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BRS Phys > Ch 5 > Flashcards

Ch 5 Flashcards

1
Q

What fraction of total body water is ICF?

A

Two Thirds

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2
Q

What fraction of total body water is ECF?

A

One Third

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3
Q

What fraction of ECFV is plasma volume?

A

One Quarter

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4
Q

What fraction of ECFV is interstitial fluid volume?

A

Three Quarters

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5
Q

What is the 20-40-60 rule?

A

TBW = 60% of body weightICF = 40% of body weight
ECF = 20% of body weight

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6
Q

What markers are used in the dilution method to measure total body water?

A

D2O, tritiated water, Antipyrene

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7
Q

What markers are used in the dilution method to measure ECFV?

A

Mannitol, inulin, sulfate

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8
Q

What markers are used in the dilution method to measure plasma volume?

A

Radiolabeled inulin, Evans blue

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9
Q

ECFV minus plasma volume is equal to…

A

Interstitial fluid volume

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10
Q

What is the formula used for the dilution method?

A

Compartment volume = (amount administered - amount lost in urine)/measured concentration after equilibration

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11
Q

How is ECF osmolarity related to ICF osmolarity?

A

They are always EQUAL

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12
Q

What occurs to normalize ICFV and ECFV and compartment osmolarities after loss of water and/or sodium?

A

WATER shifts compartments (protein/ions don’t)

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13
Q

What happens to ICFV, ECFV, ICF osmolarity, and ECF osmolarity when isotonic sodium chloride is infused?

A

ICFV - no change ECFV - increases

ICF osmolarity - no change

ECF osmolarity - no change There is no change in ICFV or either osmolarity because the main driving force for water movement across membranes is changes in osmolarity, which does not happen with addition of an isotonic solution.

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14
Q

What occurred to produce these results?

A

ICFV - unchanged
ECFV - increased
ICF osmolarity - unchanged

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15
Q

ECF osmolarity - unchanged

A

Addition of isotonic sodium chloride

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16
Q

What clinical scenario results in loss of isotonic fluid?

A

Diarrhea

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17
Q

What happens to ICFV, ECFV, ICF osmolarity, and ECF osmolarity with chronic diarrhea?

A

ICFV - no change ECFV - decreases

ICF osmolarity - no change

ECF osmolarity - no change Diarrhea is a loss of isotonic fluid. Because the fluid lost is isotonic, there is no change in osmolarity of the ECF compartment, so no water leaves the ICF, leaving ICF volume and osmolarity unchanged.

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18
Q

What occurred to produce these results?

A

ICFV - unchanged
ECFV - decreased
ICF osmolarity - unchanged

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19
Q

ECF osmolarity - unchanged

A

Chronic diarrhea (loss of isotonic fluid)

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20
Q

What two clinical scenarios result in loss of hypotonic fluid?

A

Chronic sweating and diabetes insipidus

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21
Q

What happens to ICFV, ECFV, ICF osmolarity, and ECF osmolarity with diabetes insipidus or chronic sweating?

A

ICFV - decreases ECFV - decreases

ICF osmolarity - increases

ECF osmolarity - increases These scenarios result in loss of hypotonic fluid. Loss of hypotonic fluid makes ECFV hypertonic relative to ICFV, and water shifts to correct this. Both compartments end up hypertonic.

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22
Q

What occurred to produce these results?

A

ICFV - decreased
ECFV - decreased
ICF osmolarity - increased

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23
Q

ECF osmolarity - increased

A

Diabetes insipidus or chronic sweating

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24
Q

What clinical scenario results in gain of hypotonic fluid?

A

SIADH

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25
Q

What happens to ICFV, ECFV, ICF osmolarity, and ECF osmolarity with SIADH?

A

ICFV - increases ECFV - increases

ICF osmolarity - decreases

ECF osmolarity - decreases SIADH results in gain of hypotonic fluid (water), making the ECFV hypotonic relative to the ICFV. Water shifts from into the ICFV, decreasing its osmolarity.

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26
Q

What occurred to produce these results?

A

ICFV - increased
ECFV - increased
ICF osmolarity - decreased

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27
Q

ECF osmolarity - decreased

A

SIADH (gain of hypotonic fluid)

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28
Q

What clinical scenario results in loss of NaCl?

