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Endocrine > Sodium levels > Flashcards

Sodium levels Flashcards

1
Q

How is sodium absorbed in the proximal convuluted tubule? (4)

A
  1. Active transport in the apical membrane
    * Active transport across the apical membrane of the PCT via
    - Na+/H+ exchanger
    - Sodium/Glu cotransporter (SGLT2)
  2. Active transport of Na+ across basolateral membrane via
    - Na+ / K+/ATPase pump
  3. Passive paracellular reabsorption
    - active transport of sodium into PCT cell generates osmotic gradient
    - Allows for water to follow
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2
Q

How is sodium absorbed in the thick ascending limb of the loop of Henle? (2)

A
  1. Active transport of sodium ions the apical membrane of the thick ascending limb
    - sodium-potassium-2 chloride cotransporter (NKCC2)
    - Co-transporter actively transports sodium, potassium and chloride ions
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3
Q

How is sodium reabsorbed in the distal convulated tubule? (2)

A

Sodium reabsorption in the DCT is fine-tuned and regulated by several factors:

  1. Aldosterone acts on the DCT and collecting tubules
    - Promotes synthesis of Sodium channels ENaC in the apical membrane
    - Increasing sodium reabsorption and decreasing potassium reabsorption
  2. Thiazide diuretics
    * Na+/Cl- symporter - early part of distal convulated tubule
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4
Q

How is sodium reabsorbed in the collecting duct? (3)

A

Collecting Duct
Hormones that affect sodium reabsorption include:

  1. Aldosterone:
    * It stimulates the ENaC channels in the apical membrane of collecting duct cells, leading to increased sodium reabsorption.
  2. Antidiuretic Hormone (ADH):
    - ADH increasing water permeability in the collecting duct.
    - causes water to be reabsorbed, it increases the concentration of sodium in the urine.
  3. Atrial Natriuretic Peptide (ANP):
    - ANP is released in response to increased blood volume and high blood pressure.
    - It inhibits sodium reabsorption in the collecting duct, promoting sodium excretion and water loss.
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5
Q

How is sodium ion homeostasis in the blood maintained?

A
  1. Baroreceptors detect low blood pressure which activates the sympathetic nervous system;
    * Vasoconstriction of afferent arterioles of the glomerulus
    Increased sodium reabsorption by the proximal tubules
    —> increased blood volume
    —-> increased BP
  2. RAAS activation - low BP, low renal perfusion

—> Increases renin secretion
—> Angioteniogen to Angiotensin I to Angiotensin II
—> Adrenal cortex releases aldosterone
—-> vasoconstriction + increases N+ + Cl- + water reabsorption
—> raised blood volume, raised BP

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6
Q

What is the definition of hyponatraemia?

A
  • Defined as a serum sodium concentration of <135 mmol/L.
  • It is a disorder of water balance reflected by an excess of total body water relative to electrolytes
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7
Q

What is the pathophysiology of ‘Hypertonic hyponatraemia’ (2)

A
  1. Presence of excess levels of an osmolyte/solute creates an osmotic gradient
  2. Causes water to shift from the intracellular to the extracellular compartment
  3. Thus diluting extracellular sodium.
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8
Q

What are the causes of hypertonic hyponatraemia?

A
  1. Hyperglycaemia
  2. Administration of a hypertonic fluid (e.g., mannitol, glycine, or sorbitol)
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9
Q

What is the pathophysiology of hyperglycaemia associated hyponatraemia? (4)

A
  1. Osmotic Diuresis:
    * High blood glucose levels create an osmotic gradient
    * Draws water from the body’s cells into the bloodstream.

kidneys increase urine production to eliminate the excess glucose and excess water, leading to increased urination (polyuria).

  1. Dilution of Sodium:
    * The increased urination results in the loss of both glucose and water from the body.
    * While the glucose levels are reduced, the loss of sodium is proportionally greater, causing a relative dilution of sodium in the blood.
    * This relative dilution can lead to hyponatremia.
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10
Q

What are the causes of hypovolaemic hyponatraemia?

