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MEDICINE - Renal > Electrolytes & Fluid balance > Flashcards

Electrolytes & Fluid balance Flashcards

1
Q

Man comes in who is hypernatraemic. What’s the most common cause and how does he present?

A

Water deficit.

He complains of being thirsty. Apathy, irritability, weakness, confusion, reduced consciousness, seizures, hyperreflexia, spasticity, coma.

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2
Q

What are some common causes of hypovolaemic hypernatraemia (renal and non-renal)

A
  • renal free water loses
    • osmotic diuresis (increased urination due to certain substances in the urine eg. in hyperglycaemia, uraemia, high protein tube feeding)
    • Loop diuretics
    • Intrinsic renal disease
  • Non-renal free water losses
    • excess sweating
    • burns
    • diarrhoea
    • fistulas
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3
Q

What are some renal/extra-renal causes of euvolaemic Hypernatraemia

A

Renal Losses

  • Diabetes insipidus
  • Hypodipsia (decreased thirst sensation)

Extra-renal losses

  • Insensible eg. lost in stool, skin, etc
  • Respiratory losses
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4
Q

What are some causes of hypervolaemic hypernatraemia?

A
  • primary hyperaldosteronism
  • Cushings Syndrome
  • hypertonic dialysis
  • hypertonic sodium bicarbonate
  • sodium chloride tablets
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5
Q

Explain what Diabetes Insipidus is and what’s a common differential for it?

A

Prsents as polydipsia and polyuria.

Central DI = Hypothalamus does not make ADH.

Usually due to trauma, post-op, tumours, cerebral sarcoid/TB, infection like meningitis/encephalitis, cerebral vasculitis (SLE/wegeners)

Nephrogenic = kidneys are unresponsive to ADH

Usually due to drugs (lithium, amphoterecin, demeclocycline), hypokalaemia, hypercalcaemia, tubulointerstitial disease, congenital

Differential = psychogenic polydipsia (excessive fluid intake although there is not the stimuli to drink. usually psychiatric eg. schizophrenia)

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6
Q

How would you treat DI?

A

Central = drink water to not be dehydrated, Desmopressin (basically ADH. SE is hyponatraemia if you drink too much fluids while on it and retain too much fluids)

Nephrogenic = reduce salt and proteins, thiazide diuretics, NSAIDs to reduce urine production by kidney

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7
Q

What are some causes of hyponatraemia (Udi list!)

A
  • SIADH
  • Thiazide diuretics
  • Addisons (hyperkalaemia)
  • Dehydration eg. diarrhoea, vomitting, buns etc
  • Heart failure
  • Liver failure
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8
Q

How would hyponatraemia present?

A

Decreased perception and gait disturbance, yawning, nausea, reversible ataxia, headache, apathy, confusion, seizures, coma

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9
Q

What investigations would you do to investigate a Pseudohyponatraemia?

A

Pseudohyponatraemia = serum sodium <135mEq/L in a setting of normal serum osmolality

Eg. in hyperglycaemia, uraemia, high lipids, myeloma

  • plasma osmolality (if normal/raised = pseudohyponatraemia)
  • Urine Na+ (if <20 then non-renal salt losses. If >40 then SIADH)
  • TSH and 9am cortisol
  • calcium
  • albumin
  • glucose
  • LFT
  • CT head or chest if SIADH suspected
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10
Q

What are some renal/non-renal causes for Hypovolaemic Hyponatraemia?

A

You know it’s renal if Urine Na+ <20mmol/L

  • Thiazide diuretics
  • Addisons
  • Osmotic diuresis (glucose, urea in recovering ATN)

Non-renal

  • diarrhoea, vomiting, sweating
  • third space losses (burns, bowel osbtruction, pancreatitis)
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11
Q

How would you treat Hypovolaemic Hyponatraemia?

A

IV fluids (0.9% NaCl at 1-3ml/kg/hour)

and K+ if necessary

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12
Q

What are some common causes of euvolaemic hyponatraemia?

A
  • Hypothyroidism (increased ADH)
  • Primary polydipsia (urine osmolality <100)
  • Glucocorticoid deficiency (adrenal insufficiency)
  • SIADH
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13
Q

How would you recognise SIADH?

A
  • low serum osmolality
  • inappropriately concentrated urine (urine osmolality >100)
  • Urine Na >20
  • Clinical euvolaemia
  • Not on diuretics
  • Normal renal, thyroid, adrenal function
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14
Q

How would you manage SIADH?

A

Manage:

Fluid restrict to <800ml/day.

PO Sodium Chloride and Furosemide.

Demeclocycline induces Diabetes Insipidus, reversing the effect of ADH.

Tolvaptan also suppresses ADH.

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15
Q

What are some causes of hypervolaemic hyponatraemia?

A

Congestive heart failure, liver cirrhosis, nephrotic syndrome

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16
Q

What rate should you aim to correct hyponatraemia and why?

