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electrolyte disorders Flashcards

1
Q

what is U&Es?

A

urea and electrolytes

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2
Q

how do you measure U&Es?

A

through ions and biproducts in the blood which is direct - look at sodium, potassium, chloride, bicarbonate, urea and creatinine

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3
Q

how do you estimate U&Es?

A

through deduction - rather than direct - not possible in practice - look at water

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4
Q

what are electrolyte disorders?

A

they are abnormal electrolytes

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5
Q

how can electrolyte disorders result?

A

primary disease state, secondary consequence of a multitude of disease or iatrogenic

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6
Q

why is electrolyte maintenance important?

A

maintenance of cellular homeostasis, cardiovascular physiology such as sodium for BP, renal physiology such as sodium for GFR, electrophysiology - arrhythmias

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7
Q

what is the epidemiology of electrolyte disorders?

A

commonest chemical pathology test with 100000 cases per year

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8
Q

when are electrolytes measured?

A

haemorrhage, poor intake, increased loss, D&V, diabetes insipidus and mellitus, diuretic therapy and in endocrine disorders to increase the patient outcome

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9
Q

what concepts are important in electrolyte disorders?

A

volume - need to be able to deduce
contents - cannot use to determine treatment unless have concentrations and volumes
compartments - which one is it in - intra and extracellular
concentration - does not necessarily tell us if overloaded or depleted
rates of gain and loss - dynamic therefore can retain and get overloaded

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10
Q

what is the concentration of Na?

A

inside the cell it is low and distributes at roughly 100 - potassium is higher in the cell

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11
Q

what is sodium outside the cell?

A

higher - around 140mmol/L

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12
Q

what happens to the concentration in plasma as exercise with no hydration?

A

concentration increases as volume is depleted

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13
Q

normally the system is in equilibrium, what does changing any factor do?

A

causes the new steady state to be reached

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14
Q

what is the ECF distribution of water, sodium and potassium?

A

vascular - water will be 3L, sodium 140mmol/L and K 5mmol/L

interstitial - water 16L, Na 140mmol/L and K 5mmol/L

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15
Q

what is the ICF distribution of Na, K and H2O?

A

intracellularly there will be 23L of water, 10mmol/L of Na, and 150mmol/L of K

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16
Q

what is the total volume of water in the ECF and ICF?

A

42L

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17
Q

what does loss of isotonic (similar to blood) fluid result from ?

A

can result from loss of blood or fistula fluid or haemorrhage

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18
Q

what are the characteristics of isotonic fluid loss?

A

no change in concentration of sodium, loss is from ECF, no fluid redistribution

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19
Q

what is loss of hypotonic solutions?

A

it is insensible loss such as vomiting and results in dehydration

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20
Q

where is the greatest loss in loss of hypotonic solution?

A

in the ICF - fluid is lost from the space and therefore there is a reduction in volume so increase in concentration meaning that water moves out of cells due to osmosis - cells shrink

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21
Q

what are the characteristics of insensible loss?

A

small increase in ICF sodium and fluid redistribution between the ECF and ICF

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22
Q

what are the characteristics of gain of isotonic solution?

A

this could be gain of saline drip - gain is to ECF with no change in Na concentration and no fluid redistribution. There are gains in the ECF due to gains in the blood resulting in increased BP - treatment for hypotension

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23
Q

what is a hypotonic solution gain?

A

water or dextrose - dilute patient - sodium decreases

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24
Q

what are the characteristics of gain of hypotonic solution?

A

greater gain to ICF, small decrease in sodium concentration, fluid redistribution between the ICF and ECF

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25
Q

why might a patient with a hypotonic gain show swelling or oedema?

A

the water goes into the cells and they swell

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26
Q

what causes hyponatraemia ?

A

dextrose drips have water in them - if confuse for sodium drip - kidneys need sodium to work and if not then will overload - patients can die of stroke

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27
Q

what does concentration of sodium in the blood depend on ?

A

water volume and redistribution

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28
Q

what is the result of sodium loss?

A

could be from diuretics - will lose Na in the ECF

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29
Q

what are the compensation mechanisms?

A

physiological or therapeutic

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30
Q

what comprises physiological?

