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Hyponatraemia Flashcards

1
Q

What are the three main types of hyponatraemia?

A
  • Hyponatraemia with hypovolaemia
  • Hyponatraemia with euvolaemia
  • Hyponatraemia with hypervolaemia
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2
Q

What are extrarenal causes of hyponatraemia with hypovolaemia?

A
  • Vomiting
  • Diarrhoea
  • Haemorrhage
  • Burns
  • Pancreatitis
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3
Q

What are renal causes of hyponatraemia with hypovolaemia?

A
  • Osmotic diuresis
  • Diuretics
  • Adrenocortical insufficiency
  • Tubulo-interstitial renal disease
  • Unilateral renal artery stenosis
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4
Q

What are causes of hyponatraemia with hypervolaemia?

A
  • Heart failure
  • Liver failure
  • Oliguric kidney injury
  • Hypoalbuminaemia
  • Severe hypothyroidism
  • Glucocorticoid deficiency
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5
Q

What are causes of euvolaemic hyponatraemia?

A
  • Vagal neuropathy
  • Addison’s Disease
  • Hypothyroidism
  • SIADH
  • Psychogenic polydipsia
  • Drugs
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6
Q

What are features of hyponatraemia?

A
  • Anorexia
  • Nausea
  • Malaise
  • Headache
  • Irritability
  • Confusion
  • Weakness
  • Decreased GCS/Drowsiness
  • Seizures
  • Encephalopathic
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7
Q

What is regarded biochemically as mild hyponatraemia?

A

Na+ = 130-135 mmol/L

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8
Q

What is regarded biochemically as moderate hyponatraemia?

A

Na+ = 125-130 mmol/L

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9
Q

What is regarded biochemically as profound hyponatraemia?

A

Na+ = < 125 mmol/L

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10
Q

How would you determine if someone had renal or extrarenal hypovolaemic hyponatraemia?

A

Urinary Na+ levels

  • If > 20 mmol/L = Kidney is cause
  • If < 20 mmol/L = Extrarenal
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11
Q

What volume status is SIADH associated with?

A

Euvolaemia

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12
Q

What investigations would you consider doing in someone with hyponatraemia?

A

Essential tests:

  • Serum osmolality
  • Urine osmolality
  • Urinary sodium

Optional tests:

  • ABG
  • Serum triglycerides
  • Serum protein level
  • TFTs
  • LFTs
  • Urea and creatinine
  • Random cortisol
  • Short synacthen test
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13
Q

What is the general mechanism behind hypovolaemic hyponatraemia?

A

Loss of salt in excess of water loss

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14
Q

Why do extrarenal causes of hypovolaemic hyponatraemia cause urine concentration?

A

Urinary excretion of sodium falls in response to the volume depletion, as does water excretion, leading to concentrated urine containing <10 mmol/L of sodium.

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15
Q

What does a urine Na+ of > 20 mmol/L indicate in someone with hypovolaemic hyponatraemia?

A

Renal cause

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16
Q

What are features of hypovolaemia?

A
  • Reduced skin tugor
  • Dry mucous membranes
  • Tachycardia
  • Low BP (esp. postural drop)
  • Sunken eyes
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17
Q

What are features of hypervolaemia?

A
  • Oedema
  • Raised JVP
  • LVF
  • Ascites
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18
Q

What would you particularly want to determine if someone had euvolaemic hyponatraemia?

A

If it was hypotonic hyponatraemia i.e.

  • Plasma Osm <275 mOsm/kg
  • Urine Osm > 100 mOsm/kg
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19
Q

When determining how to manage someone with hyponatraemia, what would you want to determine first?

A

Are they symptomatic of asymptomatic

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20
Q

How would you manage someone with hypovolaemic hypontraemia?

A

IV 0.9% saline

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21
Q

How would you manage acute symptomatic hyponatraemia?

