Endocrine control of body fluid volume and composition Flashcards

(51 cards)

1
Q

How does the osmolarity of the tubular fluid leaving the loop of henle compare to that of the surrounding interstitial fluid?

A

Hypo-osmotic

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2
Q

Where does the distal tubule drain to?

A

Collecting duct (cortical)

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3
Q

How does the interstitial fluid change as the collecting duct progresses?

A

Increasing osmolarity (collecting duct drills down into medulla)

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4
Q

Where in the nephron is ion and water balance mainly regulated?

A

Distal tubule and collecting duct

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5
Q

Where does most reabsorption of ions occur?

A

Proximal tubule BUT the remaining ions are essential for salt balance

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6
Q

What is the main mechanism of salt and water regulation?

A

Hormonal

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7
Q

Where do the hormones acting on the kidney act?

A

Distal tubule and collecting duct

do NOT act on proximal tubule or loop of Henle

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8
Q

How permeable is the distal tubule to water and urea? What effect does this have?

A
Not very (unless ADH levels are high)
Urea is concentrated in the tubular fluid which helps maintain the corticomedullary gradient
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9
Q

Describe what happens in the early and late parts of the distal tubule with regard to ion absorption

A
Early
 - Sodium, chlorine and potassium triple co-transporter (i.e salt reabsorption)
Late
 - Calcium reabsorption
 - Hydrogen secretion
 - Sodium reabsorption
 - Potassium reabsorption
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10
Q

Is it the early or late distal tubule that is stimulated by hormones?

A

Late

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11
Q

Describe what happens in the early and late collecting duct with regard to ion absorption

A
Early
 - Sodium reabsorption
 - Potassium reabsorption
 - Hydrogen secretion
 - Calcium reabsorption 
Late 
 - Low ion permeability 
 - Permeability to water varies with respect to ADH
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12
Q

Describe vasopressin secretion

A

Peptide hormone synthesised (supraoptic and paraventricular nuclei) in the hypothalamus >
Transported down nerves >
Stored in the posterior pituitary >
Released into blood in response to calcium dependent exocytosis (induced by action potentials)

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13
Q

Peptide hormones have a long half life. T/F

A

False - short half life

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14
Q

How does ADH increase the permeability of the collecting duct to water?

A

ADH binds to type 2 vasopressin receptors on the basolateral membranes of tubular cells >
Increase in intracellular cyclic AMP >
Increased expression of aquaporins (water channels) at the apical membrane >
Increased permeability to water

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15
Q

How is hypertonic urine formed?

A

In the presence of high ADH water moves from the collecting duct to the interstitial fluid along the osmotic gradient

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16
Q

How is hypotonic urine formed?

A

In the presence of low ADH water cannot leave the collecting duct and so is retained in the urine

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17
Q

Tubular fluid equilibrates with interstitial fluid via aquaporins under which condition?

A

High ADH

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18
Q

The collecting duct is impermeable to water so none is reabsorbed under which condition?

A

Low ADH

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19
Q

ADH affects salt and water reabsorption. T/F

A

False - ADH only has a direct effect on water reabsorption

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20
Q

Describe the ADH hormone axis

A

Increase in plasma osmolarity >
Hypothalamic osmoreceptors >
Increase in thirst and ADH secretion >
ADH causes vasoconstriction + increased distal tubular and collecting duct permeability to water >
Decreased urine output >
Increased plasma volume and decreased plasma osmolarity

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21
Q

When are left atrial volume receptors stimulated to produce ADH?

A

When there is a massive drop in ECF thus blood pressure and eventually decreased atrial stretch

22
Q

How can diabetes insipidus be classified?

A

Central

Nephrogenic

23
Q

Is diabetes insipidus hereditary?

24
Q

What are the symptoms of diabetes insipidus?

