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Renal > Renal Physiology V > Flashcards

Renal Physiology V Flashcards

1
Q

The most abundant intracellular cation

A

K+

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2
Q

In order to prevent the massive loss of filtered K+ in the excreted urine, what percentage of the filtered load of K+ is reabsorbed per day?

A

80-90%

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3
Q

As with Na+, the majority of filtered K+ (approximately 80%) isreabsorbed in the

A

Proximal tubule

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4
Q

Passive K+ reabsorption occurs via

A

Paracellular junctions

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5
Q

Active K+ reabsorption is mediated by

A

Basolateral K+ pumps and channels

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6
Q

Basically, a lot of K+ recycling between forming urine and interstitium occurs between the

A

Ascending and Descending limbs

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7
Q

In general, the ascending limb resorbs more K+ than the descending limb

A

Secretes

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8
Q

This results in a net K+ reabsorption along the

A

Loop

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9
Q

Supports an interstitial K+ gradient that tightly regulates K+ secretion

A

Medullary K+ trapping

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10
Q

K+ reabsorption is charge-driven and occurs by both paracellular and transcellular routes in the

A

Thick Ascending Limb (TAL)

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11
Q

Which two factors regulate K+ secretion in the CCT?

A
  1. ) Activity of principal cells

2. ) Rate of flow

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12
Q

Principal cells secrete K+ due to a favorable electrochemical gradient called a

A

Lumen-negative transepithelial voltage

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13
Q

This is established by the rapid reabsorption of Na+ from the forming urine in the CCT when compared to that of

A

Cl-

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14
Q

The apical membrane of the CCT contains

A

ROMK2 and K+-Cl- symporters

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15
Q

Basolateral K+ channels and Na+/K+ ATPases in the CCT support

A

K+ excretion

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16
Q

Mediate K+ reabsorption in the CCT through the coordinated actions of apical K+-H+ ATPases as well as basolateral Na+/K+ ATPases and K+ channels

A

Intercalated cells

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17
Q

Increased lumenal flow will result in a decrease in

A

Lumenal K+

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18
Q

In and of itself, this provides a favorable gradient for the secretion of K+ into the

A

Forming urine

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19
Q

This is apparent during certain diuretic regimens, an effect known as

A

Kaliuresis

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20
Q

An increase in lumenal Na+ will promote Na+ reabsorption by the tubule epithelium, and the translocation of positive charge induces cell membrane depolarization. This provides an electrochemical gradient that promotes

A

K+ secretion

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21
Q

The trade-off for aldosterone dependant Na+ reabsorption is K+ secretion within the

A

ASDN

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22
Q

This mechanism involves the acute effects of aldosterone on ENaC, whereas, the subsequent changes in membrane potential promote

A

K+ Secretion

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23
Q

However, during an episode of volume hyponatremia or volume reduction, what will we see?

A

GFR is reduced, thus lumenal flow is decreased. This signals an increase in Na+ reabsorption and a decrease in K+ secretion

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24
Q

What are the effects of decreased lumenal flow?

A

Increased Na+ reabsorption and decreased K+ secretion

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25
Q

What effect does SNS activity have on K+ secretion and excretion?

A

It reduces K+ excretion and secretion

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26
Q

Stimulate the uptake of K+ by extrarenal cells, which decreases plasma [K+] and thus lowers the filtered load of K+

A

Catecholamines

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27
Q

In addition, SNS activity directly down-modulates K+ secretion within the

A

Nephron

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28
Q

In order to maintain a healthy acid-base balance, each day the kidneys must:

  1. ) Reabsorb
  2. ) Generate
A
  1. ) Greater than 4500 meq of HCO3-

2. ) 70 meq HCO3-

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29
Q

The kidneys aggressively oversee normal acid-base balance in which three ways?

A
  1. ) Generation of HCO3-
  2. ) Reclamation of HCO3-
  3. ) Excretion of H+
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30
Q

In the kidneys, the majority of HCO3- reabsorption and generation occurs within the

A

Proximal tubule

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31
Q

However, some HCO3- reabsorption also occurs within the

A

Distal Nephron

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32
Q

In regards to the renal contribution to body acid-base balance, what is more important, prevention of HCO3- loss or excretion of H+?

A

Prevention of HCO3- loss

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33
Q

Under basal conditions, how much nonvolatile acid do humans accumulate due to metabolism and the excretion of OH- in feces?