A

thirst ADH or RAAS - ADH and RAAS can show what the patient is missing

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31
Q

what comprises therapeutic?

A

IV therapy, diuretics or dialysis

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32
Q

what is osmolality?

A

the rise of all solutes in a given volume of water

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33
Q

where is ADH produced and why?

A

it is produced by the median eminence in the brain and is released when osmolality increases/we are dehydrated. It reduces water being exctreted

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34
Q

what does ADH result in?

A

decreases renal water loss and increase thirst

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35
Q

how can you test ADH?

A

simple tests - measure plasma and urine osmolality - urine > plasma suggests that ADH is active (not actually testable - send to clinic for assay) - urine osmolality very high if kidney is working
or measure plasma and urine urea
urine far bigger than plasma means that the kidney has water retention

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36
Q

where is renin made and what does this activate?

A

it is made in the kidney and makes angiotensin in the adrenal glands made aldosterone

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37
Q

what is the role of aldosterone?

A

renal sodium retention in response to reduced IVV causing haemorrage or Na depletion

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38
Q

how can you see the action of RAAS?

A

look at urine sodium - very low means high aldosterone <10mmol/L means the RAAS is active

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39
Q

how do you replace isotonic loss?

A

with isotonic solution
in isotonic loss: lost from the ECF, same as blood so no change in sodium, therefore no fluid redistribution
add isotonic as then can just directly replace the volume still with no change in concentration or fluid redistribution
if replace with hypotonic then will decrease the sodium concentration as will have no solutes in, meaning that the equilibrium of concentration is not restored so water also moves into the cells and causes swelling and oedema

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40
Q

how would you replace hypotonic loss?

A

with hypotonic solution
in hypotonic loss the sodium concentration of the ECF rises due to removing volume but not solutes as well, meaning that there is fluid redistribution because the cells via osmosis move water out into the ECF to balance sodium concentration so they shrink
if replace with isotonic then the sodium concentration of the ECF will remain high and fluid will remain in the ECF
if you replace with hypotonic then the Na is restored as is just water going into the ECF which dilutes it and fluid can then move back into the ICF

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41
Q

what is hyponatraemia?

A

it is too little Na in the blood and ECF, there may be dilution too far and excess water in the ECF

42
Q

what is hyerpnatraemia?

A

to little water in the ECF and too much Na

43
Q

what is dehydration and what are the implications of this?

A

water deficiency and fluid deficiency (Na and water) - determine which it is so cant treat appropriately

44
Q

what is euvolaemic hyponatraemia?

A

normal sodium but excess of fluid

45
Q

what can the extravascular volume be?

A

euvolaemic, hypovolaemic or oedema

46
Q

if someone is hypovolaemic, how do you identify the cause?

A

look at urine sodium
if greater than 20 - na losing nephritis, Addisons or diuretics
if less than 20 - vomiting, diarrhoea or skin loss

47
Q

what are the causes of oedema?

A

CCF cirrhosis or nephrosis

48
Q

if someone is euvolaemic hyponatraemic what do you do?

A

look at PI osmosis - high means hypertonic hyponatraemia (reabsorption of water by molecules - false result), normal - pseudo hypoNa (false from lab), low - water overload - deficiency in water excretion

49
Q

what is hypovolaemic hyponatraemia?

A

both fluid and sodium are low

50
Q

what is oedema hyponatraemia?

A

increased fluid and sodium but fluid has larger increase than sodium

51
Q

what would you do once water overload is established?

A

look at urine sodium to identify cause - >20 is SIADH, drugs and CRF, and <20 is stress, endocrine, post surgery and hypothyroid

52
Q

what is hyponatraemia due to diuretics?

A

urine sodium reabsorption decreases leading to sodium diuresis and water loss. This means that renally more sodium is being lost than water and the concentration of urine sodium increases. Therefore intravascular volume decreases meaning that ADH will incrase so water intake rises and then plasma sodium falls again. The decrease in IVV also result in decreased GFR and increased plasma creatinine and urea

53
Q

what does sodium diuresis result in?

A

water loss, no sodium retention concentrated urine

54
Q

what is hyponatraemia due to SIADH?

