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- Y6 Endocrinology > Hyponatraemia (presentation) > Flashcards

Hyponatraemia (presentation) Flashcards

1
Q

What happens if sodium is replaced too quickly in a hyponatraemic patient?

A

Central pontine myelinolysis - pons myelin sheath is broken down due to deranged osmotic gradients. This can lead to coma and quadriplegia (pons is the light thing in the middle)

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2
Q

What are the three main systems for controlling sodium balance?

A
  1. ADH
  2. RAAS
  3. Natriuretic peptide
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3
Q

How does ADH regulate sodium balance?

A

ADH is released from the pituitary in response to:

  • reduced blood volume (carotid sinus senses this)
  • reduced sodium concentration

This is because it allows expression of AQP2 in the collecting duct

This CAN affect Na concentration

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4
Q

How does RAAS regulate sodium balance?

A
  • Trigger for RAAS is a drop in BP causing reduced stimulation of arterial baroreceptors
  • Aldosterone is important for sodium absorption and potassium excretion
  • BUT Na is absorbed with water at a 1:1 ratio
  • So there is NO EFFECT on sodium concentration
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5
Q

How do natriuretic peptides affect sodium balance?

A
  • Natriuretic peptides e.g. ANP and BNP are released by myoendocrine cells due to stretch of the arterial wall or ischaemia
  • This happens in HF due to distension of the heart (due to poor CO)
  • This causes ANP and BNP release
  • These cause natriuresis (loss of Na in urine) BUT water follows at a 1:1 ratio

Therefore Na concentration is NOT affected by natriuretic peptides

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6
Q

How is hyponatraemia categorised?

A

Hyponatraemia can be

  • hypovolaemic (= water loss)
  • euvolaemic (= endocrine)
  • hypervolaemic (= “failures”)
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7
Q

List 3 causes of hypovolaemic hyponatraemia.

A
  1. Vomiting
  2. Diarrhoea
  3. Diuretics

Water is lost with sodium but only water is then replaced. Compensation by ADH release causes this change in Na conc.

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8
Q

List 3 causes of euvolaemic hyponatraemia.

A

ALL endocrine

  1. SIADH
  2. Hypothyroidism
  3. Adrenal insufficiency - Addison’s
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9
Q

What are the most common causes of SIADH? (3)

A
  1. Lung pathology - e.g. ectopic small cell lung tumour
  2. Drugs - SSRI, TCA, opiates, PPIs, carbamazepine
  3. CNS pathology - any; meningitis, hydrocephalus etc.
  4. Surgery
  5. Tumours
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10
Q

Summarise the pathophysiology of SIADH causing euvolaemic hyponatraemia.

A
  • SIADH - high ADH release causes water to be inappropriately reabsorbed in high amounts
  • In theory you should be hypervolaemic but other systems are still working so instead you are euvolaemic
  • Urine will be concentrated and blood will have low sodium (low osmolarity)

NB: SIADH is a diagnosis of exclusion which causes abnormally high urine concentration (high osmolarity). Must exclude other endocrine causes first.

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11
Q

What is the pathophysiology of hypothyroidism causing euvolaemic hyponatraemia?

A
  • T3/T4 act on the heart to increase CO to increase blood volume (in high pressure compartments) - this is because thyroid hormones upregulate the expression of the SR Ca-activated ATPase and downregulate the phospholamban expression.
  • Hypothyroidism –> low T3/T4 –> low CO –> low BV
  • This causes less stimulation of carotid sinus receptors which leads to ADH release
  • ADH causes reduced water excretion which dilutes the Na –> hyponatraemia
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12
Q

Summarise the pathophysiology of adrenal insufficiency causing euvolaemic hyponatraemia.

A
  • Adrenal insufficiency (angiotensin II usually stimulates adrenal cortex to release aldosterone) –> no aldosterone release
  • Lack of aldosterone leads to natriuresis (loss of sodium with water 1:1 ratio)
  • Water loss in turn causes ADH release which allows retention but no Na reabsorption so there is euvolaemic hyponatraemia.
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13
Q

List 3 causes of hypervolaemic hyponatraemia.

A
  1. Renal disease
  2. HF
  3. Liver failure
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14
Q

How does renal disease cause hypervolaemic hyponatremia?

A
  • Renal disease causes a reduced GFR
  • This effectively means nothing is being excreted - neither sodium nor water
  • But more water is taken in than excreted causing hypervolaemia –> dilution of blood
  • –> hypervolaemic hyponatraemia
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15
Q

How does HF cause hypervolaemic hyponatraemia?

A
  • Reduced CO causes reduced blood volume**
  • **Blood is pooling in low pressure compartments such as veins and leaking out into third spaces - so fluid is there but in the wrong place
  • So you have low blood volume –> ADH release –> water is reabsorbed from collecting ducts –> dilution of blood –> hypervolaemic hyponatraemia
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16
Q

How does liver disease cause a hypervolaemic hyponatraemia?

A
  • Usually in cirrhosis and portal hypertension
  • Liver releases vasodilators such as NOS
  • This causes pooling of blood in the portal system etc
  • This causes reduced blood volume** (not truly)
  • –> ADH release
  • –> water reabsorption
  • –> dilution of Na
  • –> hypervolaemic hyponatraemia
17
Q

What are 3 common causes of hypernatraemia?

