T1 L10 Physiology of thirst, fluid balance and disorders Flashcards

1
Q

What does regulation of water balance ensure?

A

Plasma osmolality and extracellular fluid osmolality remains stable

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2
Q

What is the range of plasma osmolality?

A

285-295mosmol/kg

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3
Q

What are the 3 key determinants of water homeostasis?

A

ADH
Kidney
Thirst

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4
Q

What are osmoreceptors?

A

Groups of specialised cells which detect changes in plasma osmolality

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5
Q

Where are osmoreceptors located?

A

In anterior wall of third ventricle

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6
Q

How do osmoreceptors alter their volume?

A

By transmembrane flu of water in response to changes in plasma osmolality

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7
Q

What is the effect of osmoreceptors altering their volume?

A

Initiates neuronal impulses that are transmitted to the hypothalamus to synthesise ADH and to the cerebral cortex to register thirst

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8
Q

What is arginine vasopressin (AVP)?

A

Human form of ADH

Nonapeptide

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9
Q

Where is AVP synthesised?

A

In neurons in supraoptic and paraventricular nuclei of hypothalamus

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10
Q

What happens to the aquaporins when ADH is released?

A

Aquaporins are normally stored in cytoplasmic vesicle
Move and fuse with luminal membrane
Increases water permeability of renal collecting tubules to promote water reabsorption

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11
Q

Describe low plasma osmolality

A

AVP is undetectable
Dilute urine
High urine output

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12
Q

Describe high plasma osmolality

A

High AVP secretion
Concentrated urine
Low urine output

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13
Q

What happens to thirst in high plasma osmolality?

A

Increased thirst sensation

Drinking immediately transiently suppresses AVP secretion and thirst to avoid overshoot

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14
Q

What are the main causes of polyuria and polydipsia?

A

Diabetes mellitus
Cranial diabetes insipidus
Nephrogenic diabetes insipidus
Primary polydipsia

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15
Q

What is cranial diabetes insidious?

A

Lack of osmoregulated AVP secretion

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16
Q

What is nephrogenic diabetes insidious?

A

Lack of response of renal tubule to AVP

Thirst is still stimulated - polydipsia

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17
Q

What are the genetic causes of cranial diabetes insipidus?

A

Familial AD mutation of AVP gene

DIDMOAD

18
Q

What are the secondary causes of cranial diabetes insipidus?

A
Post-surgical
Traumatic
Tumours
Histiocytosis
Sarcoidosis
Encephalitis
Meningitis
Vascular insults
Autoimmune
19
Q

Describe hypothalamic syndrome

A
Disordered thirst and diabetes insidious
Disordered appetite
Disordered temperature regulation 
Disordered sleep rhythm
Hypopituitarism
20
Q

What can cause nephrogenic diabetes insipidus?

A
Idiopathic
Genetic
Metabolic: high calcium concentration or low potassium concentration
Drugs: lithium
Chronic kidney disease
21
Q

What is primary polydipsia?

A
Psychogenic
Increased fluid intake
Lower plasma osmolality
Suppressed AVP secretion
Low urine osmolality, high urine output
Lose renal interstitial solute which reduces renal concentrating ability
22
Q

How is polyuria and polydipsia investigated?

A
Medical history
Exclude diabetes mellitus
24 hour fluid balance
Exclude hypercalcaemia / hypokalaemia
Water deprivation test
23
Q

What are the steps of the water deprivation test?

A

1) Period of dehydration
2) Measure plasma and urine osmolalities and weight
3) Injection of synthetic vasopressin
4) Measure plasma and urine osmolalities

24
Q

What is the normal response of the water deprivation test?

A

Normal plasma osmolality

High urine osmolality

25
Q

What is the response of the water deprivation test in cranial diabetes insipidus?

A

Poor urine concentration after dehydration

Rise in urine osmolality after desmopressin

26
Q

What is the response of the water deprivation test in nephrogenic diabetes insipidus?

A

Poor urine concentration after dehydration

No rise in urine osmolality after desmopressin

27
Q

What is the treatment for cranial diabetes insipidus?

A

DDAVP (desmopressin)

Over treatment can cause hyponatraemia

28
Q

What is the treatment for nephrogenic diabetes insipidus?

A

Correction of cause

Thiazide diuretics / NSAIDs

29
Q

What is the treatment for primary polydipsia?

A

Explanation, persuasion

Psychological therapy

30
Q

What is hyponatraemia?

A

Sodium concentration below 135mmol/L

<125mmol/L if severe

31
Q

What are the symptoms of hyponatraemia?

A

Asymptomatic
Non-specific: headache, nausea, mood change, cramps, lethargy
If severe / sudden: confusion, drowsiness, seizures, coma

32
Q

What drugs can cause hyponatraemia?

A

Thiazide diuretics

33
Q

How can hyponatraemia be classified?

A

Hypovolaemia
Normovolaemia
Hypervolaemia

34
Q

What are the causes of hypovolaemic hyponatraemia?

A

Renal loss

Non-renal loss: D&V, burns, sweating

35
Q

What are the causes of normovolaemic hyponatraemia?

A

Hypoadrenalism
Hypothyroidism
SIADH

36
Q

What are the causes of hypervolaemic hyponatraemia?

A

Renal failure
Cardiac failure
Cirrhosis
Excess IV dextrose

37
Q

What can happen if hyponatraemia is corrected too quickly?

A

Risk of oligodendrocyte degeneration and CBS myelinolysis

38
Q

What is the diagnosis of SIADH?

A

Clinically euvolaemic patient
Low plasma sodium and low plasma osmolality
Inappropriately high urine sodium concentration and high urine osmolality

39
Q

What are the causes of SIADH?

A
Neoplasias
Neurological disorders
Lung disease
Drugs
Endocrine
40
Q

What is the treatment of SIADH?

A

Identify and treat underlying cause
Fluid restriction
Demeclocycline
Vasopressin antagonists: vaptans

41
Q

What does demeclocycline do?

A

Induces mild nephrogenic diabetes insipidus