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Digestion and Renal Sciences > Body Fluid Volume and Osmoregulation > Flashcards

Body Fluid Volume and Osmoregulation Flashcards

1
Q

What is another name for ADH?

A

ADH = anti diuretic hormone

Vasopressin

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2
Q

Where is ADH synthesised?

A

In the hypothalamus

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3
Q

Where is ADH released?

A

From the terminals of hypothalamic neurones found within the posterior pituitary

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4
Q

What does ADH increase the expression of?

A

AQP2

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5
Q

How does ADH increase the expression of AQP2?

A

ADH interacts with V2 receptor
Triggering adenylyl cyclase to produce cAMP
cAMP promotes nucleus transcription and PKA (protein kinase A)

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6
Q

Describe osmolality across the nephron

A

High in the proximal tubule
Highest in the loop of Henle
Lower in the collecting duct

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7
Q

Describe flow rate in the nephron with no ADH present

A

Highest at the start of the proximal tubule and then decreasing

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8
Q

Describe osmolality in the nephron

A

High in the proximal tubule
Highest in the loop of Henle
Lower in the convoluted tubule
Then increasing to be as high as the loop of Henle

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9
Q

Compare flow in the nephron with ADH and without

A

With ADH present flow decrease across the nephron in the same way but to a much greater extent

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10
Q

How do cells survive the very high osmolality in the nephron?

A

They have adapted to have a range of organic osmolytes within the cells
This includes sorbitol, inositol, glycerophosphororylchlorine and betaine

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11
Q

What is diabetes insipidus?

A

Loss of ADH secretion or loss of kidney sensitivity to ADH

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12
Q

What would cause a loss of sensitivity to ADH?

A

Nephrogenic diabetes insipidus

Problem with the V2 receptors

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13
Q

What are the symptoms of diabetes insipidus?

A

Unable to produce concentrated urine
Polyuria
Dehydration

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14
Q

What is central diabetes insipidus?

A

Caused by head injury, tumours or infection
Treated with desmopressin (ADH analogue)
Some treatment with thiazides

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15
Q

What causes nephrogenic diabetes insipidus?

A

Toxicity
Hyperglycaemia
Genetic mutations

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16
Q

How is nephrogenic diabetes insipidus treated?

A

Thiazide diuretic

Low salt diet

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17
Q

What is SIADH?

A

Syndromes in inappropriate ADH

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18
Q

What cause SIADH?

A

Most commonly a head injury

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19
Q

What are the symptoms of SIADH?

A

Inappropriately high levels of ADH

Concentrated urea

20
Q

How is SIADH treated?

A

With Urea

21
Q

What is the body’s mechanism against thirst?

A

Increase of osmolality of the plasma
Osmolality detected by anteroventral third ventricle AV3V
AV3V neurones extend into the hypothalamus, increasing thirst

22
Q

What happens if you drink sea water?

A

Dehydration

1kg of sea water require 1.4L of water to clear

23
Q

What is the maximum urine concentration?

A

1400mOsm

24
Q

How much urine must be produced to secrete 1400 mOsm?

A

1 litre

25
Q

What is a hyperosmolar hyperglycaemic state?

A

Hyperosmolality caused by high blood glucose levels
Leads to strong thirst
Can also cause altered mental status, seizures and increases blood viscosity

26
Q

What does the body regulate with regards to volume of water?

A

The effective circulating volume

27
Q

What is the juxtaglomerular apparatus?

A

The complex of late distal tubule and renal different arteriole

28
Q

What is the macula densa?

A

Thickening of the wall of the early distal tubule

29
Q

What system increases the effective circulating volume?

A

Renin-angiotensin-aldosterone system

30
Q

What are the two triggers for aldosterone release?

A

Angiotensin II

Hyperkalaemia

31
Q

What is spironolactone?

A

Blocks the effect of aldosterone

32
Q

How is the renin angiotensin system inhibited?

A

ACE inhibitors
AT1 receptor antagonists
Aldosterone receptor antagonists
Renin inhibition

33
Q

What is the main receptor for angiotensin II?

A

AT1 receptor

34
Q

What is the AT1 receptor coupled to?

A

Gq

35
Q

What are the five actions of angiotensin II on circulating volume?

A

Vasoconstriction
Increase Na+/H+ exchange in the proximal tubule
Increase in aldosterone release from the adrenal cortex, increasing distal Na+ absorption
Cause ADH release
Cause thirst

36
Q

What produces renin?

A

Granule cells

37
Q

What regulates renin production?

A

Sympathetic innervation of granule cells

38
Q

What are the effects of activating sympathetic innervation of the afferent arteriole?

A

Vasoconstriction upstream of granule cells causes decreased pressure sensed by them, results in a fall in blood pressure
Direct stimulation of renin release by granule cells
Afferent arteriole vasoconstriction reduces GFR

39
Q

What is the neurotransmitter in the nerves of the afferent arteriole?

A

Noradrenaline

40
Q

What causes vasoconstriction?

A

Alpha 1 adrenoreceptors that are Gq coupled

41
Q

What receptors are found on the granule cells?

A

Beta 1 adrenoreceptors that are Gs coupled

42
Q

What is another stimulus of renin release?

A

Decreased Na+ delivery to the distal tubule

A result of decreased venous tone and greater fluid loss from the filtrate

43
Q

What is atrial natriuretic peptide?

A

ANP
Released in response to increased venous return
Decreases the activity of Na+/K+/ATPase
Increases renal excretion of Na+

44
Q

What works the same as atrial natriuretic peptide?

A

Renal natriuretic, produced in the kidney

45
Q

What is the primary effect of ADH?

A

To drop osmolality

Digestion and Renal Sciences (27 decks)

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