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Electrolyte abnormalities > Electrolyte abnormalities > Flashcards

Electrolyte abnormalities Flashcards

Become confident with the management of common electrolyte abnormalities

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
Q

ADH antagonist/ vaptans
Who not to give?

A

Hypovolemic - worsens
Hepatoxic - don’t give to liver disease
stimulate thirst receptors

25
Q

Causes of hypercalcaemia

A

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
Q

PTH dependant and independant causes of hypercalcaemia

A

PTH dependant: Hyperparathyroidism,FHH, lithium

PTH independant:
Malignancy, vitamin D, thiazides, endocrine stuff, immobility

27
Q

Presentation of hypercalcaemia

A

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
Q

Investigations for hypercalcaemia

A

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
Q

ECG finding in hypercalcaemia

A
  • 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
Q

Lab findings in hyperparathyroidism

A

Calcium high
Phosphate low
PTH high

31
Q

Lab findings in malignancy

A

Calcium high
Phosphate high
PTH low (calcium -vely feeds back)

32
Q

Acute management of hypercalcaemia

A

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
Q

How do steroids work in hypercalcaemia management?

A

Steroids inhibit the conversion of vitamin D to active vitamin D - reduce GI absorption of calcium

34
Q

Cause of hypokalaemia

A

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
Q

Investigations for hypokalaemia

A

U&E, Mg, Bone profile
ECG
Digoxin level if on!

36
Q

ECG in hypokalaemia

A

PR prolonged
T wave inverted
ST depression
Q waves
QTc can be prolonged - risk of VF and torsade de pointes

37
Q

when to be cautious in potassium replacement?

A

When giving K+ to a person with renal impairment/ medications that affect kidney (NSAIDs, ACEI, ARB)

38
Q

ECG changes in hypercalcaemia

A

Bradycardic
PR prolonged, QRS prolonged - risk of bundle branch block
QTc shortened
Osbourne waves

39
Q

Acute onset of symptoms in hypercalcaemia - what to think about

A

? malignancy causing symptoms??
More chronic - think primary hyperparathyroidism

40
Q

What to think about in low K+

A

Digoxin toxicity - do they take it? If yes, then can increase risk of toxicity
Mg?

Causes,
Review medications
ECG, U&E, Mg

Electrolyte abnormalities (5 decks)

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