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*Medicine: Renal & Urology > Fluid & Electrolyte Disorders > Flashcards

Fluid & Electrolyte Disorders Flashcards

1
Q

Hyponatraemia may be caused by water excess or sodium depletion. Causes of pseudohyponatraemia include hyperlipidaemia (increase in serum volume) or a taking blood from a drip arm. Urinary sodium and osmolarity levels aid making a diagnosis

What are possible causes when the urinary sodium is > 20 mmol/l?

A

If the urinary sodium is high and they are hyponatraemic, the sodium must be going through the kidneys (so caused by things that affect kidney)

  • Sodium depletion, renal loss (patient often hypovolaemic):
    • diuretics: thiazdes + loops
    • Addison’s disease
    • diuretic stage of renal failure
  • Patient often euvolaemic:
    • SIADH (urine osmolality > 500)
    • hypothyroidism
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2
Q

What are possible causes when the urinary sodium is low?

A

If the urinary sodium is low and they are hyponatraemic, the sodium must not be going through the kidneys and must be leaving the body some other way…

  • Sodium depletion, extra-renal loss:
    • diarrhoea, vomiting, sweating
    • burns
    • rectal adenoma
  • Water XS (patient often hypervolaemic and oedematous):
    • secondary hyperaldosteronism (heart failure, liver cirrhosis)
    • nephrotic syndrome
    • IV dextrose
    • psychogenic polydipsia
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3
Q

What are clinical features of hyponatraemia?

A
  • Anorexia / Nausea
  • Malaise / Weakness
  • Headache / Irritability
  • Confusion / Reduced GCS
  • Seizures
  • Also increased risk of falls in elderly
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4
Q

What is iatrogenic hyponatraemia?

A
  • If 5% glucose infused continuously without adding 0.9% saline, glucose is quickly used, rendering the fluid hypotonic and causing hyponatraemia
  • Especially in those pts on thiazides, women and those undergoing physiological stress
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5
Q

What is the treatment for mild hyponatraemia?

A
  • Fluid restriction sufficient
  • Loop diuretics
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6
Q

What is the treatment for moderate hyponatraemia?

A
  • Cautious rehydration w/ 0.9% NaCl in first 3-4 hrs to increase Na+ > 120 mmol/l
  • Then fluid restriction (< 800ml/day) + loop diuretics
  • Rapid correction → central pontine myelinolysis
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7
Q

What is the treatment for severe hyponatraemia?

A
  • Bolus of hypertonic saline until symptom resolution
  • Can also give ADH antagonist (conviaptan)
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8
Q

What is osmotic demyelination syndrome (central pontine myelinolysis)?

A
  • AKA ‘Locked-in syndrome’
  • Can occur due to overcorrection of severe hyponatraemia
  • To avoid this, Na+ levels are only raised by 4-6 mmol/l in a 24hr period
  • Symptoms occur after 2 days are usually irreversible
  • Dysarthria / Dysphagia / Paraparesis / Seizures / Confusion / Coma
  • Patients are awake but unable to move or verbally communicate
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9
Q

Summary of hyponatraemia

A
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10
Q

Hypernatraemia results usually when water loss is greater than Na loss.

What are causes of hypernatraemia?

A
  • Fluid loss without water replacement (diarrhoea, vomiting, burns)
  • Diabetes insipidus
  • Osmotic diuresis (for diabetic coma)
  • Primary aldosteronism: rarely severe, suspect if hypertensive
  • Iatrogenic: incorrect IV fluid replacement (XS saline)
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11
Q

What are the clinical features of hypernatraemia?

A
  • Lethargy / Weakness
  • Thirst
  • Irritability
  • Confusion / Coma
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12
Q

What is the management of hypernatraemia?

A
  • Give water orally if possible
  • If not, give glucose 5% IV slowly (1L/6h) guided by urine output and plasma Na
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13
Q

What is hyperkalaemia?