A

Adrenocortical insufficiency (Addison syndrome)

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29
Q

What happens to ICFV, ECFV, ICF osmolarity, and ECF osmolarity with adrenocortical insufficiency (Addison syndrome)?

A

ICFV - increases ECFV - decreases

ICF osmolarity - decreases

ECF osmolarity - decreases Loss of NaCl causes a decrease in ECFV osmolarity. As a result, water leaves the ECF for the ICF, increasing ICFV and decreasing ICF osmolarity.

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30
Q

What occurred to produce these results?

A

ICFV - increased
ECFV - decreased
ICF osmolarity - decreased

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31
Q

ECF osmolarity - decreased

A

Adrenocortical insufficiency - loss of NaCl (Addison syndrome)

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32
Q

What is clearance?

A

The volume of plasma cleared of a substance per unit time.

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33
Q

What is the formula for clearance?

A

C = [(Urine concentration of substance) * (urine flow rate)] / Plasma concentration of substance

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34
Q

What happens to RBF with afferent arteriole vasoconstriction?

A

Decreases

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35
Q

What happens to RBF with efferent arteriole vasoconstriction?

A

Decreases

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36
Q

What does angiotensin do to renal arterioles?

A

Constricts efferent arteriole

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37
Q

What effect do ACE inhibitors have on renal arterioles?

A

Dilates efferent arteriole

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38
Q

What purpose to ACE inhibitors serve in diabetes?

A

Reduce the incidence of diabetic nephropathy by reducing GFR and thus, hyperfiltration

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39
Q

What do PGE2 and PGI2 do to renal arterioles?

A

Vasodilate

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40
Q

Explain tuboglomerular feedback

A

Increased arterial pressure increases delivery of fluid to the macula densa. Macula densa senses the increased load and causes constriction of the afferent arteriole, increasing resistance to maintain constant flow.

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41
Q

What is used to estimate RPF?

A

Clearance of PAH

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42
Q

What is used to measure RBF?

A

RBF = RPF/1-hematocrit

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43
Q

What is used to estimate GFR?

A

Clearance of inulin

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44
Q

Explain the handling of inulin by the kidney

A

It is filtered, but not reabsorbed or secreted.

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45
Q

Explain the handling of PAH by the kidney

A

It is filtered and secreted by the tubules, not reabsorbed

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46
Q

What is the definition for filtration fraction?

A

FF = GFR/RPF

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47
Q

What will happen to reabsorption with increases in filtration fraction?

A

It will increase due to increases in protein concentration in peritubular capillary blood, leading to a greater gradient for reabsorption

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48
Q

What will happen to reabsorption with decreases in filtration fraction?

A

It will decrease due to decreases in protein concentration in peritubular capillary blood, leading to a smaller gradient for reabsorption

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49
Q

Why are negatively charged proteins restricted from filtration?

A

Negatively charged glycoproteins in the filtration barrier repel them to prevent filtration

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50
Q

Which hydrostatic pressures and oncotic pressures favor filtration?

A

Glomerular capillary hydrostatic pressure and Bowman’s space oncotic pressure (which is usually zero) favor filtration

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51
Q

How does ureteral constriction cause decreases in GFR?

A

Increases Bowman’s space hydrostatic pressure, which opposes filtration

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52
Q

How does increased protein concentration cause decreases in GFR?

A

Increases glomerular capillary oncotic pressure, which opposes filtration

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53
Q

What does constriction of the afferent arteriole do to GFR?

A

Decreases it

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54
Q

What does constriction of the efferent arteriole do to GFR?

A

Increases it

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55
Q

What does constriction of the afferent arteriole do to FF?

A

No change. Afferent constriction decreases both GFR and RPF, which results in no net change in FF

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56
Q

What does constriction of the efferent arteriole do to FF?

A

Increases it. Efferent constriction increases GFR and reduces RPF, which results in a net increase in FF

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57
Q

What does increased plasma protein do to FF?

A

Decreases it. Increased plasma protein decreases GFR (increased glomerular capillary oncotic pressure), but has no effect on renal plasma flow.

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58
Q

What does a ureteral stone do to FF?

A

Decreases it. Stones decrease GFR (increased Bowman’s space hydrostatic pressure), but have no effect on renal plasma flow.

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59
Q

What is the formula for filtered load?