A

1.Gastrointestinal fluid loss(e.g., severe diarrhoea or vomiting)

  1. Third spacing of fluids- (e.g., pancreatitis, severe hypoalbuminaemia)
    * Inflammation increases vascular permeability
    * Loss of albumin : reduces oncotic pressure within the blood vessels
    - Allowing for fluid to leak into the surrounding tissues and interstitial spaces outside of the blood vessels.
  2. Cerebral salt-wasting syndrome
    - a range of intracranial pathologies such as head injury/tumor/stroke lead to excess urinary sodium loss due to unknown aietiology.

4.Mineralcorticoid deficiency
- Autoimmune destruction of adrenal cortex from Addison’s disease
- Decrease in aldosterone production increases sodium loss from kidneys

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11
Q

What is the definition of hypervolaemic hyponatraemia (2)

A

Characterized by a low concentration of sodium in the blood (hyponatremia) in the presence of increased blood volume (hypervolemia).

  • This condition typically arises due to the retention of both water and sodium by the body
  • leading to an expansion of blood volume and a dilution of sodium levels.
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12
Q

What are the causes of hypervolaemic hyponatraemia?

A
  1. Acute kidney injury/chronic kidney disease-
    - disruption the normal regulation of water and sodium excretion
    - leading to hypervolemic hyponatremia
  2. Congestive heart failure
    * heart is unable to effectively pump blood, leading to a backup of blood in the circulatory system.
    - This congestion can stimulate the release of antidiuretic hormone (ADH)
    - causing the kidneys to retain both water and sodium
    result in hypervolemic hyponatremia
  3. Cirrhosis and Nephrotic syndrome
    - In cirrhosis, the liver is damaged and less able to produce proteins, including albumin.
    - Nephrotic syndrome is a kidney disorder characterized by increased protein loss in the urine
  • leads to a reduction in oncotic pressure (the osmotic pressure that holds fluid within the blood vessels),
  • fluid to leaks into the interstitial spaces,
  • expansion of blood volume and hyponatremia.
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13
Q

What is the definition of euvolaemic hyponatraemia?

A
  1. characterized by a low concentration of sodium in the blood (hyponatremia) in the presence of normal blood volume (euvolemia)
  2. body’s total blood volume is within the normal range.
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14
Q

What is the main cause of ‘Euvolaemic Hyponatraemia’

A
  • Syndrome of inappropriate antidiuretic hormone (SIADH) is a common cause of euvolaemic hyponatraemia
  • It is a diagnosis of exclusion.
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15
Q

What are the other causes of ‘Euvolaemic hyponatraemia’ which need to be excluded before a diagnosis of SIADH can be made?

A
  1. Adrenal Insufficiency:
    * primary adrenal insufficiency (Addison’s disease), can lead to deficiencies in mineralocorticoids like aldosterone.
    * Aldosterone is responsible for regulating sodium and potassium balance.
    * Deficiency can result in sodium loss and euvolemic hyponatremia
  2. Hypothyroidism
    * Thyroid hormones play a role in regulating the responsiveness of the kidneys to aldosterone and antidiuretic hormone (ADH)
    * Low levels of thyroid hormones can lead to decreased sodium reabsorption
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16
Q

What is the definition of SIADH?

A

characterized by the excessive release of antidiuretic hormone (ADH), also known as vasopressin, from the posterior pituitary gland.

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17
Q

What are the causes of SIADH?

A
  1. Tumors:
    lung tumors, can produce and release ADH or ADH-like substances
  2. CNS disorders:
    Brain trauma/infection/tumors can distript release or regulation of ADH
  3. Lung disease:
    Pneumonia/TB.COPD can irritate lung tissue and lead to increased ADH release
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18
Q

Which medications can stimulate ADH release and cause SIADH?(2)

A
  1. thiazide diuretics - Impair urinary dilution:
  2. Antidepressants - potentiate the effects of vasopressin
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19
Q

What is the definition of serum osmolality?

A

Indicates the concentration of all particles dissolved in body fluids

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20
Q

What is pseudohyponatraemia?

A

Serum Na+ concentration < 135
with
Normal serum osmolality

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21
Q

What causes pseudohyponatraemia?

A

Common cause is due to elevated levels of cholesterol in the blood

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22
Q

What does serum osmolality > 295 indicate in hyponatraemia?

A

Hypertonic hyponatraemia
* Hypertonic hyponatraemia is due to either hyperglycaemia or the administration of hypertonic fluids (e.g., mannitol, sorbitol).

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23
Q

What does serum osmolality <275 indicate in hyponatraemia?

