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Year 2 > ENDO: Water balance, hyponatraemia and diabetes insipidus > Flashcards

ENDO: Water balance, hyponatraemia and diabetes insipidus Flashcards

1
Q

Describe the total body water composition of a 70kg male

A

42 L overall:

  1. 14L ECF (11 interstitial and 3.5L intravascular)
  2. 28L Intracellular
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2
Q

What ions are found in the ECF

A
  1. NA, Cl, HCO3-
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3
Q

What ions are found in ICF

A
  1. K+, MG3+, PO42-
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4
Q

Outline water regulation

A
  1. Decreased total body water
  2. Ingestion of water
  3. Decreased plasma osmolality
  4. Increased cellular hydration
  5. Decreased vasopressin secretion
  6. Increased urine water excretion by the kidney
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5
Q

How does Vasopressin work

A
  1. Binds to G-protein coupled 7transmembrane domain receptors
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6
Q

Role of V1a

A

Vasoconstriction

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7
Q

Role of V2

A

Reabsorption of water

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8
Q

Role of V1b

A

Pituitary regulation

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9
Q

Name two receptors that regulate vasopressin

A
  1. Osmoreceptors

2. Baroreceptors in brainstem and great vessels (emergency)

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10
Q

Where are osmoreceptors found

A

Pituitary glands

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11
Q

Where in the hypothalamus is vasopressin produced

A
  1. Supraoptic nucleus and paraventricular nucleus
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12
Q

What part of the pituitary gland releases vasopressin

A

Posterior pituitary gland

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13
Q

What are the two main drivers of water excretion by the kidney

A
  1. GFR

2. AVP

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14
Q

Define osmolality

A
  1. Concentration of particles in plasma per KILO
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15
Q

Does size of particle effect osmolality

A

No, number of size is more important

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16
Q

What ions effect osmolality

A
  1. NA
  2. K
  3. Bicarbonate
  4. Cl
  5. Urea
  6. Glucose
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17
Q

Describe the process that occurs after V2 binding

A
  1. Leads to activation go Gs protein
  2. Activation of adenyl cyclase
  3. Increases cAMP synthesis
  4. cAMP activate protein kinase A
  5. Phosphorylation of proteins to produce aquaproin-2
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18
Q

Where do aquaporin-2 channels insert

A

Apical membrane

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19
Q

How are aquaporin-2 channels subsequently broken down

A

Endocytosis

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20
Q

Clinical presentation of diabetes insipidus

A
  1. Polyuria
  2. Polydipsia
  3. NO glycosuria
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21
Q

What is diabetes insipidus

A
  1. Lagre amount of urine production + increased thirst

2. Basically where the kidneys do not properly respond to vasopressin properly

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22
Q

How is diabetes insipidus diagnosed

A
  1. Measure urine volume (>3L/day)
  2. Check renal function and serum calcium
  3. VERY dilute urine for plasma osmolality calculated
  4. Serum osmo>300 and urine osmo <200
  5. Normonatraemia or hypernatraemia
  6. Water deprivation test (GOLD STANDARD)
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23
Q

Pathophysiology of diabetes insipidus

A
  1. Caused by lack of aquaporin channels in the DCT
  2. Stops water re-absorption increasing osmolality of the blood
  3. osmoreceptors in the hypothalamus detect rise and trigger thirst centre
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24
Q

Why do we get hypernatraemia in diabetes insipidus

A

DEHYDRATION develops due to increase osmolality in the plasma

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25
Q

Define polydipsia

A

Too much thirst

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26
Q

What is cranial diabetes insipidius

A
  1. LACK OF VASOPRESSIN production by the posterior pituitary gland
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27
Q

Acquired causes of CDI

A
  1. Idiopathic
  2. Tumours (Craniopharyngioma, metastases)
  3. Traum
  4. TB, encephalitis and meningitis
  5. Aneurysms, infarctions, SCA
  6. Neurosarcoidosis, Guillain Barre, granuloma
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28
Q

What genetic causes are there for CDI

A
  1. DIDMOAD (Wolfram syndrome)
  2. Autosomal dominant
  3. Septo-optic dysplasia
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29
Q

What is wolfram syndrome

A

DIDMOAD: Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and deafness

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30
Q

What is nephrogenic diabetes insipidus

A
  1. RESISTANCE TO VASOPRESSIN
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31
Q

Acquired causes of nephrogenic diabetes insipidus

A
  1. Osmotic diuresis (diabete smellitus)
  2. Drugs (lithium, tetracycline)
  3. Chronic renal failure
  4. Post-obstructive uropathy
  5. Hypercalcaemia, hypokalaemia
  6. Amyloidosis
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32
Q

Familial causes of nephrogenic diabetes insipidus

A
  1. X-linked (V2 receptor defect)

