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BNF/Pre-Reg 2017-2018 > Electolyte Imbalances > Flashcards

Electolyte Imbalances Flashcards

1
Q

What is hypokalaemia defined as?

A

Potassium <3.5mmol/l.This is the most common electrolyte disturbance in hospitalised patients due to diuretic therapy.

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2
Q

What are the most common causes of hypokalaemia?

A
  1. Diuretic therapy2. Acute illness 3. GI losses. Increased lossess of potassium can be from the urinary tract (diuretic therapy, mineralocorticoid excess - Cushings, aldosterone excess - heart failure, renal artery stenosis Poor intake due to eating disorders. Potassium shifting to intracellular compartment (insulin therapy, salbutamol therapy - salbutamol nebules can be used to treat hyperkalaemia).
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3
Q

What are the clinical features of hypokalaemia?

A

Often asymptomatic. Weakness.Intestinal ileus. ECG changes - T wave flattening and U waves + tachyarrhythmia.Polyuria (loss of concentrating ability of kidneys)Severe muscle weakness and flaccid paralysis - when severe: <2mmol/L

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4
Q

What is the intitial treatment for the correction of severe hypokalaemia in patients who cannot swallow?

A

Potassium chloride with sodium chloride for when sufficient potassium cannot be taken by mouth.

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5
Q

In what patients may compensation for potassium loss be especially necessary?

A
  1. Patients taking digoxin or anti-arrhythmic drugs, where potassium depletion may induce arrhythmias;2. Patients whom secondary hyperaldosteronism has occured: renal artery stenosis, cirrhosis of the liver, the nephrotic syndrome, and severe heart failure. 3. Patients with excessive losses of potassium in the faeces, e.g. chronic diarrhoea associated with intestinal malabsorption or laxative abuse.
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6
Q

What is recommended for the prevention of hypokalaemia due to diuretics such as furosemide or the thiazides when they are given to eliminate oedema?

A

The use of potassium-sparing diuretics. spironolactone, amiloride, and triamterene.Epithelial sodium channel blockers: amiloride, triamterene. Aldosterone antagonists:Spironolactone, eplerenone. ACEi and ARB are not classically considered to be potassium-sparing diuretics despite a decrease in aldosterone release, which causes potassium-sparing like effects.

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7
Q

Why must smaller doses of potassium salts for the treatment of hypokalaemia (and prevention of it) be used in the elderly?

A

The elderly are more likely to have some degree of renal insufficiency and so smaller doses are required to reduce the risk of hyperkaleamia.

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8
Q

Why can potassium-sparing diuretics be preferable to the use of potassium salts?

A

They cause nausea and vomiting and poor compliance is a major limitation to their effectiveness.

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9
Q

What is acute severe hyperkalaemia defined as?

A

plasma-potassium concentration above 6.5mmol/litre or in the presence of ECG changes

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10
Q

How is acute severe hyperkalaemia (>6.5mmol/l) treated?

A

Calcium gluconate 10% by slow intravenous injection, titrated and adjusted to ECG improvement, to temporarily protect against myocardial excitability.

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11
Q

An intravenous injection of soluble insulin (5-10units) with 50mL glucose 50% given over 5-15 minutes has what effect on serum-potassium?

A

Reduces it, this can be repeated if necessary or a continuous infusion instituted.

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12
Q

Salbutamol, by nebulisation or slow intravenous infusion has what effect on serum plasma potassium levels?

A

Reduces it, unlicensed use, should be used with caution in patients with cardiovascular disease.

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13
Q

When would ion-exchange resins be used to remove excess potassium?

A

Only in mild to moderate hyperkalaemia when there are no ECG changes.

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14
Q

When would sodium bicarbonate be used by mouth?

A

For chronic acidic states such as uraemic acidosis or renal tubular acidosis. The dose for correction of metabolic acidosis is not predictable and the response must be assessed. For severe metabolic acidosis, sodium bicarbonate can be given intravenously.

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15
Q

Sodium supplements can have what unintended side effects?

A

Increased blood pressure, fluid retention, pulmonary oedema. Hypokalaemia may also be exacerbated.

