Salt and Water balance Flashcards

1
Q

What endocrine system has the predominant control over sodium

A

RAAS

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2
Q

Which endocrine system has the predominant control over water

A

ADH

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3
Q

How does hyponatraemia often present

A
  • Initially: anorexia, nausea, malaise
  • Then: Headache, irritability, confusion, weakness, decrease GCS, seizures
  • increased risk of falls in elderly
  • cardiac failure and oedema can indicate the cause
     Symptoms of salt loss – Diarrhoea & vomiting, excessive sweating
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4
Q

describe how the RAAS system works

A
  • angiotensinogen is produced from the liver
  • renin from the kidney acts on angiotensingoen and converts it to angiotensin I
  • ACE from the lung converts angiotensin I into angiotensin II
  • Angiotensin II causes an increase in sympathetic activity, causes aldosterone secretion which causes sodium retention, causes arteriolar vasoconstriction, increases ADH secretion
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5
Q

How does ADH control water

A
  • Osmoreceptors detect an increase in osmotic pressure
  • baroreceptors detect a decrease in blood pressure
  • this signals to the posterior pituitary
  • the posterior pituitary releases ADH
  • ADH causes blood vessels to vasoconstrict and causes an increased water reabsorption in the kidney
  • this leads to increased blood volume and increased blood pressure
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6
Q

What causes hyponatreaemia

A
  • Dilutional hyponatremia
  • salt deficiency or loss
  • Pseudohyponatraemia
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7
Q

Name what can cause dilutional hyponatreamia

A

Too much water ingested
- psychogenic polydipsia - psychiatric problem whereby a person drinks too much water

Too much water reabsorbed (often osmotic)

  • cirrhosis
  • Nephrotic syndrome
  • Congestive cardiac failure

Reduced excretion of water

  • syndrome of inappropriate ADH (SIADH)
  • hypoadreanlism
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8
Q

How does salt deficiency or loss cause hyponatreaemia

A

Loss from

  • kidneys
  • gut
  • skin

Hypoadrenalism

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9
Q

How does pseudohyponatraemia cause hyponatraemia

A
Lab problem 
Arterfactual low Na due to analytical problems 
- high lipids 
- high glucose 
- paraproteins
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10
Q

How do you determine the cause of hyponatraemia

A

History
 Drugs
 Water / Alcohol ingestion
 Renal / Liver problems

Examination
 Are they euvolaemic, hypovolaemic or hypervolaemic?

Investigations
 U&Es, plasma and urine osmolality, glucose, TFT, cortisol
 Urinary sodium

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11
Q

what drugs can cause hyponatraemia

A
  • Proton pump inhibitors
  • Antidepressants such as citalopram
  • thiazides
  • loop diuretics
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12
Q

How do you assess volume status

A

important in patients with hyponatremia

check:
- pulse
- postural blood pressure - look for a drop of 10mmhg
- skin turgor
- JVP - look at the neck carefully to see
- mucus membrnae
- listen to breast sound - crackles due to fluid overloaded in heart failure
- weight chart
- fluid chart

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13
Q

What does it suggest if potassium is high

A
  • suggest that you have glucocorticoid deficiency
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14
Q

what is characterstic of addisons disease

A

low sodium/high potassium

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15
Q

What does a high urea and creatine suggest

A
  • high suggests AKI/dehydration
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16
Q

What does a low cortisol suggest

A
  • very low suggests glucorticoid deficiency
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17
Q

what does it suggest if urinary sodium is low

A
  • Hypovolaemia - kidneys are trying to preserve salt and water
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18
Q

What does it suggest if urinary sodium is high

A
  • Suggests inappropriate loss of sodium e.g. SIADH
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19
Q

What is SIADH

A
  • this is a condition that is characterised by excess production of ADH that is inappropriate
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20
Q

What can SIADH be due to

A
  • malignancy
  • CNS disorders
  • Lung disease
  • endocrine disease
  • Drugs
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21
Q

describe the signs of SIADH

A
  • leads to a dilutional hyponatraemia
  • patient is euvolaemic
  • low plasma osmolality, inappropriately high urine osmolality - (too much concentrated urine and too much dilute plasma)
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22
Q

Define euvolaemic

A

Having a normal amount of body fluids

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23
Q

What is the treatment of SIADH

A
  • Treat cause of restrict fluid
  • consider salt +/- loop diuretics if severe
  • demeclocycline (ADH antagonists) - rarely used for SIADH
  • ADH receptor antagonists (Vaptans, e.g. tolvaptan)
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24
Q

what is the treatment of SIADH if the person is confused or severe CNS symptoms

A
  • Hypertonic saline

Tolvaptan

  • V2 receptor antagonists - decreases water permeability of collecting duct
  • antagonises effects of ADH
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25
Q