A

Large volumes of dilute urine

Constant thirst

25
How is diabetes insipidus managed?
ADH replacement
26
What medication (long term) induces diabetes insipidus?
Lithium as is used in bipolar disorder
27
What controls feedforward ADH secretion?
Stretch receptors in the GI tract
28
What effect do nicotine (i.e smoking) and alcohol have on ADH secretion?
Nicotine - increase ADH Alcohol - decrease ADH Nb - ecstasy also decreases ADH and thus poses a massive dehydration risk
29
How does the tubular osmolarity change across the length of the nephron
Proximal tubule - low Loop of Henle - high then low Distal tubule - low (may rise if increased ADH) Collecting duct - low (may rise if increased ADH)
30
What type of hormone is aldosterone and where is it secreted form?
Steroid | Adrenal cortex
31
What mnemonics can be used to remember the hormones secreted from the adrenal gland?
Get my = glomerulosa - mineralocorticoids (aldosterone) Freaking gun = fasiculata - glucocorticoids (cortisol) Right away = reticularis - androgens (sex hormones) Magic = medulla - adrenaline, etc (magic rush)
32
When is aldosterone secreted?
Directly in response to rising potassium Indirectly in response to falling sodium Indirectly as part of the renin-angiotensin-aldosterone system
33
What effect does aldosterone have?
Increases sodium reabsorption Increases potassium secretion Nb - remember water follows salt so inc sodium helps to increased plasma volume
34
What happens if a patient is not producing aldosterone?
Eventually leads to death due to low fluid volumes
35
Where is potassium reabsorbed? How much potassium is excreted in the urine?
90% within the proximal tubule and 10% within the distal tubule. None
36
How is potassium reabsorption affected by aldosterone?
Increase in potassium is detected by the adrenal cortex > Aldosterone release > Increased secretion of potassium
37
Decreasing sodium indirectly stimulates aldosterone release how?
Lowered sodium levels detected within the juxtaglomerular apparatus stimulates the renin-angiotensin-aldosterone system
38
Explain RAAS
Lowered ECF, sodium and BP > Kidneys detect and secrete renin > Renin acts on angiotensiogen (secreted by the liver) to covert it to angiotensin I > Angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE) in the lungs > Angiotensin II acts on the adrenal cortex to stimulate aldosterone > Aldosterone acts on the liver to decrease potassium and increase sodium reabsorption > Increased salt causing increased water retention and thus fluid repletion
39
What does angiotensin II do?
Increases thirst Stimulates aldosterone release Increases ADH Causes arteriolar vasoconstriction
40
How does the juxtaglomerular apparatus effect the RAAS?
Granular cells in the juxtaglomerular apparatus release renin in response to - decreased afferent blood pressure - decreased salt concentration - direct sympathetic stimulation
41
How does aldosterone increase sodium reabsorption at the distal tubule and collecting duct?
Promotes increased expression of apical sodium channels | Increases number and activity of basolateral sodium potassium ATPases
42
Abnormal activity of the RAAS causes what?
Hypertension
43
What is the cause of fluid retention in congestive heart failure?
RAAS
44
Where is atrial natriuretic peptide/hormone produced and stored?
Left atrium produces and atrial muscle cells store
45
What is atrial natriuretic peptide released?
In response to mechanical stretch of the left atrium due to increased circulating plasma volume
46
What does atrial natriuretic peptide do?
Increases excretion of sodium hence diuresis and thus reduction in circulating plasma volume Decreases activity of RAAS Arteriolar vasodilation Decreases sympathetic stimulation
47
Which two mechanisms control micturation?
Micturation reflex | Voluntary control
48
What initiates the micturation reflex?
Stretch receptors in the bladder wall
49
What is the micturation reflex?
Involuntary contraction of the detrusor and relaxation of the internal urethral sphincter
50
How can micturation be stopped by voluntary control?
Central pathways cause the relaxation of the detrusor and contraction of internal Voluntary contraction of external sphincter and levator ani
51
What is the difference between water diuresis and osmotic diuresis?
Water - increased urine flow but no increased salt excretion Osmotic - increase in urine flow is a result of primary increase in salt excretion