Med Term 3 > Urinary 4 > Flashcards

Urinary 4 Flashcards

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1
Q

If the osmolarity of the ECF is lower than that of the ICF then the ECF is what and water moves where?

A

hypotonic - water moves into the cells and cell will swell

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2
Q

If the osmolarity of the ECF is higher than that of the ICF then the ECF is what and water moves where?

A

hypertonic - water moves out of the cells and cell will shrink

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3
Q

What controls the release of ADH/AVP?

A

osmoreceptors in the hypothalamus

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4
Q

What does vasopressin do?

A

stimulates the exocytic insertion of AQP2 channels into the luminal membranes of the principal cells of the connecting tubule and collecting duct

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5
Q

What happens when AVP reaches the principal cells?

A

AQP2 channels are inserted into the apical membranes of the cuboidal epithelium in the connecting tubules

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6
Q

In the collecting duct, water can enter and exit via which channels?

A

enter: AQP2

exit: AQP3 and AQP4 (constitutively-expressed in the basolateral membrane)

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7
Q

With the removal of vasopressin, what happens to the AQP2 channel?

A

it is retrieved from the apical membrane by endocytosis

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8
Q

Why is the basolateral membrane of the collecting duct always permeable to water?

A

because it contains AQP3 and AQP4

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9
Q

Where are the hypothalamic osmoreceptors located?

A

supraoptic nuclei

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10
Q

What detects increase in ECF osmolarity to induce thirst?

A
  • hypothalamic osmoreceptors in the supraoptic nuclei (SON)
  • organum vasculosum of the lamina terminalis of the hypothalamus (OVLT)
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11
Q

Hypothalamic receptors are stimulated by what?

A

hypertonic plasma - which makes the hypothalamic osmoreceptors shrink

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12
Q

What stimulates thirst to induce a behavioural response to drink and replace water?

A

osmoreceptors

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13
Q

How is osmolarity primarily regulated?

A

by adjusting output (urine production)

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14
Q

Vasopressin is released in response to what?

A

high blood osmolality

low blood volume

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15
Q

Which cells synthesise and secrete AVP?

A

neurosecretory cells

(AVP is produced by the neurons located in the supraoptic and paraventricular nuclei of the hypothalamus)

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16
Q

What does AVP/ADH do?

A

regulates the permeability of the collecting duct to water

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17
Q

Production of dilute urine involves what?

Where does this occur?

A

the active removal of solute from tubular fluid in a section of the nephron that is impermeable to water

in the thick ascending limb of the Loop of Henle

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18
Q

The conservation of water by reabsorption requires the existence of what?

A

an osmotic gradient

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19
Q

What happens to the osmolarity of the interstitial fluid from the outer to the inner renal medulla?

A

increases progressively - reaching 1200mosm/l in the inner renal medulla

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20
Q

What ultimately allows vasopressin-regulated reabsorption of water from the collecting duct to occur, which allows concentration of urine?

A

hyperosmotic environment in the renal medulla

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21
Q

What is required to create hypertonicity in the renal medulla?

A

accumulation of solutes in the interstitial fluid of the renal medulla

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22
Q

The hypertonicity in the renal medulla is achieved by which mechanisms?

A
  1. countercurrent multiplication in the loop of henle
  2. accumulation of urea in the renal medulla interstitium by recycling urea from the collecting duct
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23
Q

Why is the thick ascending limb of the loop of Henle called the “diluting segment,” and what transport mechanism does it use?

A

impermeable to water, water cannot follow solutes

actively reabsorbs Na+, K+ and 2Cl- via the Na+/K+/2Cl- co transporter = removes solutes without water -> tubular fluid becomes dilute

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24
Q

The descending limb of the loop of henle is permeable to water via what channels?

