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
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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)
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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
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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.
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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
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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.
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7
Q

What causes reduced serum urea levels?

A

Non-pathological, associated with pregnancy and those on a low-protein diet.

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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
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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

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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
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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.
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