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Physio II (mine) > Renal II > Flashcards

Renal II Flashcards

1
Q

Do we lose more K or Na? And why?

A

K because the kidneys has to exchange K to reabsorbed Na and then try to recapture the K

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2
Q

Reabsorption and secretion of urea helps with what?

A

Reabsorb or lose water respectively

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3
Q

What 2 molecules are reabsorbed the least?

A

K and urea

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4
Q

What is the equation for excretion?

A

Filtration-reabsorption+secretion

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5
Q

Glomerulotubular balance (GTB)

A

Ability of each successive segment of the proximal tubule to reabsorb a constant fraction of glomerular filtrate and solutes delivered to it

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6
Q

Glomerulotubular balance prevents large swings in what when GFR is high?

A

urine volume and washout of the ECFV

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7
Q

Nephron absorbs more of what, relative or absolute amount of filtrate?

A

Absolute

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8
Q

GTB happens because a higher GFR meaning a what pressure?

A

Higher peritubular capillary oncotic pressure

GTB=absorb=onconic pressure

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9
Q

Proximal tubule has what 3 things occurring there?

A
  • Na/K ATPase
  • Na/H exchanger (NHE): Na/HCO3 co-transporter
  • Na/glucose transporters (SGLT)
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10
Q

Toxins and drugs are secreted where?

A

Proximal tubule

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11
Q

ANGII stimulates what in the proximal tubule?

A
  • Na+ / H+ ATPase
  • Na+ / HCO3- co-transporter
  • Na+ / K+ exchanger
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12
Q

Carbonic anyhydrase inhibitors cause what in proximal tubule?

A

Na and bicarbonate bind in lumen and some is excreted and lose K

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13
Q

How powerful is carbonic anyhydrase inhibitors in proximal tubule?

A

Moderately

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14
Q

Na/H exchanger (NHE): Na/HCO3 co transporter does what in proximal tubule?

A

Secretes 80% H and reabsorbs 80% bicarb via CA

CA= Carbonic Acid

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15
Q

SGLT2 inhibitors do what for SGLT in proximal tubule?

A

Allows kidneys to lower excessive blood glucose by promoting glucosuria

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16
Q

Tubular fluid/plasma concentration =1 means?

A

substance in tubular fluid = substance in plasma

-reabsorption of water has occurred at same rate as the substance in PT

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17
Q

Examples of Tubular fluid/plasma concentration =1 (2)

A
  • Na+
  • Cl-
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18
Q

Tubular fluid/plasma concentration <1 means?

A

More substance reabsorbed than water in the PT

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19
Q

Examples of Tubular fluid/plasma concentration <1 (3)

A
  • Amino Acids
  • Glucose
  • HCO3-
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20
Q

Tubular fluid/plasma concentration >1 means?

A

Substance was not reabsorbed more than water, and/or substance was secretion into the PT

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21
Q

Examples of Tubular fluid/plasma concentration >1 (2)

A
  • Urea
  • Creatinine
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22
Q

What is the point at which increases in concentration of a substance do not result in an increase in movement of a substance across a cell membrane (in kidney this means it will not be reabsorbed and thus excreted)

A

Transport maximum (Tm or Tmax)

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23
Q

What limits how fast things can be reabsorbed?

A

Tmax

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24
Q

Tmax is determined by what?

A

Saturation of a limited number of transporters

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25
Q

What is filtered load equation?

A

P[solute ] x GFR

P=plasma / Solute: Glucose or other solutes

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26
Q

Do kidneys normally regulate plasma glucose?

A

No

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27
Q

Both limbs of LOH work together to create a concentrated medullary interstitium of?

A

600-1200 mOsm

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28
Q

Predominant osmoles of LOH?

A

NaCl and urea

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29
Q

Descending limb of LOH is concentrated or diluted segment?

A

Concentrated

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30
Q

Descending limb of LOH is permeable to what?

A

H20

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31
Q

Ascending limb LOH is concentrated or diluted segment?