A

FL = GFR * plasma solute concentration

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60
Q

What is the formula for excretion rate?

A

Excretion = urine flow rate * urine solute concentration

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61
Q

What is the formula for reabsorption rate?

A

Reabsorption = Filtered load - excretion rate

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62
Q

What is the formula for secretion rate?

A

Secretion rate = Excretion rate - filtered load

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63
Q

How is glucose reaborbed in the PCT?

A

Secondary active transport (symport) with sodium

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64
Q

What is the approximate glucose concentration where transporters in the PCT are saturated?

A

350 mg/dL (note: this different from threshold, which is the glucose concentration at which glucose first appears in the urine - 250 mg/dL. The difference is due to splay)

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65
Q

What is splay?

A

The region of glucose curves between threshold (where glucose first appears in urine - 250 mg/dL) and transport maximum (when glucose transporters are saturated - 350 mg/dL)

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66
Q

What is the approximate glucose concentration where glucose first appears in the urine?

A

250 mg/dL (note this is different from the concentration at which receptors are saturated, which is 350 mg/dL. The difference is due to splay).

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67
Q

Where in the nephron is PAH secreted?

A

Primarily in the PCT

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68
Q

What is the TF/P ratio?

A

A comparison of the concentration of a substance in tubular fluid with the concentration in plasma

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69
Q

What does a TF/P ratio of 1 mean?

A

The concentration of a substance in tubular fluid is equal to its concentration in plasma. There has either been no reabsorption of the substance or reabsorption of the substance has been proportional to the resorption of water (isotonic)

70
Q

What does a TF/P ratio of <1 mean?

A

The concentration of a substance in tubular fluid is less than its concentration in plasma. The substance has been reabsorbed in the nepron at a greater rate than water.

71
Q

What does a TF/P ratio of >1 mean?

A

The concentration of a substance in tubular fluid is greater than its concentration in plasma. The substance has been reabsorbed in the nephron at a slower rate than water OR the substance is being secreted.

72
Q

Where is sodium primarily reabsorbed?

A

PCT (67%)

73
Q

The greatest amount of sodium is reabsorbed in the PCT, but fluid leaving the PCT has the same sodium concentration as did the fluid entering it. Explain.

A

Sodium is absorbed isosmotically with water. The ratio at which they are absorbed is proportional, so while there is a net less sodium present, its concentration remains constant.

74
Q

How are amino acids reabsorbed in the PCT?

A

Secondary active transport (symport) with sodium

75
Q

Explain the handling of sodium with respect to H+ ions in the PCT.

A

Sodium is reabsorbed in exchange for H+ ions in the PCT

76
Q

What does ECFV contraction do to reabsorption in the PCT?

A

Increases it (because of increases in plasma oncotic pressure) to try to regain volume

77
Q

What does ECFV expansion do to reabsorption in the PCT?

A

Decreases it (because of decreases in plasma oncotic pressure) to try to get rid of volume

78
Q

How is sodium reabsorbed in the limb of Henle?

A

In the NKCC of the thick ascending limb

79
Q

Which limb of the loop of Henle is permeable to water?

A

Descending limb

80
Q

Which limb of the loop of Henle is permeable to solutes?

A

Ascending limb (NKCC carrier)

81
Q

How is sodium reabsorbed in the early DCT?

A

Co-transport with chloride

82
Q

What is the MOA of loop diuretics?

A

Inhibit the NKCC in the thick ascending limb of Henle

83
Q

What is the MOA of thiazide diuretics?

A

Inhibit the sodium/chloride co-transporter in the DCT

84
Q

Which limb of the loop of Henle is impermeable to water?

A

Ascending limb

85
Q

Explain the function of Principal cells in the DCT

A

Reabsorb sodium (through ENaC channels)

86
Q

Secrete potassium (through K+ leak channels)

A

Both of these functions are increased by aldosterone

87
Q

Which hormone works in the DCT to increase sodium reabsorption and potassium excretion?

A

Aldosterone

88
Q

Explain how aldosterone increases sodium reabsorption and potassium excretion in the DCT.

A

Aldosterone increases insertion of ENaC channels on the lumen side, increasing sodium secretion. The drive for sodium reabsorption and potassium secretion is driven by aldosterone increasing the Na/K ATPase on the basolateral side. Increased potassium in the cell promotes secretion of potassium, while decreased sodium in the cell promotes sodium reabsorption.