A
  • K+ > 6.5 mmol/L
  • Potential emergency + needs urgent assessment
  • Can cause myocardial hyperexcitability → VF → arrest
  • Concerns if fast irregular pulse, chest pain or ECG changes
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14
Q

What are causes of hyperkalaemia?

A
  • Acute kidney injury
  • Drugs → potassium sparing diuretics, ACEi, ARBs, spironolactone, ciclosporin, heparin
  • Metabolic acidosis
  • Addison’s disease
  • Rhabdomyolysis
  • Massive blood transfusion
  • Foods → salt substitutes, bananas, oranges, kiwi, avocado, spinach, tomatoes
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15
Q

What ECG changes occur in hyperkalaemia?

A
  • Tall-tented T waves
  • Loss of P waves
  • Broad QRS complexes
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16
Q

For hyperkalaemia, precipitating factors should be addressed (eg acute renal failure) and agravating drugs stopped. Treat K+ if > 6.5mmol/L or with ECG changes.

What is the acute treatment for hyperkalaemia?

A
  • IV 10% of 10ml calcium gluconate → slowly IV; stabilises cardiac membrane; repeat dose if necessary until ECG normalises up to a max dose of 40ml
  • Dextrose/Insulin infusion → 50ml of 50% dextrose + 10U soluble human insulin; shifts potassium from ECF to ICF; check BM every hour
  • Nebulised salbutamol → also shifts K+
  • Renal replacement therapy if underlying pathology cannot be corrected
17
Q

Potassium and hydrogen can be thought of as competitors. Hyperkalaemia tends to be associated with acidosis because as potassium levels rise fewer hydrogen ions can enter the cells. Hypokalaemia (K+ < 2.5) can be with either alkalosis or acidosis.

What are causes of hypokalaemia with alkalosis?

A
  • Vomiting
  • Thiazide + loop diuretics
  • Cushing’s syndrome
  • Conn’s syndrome (primary hyperaldosteronism)
18
Q

What causes hypokalaemia with acidosis?

A
  • Diarrhoea
  • Renal tubular acidosis
  • Acetazolamide
  • Partially treated DKA

Mg deficiency may also cause hypokalaemia - normalising potassium elvle may be difficult until Mg def is corrected

19
Q

What are clinical features of hypokalaemia?

A
  • Muscle weakness
  • Hypotonia + hyporeflexia
  • Cramps
  • Tetany
  • Palpitations

Hypokalaemia also exacerbates digoxin toxicity

20
Q

What are the ECG features of hypokalaemia?

A
  • U waves
  • Small or absent T waves
  • Prolonged PR interval
  • ST depression
21
Q

What is the treatment for mild hypokalaemia?

A
  • K+ > 2.5 mmol/l
  • No symptoms
  • Give oral K+ supplement
  • Review K+ after 3 days
22
Q

What is the treatment for severe hypokalaemia?

A
  • K+ < 2.5 mmol/l
  • Dangerous symptoms
  • Infuse I K+ into large vein 10-20 mmol K+ / hr
  • Do not give K+ if oliguric
23
Q

What is Bartter’s syndrome?

A
  • Due to impaired salt transport
  • Soidum reabsorption increases further along nephron in exchange for H+ and K+
  • Therefore all cause a hypokalaemic, hypochloraemic metabolic alkalosis
  • Presents in childhood
  • Think of Bartter’s as taking lots of furosemide
24
Q

What is Fanconi syndrome?

A
  • Generalised impairment of proximal tubular function
  • Leads to glycosuria, phosphaturia, uricosuria and tubular proteinuria
  • Negative dipstick but positive urine P:CR
25
Q

What is Gitelman syndrome?

A

Milder version of Bartter’s

26
Q

What is distal (type 1) renal tubular acidosis (RTA)?

A
  • Failure of acid (H+) excretion
  • Primary genetic disease or secondary to autoimmune disease (eg. Sjogren’s, SLE), or toxins (eg. lithium)

*Medicine: Renal & Urology (23 decks)

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