Neurohypophysial disorders Flashcards
What are magnocellular neurones?
neurones that project into the neurohypophysis (with herring bodies)
What distinguishes anterior and posterior pituitary on and MRI?
Posterior pituitary is bright white on MRI
How does vasopressin work?
- VP binds to V2 receptors which are GS receptors.
- Aquaporin 2 molecules are created which move to the apical membrane (tubule lumen) in aggraphores.
- The AQA2 insert in the apical membrane to allow water reabsorption.
Osmoreceptor neurones are located in the Organum Vasculosum (has NO BBB). These neurones then project their axons into the hypothalamic paraventricular and supraoptic nuclei.
When blood osmolarity goes up, water moves out of osmoreceptor cells and the osmoreceptors shrink which triggers them to send more signals to the hypothalamus to release VP.
What happens if a normal person is water deprived?
Increased blood plasma osmolarity -> stimulation of osmoreceptors (thirst) -> increased VP release -> increased water reabsorption from renal collecting ducts -> reduction in blood plasma osmolarity & reduced urine volume (but higher urine osmolarity).
What are the two types of diabetes insipidus?
cranial (central)
nephrogenic
What are some causes of acquired and congenital central DI?
- Traumatic brain injury.
- Pituitary surgery.
- Pituitary tumours, craniopharyngioma.
- Metastasis to pituitary gland.
- Granulomatous infiltration of median eminence (e.g. TB).
CONGENITAL IS RARE
What are some causes of acquired and congenital nephrogenic DI?
The target organ (kidneys) have resistance.
- Acquired – drugs (e.g. lithium)
- Congenital – RARE (e.g. mutation in gene encoding V2 receptor, AQA2 type water channels).
What are the signs and symptoms of diabetes insipidus?
- polyuria (high volume and frequency)
- polydipsia
- nocturia
- dehydration
- fatigue
- very dilute urine (hypoosmoloar)
What is psychogenic polydipsia?
Excess fluid intake (polydipsia) and polyuria but VP secretion ability preserved.
- Frequently seen in psychiatric patients with possible aetiology being anti-cholinergic effects of medication stimulating a “dry-mouth” effect.
- May also be seen in in-patients told to “drink plenty” by healthcare professionals.
Compare the plasma osmolarity of people with DI and PP
DI people will have a high plasma osmolarity and PP people will have a low osmolarity (even though they both drink a lot of water – difference lies in differences in VP).
How is DI and psychogenic polydipsia diagnosed?
water deprivation test
- normal people will have very high urine osmolality
- those with PP will have high but slightly lower than normal as constant drinking reduces gradient in medulla
- DI will have low
- To differentiate cranial and nephrogenic give DDAVP which is synthetic AVP and cranial will have a regular response to dehydration
What things are important to watch during water deprivation test?
- Take regular weight to ensure patients don’t over dehydrate (SHOULDN’T GO LESS THAN 2% OF THEIR BODY WEIGHT)
Biochemical features of DI and PP
Diabetes Insipidus:
- Hypernatraemia (high blood sodium), raised urea, increased plasma osmolarity, hypo-osmolar urine
Psychogenic Polydipsia:
- Mild hyponatraemia, low plasma osmolarity, hypo-osmolar urine
What is important when giving DI treatment?
Remember that all vasopressin receptors will be activated – we want to target just the V2 kidney receptors.
- To treat cranial DI, we use selective VP receptor agonists:
V1 – Terlipressin
V2 – Desmopressin
(DDAVP)
Cranial diabetes insipidus treatment
Desmopressin (DDAVP)
- Can be administered as; nasal spray, orally or SC (sub-cutaneous)
- DDAVP will reduce the urine concentration and volume in cranial DI.
- The patient must be told to not continue drinking large volumes of water (which they usually do or it could lead to hyponatraemia
