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Phase 2a - Endocrinology > Vasopression and hyponatraemia > Flashcards

Vasopression and hyponatraemia Flashcards

1
Q

Where is vasopressin and oxytocin produced?

A

In the paraventricular and supraoptic nuclei of the hypothalamus.

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2
Q

How are the posterior pituitary hormones transported?

A

Through the axoplasm of the neurones.

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3
Q

Chemical characteristics of vasopression

A

9 AAs

Molecular weight: 1084

Plasma 1/2 life: 5-10 minutes

Neurohypophyseal binding protein: neurophysin II (nicotine stimulated)

Plasma binding protein: negligible

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4
Q

Chemical characteristics of oxytocin

A

9 AAs

Molecular weight: 1007

Plasma 1/2 life: 5-10 minutes

Neurophyseal binding protein: neurophysin I (oestrogen stimulated)

Plasma binding protein: negligible

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5
Q

Sensory pathways to the PVN and SON

A

Vagal nucleus and baroregulatory afferent fibres signal to the nucleus of tractus solitarius.

Signals from here go to the vasomotor centre or directly to the posteromedial nucleus.

From the posteromedial nucelus fibres go to the PVN directly and to the SON. Both of which signals to the osmoreceptor.

The thirst centre is located above the osmoreceptor.

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6
Q

Arginine vasopressin = AVP = ADH

A

Bings to G-protein coupled receptor.

V1a - vasculature - increases BP
V2 - renal collecting tubules - reabsorption of water
V1b - pituitary - pituitary ACTH release

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7
Q

Vasopressin release is controlled by

A

Osmoreceptors in the hypothalamus (day to day)

Baroreceptors in brainstem and great vessel (emergency).

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8
Q

ECF

A

14 L

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9
Q

Intravascular fluid

A

3.5 L

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10
Q

Interstitial fluid

A

10.5 L

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11
Q

Intracellular fluid

A

28 L

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12
Q

What is the major cation in ECF?

A

Na+

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13
Q

What is the major cation in ICF?

A

K+ and Mg2+

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14
Q

What are the major anions in ECF?

A

Cl- and HCO3-

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15
Q

What are the major anions in ICF?

A

(PO3)4- and proteins

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16
Q

Water excess

A

The body responds to changes in ECF osmolarity, blood pressure or blood volume by altering the amount of water reabsorbed by the kidneys and the amount of fluid ingested.

During conditions of water excess there is a fall in plasma osmolality, and an influx of water into the cells, increasing the intracellular water content.

This reduces thirst and suppresses the release of vasopressin, decreasing water intake and increasing water excretion by the kidney, respectively.

This decreases the amount of water within the body, correcting the water excess.

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17
Q

Water deficit

A

during conditions of water deprivation there is a fall in plasma osmolality, and a decrease in cellular hydration.

This stimulates thirst and the release of vasopressin, increasing water intake and reducing water excretion by the kidney.

This increases the amount of water within the body, correcting the water deficit.

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18
Q

Water loss can be

A

Insensible: stool, sweat, pulmonary

Sensible: lost in urine

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19
Q

What is the main driver for fluid intake?

A

Thirst

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20
Q

The main drivers of urine output are

A

GFR

Vasopression

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21
Q

Vasopressin binds to what?

A

V2 receptors on the renal collecting duct principle cells on basal surface causes the insertion of AQP2 channels on the apical surface.

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22
Q

Where does urine concentration take place?

A

In the nephron

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23
Q

Urine concentration and dilution is influenced by

A

Several factors, including:
Glomerular filtration rate
Sodium reabsorption
Water reabsorption
Vasopressin

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24
Q

Describe the action of vasopressin and how it controls water excretion.

A

The coupling of vasopressin to V2 receptors stimulates an intracellular signalling cascade, leading to the insertion of aquaporins (AQPs) into the apical membrane of the renal collecting duct principle cells.

In this cascade, binding of vasopressin to V2 receptors leads to activation of guanine nucleotide binding protein (Gs) which in turn activates adenylate cyclase, subsequently increasing cyclic-3’-5’-adenosine monophosphate (cAMP) synthesis within the cell.

The cAMP activates protein kinase A (PKA), which in turn phosphorylates microtubular subunits that aggregate to form aquaporin-2 (AQP-2) water channel proteins.

AQPs are then transported through the cell and inserted into the apical membrane of the renal collecting duct principal cells.