A

Diluting

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32
Q

Ascending limb of LOH is permeable to what?

A

NaCl

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33
Q

Can urea enter both ascending and descending LOH?

A

Yes

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34
Q

What are the steps of counter current multiplication (6)

A
  1. Salt is pumped out of ascending limb
  2. Increase in interstitial osmolarity
  3. Water leaves the descending limb
  4. Increased osmolarity of filtrate in descending limb of the LOH
  5. Increased osmolarity of filtrate in ascending limb of LOH
  6. Start back at #1
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35
Q

Where in the nephron is the counter current exchanger?

A

Vasa recta

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36
Q

What does the counter current exchanger create?

A

Large osmotic gradient in the nephron and interstitial fluid; water and salts are reabsorbed from the interstitial fluid into the vasa recta and brought back to the body because of this gradient

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37
Q

2 major transporters in thick ascending limb LOH?

A
  1. Na/K/Cl (NKCC2)- ~25% into cell to be reabsorbed
  2. Na/H anti porter (NHE)- 10% H secreted and HCO3 reabsorbed
38
Q

What 2 things affect NKCC2?

A
  1. ADH
  2. Loop diuretics
39
Q

How does ADH affect NKCC2?

A

Increases NKCC2 and Na/K/ATPase activity

40
Q

How does loop diuretics affect NKCC2?

A

Lose Ca2+ and Lose K+

41
Q

How powerful is loop diuretics in ascending LOH?

A

Very powerful

42
Q

What affects the Na/H antiporter (NHE)?

A

Carbonic anyhydrase inhibitors

43
Q

What does carbonic anyhydrase inhibitors do to Na/H antiporter at ascending LOH?

A

Minimal effect here, compared to PT

-less reabsorption overall

44
Q

What is the transporter in the distal tubule?

A

Na/Cl cotransporter (NCC) moves Na down concentration gradient

45
Q

What affects the NCC on the distal tubule?

A

Thiazide diuretics

-lose K+

46
Q

What do thiazide diuretics do?

A

Lower intracellular Na and help increase Ca reabsorption

47
Q

How powerful is thiazide diuretics in distal tubule?

A

Moderately

48
Q

Big picture of distal tubule (3)

A
  • 5% Na+ Cl- Ca2+ reabsorption
  • 10-50% K secretion (normal-hyper) or 2% reabsorption (hypo)
  • Water impermeable but functions as diluting segment of tubule
49
Q

Big picture on collecting duct (3)

A
  • 3% of Na+ and water reabsorption
  • 5-30% K+ secretion (normal-hyper) or 9% reabsorption (hypo)
  • 4% H+ secretion/HCO3 -reabsorption
50
Q

What are the principle cells at the collecting duct (3)

A
  • Epithelial Na channel (ENaC)
  • K channels
  • AQP channels
51
Q

What 3 things affect the principal cells at the collecting duct?

A
  • Aldosterone
  • ADH
  • Amiloride
52
Q

How does aldosterone affect the principal cells in collecting duct?

A

Increase ENaC and Na/K/ATPase to reabsorb Na

-also increase K channels expression to secrete K

53
Q

How does ADH effect principal cells in collecting duct?

A

Increase ENaC and AQP channels

54
Q

How does amiloride effect principal cells in collecting duct?

A

Blocks ENaC, K sparing

55
Q

How powerful is amiloride in the collecting duct?

A

Moderately

56
Q

A high distal flow rate at the collecting duct activates what?

57
Q

What does activation of ROMK in principal cells at the collecting duct allow for?

A

More K secretion

58
Q

Diuretics that act earlier in the nephron to prevent reabsorption of Na and water results in what?

A

High distal flow and are thus K wasting

59
Q

What are the 5 steps that occur at the collecting duct when there is an increase in flow?

A
  1. Increase flow
  2. Flow bends cilia
  3. Cilia bend activates PKD1/PKD2 and Ca entry
  4. Increase Ca activates ROMK
  5. Increase flow stimulates Na entry, which reduces Vm (membrane potential)
60
Q

What are type A intercalated cells in the collecting duct?

