Flashcards in U&Es Deck (21)
What is ammonia converted to in the liver?
Converted into urea using carbon dioxide.
Urea is a small non-toxic water-soluble molecule.
Freely filtered by the kidneys - 50% is found in the urine and 50% is reabsorbed and used to help maintain osmotic pressure and water concentration.
What causes changes in the levels or urea?
protein intake, hepatic function and renal handling.
What causes a rise in urea?
High protein diet: increased urea synthesis
Chronic starvation: increased protein catabolism
Gastrointestinal bleeding: increased intestinal protein (blood) absorption and increased urea synthesis
Dehydration: increased renal tubular reabsorption
Steroids: protein catabolism
What causes a low urea
Pregnancy (increased excretion raised GFR)
Low protein diet: less synthesised urea
Liver disease: liver failure, accumulation of ammonia
Renal causes of high urea
Dehydration causing renal reabsorption
Pre-renal: hypoperfusion of the kidney
Glomerular damage: Glomerulonephritis, diabetes
What is Creatinine
The waste product of creatine phosphate metabolism.
2% of creatine is converted to creatinine /day
All creatinine produced is removed by the kidneys, No creatinine is reabsorbed.
What is Creatinine clearance and what is its clinical significance?
Creatinine clearance reflects the glomerular filtration rate (GFR).
Creatinine Clearance is the volume of blood plasma that is cleared of creatinine per unit of time
What is GFR
It is a measurement of how much liquid and waste is passing from the blood through the glomeruli and out into the urine during each minute.
Plasma creatinine only increases when >60% of GFR is lost
What is an acute kidney injury?
An abrupt reduction in kidney function. It can complicate chronic illness or be the sole disease affecting a person. It is not inevitable in acute illness and is in many cases preventable. It is defined as;
An increase in serum creatinine of 26 µmol/l within 48 hours.
An increase in serum creatinine > 1.5 times above baseline values within 1 week.
Urine output of < 0.5ml/kg/hr for > 6 consecutive hours.
Causes of a pre-renal AKI
Heart failure, MI, arrhythmia, PE, shock, tamponade
haemorrhage, GI loss, Renal loss, skin loss, sequestration, inadequate hydration, diuretics
Afferent constriction- sepsis, drugs (NSAIDS), hypercalcaemia,
Efferent dilation– ACE Inhibitors
Thrombosis, embolism, hyperviscosity
Causes of an intra-renal AKI
- Renal artery thrombosis, malignant hypertension
Glomerular nephritis, vasculitis
Acute tubular necrosis, nephrotoxins, myoglobin
infection, inflammation, drugs
Causes of a Post renal AKI
a structural or functional hindrance of normal urine flow. It can be caused by a lesion/obstruction at any point in the urinary tract.
What are the biochemical indications for CRRT
Refractory hyperkalemia above 6.5
Serum Urea above 30
Refractory metabolic acidosis below 7.1
Refractory electrolyte disturbances
What are the clinical indications for CRRT
Urine output of less than 0.3ml/kg/her
AKI with multiple organ failure
refractory volume overload
Endo organ damage
to create intravascular space for the administration of blood products and nutrition
Severe poisoning and drug overdose
severe hypothermia or hyperthermia
What are the potential complications of AKI
What is Rhabdomyolysis>
It is a term used to describe the direct or indirect death of skeletal muscle fibres with the resultant release of their contents into the bloodstream.
Who is at risk from rhabdomyolysis
Trauma. (RTC, burns, torture, surgery)
Severe muscle exertion. (marathon runners / seizures)
Prolonged muscle compression. (unconscious)
Sickle cell trait.
Drug related. (Heroine, cocaine, ecstasy, statins)
Rare metabolic derangements.
Bacterial and Viral infections.
Rare inherited disorders (MH)
Toxins – Ethanol, envenomation.
What are the symptoms of Rhabdomyolysis
Generalised problems including malaise, fever, tachycardia, nausea, and vomiting.
Massive sodium and water shifts cause profound volume depletion. Swollen muscles uptake huge volumes of ECF – HYPOVOLAEMIC SHOCK.
Potassium shifts – severe HYPERKALAEMIA.
Calcium is absorbed into hypoxic tissues. Calcium shifts lead to calcium deposition into muscle cytosol and severe HYPOCALCAEMIA.
HYPERKALAEMIA and HYPOCALAEMIA are negative inotropes – HYPOTENSION / REDUCED CARDIAC OUTPUT.
Profuse vasodilatation (with exception of intense renal vasoconstriction)- HYPOTENSION / VERY LOW SVR.
How does rhabdomyolysis cause AKI
Baroreceptors stimulate vasoconstrictor release.
Myoglobin chelates renal nitric oxide - intense renal vasoconstriction and ischaemia.
Phosphate, purines and myoglobin are nephrotoxic (especially with underlying volume depletion, aciduria and increased urinary concentration)
Haem casts are formed in distal tubules causing obstruction and stasis – proximal tubular necrosis occurs.
Result – ACUTE KIDNEY INJURY.