Revision - Anaphylaxis & Electrolytes

Question 1

What blood test can be done to confirm anaphylaxis?

Answer 1

Serum tryptase within 6 hours of event (tryptase is released during mast cell degranulation)

Question 2

When can discharge following anaphylaxis be considered in the following scenarios:

1) good response to single dose of adrenaline

2) needed 2x doses of adrenaline

3) previously had a biphasic reaction

4) needed >2x doses of adrenaline

5) also has severe asthma

6) present late at night

Answer 2

1) min 2 hours after symptom resolution

2) min 6 hours

3) min 6 hours

4) min 12 hours

5) min 12 hours

6) min 12 hours

Question 3

What is ADH released in response to?

Answer 3

Increased serum osmolality –> leads to increased water retention in the collecting ducts in the kidneys

Question 4

How does water ingestion not lead to hyponatraemia?

Answer 4

As water ingestion causes suppression of ADH –> water is excreted in dilute urine

Question 5

How does SIADH affect sodium?

Answer 5

Hyponatraemia

Question 6

Where is ADH released from?

Answer 6

Posterior pituitary

Question 7

What are the 2 main way that sodium is lost through the kidneys?

Answer 7

1) Medications e.g. diuretics

2) Shortage of steroid hormones e.g. aldosterone, cortisol (to a lesser extent)

Question 8

Which 3 medications can lead to hyponatraemia?

Answer 8

1) Loop diuretics

2) Thiazide diuretics

3) K+ sparing diuretics

(also SSRIs)

Question 9

1st step in assessment of hyponatraemia?

Answer 9

Calculate serum osmolality –> is it a true hyponatraemia or not?

Question 10

Serum osmolality in a true hyponatraemia?

Answer 10

Low

Question 11

How does HHS cause low sodium and high osmolarity?

Answer 11

1) Blood glucose goes up very high

2) Glucose leaks into urine

3) Water & sodium follow glucose into urine

4) Concentrates glucose in blood

Question 12

Which diuretic is most likely to cause renal sodium loss?

Answer 12

Thiazide-like diuretics

Question 13

Patient is hyponatraemic and hypovolaemic.

What is cause of hyponatraemia?

Answer 13

DECREASED SODIUM

1) Sodium loss:
- renal loss
- loss from elsewhere e.g. GI, transdermal

2) Inadequate sodium intake (rare)

Question 14

Patient is hyponatraemic and hypervolaemic.

What is cause of hyponatraemia?

Answer 14

In a fluid overloaded patient, fluid accumulates in the extracellular (‘third’) space. This extra fluid causes a dilutional effect on serum sodium, causing hyponatraemia.

I.e. more water than sodium, leading to a relative sodium deficiency.

Question 15

What are the 4 main causes of hypervolaemic hyponatraemia?

Answer 15

1) CCF

2) Liver cirrhosis

3) End stage renal failure

4) Nephrotic syndrome

Question 16

How can liver cirrhosis lead to hypervolaemic hyponatraemia?

Answer 16

Hypoalbuminaemia

Question 17

How can nephrotic syndrome lead to hypervolaemic hyponatraemia?

Answer 17

Hypoalbuminaemia

Question 18

How can hypoalbuminaemia cause hyponatraemia?

Answer 18

Decreases plasma oncotic pressure –> fluid accumulates in the extracellular space

Question 19

Patient is hyponatraemic and euvolaemic.

What is cause of hyponatraemia?

Answer 19

Most commonly SIADH

Question 20

Under normal conditions, what should happen to urine osmolality when serum sodium (and serum osmolality) is low?

Answer 20

Urine osmolality should be decreased as the body attempts to conserve sodium by producing dilute urine.

Think about when you’re really hydrated!

Question 21

In euvolaemic hyponatraemia, if the urine osmolality is raised (>300mOsm/kg), what is the diagnosis?

Answer 21

SIADH.

A raised urine osmolality in the presence of low serum osmolality suggests SIADH, as the kidney is inappropriately producing concentrated urine despite low serum osmolality.

Question 22

In euvolaemic hyponatraemia, if the urine osmolality is decreased (<300mOsm/kg), what is the diagnosis?

