ADD Body fluid homeostasis Flashcards

Semester 1 year 1

1
Q

Where are antidiuretic hormones released from?

A

Posterior pituitary gland

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2
Q

How is vasopressin released?

A

Sits in vesicles where it waits for signal to be fused with the presynaptic membrane where it’s secreted

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3
Q

Where is the signal that initiates the release of antidiuretic hormones released from?

A

Neurosecretory neurons

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4
Q

What does ADH do?

A

-regulates body fluid osmolality
-conserves H2O by reducing urinary losses

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5
Q

How is blood plasma concentration returned to normal when body fluid osmolality is increased using ADH?

A

-increased blood fluid osmolality
-causes increased plasma conc.
-so increased ADH
-so less water lost in urine
-plasma conc. returned to normal

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6
Q

How is blood plasma concentration returned to normal when body fluid osmolality is decreased using ADH?

A

-decreased body fluid osmolality
-causes decreased plasma conc.
-so decreased ADH
-so more water lost in urine
-plasma conc. returned to normal

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7
Q

Where do hypothalamic osmoreceptors sit?

A

Sub-optic + paraventricular nuclei

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8
Q

How sensitive are hypothalamic osmoreceptors?

A

-very
-detect changes of +- 3 mosmol/kg H2O
-normal range = 280-300 mosmol/kg H2O

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9
Q

What are hypothalamic osmoreceptors stimulated by and what is their response?

A

-stimulated by increased osmolality
-release ADH from posterior pituitary
-feeling of thirts

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10
Q

What causes an increased osmolality plasma?

A

-solute ingestion or H2O deficiency
-stress + drugs (nicotine, ecstasy)

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11
Q

What causes a decreased osmolality plasma?

A

-excessive fluid ingestion
-alcohol

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12
Q

At normal plasma osmolality, is there ADH circulating?

A

Yes

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13
Q
A
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14
Q

Does urine osmolality go to 0?

A

-no
-we can never not produce urine
-always have to excrete waste products of metabolism

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14
Q

As plasma ADH increases, what happens to urinary osmolality?

A

It increases

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15
Q

Describe the principal cell H2O model

A

-ADH binds to V2 receptor, initiating signalling cascade
-activates PKA creating active PKA
-phosphorylates proteins in vesicle membranes
-causes vesicles containing AQP2 H2O channels to fuse with principal cell membrane
-more AQP2 channels in membrane

16
Q

What protein channels aren’t regulated by ADH?

A

-AQP3
-AQP4

17
Q

What does having more AQP2 channels in the apical membrane of principal cells lead to?

A

-increased H2O reabsorption
-dilution of plasma
-fall in body fluid osmolality
-fast response - around 15 mins

18
Q

What is the effect of diabetes insipidus?

A

Create copious quantities of dilute urine

19
Q

Describe central diabetes insipidus and how it can be treated

A

-no release of ADH
-treatment - nasal spray desmopressin

20
Q

Describe nephrogenic diabetes insipidus and how it can be treated

A

-no response to ADH
-caused by gene mutations in the genes coding for V2 receptors or AQP2 channels
-range of treatments

21
Q

What is aldosterone?

A

-classed as a mineralocorticoid
-regulates plasma Na+ content, K+ content + body fluid volume

22
Q

Where is aldosterone released from?

A

Cortex of adrenal gland by the layer zona glomerulosa

23
Q

What is aldosterone released in response to?

A

-increased plasma K+
-decreased plasma Na+ –> usually maintained by osmoregulation (ADH)
-decreased ECF volume - in conjunction with renin-angiotensin system

24
Q

What does aldosterone act on?

A

-late distal tubule
-cortical + medullary collecting duct

25
Q

What happens as a result of aldosterone?

A

-increased Na+ reabsorption, causing increased H2O reabsorption
-increased secretion of K+ and H+

26
Q
A