A

Hypovolaemic hyponatraemia

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24
Q

What does normal serum osmolality indicate in hyponatraemia?

A

275 - 295

Isotonic pseudohyponatraemia

25
Q

What are the two possible urine sodium concentration results seen in ‘Hypovolaemic hyponatraemia’ and what does this show? (4)

A
  1. Urine sodium concentration >20 mmol/L: indicates renal sodium losses (e.g., diuretics)
  2. Urine sodium concentration ≤20 mmol/L: indicates hypovolaemia with non-renal sodium losses (e.g., gastrointestinal losses).
26
Q

What are the two possible urine sodium concentration results seen in ‘Hypervolaemic hyponatraemia’ and what does this show? (4)

A

Urine sodium concentration >20 mmol/L: indicates renal sodium losses (e.g., diuretics)

Urine sodium concentration ≤20 mmol/L: indicates hypovolaemia with non-renal sodium losses (e.g., gastrointestinal losses).

27
Q

What is the urine sodium concentration seen in patients with ‘Euvolaemic Hyponatraemia’?

A
  • Urine sodium concentration is >20 mmol/L in most patients
  • however, patients with a concomitant low sodium intake may have a low urinary sodium.
28
Q

What the definition of urine osmolality?

A

The concentration of particles dissolved in the urine

29
Q

What is the significance of urine osmolality?

A

Urine osmolality can be used to further identify causes of ‘Euvolaemic hyponatraemia’

  • Urine osmolality is >300 (high) : Hyper/hypovolaemic hyponatraemia

* Urine osmolality is variable in euvolaemic hyponatraemic depending on the cause

30
Q

What does >300 urine osmolality indicate in euvolaemic hyponatraemia?

A

SIADH due to the inappropriate dilution of plasma as a result of pathological vasopressin release
- may be due to drug-related effects

31
Q

What does 150-300 mml/kg urine osmolality indicate in euvolaemic hyponatraemia?

A

partial effect of medications or mild SIADH in conjunction with high fluid intake

32
Q

What does <150 mmol/kg urine osmolality indicate in euvolaemic hyponatraemia?

A

Low - indicates primary polydipsia

33
Q

What are the clinical features of acute hyponatraemia?

A
  • Acute onset < 48 hours
  • Cerebral oedema : nausea/vomiting, altered mental status, somnolence, seizures, coma
34
Q

What is the management of acute hyponatraemia? (3)

A
  1. IV hypertonic 3% saline - 100ml over 10 mins as a bolus until symptom improvement occurs.
  2. Once desired serum sodium concentration is achieved - cease hypertonic 3% saline
  3. Continue IV fluid repletion with suitable fluids
35
Q

What is the rate of sodium correction to preven myelinolysis in hyponatraemia?

A

<8 mmol/L/day to prevent myelinolysis

36
Q

What are the clinical features of chronic hyponatraemia?

A

Onset > 48 hours
Asymptomatic or mild symptoms only

37
Q

What is the management of chronic hypovolaemic hyponatraemia?

A
  1. IV isotonic fluids e.g. normal saline 0.9%
    Give as 250-1000ml bolus initially
    IV infusion of 1ml/kg/hour } replete intravascular volume until signs and symptoms are no longer present
  2. Avoid hypotonic fluids in these patients
  3. Treat underlying cause
38
Q

What are hypovolaemic fluids?

A
39
Q

What are euvolaemic fluids?

A
40
Q

What is the management of Hypervolaemic or Euvolaemic hyponatraemia?

A
  1. First line : Fluid restriction of 1L
    - adjusted measured on urine output and set at 500ml less than daily urine volume
  • Treat underlying cause such as AKI or SIADH
  1. Second line ; Vasopressing receptor anatagonist and discontinue fluid restriction
    * If fluid restriction fails - consider vasopressin receptor antagonist (also known as a vaptan)
    * fluid restriction is lifted in order to prevent overcorrection of Na+
41
Q

What is the mechanism of action of Vaptan and when is it indicated?

A

Vaptan MOA : directly block the action of vasopressin on the kidneys, thereby reducing water retention. They have been shown to be safe and effective at slowly correcting serum sodium levels.

Indication : If fluid restriction fails in the management of hyper/euvolaemic hyponatraemia

42
Q

What is the definition of hypernatraemia?