A

1mmole of nonvolatile acid/Kg body weight/day

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34
Q

A simple relationship defines net urinary acid secretion. It is simply the difference bewteen HCO3- secretion in the urine and the collective loss of H+ in the forms of

A

H2PO4-, uric acid, NH4+ and/or H+ bound to creatinine

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35
Q

Keep in mind that all secreted H+ is no excreted. In fact much of the secreted H+ is used for the

A

Regeneration of HCO3- within the nephron

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36
Q

Interestingly, the pathways that facilitate the excretion of H+ in the forms of H2PO4- and NH4+ also promote

A

HCO3- generation

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37
Q

Is HCO3- within the filtrate simply just absorbed?

A

No (that is biochemically cumbersome)

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38
Q

Instead, filtered HCO3- reacts with

A

Carbonic Anhydrous Type IV (CAIV)

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39
Q

CAIV is located within the

A

Apical membrane of tubule epithelium

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40
Q

CAIV catalyzes the dissociation of HCO3- into

A

OH- and CO2

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41
Q

Rapidly and passively diffuses into the epithelium

A

CO2

42
Q

In the meantime, the lumenal OH- reactes with

A

Secreted H+ (forms H2O)

43
Q

By providing OH- to react with secreted H+, CAIV in effect maintains a favorable gradient for

A

Proton secretion

44
Q

Like CO2, H2O rapidly diffuses into the tubule epithelium. What happens once H2O is in the cells?

A

It dissociates into H+ and OH-

45
Q

Within the epithelial cytosol, the formationof HCO3- from OH- and CO2 is catalyzed by

A

CA type II (CAII)

46
Q

Then the HCO3- is rapidly reabsorbed into the interstitium and delivered back into

A

Circulation

47
Q

Is the exact molecule of HCO3- that was filtered from glomerular circulation the same molecule that is then reabsorbed?

A

No

48
Q

The mechanism by which H+ is buffered within the distal nephron utilizes secreted

A

Ammonia (NH3) and H+ to form NH4+

49
Q

As within the proximal nephron, H+ in the distal nephron is freed from H2O resulting in

A
  1. ) H+ secretion and buffering by NH3

2. ) Production of HCO3-

50
Q

Within the proximal tubule, NH3 serves to buffer secreted H+ by forming

A

NH4+

51
Q

This NH4+ travels within the forming urine until it is reabsorbed at the

A

Thick Ascending limb

52
Q

NH4+ actually competes for the K+ binding site on

A

NKCC

53
Q

Once inside the less acidic tubule epithelium, NH4+ dissociates. The NH3 then freely diffuses into the

A

Renal Medullary intersitium

54
Q

Once there, NH3 follows gradients to regions of relatively low NH3 concentrations, one of which is the

A

Proximal tubule (WHERE NH3 combines with an H+ to once again become NH4+)

55
Q

However, some of the NH3 from the tubule epithelium follows concentration gradients to the

A

Collecting tubule (where it forms NH4+ too)

56
Q

What is the fate of the NH4+ formed in the collecting tubule?

A

Remains in forming urine and is excreted (thus reducing some of the acid load)

57
Q

When faced with an alkaline load, the kidneys do not necessarily upregulate HCO3- excretion. Rather, their initial response is to

A

Lower excretion of NH4+

58
Q

Remember that each NH4+ that is resorbed also generates

A

HCO3-

59
Q

Thus, by dampening urinary acid excretion, the renal sytem in effect suppresses

A

HCO3- reclamation

60
Q

Usually involves a defect in renal HCO3- secretion and excretion due to effective volume depletion and Cl- loss

A

Maintained Metabolic alkalosis

61
Q

Which two conditions are common with metabolic alkalosis?

A

Hypokalemia and hypochloremia

62
Q

Abnormally increased K+ excretion may induce

A

Metabolic alkalosis

63
Q

Volume contraction, diminished GFR, and aldosterone excess also often accompany

A

Metabolic Alkalosis

64
Q

What three ways is H+ secretion stimulated?