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16
Q

When hyperchloraemic acidosis is associated with potassium deficiency, as in some renal tubular and GI disorders, it may be appropriate to give oral what?

A

Potassium bicarbonate but acute or severe deficiency should be managed by IV therapy.

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17
Q

Isotonic solutions may be infused safely into a peripheral vein. Solutions more concentrated than plasma, e.g. __% glucose, are best given through what?

A

20% glucose, an indwelling catheter positioned in a large vein.

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18
Q

Sodium depletion can occur from conditions (not drug induced) such as? [4]

A

Gastro-enteritits, Diabetic ketoacidosis,Ileus,Ascities

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19
Q

Chronic hyponatraemia rising from inappropriate secretion of antidiuretic hormone should ideally be corrected by what?

A

Fluid restriction. However, if sodium chloride is required for acute or chronic hyponatraemia, regardless of the cause, the deficit should be corrected slowly to avoid the risk of osmotic demyelination syndrome and the rise in plasma-sodium concentration should not exceed 10mmol/litre in 24 hours. In severe hyponatraemia, sodium chloride 1.8% may be used cautiously.

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20
Q

Why would Hartmann’s solution (compound sodium lactate) be used instead of isotonic sodium chloride solution during or after surgery, or in the initial management of the injured or wounded?

A

Reduced risk of hyperchloraemic acidosis.

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21
Q

Why should initial potassium replacement therapy not involve glucose infusions?

A

Because glucose may cause a further decrease in the plasma-potassium concentration.

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22
Q

Sodium bicarbonate is used to control severe metabolic acidosis, which is defined as a pH value of what?

A

pH <7.1

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23
Q

Mild metabolic acidosis associated with volume depletion should first be managed by what? and why?

A

Appropriate fluid replacement because acidosis usually resolves as tissue and renal perfusion are restored.

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24
Q

Why is sodium lactate IV infusion no longer used in metabolic acidosis?

A

Becase of the risk of producing lactic acidosis, particularly in seriously ill patients with poor tissue perfusion or impaired hepatic function.

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25
Q

What antibiotics and antifungals have the potential to causes hypokalaemia?

A

Ampicillin, high-dose penicillins. Azoles.Amphotericin BEchinocandins. Gentamicin.

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26
Q

What drugs can cause hypokalaemia in overdose?

A

Verapamil and Quetiapine

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27
Q

What are the clinical features of hyperkalaemia?

A

When present, can be:Muscle weakness and fatigue.Frank muscle paralysis. Shortness of breath. Palpitations or sometimes chest pain. .

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28
Q

The most common causes of hyperkalaemia are due to what?

A

Decreased renal potassium excretion caused by: renal failure, potassium sparing diuretics, ACEi, ARBs and NSAIDs.

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29
Q

What is hypernatraemia defined as?

A

serum sodium levels of more than 145mmol/l (severe symptoms typically only occur when levels are above 160mmol/L)

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30
Q

What are normal serum sodium levels?

A

135-145mmol/L

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31
Q

What are the early symptoms of hypernatraemia?

A

Strong feeling of thirst. Weakness.Nausea. Loss of appetite.

32
Q

What are the severe symptoms of hypernatraemia?

A

Confusion, muscle twitching and bleeding in or around the brain.

33
Q

The most important signs of hypernatraemia result from what?

A

Brain cell shrinkage: confusion, muscle twitching or spasms.

34
Q

Hypernatraemia is typically classified by what?

A

A persons fluid status:Low volumeNormal volumeHigh volume.

35
Q

Common low volume causes of hypernatraemia include:

A

SweatingVomitingDiarrhoeaDiuretic medication Kidney disease

36
Q

Common normal volume causes of hypernatraemia include:

A

Fever, inappropriately decreased thirst, prolonged increased breath rate, diabetes insipidus and due to lithium.

37
Q

Common high volume causes of hypernatraemia include:

A

HyperaldosteronismToo much IV salineToo much salt from drinking sea water or soy sauce.

38
Q

What is the mainstay treatment for hypernatraemia?

