Jackson 6 Flashcards

1
Q

Two modes of transport

A

transcellular –

paracellular –

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2
Q

transcellular –

A

molecules move through tubular cells

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3
Q

paracellular –

A

molecules move between tubular cells

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4
Q

osmosis – diffusion of water
solvent drag results from ——-

rate of water diffusion can be regulated by ——-

A

solutes being carried by water in paracellular transport

aquaporins

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5
Q

endocytosis and exocytosis –

A

vesicular transport

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6
Q

Sodium can be reabsorbed in all but one segment of a nephron - reabsorption occurs in the

A

proximal tubule, the ascending limbs of the loop of Henle, the distal tubule, and the collecting duct. The transport mechanism used varies.

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7
Q

proximal tubule reabsorption–

Most of the reabsorption (65%) occurs in the

A

proximal tubule. In the latter part it is favoured by an electrochemical driving force, but initially it needs the cotransporter SGLT and the Na-H antiporter. Sodium passes along an electrochemical gradient (passive transport) from the lumen into the tubular cell, together with water and chloride which also diffuse passively. Water is reabsorbed to the same degree, resulting in the concentration in the end of the proximal tubule being the same as in the beginning. In other words, the reabsorption in the proximal tubule is isosmotic.

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8
Q

thick ascending limb reabsoprtion–

Sodium is reabsorbed in the thick ascending limb of loop of Henle, by

A

Na-K-2Cl symporter and Na-H antiporter. It goes against its chemical driving force, but the high electrical driving force renders the overall electrochemical driving force positive anyway, availing some sodium to diffuse passively either the transcellular or paracellular way..

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9
Q

distal tubule reabsoprtion –

In the distal convoluted tubule sodium is transported against an

A

electrochemical gradient by sodium-chloride symporters.

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10
Q

collecting duct reabsorption -

The principal cells are the

A

sodium-transporting cells in the collecting duct system.

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11
Q

Reabsorption in the proximal tubule

1. Glucose and amino acids are rebsorbed with

A

Na+ using symporters

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12
Q

Reabsorption in the proximal tubule

  1. Active transport on
A

basal side, keeps intracellular Na+ low

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13
Q

Reabsorption in the proximal tubule

  1. Water (and solutes) move via
A

paracellular transport; keeps the osmolarity of the tubular fluid constant

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14
Q

Reabsorption in the proximal tubule

  1. Na+ reabsorption also occurs in conjunction with
A

bicarbonate reabsorption using a Na+/H+ antiporter

reabsorption is not direct……H+ secretion = HCO3- reabsorption

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15
Q

Reabsorption in the proximal tubule

CA reaction produces

A

H+ and HCO3- in tubule cell à HCO3- is transported into blood à H+ transported into tubular fluid where it recombines with a filtered HCO3-

Net effect is bicarbonate reabsorption

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16
Q

The proximal tubule also has transporters for

A

organic cations and anions so such molecules are secreted into the tubular fluid. Many drugs are organic ionic compounds. They are commonly bound to plasma proteins so they are not filtered at the glomerulus, must be secreted in order for them to be excreted in the urine.

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17
Q

Proximal tubule The transporters have low

A

specificity and can be saturated.

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18
Q

To summarize: by the end of the proximal tubule –

A

To summarize: by the end of the proximal tubule –

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19
Q

Reabsorption in the loop of Henle

In the loop of Henle,

A

25% of filtered NaCl and 15% of water is reabsorbed

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20
Q

Descending thin limb -

A

impermeable to salt, but permeable to water

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21
Q

Ascending thin limb -

A

impermeable to water, but permeable to salt.

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22
Q

Reabsorption in thin limb segments is

A

passive

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23
Q

In the ascending thick limb (ATL; see diagram at right), fluid is

A

diluted

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24
Q

ATL: Na+ K+ 2Cl- symporter in

A

apical membrane

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25
Q

ATL: Na+ K+ ATPase in

A

basolateral membrane

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26
Q

ATL: paracellular transport of monovalents and divalents NOT due to

A

solvent drag.

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27
Q

Tubular fluid becomes positive when

A

Cl- reabsorbed so cations diffuse along an electrical gradient

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28
Q

Fluid leaving loop is

A

hyposmotic, but the renal countercurrent mechanism has established an osmotic gradient required for formation of hyperosmotic urine.

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29
Q

Concentration of the tubular fluid will occur in the

A

collecting duct if antidiuretic hormone (ADH/vasopressin) is present.

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30
Q

The peritubular capillaries are permeable to

A

NaCl and water so plasma osmolarity changes as the capillaries follow the loop, but the osmolarity of the blood leaving the kidney (to veins) is normal.

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31
Q

Reabsorption in the distal tubule and collecting duct

The initial segment of the distal tubule, reabsorbs

A

~8% of filtered NaCl via a Na+ Cl- symporter in apical membrane and Na+ K+ ATPase in basolateral membrane

32
Q

reabsorption of K+, H+ and water in distal tubule is

A

variable

33
Q

Sodium reabsorption in the latter half of distal tubule and the collecting duct is

A

similar

34
Q

There are two cell types in the collecting duct and late distal tubule

A

principal cells have epithelial sodium channels (ENaC)

intercalated cells

35
Q

epithelial sodium channels (ENaC) that reabsorb

A

Na+ and secrete K+

36
Q

ENaC:

Na+ reabsorption drives

A

paracellular Cl- reabsorption

37
Q

ENaC:

