Week 2 Altered Sodium/ Water Homeostasis Flashcards

1
Q

In the body overall where is most of the sodium and most of potassium?

A

Most of the potassium in intracellular and most of the sodium is extracellular

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2
Q

What happens to water movement between the intra/extra cellular spaces if we add sodium to the body?

A

Sodium primarily exists in the extracellular space therefore water will get drawn out of the intracellular space and into the extracellular

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3
Q

What is the relationship between volume status and hyponatraemia?

A

None, you can have normal volume or be hypo/hyper volaemic depending on the reason for hyponatraemia

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4
Q

What are the different ypes of hyponatraemia based on volume?

A

Norvolaemic hyponatraemia
Hypovolaemic hyponatraemia
Hypervolaemic hyponatraemia

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5
Q

Why can be hard to tell whether or not someone is normovolaemic?

A

We only get clinical signs when the ratios between intra and extra cellular fluid are different.

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6
Q

What is the result of the following (potassium stays the same):

An increase in water

A decrease in water

An increase in sodium

A decrease in sodium

A

An increase in water - hyponatraemia (I/X volume ratio stays the same, [Na] goes down)

A decrease in water - hypernatraemia (I/X volume ratio stays the same, [Na] goes up)

An increase in sodium - hypervolaemia (I -> X until [Na] normal)

A decrease in sodium - hypovalaemia (X -> I until [Na] normal)

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7
Q

Thinking about water and sodium gain/loss how would each of these states be acheived:

Norvolaemic hyponatraemia
Hypovolaemic hyponatraemia
Hypervolaemic hyponatraemia

A

Norvolaemic hyponatraemia - pure water gain (although in reality slightly hypervolaemic as extracellular fluid is increased, there is never odeama so is clinically normovolaemic)

Hypovolaemic hyponatraemia - Water and salt gain (water more than salt)

Hypervolaemic hyponatraemia - Water and salt loss (salt more than water)

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8
Q

Examples of Normovolaemic / hypervolaemic hyponatraemia ( pure water gain )

A

SIADH
hypothyroidism
Iatrogenic

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9
Q

A 72 year old lady becomes confused 3 days after a hip replacement; electrolytes reveal:
urea: 2.4 mmol/l
creatinine: 78 umol/l
potassium: 3.4 mmol/l
sodium: 122 mmol/l
Clinical examination reveals a trace of
oedema.
What has happened ?
Why is she confused ?

A

She has been given hypotonic fluid.

Dilute extracellular space (slight odema)
-> hyponatraemia ->
Fluid moves to hypertonic cellular space due to osmotic & hydrostatic forces ->
Cerebral oedema

This is an example or normo/hypervolaemic hyponatraemia. Although slightly hypervolaemic it is not enough to cause significant interstitial oedema, instead the movement into the cellular is more significant and causes cerebral oedema.

I think this is because as water is added, BP increases, therefore RAAS is surpressed, resulting in more sodium excretion and hence further hyponatraemia, hence water keeps going into the intracellular even more than the extra cellular.

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10
Q

A 38 year old lady is brought in to hospital having collapsed at home. She has Crohn’s disease with a high-output ileostomy; she caught gastroenteritis from her son 5 days ago.
Tests reveal a sodium of 128mmol/l.
Her blood pressure is 90/40mmHg in bed

Why did she collapse ?

A

Salt-rich diarrhoea ++++
water loss cannot compensate for Na+ loss.
Hydrostatic forces favour water movement from cells to interstitium, however, Osmotic forces favour the reverse. This results in the cellular volume not fully able to compensate for the extracellular and hence hypovolaemia persists.

Vascular depletion causes hypotension

Standing up causes postural hypotension & collapse

This is an example of hypovolaemic hyponatraemia

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11
Q

When can hypovolaemic hyponatraemia occur?

A

any case where salt & water loss occur, but water loss is insufficient to concentrate the sodium

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12
Q

When can hypervolaemic hyponatraemia occure?

