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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
What is osmolality?
Concentration in plasma. Size of particle is NOT important - it is all about the NUMBER of particles.
26
What endogenous products affect osmolality?
Sodium, potassium, chloride, bicarbonate, urea and glucose.
27
What exogenous solutes may affect osmolality?
Alcohol Methanol Polyethylene glycol Mannitol
28
How can plasma osmolality be calculated?
Na+ (2x) (accounts for anions associated with Na) + Glucose + Urea
29
Plasma osmolality normal values are
Between 282-295 mOsmol/kg
30
AVP deficiency (cranial diabetes insipidus)
Lack of vasopressin - uncommon but life threatening.
31
AVP resistance (nephrogenic diabetes insipidus)
Resistance to action of vasopressin - not common but life threatening.
32
SIAD
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
AVP deficiency and resistance symptoms
Polyuria Polydypsia No glucosuria
34
AVP deficiency and resistance Dx
- 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
AVPR (nephrogenic DI)
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
Copeptin
When vasopressin is cleaved - copeptin is released which can be measured.
37
Management of AVP deficiency
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
Management of AVP resistance
Try and avoid precipitating drugs. Congenital DI - very difficult free access to water very high dose desmopressin
39
Hyponatraemia
Common Symptomatic vs. asymptomatic Most often caused by excess water rather than salt loss.
40
What is the normal serum sodium level?
135-144 mmol.
41
Definition of hyponatraemia
Serum sodium is < 135 mmol/L
42
Biochemical severe
Serum sodium is < 125 mmol/L
43
Sign and symptoms of hyponatraemia
No or mild symptoms. Moderate symptoms. Severe symptoms.
44
What are the moderate symptoms of hyponatraemia?
Headache Irritability Nausea/Vomiting Mental slowing Unstable gait/falls Confusion/delirium Disorientation
45
What are the severe symptoms of hyponatraemia?
Stupor/coma Convulsions Respiratory arrest
46
In gradual onset hyponatraemia, the brain undergoes what?
Volume adaptation. Normal brain > water gain > loss of sodium, potassium, and chloride > Loss of organic osmolytes.
47
Biochemical classification of hyponatraemia
Mild 130-135 mmol/L Moderate 125-129 mmol/L Severe <125 mmol/L
48
Aetiology of hyponatraemia
Hypovolaemic Euvolaemic Hypervolaemic
49
Acuity of onset
Acute <48 hours Chronic >48 hours
50
What to do with someone in hospital who is hyponatraemic?
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
Assessment and management of chronic hyponatraemia in dehydrated person.
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
Assessment and management of chronic hyponatraemia in normovolaemic individuals
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
Assessment and management of chronic hyponatraemia in fluid overload
Cirrhosis of liver/liver failure CCF Inappropriate IV fluids Fluid restriction 500-1000 mL/24 hours.
54
SIAD
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
What CNS disorders cause SIAD?
Head injury Meningitis Encephalitis Brain tumour Brain abscess Cerebral haemorrhage/thrombosis Guillain-Barre syndrome Acute intermittent porphyria
56
What tumours cause SIAD?
Carcinoma (lung especially) Lymphoma Leukaemia Thymoma Sarcoma Mesothelioma
57
What are the respiratory causes of SIAD?
Pneumonia Tuberculosis Severe Asthma Pneumothorax Positive-pressure ventilation Emphysema
58
What drugs cause SIAD?
carbamazapine, clofibrate, chlorpropramide, thiazides, phenothiazines, MAO inhibitors, cytotoxics, desmopressin, vasopressin, oxytocin, Selective serotonin reuptake inhibitors, PPI’s
59
Treatment goals of SIAD
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
SIAD management
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
If improper therapy is given to gradual onset hyponatraemia, that can lead to
Osmotic demyelination.
62
Osmotic demyelination syndrome
White areas in the middle of the pons Massive demyelination of descending axons May take up to 2 weeks to manifest
63
What are the risk factors for osmotic demyelination syndrome?
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
Other management
Selective V2 receptor oral antagonist - ‘tolvaptan’ -competitive antagonist to AVP cause a profound ‘aquaresis’ licensed for SIAD -expensive tablet
65
Management of acute severe symptomatic hyponatraemia
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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