A

Move to level 2 care

  • Administer hypertonic saline
    1. 150 ml 3% saline over 15-20 minutes
    2. Check Na+ and Repeat 150 ml after 20 mins if no clinical improvement
    3. Stop hypertonic, administer slow 0.9% saline
    4. Check Na+ every 6 hours - Aim for correction no more than 10 mmol/L in first 24 hours. Thereafter, aim for 8 mmol/L
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22
Q

What can be a complication of giving sodium too quickly - i.e raising sodium too quickly?

A

From low to high - the pons will DIE

Osmotic pontine demyelination syndrome - encompasses central pontine myelinolysis and extrapontine myelinolysis

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23
Q

What is osmotic demyelination syndrome?

A

Neurones reclaim organic osmolytes slowly in the phase of rapid correction of hyponatraemia, resulting in an hypo-osmolar intracellular compartment and lead to shrinkage of cerebral vascular endothelial cells.

Consequently the blood–brain barrier is functionally impaired, allowing lymphocytes, complement, and cytokines to enter the brain, damage oligodendrocytes, activate microglial cells and cause demyelination.

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24
Q

What rate should Na+ be corrected in the first 24 hours?

A

8 mmol/L

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25
Q

What are features of osmotic central pontine myelinolysis?

A
  • Dysarthria
  • Dysphagia
  • Flaccid symmetric quadraparesis
  • Locked in syndrome and death if severe
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26
Q

What are features of extrapontine myelinolysis?

A
  • Tremor
  • Ataxia
  • Movement disorders
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27
Q

What are regarded as essential tests to perform in someone with hyponatraemia?

A
  • Serum osmolality
  • Urine osmolality
  • Urinary sodium
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28
Q

What physiologically occurs in the kidenys in response to dehydration?

A

ADH is secreted, along with activation of RAAS system, inparticular aldosterone. This leads to salt and water retention. This will generally give a urinary sodium of <20 mmol/L

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29
Q

What situations can give rise to low urinary sodium hyponatraemia?

A

Represent a normal RAAS response to hypovolemia, or an abnormal overreaction to an “apparent” low volume state:

  • Dehydration/True hypovolaemia
  • Heart Failure
  • Advanced cirrhosis
  • Nephrotic syndrome
  • Polydipsia
  • Inappropriate IV fluids
  • Beer potomania
  • Reset osmostat
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30
Q

What is the most important step to perform in terms of investigations once recognising that someone is hyponatraemic?

A

Determine serum osmolality

31
Q

If someone had hypo-osmotic (serum) hyponatraemia, what would you consider looking at/investgating to narrow the differential?

A

Urinary osmolality

32
Q

If someone had a hypo-osmotic hyponatraemia with high urine osmolality, what might this indicate about the body’s response to hyponatraemia?

A

This represents an abnormal response to hyponatraemia - kidney’s have lost the ability to make urine dilute. Producing copious amounts of dilute urine is the only sensible way you can physiologically restore your tonicity, short of engaging in high-risk sodium seeking behaviour. Ergo, a hypoosmolar hyponatremic person should pee buckets, and their urine should resemble tap water.

33
Q

For someone with hypoosmotic hyponatraemia who’s urinary osmolality you have determined as being high/low, what test would you consider looking at/doing to narrow down a diagnosis?

A

Urinary sodium

34
Q

What can cause hypo-osmotic hyponatraemia with a high urine osmolality and a high urinary sodium?

A

This means renal soidum loss is high, despite low sodium, and water reabsoprtion mechanisms remain intact.

  • Thiazide diuretics
  • Polyuric phase of ATN
  • Post-obstructive diuresis
  • CKD
  • Mineralocorticoid deficiency
  • Hypothyroidism
  • SIADH
  • Cerebral salt wasting
35
Q

What is cerebral salt wasting syndrome?

A

Another potential cause of hyponatremia in those with CNS disease, particularly patients with subarachnoid hemorrhage. CSW is characterized by hyponatremia and extracellular fluid depletion due to inappropriate sodium wasting in the urine. However, some authorities contend that CSW does not really exist and is only a misnomer for what is actually SIADH, with the putative salt wasting being due to unappreciated volume expansion

36
Q

How might you distinguish between cerebral salt wasting and SIADH?