How do you treat hypovolaemic hyponatraemia

A
  • replacement with oral or IV salt
26
Q

What is hypovolaemic hyponatraemia caused by

A

Due to salt loss

27
Q

What is hypervolaemic hyponatraemia caused by

A
  • Due to fluid excess e.g. Congestive Cardiac Failure (CCF), cirrhosis, nephrotic syndrome
28
Q

How do you treat hypervolaemic hyponatraemia

A

 Difficult to treat as diuretic use will lower sodium

 Diuretic, fluid restriction, vaptans

29
Q

What are the causes of hypernatraemia

A
  • Severe dehydration - loss of water from the renal/gut/skin
  • Diabetes insipidius
30
Q

What are the two causes of diabetes insipidus

A

 Central (Cranial) – failure of production of ADH from the posterior pituitary

 Nephrogenic – failure of response of kidneys to circulating ADH

31
Q

What causes central (cranial) cause of diabetes inspidius

A
 Trauma
 Brain tumour (craniopharyngioma) 
 Infection / inflammation
 DIDMOAD - woffarn syndrome - genetic syndrome that is associated with those conditions
- idiopathic 
- congenital 
- hypophysectomy 
- autoimune hypophysitis 
- infiltration - histiocytosis, sarcoidosis 
- vascular - haemorrhage
32
Q

What causes Nephrogenic diabetes inspidius

A
 Drugs – lithium, demeclocycline 
- post obstructive uropathy 
 CKD
 High Ca2+
 Low K+
33
Q

How do you investigate diabetes insipidus

A

 Urinary volume is high – production of large quantities of dilute urine - in hospital you can measure it
 Low urine osmolality – urine is dilute (inappropriately)
 High or normal serum Na+
 MRI – to look for a structural cause – pituitary or hypothalamic lesion

34
Q

how do you determine the cause of diabetes inspidius or to prove it

A

Water deprivation test

35
Q

How does water deprivation test work

A
  • Tests kidneys ability to concentrate urine and localise the cause
  • fasting and no fluids for 8 hours
  • monitor serum and urine osmolarity, urine vole and weight hourly for up to 8 hours
  • abandon fluid deprivation if weight loss >3% occurs
  • if serum osmolality is >300mOsm/kg and/or urine <600mOsm/kg = give demopressin 2ug IM at end of test
  • allow free fluid but measure urine osmolality for 2-4 hours
36
Q

Name the results of the water deprivation test for

  • cranial diabetes insipidus
  • Nephrogenic diabetes insipidus
A

Cranial

  • urine osmolality is dilute
  • after desmopressin is given the urine osmolality stays dilute

Nephrogenic

  • urine osmolality is dilute
  • after desmopressin is given the urine osmolality stays dilute
37
Q

What is the management of

  • cranial diabetes insipidus
  • Nephrogenic diabetes insipidus
A

Cranial DI
 Replace ADH with oral, im or nasal desmopressin

Nephrogenic DI
 Correct cause
 Thiazides may help - make the collecting tubule more responsive to ADH

38
Q

What is plasma sodium dependent on

A
  • Sodium and water is what plasma sodium is dependent on

- hyponatraemia doesn’t necessarily imply sodium depletion

39
Q

describe the causes of hyponatraemia

A

Is the patient dehydrated?

Yes
- is urinary Na > 20mmol/L
if yes
- sodium and water is lost via kidneys
- caused by renal failure, diuretic excess, osmolar diuresis, Addison’s disease
if no
- sodium and water form somewhere other than the kidneys
- due to diarrhoea, vomiting, burns, trauma, small bowel obstruction, fistulae

No
- is the patient oedematous? 
if yes 
- heart failure 
- renal failure 
- nephrotic syndrome 
- liver cirrhosis 
if No 
- is urine osmolality >500mmol/kg 
if yes - SIADH 
if no - water overload, severe hypothyroidism, glucocorticoid insufficiency
40
Q

What is iatrogenic hyponatraemia

A
  • if 5% glucose is infused continuously without adding 0.9% saline, then glucose is quickly used, rendering the fluid hypotonic and causing hyponatraemia - especially in those on thiazide diuretics, women, those undergoing physiological stress
41
Q

What is the diagnosis of SIADH

A
  • concentrated urine - urine Na>20mmol/L and osmolality >100mOsm/Kg
  • Hyponatraemia - plasma Na<125mmol/L and low plasma osmolality <260mOsm/kg
  • absence of hypovolaemia, oedema, diuretics
42
Q