A

Aim to correct at <12mmol/L/day

Central Osmotic Myelinosis!!! (Most commonly affected is the pons)

Rapid increase in Na+ causes H2O to shift out of brain cells, causing destruction of myelin and nerve fibres.

Symptoms show 2-3 days after hyponatraemia correction = decreased awareness, dysarthria, dysphagia.

Eventually locked in syndrome, coma.

17
Q

What are the basic concepts of treating Acute and Chronic (symptomatic/asymptomatic) Hyponatraemia?

A

Acute

  • 3% hypertonic saline IV boluses with Furosemide

Chronic

  • If symptomatic - isotonic saline and furosemide
    • hypertonic saline boluses if seizures
  • If asymptomatic - water restriction, stop offending drug.
    • If dehydrated - restore with fluids!
    • If overloaded - Na and H2O restriction and diuretics.
18
Q

What are some causes of hyperkalaemia (Udi list!!)

A
  • Pseudohyperkalaemia (RBC lysis due to poor blood drawing)
  • Addisons
  • Periodic Paralysis (rare)
  • Gordon’s syndrome (rare)
  • K+ rich diet in CKD (dried fruit, potatoes, oranges, tomatoes, avo, nuts)
  • Drugs eg. Ace inhibitors, ARBs, K+ sparing (amiloride, spironolactone), NSAIDs, Heparin, LMWH, cyclosporin or calcineurin inhibitors, high dose Trimethoprim, Digoxin toxicity, B Blockers
  • Succinylcholine use
  • Rhabdomoyolysis, tumour lysis, massive haemolysis
  • Acidosis
  • DKA
19
Q

What is Hyporeninaemic Hypoaldosteronism?

A

Hyperkalaemic Hypochloraemic metabolic acidosis, associated with some renal insufficiency (a reduced eGFR). Often Hypertensive.

Common in diabetes nephropathy, acute GN (nephritis), sickle cell, NSAIDs, Calcineurin Inhibitors, Lupus Nephritis

Treat with low potassium diet and Loop/Thiazide diuretic to excrete K+.

20
Q

How does hyperkalaemia present clinically?

A
  • cardiac arrhythmias eg. VF
    muscle weakness, paralysis, paraesthesia
  • decreased deep tendon reflexes (due to persistent depolarisation of Na+ channels)
  • nausea, vomiting, diarrhoea
21
Q

How does hyperkalaemia present on an ECG?

A
22
Q

How would you manage hyperkalaemia?

(Theres 3 main principles)

A

1) Stabilise the myocardium to prevent arrhythmias

  • 10mls of 10% Calcium Gluconate over 5-10 mins

2) Shift K+ back into intracellular space

  • 10 units IV fast acting insulin (actrapid)
  • 50mls IV glucose/dextrose 50%
  • 500mls of 1.4% Sodium Bicarbonate (only useful in acidotic patients)
  • 5-10mg Salbutamol via nebulizer

3) Eliminate Potassium from the body

  • 15-45g oral/rectal Calcium Resonium mixed with sorbitol/lactulose
  • Furosemide
  • Haemodialysis if resistant to medical treatment
23
Q

How would hypokalaemia present?

A

Fatigue, constipation, proximal muscle weakness, paralysis, cardiac arrhythmias eg. VFib, worsened glucose control in diabetics, nausea, vomiting, hypertension

24
Q

What are some causes of hypokalaemia?

A
  • Pseudohypokalaemia - acute leukaemia
  • GI losses eg. vomiting, NG losses, diarrhoea, laxatives, Zollinger Ellison, Ileostomy, enteric fistula
  • Inadequate PO intake
  • Redistribution (eg. caused by increased stimulation of Na+/K+/ATPase so K+ out of cell) eg. beta agonists, insulin, caffeine, theophylline, alpha blockers (Doxazosin)
  • Hypokalaemic periodic paralysis (muscle disease characterised by weakness that is proximal, symmetric, flaccid paralysis)
  • Refeeding syndrome
  • Alkalosis
  • Primary Hyperaldosteronism (Conns)
  • Cushings
  • Renal losses (Diuretics, Renal Tubular Acidosis, Tubulopathies, liquorice, glucocorticoids, hypomagnesaemia)
    *
25
Q

How does hypomagnesaemia cause hypokalaemia?

A

Decreased Na+ absorption in the Loop of Henle and PCT via Na+/K+ ATPase.

This causes increased Na+ in the lumen that distally causes increased Na+ reabsorption and K+ secretion by principal cells.

Mg2+ also inhibits ROMK. So when Mg2+ degreases, ROMK activity goes up, secreting more K+

26
Q

What are some ECG signs seen in hypokalaemia?

A
  • Small/flattened/inverted T waves
  • prolonged U wave
  • Increased PR interval
27
Q

How would you treat hypokalaemia?

A
  • Replace magnesium
  • Oral K+ replacements
  • IV K+ replacement + 0.9% NaCl (dextrose would induce further hypokalaemia)
  • If diuretic induced, discontinue or add K+ sparing

MEDICINE - Renal (3 decks)

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