A

AQP1 channels

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25
Which segment of the nephron is impermeable to water but actively reabsorbs Na⁺, K⁺, and 2Cl⁻?
thick ascending limb of the loop of Henle - uses the Na+/K+/2Cl- cotransporter = creates a dilute tubular fluid and concentrating the medullary interstitium
26
What is the mechanism of action of loop diuretics? Give an example.
inhibit the Na+/K+/2Cl- cotransporter in the thick ascending limb - prevents solute reabsorption furosemide
27
How do loop diuretics affect the medullary interstitium and urine concentration?
blocking solute reabsorption reduces the medullary osmotic gradient -> collecting ducts cannot reabsorb water efficiently because the gradient is lost -> copious, dilute urine is produced (medullary interstitium becomes isosmotic - water cannot be reabsorbed even in the presence of ADH)
28
29
What happens to NaCl in the ascending limb? What is the result of this?
it is transported out of the ascending limb by the NaK2Cl co-transporter gain of NaCl in the medullary interstitium raises the osmotic pressure in the interstitium (and decreases osmotic pressure in the ascending limb)
30
The NaK2Cl pump re-establishes a gradient of how many mosm/l between the ascending limb and the interstitium?
200 mOsm/l
31
What is the name of the only blood vessels in the renal medulla?
vasa recta
32
What is the purpose of the Vasa Recta? What happens in the descending and ascending limb of the Vasa Recta?
to shunt water from the descending limb to the ascending limb to prevent the dilution of the medullary concentration gradient established by the loop of Henle (blood in the vasa recta removes water leaving the loop of Henle) descending: water leaves and solutes like NaCl and urea enter ascending: solutes move out and water moves in
33
The Vasa Recta acts as a what?
countercurrent exchanger
34
What accounts for approx 50% of the inner medulla tonicity?
urea
35
Beyond the proximal tubule, how does the nephron handle urea permeability?
the nephron is largely impermeable to urea until the inner medullary collecting duct (IMCD)
36
How does urea concentration change along the nephron?
it increases along the nephron because water is reabsorbed but urea is "trapped" until the IMCD
37
Which hormone regulates urea absorption in the IMCD?
ADH/AVP
38
Which transporters does ADH stimulate in the IMCD to move urea?
urea transporters UT-A1 and UT-A3
39
How does urea move out of the IMCD into the medulla?
passive diffusion through UT-A1 and UT-A3
40
Why is urea reabsorption into the medulla important?
strengthens the medullary conc gradient - allows more water reabsorption and concentrated urine formation
41
What effect does a low-protein diet have on renal urea handling?
reduces urea synthesis -> less medullary tonicity -> impaired ability to concentrate urine
42
Where is urea passively reabsorbed in the nephron? What percentage is reabsorbed?
45% - PCT
43
Urea recycling increases under the influence of what? What is this triggered by?
vasopressin (AVP/ADH) increase in plasma osmolarity (to reabsorb lots of water against steep gradients, kidney needs an extra strong osmotic "pull" - comes from urea as well as NaCl) (when plasma osmolarity rises, kidney needs the medullary interstitium to be much saltier than plasma - urea recycling is what makes this possible)
44
Which hormone is responsible for central control of urine volume in humans?
AVP
45
What is desmopressin?
synthetic analogue of vasopressin / AVP
46
After taking desmopressin, there is no change in the patient's urine production. a. Explain these results. b. Diagnose this patient as either a central DI patient or a nephrogenic DI patient.
a. vasopressin (or desmopressin) causes concentration of urine b. nephrogenic DI - central DI pts produce no AVP and if given AVP their symptoms correct nephrogenic DI patients do not produce AVP and their kidneys also do not respond to it, giving standard dose of vasopressin analogue has no effect
47
How frequently do adult humans normally pass urine each day? Under normal conditions, approximately what volume of urine would you expect a healthy adult to pass each day?
approx 4-6 times a day between 0.7l to 3l of urine each day
48
What is the medical term used to describe the passing of excessively large volumes of urine?
polyuria
49
1. What will be the effect of this on his plasma osmolarity and why? 2. What response limits this effect, and how is it stimulated?
1. it will increase because he is losing more water than solute in his urine 2. osmoreceptors in the hypothalamus detect increased osmolarity and stimulate thirst - increasing drinking
