U&Es Flashcards
Causes of abnormal electrolytes
- 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
Physiological Compensatory Mechanisms
Thirst, ADH, Renin-Angiotensin-Aldosterone System
Therapeutic Compensatory Mechanisms
IV Therapy, Diuretics, Dialysis
Loss of 2L of isotonic fluid (e.g. blood, fistula fluid)
Loss is from ECF. No change in [Na]. No fluid distribution.
Replacement of loss of 2L of isotonic fluid
“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).
Loss of 3L of hypotonic fluid (e.g. insensible loss)
- 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)).
Replacement of loss of 3L of hypotonic fluid
“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.
ADH
Stimulated in response to a rise in concentration of osmotically active particles - decreases renal water loss, increases thirst.
RAAS
- 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).
Simple test used to measure RAAS status?
- measure plasma and urine Na
- if urine <10mmol/l suggests RAAS active
- if not active could be due to a derangement of mineralocorticoids
Urea
- 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.
Creatinine
- 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.
What influences GFR?
Renal perfusion pressure, renal vascular resistance, glomerular damage, post-glomerular resistance.
eGFR
- estimated GFR
- used to aid staging of chronic kidney disease
AKI Flag
- used to flag up incipient Acute Kidney Injury
- Highlights subtle changes in renal function
Psuedohyponatraemia
Less sodium because there is less water due to displacement
Low Sodium Causes
- 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.
Relationship between K+ and H+
- 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.
Causes of High K+
- 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.
Causes of Low K+
- 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
Effects of K+ Depletion (<2.5 mmol/l)
- 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
Suspect K+ depletion when..
- diarrhoea, vomiting, drugs (diuretics, digoxin)
- alkalosis - raised HCO3
- Symptoms of lethargy/weakness
- Cardiac arrhythmias