A
  • SIADH - normovolaemic, low urine output
  • CSW - Hypovolaemic, high urine output
37
Q

If someone had a hypo-osmotic hyponatraemia with low urine osmolality, what might this indicate about the body’s response to hyponatraemia?

A

A normal response to hyponatraemia - kidney’s have retained the ability to make urine dilute. Producing copious amounts of dilute urine is the only sensible way you can physiologically restore your tonicity, short of engaging in high-risk sodium seeking behaviour. Ergo, a hypoosmolar hyponatremic person should pee buckets, and their urine should resemble tap water.

38
Q

What investigations might you consider doing in someone with hypo-osmotic, hyponatramia with high urine osmolality and low urinary sodium?

A
  • LFTs
  • TTE
  • 24hr urinary protein
39
Q

What investigations would you consider doing if someone had hypo-osmotic hyponatraemia with high urine osmolality and high urinary sodium?

A
  • TFTs
  • Cortisol Level
40
Q

What investigations would you consider doing/looking at if someone with hypo-osmotic hyponatraemia has low urine osmolality?

A

Measure urinary sodium

41
Q

What would you consider as a cause of hypo-osmotic hyponatraemia with low urine osmolality with low urinary sodium?

A

Sodium retention, water loss - Water excretion mechanism maintained, but free water intake is abnormally high

  • Polydipsia
  • Inappropriate IV fluid
  • Beer potomania
  • Malnutrition
  • Reset osmostat
42
Q

What would you consider as a cause of hypo-osmotic hyponatraemia with low urine osmolality and high urinary sodium?

A

Sodium and water wasting - both water and sodium resorption mechanisms have failed:

  • Renal sodium loss
    • Post-obstructive diuresis
    • Polyuric phase of ATN
    • AKI
43
Q

What are causes of hypo-osmotic hyponatraemia with high urine osmolality and low urinary sodium?

A

Sodium and water retention - There is an attempt being made to retain sodium as well as water, for whatever reason

  • True hypovolaemia
  • Heart failure
  • Cirrhosis
  • Nephrotic syndrome
44
Q

In terms of sodium and water retention/wasting, what physiologically occurs in hypo-osmotic hyponatraemia with high urine osmolality and low urinary sodium?

A

Sodium and water retention

45
Q

What are causes of hyponatraemia with high urinary sodium?

A

A high urine sodium in the face of serum hyponatremia suggests that there is some sort of sodium wasting disorder taking place, but these are uncommon

  • Hypoadrenalism
  • Hypothyroidism
  • Acute or chronic renal failure
  • SIADH
  • Cerebral salt wasting
  • Post-obstructive diuresis
  • The polyuric phase of acute tubular necrosis
  • Diuretic use
46
Q

In terms of sodium and water retention/wasting, what physiologically occurs in hypo-osmotic hyponatraemia with high urine osmolality and high urinary sodium?

A

Sodium wasting, water retention

47
Q

In terms of sodium and water retention/wasting, what physiologically occurs in hypo-osmotic hyponatraemia with low urine osmolality and high urinary sodium?

A

Sodium and water wasting

48
Q

In terms of sodium and water retention/wasting, what physiologically occurs in hypo-osmotic hyponatraemia with low urine osmolality and low urinary sodium?

A

Sodium retention and water wasting

49
Q

What does high urine osmolality indicate in terms of water wasting/retention?

A

Water retention

50
Q

What does low urine osmolality indicate in terms of water retention/wasting?

A

Water wasting

51
Q

How does hyperglycaemia cause Hyperosmolar Hyponatraemia?

A

In the context of HHS, glucose overloads the system and acts osmotically

52
Q

What are causes of hyperosmolar hyponatraemia?

A
  • Glucose
  • Mannitol
  • Glycine
  • Alcohol intoxication - within the first few hours of drinking.
53
Q

What is isoosmolar hyponatraemia also known as?

