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Phase 2 3. Endocrinology > Disorders of calcium and sodium regulation > Flashcards

Disorders of calcium and sodium regulation Flashcards

1
Q

Why is fluid and electrolyte distribution important?

A

ECF and ICF must be in osmotic equilibrium

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2
Q

How is osmotic equilibrium maintained?

A

by the movement of water

  • Water moves freely across most membranes (electrolytes do not)
  • Osmolality is maintained at expense of volume
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3
Q

Where is the majority of fluid in the body?

A

(Relatively small amount of fluid circulates in the blood vessels)

Majority of fluid in the body is contained in the intracellular space

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4
Q

What is plasma osmolality?

A

ratio of plasma solutes (sodium,

glucose and urea) and plasma water

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5
Q

How is serum osmolality determined?

A

Sodium is the major contributor to calculating osmolality

Serum sodium concentration (osmolality) is mainly determined by amount of extracellular water
o Regulate sodium balance by changing intake or output of water

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6
Q

What mechanisms regulate water status?

A
  • thirst

- Anti-diuretic hormone

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7
Q

What is ADH?

A

vasopressin

- main role in regulating water status

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8
Q

When is ADH produced?

A

o decreased plasma volume (sensed by baroceptors in atria/veins/carotids)
o increased plasma osmolality (sensed by osmoreceptors in hypothalamus)

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9
Q

Where does ADH work?

A

acts mainly via the AVP 2 receptor

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10
Q

Describe the AVPR2

A

found on the basolateral membrane of kidney collecting ducts

Inserts aquaporin channels to increase renal water
reabsorption

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11
Q

How is increased blood osmolality sensed?

A

osmoreceptors in the hypothalamus

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12
Q

How is ADH secreted?

A

Increased blood osmolality is sensed by osmoreceptors in hypothalamus => release ADH which will increase
water reabsorption from kidney collecting ducts

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13
Q

What is ADH’s action?

A

will decrease plasma osmolality

also trigger thirst reflex

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14
Q

How is effective arterial volume regulated?

A
  • renin angiotensin system
  • carotid/ aortic baroreceptors
  • cardiac receptors
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15
Q

How does the renin-angiotensin system regulate effective arterial volume?

A

Reduced volume sensed by JGA of kidneys (secrete
renin)

o Angiotensin II:

  • Potent vasoconstrictor
  • Promotes aldosterone release
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16
Q

How do carotid/aortic baroreceptors regulate the effective arterial volume?

A
  • Increase sympathetic nervous system activity

- Causes vasoconstriction and increased cardiac output

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17
Q

How do cardiac receptors regulate the effective arterial volume?

A

Atrial natriuretic peptide release

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18
Q

What is the principle target organ of aldosterone?

A

kidney

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19
Q

What is ENaC?

A

Epithelial sodium channel

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20
Q

What is aldosterones effect on the kidney?

A

Aldosterone increases sodium reabsorption and potassium excretion in the distal nephron

This increase in sodium status also increases plasma volume and raises blood pressure

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21
Q

What is hyponatraemia?

A

= serum sodium < 135 mmol/l

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22
Q

What is a normal sodium range?

A

(135-145 mmol/L is normal range)

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23
Q

What causes hyponatraemia?

A

disorder of water balance, not sodium deficiency

1) Inability to suppress ADH release so inappropriate retention of water
2) Renal impairment
3) Diuretic effect (especially thiazides)

Excess water retention dilutes plasma sodium concentration

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24
Q

What is euvolemia

A

normal total body sodium but hyponatraemia results due to excessive water retention. Most
common presentation

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25
Q

What causes euvolemia?

A

1) Adrenal failure (steroid deficiency)
2) Consequence of medications
3) SIADH

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26
Q

What is hypervolemia

A

patients look fluid overloaded. Increase in sodium but a bigger increase in total body water,
causing hyponatremia

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27
Q

What is syndrome of inappropriate anti-diuretic hormone (SIADH)

A

Excess ADH or inappropriate ADH relative to plasma osmolality

Often seen in the elderly

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28
Q

What are the causes of SIADH

A

o Cancer: lung/lymphoma/leukaemia
o Chest disease: pneumonia
o CNS disorders: infections, injury
o Drugs: opiates, thiazides, anti-convulsants, proton pump inhibitors, anti-depressants

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29
Q

What are the five criteria for SIADH?

A

1) Hyponatraemia with inappropriate low plasma osmolality
2) Urine osmolality > plasma osmolality (urine is being concentrated)
3) Urine sodium > 20 mmol/l (inappropriate sodium excretion)
4) Absence of adrenal, thyroid, pituitary or renal insufficiency
5) No recent use of diuretic agents

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30
Q

What are the consequences of hyponatraemia on the brain?