2. Aquaporin 2 defect

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33
Q

How do we see a difference between NDI and CDI in water deprivation test

A
  1. NDI should see a constant increase in osmolality whilst CDI will decrease after 2 micrograms of IM DESMOPRESSIN is given
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34
Q

How can desmopressin be given to manage CDI

A
  1. Tablets (100-1200 mg/day)
  2. Nasal spray (10-40)
  3. Injection (1-2)
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35
Q

How’s nephrogenic DI treated

A
  1. Avoid precipitating drugs
  2. Free access to water
  3. HIGH dose desmopressin
  4. Hydrochlorothiazide
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36
Q

What defines hyponatraemia

A

Na< 135 mmol/L

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37
Q

What defines severe hyponatraemia

A

<125 mol/L

38
Q

Normal serum levels of Na

A

137-144 mol

39
Q

Clinical presentation of hyponatraemia

A
  1. Headache
  2. Lethargy
  3. Anorexia and abdo pain
  4. Weakness
  5. Confusion/Hallucinations
  6. Agitation
  7. Decreased consciousness
  8. Fitting
  9. Coma

Quicker onset = greater the symptoms

40
Q

How doe the brain adapt to hyponatraemia

A
  1. Water moves into the brain causing brain oedema
  2. Brain tries to normalise the volume by losing Na, K and cl ions
  3. Brian volume normalises and adapts to hyponatraemia
41
Q

Acute vs chronic hyponatraemia

A
  1. Acute - 48 hours (after subarachnoid haemorrhage) can be corrected rapidly
  2. Chronic (CNS adapts) so correction has too slow
42
Q

Rate at which Na is given in chronic hyponatraeima

A

<8 mol/24 hours

43
Q

Diagnostics for hyponatraemia

A
  1. Plasma osmolality
  2. Urine osmolality
  3. Plasma glucose
  4. Urine sodium
  5. Urine dipstick for protein
  6. TSH
  7. Cortisol
  8. Short synacthen if cortisol <500 mol/L
  9. Consider alcohol

OR you can just get them off thiazide to see if it helps

44
Q

What is the syncathen test

A

ACTH test to assess functioning of adrenal glands

45
Q

3 ways we get hyponatraemia

A
  1. Fluid overload
  2. normovolaemic
  3. Dehydration
46
Q

Two ways fluid overload can cause hyponatraemia

A
  1. Cirrhosis of liver

2. Congestive heart fialure

47
Q

How to spot normovolaemic hyponatraemia

A
  1. Spot urine > 30mmol/L
  2. TSH is normal
  3. Cortisol > 500 nmol/L
48
Q

What condition can cause normovolaemic hyponatraemia

A
  1. Syndrome of inappropriate antidiuretic hormone
49
Q

What is seen in the blood in SIADH

A

High Urine osmolality

High Urine Na

50
Q

How is normovolaemic and fluid overload (liver cirrhosis and heart failure) hyponatreamia treated

A

Fluid restriction (750-1000ml/24 hours)

51
Q

What will cause low urine Na (dehydration)

A
  1. Vomiting and diarrhoea
  2. Burns
  3. Pancreatitis
  4. Sodium depletion after diuretics
52
Q

What will cause high urice Na (Dehydration)

A
  1. Diuretics
  2. Addison’s
  3. Cerebral salt wasting
  4. Salt wasting nephropathy
53
Q

How is dehydration treated

A

IV SALINE

54
Q

What is SIADH

A

too much AVP secretion

55
Q

What happens to osmolality in SIADH

A

LOW and plasma N his low

56
Q

What is seen in the urine

A

High CONC

57
Q

Clinical presentation of SIADH

A
  1. NORMAL CIRCULATING VOLUME
  2. NO OEDEMA
ECF increased due to water retention 
Increased GFR (less Na reabsorbed in PCT

Normal thyroid and adrenal function

58
Q

Na urine levels in SIADH

A

> 30 mol/L

59
Q

What causes SIADH

A

CNS: Meningitis, Brain tumour, encephalitis, brain abscess, Guillain-Barre syndrome

Tumours: Carcinoma, Lymphoma, Leukaemia, Sarcoma, Mesothelioma

Respiratory causes: Pneumonia, TB, Pneumothorax, Emphysema, Positive-pressure ventilation

Drugs: Carbamazepine, MAO inhibitors, Desmopressin, vasopressin, PPIs, Selective serotonin reuptake inhibitors

60
Q

How is SIADH managed

A
  1. treat underlying condition
  2. Fluid restriction <1L/24 hours
  3. Demeclocycline (tetracycline)
  4. VAPTANS
61
Q