A

Electrolyte imbalance consisting of a rise in sodium concentration.
Defined as ; Na+ > 145 mmol/L
Severe hypernatraemia >152 mol

43
Q

What is the pathophysiology of hypernatraemia?

A
  • Increased loss of water compared to Na+ loss
  • Occurs when water loss is not replaced by increased water intake

Lack of normal renal function such as kidney dysfunction or diabetes insidious will prevent concentration and secretion of Na+ ions via the urine

44
Q

What is the pathophysiology of acute hypernatraemia < 48 hours?

A
  • High Na+ concentration extracellularly increases osmolarity
  • Water leaves cells and enters the blood via osmosis
  • In the brain - osmosis of water, causes the brain the shrink, leading to neurological side effects.
45
Q

What are the clinical features of acute hypernatraemia?

A

Lethargy, weakness
Irritability
Sizures
IC haemorrage
Coma

46
Q

Why are there fewer clinical features in chronic hypernatraemia?

A

Brain cells are able to adapt by increasing intracellular brain solutes by retaining more electrolytes
thus reduced brain shrinkage and neurological side effects.

47
Q

What are the causes of hypernatraemia?

A
  1. Free water losses;
  2. Excessive urination : Diabetes (DKA or HHS), use of diuretics
  3. GI losses : severe diarrhoea, prolonged vomittin
  4. Insensible losses : fever, burns, exercise
  5. Diabetes insipidus
  6. Sodium overload
    * Excess IV hypertonic saline
    * Excess mineralcorticoids : Cushings or primary aldosteronism
48
Q

Which endocrine disorders may lead to hypernatraemia and how?

A
  1. Cushing’s syndrome : activates RAAS
  2. Hyperaldosteronism : increased sodium retention in the distal and collecting ducts
49
Q

What are the risk factors for hypernatraemia?

A

High urine or stool output e.g. Renal dysfunction, C. Diff infection
Inability to drink - dementia patients, ventilated/intubated or impaired mental status
Inability to concentrate urine - Diabetes inspitidus, renal failure

50
Q

Which medication may cause hypernatraemia?

A
  1. Nephrogenic diabetes insipidus
    * Lithium : assoc with nephrogenic diabetes due to down regulation of aquaporin 2 ducts
    * Demeclocycline, Aminoglycocide, Phenytoin
  2. Loop diuretics; increase free water excretions
  3. IV mannitol : can cause osmotic diuresis
  4. Laxative : can cause severe diarrhoea
  5. Corticosteroids : increased risk of hypernatraemic when used in high doses
51
Q

What are the clinical features of hypernatraemia?

A

Signs of hypovalaemia
* Oliguria
* Orthostatic hypotension
* Tachycardia
* Dry mucous membranes

Signs of Diabetes insidious; output of large volumes of dilute urine

52
Q

Which investigations are indicated in hypernatraemia?

A
  1. Bloods : Full electrolytes, plasma glucose
    - Plasma osmolality
  2. Urine :
    Urine osmolality
    Urine electrolytes
    Urine flow rate
53
Q

How is Diabetes Insipidus diagnosed?

A
  1. Desmopressin challenge
    Definition : to differentiate between central vs nephrogenic diabetes insidious
  • Exogenous vasopressin is administrated
  • Central DI - respond with decreased urine output and increased urine osmolality as kidneys are still responsive
  • Nephrogenic DI : no change
54
Q

Hypernatraemia : what does urine osmolality (>500) > plasma osmolalaity indicate?

A

Cause : Volume depletion 2nd to GI or insensible losses

  • Evidence of kindeys functioning properly as they are filtering out the excess Na+
55
Q

Hypernatraemia : what does urine osmolality = plasma osmolalaity indicate?

A

Cause : Renal concentrating defect due to renal failure, use of diuretics

56
Q

What is the management of chronic hypernatraemia?

A

Chronic hypernatraemia :
* correction rate of 0.5 mmol/L/hour
* IV fluid administered - Dextrose 5%
Monitor electrolytes and urine output and adjust accordingly

57
Q

What is the management of central Diabetes Insipidus?

A
  • Desmopressin (synthetic analogue of ADH)
58
Q

What is the management of nephrogenic diabetes insipidus?

A

Thiazide diuretic - increases proximal reabsorption of sodium and water, thus decreasing urine output.

Endocrine (11 decks)

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