electrolyte disorders Flashcards
(100 cards)
1
Q
what is U&Es?
A
urea and electrolytes
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
3
Q
how do you estimate U&Es?
A
through deduction - rather than direct - not possible in practice - look at water
4
Q
what are electrolyte disorders?
A
they are abnormal electrolytes
5
Q
how can electrolyte disorders result?
A
primary disease state, secondary consequence of a multitude of disease or iatrogenic
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
7
Q
what is the epidemiology of electrolyte disorders?
A
commonest chemical pathology test with 100000 cases per year
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
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
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
11
Q
what is sodium outside the cell?
A
higher - around 140mmol/L
12
Q
what happens to the concentration in plasma as exercise with no hydration?
A
concentration increases as volume is depleted
13
Q
normally the system is in equilibrium, what does changing any factor do?
A
causes the new steady state to be reached
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
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
16
Q
what is the total volume of water in the ECF and ICF?
A
42L
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
18
Q
what are the characteristics of isotonic fluid loss?
A
no change in concentration of sodium, loss is from ECF, no fluid redistribution
19
Q
what is loss of hypotonic solutions?
A
it is insensible loss such as vomiting and results in dehydration
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
21
Q
what are the characteristics of insensible loss?
A
small increase in ICF sodium and fluid redistribution between the ECF and ICF
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
23
Q
what is a hypotonic solution gain?
A
water or dextrose - dilute patient - sodium decreases
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
25
why might a patient with a hypotonic gain show swelling or oedema?
the water goes into the cells and they swell
26
what causes hyponatraemia ?
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
27
what does concentration of sodium in the blood depend on ?
water volume and redistribution
28
what is the result of sodium loss?
could be from diuretics - will lose Na in the ECF
29
what are the compensation mechanisms?
physiological or therapeutic
30
what comprises physiological?
thirst ADH or RAAS - ADH and RAAS can show what the patient is missing
31
what comprises therapeutic?
IV therapy, diuretics or dialysis
32
what is osmolality?
the rise of all solutes in a given volume of water
33
where is ADH produced and why?
it is produced by the median eminence in the brain and is released when osmolality increases/we are dehydrated. It reduces water being exctreted
34
what does ADH result in?
decreases renal water loss and increase thirst
35
how can you test ADH?
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
36
where is renin made and what does this activate?
it is made in the kidney and makes angiotensin in the adrenal glands made aldosterone
37
what is the role of aldosterone?
renal sodium retention in response to reduced IVV causing haemorrage or Na depletion
38
how can you see the action of RAAS?
look at urine sodium - very low means high aldosterone <10mmol/L means the RAAS is active
39
how do you replace isotonic loss?
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
40
how would you replace hypotonic loss?
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
41
what is hyponatraemia?
it is too little Na in the blood and ECF, there may be dilution too far and excess water in the ECF
42
what is hyerpnatraemia?
to little water in the ECF and too much Na
43
what is dehydration and what are the implications of this?
water deficiency and fluid deficiency (Na and water) - determine which it is so cant treat appropriately
44
what is euvolaemic hyponatraemia?
normal sodium but excess of fluid
45
what can the extravascular volume be?
euvolaemic, hypovolaemic or oedema
46
if someone is hypovolaemic, how do you identify the cause?
look at urine sodium
if greater than 20 - na losing nephritis, Addisons or diuretics
if less than 20 - vomiting, diarrhoea or skin loss
47
what are the causes of oedema?
CCF cirrhosis or nephrosis
48
if someone is euvolaemic hyponatraemic what do you do?
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
what is hypovolaemic hyponatraemia?
both fluid and sodium are low
50
what is oedema hyponatraemia?
increased fluid and sodium but fluid has larger increase than sodium
51
what would you do once water overload is established?
look at urine sodium to identify cause - >20 is SIADH, drugs and CRF, and <20 is stress, endocrine, post surgery and hypothyroid
52
what is hyponatraemia due to diuretics?
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
what does sodium diuresis result in?
water loss, no sodium retention concentrated urine
54
what is hyponatraemia due to SIADH?
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
what is the result of hypernatraemia due to decreased water intake?
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
what happens in osmotic diuresis in hypernatraemia?
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
what happens with hypernatraemia due to aldosterone?
