neurohypophysial disorders Flashcards
what are magnocellular neurones?
neurones that project into neurohypophysis (with herring bodies)
what are the 2 neurohypophysis hormones?
oxytocin
vasopressin
where does VP act?
by increasing water reabsoprtion from renal cortical and medullary collecting ducts via V2 receptors
describe the VP action
- VP binds to V2 receptors (Gs receptors)
- aquaporin 2 molecules are created which move to apical membrane in aggraphores
- AQA2 insert in apical membrane to allow water reabsorption
where do osmoreceptor neurones located? where do they project?
in organum vasculosum (no BBB)
neurones project axons into hypothalamic paraventricular and supraoptic nuclei
what happens when blood osmolarity goes up?
- water moves out of osmoreceptor cells
- osmoreceptors shrink
- triggers them to send more signals to hypothalamus to release VP
describe what happens in water deprivation
- inc. blood osmolarity
- stimulation of osmoreceptors (thirst)
- inc. VP release
- inc. water reabsorption from renal collecting ducts
- reduction in blood plasma osmolarity
- reduced urine volume
what are the 2 forms of DI?
- central/cranial: not making enough VP
- nephrogenic: target organ (kidneys) have resistance
what are the acquired and congenital causes of cranial DI?
Acquired: - TBI - pituitary surgery - pituitary tumours - metastasis to pituitary gland - granulomatous infiltration of median eminence Congenital: rare
what are the acquired and congenital causes of nephrogenic DI?
acquired: drugs
congenital: rare
what are the signs and symptoms of DI?
- polyuria
- very dilate urine
- polydipsia
- dehydration
- disruption to sleep and fatigue
what is psychogenic polydipsia?
- excess fluid intake and polyuria
- but VP secretion ability preserved
what is psychogenic polydispia seen in?
- psychiatric patients
- anti-cholinergic effects of medication stimulating dry mouth
- seen in patients told to drink plenty
what is the differene between the plasma osmolarity in people with DI and PP?
DI = HIGH plasma osmolarity PP = LOW plasma osmolarity
what is DDAVP?
synthetic AVP
differentiates cranial and central
what are the biochemical features of DI?
- hypernatraemia
- raised urea
- inc. plasma osmolarity
- hypo-osmolar urine
what are the biochemical features of PP?
- mild hyponatraemia
- low plasma osmolarity
- hypo-osmolar urine
where are V1 receptors?
- VSM
- NVSM
- anterior pituitary
- liver
- platelets
- CNS
where are V2 receptors?
- kidney
- endothelial cells
how do you treat DI?
remember ALL vasopressin receptors will be activated
but want to target just V2 receptors
to treat cranial use selective VP receptive agonists
V1: Terlipressin
V2: Desmopressin (DDAVP)
what will DDAVP do? what must a patient be told not to do?
- reduces urine conc and volume in cranial DI
- patient must be told not to continue drinking large volumes of water
- could lead to hyponatraemia
what is the possible mechanism for thiazides in the treatment of nephrogenic DI?
- inhibits Na/Cl transport in DCT in kidneys
- volume depletion
- inc. in Na reabsorption in PCT
- inc. water reabsorption in PCT
- reduced urine volume
what is SIADH?
excessively high ADH
what is natriuresis?
excretion of sodium in urine
what is evolaemia?
state of normal body fluid volume
what are the signs and symptoms of SIADH?
- small volumes of concentrated urine, hyponatraemia
- if hyponatraemic, then weak, poor mental function and nausea or then coma and death
what are the causes of SIADH?
CNS - SAH, stroke, tumour, TI Pulmonary disease - penumonia, bronciesctasis Malignancy - lung (small cell) drug-related idiopathic
how do you reduce the immediate concern in SIADH?
immediate - fluid restriction
long term - demeclocycline (prevent VP action in kidneys)
what are VAPTANS?
- non-competitive V2 receptor antagonists
- inhibit AQA2 synthesis and transport
- aquaresis: solute-sparing renal excretion of water
