Na, K, H20 and electrolyte disorders Flashcards

(34 cards)

1
Q

What is measured in U and Es?

A
Na
K
Cl
Bicarbonate (HCO3)
Urea
Creatinine
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2
Q

What is estimated in U and Es?

A

Water

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3
Q

What is electrolyte balance important?

A

Maintenance of cellular homeostasis
Cardiovascular electrophysiology
renal physiology

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4
Q

Clinical examples of poor electrolyte balance

A
haemorrhage 
poor intake - food and water 
diuretic therapy 
Diabetes
endocrine disorders- ADH, aldoesterone etc.
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5
Q

What are the concepts looked for in U and Es?

A

Concentrations, compartments, contents, volume, rates of gain and loss

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6
Q

What happens to a cell if you decrease the volume?

A

Will decrease the concentration of any solute

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7
Q

What happens to a cell if you increase the excretion of a solute?

A

The solute concentration will decrease

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8
Q

What is the normal Na level within cells?

A

10 mmol/L

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9
Q

what is the normal Na level within ECF?

A

140 mmol/L

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10
Q

What is the normal K level within cells?

A

150

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11
Q

What is the normal K level in the ECF?

A

5

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12
Q

What is isotonic solution?

A

similar to blood or blood

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13
Q

What happens during a loss of isotonic solution?

A

Loss in ECF
No change in Na
No fluid redistribution

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14
Q

What is hypotonic solution?

A

water

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15
Q

What happens during a loss of hypotonic solution?

A

Greater loss from ICF than ECF (not sure why need to check)
No change in Na
No fluid redistribution

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16
Q

What happens during a gain of hypotonic solution?

A

Greater gain to ICF than ECF
Small decrease in Na
Fluid redistribution between ECF an ICF

17
Q

What does ADH do? Where is it produced and how do we test for it?

A

Anti- diuretic hormones
Produced by eminence and release increases with rising osmolity, decreases renal water loss
Induced thirst
Test ADH status via plasma and urine osmolity

18
Q

What does the RAAS system do? How do we test for it?

A

Activated by Intravascular volume (decrease such as haemorrhage)
Test using measurement of plasma and urine Na
If urine

19
Q

What would happen if you replaced an isotonic fluid loss with

a. Isotonic fluid
b. hypotonic fluid

A

a. No change in Na or fluid redistribution- this is the correct one to do
b. Fall in Na and a fluid redistribution- this would dry out the patient

20
Q

What would happen is you replaced a hypotonic fluid loss with

a. isotonic fluid
b. hypotonic fluid

A

a. Na slightly increased but no fluid redistribution- this would over hydrate the patient
b. Na is restored and there is no fluid redistribution, this is the correct one to do

21
Q

What is hyponatraemia?

A

Too much H20, too little Na both in ECF

22
Q

What is hypernatremia?

A

Too much Na and too little H20 both in ECF

23
Q

What values within the ECF for K are potentially dangerous? What problems would it cause?

A

6

Cardiac conduction defects, abnormal neuromuscular

24
Q

What are the problems with measuring serum K? How would you determine total body K?

A

Most K is within the ICF therefore is not an accurate representation
Total body potassium determined by total cell mass

25
What sort of things cause ECF-ICF exchanges in K?
Acidosis or alkalosis Insulin/glucose therapy adrenaline Rapid cellular incorporation e.g TPN, leukaemia
26
What is the usual total mmol of K within the plasma?
70
27
What is the usual total mmol of K within the ICF?
3400
28
What do K and H both bind to?
negatively charged proteins e.g. Hb
29
What does Acidosis and Alkalosis do in terms of K concentration in the ECF?
Acidosis- H+ ions move into cell and displace K+ therefore it moves into ECF = HYPERKALCAEMIA Alkalosis - Less H+ therefore K moves into cell and there is less in ECF = HYPOKALCAEMIA
30
What are the artefactual, renal, mineralocorticoid, cell death and intercellular exchange causes of hypercalcaemia?
Artefactual- delay in sample testing, haemolysis (breakage of cells during sample taking releases K) and drug therapy Renal- ARfailure can increase K as it is not filtered out and chronic Rfailure Intracellular exchange- acidosis Mineralocorticoid - adrenocortical failure, use of spironolactone Cell death- chemo, large release of dead cell component s
31
How can we treat hyperkalaemia?
Correct acidosis- but be careful not to decrease it too much stop unnecessary supplements Give glucose and insulin- drives K back into cells Ion exchange resins- helps GIT K binding Dialysis- short term solution
32
What are the causes of K depletion?
Low intake increased urine loss - diuretics, tubular defects, mineralocorticoid excess (steroid therapy) GIT losses-vomiting, fistulae etc. Hypokalaemia without depletion-alkalosis, insulin/glucose therapy
33
Effects of K depletion? Acute and chronic
Acute-Neuromuscular- lethargy, weakness, heart arthymias Chronic- same neuromuscular as acute Kidney -polyuria and alkalosis due to increase in renal bicarbonate (due to damage of the kidneys) Gut can seize up Vascular
34
How do you treat a depletion is K? Prevention, replacement and who would you monitor closely?
Prevention- by using K sparing diuretics, adequate supplementation Replacement deficit- Oral 48mmol/day + diet IV