A

Pseudohyponatraemia

54
Q

What is the most common cause of isosmolar hyponatraemia?

A

Hypertriglyceridaemia

55
Q

What are causes of isosmolar hyponatraemia?

A
  • Hypertriglyceridaemia
  • Turp Syndrome
  • Paraproteinaemia
56
Q

What is the physiological effect of psychogenic polydipsia?

A

Water will distribute evenly among all the compartments, and the compartments will now have an osmolality of about 250mOsm/Kg

57
Q

How would you manage fluid intake in psychogenic polydipsia?

A

Gradual reduction in water consumption - if to quick - central pontine demyelination

58
Q

How does post obstructive diuresis cause hyponatraemia?

A

During obstructed period, numerous diuretic factors are released, and their effect becomes evident after the obstruction is released. The effect is that of proximal tubule dysfunction; massive dilute diuresis and uncontrollable sodium excretion ensue. The pent-up serum urea is now free to escape via the glomerulus, and it also acts as an osmotic diuretic, increasing urine volume and maintaining urine osmolality somewhat above the “maximal” dilution.

Additonally, Na+/K+ ATPase in the distal tubule stops working; if the sodium is not being pumped out of the cell effectively, no gradient for sodium reabsorption can be maintained, and consequently sodium and water are not reabsorbed.

59
Q

What is the pathophysiology of the polyuric phase of ATN?

A

Sodium transport in the proximal tubule relies on the action of Na+/K+ ATPase sucking sodium out of the cell (and into the peritubular capillary), maintaining a gradient to drive the Na+/H+ antiporter which gets sodium out of the tubular lumen. This demands vast quantities of ATP. In a state of ischaemia, this process breaks down, and sodium remains in the proximal tubule lumen.

Furthermore, tubules and collecting duct are resistant to aldosterone and ADH. The result is a failure to reabsorb the sodium as it travels down the tubule, as well as a failure to reabsorb water. Once the glomerulus recovers, it sends a normal amount of fluid through the tubule, but the tubule simply doesn’t care.

60
Q

What is the physiology behind hypoosmolar hyponatraemia with concentrated (hyperosmolar) urine and low urinary sodium?

A

Hypoosmolar hyponatremia with concentrated urine and low urine sodium is a state where there is either an actual low extracellular volume (and water and sodium are being appropriately retained by the kidneys), or a volume overloaded state where the renal mechanisms have been fooled into retaining sodium and water by some other pathological process.

61
Q

What is the basic physiology behind hypervolaemic hypoosmolar hyponatraemia?

A

In these situations, the renin-angiotensin-aldosterone system is activated inappropriately. Whereas in fact oedema and fluid overload may be the reality, the kidneys are convinced that there is an extracellular fluid deficit.

All of these forms of hyponatremia are treatable by ACE-inhibition and with loop diuretics

62
Q

How does heart failure cause hypervolaemic hyposmolar hyponatraemia?

A

A low output state (where the cardiac output is reduced) results in a decreased salt delivery to the macula densa, which in turn activates the renin-angiotensin-aldosterone system. Sodium and water retention are the result; this oedematous patient will have low serum sodium as well as a low urine sodium, with a decreased volume of concentrated urine.

63
Q

How does cirrhosis with ascites cause hyposmolar hypervolaemic hyponatraemia?

A

Cirrhosis may actually be a high-output state (with a hyperdynamic circulation) - but the arterial blood pressure is still low, owing to the systemic vasodilation. Why the vasodilation? Anybody’s guess, really. It is though that nitric oxide secretion plays a role; it is thought that intestinal bacterial endotoxins cause this, as they are no longer being cleared from the portal blood by the useless wooden liver.

In any case, the arterial vasodilation activates the renin-angiotensin-aldosterone system, and again water and sodium is retained. It does not help that the liver is responsible for the metabolism of about 1/3rd of the secreted vasopressin.

64
Q

How does nephrotic syndrome cause hypervolaemic hypoosmotic hyponatraemia?