If Na+ <125 mol AND fitting how is it managed

A

Hypertonic N/Saline on ITU

62
Q

How is chronic Na treated

A

8mmol/L per 24 horus

63
Q

Side-Effects of SIADH management

A

Central pontine myelinolysis

64
Q

What is central pontine myelinolysis

A

Breaking down of myelin in the pons nerve cells

65
Q

Side-Effects of demeclocycline

A

Skin rash/photosensitivity

66
Q

When is hypertonic saline given

A

Symptomatic hyponatraemia

67
Q

How is hypertonic saline dleivered

A

1.8% N Saline 300mls over 20 minutes and repeat after 20 minutes

68
Q

Limits of hypertonic saline conc in chronic hyponatraemia

A
  1. 10 mol/L in 24 hours

2. 18 mol/L in 48 hours

69
Q

What are VAPTANS

A
  1. Selective V2 receptor oral antagonist
70
Q

Name a captain

A

Tolvaptan

71
Q

Disadvantage of VAPTANS

A
  1. EXPENSIVE (fluid restriction is free)

2. rise in Na could be too rapid

72
Q

Advantages of VAPTANS

A
  1. Allows more normal drinking (improves QoL)
  2. Titrate dose against effect on Na
  3. Less expensive as shorter hospital stays
73
Q

What is desmopressin

A

Vasopressin analogue

74
Q

Value for polyuria

A

15L in 24 hours

75
Q

What is Addison’s disease

A
  1. Where the adrenal glands do not produce enough steroid hormones due to detsurtcion of whole adrenal cortex (mineralocorticoids, glucocorticoids and sex steroids)
76
Q

Clinical presentation of addison’s

A
  1. Fatigue
  2. Postural hypotension
  3. Fever
  4. Nausea
  5. Headache
  6. Sweating
  7. Hyperpigmentation of skin (palmer creases, border of the lips)
  8. Low BP
77
Q

Why do we get hyper pigmentation of the skin in addison’s

A

As MSH and ACTH share the same precursor molecule POMC

78
Q

What conditions is addison’s associated with

A
  1. Type I diavetes
  2. Hashimoto’s thyroiditis
  3. Coeliac’s
  4. Vitiligo
79
Q

What is the Addisonian crisis

A

Caused by undiagnosed addison’s disease causing adrenal haemorrhage or trauma

  1. Sudden pain in legs, back and abdo
  2. VOmtiing and diarrhoea (dehydration
  3. Syncope
  4. Hypoglycaemia
  5. Hyponatraemia
  6. Hyperkalaemia
  7. Convulsions
  8. Fever
  9. Shock
80
Q

What causes addison’s

A
  1. Destruction of adrenal cortex by reaction against 21-hydroxylase
  2. Adrenoleukodystrophy (when metastatic cancer spreads to adrenal glands)
81
Q

What usually causes addison’s

A

TB
Long steroid use
HIV (CMV)

82
Q

FBC for addison’s

A

1, Hyponatraemia

  1. Hypokalaemia (decreased aldosterone)
  2. hypoaldosteronism
  3. Low cortisol
  4. uraemia
  5. Raised Ca
  6. Eosinophilia as cortisol has anti-inflammatory effects which causes raised WCC
  7. Anaemia
83
Q

Diagnostics for addison’s

A
  1. Short ACTH stimulation test
  2. Adrenal antibodies (21 hydroxyls)
  3. 9 AM ACTH levels (high in addison’s)
  4. AXR/CXR
84
Q

What is the short ACTH stimulation test

A
  1. Measure plasma cortisol before and 30 mins after IM TETROCOSACTIDE

synACTHen - ACTH analogue

Addison’s excluded if 30 min cortisol > 500 nmol/L

85
Q

Why is CXr done for addison’s

A

TB history (look for upper zone fibrosis or adrenal calcification)

86
Q

How is Addison’s treated

A
  1. IV HYDROCORTISONE
  2. IV 0.9% SALINE
  3. GLUCOSE infusion if there is hypoglycaemia

Replace steroids daily three times a day to mimic circadian rhythm:
ORAL HYDROCORTSIONE
ORAL FLUDROCORTSIONE
Double dose in infection/surgery or nightshift work

87
Q

How is addison’s crisis treated

A

IV HYDROCORTSIONE

88
Q

What is secondary hypoadrenalism

A
  1. Pituitary problem not the adrenal glands
89
Q

What causes secondary hypoadrenalism

A

Due to long-term steroid therapy leading to suppression of pituitary-adrenal axis

DECREASED ACTH production and cortisol

Mineralocorticoid production is the same

90
Q

Clinical presentation of hypoadrenalism

A
  1. NO SKIN HYPERPIGMENTATION as ACTH is reduced not increased
  2. Not feeling well
91
Q

How is secondary hypoadrenalism diagnosed

A
  1. ACTH low and mineralcorticosteroid is intact
92
Q

How is secondary hypoadrenlaim treated

A
  1. ORAL HYDROCORTISONE

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