A
  1. ) Aldosterone excess
  2. ) Hypovolemia
  3. ) Hypokalemia
65
Q

In general, acidosis causes a net decrease in

A

Tubular K+ secretion

66
Q

Suppresses H+ secretion within the renal tubules

A

Hyperkalemia

67
Q

Within the principal cells, aldosterone-dependant Na+ reabsorption creates a lumen negative potential which drives

A

H+ secretion

68
Q

Within the intercalated cells, aldosterone stimulates a H+- K+ exchanger, as well as a H+ ATPase, which each mediate

A

H+ Secretion

69
Q

Although there is no evidence that acid-base disturbances directly alter aldosterone secretion, hyper- and hypoaldosteronisms can affect

A

Acid-base balance

70
Q

A metabolic acidosis resulting from impaired net H+ secretion from the kidney

A

Renal Tubule Acidosis (RTA)

71
Q

There are three types of RTAs which are subcategorized into

A
  1. ) Proximal (type 2)

2. ) Distal (types 1 and 4)

72
Q

Can be autoimmune in origin or can be induced by certain drugs and toxins

A

Type 1 RTA

73
Q

During a type 1 RTA, within the kidneys there is a net reduction in H+ secretion within the

A

Collecting tubules

74
Q

Type 1 RTA involves an impairment in the secretion of

A

NH4+ and titratable acid

75
Q

Since acid secretion is suppressed, one clinical sign of Type 1 RTA is a urine pH of

A

Greater than 5.3 in adults and greater than 5.6 in children

76
Q

A normal anion gap (hyperchloremic) acidosis

-believed to be due to impaired H+ ATPase and Cl-/HCO3- exchanger

A

Type 1 RTA

77
Q

It is of clinical importance to note that chronic acidemia results in the release of

A

CaPO4 from bone

78
Q

Therefore, other signs of a type 1 RTA include

A

Hypercalciuria, hyperphosphaturia, and nephrolithiasis

79
Q

High pH in the forming urine is conductive to forming Ca2+ precipitates and thus

A

Nephrolithiasis (Kidney stones)

80
Q

Type 1 RTA can also be accompanied by either

A

Hyp- or hyperkalemia

81
Q

A proximal RTA that is usually accompanied by the urinary loss of not only HCO3-, but also glucose, amino acids, and phosphate

A

Type 2 RTA

82
Q

Interestingly, during a type 2 RTA, what do we see with HCO3- reabsorption impairment?

A

Proximal tubule reabsorption is impaired but distal tubule reabsorption is in tact

83
Q

However, the HCO3- resorptive capacity of the distal tubule is much less than that of the proximal tubule; therefore, this becomes the limiting factor for maintaining

A

Plasma HCO3-

84
Q

Generally, in a type 2 RTA, plasma HCO3- achieves a new steady state t around

A

14-20 meq/L

85
Q

Defects in the Na+/ H+ exchanger, Na+/K+ ATPase, and/or carbonic anhydrase are all implicated as
mechanisms controlling

-all assist with HCO3- reabsorption from the proximal tubule

A

Type 2 RTA

86
Q

In a type 2 RTA, disruptions in proximal HCO3- transport set in motion electrochemical cascades which impair the reabsorption of

A

K+ and NaCl

87
Q

This collectively leads to

A

Na+ wasting and hyperaldosteronism

88
Q

Hyperaldosteronism exacerbates the hypokalemia that is associated with

A

Type 2 RTA

89
Q

What are two other common things seen in a type 2 RTA?

A

Phosphate wasting and vitamin D deficiency

90
Q

A relatively mild form of hyperchloremic metabolic acidosis that is due to aldosterone deficiency or resistance

A

Type 4 RTA

91
Q

What are the 3 hallmarks of patients with type 4 RTAs?

A

1/) Volume depleted

  1. ) hyperkalemic
  2. ) Plasma HCO3- of no less than 15 meq/L
92
Q

Type 4 RTAs are caused by the lowered level of tubule

A

H+-ATPase activity

93
Q

The hyperkalemic state associated with a type 4 RTA impedes NH4+ production and excretion, which blocks

A

NH4+ recycling and NH3 secretion in distal nephron

94
Q

Since the excretion of NH4+ and titratable acid is disrupted in a type 4 RTA, urine is not acidified below approximately

A

pH 5.5

-results in positive acid balance

95
Q

UAG is only useful for helping to diagnose

A

Normal AG metabolic acidosis

96
Q

Assuming the kidneys are healthy and the metabolic acidosis is being driven by diarrhea, when pH drops, the kidneys will excrete H+, most of which is in the form of NH4+. This is the proccess of

A

Distal acidification

97
Q

In order to maintain electroneutrlity, what is excreted with the NH4+?

A

Cl-

98
Q

The nitrogenous end-product of protein (amino acid) metabolism

-generated from NH4+

A

Urea

99
Q

For urea, is the amount reabsorbed greater than or less than that secreted?

A

Greater reabsorption than secretion

100
Q

However, very little of the filtered load of urea is returned to

A

Systemic circulation

Renal (10 decks)

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