Electrolyte abnormalities Flashcards

Become confident with the management of common electrolyte abnormalities (41 cards)

1
Q

Causes of nephrogenic diabetes insipidus

A

Lithium
Head injury

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1
Q

Things to consider with a hypernatremia patient (broadly speaking)

A

1) Dehydration/ impaired thirst mechanism/ impaired access to water e.g., cognitive impairment, learning difficulty

2) Check a glucose ? diabetic with HHS !

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2
Q

Causes of hypernatraemia

A

Not reabsorbing water
No ADH: Central diabetes insipidus
ADH produced, but not working on the kidneys: Nephrogenic diabetes insipidus

ADH produced, but impaired thirst mechanism/ no access to water

Loosing water via
GI tract: Vomiting, diarrhoea, stoma, laxatives

Renal: Diuretics (loop) high glucose (osmotic diuresis) Insensible losses (sweat, increased RR)

Too much sodium
- Hypertonic saline, hypertonic dialysis
- Increase in aldosterone (Conn’s, cushing’s)

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3
Q

Consequences/ risks of hypernatraemia

A

High blood osmolality, get fluid shift from cells to the blood, causes cell shrinkage

In the brain, can cause tearing of the arteries -> cause ICH

Shrinking of brain cells = death of brain cells

Osmotic demyelination syndrome (shrink of cells in the pons, where corticobulbar (speech), spinothalamic(paralysis), VI, run through (palsy) reticular formation (consciousness reduced)

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4
Q

Symptoms of hypernatremia

A

Nausea and vomiting
Thirsty, loss of appetite
Lethargy and weakness
Confusion (brain cells dying)

Severe: Seizure, myoclonic jerks, coma, ICH, coma, death

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5
Q

Approach to hypernatraemia patient

A

Why - think of the causes
ADH working = urine osmolality low
- Losing water, ADH, not drinking (GI loss, renal loss)
- low urinary sodium, as RAAS is working
- Given extra sodium, ADH working, losing sodium in urine as so much in blood!

ADH not working = urine osmolality high
- Diabetes insipidus (central, nephrogenic)

NEWS & BM
Fluid balance
Blood-type - electrolytes (U&E, bone profile, magnesium) glucose
Urine and serum osmolality and sodium

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6
Q

Management of hypernatraemia

A

Fluids, calculate free water deficit, monitor sodium, > 160 ? ITU, fluid balance

Hypotensive: NaCL until BP normal

Non-diabetic: IV dextrose e.g. bag over 6 hours, check sodium 4-6 hours after start to ensure rate falling is okay (12 mmol in 24 hrs, 0.5 an hour)

Diabetic: Saline dex, monitor BMs - dex can make worse as cause osmotic diuresis, ? HHS if high glucose before starting!

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7
Q

Approach to hyponatraemia

A

exclude spurious result
1) Severity
2) Onset - acute VS chronic
3) Symptoms - unlikely with mild
4) Serum osmolality
5) Fluid balance - hypovolemic, euvolemic, hypervolemic
6) Review meications

Think SOS
Serum osmolality, fluid status, review medications

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8
Q

Causes of hyponatraemia

A

Hypovolemic - ADH activated as low blood volume
Renal: Diuretics (thiazide! loop) low aldosterone (Addinson’s)
cerebral and renal salt wasting

GI loss - vom, diarrhoea, stoma
Insensible loss - sweat, burn, ventilation
Third spacing
Blood loss

Euvolemic - ADH not activated
Tea & toast
Beer potomania
Primary polydipsia
SIADH
Low cortisol, hypothyroidism
Drugs

Hypervolemic - third spacing, ADH activation
CCF, nephrotic syndrome, cirrhosis

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9
Q

Non ADH dependant causes of hyponatraemia

A

Tea and toast
Beer potomania
Primary polydipsia - anticholinergic medications, psych
SIADH
Medications - thiazide and loop diuretics, SSRI, AED, antipsychotic drugs
Low cortisol
Hypothyroid - bad!

