Osmoregularitiy

Question 1

what monitors water content?

Answer 1

the hypothalamus

Question 1

where is ADH synthesised and released?

Answer 1

ADH is synthesised in the hypothalamus and released from terminals of hypothalamic neurons in the pituitary gland

Question 2

why can ADH be tightly controlled?

Answer 2

short half-life so its levels can be changed quickly = tight control

Question 3

what channels does ADH increase in the CD?

Answer 3

AQP2
causes insertion of the urea transporter U1-A1 into to collecting duct, allowing it to leave and increase osmolality at the loop of Henle = increase water uptake

Question 4

what receptors does ADH bind to ?

Answer 4

V2 receptor is a G protein coupled receptor linked to Gs. Gs stimulates adenyl cyclase leading to increased cAMP levels.

Question 5

how does increased cAMP levels effect the CD cell

Answer 5

cAMP stimulates PKA which triggers AQP2 in vesicles to fuse with the cell membrane
cAMP also promotes synthesis of new AQP2 to replace what was lost

Question 6

how do cells in the medulla combat the high osmolarity?

Answer 6

accumulating organic osmolytes within their cytoplasm’s they include inositol and sorbitol

Question 7

what are the 2 types of diabetes insipidus?

Answer 7

Type 1 - deficiency in ADH secretion (central diabetes insipidus) , Type 2 not responsive to ADH often due to a problem with V2 receptor (nephrogenic diabetes insipidus )

Question 8

what are the symptoms of diabetes insipidus?

Answer 8

individuals can’t concentrate urine, leading to dehydration, polyuria (abnormal urine production) causing polydipsia (drinking too much)
hypernatreamic (too high Na), due to the loss of water increasing conc

Question 9

what are the causes of central diabetes insipidus?

Answer 9

head injuries, infections

Question 10

what are the treatments for central diabetes insipidus?

Answer 10

desmopressin an ADH analogue which is produced in a lab and has a longer half life
also thiazide drugs can be used (increase Na, in PCT)

Question 11

causes of nephrogenic diabetes insipidus

Answer 11

toxicity e.g. due to excess lithium in drugs used to treat bipolar , hypercalcemia, genetic due to mutations in V2 or AQP2

Question 12

what are the treatments for nephrogenic diabetes insipidus ?

Answer 12

low salt diet / thiazide diuretic (increase Na reabsorption in the PCT)

Question 13

what does SAIDH stand for?

Answer 13

Syndromes in Inappropriate ADH secretion

Question 14

what are the symptoms of SAIDH?

Answer 14

very concentrated urine and become hyponatraemic, fluid overload,

Question 15

what are the treatments for SAIDH?

Answer 15

fluid restriction and V2 receptor antagonists that block the ADH from binding and causing a response

Question 16

what part of the brain detects osmolarity and controls ADH secretion?

Answer 16

• Osmolality of the blood is detected in the anteroventral third ventricle (AV3V) region, which also regulates ADH release

Question 17

how does ADH increase thirst?

Answer 17

AV3V is also connected to the median preoptic area of the hypothallus which increases thirst

Question 18

why does diabetes mellitus cause increase in urine production?

Answer 18

high glucose in the blood contributing to osmolality it can be a huge contributor
= excess urine production
large increase in thirst
* It often occur when glucose conc is above 33mM giving osmolality of around 320osmKG-1

Question 19

what are the symptoms of the high osmolarity in the blood in diabetes mellitus ?

Answer 19

a strong thirst drive, if not enough water is taken in to counteract the effects it can lead to cellular dehydration, hypernatraemia
* This cause altered mental status, seizures and increases blood viscosity