A

The administration of water to correct the relative water deficit. Orally or IV - although water cannot be given alone intravenously (due to osmolarity issues) it can be given in addition to dextrose or saline infusion solutions.

39
Q

Why should water alone never be given intravenouslly to treat hypernatraemia?

A

Rapidly lowering the sodium concentration with free water causes water to flow into brain cells and cause them to swell. This can lead to cerebral oedema, potentially resulting in seizures.

40
Q

What is hyponatraemia defined as?

A

<135mmol/L Severe hyponatraemia is <120mmol/litre.

41
Q

What are the mild symptoms of hyponatraemia? (<135 but >120mmol/L)

A

Decreased ability to think.Headaches. NauseaPoor balance.

42
Q

Whar are the symptoms of severe hyponatraemia? (<120mmol/L)

A

Confusion, seizures and coma.

43
Q

Hypothyroidism causes what type of sodium imbalance?

A

low sodium.

44
Q

What is the treatment of hyponatraemia?

A

IV saline at a rate which is patient and cases specific.

45
Q

What is hypermagnesemia defined as?

A

Magnesium levels higher than 1.1mmol/L.

46
Q

What symptoms might indicate hypermagnesemia?

A

Weakness, confusion, decreased breathing rate and cardiac arrest.

47
Q

Why does hypermagnesemia occur rarely?

A

Because the kidney is highly efficient at excreting excess magnesium.

48
Q

When does hypermagnesemia typically occur?

A

In kidney failure, in those given high dose magnesium salts, or use antacids/laxatives containing high levels of magnesium.

49
Q

Intoxication/toxicity from which drug can predispose to mild hypermagnesemia?

A

Lithium.

50
Q

What are the treatment options for hypermagnesmia?

A

> 1.1mmol/LWithdrawal of magnesium supplementation.In more severe cases: - intravenous calcium gluconate- intravenous diuretics (normal kidney function)- dialysis (kidney impairment)

51
Q

Why does intravenous calcium gluconate work in the treatment of severe hypermagnesemia?

A

The actions of magnesium in neuromuscular and cardiac function are antagonised by calcium.

52
Q

What is hypermagnesemia defined as?

A

Levels less than 0.6mmol/L

53
Q

What symptoms accompany hypomagnesemia?

A

TremorNystagmus (involuntary eye movement)SeizuresCardiac arrest (inlcuding tosade de pointes)

54
Q

What is the most common cause of hypomagnesemia?

A

Loop and thiazide diuretic use.

55
Q

Why can aminoglycosides, amphotericin, pentamidinem, gentamicin, tobramycin and viomycin cause hypomagnesemia?

A

They block magnesium resorption in the loop of henle.

56
Q

Long term use of proton-pump inhibitors such as omeprezale can cause what electrolyte imbalance?

A

hypomagnesemia.

57
Q

How do cisplatin and ciclosporin both cause hypomagnesemia?

A

They both stimulate renal magnesium excretion.

58
Q

Intravenous MgSO4 has been suggested as having a potential use in asthma, why is this?

A

Magnesium exerts a bronchodilator effect, probably by antagonising calcium-mediated bronchoconstriction.

59
Q

Hypercacaemia is defined as what?

A

levels greater than 2.6mmol/l.

60
Q

What are the symptoms of hypercalcaemia of high severity of rapid onset mild severity?

A

Abdominal pain, bone pain, confusion, depression, weakness, kidney stones or an abnormal heart rhythm including cardiac arrest.

61
Q

What causes 90% of hypercalcaemia?

A

Primary hyperparathryoidism and malignancy.

62
Q

Lithium use can increase the risk of hypercalcaemia. Why is this?

A

Lithium use can increase the incidence of hyperparathyroidism.Primary hyperparathyroidism and malignancy account for about 90% of cases of hypercalcaemia. `

63
Q

High-bone turnover can cause hypercalcaemia. What can cause high-bone turnover rates?

A

Hyperthyroidism. Multiple myeloma. Prolonged immobilisation. Paget’s disease. Thiazide use. Vitamin A intoxication.