K+ secreted due to

A

Na+ K+ ATPase activity in basal membrane

38
Q

intercalated cells involved with

A

acid-base balance; can also reabsorb K+

39
Q

The activity of transport mechanisms can be modified to maintain

A

blood volume. A positive or negative shift in water balance shifts extracellular volume away from euvolemia (normal volume). Hormonal and neural responses to this shift help re-establish euvolemia

40
Q

Hormonal regulation of blood volume -

A

ADH

Vasopressin or antidiuretic hormone (ADH) released from the posterior pituitary

41
Q

Vasopressin or antidiuretic hormone (ADH)
release is stimulated by
high pressure baroreceptors in aortic arch and carotid sinus response to a decrease in blood pressure

A

changes in osmolality of body fluids

42
Q

Vasopressin or antidiuretic hormone (ADH

respond to osmolality above a set point of

A

275-290 mOsm/kg H2O

43
Q

Vasopressin or antidiuretic hormone (ADH

release can also be stimulated by

A

changes in blood volume/pressure

44
Q

Vasopressin or antidiuretic hormone (ADH

low pressure baroreceptors in

A

left atrium and large pulmonary vessels respond to a decrease in blood volume

45
Q

Actions of ADH:

increases the permeability of the late distal tubule and the collecting duct to water by increasing

A

aquaporins into the apical membrane (basolateral membrane is freely permeable to water)

46
Q

Actions of ADH

also increases permeability of

A

medullary collecting duct to urea

47
Q

Actions of ADH

If ADH low (diuresis) – solutes reabsorbed in

A

distal tubule and collecting duct, but no water reabsorption; urine as dilute as 50 mOsm/kg H2 O

48
Q

Actions of ADH

If ADH high (antidiuresis) – water reabsorbed as

A

fluid passes through collecting duct; urine can be concentrated up to 1200 mOsm/kg H2O

49
Q

The renin-angiontensin-aldosterone system stimulates events that increase

A

reabsorption of sodium and water (combat volume contraction)

50
Q

renin-angiontensin-aldosterone system:

renin released in response to a drop in

A

perfusion pressure, decreased NaCl delivery to macula densa, or sympathetic input to juxtaglomerular cells

51
Q

renin-angiontensin-aldosterone system

renin converts

A

angiotensinogen to angiotensin I

52
Q

renin-angiontensin-aldosterone system

angiotensin I converted to

A

angiotensin II by angiotensin converting enzyme (ACE)

53
Q

renin-angiontensin-aldosterone system

angiotensin II has multiple effects

A

vasoconstriction

stimulate release of ADH

increase sympathetic activity

stimulate aldosterone secretion

54
Q

renin-angiontensin-aldosterone system

aldosterone from the adrenal cortex acts to increase

A

NaCl reabsorption in the distal tubule and collecting duct by increasing transport protein synthesis

55
Q

Natriuretic peptides are hormones secreted when the

A

heart dilates (during volume expansion)

56
Q

Natriuretic peptides:

Atrial natriuretic peptide

A

from the atria

57
Q

Natriuretic peptides

Brain natriuretic peptide from the

A

ventricles

58
Q

Natriuretic peptides

The effects of natriuretic peptides include

A

vasodilation of afferent arterioles

vasoconstriction of efferent arterioles

inhibition of renin (and aldosterone)

inhibition of ADH secretion

59
Q

Natriuretic peptides

Net effect is to increase the excretion of

A

NaCl and water.

60
Q

Why is potassium regulation important?

K+ is a major determinant of

A

membrane resting potential. Therefore, it can affect electrically excitable cells.

61
Q

Why is potassium regulation important?

hyperkalemia will

A

depolarize Vm

62
Q

Why is potassium regulation important?

hypokalemia will

A

hyperpolarize Vm

63
Q

Why is potassium regulation important?

changes in K+ can cause

A

cardiac arrhythmias

64
Q

How is potassium regulated?

ingested K+ is

A

fast shifted into cells – mediated by insulin, epinephrine, and aldosterone

65
Q

kidneys typically excrete ——– of ingested K+

A

90-95%

66
Q

Reabsorption and secretion of K+ in the nephron

In the glomerulus K+

A

is freely filtered.

67
Q

In the proximal tubule about 67% of filtered K+ is

A

reabsorbed, mostly by paracellular transport / solvent drag as previously discussed for Na+.

68
Q

In the thick ascending limb have reabsorption by

A

Na+K+2Cl- symporter and paracellular transport (non-solvent drag)

69
Q

In the late distal tubule and collecting duct

K+ secreted by

A

principal cells depending on ATPase activity, K+ gradient, and/or apical K+ permeability

or intercalated cells reabsorb K+ when potassium is depleted

70
Q

Factors affecting excretion of potassium include

plasma [K+] - increased K+ stimulates

A

aldosterone release, and aldosterone increases Na+ K+ ATPases in principal cells

71
Q

Factors affecting excretion of potassium include

flow rate of tubular fluid – increased flow rate increases

A

K+ secretion

local response to bending of cilia

72
Q

Factors affecting excretion of potassium include

↑ flow –> ↑ —- in collecting duct –> ↑Na+ —– –> favors ↑ —– secretion

A

Na+

reabsorption

K+

73
Q

Compare renal handling of potassium relative to plasma concentrations of potassium:

Reabsorption in proximal tubule and thick ascending limb changes

A

very little

74
Q

Compare renal handling of potassium relative to plasma concentrations of potassium

Distal tubule and cortical collecting duct will

A

reabsorb potassium when plasma concentrations are low

75
Q

Compare renal handling of potassium relative to plasma concentrations of potassium

If plasma K+ is high, secretion

A

increases in distal tubule and cortical collecting duct