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Pathology (Guide) > Chemical Pathology - Sodium > Flashcards

Chemical Pathology - Sodium Flashcards

1
Q

How much sodium is freely exchanged, and where is the rest found?

A
  • 70% freely exchangable
  • The rest is complexed in bone
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2
Q

What is sodium?

A

Predominantly an extracellular cation, largely maintained by active pumping from ICF to ECF by Na/K ATPase

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3
Q

What is ECF volume directly dependent on?

A

Sodium

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4
Q

What is the treatment of mild/moderate hyponatraemia?

A

Treat underlying cause (unless severe and symptomatic)

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5
Q

How are mild and severe hyponatraemias defined?

A

Mild = 130-135 mmol/L
Moderate = 125-130 mmol/L
Severe = <125 mmol/L

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6
Q

What are the symptoms of Symptomatic hyponatraemia and when do they arise?

A
  • Nausea + Vomiting: <134 mmol/L
  • Confusion: <131 mmol/L
  • Seizures, non-cardiogenic pulmonary oedema: <125 mmol/L
  • Coma: <117 mmol/L + eventual death

MEDICAL EMERGENCY

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7
Q

What is the pathogenesis of true hyponatraemia?

A

Increased extracellular water

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8
Q

What are some causes of hyponatraemia with a high osmolality?

A
  • Glucose/mannitol
  • Infusion
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9
Q

What are some causes of hyponatraemia with a normal osmolality?

A
  • Spurious
  • Drip arm sample
  • Pseudohyponatraemia (hyperlipidaemia/paraproteinaemia)
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10
Q

What is the cause of hyponatraemia with a low osmolality

A

True hyponatraemia

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11
Q

What is TURP syndrome (transurethral resection of the prostate)?

A

Hyponatraemia from irrigation aborbed through damaged prostate

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12
Q

What is used to irrigate during TURP (transurethral resection of the prostate)?

A

Glycine 1.5%

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13
Q

How is the clinical presentation of TURP caused?

A

Due to metabolism of glycine and hyponatraemia caused by dilution

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14
Q

What is the process of water reabsorption?

A

ADH acts on V2 receptors in the collecting duct, thus inserting Aquaporin-2 into the cell membrane, causing water reabsorption

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15
Q

What processes cause an increase in ADH release?

A
  • An increased osmolality is detected by osmoreceptors causing an increase in ADH release
  • A decrease in blood volume/pressure is detected by baroreceptors in the heart causing an increase in ADH release
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16
Q

What is the cause of hyponatraemia with elevated plasma osmolality?

A

An excess of osmotically active solutes into the plasma
- Often glucose (in HHS), can be mannitol
- Solutes draw water from ceclls into plasma, which dilutes the sodium

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17
Q

What are some symptoms of hypovolaemia?

A
  • Tachycardia
  • Postural hypotension
  • Dry mucous membranes
  • Reduced skin turgor
  • Confusion/drowsiness
  • Reduced urine output
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18
Q

What are some symptoms of hypervolaemia?

A
  • Raised JVP
  • Bibasasl crackles
  • Peripheral oedema
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19
Q

What is the basic MoA of cardiac failure in causing hyponatraemia?

A

The heart pumps less so the BP is lowered

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20
Q

What is the basic MoA of liver cirrhosis in causing hyponatraemia?

A

There is an increase in release of vasodilators which causes the BP to drop

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21
Q

What is the basic MoA of renal failure in causing hyponatraemia?

A

There is reduced water excretion

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22
Q

What are initial steps of treating a hyponatraemic patient?

A

Assess volume status, urine sodium + osmolality

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23
Q

If a patient has hypovolaemic hyponatraemia, how are they managed?

A
  • Fluid replacement with 0.9% NaCl (isotonic saline)
  • Treat the cause
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24
Q

If a patient has hypervolaemic hyponatraemia, how are they managed?

A

Fluid restriction +/- diuresis
- Treat the cause
- Cirrhois usually requries specialist input

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25
Q

If a patient has euvolaemic hyponatraemia, what further investigations would you consider?

A
  • TFTs
  • Short Synacthen test
  • Paired urine and serum osmolalities
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26
Q

If a patient has euvolaemic hyponatraemia, how are they managed?

A
  • Dependent on the cause
27
Q

What are some causes of hypovolaemic hyponatraemia, with a urine osmolality >20?

A
  • Adrenocortical deficiency
  • Renal failure/disease
  • Diuretics
  • Cerebral salt wasting
28
Q

What are some causes of hypovolaemic hyponatraemia, with a urine osmolality <20?

A
  • Vomiting
  • Diarrhoea
  • Skin loss (sweat/burns)
29
Q

What are some causes of hypervolaemic hyponatraemia, with a urine osmolality >20?

A
  • Renal failure
30
Q

What are some causes of hypervolaemic hyponatraemia, with a urine osmolality <20?

A
  • Heart Failure
  • Cirrhosis
  • Nephrotic syndrome
  • Primary polydipsia
31
Q

What are some causes of euvolaemic hyponatraemia, with a urine osmolality <100?

A
  • Acute water load
  • Psychogenic polydipsia
  • Tea + toast/beer diets
32
Q

What are some causes of euvolaemic hyponatraemia, with a urine osmolality >100?

A
  • SIADH
  • Glucocorticoid deficiency
  • Chronic hypothyroidism
  • Acute water load
33
Q

When can hypertonic (3%) saline be used in a hyponatraemic patient?

