Q

What can cause artefactually high K?

A
  • Haemolysed blood sample
  • Improper collection
  • Delay in processing blood sample
  • Markedly raised platelets, leukocytes, or erythrocytes
69
Q

Give 2 ways in which improper collection can cause a falsely raised K?

A
  • EDTA contamination

- Squeezed sample

70
Q

Why is it essential that treatment for hyperkalaemia is started as soon as possible?

A

Severe hyperkalaemia can precipitate cardiac arrhythmias

71
Q

How is hyperkalaemia treated?

A
  • Measures to internalise potassium from extracellular to intracellular
  • Potassium binders
  • Stabilise myocardium
72
Q

What measures can internalise potassium from extracellular to intracellular?

A
  • Correction of acidosis
  • Insulin glucose infusion
  • Beta 2 agonist e.g. salbutamol
73
Q

How is acidosis corrected in the treatment of hyperkalaemia?

A

Bicarbonate

74
Q

Give an example of a potassium binder?

A

Calcium resonium resin

75
Q

How do potassium binders work in hyperkalaemia?

A

They decrease the body potassium store

76
Q

How is the myocardium stabilised in hyperkalaemia?

A

IV calcium gluconate

77
Q

What is the first step in identifying the underlying aetiology of hyperkalaemia?

A

Assessment of renal function

78
Q

Why is assessment of renal function the first step in the identified of the cause of hyperkalaemia?

A

Renal failure from any cause will lead to hyperkalaemia

79
Q

What can aggravate hyperkalaemia caused by renal failure?

A

Other coincidental factors, e.g.;

  • Use of drugs
  • Increased K load
80
Q

What drugs can contribute to hyperkalaemia?

A
  • ACEi
  • ARBs
  • Beta blockers
  • Trimethoprim
81
Q

What can cause an increased K load?

A
  • Tumour lysis syndrome
  • Intravascular haemolysis
  • Rhabdomyolysis
82
Q

What are the causes of hyperaemia?

A
  • Renal failure
  • Acidosis
  • Adrenal insufficiency
  • Cell lysis
  • Excessive potassium intake
83
Q

What needs to be excluded as a cause of hyperkalaemia in the critically ill neonate?

A

Inadequate cardiac output

84
Q

What is hyperkalaemia in the presence of normal GFR usually due to?

A
  • Failure of delivery of sodium to distal tubules

- Aldosterone deficiency/resistance

85
Q

What can cause failure of delivery of sodium to the distal tubules?

A

Hypovolaemia

86
Q

Give 2 causes of aldosterone deficiency/resistance?

A
  • Congenital adrenal hyperplasia

- Primary hypoaldosteronism

87
Q

What is hypokalaemia defined as?

A

K <3.5mmol/L

88
Q

How can hypokalaemia present?

A
  • Lethargy
  • Confusion
  • Muscle weakness
  • Intestinal ileus
89
Q

How can muscle weakness caused by hypokalaemia progress in severe cases?

A

To paralysis

90
Q

What are the potential pathological processes causing hypokalaemia?

A
  • Decrease in total body potassium

- Shift of potassium to the intracellular space

91
Q

What are the causes of hypokalaemia?

A
  • Diarrhoea
  • Alkalosis
  • Volume depletion
  • Primary hyperaldosteronism
  • Diuretic abuse
92
Q

What suggests renal loss in hypokalaemia?

A

A fractional excretion of >10%

93
Q

What can cause hypokalaemia with volume excess?

A
  • Aldosterone excess

- Renal artery stenosis

94
Q

What is hypokalaemia and volume excess due to hyperaldosteronism known as?

A

Conn’s syndrome

95
Q

What causes hypokalaemia with acidosis?

A

Renal tubular acidosis

96
Q

What causes hypokalaemia with low urinary potassium?

A

Extrarenal loss of potassium, e.g. diarrhoea

97
Q

When is IV potassium treatment required in hypokalaemia?

A

If cardiac arrhythmias or respiratory insufficiency secondary to paralysis

98
Q

Why should very rapid infusion of potassium be avoided in hypokalaemia?

A
  • Potential to cause major adverse effects

- Very concentrated potassium solutions damaging to peripheral veins

99
Q

What is considered to be a ‘very concentrated’ potassium solution?

A

> 40mmol/L

100
Q

What safety measures should be taken when emergency IV potassium replacement is required?

A
  • Under ECG monitoring

- In PICU

101
Q

What other electrolyte should be checked in hypokalaemia?

A

Magnesium

102
Q

Why is it important to treat low serum magnesium in hypokalaemia?

A

It can increase the risk of cardiac arrhythmias

TAS Nephrology (16 decks)

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