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
How do you treat hypovolaemic hyponatraemia
- replacement with oral or IV salt
26
What is hypovolaemic hyponatraemia caused by
Due to salt loss
27
What is hypervolaemic hyponatraemia caused by
- Due to fluid excess e.g. Congestive Cardiac Failure (CCF), cirrhosis, nephrotic syndrome
28
How do you treat hypervolaemic hyponatraemia
 Difficult to treat as diuretic use will lower sodium |  Diuretic, fluid restriction, vaptans
29
What are the causes of hypernatraemia
- Severe dehydration - loss of water from the renal/gut/skin - Diabetes insipidius
30
What are the two causes of diabetes insipidus
 Central (Cranial) – failure of production of ADH from the posterior pituitary  Nephrogenic – failure of response of kidneys to circulating ADH
31
What causes central (cranial) cause of diabetes inspidius
```  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
What causes Nephrogenic diabetes inspidius
```  Drugs – lithium, demeclocycline - post obstructive uropathy  CKD  High Ca2+  Low K+ ```
33
How do you investigate diabetes insipidus
 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
how do you determine the cause of diabetes inspidius or to prove it
Water deprivation test
35
How does water deprivation test work
- 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
Name the results of the water deprivation test for - cranial diabetes insipidus - Nephrogenic diabetes insipidus
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
What is the management of - cranial diabetes insipidus - Nephrogenic diabetes insipidus
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
What is plasma sodium dependent on
- Sodium and water is what plasma sodium is dependent on | - hyponatraemia doesn't necessarily imply sodium depletion
39
describe the causes of hyponatraemia
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
What is iatrogenic hyponatraemia
- 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
What is the diagnosis of SIADH
- 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
What cancers cause SIADH
- lung small cell - pancreas - prostate - thymus - lymphoma
43
What CNS disorders cause SIADH
- meningoencephalitis - abscess - stroke - subarachnoid or subdural haemorrhage - head injury - neurosurgery - Guillain-Barre - vasculitis - SLE
44
What lung disease causes SIADH
- TB - pneumonia - abscess - aspergillosis - small-cell lung cancer
45
how does endocrine disease cause SIADH
- hypothyroidism (not true SIADH but due to excess ADH release from carotid sinus baroreceptors triggered by low CO)
46
What drugs cause SIADH
- opiates - carbamazepine - chlorpropramide - sulfonylureas - SSRIs - TCAs - cytotoxic - lithium - MDMA - tramadol - haloperidol - vincristine - desmopressin - fluphenazine
47
How can you treat asymptomatic chronic hyponatraemia
- fluid restriction - often sufficiency | - demeclocyline may be required; if hypovolaemic (cirrhosis, CCF) treat underlying disorder first
48
How can you treat acute or symptomatic hyponatraemia or dehydrated
- 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
How do you treat emergency hyponatraemia
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
What is the presentation of hypernatraemia
- lethargy - thirst - weakness - irritability - confusion - coma - fits - signs of dehydration - lab features: increase sodium, increase PCV, increase albumin and increase urea
51
What are the causes of hypernatraemia
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
What is the management of hypernatraemia
- 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
How do you present diabetes insipidus
- polyuria - polydipsia - excessive and can be uncontrollable - dehydration - symptoms of hypernatraemia
54
Define diabetes insipidus
- passage of large volumes of water (>3L/day) of dilute urine due to impaired water resorption by the kidney
55
What is normal plasma osmolality
285-295 mOsm/kg
56
What investigations do you use for diabetes insipidus
- U&Es - serum calcium - serum glucose (exclude DM) - serum and urine osmolality = 2 x (Na+K) + urea + Glucose
57
How do you manage cranial Diabetes insipidus
- MRI head - test anterior pituitary function - give demopressin (synthetic ADH)
58
How do you manage nephrogenic diabetes insipidus
- 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
How do you treat mild moderate and severe hyponatremia and what are the symptoms
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
What are the causes of cranial and nephrogenic DI
``` Cranial DI - Idiopathic - Post head injury - Pituitary surgery - Craniopharyngiomas - DIDMOAD Nephrogenic DI - Genetic - hypercalcaemia and hypokalaemiea - Lithium - Demeclocycline ```