A

plasma sodium, urea and osmolality is very low, but the urine sodium, urea and osmolality is very high. This shows a problem with ADH. ADH increase results in decrease in urine volume and incrase in concentration. Increase in ADH also result in renal water reabsorption resulting in increased IVV and urine osmolality. IVV increase leads to decreased Na renal reabsorption leading to increased urine Na concentration. IVV increase also leads to haemodilution resulting in decreased plasma osmolality, sodium concentration and creatinine and urea concentration

55
Q

what is the result of hypernatraemia due to decreased water intake?

A

urine has high sodium and urea plasma concentration and lower sodium and urea and sodium urine (still high) concentration. water intake decrease results in haemoconcentration resulting in increased plasma sodium and osmolality. water decreased also leads to decreased IVV and therefore decreased RBF and GFR meaning that urine volume decreases but osmolality increases (also acted upon by increased ADH). Decreased IVV leads to incrased RAA and increased renal NA reabsorption leading to decreased urine concentration.

56
Q

what happens in osmotic diuresis in hypernatraemia?

A

plasma na, urea and glucose are high and sodium and urea in urine lower (still high). plasma glucose increase leads to osmotic diuresis leading to increased renal loss and urine sodium. Inreased glucose also leads to increase plasma osmolality leading to incrased ADH and urine osmolality. Also contributing to plasma osmolality is incrased haemoconentration from renal water loss which icnrases plasma osmolality and plasma sodium. Renal water loss can also result in decreased IVV, GFR and therefore increased plasma creatinine/urea concentration

57
Q

what happens with hypernatraemia due to aldosterone?

A

increase urine Na absoprtion but decreased K reabsoprtion. Therefore renal loss of water is greater that sodium. The decreased sodium renal loss leads to decreased sodium urine conc but increased K urine conc, an overall increase in IVV (increase in GFR and therefore decreased in plasma creatinine and urea) and increased plasma Na and decreased plasma K. This also is influenced by reduced ADH from the increased IVV, resulting in more water loss.

58
Q

what is the reference range of metabolism?

A

3.6-5mmol/L

59
Q

what are the effects of abnormal potassium?

A

less than 3 or more than 6 - cardiac conduction defects,l abnormal neuromuscular excitability

60
Q

what are the iatrogenic causes of potassium disorder?

A

commonly is the inappropriate use of IV fluids or drugs

61
Q

what is measured for potassium?

A

the plasma potassium - it reflects a small proportion of the body potassium

62
Q

why is serum potassium not often used?

A

serum potassium does not reflect body potassium

63
Q

how do you determine the total body potassium?

A

through the total cell mass

64
Q

what affects the plasma potassium significantly?

A

the exchange of ICF/ECF - potassium is pumped across membranes

65
Q

what causes changes in the exchange of ICF/ECF?

A

acidosis, glucose/insulin therapy - potassium moved into cells, adrenaline - deficiency when going fast, rapid cellular incorporation in TPN or leukaemia

66
Q

where is a large amount of potassium found?

A

intracellular fluid space - 98% - 3400 mmol

2% is found in plasma/interstitial fluid at a total of 70mmol

67
Q

what is exchanged across the membrane for potassium?

A

H+ - both will bind to negatively charged proteins such as Hb

68
Q

how do changes in the pH affect the equilibrium?

A

acidosis - potassium moves out of cells - hyperkalaemia

alkalosis - potassium moves into cells - hypokalaemia

69
Q

what happens in acidosis?

A

the potassium in the plasma can overstep the safe threshold

70
Q

what happens in chronic acidosis?

A

high potassium is tolerated - cell produces more H+ and therefore they cannot escape so will shift K+ out

71
Q

what differes from hyperkalaemia in chronic vs acute settings?

A

in acute setting cannot be tolerated - can lead to arrhythmia - ventilate to allow the heart to work properly but reducing acid

72
Q

what can potassium depletion affect?

A

acid base status

73
Q

what is the basis of acidosis?

A

H+ push into the cell and push K+ out so increase the concentration in plasma

74
Q

what are the causes of hyperkalaemia?

