regulation of osmolarity Flashcards

1
Q

what is water regulation controlled by

A

ADH (vasopressin)

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2
Q

where is ADH synthesised

A

in the supraoptic an dparaventricular nuclei of the hypothalamus in brain

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3
Q

where is ADH released from

A

posterior pituitary

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4
Q

what effects ADH secretion

A

primary control is plasma osmolarity

also ECF volume

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5
Q

what happens to ADH secretion when plasma osmolarity increases

A

increase release of ADH

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6
Q

what are changes in neuronal discharge mediated by

A

osmoreceptors

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7
Q

osmoreceptors: increased osmolairy

A

H2O leaves cell
cell shrinks - stretch sensitive ion channel activated
inc neural dischare
inc ADH secretion

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8
Q

osmoreceptors: decreased osmolarity

A

H2O enters cell
cell swells
decrease neural discharge
dec ADH secretion

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9
Q

normal plasma osmolality

A

280-290mOsm/kg H2O

regulated very preciscely

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10
Q

why ‘effecitive’ osmolarity

A

an increase in osmolarity that does not cause an increase in tonicity is ineffective in causing increase in ADH

solutes that can penetrate membranes move together with water and don’t produce any ‘osmotic drag’ or tonictiy

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11
Q

what does amount of urine produced depend on

A

[ADH]

amount of solute to be excreted

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12
Q

ingestion of hypertonic solutions (e.g. seawater)

A

increase solute load to be excreted –> inc urine flow –> dehydration as more water required to excrete solute load than was ingested with it

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13
Q

what does ADH act on to control permeability collecting duct

A

H2O channels in luminal membrane (aquaporins)

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14
Q

if ADH is present

A

water is able to leave collecting duct

this means cortical CD becomes equilibrated with that of cortical interstitium ie 300

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15
Q

with maximal ADH

A

produce small volume of highly concentrated urine

  • relatively less of filtered water than solute
  • compensate for water deficit
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16
Q

absence of ADH

A

collecting duct impermeable to water

large volume of dilute urine is excreted
-compensate for water excess

17
Q

role of urea

A

in presence of ADH, water moves out CF and greatly concentrates urea. CD is relatively permable to urea, esp at medullary tips

as urea approaches medullary tips it moves out down conc gradien into interstitium where it acts to reinforce the interstition gradient in the region of asc loops of henle

18
Q

urea recycling during maximum anti-diuresis

A

in anti-diuresis with high levels ADH, urea is retained in order to save water and reinforce medullary gradient at ascending limb LoH

ureaemia occurs

19
Q

what would happen iif urea wasnt reabsorbed

A

it would remain in tubule and exert osmotic effects to hold water in tubule and reduce potential for rehydration

20
Q

how does ECF volume effect ADH secretion

A

inc ECF volume –> less ADH

dec ECF volume –? more ADH

21
Q

where are low P receptors located

A

L and R atria

great veins

22
Q

where are high P receptors located

A

carotid and aortic arch baroreceptors

23
Q

relationship between ADH secertion and discharge of stretch P receptors

A

inverse relationship between rate of ADH secretion and rate of discharge of stretch receptor afferents in the low and high P areas of circulation

24
Q

other stimuli affecting ADH: more ADH

A
pain 
emotion 
stress
excercise
nicotine 
morphine
25
Q

other stimuli affecting ADH: less ADH

A

alcohol

26
Q

diabetes insipidu s

A

ADH deciciency