Renal Medicine - Electrolytes and Fluid Balance Flashcards
Give the criteria for the WHO performance status:
0
1
2
3
4
5
0: fully active without restriction
1: restricted in physically strenuous activity, but ambulatory and able to carry out light work
2: ambulatory and capable of self-care, but unable to carry out light work
3: capable of limited self-care, confined to bed or chair >50% of the time
4: completed disabled and confined to bed or chair; cannot self care
5: dead
Interpret the following VBG result:
PaO2: 14 (11 – 13 kPa)
pH: 7.33 (7.35 – 7.45)
PaCO2: 3.0 (4.7 – 6.0 kPa)
HCO3–: 17 (22 – 26 mEq/L)
Metabolic acidosis - partially compensated by respiratory alkalosis.
Interpret the following VBG result:
PaO2: 12.7 kPa (11 - 13 kPa)
pH: 7.50 (7.35 - 7.45)
PaCO2: 5.5 kPa (4.7 - 6.0 kPa)
HCO3-: 29 (22 - 26 mEq/L)
BE: +3
Metabolic acidosis - not compensated
Give some causes of metabolic alkalosis.
GI losses (e.g. diarrhoea / vomiting)
Renal losses (e.g. primary hyperaldosteronism, diuretics)
Intracellular shift (e.g. hypokalaemia)
What is the anion gap?
A calculation that is useful to work out what is the cause of metabolic acidosis?
Anion gap = sodium - (chloride + bicarbonate)
Normal anion gap 8-12
Give some causes of a metabolic acidosis, with anion gap >12.
Acidosis due to increased acid, for example:
- lactic acidosis in anaerobic exercise, sepsis and organ ischaemia
- ketoacidosis (e.g. diabetic, alcohol abuse)
- toxins (e.g. isoniazid, aspirin, methanol)
- renal failure
Give some causes of a metabolic acidosis, with anion gap <8.
Acidosis due to reduced alkali, for example:
- GI losses of HCO3 in vomiting and diarrhoea
- renal losses of HCO3 in renal tubular acidosis and Addison’s
- toxins (e.g. ammonium chloride, acetazolamide)
What are the causes of hypernatraemia?
Hypovolaemic hypernatraemia due to dehydration (e.g. diuretics, excess sweating, burns, diarrhoea).
Euvolaemic hypernatraemia due to renal losses (e.g. diabetes insipidus) and extra-renal losses (e.g. insensible and respiratory losses).
Hypervolaemic hypernatraemia due to sodium gains (e.g. primary hyperaldosteronism, Cushing’s syndrome, sodium chloride tablets)
What are the symptoms of hypernatraemia?
- thirst
- apathy
- irritability
- weakness
- seizures
- hyperreflexia
- coma
What is diabetes insipidus?
The lack of ADH, preventing the kidneys from being able to concentrate the urine, leading to polyuria.
How is hypernatraemia usually treated?
Free water
What are the causes of hyponatraemia?
Hypovolaemic hyponatraemia (e.g. diuretics, Addison’s, diarrhoea, vomiting).
Euvolaemic hyponatraemia (e.g. hypothyroidism, SIADH, adrenal insufficiency).
Hypervolaemic hyponatraemia (e.g. congestive heart failure, nephrotic syndrome, liver cirrhosis).
What is SIADH?
An excessive release of ADH causing excessive water reabsorption, causing a euvolaemic hyponatraemia.
How is hyponatraemia managed?
Acute - IV 3% saline solution + furosemide
Chronic - IV 0.9% saline + furosemide
Why is is dangerous to correct chronic hyponatraemia too quickly?
A rapid correction of chronic hyponatraemia can cause osmotic demyelination syndrome, whereby the myelin sheath within the pons is destroyed.
What is the main complication of hyperkalaemia?
Cardiac arrhythmias such as ventricular fibrillation.