A

When the serum [Na] is low, water moves into cells to increase plasma osmolality, causing cell swelling

The brain is encased by the skull, so there is little room for swelling

Cerebral oedema can result

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31
Q

What is the pathophysiology of cerebral oedema?

A

o Water rushes into the brain to try and increase the plasma osmolality
o Can cause seizures and even death
o Plasma dilution decreases serum osmolality, resulting in a higher osmolality in the brain compared
to the serum.
o This creates an abnormal pressure gradient and movement of water into the brain, which can cause
progressive cerebral oedema, resulting in a spectrum of signs and symptoms from headache and
ataxia to seizures and coma.

32
Q

What are the consequences of fast sodium normalisation?

A

water leaves the brain to bring the osmolality back down, and
can cause osmotic demyelination

(due to brain adapting & minimising ill effects)

33
Q

What is a significant cause of acute hyponatraemia?

A

Patients who have ran the marathon

34
Q

What is Osmotic delmyelination syndrome

A

neurological disorder caused by severe damage to themyelin sheathofnerve cells in the pons

35
Q

What is the cause of osmotic demyelination syndrome

A

overly rapid correction of hyponatremia

36
Q

How does the brain compensate in hyponatraemia?

A

withchronic hyponatremia, the brain compensates by decreasing the levels of osmolytes within the cells, so that they can remain relatively isotonic with their surroundings and not absorb too much fluid.

37
Q

How does the brain compensate in hypernatraemia?

A

the cells increase their intracellular osmolytes so as not to
lose too much fluid to the extracellular space.

38
Q

What are the clinical features of hyponatraemia?

A 
 Often asymptomatic
 Mild confusion
 Gait instability
 Marked confusion
 Drowsiness
 Seizures
  • symptoms worsen as plasma sodium falls
39
Q

How is severe and acute hyponatraemia managed?

A

(Unconscious or seizures) - unusual
o Give infusion of hypertonic (3%) saline
o Can increase quickly

40
Q

How is less severe/chronic hyponatraemia managed?

A

o Try to establish cause (might be easily reversible, e.g. stopping omeprazole) and treat underlying
cause
o Usually fluid restriction is correct management
o Increase slowly
o 2nd line treatment is controversial
 Can consider AVPR2 antagonists (‘vaptans’), very occasionally used

41
Q

How is hypernatraemia managed?

A

 Most usually due to water loss (‘dehydration’) and inability to access water

42
Q

What are the causes of hypernatraemia?

A

Main causes:
o Insensible/sweat losses (severe burns/sepsis)
o GI losses
o Diabetes Insipidus
o Osmotic diuresis due to hyperglycaemia (HHS/DKA)

(Seen a lot in patients with dementia => no intact thirst mechanisms)

43
Q

How is hypernatraemia managed?

A 
 Treat underlying cause!
 Estimate total body water deficit if possible to guide fluid regimen
 Avoid overly rapid correction
o Aim for ↓ 10 mmol/l in 24 hours
o Concern is cerebral oedema
 Use IV 5% dextrose
44
Q

Where in the body are the main sources of calcium?

A
  • GI tract
  • Bones
  • Kidney
45
Q

Describe the GIT as a calcium source

A

Absorbed throughout small intestine from dietary sources (only approx 10% of ingested calcium is
absorbed)
o Vitamin D dependent process

46
Q

Describe the bones as a calcium source

A

Calcium reservoir

o Regulates plasma Ca via action of osteoblasts and osteoclasts

47
Q

Describe the kidney as a calcium source

A

Free Ca filtered by glomerulus

o 97-99% is reabsorbed

48
Q

What is vitamin D’s role in calcium?

A

o Increases GI absorption
o Increases bone resorption
o Increased renal reabsorption

49
Q

How is calcium regulated?

A

PTH secreted by the parathyroid glands – normally located on posterior
surface of thyroid gland

50
Q

What is hypercalcaemia?

A

high calcium (Ca2+) level in the blood serum. The normal range is 2.1–2.6 mmol/L (8.8–10.7 mg/dL, 4.3–5.2 mEq/L) with levels greater than 2.6 mmol/L defined as hypercalcemia.

51
Q

What are the clinical features of hypercalcaemia?

A

 Moans = depression/slowed down
 Bones = bone pain, muscle weakness, osteopaenia
 Stones = predisposed to nephrocalcinosis/nephrolithiasis
 Abdominal Groans = vomiting, constipation
 Also increased thirst and polyuria  can cause nephrogenic diabetes

52
Q

What cardiac symptoms can be seen in hypercalcaemia?

A

ECG changes:

 Can predispose to dysrhythmia
 Shortened QTc interval
 Bradycardia

53
Q

What are the causes of hypercalcaemia?

A
  • primary hyperparathyroid

- malignancy

54
Q

How does primary hyperparathyroidism cause hypercalcaemia?

