U&Es

Question 1

Causes of abnormal electrolytes

Answer 1

• Primary disease state - elderly/poor intake, haemorrhage, increased losses (pyrexia and heat). endocrine disorders (diabetes insipidus, diabetes and mellitus , disorders of ADH, aldosterone, etc).
• Secondary consequence of a multitude of diseases
• Iatrogenic (caused by examination or treatment) problems are very common - diuretic therapy

Question 2

Physiological Compensatory Mechanisms

Answer 2

Thirst, ADH, Renin-Angiotensin-Aldosterone System

Question 3

Therapeutic Compensatory Mechanisms

Answer 3

IV Therapy, Diuretics, Dialysis

Question 4

Loss of 2L of isotonic fluid (e.g. blood, fistula fluid)

Answer 4

Loss is from ECF. No change in [Na]. No fluid distribution.

Question 5

Replacement of loss of 2L of isotonic fluid

Answer 5

“Like with like” (isotonic fluid) works best. Does not change {Na] or fluid distribution.

If you were to try to replace with hypotonic fluid, it would cause a fall in [Na] and fluid distribution (more moves intracellularly).

Question 6

Loss of 3L of hypotonic fluid (e.g. insensible loss)

Answer 6

• Greater loss from ICF (1L) than ECF (2L).
• Small increase in [Na].
• Fluid redistribution between ECF and ICF (initial loss is from ECF (3L) then ICF replaces loss from ECF partially (2L), so more lost from ICF (2L)).

Question 7

Replacement of loss of 3L of hypotonic fluid

Answer 7

“like with like” Replace with Hypotonic, [Na] restored, fluid distribution.

If replaced with isotonic fluid, [Na] remians slightly increased and theres no fluid distribution meaning ECF is high and ICF is low.

Question 8

ADH

Answer 8

Stimulated in response to a rise in concentration of osmotically active particles - decreases renal water loss, increases thirst.

Question 9

RAAS

Answer 9

• Activated by reduced intra-vascular volume (IVV) which can be caused by Na depletion or haemorrhage.
• Aldosterone induces renal Na retention (which brings water with it).

Question 10

Simple test used to measure RAAS status?

Answer 10

• measure plasma and urine Na
• if urine <10mmol/l suggests RAAS active
• if not active could be due to a derangement of mineralocorticoids

Question 11

Urea

Answer 11

• Normal breakdown product of protein, filtered at glomerulus and major component of urine. Approx 800mmol/l is filtered per day.
• Sensitive marker for dehydration
• Sodium and urea concs often parallel each other during fluid correction.
• Elevated urea often found in gastric bleed, CCF, shock, MI, and severe burns.
• Low urea with low protein intake, increase IV fluids.

Question 12

Creatinine

Answer 12

• Breakdown product of protein and muscle.
• Usually filtered freely at the glomerulus.
• Plasma and urine values typically reflect muscle mass - mo’ muscle, mo’ creatinine.
• Marker of renal dysfuction.

Question 13

What influences GFR?

Answer 13

Renal perfusion pressure, renal vascular resistance, glomerular damage, post-glomerular resistance.

Question 14

eGFR

Answer 14

• estimated GFR

- used to aid staging of chronic kidney disease

Question 15

AKI Flag

Answer 15

• used to flag up incipient Acute Kidney Injury

- Highlights subtle changes in renal function

Question 16

Psuedohyponatraemia

Answer 16

Less sodium because there is less water due to displacement

Question 17

Low Sodium Causes

Answer 17

• Hypovolaemic - if urine sodium is >20 then Diuretics, Addison’s or Na-losing Nephritis. If urine sodium <20 then vomiting, diarrhoea, skin loss.
• Oedema - Congestive Cardiac Failure Cirrhosis and Nephrosis
• Euvolaemic - with normal plasma osmolality, pseudohyponatraemia. With high plasma osmolality, hypertonic hyponatraemia. With low plasma osmolality, water overload. Water overload’s underlying cause can be divided into further two subdivisions: Urine sodium >20 SIADH, Drugs, and Chronic Renal Failure; Urine sodium <20 stress, post surgery and hypothyroidism.

Question 18

Relationship between K+ and H+

Answer 18

• They exchange across the cell membrane.
• Acidosis - K+ out of cell, H+ in. - High potassium.
• Alkalosis - K+ into cell, H+ out. - Low potassium
• Potassium levels can affect acid-base status.

Question 19

Causes of High K+

Answer 19

• Artefactual - delay in sample analysis, haemolysis (when samples are taken out of the body, K+ pumps become slower so longer the delay, slower the pumps, so there in a rise in [K+]), drug therapy - excess intake.
• Renal - acute or chronic renal failure.
• Acidosis
• Minerlocorticoid Dysfunction - adrenocorticoid failure or mineralocorticoid resistance e.g. spironolactone.
• Cell Death - cytotoxic therapy.

Question 20

Causes of Low K+

Answer 20

• Low Intake
• Increased urine loss - diuretics/osmotic diuresis, tubular dysfunction, mineralocorticoid excess
• Gastrointestinal losses - vomiting, diarrhoea/laxatives, fistulae
• Low serum K+ without depletion - alkalosis, insulin/glucose therapy

Question 21

Effects of K+ Depletion (<2.5 mmol/l)

Answer 21

• Acute changes in ICF/ECF ratios - neuromuscular: lethargy, muscle weakness, heart arrhythmias
• Chronic losses from the ICF - neuromuscular: lethargy, muscle weakness, heart arrhythmias
• Kidney - polyuria, alkalosis (increases renal HCO3- production)
• Vascular
• Gut

Question 22

Suspect K+ depletion when..

Answer 22

• diarrhoea, vomiting, drugs (diuretics, digoxin)
• alkalosis - raised HCO3
• Symptoms of lethargy/weakness
• Cardiac arrhythmias