A

3 classic cases:
heart failure - a good example
liver failure
nephrotic syndrome

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13
Q

How is hypervolaemic hyponatraemia acheived in heart failure?

A

Heart perfusion and BP drops hence RAAS and ADH kicks in as body thinks it’s hypovolaemic. RAAS retains sodium and water however ADH only retains water hence things still become a bit hyponatraemic.

Fluid is retained putting further stress in the LV.

Cycle continues.

In this case as the body isn’t particularly hyponatraemic hence not much goes into the extracellular space.

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14
Q

Combinations of water/Na gain/loss that oculd lead to hypernatraemia?

A

pure water loss
water gain < Na+ gain
Na+ loss < water loss
pure Na+ gain ( possible  )

Na+ gain and water loss

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15
Q

Is hypernatraemia often hypovolaemic or hypervolaemic?

A

Hypovolaemia is almost always the case

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16
Q

How does the list of eitiologies for hypernatraemia compare to hyponatraemia?

A

The list of potential aetiologies is very similar to that for hypovolaemic hyponatraemia:

The difference is the sodium : water balance

17
Q

A 38 year old lady is brought in to hospital having collapsed at home. She has Crohn’s disease with a high-output ileostomy; she caught gastroenteritis from her son 5 days ago.
Tests reveal a sodium of 128mmol/l.
Her blood pressure is 90/40mmHg in bed

Why did she collapse ?

A
  • Colonic secretions are water&raquo_space; salt
    ( salt absorbed in small bowel )
  • water loss causes hypernatraemia
  • osmotic and hydrostatic forces favour shifts from cells to ECF
    ( but not enough )
  • Hypovolaemia
  • Orthostatic hypotension?
18
Q

What does volaemia refer to?

A

The volume fo extracellular fluid e.g. interstitial and circulating

19
Q

Specific causes of hypernatraemia?

A

Pure water loss:
* fever ( sweat +++ )
* hyperventilation
* diabetes insipidus ( see later )

Reduced water intake:
* iatrogenic
* psychosocial - elderly, infants, apathetic etc.
* stroke, coma, confusion etc.

High sodium intake:
* iatrogenic -
concentrated feeds
emetics
(uncommon)

19
Q

Things that can cause SIADH?

A

Pituitary hypersecretion / direct effect:
Neurological:
mening / encephalitis, head injury, stroke etc.
hypothalamic tumour
NOT pituitary macroadenoma (these tend to surpress ADH)

Ectopic secretion:
Malignancy:
SCLC, pancreas, bladder, prostate etc
Pulmonary ( non-malignant ):
TB, pneumonia etc.

20
Q

Causes of diabetes insipidus

21
Q

Rough plasma/ urine osmolalities for SIADH vs DI

22
Q

Ways to give water

A

The oral route is the best

Water cannot be given IV (local cells will burst!!!):
* 5% dextrose is the usual form of IV water

23
Q

Best ways to alter water balance in a patient

A
  • Restrict intake - restrict drinking, remove feeds
  • Give water - give orally, give IV int he form of 5% dextrose
24
Therepies for cranial DI and nephrogenic DI
Cranial DI: synthetic ADH ( DDAVP ) Nephrogenic DI: supraphysiological ADH diuretics ( paradoxically ) NSAIDs largely unsatisfactory
25
What is central pontine myelinolysis?
A demyelinating condition that results from correcting chronic hyponatraemia too quickly. In chronic hyponatraemia: * Brain cells adapt by losing osmolytes to prevent swelling from excess water. * If you correct sodium too quickly, extracellular osmolality rises rapidly → water rushes out of brain cells. * This causes cells to shrink rapidly, damaging oligodendrocytes and leading to demyelination, particularly in the pons.
26
What is the reccomended rate to correct for hyponatraemia in order to prevent central pontine myelinolysis?
recommended rate of correction: * 4-10 mmol/l/day if asymptomatic * 8-12 mmol/l/day if symptomatic
27
What are signs and symptoms of hypovolaemia/ dehydration?
28
What are the signs and symptoms of hypervolaemia/ overhydration?