neurohypophysial disorders

Question 1

posterior pituitary location DIAGRAM

Answer 1

dk

Question 2

define diuresis and what vasopressin is

Answer 2

increase in urine production anti-diuretic

Question 3

mechanism of vasopressin DIAGRAM

Answer 3

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

Question 4

location of osmoreceptors and what they do

Answer 4

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

Question 5

response to water deprivation

Answer 5

increased osmolality= osmoreceptors stimulated (thirst increases)= more VP release= more water reabsorption= less urine+ increased urine osmolality+ lower plasma osmolality

Question 6

diabetes insipidus define and types

Answer 6

issue with vasopressin, NOT glucose cranial/central or nephrogenic

Question 7

causes of cranial type

Answer 7

acquired- damage to neurohypophysial system by traumatic brain injury, pituitary tumours/surgery, or inflammation of median eminence from TB congenital is rare

Question 8

causes of nephrogenic type

Answer 8

congenital rare (mutation in receptor/water channel) acquired- drugs like lithium

Question 9

symptoms of diabetes insipidus

Answer 9

polyuria, hypo-osmolar urine (not HYPER like mellitus), polydipsia, dehydration, and hence sleep disruption

Question 10

flowchart of insipidus

Answer 10

lack of VP, so poluria= increased plasma osmolality+ lower volume= polydipsia= dehydration if no water access

Question 11

psychogenic polydipsia and flow chart

Answer 11

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

Question 12

effects of fluid deprivation DIAGRAM

Answer 12

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

Question 13

biochemical features of DI

Answer 13

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?

Question 14

biochemical features of psychogenic

Answer 14

mild hyponatraemia, hypo-osmolar urine, low plasma osmolality

Question 15

treatment of DI; how it’s given and caution

Answer 15

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

Question 16

treatment of nephrogenic

Answer 16

thiazides (diuretics), NOT desmopressin

Question 17

define SIADH (syndrome of inappropriate ADH)

Answer 17

plasma vasopressin too high for plasma osmolaity (ie nothing wrong with water balance initially- just too much vasopressin)

Question 18

mechanism of SIADH

Answer 18

high VP- high reabsorption= high ECF= ANP released from right atrium= natriuresis (sodium excretion)= euvolaemia (normal ECF) but hyponatraemia

Question 19

signs and symptoms of SIADH

Answer 19

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

Question 20

SIADH causes

Answer 20

CNS- stroke/tumour/subarachnoid haemorrhage pulmonary- pneumona lung cancer- ectopic drug-related= carbamazepine idiopathic- unknown

Question 21

treatment of SIADH

Answer 21

treatment for cause eg lung cancer hyponatreaemia immediately reduced by fluid restriction, or drugs preventing VP for longer term eg V2 receptor antagonists

Question 22

vaptans and issue

Answer 22

non-competitive V2 receptor antagonists, preventing AQP2 synthesis= aquaressi (excretion of water without electrolyte loss) very expensive