A

artefactual, renal, acidosis, cell death and mineralocorticoid dysfunction

75
Q

what is artefactual?

A

it is when there is a delay in sampling so when the cells are in the small tube they break up on edges and this is haemolysis or can be from drug therapy where there is excess intake

76
Q

what is the difference between acute and chronic renal failure in hyperkalaemia?

A

worry more in acute as this can cause the patient to become acidotic with high potassium and acute onset - renal failure
chronic - compensation systems in place

77
Q

what is acidosis from?

A

intracellular exchange

78
Q

how can mineralocorticoid dysfunction result in hyperkalaemia?

A

in adrenocortical failure we are not producing angiotensin and therefore blood pressure is reduced and sodium is not retained - excess potassium due to diuresis not occuring effectively - results in Addisons - usually chronic
mineralocorticoid resistance from drugs such as spironolactone - potassium sparing diuretic

79
Q

what happens in cell death?

A

in cytotoxic therapy such as chemo there are large amount of cell breakdown and therefore a large amount of K released

80
Q

what is the treatment of hyperkalaemia?

A

stop the underlying cause, stop taking unnecessary supplements, give glucose or insulin to drive potassium into the cells, ion exchange resins which are for GIT potassium binding and dialysis which can be short or long term and renal perfusion or infiltration

81
Q

what are causes of potassium depletion?

A

low intake, increased urine loss, GIT losses, hypokalaemia without depletion

82
Q

what does low intake result in?

A

malnourishement

83
Q

what is the main cause of increased urine loss?

A

diuretic - iatrogenic - common - osmotic diuresis or diuretics

84
Q

what are other causes of increased urine loss?

A

tubular dysfunction - intrinsic renal problem resulting in renal failure - may be missing pumps or
mineralocorticoid excess - cushings or
disease of adrenal glands - tumours resulting in excess aldosterone

85
Q

how do GIT losses occur?

A

vomiting, diarrhoea, laxatives, fistulae - bypass internal connections and get abnormal linkages

86
Q

how can you have hypokalaemia without depletion?

A

alkalosis or insulin or glucose therapy

87
Q

what is the threshold value for potassium depletion?

A

<2.5mmol/L

88
Q

what are the effects of potassium depletion?

A

acute changes on the ICF/ECF ratios or chronic losses from the ICF

89
Q

what happens in acute changes in the ICF/ECF ratios?

A

this is particularly common with the elderly on too many diuretics and can have neuromusclular effects including muscle weakness, lethargy and heart arrhythmias

90
Q

what results from chronic losses from the ICF?

A

this can be due to the kidney and again has the same neuromuscular effects, as well as polyuria (which can exacerbate situation and alkalosis (HCO3- production) in the kidney, vascular and gut effects

91
Q

what are the gut effects of potassium depletion?

A

the ileus will seize up and not move due tpo absence of potassium as the muscular system breaks down - stasis of movement and blockage of bowel - needs suction to remove excess and drip of electrolytes post surgery

92
Q

how would potassium depletion be detected?

A

history, electrolyte investigation and clinical suspicion

93
Q

what is included in the history?

A

symptoms and lethargy and weakness, cardiac arrhythmia and diarrhoea, vomiting and drugs such as digoxin and diuretics

94
Q

what is included in the electrolyte investigation in potassium depletion?

A

hypokalaemia and alkalosis with high HCO3-

95
Q

what is the issue with potassium depletion?

A

it is easy to miss

96
Q

what is the treatment of potassium depletion?

A

prevention. replacement of deficit and monitor the plasma potassium regularly

97
Q

what is involved in prevention?

A

adequate supplementation and potassium sparing diuretics to stop depletion

98
Q

how would you replace deficit of potassium?

A

oral - 48mmol/day + diet (most effective way) - can overload if take any more
IV - <20mmol/day - slow as can push into hyperkalaemic state and cause arrhythmia if not careful

99
Q

what are the main conditions where plasma potassium needs to be monitored regularly?

A

in support of IV resuscitation from DM ketoacidosis
diuretic therapy
digoxin therapy
compromised renal function

100
Q

what is the issue with digoxin?

A

can become toxic and lead to potassium depletion

EMS MOD (28 decks)

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