64
Q

Initial therapy for hypercalaemia is what?

A

Fluids and diuretics. Hydration is needed due to vomiting or kidney defects in concentrating urine. After rehydration, a loop diuretic such as furosemide can be given to permit continued large volume IV salt and water replacement whilst preventing blood volume overload.

65
Q

All people with cancer-associated hypercalcaemia should receive treatment with what?

A

Bisphosponates as first line hydration and diuretic therapy cannot be continued indefinitely.

66
Q

How do bisphosphonates function?

A

They are pyrophosphate analogues with high affinity for bone - they are taken up by osteoclasts and inhibit osteoclastic bone resorption.

67
Q

What are the most potent bisphosphonates?

A

EtidronateTiludronateIV pamidronateAlendronateZoledronateRisedronate

68
Q

When is calcitonin used? how does it work?

A

Caclitonin is used in life-threatening hypercalcaemia along with rehydration, diruesis and bisphosphonates.Calcitonin blocks bone resorption and increases urinary calcium excretion by inhibiting calcium reabsorption by the kidney.

69
Q

What is hypocalcaemia defined as?

A

Levels less than 2.1mmol/L

70
Q

What are the symptoms of hypocalcaemia?

A

NumbnessMuscle spasmsSeizuresConfusion Cardiac arrest.

71
Q

What are the most common causes of hypocalcaemia?

A

Hypoparathyroidism and Vit D deficiency. Other causes:Kidney failure, pancreatitis, calcium channel blocker overdose, rhabdyomylolysis, tumour lysis syndrome, bisphosphonates.

72
Q

Why do reduced calcium levels result in symptoms such as convulsions, arrhythmias, tetany and numbness?

A

Calcium blocks sodium channels and inhibits depolarisation of nerve and muscle fibres, reduced calcium lowers the threshold for depolarisation.

73
Q

How does hypoparathyroidism result in hypocalcaemia?

A

Calcium levels are tightly regulated by the parathyroid hormone (PTH). Low calcium levels leads PTH to:1) induce the kidneys to reabsorb calcium2) induce the kidneys to increase production of calcitriol (active form of vit D) thereby increasing intestinal absorption of calcium3) induce the bones to release calcium.

74
Q

The management of hypocalcaemia involves what?

A

Intravenous calcium gluconate 10% or if severe, calcium chloride.

75
Q

The use of intravenous calcium gluconate 10% or if severe, calcium chloride in the management of hypocalcaemia is only appropriate when?

A

When the hypocalcaemia is acute and has occured over a relatively short time frame. If the hypocalcaemia has been severe and chronic, then the regimen can actually be fatal, because there is a degree of acclimatization.

76
Q

A patient has serum K+: 2.3mmol/L (ref 3.5-4.7) and the ECG shows small T waves. How should she be managed?

Co-amilofruse 5/40 1 tablet orally
Potassium chloride 40mmol in 1L NaCl IV over 2 hours
Potassium chloride 40mmol in 1L Glucose 5% over 1 hour.
Potassium chloride/bicarbonate (Sando-K) 3 tablets orally
Ramipril 5mg orally

A

Potassium chloride 40mmol in 1L NaCl over 2 hours.

Hypokalaemia: can cause arrhythmias, <2.5mmol/L is considered to be severe and this warrants IV treatment.

Co-amilofruse 5/40 is a combination of a loop diuretic (furosemide) and a (weak) potassium-sparing diuretic (amiloride) - if hypokalaemia were to occur with furosemide treatment it may be appropriate to swap to this combination product but in the acute scenario it is not an appropriate option.

KCl 40mmol in 1L 5% Glucose over 1 hour is too fast! on the ward setting, the rate would not exceed 20mmol/hr. Also it is generally better to treat hypokaleamia using a NaCl based fluid.

Oral potassium is fine for non-severe hypokalaemia and while ramipril does raise K+ levels, ACEi should ideally be avoided in patients who are acutely unwell due to risk of acute kidney injury.

BNF/Pre-Reg 2017-2018 (144 decks)

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