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tubular function Flashcards

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1
Q

when urine volume is 23 L how much water is reabsorbed

A

87%

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2
Q

obligatory water reabsorption

A

represents 87% of water reabsorbed without adh

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3
Q

segments where water is reabsorbed

A

PCT - 65%
loop of Henle - 15%
DCT - 5%
CD - 2%

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4
Q

movement of water in proximal convoluted tube

A

water moves out passively out of tubules

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5
Q

water channels where water reabsorption takes place

A

aquaporin-1

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6
Q

tubular fluid is

A

isotonic

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7
Q

receives isotonic fluid

A

descending loop of henle

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8
Q

fluid in the descending limb becomes

A

hypertonic as water move into hypertonic interstitium

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9
Q

hypertonicity of tip of renal pyramids

A

1200-1400 mosm/L

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10
Q

impermeable to water

A

ascending loop of henle and thick ascending limb

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11
Q

ascending loop of hence is permeable to

A

sodium & chloride

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12
Q

poor permeability to solutes

A

thick ascending limb

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13
Q

as it ascends

A

tubular fluid becomes more hypotonic area is called diluting segment

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14
Q

relatively impermeable to water

A

distal convoluted tubule

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15
Q

tonicity of fluid in dct

A

remains hypotonic

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16
Q

ADH controls

A

facultative water reabsorption aka

late DCT
cortical CD
medullary CD

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17
Q

adh relationship with collecting duct

A

increase in adh permeability to water increases in collecting duct

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18
Q

adh stimulates reabsorption of about

A

12.7% of the total
8% in the late DCT cortical CD
4.7% in the medullary CD

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19
Q

receptors of adh

A

V2

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20
Q

receptor v2 of adh is located in

A

basolateral membrane of the principal cells

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21
Q

mechanism of adh

A
  • ADH binds to V2 receptors on the basolateral membrane
    of the principal cell
  • activate adenylate cyclase enzyme.
  • this increases the intracellular cAMP which activate
    protein kinase A
  • protein kinase A activate translocation of aquaporins-2
    channels from intracellular vesicles to the apical
    membrane
  • water moves passively through aquaporins-2 channels.
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22
Q

in the presence of adh

A

water moves passively
tubular fluid is isotonic
8% of filtered water is reabsorbed
urine is highly concentrated 1400 mosm/L
99.7% of water is reabsorbed
4.7% of filtered water is reabsorbed into the hypertonic medullary interstitium

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23
Q

in the absence of adh

A
  • collecting duct is relatively impermeable to water
  • tubular fluid remain hypotonic
  • large volume of diluted urine is excreted.
  • Urine volume reach 23L/day & its osmolarity is only 30
    mosm/L
  • 13% of filtered water may be excreted
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24
Q

caused by ADH deficiency

A

neurogeneic diabetes insipidus

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25
respond to treatment with ADH agonist
neurogeneic diabetes insipidus
26
failure to respond to ADH
nephrogenic diabetes insipidus
27
collecting ducts failure to respond to ADH it may be due to
the gene for V2 receptors is mutated making the | receptors un responsive or defect in aquaporin-2 channels due to mutation in its gene
28
does not respond to treatment with ADH agonist
nephrogenic diabetes insipidus
29
mechanism of urine concentration
depend on the maintenance of a gradient of osmolarity along the medullary interistitum
30
hyperosmolarity of medullary interistitum is produced by
operation of the LH as countercurrent multipliers operation of vasa recta as countercurrent exchangers urea recycling sluggish medullary blood flow
31
countercurrent multiplier system
between the descending & ascending limbs of LH of the juxtamedullary nephrons
32
function of countercurrent multiplier system
is the process of using energy to generate an osmotic gradient that enables you to reabsorb water from the tubular fluid and produce concentrated urine mechanism is due to loop of henle
33
Na+ & CL- diffuse passively into MI, so that hyperosmolarity is developed in the MI
thin ascending limb of loop of henle
34
Na+ & CL- are actively transported from the tubular lumen into the MI by 1Na+ ,1K +, 2CL- co-transporter
thick ascending limb of loop of henle
35
transporter and co transporter of actively transported Na+ & CL-
Na+ ,1K +, 2CL- co-transporter
36
countercurrent exchanger system
between the descending & ascending limb of vasa recta
37
main function of vasa recta is to
maintain MI hyperosmolarity
38
mechanism of vasa recta
it provide a trapping mechanism for Na+ & CL- in the MI | it remove excess water in the MI
39
in the descending limb of vasa recta
solutes diffuse from MI into the blood while water diffuse from blood into MI (the blood osmolarity ↑).
40
blood osmolarity increases in
descending limb of vasa recta
41
in the ascending limb of vasa recta
solutes diffuse from the blood into the MI while water diffuses from MI to blood (blood osmolarity↓)
42
blood osmolarity decreases in
ascending limb of vasa recta
43
contributes by about 40 % of hyperosmolarity of the MI
urea
44
urea moves out of the PCT
passively
45
tubules impermeable for urea
all except medullary collecting duct become highly permeable under effect of ADH
46
in the presence of ADH urea
passively diffuses from the MCDs to the MI adding to its hyperosmolarity
47
sodium is filtered into
Bowman's capsule
48
osmolarity of sodium in urine
150mmol/d
49
percentage of sodium that is reabsorbed
96-99%
50
90% of the energy consumed by kidney used for
active transport of Na+
51
Na+ reabsorption is coupled with
Reabsorption of most solutes by secondary active transport Reabsorption of water by osmosis Secretion of H+ & K+ Reabsorption of HCO3 & H+
52
reabsorbs 65% of the filtered Na+
PCT
53
reabsorption of sodium at PCT occurs actively by
Na+ -K+ pump on the basolateral membrane
54
reabsorbs 25% of the filtered Na+
loop of henle
55
does not reabsorb Na+
descending limb
56
reabsorbs Na+ passively
thin ascending limb
57
reabsorbs Na+ actively by Na+ -K+ -2CL- co-transporter.
thick ascending limb
58
called cortical diluting segment
early DCT
59
reabsorption of NaCL by Na+ CL- cotransport
early DCT
60
Na+ reabsorption is hormonally dependent according to the need of the body
late DCT and CD
61
less than 10% of filtered Na+ is reabsorbed
late DCT and CD
62
adh relationship with sodium in late dct and cd
adh increases sodium reabsorption and is associated with potassium or hydrogen
63
aldosterone
steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland. It is essential for sodium conservation in the kidney, salivary glands, sweat glands and colon.
64
aldosterone binds to
cytoplasmic receptors in the principle cell
65
regulation of sodium excretion
glomerulotubular balance | rate of tubular flow
66
regulation of sodium excretion occurs in
pct mostly bc its hormone independent
67
constant percentage of filtered Na+
65%
68
slow rate of tubular flow
increase tubular reabsorption of Na+
69
Effect of ABP on tubular reabsorption pressure natriuresis & pressure diuresis
pressure natruresis: ↑ in ABP → marked ↑ in urinary excretion of sodium & water

Physiology (4 decks)

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