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Flashcards in U&Es Deck (21)
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1

What is ammonia converted to in the liver?

Converted into urea using carbon dioxide.

2

Describe urea?

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.

3

What causes changes in the levels or urea?

protein intake, hepatic function and renal handling.

4

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

5

What causes a low urea

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

6

Renal causes of high urea

Dehydration causing renal reabsorption

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

7

What is Creatinine

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.

8

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

9

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

10

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.

11

Causes of a pre-renal AKI

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

12

Causes of an intra-renal AKI

Vascular:
- Renal artery thrombosis, malignant hypertension

Glomerular:
Glomerular nephritis, vasculitis

Tubular:
Acute tubular necrosis, nephrotoxins, myoglobin

Interstitial:
infection, inflammation, drugs

13

Causes of a Post renal AKI

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.

14

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

15

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

16

What are the potential complications of AKI

Hyperkalemia
Acidosis
Pulmonary oedema
Uremic encephalopathy/pericarditis

17

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.

18

Who is at risk from rhabdomyolysis

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.

19

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.

20

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.

21

What is the main diagnostic test for Rhabdomyolysis

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