neurohypophysial disorders Flashcards
posterior pituitary location DIAGRAM
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define diuresis and what vasopressin is
increase in urine production anti-diuretic
mechanism of vasopressin DIAGRAM
binds to V2 receptor on basolateral side, causing ATP=cAMP, activating PKA, which causes synthesis of AQP2, which is inserted into aggraphores and migrates to apical side H20 diffuses in, then into blood via AQP3/4
location of osmoreceptors and what they do
in organum vasculosum, communciates with systemic circulation as no BBB senses changes in osmolality (ie Na+) and shrinks which increases firing, and projects to paraventricular nucleus and supraoptic nucleus
response to water deprivation
increased osmolality= osmoreceptors stimulated (thirst increases)= more VP release= more water reabsorption= less urine+ increased urine osmolality+ lower plasma osmolality
diabetes insipidus define and types
issue with vasopressin, NOT glucose cranial/central or nephrogenic
causes of cranial type
acquired- damage to neurohypophysial system by traumatic brain injury, pituitary tumours/surgery, or inflammation of median eminence from TB congenital is rare
causes of nephrogenic type
congenital rare (mutation in receptor/water channel) acquired- drugs like lithium
symptoms of diabetes insipidus
polyuria, hypo-osmolar urine (not HYPER like mellitus), polydipsia, dehydration, and hence sleep disruption
flowchart of insipidus
lack of VP, so poluria= increased plasma osmolality+ lower volume= polydipsia= dehydration if no water access
psychogenic polydipsia and flow chart
polydipsia and polyuria, but nothing wrong with vasopressin- may be due to anti-cholinergic effects of medication polydipsia= LOWER osmolality (unlike insipidus)= less VP= poluria= EC fluid back to normal
effects of fluid deprivation DIAGRAM
in normal patient and one with psychogenic polydipsia- vasopressin increases= low urine and concentrated for both types of insipidus, cannot reabsorb water, so urine osmolality stays low
biochemical features of DI
hypernatremia, high uria, high plasma osmolality and hypo-osmolar urine those with polyuria/dipsia should be checked for mellitus (blood glucose)- if normal, is it psycogenic or insipidus?
biochemical features of psychogenic
mild hyponatraemia, hypo-osmolar urine, low plasma osmolality
treatment of DI; how it’s given and caution
all vasopressin receptors activated if vasopressin given- for V1 specific is terlipressin, for V2 specific is DDAVP (desmopressin) given nasally, orally or via injection, and reduces urine volume/conc in ONLY CRANIAL caution- should not drink too much water as can cause hyponatraemia
treatment of nephrogenic
thiazides (diuretics), NOT desmopressin
define SIADH (syndrome of inappropriate ADH)
plasma vasopressin too high for plasma osmolaity (ie nothing wrong with water balance initially- just too much vasopressin)
mechanism of SIADH
high VP- high reabsorption= high ECF= ANP released from right atrium= natriuresis (sodium excretion)= euvolaemia (normal ECF) but hyponatraemia
signs and symptoms of SIADH
high urine osmolality+ low urine volume initially, but then hyponatraemia often symptomless but can cause weakness, nausea and lethargy if [NA+] below 120 mM, if below 110, causes confusion= coma
SIADH causes
CNS- stroke/tumour/subarachnoid haemorrhage pulmonary- pneumona lung cancer- ectopic drug-related= carbamazepine idiopathic- unknown
treatment of SIADH
treatment for cause eg lung cancer hyponatreaemia immediately reduced by fluid restriction, or drugs preventing VP for longer term eg V2 receptor antagonists
vaptans and issue
non-competitive V2 receptor antagonists, preventing AQP2 synthesis= aquaressi (excretion of water without electrolyte loss) very expensive