A

Third space distribution of fluid is the key factor in the mechanism of hyponatremia due to nephrotic syndrome. Because of the low serum protein, oncotic pressure is reduced and fluid migrates out of the intravascular compartment, reducing the effective circulating volume. Again, the renin-angiotensin-aldosterone system responds by increasing sodium and water retention

65
Q

How do thiazide diuretics cause inappropriate sodium loss causing hypoosolar hyponatraemia with concentrated urine and high urinary sodium?

A

The mechanism of this hyponatremia rests on the tendency of diuretics to produce volume depletion, which in turn causes ADH secretion, which in turn causes water retention - with ongoing sodium loss (so the urine ends up being more sodium-rich than the plasma!). Unlike the loop diuretics, the thiazides do not impair the medullary osmotic gradient, and ADH can still cause the reabsorption of water into the medulla (whereas the loop diuretics interfere with the medullary gradient, rendering ADH less effective). The result is a failure to dilute urine, combined with a failure to reabsorb sodium.

66
Q

How does acute/chronic renal failure result in hypo-osmolar hyponatraemia with high urinary sodium and concentrated urine?

A

In acute renal failure, the urine osmolality is unpredictable. A combination of tubule dysfunction and reduced urine delivery to the distal nephron reduces its ability to reclaim sodium from the tubular lumen; however the ability to concentrate urine (i.e. ADH responsiveness of the collecting duct) may still be preserved. In chronic renal failure, the urine osmolality trends towards about 300mOsm/Kg (“isosthenuria”). Water intake in these patients is not matched by excretion, and a dilutional hyponatremia develops; the sodium loss occurs because of insufficient efforts to reclaim it from the tubules.

67
Q

How does corticosteroid deficiency cause hypoosmolar hyponatraemia with concentrated urine and high urinary sodium?

A

Aldosterone activates the ENaC channel in the collecting duct, which causes resorption of sodium (and thus forces excretion of potassium). Loss of aldosterone, eg. Addisons disease, results in decreased sodium resoprtion, and increased potassium retention – thus the hyponatremia and hyperkalemia. Not only that - but cortisol itself acts an inhibitor of ADH secretion; less circulating cortisol means more circulating vasopressin. The result is water retention, and concentrated sodium-rich urine.

68
Q

How does hypothyroidism cause hyposmolar hyponatraemia with concentrated urine and high urinary sodium?

A

The vasopressin levels are usually high in these people but the mechanism seems to be a matter of ADH-induced water retention, in response to a decreased cardiac output which causes decreased renal blood flow. The situation is therefore analogous to the hyponatremia of cardiac failure.

69
Q

What is the pathophysiology behind cerebral salt wasting syndrome?

A

MAY NOT EVEN BE A THING

Natriuretic peptides such as BNP and ANP are thought to be the cause of this. One can imagine the injured brain releasing BNP as its cells decompose; however in humans there is not much BNP in brain tissue (it was first named after being discovered in porcine brains, where it for some reason exists in higher concentration). Whatever the (poorly understood) cause, a diuresis with natriuresis occurs, and the brain-injured patient dehydrates gradually as electrolyte-rich urine issues forth.

70
Q

How might you distinguish between CSW and SIADH?

A

The key feature if hypovolemia. These patients are dry and they produce a high urine output; in contrast SIADH patients are normovolemic, and have low urine output. The trick to discriminating between these two conditions lies in the ability to demonstrate that the body fluid volume is decreased. In both conditions the ADH level is elevated, but in cerebral salt wasting the ADH is elevated appropriately because the patient is hypovolemic, and so it cannot possibly be SIADH by definition.

71
Q

How might you manage someone with hypervolaemic hyponatraemia?

A

Fluid restriction

72
Q

Hopw would you manage euvolaemic hyponatraemia?

A

Fluid restriction

73
Q

How would you treat hypovolaemic hypontraemia?

A

Isotonic saline

74
Q

How would you calculate sodium deficit?

A

Sodium deficit = 0.6 (men) or 0.5 (women) × body weight × (desired concentration - current concentration)

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