A

o Usually a single parathyroid adenoma
o One PTH gland becomes overactive, churning out PTH
o Increased bone resorption and GI absorption

55
Q

How does malignancy cause hypercalcaemia?

A

o Usually due to secretion of PTH-related peptide - secreted by a lot of cancers. Acts at PTH receptor
o Breast, lung and multiple myeloma are commonest tumours
o Also, seen in bone metastases due to direct osteolysis and release of calcium from bones

56
Q

How do you differentiate between hypercalcaemia causes?

A

Measure PTH:

o If ↓ then malignancy is likely (PTHrP has negative feedback effect on PTH production)
o If ‘normal’ or ↑ then primary hyperparathyroidism

57
Q

How is hypercalcaemia managed?

A
  • rehydration
  • bisphosphonate therapy
  • calcitonin
  • parathyroidectomy
58
Q

How is severity of hypercalcaemia determined?

A

o Mild < 3mmol/l
o Moderate 3-3.5 mmol/l
o Severe > 3.5 mmol/l

59
Q

Why is hydration used to treat hypercalcaemia?

A

 Patients are often hypovolaemic

  • Hypercalcaemia can cause AKI
  • Hypovolemiaexacerbateshypercalcemiaby impairing the renal clearance of calcium

 Isotonic (0.9%) saline infusion corrects hypovolaemia – be careful of fluid overload
 Will not normalise calcium unless only mildly elevated

60
Q

Why is bisphosphonate therapy used to treat hypercalcaemia?

A

 Inhibit bone resorption (and therefore calcium release from bones) by inhibiting osteoclasts
o Commonly used to treat osteoporosis

 Agents of choice for treating hypercalcaemia of malignancy (underlying cause may be incurable)
o Zolendronic acid is most commonly used

 Delayed effect, maximal at 2-4 days after treatment

61
Q

Why is calcitonin used to treat hypercalcaemia?

A 
o Has opposite effects to PTH
o Increases renal calcium excretion
o Decreases bone resorption (increases osteoblast activity)
o Only effective for 48 hours
o Given as subcutaneous injection
62
Q

Why are glucocorticoids used to treat hypercalcaemia?

A

inhibit vitamin d production

63
Q

Why is parathyroidectomy used to treat hypercalcaemia?

A

o Primary hyperparathyroidism
o Only if resistant to treatment
o Rarely indicated urgently, usually done as elective surgery

64
Q

What are the cardiac complications of hypocalcaemia?

A

o Dysrhythmia

o Hypotension

65
Q

What is the link between hyperventilation and hypocalcaemia?

A

hyperventilation causes very mild and transient hypocalcaemia due to
alkalosis =>tingling in hands

Alkalemia induces tetany due to a decrease in ionized calcium, whereas acidemia is protective.

66
Q

What is the main outcome of hypocalcaemia?

A

Tetany, as calcium is important as a neurotransmitter

67
Q

What is tetany?

A

Increased neuromuscular excitability

68
Q

How does tetany occur?

A

Low ionized calcium levels in the extracellular fluid increase the permeability of neuronal
membranes to sodium ion, causing a progressive depolarization, which increases the possibility of
action potential

If the plasma Ca 2+ decreases to less than 50% of the normal value, action potentials may be
spontaneously generated, causing contraction of peripheral skeletal muscles.

69
Q

What is the role of calcium in the brain?

A

calcium ions interact with the exterior surface ofsodium channelsin theplasma
membrane

When calcium ions are absent, the voltage level required to open voltage gated sodium channels is
significantly altered (less excitation is required).
70
Q

What are the symptoms of tetany?

A

Peri-oral numbness, muscle cramps, tingling of hands/feet

If severe: carpopedal spasm, laryngospasm, seizures

71
Q

What are the causes of hypocalcaemia?

A
  • Low PTH
  • High measured PTH
  • Drugs
  • Hypomagnesaemia
72
Q

What can cause low PTH?

A
  • after parathyroid surgery

- autoimmune hypoparathyroidism

73
Q

What can cause high measured PTH in hypocalcaemia?

A

o Vitamin D deficiency => PTH level increases to try and increase vitamin D levels, but this may be
insufficient to prevent hypocalcaemia

o Chronic renal failure => reduced ability to hydroxylate vitamin D

o Loss of Calcium => unusual but possible

74
Q

How can hypomagnesaemia effect hypocalcaemia?

A

o often results from PPIs and is required for PTH to cause effects
o correcting calcium without correcting magnesium will not solve underlying problem
o Leads to PTH resistance

75
Q

What is the treatment of hypocalcaemia?

A 
 Intravenous calcium replacement if tetany or cardiac manifestations
 May also need magnesium infusion
 Chronic management:
o Vitamin D (D2 or D3)
o Oral calcium salts
 Treat underlying cause

Phase 2 3. Endocrinology (25 decks)

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