Renal II Flashcards

1
Q

What is the normal pH range of body fluids?

A

7.35-7.45

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2
Q

What pH values are not life sustainable?

A

< 6.8

> 7.8

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3
Q

T/F: Fluids are at greater risk for becoming too basic than too acidic.

A

False

Body takes in and produces more acid

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4
Q

How is the majority of volatile acid excreted?

A

Exhalation

Ex. CO2

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5
Q

How are nonvolatile acids excreted?

A

Urine

Must be neutralized with HCO3

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6
Q

T/F: Volatile acids are regulated in the renal system.

A

False

Nonvolatile

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7
Q

How does the kidney neutralize the acids produced by the body?

A

Reabsorbes all of the filtered bicarbonate and produces new bicarbonate

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8
Q

______ allow us to keep urine pH at 4.4, yet still excrete the necessary amount of acids.

A

Buffers

Bind to excess H+

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9
Q

What molecules does the renal system use as buffers?

A
  1. Bicarbonate
  2. Phosphate
  3. Ammonium
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10
Q

Which buffer is used first?

A

Phosphate

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11
Q

Of the three forms of excreted acids, which are titratable?

A

H+ and HPO4

NH4 is NOT titratable

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12
Q

T/F: Net acid excretion should remove all volatile acid from the body.

A

False

Nonvolatile

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13
Q

The kidney regulates acidity of the urine by regulating ______ reabsorption.

A

bicarbonate

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14
Q

How can the renal system decrease the body pH?

A

Not reabsorbing all HCO3

Produces basic urine and acidic body fluids

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15
Q

What will be the result of the renal system resorbing all HCO3?

A

No effect on body pH and the urine will have a neutral pH

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16
Q

How can the renal system increase the bodies pH?

Typical state of the body

A

Reabsorb all HCO3 and produce more

Produces acidic urine and makes body fluids basic

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17
Q

Why does the urine become more acidic when HCO3 is resorbed?

A

Reaction results in H+ being secreted

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18
Q

T/F: 80% of HCO3 is resorbed in the proximal tubule.

A

True

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19
Q

What produces H+ and HCO3?

A

Carbonic anhydrase in tubular epithelium

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20
Q

Which cells in the collecting duct produce H+ and HCO3?

A

Intercalated cells

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21
Q

Differentiate between mechanisms of H+ secretion in the proximal tubule and the collecting duct.

A

Tubules have an Na+/H+ anti porter and ducts do not

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22
Q

How is HCO3 reabsorbed?

A

Transported across basolateral membrane

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23
Q

T/F: There are intercalated cells that reverse the process to reabsorb H+ and secrete HCO3.

A

True

Activity very low

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24
Q

T/F: Cells in the proximal tubule can alter CA activity based on intracellular pH.

A

True

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25
Q

If the body is acidic ______ will be used as an additional buffer to increase H+ excretion.

A

phosphate

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26
Q

After HCO3 has been reabsorbed and phosphate has been depleted, the kidney will produce _______ to increase H+ excretion.

A

Ammonium

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27
Q

Why can’t ammonium enter the body?

A

Will convert to urea and produce H+

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28
Q

Where is ammonium produced?

A

Proximal tubules via glutamine metabolism

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29
Q

What are the two products of glutamine metabolism?

A

Ammonium: goes into tubular fluid

Bicarbonate: goes into blood

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30
Q

What process allows for more ammonium to be added to the urine?

A

Diffusion trapping between loop and collecting duct

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31
Q

Respiratory acidosis is related to ___ build up.

A

CO2

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32
Q

What are the renal responses to respiratory acidosis and alkalosis?

A

Acidosis: produce HCO3

Alkalosis: excrete HCO3

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33
Q

What is metabolic acidosis?

A

Low pH due to low HCO3

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34
Q

Is there a respiratory response to metabolic acidosis/alkalosis?

A

Acidosis: hyperventilate
Alkalosis: hypoventilate

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35
Q

How much of ECF calcium can be filtered at the glomerulus?

A

A little over half

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36
Q

Where is the majority of calcium?

A

Bone

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37
Q

_______ can lead to increased excitability of neural and muscle tissue (tetany).

A

Hypocalcemia

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38
Q

________ can lead to cardiac arrhythmia and disorientation (possibly death).

A

Hypercalcemia

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39
Q

T/F: A decrease in plasma pH will increase the amount of free calcium.

A

True

Alkalosis can lead to hypocalcemia

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40
Q

Where are calcium sensing receptors found?

A
  1. Parathyroid gland
  2. Thyroid parafollicular cells
  3. Proximal tubule
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41
Q

What are the three hormones that help regulate calcium?

A
  1. Parathyroid hormone
  2. Calcitriol (1,25 dihydroxyvitamin D)
  3. Calcitonin
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42
Q

PTH is released during ________ and stimulates ________ production.

A

hypocalcemia; calcitriol

43
Q

Which hormone is released in response to hypercalcemia?

A

Calcitonin

Increases bone deposition

44
Q

How is calcium reabsorbed in the proximal tubule?

A

paracellular transport (solvent drag)

45
Q

How is calcium reabsorbed in the thick ascending limb?

A

Transcellular and paracellular (not solvent drag)

46
Q

Transcellular reabsorption of Ca in the distal tubule is regulated by ____.

A

PTH

47
Q

What is diuresis?

A

Excess urine output

48
Q

T/F: Diuretics decrease urine output due to actions on the kidney.

A

False

Increase

49
Q

T/F: Diuretics inhibit water reabsorption.

A

True

50
Q

What are two reasons for taking diuretics?

A
  1. Congestive heart failure

2. Hypertension

51
Q

What parts of the nephron do osmotic diuretics work on?

