3. Electrolytes and the Kidney Flashcards

1
Q

what is urea

A

produced in the liver
excretion of ammonia and breakdown products of amino acids
excreted in urine

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2
Q

normal serum urea

A

1.7 - 8.3 mmol/l

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3
Q

urea levels in disease

A

decreased in liver disease

increased in intravascular depletion, blood meal (GI haemorrhage) and renal failure

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4
Q

symptoms when urea >20mmol/l

A
nausea
decreased appetite 
itchiness 
tiredness
smelly breath 
metallic taste in mouth
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5
Q

symptoms when urea >60mmol/l

A

extreme uraemic frost
uraemic pericarditis
encephalopathy

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6
Q

what is creatinine

A

breakdown of creatinine phosphate in muscle
usually produced at fairly constant rate by the body
not toxic itself
less affected by fluid shifts

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7
Q

how is creatinine cleared

A

only cleared by the kidney

the less the number of nephrons, the more build up of creatinine

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8
Q

normal creatinine level

A

62 - 106 umol/l - dependent on muscle mass
old lady - 63 umol/l
muscular male - 106 umol/l

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9
Q

eGFR at CKD stages

A
CKD 1 - >90mls 
CKD 2 - >60mls 
CKD 3a - >45mls 
CKD3b - >30mls
CKD 4 - >15mls 
CKD 5 - <15mls
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10
Q

calculations for eGFR

A

MDRD

Cockroft and Gault

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11
Q

hyponatraemia and disorders of urine dilution

A

disorders of urine dilution underlie hyponatraemia
defect with Na/Cl transport out of thick ascending loop/distal convoluted tubule
continued secretion of ADH, stimulated by non-osmotic mechanism

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12
Q

hyponatraemia diagnostic approach

A

assess volume status

  • hypovolaemia: measure urinary Na+
  • euvolaemia
  • hypervolaemia: measure urinary Na+
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13
Q

hyponatraemia and hypovolaemia with urinary Na+>20mmol/l

A

renal losses

  • diuretic excess
  • mineralocorticoid deficiency
  • salt-losing neophripathy
  • bicarbonaruria with renal tubular acidosis and metabolic alkalosis
  • ketonuria
  • osmotic diuresis
  • cerebral salt wasting
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14
Q

hyponatraemia and hypovolaemia with urinary Na+<20mmol/l

A

extrarenal losses

  • vomiting
  • diarrhoea
  • third spacing of fluids in burns, pancreatitis, trauma
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15
Q

hyponatraemia and euvolaemia

A
  • glucocorticoid deficiency
  • hypothyroidism
  • stress
  • drugs
  • SIADH
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16
Q

hyponatraemia and hypervolaemia with urinary Na+>20mmol/l

A

acute or chronic renal failure

17
Q

hyponatraemia and hypervolaemia with urinary Na+<20mmol/l

A
  • nephrotic syndrome
  • cirrhosis
  • cardiac failure
18
Q

how is potassium abrosbed

A

efficiently absorbed from GI tract

present in most foods (bread, avocado, chocolate, leafy green veg)

19
Q

where is potassium distributed

A

major cellular cation

however, is distributed intracellularly and intracellularly

20
Q

normal serum K+

A

3.2 - 5.1 mmol/L

21
Q

causes of hypokalaemia

A

redistribution:
- insulin
- theophylline
- adrenergic use
non-renal loss:
- sweating
- vomiting
-diarrhoea
poor diet
renal loss

22
Q

hypokalaemia caused by renal loss

A

drugs - diuretics, aminoglycosides, amphotericin
RTA or metabolic acidosis
Low BP - Bartter’s or Gittleman’s
High BP
high aldosterone, normal cortisol - hyperaldosteronism
low aldoseterone, normal cortisol - Liddle’s
low aldosterone, high cortisol -Cushing’s

23
Q

cardiovascular complications in chronic hypokalaemia

A

hypertension

ventricular tachycardia

24
Q

endocrine complications in chronic hypokalaemia

A

impairs insulin and sensitivity

25
Q

muscular complications in chronic hypokalaemia

A

impairs muscle contraction

26
Q

renal complications in chronic hypokalaemia

A

mild tubulointerstitial fibrosis
renal cyst formation
metabolic alkalosis (increased net renal excretion)
polyuria

27
Q

liver complications in chronic hypokalaemia

A

increased renal ammonia production - may worse hepatic encephalopathy

28
Q

hyperkalaemia

A

present <1% healthy adults
kidneys have very large capacity to excrete K+
indicates impaired renal excretion

29
Q

causes of hyperkalaemia

A

impaired renal excretion - CKD 4/5
drugs imparing secretion - spironolactone, amiloride, ACE inhibitors, ARBs
increased K+ load - rhabdomyolysis, haemolysis, GI bleed
increased intake
peusdohyperkalaemia - haemolysis (during blood collection/storage, rheumatoid/infectious mononucleosis)

30
Q

drugs that impair K+ secretion

A

spironolactone
amiloride
ACE inhibitors
ARBs

31
Q

hyperkalaemia treatment

A
back into cells:
- salbutamol 
- insulin and dextrose 
- sodium bicarbonate (if acidotic) 
stablisation: calcium gluconate
removal: 
- pee it out, iv fluids and diuretics 
dialysis
32
Q

body pH

A

7.35 - 7.45

essential for functioning of proteins, enzymes etc

33
Q

how is body pH maintained

A

large net acid production: 1mmol H+/kg
buffers provide immediate defence against acid/alkali
resp system regulates CO2 tension
kidneys regulate HCO3 tension

34
Q

how is HCO3 recovered in kidneys?

A

in proximal tubule:
- broken down into water and CO2 in lumen
- combines with OH- in cell to reform HCO3
- transported out to interstitium
in cortical collecting duct:
- water and CO2 in cell broken to make HCO3-
- transported out of cell - exchanged with Cl-

35
Q

managing acid-base disturbance

A

determine underlying cause (drugs, AKI, CKD, dehydration)
reverse underlying cause
replace/remove
renal interventions

36
Q

sodium bicarbonate in severe metabolic acidaemia

A

generally safe to give isotonic NaHCO3 1.26%

removing stimulus to production of lactate/ketones will allow oxidative mechanisms