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
what is the reference range of metabolism?
3.6-5mmol/L
59
what are the effects of abnormal potassium?
less than 3 or more than 6 - cardiac conduction defects,l abnormal neuromuscular excitability
60
what are the iatrogenic causes of potassium disorder?
commonly is the inappropriate use of IV fluids or drugs
61
what is measured for potassium?
the plasma potassium - it reflects a small proportion of the body potassium
62
why is serum potassium not often used?
serum potassium does not reflect body potassium
63
how do you determine the total body potassium?
through the total cell mass
64
what affects the plasma potassium significantly?
the exchange of ICF/ECF - potassium is pumped across membranes
65
what causes changes in the exchange of ICF/ECF?
acidosis, glucose/insulin therapy - potassium moved into cells, adrenaline - deficiency when going fast, rapid cellular incorporation in TPN or leukaemia
66
where is a large amount of potassium found?
intracellular fluid space - 98% - 3400 mmol
| 2% is found in plasma/interstitial fluid at a total of 70mmol
67
what is exchanged across the membrane for potassium?
H+ - both will bind to negatively charged proteins such as Hb
68
how do changes in the pH affect the equilibrium?
acidosis - potassium moves out of cells - hyperkalaemia
| alkalosis - potassium moves into cells - hypokalaemia
69
what happens in acidosis?
the potassium in the plasma can overstep the safe threshold
70
what happens in chronic acidosis?
high potassium is tolerated - cell produces more H+ and therefore they cannot escape so will shift K+ out
71
what differes from hyperkalaemia in chronic vs acute settings?
in acute setting cannot be tolerated - can lead to arrhythmia - ventilate to allow the heart to work properly but reducing acid
72
what can potassium depletion affect?
acid base status
73
what is the basis of acidosis?
H+ push into the cell and push K+ out so increase the concentration in plasma
74
what are the causes of hyperkalaemia?
artefactual, renal, acidosis, cell death and mineralocorticoid dysfunction
75
what is artefactual?
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
what is the difference between acute and chronic renal failure in hyperkalaemia?
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
what is acidosis from?
intracellular exchange
78
how can mineralocorticoid dysfunction result in hyperkalaemia?
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
what happens in cell death?
in cytotoxic therapy such as chemo there are large amount of cell breakdown and therefore a large amount of K released
80
what is the treatment of hyperkalaemia?
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
what are causes of potassium depletion?
low intake, increased urine loss, GIT losses, hypokalaemia without depletion
82
what does low intake result in?
malnourishement
83
what is the main cause of increased urine loss?
diuretic - iatrogenic - common - osmotic diuresis or diuretics
84
what are other causes of increased urine loss?
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
how do GIT losses occur?
vomiting, diarrhoea, laxatives, fistulae - bypass internal connections and get abnormal linkages
86
how can you have hypokalaemia without depletion?
alkalosis or insulin or glucose therapy
87
what is the threshold value for potassium depletion?
<2.5mmol/L
88
what are the effects of potassium depletion?
acute changes on the ICF/ECF ratios or chronic losses from the ICF
89
what happens in acute changes in the ICF/ECF ratios?
this is particularly common with the elderly on too many diuretics and can have neuromusclular effects including muscle weakness, lethargy and heart arrhythmias
90
what results from chronic losses from the ICF?
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
what are the gut effects of potassium depletion?
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
how would potassium depletion be detected?
history, electrolyte investigation and clinical suspicion
93
what is included in the history?
symptoms and lethargy and weakness, cardiac arrhythmia and diarrhoea, vomiting and drugs such as digoxin and diuretics
94
what is included in the electrolyte investigation in potassium depletion?
hypokalaemia and alkalosis with high HCO3-
95
what is the issue with potassium depletion?
it is easy to miss
96
what is the treatment of potassium depletion?
prevention. replacement of deficit and monitor the plasma potassium regularly
97
what is involved in prevention?
adequate supplementation and potassium sparing diuretics to stop depletion
98
how would you replace deficit of potassium?
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
what are the main conditions where plasma potassium needs to be monitored regularly?
in support of IV resuscitation from DM ketoacidosis
diuretic therapy
digoxin therapy
compromised renal function
100
what is the issue with digoxin?
can become toxic and lead to potassium depletion
