Physiology of Thirst and Fluid Balance Flashcards
1
Q
What are the two main types of the pathophysiology associated with Thirst and Fluid Balance?
A
- Polyuria and polydipsia
- Diabetes Insipidus (DI)
- Hyponatraemia
- Syndrome of inappropriate ADH secretion (SIADH)
2
Q
What is the importance of water homeostasis and what are its 3 key determinants?
A
- water homeostasis ensures plasma and extracellular fluid osmolality remains stable
- there is a narrow plasma osmolality range 285-295mosmol/kg
-
ADH
- osmotically stimulated secretion
- acts on renal tubule to allow increased reabsorption of water
-
Kidney function
- __wide variation in urine output
-
Thirst
- __osmoregulated
- stimulates fluid intake behaviour
3
Q
What are osmoreceptors how do they function?
A
- groups of specialised cells which detect changes in plasma osmolality (esp sodium)
- Located in the anterior wall of 3rd ventricle
- Fenestrations in the blood-brain barrier allow circulating solutes (osmoles) to influence brain osmoreceptors
- they alter their volume by a transmembrane flux of water in response to changes in plasma osmolality
- This initiates neuronal impulses that are transmitted to the hypothalamus to synthesise ADH, and to the cerebral cortex to register thirst
4
Q
What is the human ADH and how is it formed?
A
- Arginine vasopressin (AVP) is the human form of ADH
- it is a nonapeptide synthesised in the
- Supraoptic and
- Paraventricular nuclei of the hypothalamus
- Secretory granules migrate down axons to the posterior pituitary where it is released
5
Q
Where are the Paraventricular and Supraoptic nucleus located in relation to the 3rd ventricle and pituitary gland?
A
6
Q
What is the action of ADH?
A
- action is mediated by V2 receptors
- increases the number of aquaporins that bind to the collecting tubules in the kidney
- increases reabsorption of water
7
Q
How is osmoregulation controlled by AVP and the kidney?
A
- Low plasma osmolality
- AVP undetectable
- Dilute urine
- High urine output
- High plasma osmolality
- High AVP secretion
- Concentrated urine
- Low urine output
8
Q
How is osmoregulation controlled by thirst?
A
- Low plasma osmolality
- No thirst
- High osmolality
- Increased thirst sensation
- Drinking immediately transiently suppresses AVP secretion and thirst
- Avoids ‘overshoot’
9
Q
What are the causes of Polyuria and Polydipsia?
A
- Cranial (central) diabetes insipidus (DI)
- Lack of osmoregulated AVP secretion
- Nephrogenic diabetes insipidus (DI)
- Lack of response of the renal tubule to AVP
- Primary polydipsia
- Psychogenic polydipsia, social/cultural
- Diabetes mellitus must be excluded for these causes
- these may be all partial pathologies
10
Q
What is Cranial Diabetes Insipidus and what are its causes?
A
- excessive excretion of water due to insufficient secretion or synthesis of AVP –> poluria and if thirst sensation remains intact polydipsia
- Idiopathic (27%)
- Genetic (<5%)
- Familial (AD) mutation of AVP gene
- DIDMOAD (Wolfram) (Ar, incomplete penetrance)
- Secondary (commonest causes)
- Post-surgical (pituitary / other brain operations)
- Traumatic (head injury, including closed injury)
- Rarer causes
- Tumours, histiocytosis, sarcoidosis, encephalitis, meningitis, vascular insults, autoimmune
11
Q
What pathology is this a CT of?
- what is the impact of this pathology?
A
- Disordered thirst and Diabetes Insipidus
- Disordered appetite (hyperphagia)
- Disordered temperature regulation
- Disordered sleep rhythm
- Hypopituitarism
12
Q
What is nephrogenic Diabetes Insipidus, and what are its causes?
A
- when the renal tubules are resistant to the action of AVP causing polyuria but thirst is still stimulated –> polydipsia
- Idiopathic
- Genetic (rare) Xr or Ar
- Mutations of V2 receptor gene/aquaporin gene
- Metabolic
- High [calcium] or low [potassium]
- Drugs
- Lithium (bipolar disorder)
- Chronic kidney disease
13
Q
What is Primary Polydipsia, and what are the causes?
A
- increased fluid intake
- lower plasma osmolality
- suppressed AVP secretion
- low urine osmolality, high urine output
- polyuria
- Also lose renal interstitial solute, reducing the renal concentrating ability
14
Q
How would you investigate Polyuria and Polydipsia?
A
- Medical History
- exclude diabetes mellitus
- document 24 hr fluid balance
- input vs output
- Exclude hypercalcaemia/ hypokalaemia
- Water deprivation test
- have a period of dehydration: measure plasma & urine osmolalities & weight
- Injection of synthetic vasopressin: measure plasma & urine osmalities
- Desmopressin (DDAVP)
15
Q
Explain the different outcomes of a Water Deprivation Test
A
- have a period of dehydration: measure plasma & urine osmolalities & weight
- Injection of synthetic vasopressin: measure plasma & urine osmolalities
- Desmopressin (DDAVP)
- Normal response to dehydration
- Normal plasma osmolality, high urine osmolality
- Cranial diabetes insipidus response
- Poor urine concentration after dehydration
- Rise in urine osmolality after desmopressin
- Nephrogenic diabetes insipidus
- Poor urine concentration after dehydration
- No rise in urine osmolality after desmopressin
