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Physiology > tubular function > Flashcards

tubular function Flashcards

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
Q

respond to treatment with ADH agonist

A

neurogeneic diabetes insipidus

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26
Q

failure to respond to ADH

A

nephrogenic diabetes insipidus

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27
Q

collecting ducts failure to respond to ADH it may be due to

A

the gene for V2 receptors is mutated making the

receptors un responsive or defect in aquaporin-2 channels due to mutation in its gene

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28
Q

does not respond to treatment with ADH agonist

A

nephrogenic diabetes insipidus

29
Q

mechanism of urine concentration

A

depend on the maintenance of a gradient of osmolarity along the medullary interistitum

30
Q

hyperosmolarity of medullary interistitum is produced by

A

operation of the LH as countercurrent multipliers
operation of vasa recta as countercurrent exchangers
urea recycling
sluggish medullary blood flow

31
Q

countercurrent multiplier system

A

between the descending & ascending limbs of LH of the juxtamedullary nephrons

32
Q

function of countercurrent multiplier system

A

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
Q

Na+ & CL- diffuse passively into MI, so that hyperosmolarity is developed in the MI

A

thin ascending limb of loop of henle

34
Q

Na+ & CL- are actively transported from the tubular lumen into the MI by 1Na+ ,1K +, 2CL- co-transporter

A

thick ascending limb of loop of henle

35
Q

transporter and co transporter of actively transported Na+ & CL-

A

Na+ ,1K +, 2CL- co-transporter

36
Q

countercurrent exchanger system

A

between the descending & ascending limb of vasa recta

37
Q

main function of vasa recta is to

A

maintain MI hyperosmolarity

38
Q

mechanism of vasa recta

A

it provide a trapping mechanism for Na+ & CL- in the MI

it remove excess water in the MI

39
Q

in the descending limb of vasa recta

A

solutes diffuse from MI into the blood while water diffuse from blood into MI (the blood osmolarity ↑).

40
Q

blood osmolarity increases in

A

descending limb of vasa recta

41
Q

in the ascending limb of vasa recta

A

solutes diffuse from the blood into the MI while water diffuses from MI to blood (blood osmolarity↓)

42
Q

blood osmolarity decreases in

A

ascending limb of vasa recta

43
Q

contributes by about 40 % of hyperosmolarity of the MI

A

urea

44
Q

urea moves out of the PCT

A

passively

45
Q

tubules impermeable for urea

A

all except medullary collecting duct become highly permeable under effect of ADH

46
Q

in the presence of ADH urea

A

passively diffuses from the MCDs to the MI adding to its hyperosmolarity

47
Q

sodium is filtered into

A

Bowman’s capsule

48
Q

osmolarity of sodium in urine

A

150mmol/d

49
Q

percentage of sodium that is reabsorbed

A

96-99%

50
Q

90% of the energy consumed by kidney used for

A

active transport of Na+

51
Q

Na+ reabsorption is coupled with

A

Reabsorption of most solutes by secondary active transport
Reabsorption of water by osmosis
Secretion of H+ & K+
Reabsorption of HCO3 & H+

52
Q

reabsorbs 65% of the filtered Na+

A

PCT

53
Q

reabsorption of sodium at PCT occurs actively by

A

Na+ -K+ pump on the basolateral membrane

54
Q

reabsorbs 25% of the filtered Na+

A

loop of henle

55
Q

does not reabsorb Na+

A

descending limb

56
Q

reabsorbs Na+ passively

A

thin ascending limb

57
Q

reabsorbs Na+ actively by Na+ -K+ -2CL- co-transporter.

A

thick ascending limb

58
Q

called cortical diluting segment

A

early DCT

59
Q

reabsorption of NaCL by Na+ CL- cotransport

A

early DCT

60
Q

Na+ reabsorption is hormonally dependent according to the need of the body

A

late DCT and CD

61
Q

less than 10% of filtered Na+ is reabsorbed

A

late DCT and CD

62
Q

adh relationship with sodium in late dct and cd

A

adh increases sodium reabsorption and is associated with potassium or hydrogen

63
Q

aldosterone

A

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
Q

aldosterone binds to

A

cytoplasmic receptors in the principle cell

65
Q

regulation of sodium excretion

A

glomerulotubular balance

rate of tubular flow

66
Q

regulation of sodium excretion occurs in

A

pct mostly bc its hormone independent

67
Q

constant percentage of filtered Na+

A

65%

68
Q

slow rate of tubular flow

A

increase tubular reabsorption of Na+

69
Q

Effect of ABP on tubular reabsorption pressure natriuresis & pressure diuresis

A

pressure natruresis: ↑ in ABP → marked ↑ in urinary excretion of sodium & water

Physiology (4 decks)

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