89
Q

What do intercalated cells do with H+ ions in the DCT?

A

Secrete

90
Q

What function does ADH have and where does it work?

A

Inserts water channels to facilitate water reabsorption in the late DCT and early collecting duct

91
Q

What receptor does ADH bind in the kidney to cause water reabsorption and what is the molecular effect of its binding?

A

V2 receptor, increases cAMP to increase aquaporin channel insertion on the basolateral membrane

92
Q

Patient has a massive K+ shift into their cells. Dx?

A

Hypokalemia

93
Q

Patient has a massive K+ shift out of their cells. Dx?

A

Hyperkalemia

94
Q

Where is most potassium reabsorbed in the nephron?

A

PCT (67%)

95
Q

The greatest amount of potassium is reabsorbed in the PCT, but fluid leaving the PCT has the same sodium concentration as did the fluid entering it. Explain.

A

Potassium is absorbed isosmotically with water. The ratio at which they are absorbed is proportional, so while there is a net less sodium present, its concentration remains constant.

96
Q

How is potassium reabsorbed in the limb of Henle?

A

Via the NKCC transporter with sodium and chloride

97
Q

Which cells secrete potassium?

A

Principal cells of DCT

98
Q

What does insulin do to potassium concentration?

A

Decreases plasma concentration of potassium by shifting it into cells

99
Q

What does sympathetic activation do to potassium concentration?

A

Decreases plasma concentration of potassium by shifting it into cells

100
Q

How does acidosis cause hyperkalemia?

A

Since the blood contains excess H+, H+ enters cells in exchange for K+ (H/K ATPase). Since K+ concentration in cells is lower, it is not secreted as well, resulting in hyperkalemia.

101
Q

How does alkalosis cause hypokalemia?

A

Since blood contains too little H+, H+ leaves cells in exchange for K+. Excess K+ in cells increases excretion of K+, resulting in hypokalemia.

102
Q

What do thiazide and loop diuretics do to potassium secretion?

A

Increase it, causing hypokalemia

103
Q

What is the MOA of potassium sparing diuretics?

A

Block ENaC in the principal cells of the DCT. Sodium isn’t reabsorbed as well, so potassium isn’t secreted as effectively.

104
Q

What does ADH do to urea reasbsorption?

A

Increases

105
Q

What does PTH do to phosphate excretion?

A

Increases it (PTH - Phosphate Trashing Hormone)

106
Q

What is the main way the nephron handles phosphate?

A

Reabsorbs 85% of it, in the PCT

107
Q

What GPCR is activated in the kidney as a result of PTH binding?

A

Gs - activates AC, which activates cAMP

108
Q

What 2 things should you look for in the urine if you suspect someone of having too high of PTH levels?

A

Phosphate and cAMP

109
Q

What do thiazide diuretics do to calcium reabsorption?

A

Increase it

110
Q

What do loop diuretics to do calcium reabsorption?

A

Decrease it - patients on loop diuretics lose calcium

111
Q

What role does ADH play with respect to urea?

A

ADH increases cycling of urea between the collecting duct and medulla, increasing osmolarity of the interstitium

112
Q

What will TF/P be in the PCT?

A

1, because water is reabsorbed isosmotically with solute

113
Q

Explain the body’s response to water deprivation.

A

Water deprivation causes increased plasma osmolarity, which is sensed by osmoreceptors in the hypothalamus. As a result, ADH is secreted from the supraoptic nucleus of the posterior pituitary. ADH acts on principal cells in the DCT/CD to increase aquaporin channel insertion, increasing water reabsorption, which decreases the plasma osmolarity towards normal. Urine osmolarity will be increased, and urine volume will be decreased.

114
Q

Explain the body’s response to increased water intake.

A

Excess water intake decreases plasma osmolarity, inhibiting osmoreceptors in the hypothalamus. As a result, ADH secretion from the posterior pituitary is inhibited. This decreases the insertion of aquaporin channels on the DCT/CD, resulting in decreased water reabsorption, bringing raising plasma osmolarity back to normal. Urine volume is increased, and urine osmolarity is decreased.

115
Q

What is the osmolarity of fluid leaving the ascending limb of Henle with respect to plasma osmolarity?