What cancers cause SIADH

A
  • lung small cell
  • pancreas
  • prostate
  • thymus
  • lymphoma
43
Q

What CNS disorders cause SIADH

A
  • meningoencephalitis
  • abscess
  • stroke
  • subarachnoid or subdural haemorrhage
  • head injury
  • neurosurgery
  • Guillain-Barre
  • vasculitis
  • SLE
44
Q

What lung disease causes SIADH

A
  • TB
  • pneumonia
  • abscess
  • aspergillosis
  • small-cell lung cancer
45
Q

how does endocrine disease cause SIADH

A
  • hypothyroidism (not true SIADH but due to excess ADH release from carotid sinus baroreceptors triggered by low CO)
46
Q

What drugs cause SIADH

A
  • opiates
  • carbamazepine
  • chlorpropramide
  • sulfonylureas
  • SSRIs
  • TCAs
  • cytotoxic
  • lithium
  • MDMA
  • tramadol
  • haloperidol
  • vincristine
  • desmopressin
  • fluphenazine
47
Q

How can you treat asymptomatic chronic hyponatraemia

A
  • fluid restriction - often sufficiency

- demeclocyline may be required; if hypovolaemic (cirrhosis, CCF) treat underlying disorder first

48
Q

How can you treat acute or symptomatic hyponatraemia or dehydrated

A
  • Cautious rehydration with 0.9% saline
  • max rise in serum sodium 15mmol/L per day if chronic or 1mmol/L per hour if acute
  • do not correct changes rapidly as central pontine myelinolysis may result
  • consider furosemide when not hypovolaemic to avoid fluid overload
49
Q

How do you treat emergency hyponatraemia

A

seizures and coma

  • hypertonic saline (1.8%) at 70mmol sodium +/- furosemide
  • aim for gradual increase in plasma sodium to - 125mmol/L
  • Beware heart failure and CPM
50
Q

What is the presentation of hypernatraemia

A
  • lethargy
  • thirst
  • weakness
  • irritability
  • confusion
  • coma
  • fits
  • signs of dehydration
  • lab features: increase sodium, increase PCV, increase albumin and increase urea
51
Q

What are the causes of hypernatraemia

A

usually due to water loss in excess of sodium loss

  • fluid loss without replacement - diarrhoea, vomiting, burns
  • diabetes insipidus - suspect if polyuria, may follow head injury or CNS surgery
  • osmotic diuresis
  • primary aldosteronism - rarely severe, suspect if increase in blood pressure, decrease in potassium, alkalosis
  • iatrogenic - incorrect IV fluid replacement
52
Q

What is the management of hypernatraemia

A
  • give water orally if possible
  • if not give 5% glucose IV slowly guided by urine output and plasma sodium
  • use 0.9% saline IV if hypovolaemic as fluid shifts are less marked and is hypotonic in a hypertonic patient
53
Q

How do you present diabetes insipidus

A
  • polyuria
  • polydipsia - excessive and can be uncontrollable
  • dehydration
  • symptoms of hypernatraemia
54
Q

Define diabetes insipidus

A
  • passage of large volumes of water (>3L/day) of dilute urine due to impaired water resorption by the kidney
55
Q

What is normal plasma osmolality

A

285-295 mOsm/kg

56
Q

What investigations do you use for diabetes insipidus

A
  • U&Es
  • serum calcium
  • serum glucose (exclude DM)
  • serum and urine osmolality = 2 x (Na+K) + urea + Glucose
57
Q

How do you manage cranial Diabetes insipidus

A
  • MRI head
  • test anterior pituitary function
  • give demopressin (synthetic ADH)
58
Q

How do you manage nephrogenic diabetes insipidus

A
  • treat cause
  • if persisting - bendroflumethiazide 5mg PO/24 hour
  • NSIADS - lower urine volume and plasma sodium by inhibiting prostaglandin synthesis (locally inhibit action of ADH)
59
Q

How do you treat mild moderate and severe hyponatremia and what are the symptoms

A

Mild hyponatremia
- Non-specific symptom’s such as headache, lethargy, nausea, vomiting, dizziness, confusion and muscle cramps
- Manage with fluid restriction and loop direutics
Moderate hyponatremia
- Same as mild
- Hypertonic saline in first 3-4 hours to increase Na+>120mmol/l
Severe hyponatremia
- Seizures, coma, and respiratory arrest
- Bolus of hypertonic saline until symptom resolution with or without conivaptan

60
Q

What are the causes of cranial and nephrogenic DI

A
Cranial DI 
-	Idiopathic 
-	Post head injury 
-	Pituitary surgery 
-	Craniopharyngiomas
-	DIDMOAD
Nephrogenic DI 
-	Genetic 
-	hypercalcaemia and hypokalaemiea 
-	Lithium
-	Demeclocycline