A
  • Uncompensated water loss
  • Diabetes insipidus
  • Hyperaldosteronism
18
Q
A

Hypernatraemia

19
Q

How does diabetes insipidus cause hypernatraemia?

A
  • DI is the opposite of SIADH
  • This means there is no ADH release/nephrons are not sensitive to ADH (cranial/nephrogenic)
  • Water is lost
  • Sodium is retained
20
Q

What is a common drug which causes diabetes insipidus?

A

Lithium (mood stabiliser) is excreted by the kidney and eventually causes nephrogenic diabetes insipidus

21
Q

She is also in respiratory acidosis.

A
  • Pneumonia
  • CURB65
  • It is not small cell lung cancer because it doesn’t cause ABG abnormalities.
  • Not HF because it doesn’t cause ABG changes either
  • Diarrhoeal illness would cause metabolic problem
22
Q

typically, below what level of Na would you have to keep the patient admitted for further testing?

A

<128 mmol/L

Do not discharge if Na is below this; you must find the diagnosis.

23
Q

“Is it real” - what factors can cause a reading of hyponatraemia in a laboratory?

A
  1. High triglycerides
  2. High protein in liver dysfunction
  3. High glucose
24
Q

What calculations can be used to calculate osmolarity?

A

Osmolarity = 2 (Na+) + 2 (K+) + Glucose + Urea (all in mmol/L);

OR

Osmolarity = 2 (Na+) + Glucose + Urea (all in mmol/L).

25
Q

What is the relationship between glucose and Na in blood?

A

For every 3 that glucose goes up, Na goes down by 1.

26
Q

Clinically how do you evaluate volume status (i.e. whether patient is hypovolaemic, euvolaemic or hypervolaemic)?

A
  • JVP (can do BNP to confirm)
  • BP and pulse pressure
  • Skin turgor
27
Q

What is meant by the term “volume overrides the loss of tonicity”?

A

When blood is lost, a lower serum osmolality is tolerated.

28
Q

What is the difference in units between osmolality and osmolarity?

A

Osmolality - osmoles of solute per kilogram of solvent (Osm/kg)

Osmolarity - osmoles of solute per liter of solution (Osm/L)

29
Q

What is the sequence of questions to address in a hyponatraemic patient?

A
  1. Is the hoponatraemia real, or due to lab error?
  2. What is the volume status?
  3. What is the urine sodium? - in hypo and hypervolaemia the urine sodium will be low (<20mmol/L)
  4. Investigate with a CT head and CAP
  5. Management - fluid restrict+ diuretic OR increase solute intake

From Dr Cox

30
Q

What kind of saline should you give to a patient with hyponatraeamia, if their urine osmolarity is 600mmol/L?

A
  • The osmolarity of the saline needs to be at least 600mmol for them not to take up any additional fluid.
  • So you give triple concentration of normal saline
  • Normal saline concentration is 300mmol/L (150 Na + 150 Cl)
  • So triple concentrated is 900 mmol/L so the patient would lose some fluid with that and keep some Na (if it were 600 mmol/L then they would stay the same).

From Dr Cox

31
Q

What is the typical intake of sodium?

A

10mOsm/kg

32
Q

What are the limits for increasing sodium initially and in each 24 hr period thereafter?

A

Initially, increase by <10

Thereafter, in each 24hr perdiod <8

Never more as this could lead to central pontine myelinolysis.

33
Q

Name two drugs which are ideal treatments for SIADH (but too expensive to use on the NHS).

A

Tolvaptan - an aquaretic drug that functions as a selective, competitive vasopressin receptor 2 (V2) antagonist

Colivaptan - non-peptide inhibitor of the receptor for anti-diuretic hormone

34
Q

At what point should you stop treatment for hyponatraemia? (Na concentration value)

A

130 mmol/L - do not overshoot as this could have serius consequences

35
Q

Which drug is used in palliative patients for treatment of hyponatraemia resulting from SIADH, if fluid restriction alone does not restore sodium concentration or is not tolerable?

A

Demeclocycline but doesn’t work very well. Usually given to palliative resp patients if you do not want to fluid restrict.

36
Q

If you see….

  • hypoglycaemia
  • hypothermia
  • hypovolaemia

…what is the likely diagnosis to do with?

A

Thyroid function - hypothyroid

Cortisol release - Addison’s disease

37
Q

Which compartements does… migrate to when given to a patient?

  1. Normal saline
  2. 5% dextrose
A
  1. Normal saline- extracellular only…
    • 1/3 intravascular
    • 2/3 exravascular
  2. 5% dextrose
    • 2/3 intracellular
    • 1/3 extracellular of which
      • 1/3 intravascular
      • 2/3 extravascular

So saline better for increasing BP after surgery (according to DrCox)

38
Q

Why do post-operative patients become hyponatraemic? Name 3 factors.

A
  1. Pain
  2. General anaesthetic
  3. Opiates

These all increase ADH release so hyponatraemia is likely to result.

39
Q

Summarise the management of hyponatraemia.

A

- Y6 Endocrinology (33 decks)

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