The presence of AQPs on the apical membrane allows water to be reabsorbed from the renal collecting duct, transported through the collecting duct cell and returned to the bloodstream.

When the stimulus for water reabsorption ends, AQP-2 is removed from the apical membrane by endocytosis.

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25
Q

What is osmolality?

A

Concentration in plasma.

Size of particle is NOT important - it is all about the NUMBER of particles.

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26
Q

What endogenous products affect osmolality?

A

Sodium, potassium, chloride, bicarbonate, urea and glucose.

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27
Q

What exogenous solutes may affect osmolality?

A

Alcohol
Methanol
Polyethylene glycol
Mannitol

28
Q

How can plasma osmolality be calculated?

A

Na+ (2x) (accounts for anions associated with Na)
+
Glucose
+
Urea

29
Q

Plasma osmolality normal values are

A

Between 282-295 mOsmol/kg

30
Q

AVP deficiency (cranial diabetes insipidus)

A

Lack of vasopressin - uncommon but life threatening.

31
Q

AVP resistance (nephrogenic diabetes insipidus)

A

Resistance to action of vasopressin - not common but life threatening.

32
Q

SIAD

A

Syndrome of antidiuretic hormone secretion - too much vasopressin release when it should not be released. (Ectopic - carcinoma of lung)

Really common - can be life threatening.

33
Q

AVP deficiency and resistance symptoms

A

Polyuria
Polydypsia
No glucosuria

34
Q

AVP deficiency and resistance Dx

A
  • measure urine volume, if <3L/day it is unlikely
  • renal function and serum calcium

Biochemistry examination:
- inappropriately dilute urine for plasma osmolality
- serum osmo >300 and urine osmo<200 consistent with AVPD or AVPR
- normonatraemia or hypernatraemia
- hypertonic saline infusion and measurement of AVP

35
Q

AVPR (nephrogenic DI)

A

Familial - rare
- X-linked (V2 receptor defect)
- Autosomal (AQP2 defect)

Acquired - either reduction in medullary concentrating gradient or antagonism of effects of AVP.

Osmotic diuresis (DM)
Drugs: lithium, tetracycline
Chronic renal impairment
Post obstructive nephropathy
Metabolic - hypercalcaemia/hypokalaemia
Renal infiltration (amyloid)

36
Q

Copeptin

A

When vasopressin is cleaved - copeptin is released which can be measured.

37
Q

Management of AVP deficiency

A

Treat any underlying condition.

Desmopressin - high activity at V2 receptor
tbl: 100-600 micrograms/day
nasal spray: 10-20 micrograms/day
injection: 1-2 micrograms/day

38
Q

Management of AVP resistance

A

Try and avoid precipitating drugs.

Congenital DI - very difficult
free access to water
very high dose desmopressin

39
Q

Hyponatraemia

A

Common

Symptomatic vs. asymptomatic

Most often caused by excess water rather than salt loss.

40
Q

What is the normal serum sodium level?

A

135-144 mmol.

41
Q

Definition of hyponatraemia

A

Serum sodium is < 135 mmol/L

42
Q

Biochemical severe

A

Serum sodium is < 125 mmol/L

43
Q

Sign and symptoms of hyponatraemia

A

No or mild symptoms.

Moderate symptoms.

Severe symptoms.

44
Q

What are the moderate symptoms of hyponatraemia?

A

Headache
Irritability
Nausea/Vomiting
Mental slowing
Unstable gait/falls
Confusion/delirium
Disorientation

45
Q

What are the severe symptoms of hyponatraemia?

A

Stupor/coma
Convulsions
Respiratory arrest

46
Q

In gradual onset hyponatraemia, the brain undergoes what?

A

Volume adaptation.

Normal brain > water gain > loss of sodium, potassium, and chloride > Loss of organic osmolytes.

47
Q

Biochemical classification of hyponatraemia

A

Mild 130-135 mmol/L
Moderate 125-129 mmol/L
Severe <125 mmol/L

48
Q

Aetiology of hyponatraemia

A

Hypovolaemic
Euvolaemic
Hypervolaemic

49
Q

Acuity of onset

A

Acute <48 hours
Chronic >48 hours

50
Q

What to do with someone in hospital who is hyponatraemic?

A

Stop hypotonic fluids.

Review drug card (PPI).