A

Water permeable segments - PT and descending loop of Henle

52
Q

Where is the major site of action for CA inhibitors?

A

Proximal tubule

Reduce H20 reabsorption by reducing Na+ reabsorption

53
Q

Where do loop diuretics act in the nephron?

A

TAL - inhibit Na+K+2Cl- symporter

54
Q

Where do thiazides act in the nephron?

A

Early distal tubule - block Na+Cl- symporter

55
Q

What are the two classes of K+ sparing diuretics and where do they act?

A
  1. Aldosterone antagonists
  2. ENAC blockers

Late distal tubule/collecting duct

56
Q

How do K+ sparing diuretics work?

A

Inhibit Na+ reabsorption and K+ secretion

Spare K+

57
Q

_______ work by acting as an ADH antagonist.

A

Aquaretics

58
Q

T/F: Osmotic diuretics increase osmotic pressure in tubular fluid.

A

True

59
Q

What are two examples of osmotic diuretics?

A

Mannitol and glucose

60
Q

What is a secondary effect of osmotic diuretics?

A

As H2O reabsorption decreases so does Ca reabsorption via less solvent drag

61
Q

How do osmotic diuretics gain access to the tubules?

A

Glomerular filtration

62
Q

T/F: CA inhibitors will reduce amount of H+ available inside the epithelial cell.

A

True

CA produces H+ to be used with H+/Na+ symporter. If Na+ can not get in the epithelial cell than it can not be pushed out into the blood

63
Q

What is a common CA inhibitor?

A

Acetazolamide

64
Q

T/F: CA inhibitors gain access to the tubule via glomerular filtration.

A

False

Secretion

65
Q

T/F: CA inhibitors have the strongest diuretic effect.

A

False

Relatively weak

66
Q

T/F: Loop diuretics have the strongest diuretic effect.

A

True

67
Q

What is an example of a loop diuretic?

A

Furosemide

68
Q

Loop diuretics gain access to the tubules via _______.

A

secretion

69
Q

T/F: When loop diuretics are used, the urine that is excreted is much more dilute than the urine entering the collecting duct.

A

True

70
Q

What is an example of a thiazide diuretic?

A

Chlorothiazide

71
Q

Thiazides enter the tubules via ______.

A

secretion

72
Q

T/F: Thiazides block water reabsorption in the collecting duct.

A

False

Works in early distal tubule

73
Q

Aldosterone antagonists (spironolactone) block aldosterone receptors in the ________ cells.

A

principal

74
Q

T/F: Cortical nephrons are more superficial than juxtamedullary nephrons.

A

True

75
Q

T/F: ENaC blockers (amiloride) must be in the principal cell to act.

A

False

Can act on apical membrane from in the tubular fluid

76
Q

Tolvaptan is an example of an _________.

A

Aquaretic

77
Q

T/F: Aquaretics eliminate water without the loss of solutes.

A

True

78
Q

What is the diuretic braking phenomenon?

A

Continued use of diuretics makes them less effective via compensatory mechanisms

79
Q

How is the sympathetic nervous system involved in diuretic braking?

A

Reduced BP from diuretics -> increased symp activity -> decrease GFR -> increase proximal tubule reabsorption and increased renin

80
Q

How does the increase in renin during diuretic braking counteract the diuretic?

A

Increased renin -> increased angiotensin II -> increased aldosterone -> decreased Na excretion

81
Q

T/F: ADH release is stimulated during diuretic braking and inhibits the excretion of water.

A

True

82
Q

K+ excretion is a secondary effect of all but what type of diuretics?

A

K+ sparing diuretics

83
Q

________ lead to metabolic acidosis.

A

CA inhibitors and K+ sparing diuretics

84
Q

__________ lead to metabolic alkalosis.

A

Loop and thiazide diuretics

85
Q

All diuretics except for ________ alter calcium excretion.

A

K+ sparing diuretics

86
Q

Osmotic and CA inhibitors act in the _________ and ________ reabsorption of calcium in that area.

A

proximal tubule; reduce

87
Q

Loop diuretics increase calcium excretion by altering _________ transport of Ca.

A

paracellular

88
Q

_________ stimulate reabsorption of calcium in the distal tubule.

A

Thiazide diuretics

89
Q

T/F: In a dialyzer, the blood and fluid move in countercurrent directions.

A

True

90
Q

Which molecules diffuse from the blood to the dialysis fluid?

A

Urea, potassium, and phosphate

91
Q

Which molecule diffuses into the blood from the dialysis fluid?

A

Bicarbonate

92
Q

T/F: NaCl concentrations in dialysis fluid are similar to that in blood.

A

True

93
Q

What is the preferred way to access blood for long-term dialysis?

A

AV fistula

94
Q

What are some risks of accessing blood through a catheter for dialysis?

A

scarring, vessel narrowing and occlusion

95
Q

A _______ uses an artificial vessel to join an artery and vein.

A

AV graft

96
Q

When would you use an AV graft?

A

Vascular problems prevent use of a fistula

97
Q

What are some long-term consequences of dialysis?

A

Sepsis, endocarditis, and osteomyelitis

Amyloid deposits in joints

98
Q

Patients with chronic renal failure are almost always diagnosed with _______.

A

anemia

Kidneys stop producing erythropoietin (EPO)

99
Q

Where in the kidney is EPO produced?

A

Interstitial fibroblasts in renal cortex

100
Q

EPO production is stimulated when _____ is low.

A

P(O2)

101
Q

Which transcription factors regulate EPO synthesis?

A

HIF-1 and HIF-2

102
Q

Patients with anemia are often treated with __________ to stimulate erythropoiesis.

A

Procrit

103
Q

What are the side effects of Procrit?

A

Flu-like symptoms, headaches, high BP and CV problems