U&Es

Question 1

What is ammonia converted to in the liver?

Answer 1

Converted into urea using carbon dioxide.

Question 2

Describe urea?

Answer 2

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.

Question 3

What causes changes in the levels or urea?

Answer 3

protein intake, hepatic function and renal handling.

Question 4

What causes a rise in urea?

Answer 4

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

Question 5

What causes a low urea

Answer 5

Pregnancy (increased excretion raised GFR)
Low protein diet: less synthesised urea
Liver disease: liver failure, accumulation of ammonia

Question 6

Renal causes of high urea

Answer 6

Dehydration causing renal reabsorption

Pre-renal: hypoperfusion of the kidney
Glomerular damage: Glomerulonephritis, diabetes
Tubular disease
Urinary obstruction

Question 7

What is Creatinine

Answer 7

The waste product of creatine phosphate metabolism.
2% of creatine is converted to creatinine /day
Non-toxic
All creatinine produced is removed by the kidneys, No creatinine is reabsorbed.

Question 8

What is Creatinine clearance and what is its clinical significance?

Answer 8

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

Question 9

What is GFR

Answer 9

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

Question 10

What is an acute kidney injury?

Answer 10

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.

Question 11

Causes of a pre-renal AKI

Answer 11

Cardiac:
Heart failure, MI, arrhythmia, PE, shock, tamponade

Volume:
haemorrhage, GI loss, Renal loss, skin loss, sequestration, inadequate hydration, diuretics

Vasomotor factors:
Afferent constriction- sepsis, drugs (NSAIDS), hypercalcaemia,
Efferent dilation– ACE Inhibitors

Obstruction:
Thrombosis, embolism, hyperviscosity

Question 12

Causes of an intra-renal AKI

Answer 12

Vascular:
- Renal artery thrombosis, malignant hypertension

Glomerular:
Glomerular nephritis, vasculitis

Tubular:
Acute tubular necrosis, nephrotoxins, myoglobin

Interstitial:
infection, inflammation, drugs

Question 13

Causes of a Post renal AKI

Answer 13

Obstructive uropathy
a structural or functional hindrance of normal urine flow. It can be caused by a lesion/obstruction at any point in the urinary tract.

Question 14

What are the biochemical indications for CRRT

Answer 14

Refractory hyperkalemia above 6.5
Serum Urea above 30
Refractory metabolic acidosis below 7.1
Refractory electrolyte disturbances

Question 15

What are the clinical indications for CRRT

Answer 15

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

Question 16

What are the potential complications of AKI

Answer 16

Hyperkalemia
Acidosis
Pulmonary oedema
Uremic encephalopathy/pericarditis

Question 17

What is Rhabdomyolysis>

Answer 17

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.

Question 18

Who is at risk from rhabdomyolysis

Answer 18

Trauma. (RTC, burns, torture, surgery)
Ischaemic events.
Severe muscle exertion. (marathon runners / seizures)
Hyper Hypothermia.
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.

Question 19

What are the symptoms of Rhabdomyolysis

Answer 19

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.

Question 20

How does rhabdomyolysis cause AKI

Answer 20

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.

Question 21

What is the main diagnostic test for Rhabdomyolysis

Answer 21

The primary diagnostic indicator is an elevated serum creatine phosphokinase (CK) to at least five times the normal value. (normal approx 180 – 200 iuL)