U&E Interpretation Flashcards
1
Q
What does a standard urea and electrolyte profile account for?
A
- Serum creatinine
- Estimated glomerular filtration rate (eGFR)
- Serum urea
- Serum sodium
- Serum potassium
2
Q
Why check U&Es?
A
- Renal impairment can lead to imbalances in certain electrolytes
- Kidney excretes urea and creatinine - used as markers of renal function
- Assessing urea levels in the case of suspected upper gastrointestinal haemorrhage.
- Suspected electrolyte disturbances due to non-renal causes, medication monitoring (e.g. after starting ACE inhibitors)
3
Q
What are some drugs that may require U&E monitoring?
A
- ACE inhibitors and ARBs
- Diuretics: spironolactone, thiazide diuretics (e.g. indapamide), loop diuretics (e.g. furosemide)
- Direct-acting oral anticoagulants (DOACs)
- Carbamazepine
- Lithium
- Digoxin
4
Q
Describe creatinine.
A
- Waste product of muscle metabolism excreted entirely by the kidney
- Levels determined by extent of filtration from bloodstream by kidney - high levels indicate renal dysfunction
- As the serum creatinine rises, the eGFR will decrease, indicating worsening kidney dysfunction.
5
Q
Describe urea.
A
- Waste product of protein breakdown produced in the liver.
- Kidneys predominantly excrete urea, and it can be used as a surrogate marker of renal function
6
Q
What causes raised serum urea levels?
A
- Renal dysfunction: decreased excretion of urea into the urine.
- Dehydration: urea rises quickly in dehydration, even in the presence of normally functioning kidneys. This is physiologically mediated by anti-diuretic hormone (ADH), released from the posterior pituitary gland in response to intravascular volume depletion. ADH increases urea and water reabsorption in the collecting ducts.
- Upper gastrointestinal bleeding: blood in the upper GI tract is broken down into proteins, which are transported to the liver via the portal vein and metabolised into urea.
7
Q
What causes reduced serum urea levels?
A
Non-pathological, associated with pregnancy and those on a low-protein diet.
8
Q
Describe sodium.
A
- Main determinant of plasma osmolality, and serum levels are closely related to hydration (volume) status and regulated by ADH
- Symptoms of both hypernatremia and hyponatremia are primarily neurological. Mild symptoms include fatigue, weakness and confusion, but can progress to severe symptoms such as seizures and coma
9
Q
Describe hypernatraemia. PART 1
A
- Serum sodium level >146mmol/L. It is most commonly caused by dehydration (e.g. unreplaced skin or GI losses of hypotonic fluid)
Rarer causes of hypernatraemia include:
- Diabetes insipidus
- Drugs (e.g. loop diuretics)
- Osmotic diuresis (e.g. in hyperglycemic states)
- Extreme levels of salt ingestion
10
Q
Describe hypernatraemia. PART 2
A
- In most cases, where there is a clear history implicating dehydration (e.g. vomiting/diarrhoea), treatment involves gentle rehydration with intravenous hypotonic fluids (e.g. 5% dextrose).
- Essential to monitor sodium levels during treatment, as correcting the hypernatraemia too rapidly can lead to intracerebral fluid shifts and central pontine myelinolysis
11
Q
Describe hyponatraemia.
A
- Serum sodium level <135mmol/L. It is often caused by a failure to excrete water normally i.e an excess of water in the body in relation to sodium (e.g. SIADH)
- Treatment can vary according to the underlying cause and the patient’s fluid status. Important to regularly monitor sodium levels to avoid rapid correction.