Specifics:
Plasma and Urine Osmolality
Urinary Na+
glucose
TFT’s
+/- Assessment of Cortisol
Assessment of underlying causes eg chest imaging

51
Q

Assessment and management of chronic hyponatraemia in dehydrated person.

A

Saline replacement if dehydrated.

Low urine Na because of:
Vomiting and diarrhoea
Burns
Pancreatitis
Sodium depletion after diuretics

Urine Na > 40mmol/L
Diuretics
Addison’s
Cerebral salt wasting
Salt wasting nephropathy

52
Q

Assessment and management of chronic hyponatraemia in normovolaemic individuals

A

Serum and urine osmolalities
Sport urine sodium
TSH normal
Cortisol > 430 nmol/L

SIAD
P Osm <275 mOsmol/kg
U Osm >100 mOsmol/kg
U Na . 40 mmol/L

Fluid restriction 500-1000 mL/24 hours

53
Q

Assessment and management of chronic hyponatraemia in fluid overload

A

Cirrhosis of liver/liver failure
CCF
Inappropriate IV fluids

Fluid restriction 500-1000 mL/24 hours.

54
Q

SIAD

A

common in clinical practice - 25% of all hyponatraemia
BUT not the only cause………………

Too much AVP, when it should not be being secreted
Low osmolality
Plasma sodium is low
Urine is inappropriately concentrated
Water retention - ECF volume increased mildly
Increase GRF - less Na reabsorption in PCT
thus - urine Na+ usually >30mmol/l
normal thyroid and adrenal function

Clinically: NORMAL CIRCULATING VOLUME
No Oedema

55
Q

What CNS disorders cause SIAD?

A

Head injury
Meningitis
Encephalitis
Brain tumour
Brain abscess
Cerebral haemorrhage/thrombosis
Guillain-Barre syndrome
Acute intermittent porphyria

56
Q

What tumours cause SIAD?

A

Carcinoma (lung especially)
Lymphoma
Leukaemia
Thymoma
Sarcoma
Mesothelioma

57
Q

What are the respiratory causes of SIAD?

A

Pneumonia
Tuberculosis
Severe Asthma
Pneumothorax
Positive-pressure ventilation
Emphysema

58
Q

What drugs cause SIAD?

A

carbamazapine, clofibrate, chlorpropramide, thiazides, phenothiazines, MAO inhibitors, cytotoxics, desmopressin, vasopressin, oxytocin, Selective serotonin reuptake inhibitors, PPI’s

59
Q

Treatment goals of SIAD

A

ensure correct diagnosis
allow/facilitate increase in serum Na+
treat any underlying condition
identify and stop any causative drug (if possible)
in acute setting - daily U+E - hospital
in chronic setting - weekly to monthly U+E - hospital/GP
frequent co-morbidity
Na+>130 mmol/l - usually no need for urgent intervention

60
Q

SIAD management

A

Diagnose and treat underlying condition

fluid restriction <1L/24 hour

sometimes demeclocycline/ vaptan

if Na+ <115 mmol/l AND fitting hypertonic N/Saline on ITU

<8mmol/l increase in Na+ per 24 hour if chronic

Potential risk of central pontine myelinolysis

61
Q

If improper therapy is given to gradual onset hyponatraemia, that can lead to

A

Osmotic demyelination.

62
Q

Osmotic demyelination syndrome

A

White areas in the middle of the pons

Massive demyelination of descending axons

May take up to 2 weeks to manifest

63
Q

What are the risk factors for osmotic demyelination syndrome?

A

Serum Na+ <105mmol/L
Hypokalaemia
Chronic excess alcohol
Malnutrition
Advanced Liver disease
>18mmol/L Na+ increase in 48 hour

LIMITS (not targets) for NA+ rise
High risk <8mmol/l in any 24 hour period
Normal <10-12mmol/l in any 24 hour period

64
Q

Other management

A

Selective V2 receptor oral antagonist - ‘tolvaptan’
-competitive antagonist to AVP
cause a profound ‘aquaresis’
licensed for SIAD
-expensive tablet

65
Q

Management of acute severe symptomatic hyponatraemia

A

IV 150mL of 3% saline or equivalent over 20mins.

Check serum Na+.

Repeat twice until 5mmol/L increase Na+

After 5mmol/L increase:
- stop hypertonic saline
- establish diagnosis
- Na+ 6 hourly for 1st 24 hours
Limite increase to 10 mmol/L first 24 hours

Phase 2a - Endocrinology (11 decks)

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