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10
Q

Causes of SIADH

A

Malignancy -> GI, lung
Pulmonary disease -> COPD, pneumonia
Medications - SSRIs, AED, AP
Intracranial pathology e.g., SAH, stroke

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11
Q

What is SIADH

A

No trigger for the release of ADH (blood volume fine, perfusion of kidneys okay)

ADH released w/o a cause!

RAAS not activated, so no sodium reabsorption from aldosterone! Higher sodium in urine!

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12
Q

Symptoms of hyponatraemia

A

Mild, can be asymptomatic!

Due to cerebral oedema
- nausea, vomiting
- headaches
- drowsy

severe: seizures, reduced GCS, cardio-rsp arrest, coma

Chronic: Gait instability, altered mental status, reduced concentration

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13
Q

Investigations for hyponatraemia

A
  • Serum and urine osmolality and sodium (ADH working or not)
  • Urine dipstick (nephrotic syndrome)
  • Bloods: U&E albumin (indicated dehydration, nephrotic syndrome), LFTs (cirrhosis) pro BNP (CCF) TFTs (? low), 9am cortisol (? low)
  • CXR - ? CCF
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14
Q

What requires emergency treatment with hyponatraemia

A

Severity - severe
Onset - acute
Symptoms - severe YES

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15
Q

What makes person more at risk of seizures in hyponatraemia?

A

Epilepsy! (more at risk of seizures)
Brain injury e.g., previous stroke, mass (more at risk of herniation)

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16
Q

Consequences of hyponatraemia

A

Cerebral oedema
- Brain herniation
- Increase neurone irritability = seizures

17
Q

Emergency treatment for hyponatraemia

A

IV 3% NaCl over 20 minutes
Check sodium after
Not reduce more than 8-10 mmol/ ml in 24 hours - risk ODS
Find cause
Give fluids
Regular monitoring of sodium

18
Q

Complications/ to think about when correcting hyponatraemia

A

1) ODS
2) Chronic = ODS risk higher
3) Low K+ -> chucks Na out of cells when going into cell, increase osmolality even more

19
Q

Osmotic demyelination syndrome

A

Over correction of hyponatraemia, increase osmolality of blood, fluid shift out from cells = shrink = die
astrocyte responsible for myelination, these die = demyelination

In pons have tracts running through
Corticobulbar = speech lost
spinothalamic = paralysis
VI = palsy
reticular formation = consciousness

symptoms develop 2 days after, dysphagia, dysarthria, paraparesis, quadriparesis

max correction 4-6 mmol in 24 hours!

20
Q

Management of non-emergency hyponatraemia hypovolemic

A

work out cause
mild and mod, no symptoms, fluid status assessment, review medications

  • Hypovolemic: NaCl replace fluids, if sodium improves supports diagnosis,
    if falls - alternative diagnosis ? SIADH

monitor sodium and fluid balance

21
Q

Sudden acute drop to think

A

Taken from a drip arm?
Yes = repeat (VBG)
No = treat as appropriate ?emergency

22
Q

Management of non-emergency SIADH hyponatraemia

A
  • SIADH: FR 500-1000ml a day -> vaptans can be used (ADH antagonist)

Monitor sodium! Fluid balance!

23
Q

Management of non-emergency hypervolemic hypernatraemia

A

Fluid restrict 500-1000ml a day
monitor sodium and fluid balance
consider loop diuretics