Answer 22

Water intoxication may be the cause (primary polydipsia).

Question 23

Who is primary polydipsia seen in?

Answer 23

• psychiatric disturbances
• use of ectasy
• severe hypothyroidism
• glucocorticoid deficiency.

Question 24

Managemnt of acute hyponatraemia with severe neurological symptoms (e.g. seizures, severe drowsiness)?

Answer 24

Medical emergency

1) IV hypertonic saline bolus (100ml 3% NaCl)

2) Close monitoring of serum sodium

Question 25

Goal of sodium correction rate in hyponatraemia without severe neuro symptoms?

Answer 25

No more than 6 mmol/L in the first 6 hours

No more than 10 mmol/L in the first 24h

Question 26

If the sodium is corrected too quickly in hyponatraemia, what is the patient at risk of?

Answer 26

Osmotic demyelination syndrome

Question 27

Management of hypovolaemic hyponatraemia?

Answer 27

Rehydration with IV 0.9% normal saline, with regular monitoring of serum sodium.

Question 28

Management of hypervolaemic hyponatraemia?

Answer 28

Fluid restriction (<1.5L/24h), with regular monitoring of serum sodium.

Question 29

Management of euvolaemic hyponatraemia?

Answer 29

Fluid restriction (1.5L/24h), with regular monitoring of serum sodium.

Question 30

When does osmotic demyelination syndrome typically present?

Answer 30

2-4 days after treatment

Question 31

What are 3 drugs that can cause SIADH?

Answer 31

1) SSRIs

2) Amitriptyline

3) Carbamazepine

Question 32

What hormonal abnormality can cause SIADH?

Answer 32

Hypothyroidism

Question 33

What are the 6 features that must be present for a diagnosis of SIADH to be made?

Answer 33

1) hyponatraemia

2) low plasma osmolality

3) euvolaemia

4) inappropriately elevated urine osmolality (i.e. greater than plasma osmolality)

5) urine [Na+] >40 mmol/L despite normal salt intake

6) normal thyroid and adrenal function

Question 34

Mx of SIADH?

Answer 34

Fluid restriction

Question 35

ECG features of hyperkalaemia vs hypokalaemia

Answer 35

Hyperkalaemia:
- flattended p waves
- tall t waves
- PR prolongation
- wide QRS

Hypokalaemia:
- U waves
- T wave inversion
- ST depression

Question 36

How can trauma or burns lead to hyperkalaemia?

Answer 36

Tissue damage sustained secondary to trauma or burns results in the release of significant volumes of potassium from damaged cells.

Question 37

When is oral vs IV potassium replacement indicated in hypokalaemia?

Answer 37

1) If potassium is >3mmol/L, the patient is asymptomatic, and there are no ECG changes –> oral potassium replacement can be given.

2) If potassium is <3mmol/L (severe hypokalaemia) or ECG changes are present –> IV potassium replacement is indicated.

Question 38

What is a ‘corrected’ calcium?

Answer 38

Most laboratories report a ‘corrected calcium’ alongside total calcium, in which the serum calcium level is adjusted for the serum albumin level.

Question 39

What can sometimes be used in hypercalcaemia mx in patients who cannot tolerate aggressive fluid rehydration?

Answer 39

Loop diuretics

Question 40

What 2 electrolyte disturbances can cause torsades de pointes?

Answer 40

1) hypokalaemia

2) hypomagnesaemia

Question 41

What precipitates torsades de pointes?

Answer 41

Prolonged QT

Question 42

Mx of mild/moderate hypocalcaemia vs severe hypocalcaemia (e.g. prolonged QT, carpopedal spasm etc)?

Answer 42

Mild/moderate –> oral calcium repalcement e.g. calcium carbonate

Severe –> IV calcium gluconate (10ml 10%)

Question 43

What is cinacalcet?

Answer 43

a calcium-sensing receptor agonist that reduces PTH secretion

(used in mx of hyperparathyroidism)

Question 44

What electrolyte disturbance presents similarly to hypocalcaemia?

Answer 44

Hypomagnesaemia