A

H/K/ATPase: K reabsorbed and H secreted

61
Q

What affects the H/K/ATPase in the type A intercalated cells of the collecting duct?

A

Aldosterone

62
Q

How does aldosterone affect the H/K/ATPase in type A intercalated cells of collecting duct?

A

Increase H ATPase, K/H exchanger and Na/K pump

63
Q

What does type B intercalated cells do?

A

Work in reverse of type A cell; secret bicarb

64
Q

When are type B cells used predominantly?

A

In states of alkalosis

65
Q

What is steady-state for diuretics?

A

Na intake and exception are equal; this leads to a set of ECFV and urine output

66
Q

Diuretics reduce what and increase what?

A

Reduce Na reabsorption and increase rate of urine volume output

67
Q

What is the overall goal of diuretics?

A

Decrease ECFV to decrease edema and/or HTN

68
Q

When does a new balance between Na and water intake and renal output occur?

A

During chronic diuretic therapy

69
Q

What are the compensatory mechanisms for getting a new balance between Na and water during chronic diuretic therapy?

A

Decrease ECFV=Decrease MAP&GFR=Increase RAAS=Decrease Na excretion and urine output

70
Q

What are the 2 things that occur during CKD?

A
  1. Damage to glomerulus causes less NaCl at macula densa
  2. Tubuloglomerular feedback induces renin release, ANGII formation, and EA constriction to drive up PGC
71
Q

CKD can be magnified by what other disease? (2)

A
  1. HTN
  2. Diabetes
72
Q

What 2 products are dependent on filtration and are not reabsorbed?

A

Waste products (Creatinine and urea)

73
Q

Decrease in GFR manifests itself in a proportionate of what to plasma concentrations of urea and creatinine?

74
Q

What products are maintained until GFR falls under ~30% of normal. And they rise but not in proportion to the decline in GFR, as the kidney has high baseline excretion rates and hormonal influences as well.

A

Phosphate and H+

75
Q

What products are maintain more tightly until renal failure, as reabsorption is tightly regulated by powerful and sensitive hormonal and renal systems, and thus we can adjust reabsorption/excretion. And only see problems here in during end stage renal failure and we need to use dialysis to help compensate particularly for ECFV.

A

Electrolytes (Na and Cl)

76
Q

ADH is regulated by what 2 things?

A

Osm and volume/pressure

77
Q

ADH responds best to changes in what?

A

plasma Na+

78
Q

RAAS responds best to changes in what?

A

Plasma volume

79
Q

ADH controls ECF via urine concentration where?

A

Distal nephron

80
Q

What 4 things does ADH cause?

A
  1. Increase Na reabsorption
  2. Increase lots of urea reabsorption and so hypotonic reabsorption of water
  3. Constriction of EA
  4. Increases thirst
81
Q

If plasma increases from 300 to 320 mOsm, what does the urine look like?

A

Small volume of concentrated urine

82
Q

If plasma decreases from 300 to 280 mOsm, what does the urine look like?

A

Large volume of dilute urine

83
Q

What is the goal of RAAS activation?

A

Increase ECFV via Na and water reabsorption

84
Q

How powerful is the effect on Na reabsorption to pull water by the activation of RAAS?

85
Q

Where does ANGII work on the nephron?

86
Q

Where does aldosterone work on the nephron?

87
Q

Hyperkalemia causes K secretion by promoting it how?

A

Directly and by recruiting aldosterone to increase the expression of ENaC and K channels

88
Q

What can aldosterone blockade lead to?

A

Hyperkalemia

89
Q

What regulates the Na transport?

A

ANP/BNP release

90
Q

What is the goal of ANP/BNP?

A

Oppose RAAS and lower ECFV via Na and water excretion

91
Q

What 3 things can cause ANP/BNP?

A
  1. Cardiac distention
  2. Sympathetic stimulation (baroreceptor)
  3. ANGII

Physio II (mine) (6 decks)

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