Water, electrolytes, acid-base Flashcards

1
Q
  1. Why do conditions that cause retention of sodium, such as cardiac
    failure, result in low serum sodium?
A

One explanation is the non-osmotic release of antidiuretic hormone
(ADH), due to arterial underfilling causing the retention of water and a
dilutional hyponatraemia. A second explanation is that reduced delivery
of chloride to the diluting segment of the ascending loop of Henle
because of avid reabsorption of sodium and chloride in the proximal
tubule. This results in a reduced ability to generate ‘free water’ and
produce a dilute urine so hyponatraemia occurs due to water excess.

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2
Q

Why is there a difference in the pattern of oedema in nephrotic syndrome
and cardiac oedema? How is it related to the interstitial spaces and all
that? I am confused.

A

In all conditions associated with oedema there is increased extracellular
volume associated with renal sodium chloride retention.
The oedema in all conditions is usually in the ankles in all patients but
this depends on body position. Patients with the nephrotic syndrome are
not usually breathless and so lie flat and the oedema occurs in the face.
The reverse is true for cardiac failure.

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3
Q

What is meant by ‘free water’?

A

The term ‘free water’ is a concept that is used to describe the
movement of water independent of sodium.

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4
Q

What treatment is recommended for recurrent attacks of generalized
swelling, with angio-oedema, in a middle-aged female patient?

A

This sounds like idiopathic oedema of women. It might respond to
diuretics. Antidiuretic hormone (ADH) acts on vasopressin (V2) receptors
located on principal cells. ADH promotes water reabsorption in the
collecting ducts and this might be a factor in the cause of the oedema.
V2 receptor antagonists are now available.

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5
Q

Is an osmotic diuresis, due to hyperglycaemia for instance, a cause of
both hyponatraemia and hypernatraemia. Please explain how this can be
the case.

A

Hypernatraemia is due to loss of Na

and water with the osmotic
diuresis. This causes dehydration and hypernatraemia. Hyponatraemia
occurs because antidiuretic hormone (ADH) stimulates thirst; excess
water compared to sodium is drunk, and hyponatraemia occurs

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6
Q

What is the mechanism of β2-agonists (albuterol) in correcting
hyperkalaemia in emergency? How does it cause a shift of potassium?

A

β2-adrenergic receptors increase the activity of the sodium–potassium
ATPase pump in the cell membrane. This is followed by the excretion of
excess potassium in the urine.

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7
Q

Why do we give sodium lactate along with sodium bicarbonate in
acidotic patients? How does sodium lactate then act?

A

Sodium lactate intravenous infusion is obsolete for the treatment of
metabolic acidosis. It carries the risk of lactic acidosis and should not be used.

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8
Q

How does hypochloraemia alone cause a metabolic alkalosis?

A

If chloride is lost either through the kidney or via the stomach, there is a
preferential absorption of bicarbonate in the distal tubule. This leads to
metabolic alkalosis.

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9
Q
  1. Why is there a higher concentration of anions (18) on measuring the
    anion gap while there is a high concentration of immeasurable anions?
    I would have expected a higher concentration of cations because most
    of them are measurable.
  2. Could you explain to me in more details how NaCO3 loss or HCl
    retention could lead to normal anion gap acidosis?
A
  1. Normally there is an anion gap of approximately 12 mmol/L. Albumin
    normally makes up the largest portion of these unmeasured anions.
  2. The loss of bicarbonate, e.g. from the gastrointestinal tract, is initially
    compensated but eventually the increased loss of bicarbonate leads to
    hydrogen ion excess; that is, acidosis
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10
Q

formula for calculating the serum anion gap?

A

(Na + K) - (Cl + HCO3)

normal 6-12

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11
Q

What is the role of IV saline in the management of a cirrhotic patient with
a serum sodium of 120mmol/L?

A

The initial management is with water restriction as the hyponatraemia is
dilutional. IV saline therapy depends on:
● the rapidity of the development of hyponatraemia
● whether the patient is symptomatic.
In most patients with liver disease, the onset is slow and the patient is
consequently asymptomatic; Hypertonic saline 3% should only be given
to patients with neurological symptoms and signs and must be given
extremely slowly so that the change in serum sodium should not exceed
15 mmol over 48 hours.

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12
Q

immediate tx severe

hyperkalaemia?

A

Attach ECG monitor and IV access
Protect myocardium
● 10 mL of 10% calcium gluconate IV over 5 min
● Effect is temporary but dose can be repeated after 15 min
Drive K into cells
● Insulin 10 units 50 mL of 50% glucose IV over 10–15 min followed by
regular checks of blood glucose and plasma K
● Repeat as necessary
● and/or correction of severe acidosis (pH6.9): infuse NaHCO3 (1.26%)
● and/or salbutamol 0.5mg in 100mL of 5% glucose over 15min (rarely
used)

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13
Q

Can you explain the respiratory alkalosis and metabolic acidosis in
salicylate poisoning?

A

Initially, there is stimulation of the respiratory centre with
hyperventilation leading to respiratory alkalosis. Metabolic acidosis
ensues because of compensatory mechanisms including the renal
excretion of bicarbonate and potassium as well as the accumulation of
lactate, pyruvate and ketone bodies.

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14
Q

In an elderly patient with oedema due to heart failure, which is the best
diuretic to start treatment with? Some books recommend thiazides
whereas others use loop diuretics.

A

Bendroflumethiazide is a cheap, effective agent that, if given early in the
day, causes a diuresis that does not interfere with sleep. Chlortalidone,
another thiazide, has a longer action and can be given on alternate days.
It is useful if a patient has prostatic symptoms as it produces a slower
diuresis. Loop diuretics, e.g. furosemide and bumetanide, act within
1 hour of administration and would be used as first line in a severe acute
situation, e.g. pulmonary oedema.

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15
Q

later tx severe hyperkalaemia

A

Later
Deplete body K (to decrease plasma K over the next 24 h):
● Polystyrene sulphonate resins:
● 15 g orally up to three times daily with laxatives
● 30 g rectally followed 3–6 hours later by an enema
● Haemodialysis or peritoneal dialysis if the above fails

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