50
Normally, an increase in plasma osmolarity would lead the body to reabsorb more water (from the nephrons into the blood), thereby leading to the production of small volumes of concentrated urine. What is the most likely explanation for this not happening in this case?
most likely that the head trauma inflicted on the man has caused damaged to the hypothalamus or posterior pituitary gland - which has resulted in an inability to secrete AVP / vasopressin
51
What will be different about the cells lining the collecting duct in this patient compared to a normal patient with increased plasma osmolarity?
they will be impermeable to water because there is no vasopressin to stimulate the formation of aquaporins and their insertion into the cell membranes
52
In a normal patient what a) causes and b) permits water to leave the filtrate in the medullary collecting duct?
a) osmotic gradient between the filtrate and hypertonic renal medulla b) water permeability of collecting duct cells because of membrane aquaporins (by AVP)
53
How are the conditions that cause water to leave the collecting duct established?
counter-current exchange in the loop of Henle urea recycling between the collecting duct and loop of henle generates a hypertonic renal medulla
54
What is the: a) Minimum urine osmolality in humans. b) The maximum urine osmolality in humas? c. Adults must excrete 600 mOsm of waste products in the urine every day. Calculate the minimum volume of urine an adult human can produce in one day in ml.
a. 50 mOsm/kg b. 1400 mOsm/kg c. max = 1400 - 600 / 1400 = 0.43kg = 0.43L - 0.43 x 1000 = 430 ml
55
What type of drug would you use to treat this patient?
vasopressin mimetic
56
List 2 other possible effects of damage to structures around the hypothalamus.
- disorders of anterior pituitary secretion - visual disturbances due to damage to optic nerve and optic chiasm
57
Describe how sweat glands produce sweat from ECF.
primary secretion isotonic with plasma is secreted in acini of sweat glands solute Na+ is removed from this secretion as it passes through conducting portion of the sweat gland (i.e sweat ducts) to the surface of the skin to yield a hypotonic solution that evaporates from the body surface
58
What happens to the composition of sweat as the rate or production increases?
sweat will progressively contain more sodium ions as rate of reabsorption of sodium ions will always remain the same - hence there will be less of an opportunity to remove salt from the sweat at higher flow rates
59
As the rate of perspiration increases, what will happens to the following: a. plasma osmolarity b. plasma sodium ion concentration c. amount of sodium in the ECF and why
sweat always hypotonic to plasma - therefore, more water than salt is lost a. increase b. increase c. decrease
60
What will happen to the following: a. The urine osmolarity b. Water intake if water is available to drink
a. urine will become concentrated as vasopressin is secreted in response to the increased osmolarity of plasma b. thirst will be stimulated, more water will be consumed to restore plasma osmolarity
61
After a prolonged period of sweating, what will have happened to her plasma volume, even if there was plenty of water to drink, and why?
during sweating, you lose water and sodium in sweat - sweat is hypotonic - prolonged sweating = more Na+ is lost relative to water if she keeps drinking water, she will replace water but not lost sodium, sodium conc in ECF will fall = hyponatreamia risk
62
1. When her water ran out, what would have happened to her circulating plasma volume and why? 2. What effect would the lowering of plasma volume have had on her cardiac output, and why? How will this effect arterial BP?
1. plasma volume will fall even more as water will not be replaced, osmolarity will continue to rise as more water is lost than sodium 2. it would fall as the venous pressure is reduced, and by Starling's law - cardiac output will fall, arterial BP will also fall
63
1. What will have likely happened to he TPR, and what impact will this have on her arterial blood pressure? 2. What will eventually happen to her circulation if she carries on walking in a dehydrated state?
1. while peripheral vasodilation necessary to lose heat would have lowered her BP, TPR will likely be increased to compensate for her low BP - overall effect of this on her BP would be to increase it 2. hypovolaemic shock due to inadequate perfusion of key organs
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