A

Fluid leaving the ascending LOH has an osmolarity of 100 mOsm/L, much lower than plasma osmolarity (TF/P <1).

116
Q

What is the TF/P in the collecting duct?

A

TF/P >1, because urine is concentrated to become hyperosmolar

117
Q

What value is used to estimate the kidney’s ability to concentrate or dilute the urine?

A

Free water clearance

118
Q

What is the formula for free water clearance?

A

Free water clearance = Urine flow rate - Osmolar clearance

119
Q

What happens to free water clearance with increased ADH? Decreased ADH?

A

Increased ADH - free water clearance decreases Decreased ADH- free water clearance increases

120
Q

What happens to ADH levels in primary polydipsia?

A

Decrease - want to get rid of water

121
Q

What happens to ADH levels in central diabetes insipidus?

A

Decrease

122
Q

What happens to serum osmolarity in primary polydipsia?

A

Decreases

123
Q

What happens to serum osmolarity in central and nephrogenic diabetes insipdus?

A

Increases, because of excretion of too much H2O

124
Q

What happens to ADH levels in neprogenic diabetes insipidus?

A

INCREASE

125
Q

What happens to ADH levels in water deprivation?

A

Increase, trying to save water

126
Q

What happens to ADH levels in SIADH?

A

Increase

127
Q

What happens to serum osmolarity in water deprivation?

A

Increases

128
Q

What happens to serum osmolarity in SIADH?

A

Decreases due to reabsorption of too much H2O

129
Q

List 3 causes of increased free water clearance

A

Central/Nephrogenic diabetes insipidus Primary polydipsia

130
Q

List 2 causes of decreased free water clearance

A

Water deprivation SIADH

131
Q

What is the major extracellular buffer?

A

Bicarbonate

132
Q

Where on the titration curve are buffers most effective?

A

+/- 1.0 pH unit of the pKa

133
Q

Is deoxy or oxyhemoglobin a better buffer at physiologic pH?

A

Deoxyhemoglobin

134
Q

What is the Henderson-Hasselbalch equation?

A

pH = pKa + log (A-)/(HA)

135
Q

When concentrations of A- and HA are equal, what is the pH of a solution?

A

Equal to the pKa

136
Q

Explain the handling of HCO3 in the PCT

A

HCO3- is freely filtered at the glomerulus. In the PCT, it combines with H+ ions, which are being secreted in an antiport with sodium (controlled by AT II). The secreted hydrogen ions combine with filtered bicarbonate to form H2CO3, which is converted into H2O and CO2 by carbonic anhydrase in the lumen. The water and carbon dioxide are then taken into the cell, where carbonic anhydrase reverses the above reaction. The resultant HCO3- is reabsorbed (a NET GAIN of bicarbonate), and the H+ ion is re-secreted in a cyclic fashion to cause reabsorption of bicarbonate.

137
Q

Explain renal compensation for respiratory acidosis

A

Increased intracellular PCO2 results in increased rates of HCO3- reabsporption, because more intracellular H+ is available to be secreted to cause reabsorption of HCO3-, so HCO3- is gained.

138
Q

Explain renal compensation for respiratory alkalosis

A

Decreased intracellular PCO2 results in decreased rates of HCO3- reabsporption, because not as much H+ is available to be secreted to cause reabsorption of HCO3-, so HCO3- is lost.

139
Q

Explain how an increase in angiotensin II causes alkalosis in a volume contracted state.

A

Increased AT II occurs with volume depletion. AT II stimulates Na reabsorption & H+ secretion (via the Na/H antiporter) in the PCT, thus increasing overall net bicarbonate reabsorption.

140
Q

Explain the two mechanisms by which the body gets rid of excess H+ ions

A

H+ ion secreted into the tubule complexes with HPO4 or NH3. Because it is not complexing with HCO3-, the H+ ion is not reabsorbed into the tubule, and is “lost”

141
Q

What is the primary disturbance in metabolic acidosis?

A

Reduced arterial HCO3-

142
Q

What is the respiratory compensation for metabolic acidosis?

A

Kussmaul breathing - blowing off lots of CO2 to try to increase pH

143
Q

What is the formula for anion gap?

A

Anion gap = Sodium concentration - chloride concentration - bicarbonate concentration

144
Q

What is the normal anion gap range?

