Disorders of sodium concentration Flashcards

1
Q

What is Hyponatraemia?

A

low plasma sodium (Na+) concentration less than 135 mmol/L.

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2
Q

What is the normal range for sodium?

A

135-145 mmol/L

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3
Q

How is mild, moderate and sever hyponatraemia classified?

A

Mild hyponatraemia: serum Na+ 130-135 mmol/L.

Moderate hyponatraemia: serum Na+ 125-129 mmol/L.

Severe hyponatraemia: serum Na+ < 125 mmol/L.

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4
Q

What is the difference between acute and chronic hyponatraemia?

A

Acute: duration < 48 hours.

Chronic: duration > 48 hours

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5
Q

Which hormone is the key hormone responsible for osmoregulation? Where is this hormone produced?

A

Antidiuretic hormone

Produced by the magnocellular neurons in the paraventricular and supraoptic nuclei of the hypothalamus.

It is stored and released by the posterior pituitary in response to rising plasma osmolality.

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6
Q

How does Antidiuretic hormone regulate plasma osmolality?

A

Normal plasma osmolality is approximately 275-295 mOsm/L.

ADH release begins at a plasma osmolality of around 280 mOsm/kg

Thirst begins at 290 mOsm/kg

ADH acts on the distal convoluted tubule and collecting duct to increase water reabsorption

ADH stimulates the insertion of aquaporin-2 channels onto the luminal membrane of kidneys, allowing the free entry of water.

ADH also causes vasoconstriction of arterioles.

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7
Q

What are the 3 main categories of hypovolemia based on fluid status?

A

hypovolaemia (reduction in extracellular fluid volume), euvolaemia, hypervolaemia

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8
Q

What are the causes of hyponatraemia with hypovolaemia

A

Extrarenal causes (urinary sodium <20 mmol/L)

  • Vomiting
  • Diarrhoea
  • Haemorrhage
  • Burns
  • sweating
  • Pancreatitis
  • Sepsis
  • Cerebral salt wasting

Kidney (urinary sodium >20 mmol/L)

  • Osmotic diuresis (e.g. hyperglycaemia, severe uraemia)
  • Diuretics (mainly but not only thiazide diuretics)
  • Adrenocortical insufficiency (Addison’s)
  • Tubulointerstitial renal disease
  • Unilateral renal artery stenosis
  • Recovery phase of acute tubular necrosis
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9
Q

What are the signs and symptoms associated with someone who is hypovolaemic? (9)

A
  • Thirsty
  • Hypotensive
  • Low urine output
  • Tachycardic (hypovolaemia can active a vagal mechanism that can cause bradycardia)
  • Reduced skin turgor
  • Dry mucous membranes
  • Capillary refill time > 2 seconds
  • Dizziness
  • Postural drop in systolic blood pressure- Low JVP (can only be seen if patient is lying completely flat)
  • Cold peripheries
  • Early warning signs >3
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10
Q

How does vomiting lead to Hypovolaemia hyponatraemia?

A
Vomiting causes water loss
HCL acid and electrolytes are also lost.
Loss of HCL causes alkalaemia 
Kidneys compensate by excreting bicarbonates with sodium 
This increases sodium excretion
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11
Q

How does diarrhoea lead to hyponatraemia?

A

There is a loss of water and electrolytes in the form of sodium bicarbonate. Loss of bicarbonate = Academia

The kidneys as a result will excrete hydrogen ions to increase the serum PH

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12
Q

What are some causes of hypoaldosteronism and how does it cause Hypovolaemia hyponatraemia?

A

Addison’s disease
Spironolactone

Aldosterone is realised from the adrenal cortex. Aldosterone acts on the kidneys to reabsorb sodium in exchange for potassium

Low aldoserone will decrease the effect aldosterone has on the distal tubules and collecting ducts in the kidneys

There will be decreased expression of the sodium/ potassium ATP pump and aldosterone dependant sodium channels

Aldosterone can not retain sodium, increasing sodium and water excretion (water follows sodium)

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13
Q

What are the causes of hyponatraemia with Euvolaemia?

A

Abnormal antidiuretic hormone release

  • Vagal neuropathy (failure of inhibition of ADH release)
  • Deficiency of adrenocorticotrophic hormone (ACTH) or glucocorticoids (Addison’s disease)
  • Hypothyroidism
  • Severe potassium depletion

Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

Psychiatric illness

  • Psychogenic polydipsia’
  • Antidepressant therapy

Increased sensitivity to ADH

  • Chlorpropamide
  • Tolbutamide

ADH like substances

  • Oxytocin
  • Desmopressin

osmotically active substances stimulating osmotic ADH release

  • Glucose
  • Chronic alcohol use
  • Mannitol
  • Sickle cell syndrome

High water, low solute intake (i.e. primary polydipsia, anorexia nervosa)

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14
Q

What are the causes of hyponatraemia with hypervolaemia?

A

Heart failure - congestive heart failure
Liver failure - Cirrhosis
Oliguric kidney injury
Hypoalbuminaemia - nephrotic syndrome

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15
Q

What are some cause of pseudo hyponatraemia?

A
High glucose 
hyperlipidaemia 
hyperproteinaemia 
Paraoriteins 
Arm being infused with fluid containing low sodium 
Mannitol
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16
Q

Which drugs can cause postural hypotension?

