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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
Define polydipsia
Too much thirst
26
What is cranial diabetes insipidius
1. LACK OF VASOPRESSIN production by the posterior pituitary gland
27
Acquired causes of CDI
1. Idiopathic 2. Tumours (Craniopharyngioma, metastases) 3. Traum 4. TB, encephalitis and meningitis 5. Aneurysms, infarctions, SCA 6. Neurosarcoidosis, Guillain Barre, granuloma
28
What genetic causes are there for CDI
1. DIDMOAD (Wolfram syndrome) 2. Autosomal dominant 3. Septo-optic dysplasia
29
What is wolfram syndrome
DIDMOAD: Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and deafness
30
What is nephrogenic diabetes insipidus
1. RESISTANCE TO VASOPRESSIN
31
Acquired causes of nephrogenic diabetes insipidus
1. Osmotic diuresis (diabete smellitus) 2. Drugs (lithium, tetracycline) 3. Chronic renal failure 4. Post-obstructive uropathy 5. Hypercalcaemia, hypokalaemia 6. Amyloidosis
32
Familial causes of nephrogenic diabetes insipidus
1. X-linked (V2 receptor defect) | 2. Aquaporin 2 defect
33
How do we see a difference between NDI and CDI in water deprivation test
1. NDI should see a constant increase in osmolality whilst CDI will decrease after 2 micrograms of IM DESMOPRESSIN is given
34
How can desmopressin be given to manage CDI
1. Tablets (100-1200 mg/day) 2. Nasal spray (10-40) 3. Injection (1-2)
35
How's nephrogenic DI treated
1. Avoid precipitating drugs 2. Free access to water 3. HIGH dose desmopressin 4. Hydrochlorothiazide
36
What defines hyponatraemia
Na< 135 mmol/L
37
What defines severe hyponatraemia
<125 mol/L
38
Normal serum levels of Na
137-144 mol
39
Clinical presentation of hyponatraemia
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
How doe the brain adapt to hyponatraemia
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
Acute vs chronic hyponatraemia
1. Acute - 48 hours (after subarachnoid haemorrhage) can be corrected rapidly 2. Chronic (CNS adapts) so correction has too slow
42
Rate at which Na is given in chronic hyponatraeima
<8 mol/24 hours
43
Diagnostics for hyponatraemia
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
What is the syncathen test
ACTH test to assess functioning of adrenal glands
45
3 ways we get hyponatraemia
1. Fluid overload 2. normovolaemic 3. Dehydration
46
Two ways fluid overload can cause hyponatraemia
1. Cirrhosis of liver | 2. Congestive heart fialure
47
How to spot normovolaemic hyponatraemia
1. Spot urine > 30mmol/L 2. TSH is normal 3. Cortisol > 500 nmol/L
48
What condition can cause normovolaemic hyponatraemia
1. Syndrome of inappropriate antidiuretic hormone
49
What is seen in the blood in SIADH
High Urine osmolality | High Urine Na
50
How is normovolaemic and fluid overload (liver cirrhosis and heart failure) hyponatreamia treated
Fluid restriction (750-1000ml/24 hours)
51
What will cause low urine Na (dehydration)
1. Vomiting and diarrhoea 2. Burns 3. Pancreatitis 4. Sodium depletion after diuretics
52
What will cause high urice Na (Dehydration)
1. Diuretics 2. Addison's 3. Cerebral salt wasting 4. Salt wasting nephropathy
53
How is dehydration treated
IV SALINE
54
What is SIADH
too much AVP secretion
55
What happens to osmolality in SIADH
LOW and plasma N his low
56
What is seen in the urine
High CONC
57
Clinical presentation of SIADH
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
Na urine levels in SIADH
>30 mol/L
59
What causes SIADH
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
How is SIADH managed
1. treat underlying condition 2. Fluid restriction <1L/24 hours 3. Demeclocycline (tetracycline) 4. VAPTANS
61
If Na+ <125 mol AND fitting how is it managed
Hypertonic N/Saline on ITU
62
How is chronic Na treated
8mmol/L per 24 horus
63
Side-Effects of SIADH management
Central pontine myelinolysis
64
What is central pontine myelinolysis
Breaking down of myelin in the pons nerve cells
65
Side-Effects of demeclocycline
Skin rash/photosensitivity
66
When is hypertonic saline given
Symptomatic hyponatraemia
67
How is hypertonic saline dleivered
1.8% N Saline 300mls over 20 minutes and repeat after 20 minutes
68
Limits of hypertonic saline conc in chronic hyponatraemia
1. 10 mol/L in 24 hours | 2. 18 mol/L in 48 hours
69
What are VAPTANS
1. Selective V2 receptor oral antagonist
70
Name a captain
Tolvaptan
71
Disadvantage of VAPTANS
1. EXPENSIVE (fluid restriction is free) | 2. rise in Na could be too rapid
72
Advantages of VAPTANS
1. Allows more normal drinking (improves QoL) 2. Titrate dose against effect on Na 3. Less expensive as shorter hospital stays
73
What is desmopressin
Vasopressin analogue
74
Value for polyuria
15L in 24 hours
75
What is Addison's disease
1. Where the adrenal glands do not produce enough steroid hormones due to detsurtcion of whole adrenal cortex (mineralocorticoids, glucocorticoids and sex steroids)
76
Clinical presentation of addison's
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
Why do we get hyper pigmentation of the skin in addison's
As MSH and ACTH share the same precursor molecule POMC
78
What conditions is addison's associated with
1. Type I diavetes 2. Hashimoto's thyroiditis 3. Coeliac's 4. Vitiligo
79
What is the Addisonian crisis
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
What causes addison's
1. Destruction of adrenal cortex by reaction against 21-hydroxylase 2. Adrenoleukodystrophy (when metastatic cancer spreads to adrenal glands)
81
What usually causes addison's
TB Long steroid use HIV (CMV)
82
FBC for addison's
1, Hyponatraemia 2. Hypokalaemia (decreased aldosterone) 3. hypoaldosteronism 4. Low cortisol 5. uraemia 6. Raised Ca 7. Eosinophilia as cortisol has anti-inflammatory effects which causes raised WCC 8. Anaemia
83
Diagnostics for addison's
1. Short ACTH stimulation test 2. Adrenal antibodies (21 hydroxyls) 3. 9 AM ACTH levels (high in addison's) 4. AXR/CXR
84
What is the short ACTH stimulation test
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
Why is CXr done for addison's
TB history (look for upper zone fibrosis or adrenal calcification)
86
How is Addison's treated
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
How is addison's crisis treated
IV HYDROCORTSIONE
88
What is secondary hypoadrenalism
1. Pituitary problem not the adrenal glands
89
What causes secondary hypoadrenalism
Due to long-term steroid therapy leading to suppression of pituitary-adrenal axis DECREASED ACTH production and cortisol Mineralocorticoid production is the same
90
Clinical presentation of hypoadrenalism
1. NO SKIN HYPERPIGMENTATION as ACTH is reduced not increased 2. Not feeling well
91
How is secondary hypoadrenalism diagnosed
1. ACTH low and mineralcorticosteroid is intact
92
How is secondary hypoadrenlaim treated
1. ORAL HYDROCORTISONE

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