A

8-16 mEq/L

145
Q

Explain the mnemonic MUDPILES

A

MUDPILES is representative of things that cause high anion gap metabolic acidosis Methanol, Uremia, DKA, Propylene glycol, INH/Iron, Lactic acid, Ethanol/Ethylene glycol, Salicylates (aspirin)

146
Q

What does the body do to maintain electroneutrality in normal anion gap metabolic acidosis?

A

Increases chloride ion concentration

147
Q

What type of acid/base disturbance does vomiting cause?

A

Metabolic alkalosis (loss of H+ from gastric contents)

148
Q

What type of acid/base disturbance does hyperaldosteronism cause?

A

Metabolic alkalosis (increased H+ secretion by DCT)

149
Q

What type of acid/base disturbance does opioid overdose cause?

A

Respiratory acidosis (retain CO2)

150
Q

What type of acid/base disturbance does COPD cause?

A

Respiratory acidosis (retain CO2)

151
Q

What type of acid/base disturbance does pneumonia cause?

A

Respiratory alkalosis (hypoxia increases respiratory drive)

152
Q

What type of acid/base disturbance does PE cause?

A

Respiratory alkalosis (hypoxia increases respiratory drive)

153
Q

What TWO types of acid/base disturbances does aspirin (salicylate) poisoning cause?

A

Metabolic acidosis AND respiratory alkalosis (Salicylates directly stimulate respiratory centers to cause increased ventilation rate)

154
Q

What type of acid/base disturbances does diarrhea cause?

A

Normal anion gap metabolic acidosis (hyperchloremic - body increases chloride to compensate for loss of HCO3- with diarrhea)

155
Q

What is the primary disturbance in metabolic alkalosis?

A

Increase in arterial HCO3-

156
Q

What is the primary disturbance in respiratory alkalosis?

A

Decreased PCO2

157
Q

What is the primary disturbance in respiratory acidosis?

A

Increased PCO2

158
Q

A patient who is hyperventilating has tingling, numbness, and muscle spasms. What is causing this?

A

Hyperventilation caused respiratory alkalosis. Decreased H+ in the blood means less H+ is available to compete with calcium for binding on plasma proteins. This results in hypocalcemia, because calcium is increasingly bound by plasma proteins. The symptoms of hypocalcemia are tingling, numbness, and muscle spasm.

159
Q

Fenestrated capillary epithelium rejects filtration of objects based on…

A

Size

160
Q

Clearance > GFR means what with respect to the handling of a solute?

A

The solute was secreted

161
Q

Clearance < GFR means what with respect to the handling of a solute?

A

The solute was reabsorbed

162
Q

Clearance = GFR means what with respect to the handling of a solute?

A

There was no NET reabsorption or secretion of the solute

163
Q

What do beta blockers do to renin release?

A

Decrease it. Beta-1 receptors cause renin release at the JGA

164
Q

What effect on K+ balance does digoxin have?

A

Causes hyperkalemia (by inhibiting the Na/K ATPase)

165
Q

What is Winter’s formula used to predict?

A

CO2 level necessary for compensation of a metabolic acidosis

166
Q

What is Winter’s formula?

A

PCO2 to compensate for a metabolic acidosis= 1.5 (HCO3-) +8 (+/- 2)

167
Q

Winter’s formula gives a higher PCO2 than predicted. What does this mean?

A

Concomitant respiratory acidosis on top of the metabolic acidosis

168
Q

Winter’s formula gives a lower PCO2 than predicted. What does this mean?

A

Concomitant respiratory alkalosis on top of the metabolic acidosis (over-compensated)

169
Q

What happens in type 1 renal tubular acidosis?

A

Defect in collecting tubules ability to excrete H+. Untreated patients have a urine pH >5.5. It is associated with hypokalemia

170
Q

What happens in type 2 renal tubular acidosis?

A

Defect in proximal tubule HCO3- reabsorption. Seen with Fanconi syndrome, multiple myeloma. Patients have urine pH <5.5.

171
Q

What happens in type 4 renal tubular acidosis?

A

Hypoaldosteronism or lack of collecting tubule response to aldosterone. Hyperkalemia results in ammonia generation, leading to decreased buffering capacity and decreased urine pH

BRS Phys (6 decks)

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