A
Tricyclic antidepressants
Nitrates
Calcium-channel blockers
α-Adrenoceptor-blocking drugs
Beta blockers
17
Q

How is Hyponatraemia with hypovolaemia managed?

A

In healthy patients -

  • oral electrolyte–glucose mixtures
  • Increase salt intake with slow sodium 60–80 mmol/day

In a patient with vomiting or severe volume depletion -
- Give intravenous fluid with potassium supplements, i.e. 1.5–2 L 5% glucose (with 20 mmol K+) and 1 L 0.9% saline over 24 h plus measurable losses.

Correction of acid–base abnormalities is usually not require

18
Q

How is Hyponatraemia with euvolaemia managed?

A

Most cases are simply managed by restriction of water intake (to 1000 or even 500 mL/day) with review of diuretic therapy. Magnesium and potassium deficiency must be corrected. In mild sodium deficiency, 0.9% saline given slowly (1 L over 12 h) is sufficient.

19
Q

What is the commonest cause of acute onset hyponatraemia?

A

Postoperative iatrogenic hyponatraemia

20
Q

What are common causes of hyponatraemia?

A

Postoperative iatrogenic
hyponatraemia

Excessive water intake associated with psychosis,

Marathon running

Use of Ecstasy

Medical emergency with aggressive treatment

21
Q

If someone is suffering from acute hyponatremia with neurological symptoms, which symptoms would you expect to see and how is this condition treated?

A

fits, coma or cerebral oedema

hypertonic saline (3%, 513 mmol/L)

It must be given very slowly (not more than 70 mmol/h), the aim being to increase the serum sodium by 4–6 mmol/L in the first 4 hours, but the absolute change should not exceed 15–20 mmol/L over 48 hours.

22
Q

Which neurological complication can occur is a patients extracellular osmolality rises too quickly?

A

osmotic demyelination syndrome

23
Q

When treating someone with hyponatremia, how much should their plasma sodium concentration rise daily?

A

should not rise by more than 8 mmol/L per day

The rate of rise of plasma sodium should be even lower in patients at higher risk for osmotic demyelination syndrome (ODS)

24
Q

What are the risk factors for a patient to develop osmotic demyelination syndrome?

A
  • alcohol excess,
  • cirrhosis,
  • malnutrition
  • hypokalaemia
  • pre-existing hypoxaemia
  • central nervous system radiation
25
Q

How is osmotic demyelination syndrome diagnosed?

A

hypointense lesions on T1-weighted MRI

hyperintense lesions on T2-weightedMRI

can take 2 weeks or more to appear.

26
Q

Reversing hyponatraemia can cause hypernatremia. Why does this happen and how is it treated?

A

When the cause of water retention is reversed ADH levels fall and plasma sodium levels rise due to the excretion of dilute urine.

This excessive water diuresis should be anticipated and prevented by use of desmopressin

27
Q

Which new drug has been approved to be used in euvolemic hyponatraemia patients and those with SIADH?

A

Tolvaptan
Vasopressin V2 receptor antagonists

(conivaptan in some countries)

28
Q

What are the signs and symptoms of Hypervolaemia?

A
Raised JVP
Bibasal crackles
Gallop rhythm
Peripheral oedema
Hypertensive
29
Q

What is hypernatraemia?

A

When Na concentration above 145mmol/L

30
Q

What type of blood osmolality is associated with hypernatraemia? How is hypernatremia classified using this?

A

Blood osmolality is usually hypertonic -

31
Q

How is hypernatremia classified

A

Blood volume is the o altered - It can be normal, reduced or expanded extracellular volume,

Hypervolemic

Hypovolemic (salt and water is lost but more water than salt is lost - sodium concertation goes up)

Isovolumic

32
Q

What is the cause of hypovolemic hypernatremia?

A
Non renal (sodium concertation >10 in urine)
Sweating, diarrhoea, Dehydration (kidney holds on to sodium and fluid) 

Osmotic diuresis - e.g mannitol. Water is lost in kidneys causing sodium to go up.
Sodium in urine is above >20

33
Q

What is the cause of hypervolemic hypernatremia? How is it treated?

A

Results in sodium and water retention, but more sodium is being retained more than water

Non renal-
- Over resuscitation with IV fluids - hypertonic sodium solutions

  • Too much sodium bicarbonate in a code situation after cardiac arrest
  • Giving drugs with high sodium content (piperacillin)
  • Mineralocorticoid excess (Cushing’s syndrome)

Diuretics (esp. sodium wasting) and free water

Renal -

34
Q

What is the cause of Euvolemic hypernatremia? How is it treated?

A
  • Loss of free water
    Non renal-
  • Reduction in antidiuretic hormone ( not being secreted in posterior pituitary - Pituitary diabetes insipidus or not making it in hypothalamus) to reabsorb free water from collecting tubules (diabetes insipidus)
  • Nephrogenic diabetes insipidus (kidneys are not responding to the antidiuretic hormone ADH)

Treatment- free water replacement

35
Q

Which conditions can cause Insensitivity to ADH (nephrogenic diabetes insipidus)?

A

Acute tubular necrosis
Osmotic diuresis
Total parenteral nutrition
Hyperosmolar hyperglycaemic state

36
Q

Which drugs can cause Insensitivity to ADH (nephrogenic diabetes insipidus)?

A

Lithium
Tetracyclines
Amphotericin B