Renal 2 Flashcards

1
Q

where is glucose reabsorbed?

A

proximal tubule

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2
Q

glucose reabsorption occurs by –

A

secondary active transport (cotransport) coupled to sodium ion

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3
Q

where is urea reabsorbed?

A

proximal tubule then distal tubule, cortical collecting duct, and medullary collecting duct

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4
Q

urea reabsorption in the proximal tubule is by –

A

diffusion, secondary to water removal

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5
Q

As water leaves proximal tubule, urea becomes concentrated and –

A

diffuses down its concentration gradient from tubular lumen into peritubular capillaries

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6
Q

T/F: urea is just a waste product

A

false

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7
Q

urea contributes to – in medulla

A

maintaining the hyperosmotic gradient

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8
Q

Is urea freely filtered?

A

yes

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9
Q

how does urea move through kidney?

A

simple and mediated diffusion

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10
Q

approximately 50% of filtered urea is reabsorbed in the proximal tubule it follows –

A

Na+ and H2O reabsorption

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11
Q

the remaining 50% of urea that is not reabsorbed –

A

enters loop of Henle

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12
Q

urea that has accumulated in the – is secreted back into thin descending and ascending loops of Henle

A

inner medulla intersitium

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13
Q

how does urea secreted back into the loop of Henle

A

facilitated diffusion

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14
Q

– urea is reabsorbed in distal tubule and cortical collecting duct

A

30%

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15
Q

– urea is reabsorbed in medullary collecting duct

A

55%

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16
Q

– urea is excreted

A

15%

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17
Q

cycling traps urea in –

A

inner medulla

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18
Q

sources of water gain

A

water from ingestion of liquids and “solid” food and from metabolism

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19
Q

sources of water loss

A

urine, feces, sweat and insensible loss through skin, lungs and menstruating

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20
Q

sources of Na+ gain

A

ingestion of food

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21
Q

sources of Na+ loss

A

urine, feces, and sweat

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22
Q

what is the mechanism of Na+ reabsorption?

A

Na/K-ATPase pumps sodium of the cell = keeps intracellular [Na+] low –> sodium moves downhill out of lumen into tubular epithelial cells

23
Q

na+ reabsorption drives the reabsorption of the cotransported substances and the secretion of –

A

H+

24
Q

water reabsorption is a – process

A

passive

25
Q

active reabsorption of ions coupled to Na+ reabsorption decreases the osmolarity of the tubular fluid which – the water concentration

A

raises

26
Q

active reabsorption of ions coupled to Na+ reabsorption – the osmolarity in the interstitial fluid

A

raises (lower [water])

27
Q

water permeability varies from epithelial tubular segment to segment and depends on –

A

presence of aquaporins

28
Q

vasopressin stimulates insertion, by exocytosis, of a particular group of – into luminal membrane

A

aquaporin water channel

29
Q

vasopressin acts on cells of –

A

cortical and medullary collecting ducts

30
Q

effect of vasopressin

A

increase permeability of collecting ducts to water = water reabsorption

31
Q

along entire length of ascending limb of loop of Henle, – are reabsorbed into the medullary interstitial fluid

A

Na+ and Cl-

32
Q

ascending limb is relatively – to water

A

impermeable (so little water follows salt reabsorption here)

33
Q

after Na+/Cl- reabsorption, the interstitial fluid of medulla becomes – compared to fluid in ascending limb

A

hyperosmotic

34
Q

descending limb is highly permeable to –

A

water

35
Q

descending limb does not reabsorb –

A

NaCl

36
Q

– stimulates hypothalamus and ADH secretion from posterior pituitary

A

increased plasma osmolarity

37
Q

effect of ADH secretion on permeability of principle cells

A

increase water permeability

38
Q

increase water permeability of principal cells – water reabsorption

A

increases

39
Q

increased water reabsorption – urine osmolarity

A

increase

40
Q

increased water reabsorption – urine volume

A

decrease

41
Q

low plasma osmolarity – osmoreceptors in hypothalamus

A

inhibits

42
Q

low plasma osmolarity’s effect on ADH secretion

A

lowers

43
Q

SIADH secretes –

A

too much ADH

44
Q

depletes posterior pituitary gland of ADH stores

A

central diabetes insipidus

45
Q

principal cells are unresponsive to ADH

A

nephrogenic diabetes insipidus

46
Q

when is SIADH secreted?

A

head injury or inappropriate ADH secretion from lung tumor

47
Q

SIADH secretes ADH when it is –

A

not needed

48
Q

how do you treat SIADH

A

inhibitory drug on ADH

49
Q

when does central diabetes insipidus occur

A

head injury

50
Q

treatment for central diabetes insipidus

A

ADH analogues

51
Q

how is nephrogenic diabetes insipidus treated?

A

thiazide drugs

52
Q

thiazide drugs treat nephrogenic diabetes insipidus by – in early distal convoluted tubule which prevents dilution of filtrate/urine so it has more NaCl

A

inhibit Na+ reabsorption

53
Q

thiazide drugs treat nephrogenic diabetes insipidus by reducing – which reduces extracellular fluid so less water will be filtered and more reabsorbed and less water is excreted

A

GFR