A

If they have status epilepticus secondary to hyponatraemia (only on advice of specialist, usually in ITU)

34
Q

What can happen with rapid correction of hyponatraemia, and how can this be avoided?

A
  • Central pontine myelinolysis (pseudobulbar palsy, paraparesis, locked-in syndrome)
  • Aim to increase sodium by no more than 8-10mmol/L per 24hrs
35
Q

What can cause hyponatraemia post-surgery?

A
  • Overhydration with hypotonic IV fluids
  • Transient increase in ADH due to stress of the surgery
36
Q

What does demeclocycline do?

A

Reduces the cells responsiveness to ADH

37
Q

What does tolvaptan do?

A

Antagonist to V2 receptor

38
Q

What is the diagnostic criteria for SIADH?

A
  • True hyponatraemia (<135)
  • Low plasma/serum osmolality (<270)
  • High urine sodium (>20)
  • High urine osmolality (>100)
  • No adrenal/thyroid/renal dysfunction
39
Q

What is SIADH?

A

An inappropriate ADH secretion, not in response to a stimulus

40
Q

What is the mechanism of SIADH?

A

Increased ADH causes increased water reabsorption leading to a low plasma osmolality (secondary to dilution) causing less water to be excreted in the urine and causing a high urine osmolality

41
Q

How do you confirm the diagnosis of SIADH?

A
  • Normal 9am cortisol
  • Normal TFTs

Diagnosis of exclusion

42
Q

What are some causes of SIADH?

A
  • Malignancy: SMALL CELL LUNG CANCER (most common), pancreas, prostate, lymphoma
  • CNS disorders: meningoencephalitis, haemorrhage, abscess
  • Chest disease: TB, pneumonia, abscess
  • Drugs: opiates, SSRIs, TCAs, carbamazepine, PPIs
43
Q

What is the treatment of SIADH?

A
  • Fluid restriction
  • Treat the cause
  • Demeclocycline + tolvaptan can induce state of DI that may help correct SIADH (cost is prohibitive)
  • IF SEVERE: slow IV hypertonic 3% saline
44
Q

What would be some concurrent investigation findings in a hypernatraemic patient?

A

Raised urea, albumin + PCV

45
Q

Which is more common - hyponatraemia or hypernatraemia?

A

Hyponatraemia

46
Q

Which type of patients are usually hypernatraemic?

A
  • ITU patients
  • Elderly
  • Infants
47
Q

What is the pathogenesis of hypernatraemia?

A

Decreased extracellular water

48
Q

How can the symptoms progress in a hypernatraemic patient?

A

Thirst leads to confusion, leading to seizures and ataxia leading to a coma

49
Q

What are some causes of a hypovolaemic hypernatraemic patient with a urinary sodium <20

A
  • GI loss (vomiting, diarrhoea)
  • Skin loss (excessive sweating, burns)
50
Q

What are some causes of a hypovolaemic hypernatraemic patient with a urinary sodium >20?

A
  • Loop diuretics
  • Osmotic diuresis (uncontrolled DM, gluce, mannitol)
  • Diabetes insipidus
  • Renal disease
51
Q

What are some causes of a euvolaemic hypernatraemic patient?

A
  • Respiratory (tachypnoea)
  • Skin (sweating, fever)
  • Diabetes insipidus
52
Q

What are some causes of a hypervolaemic hypernatraemic patient?

A
  • Mineralocorticoid excess (Conn’s syndrome)
  • Inappropriate saline
53
Q

What is the management of hypernatraemia?

A

Slow fluids/replace water (5% dextrose)

  • IF really dry, replace initially with 0.9% NaCl
54
Q

What are some clinical features of diabetes insipidus?

A
  • Hypernatraemia (lethargy, thirst, irritability, confusion, coma, fits)
  • Clinically euvolaemic
  • Polyuria + polydipsia
  • Urine plasma osmolality <2
55
Q

What are some causes of cranial diabetes inspidius?

A
  • Surgery
  • Trauma
  • Tumours (craniopharyngioma)
  • Autoimmune hypophysitis
  • Irradiation
56
Q

What is the management of cranial diabetes insipidus?

A

Desmopressin

57
Q

What is cranial diabetes insipidus?

A

Lack of/no ADH production

58
Q

What is nephrogenic diabetes insipidus?

A

Receptor defect - insensitivity to ADH

59
Q

What are the causes of nephrogenic diabetes insipidus?

A
  • Inherited channelopathies
  • Drugs: litium, demeclocycline
  • Electrolyte disturbances: hypokalaemia, hypercalcaemia
60
Q

What is the management of nephrogenic diabetes insipidus?

A

Thiazide diuretics (e.g. bendroflumethiazide)

61
Q

What are the five steps to diagnose diabetes insipidus?

A
  1. Serum glucose (exclude DM)
  2. Serum potassium (exclude hypokalaemia)
  3. Serum calcium (exclude hypercalcaemia)
  4. Plasma + urine osmolality
  5. 8-hour water deprivation test (DIAGNOSTIC)
62
Q

What is the exclusion criteria for diabetes insipidus?

A

Urine : Plasma osmolality ratio > 2:1
- Plasma osmolality <296mOsmol/kg

63
Q

How can you distinguish between cranial and nephrogenic diabetes insipidus?

A

8-hour water deprivation test
- Cranial: urine osmolality increases >600mOsmol/kg ONLY after desmopressin administration
- Nephrogenic: no increase in urine osmolality, even after desmopressin

  • Primary polydipsia: urine concentrates but less than normal (400-600mOsmol/kg)

Pathology (Guide) (84 decks)

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