24
ADH antagonist/ vaptans Who not to give?
Hypovolemic - worsens Hepatoxic - don't give to liver disease stimulate thirst receptors
25
Causes of hypercalcaemia
Hyperparathyroidism Primary - benign hyperplasia, adenoma (most common), malignancy (MEN1, 2a) Tertiary - secondary to chronic kidney disease, chronic low vit D - parathyroid gland increase PTH production and hypertrophy Malignancy - PTHrP released - 1000x more potent than PTH - Bone lysis/ lytic lesions - mets to bone - myeloma - cytokine increase OC activity Increased in vitamin D - Oral/ OTC - Granuloma e.g., sarcoidosis, make own vitamin D FHH - sensors need a higher level of calcium before -ve feedback Medications; thiazide diuretics (increase calcium reabsorption DCT) and lithium (increase PTH) Endocrine: Acromegaly, Addison's, thyrotoxicosis, phaeochromocytoma Prolonged immobolisation = high bone turnover
26
PTH dependant and independant causes of hypercalcaemia
PTH dependant: Hyperparathyroidism,FHH, lithium PTH independant: Malignancy, vitamin D, thiazides, endocrine stuff, immobility
27
Presentation of hypercalcaemia
High calcium = stabilise voltage-gated sodium channels, reduced excitability - Slower or absent reflexes - Slow muscles: Myalgia, weakness - Slow GI muscles: Constipation, nausea, vomiting, bloating - Confusion, psychosis More calcium exreted in urine, osmotic diuresis - polyuria, polydipsia, dehydration - Renal stones (high calcium oxalate, and dehydrated) - Bone breakdown Bone pain - Calcium mediated gastric acid release Dyspepsis severe - arrythmia chronic more likely hyperparathyroidism, is more gradual acute - think more malignancy
28
Investigations for hypercalcaemia
Calcium levels Phosphate PTH Magnesium (high calcium, reduce magnesium) Vitamin D Albumin LFTs - ALP rise in bone lysis U&E - renal function FBC ECG
29
ECG finding in hypercalcaemia
- Bradycardic - Short QTc interval - PR, QRS prolonged risk of AV node branch blocks - Osbourne wave - +ve deflection @ J point between QRS and ST segment
30
Lab findings in hyperparathyroidism
Calcium high Phosphate low PTH high
31
Lab findings in malignancy
Calcium high Phosphate high PTH low (calcium -vely feeds back)
32
Acute management of hypercalcaemia
Mild: encourage oral, review meds, repeat > 3.5 or > 3 with symptoms Aggressive IV NaCl 3-4 litres for 2-3 days, increases filtration and excretion of calcium, careful in overload Loop diuretics, inhibit calcium reabsorption in DCT, give after fluids or if cannot have, deranged electrolytes (K+, Na+) Bisphosphonates: Take 2-3 days to work, inhibit OC of bone, indicated in hypercalcaemia of malignancy! Steroids - Inhibit vitamin D conversion to active vitamin D, vit D excess, granuloma, haematological malignancy -
33
How do steroids work in hypercalcaemia management?
Steroids inhibit the conversion of vitamin D to active vitamin D - reduce GI absorption of calcium
34
Cause of hypokalaemia
1) Drip arm with no K+ in 2) Reduced intake Oral, IV, TPN Malabsorption Low magnesium (lose K+ in urine, body can alter reabsorption!) 2) Extracellular to intracellular Alkalosis (e.g. loss HCL in vomiting), insulin, adrenaline, beta-2-agonist 3) Increased losses GI: Vom, diarrhoea, laxative abuse, stoma Renal: Loop & thiazide diuretics, high aldosterone (conn's, cushings) (Na+ high, K+ low), renal tubular acidosis Insensible losses
35
Investigations for hypokalaemia
U&E, Mg, Bone profile ECG Digoxin level if on!
36
ECG in hypokalaemia
PR prolonged T wave inverted ST depression Q waves QTc can be prolonged - risk of VF and torsade de pointes
37
when to be cautious in potassium replacement?
When giving K+ to a person with renal impairment/ medications that affect kidney (NSAIDs, ACEI, ARB)
38
ECG changes in hypercalcaemia
Bradycardic PR prolonged, QRS prolonged - risk of bundle branch block QTc shortened Osbourne waves
39
Acute onset of symptoms in hypercalcaemia - what to think about
? malignancy causing symptoms?? More chronic - think primary hyperparathyroidism
40
What to think about in low K+
Digoxin toxicity - do they take it? If yes, then can increase risk of toxicity Mg? Causes, Review medications ECG, U&E, Mg