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FA Active Learning > FA - Renal Physiology > Flashcards

FA - Renal Physiology Flashcards

1
Q

What is the course of the ureters in relation to the surrounding vasculature?

A

Ureters pass under the uterine artery and under the ductus deferens (water under the bridge)

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2
Q

What is the distribution of water in the body?

A

60% total body water; 40% ICF (2/3), 20% ECF (1/3)

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3
Q

What is the breakdown of extracellular fluid in the body?

A

1/4 plasma volume, 3/4 interstitial volume

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4
Q

What is the osmolarity of the body?

A

290 mOsm/L

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5
Q

What are the components of the glomerular filtration barrier?

A

Composed of

  • Fenestrated capillary endothelium (size barrier)
  • Fused basement membrane with heparan sulfate (negative charge)
  • Epithelial layer consisting of podocyte foot processes
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6
Q

How is the glomerular filtration barrier affected in nephrotic syndrome?

A

Charge barrier is lost, resulting in albuminuria, hypoproteinemia, generalized edema, and hyperlipidemia

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7
Q

How is renal clearance calculated?

A

Cx=Ux*V/Px

V=urine flow rate

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8
Q

What is an example of clearance < GFR and what does it indicate?

A

Urea; indicates net tubular reabsorption

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9
Q

What is an example of clearance = GFR and what does it indicate?

A

Inulin; indicates no net secretion or reabsorption

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10
Q

What is an example of clearance > GFR and what does it indicate?

A

Creatinine; indicates net tubular secretion

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11
Q

How can GFR be estimated?

A

Inulin clearance

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12
Q

How can effective renal plasma flow be estimated?

A

PAH clearance; underestimates by 10%

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13
Q

How is renal blood flow calculated?

A

RBF=RPF/(1-Hct)

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14
Q

What is a typical value for GFR?

A

100 mL/min

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15
Q

What is the equation for filtration fraction and what is an average value?

A

FF=GFR/RPF
=GFR/((1-Hct)(RBF))
= ~20%

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16
Q

What is the effect of prostaglandins on FF?

A

Causes dilation of afferent arteriole –>increased RPF, increased GFR, FF unch

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17
Q

What is the effect of NSAIDs on FF?

A

Inhibits actions of prostaglandins –> less renal perfusion; may precipitate acute renal failure

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18
Q

What is the effect of Ang II on FF?

A

Causes constriction of efferent arteriole –>decreased RPF, increased GFR –>increased FF (autoregulation)

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19
Q

What is the effect of ACEi on FF?

A

Prevents autoregulatory constriction of efferent arteriole –>decreased FF

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20
Q

What is the effect of afferent arteriolar constriction on RPF, GFR, FF?

A

Dec RPF, dec GFR, FF unchanged

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21
Q

What is the effect of efferent arteriolar constriction on RPF, GFR, FF?

A

Dec RPF, Inc GFR, Inc FF

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22
Q

What is the effect of increased plasma protein concentration on RPF, GFR, FF?

A

NC RPF, Dec GFR, Dec FF

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23
Q

What is the effect of decreased plasma protein concentration on RPF, GFR, FF?

A

NC RPF, Inc GFR, Inc FF

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24
Q

What is the effect of ureteral constriction on RPF, GFR, FF?

A

NC RPF, Dec GFR, Dec FF

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25
Q

How do you calculate filtered load?

A

Filtered load = GFR x Px

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26
Q

How do you calculate excretion rate?

A

Excretion rate = V x Ux

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27
Q

How do you estimate reabsorption?

A

=Filtered-excreted

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28
Q

How do you estimate secretion?

A

=Excreted-filtered

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29
Q

What is the clearance of glucose?

A

Plasma level <160 mg/dL is completely reabsorbed by Na+/glucose co-transport

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30
Q

At what concentration of glucose are the transporters saturated?

A

Tm=350 mg/dL

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31
Q

How is glucose and amino acid metabolism affected in pregnancy?

A

Both are reduced, leading to glycosuria and aminoaciduria

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32
Q

How are amino acids reabsorbed in the proximal tubule?

A

AAs are reabsorbed via sodium-dependent transporters in prox. tubule

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33
Q

What is Hartnup’s disease characterized by?

A

Deficiency of neutral AA (tryptophan) transporter –>cannot synthesize niacin –>pellagra

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34
Q

What substances are 67-70% reabsorbed in the proximal tubule?

A

Water, Na+, Cl-, Ca++

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35
Q

What substances are 100% reabsorbed in the proximal tubule?

A

Large macromolecules (glucose, AAs, phosphate), HCO3-

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36
Q

What substances are secreted in the proximal tubule?

A

H+, organic cations and anions

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37
Q

What are features of the proximal tubule?

A
  • Contains brush border
  • Isotonic absorption
  • Generates and secretes ammonia (buffer for secreted H+)
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38
Q

What is the effect of PTH in the proximal tubule?

A

Inhibits Na+/phosphate co-transport –>increased phosphate excretion

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39
Q

What is the effect of ANGII in the proximal tubule?

A

Stimulates Na+/H+ exchange –>increased Na+, H2O, HCO3- reabsorption (permits contraction alkalosis)

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40
Q

What are features of the thin descending loop of Henle?

A

Passively reabsorbs water via medullary hypertonicity (impermeable to sodium) –>makes urine more hypertonic

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41
Q

What are features of the thick ascending loop of Henle?

A
  • Actively reabsorbs Na+, K+, and Cl-.
  • Indirectly induces the paracellular reabsorption of Mg++ and Ca++ through (+) lumen pot’l generated by K+ backleak
  • Impermeable to H2O –>makes urine less concentrated
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42
Q

How much Na+ is reabsorbed in the TAL?

A

10-20%

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43
Q

What are features of the distal convoluted tubule?

A

-Actively reabsorbs Na+, Cl- –> makes urine more hypotonic

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44
Q

What is the effect of PTH on the DCT?

A

Increases Ca++/Na+ exchange –>increased Ca++ reabsorption

45
Q

How much Na+ is reabsorbed in the DCT?

A

5-10%

46
Q

What are features of the collecting duct?

A

Reabsorb Na+ in exchange for secreting K+ and H+ (regulated by aldosterone)

47
Q

What is the effect of aldosterone on the collecting duct?

A

Acts on MR –>insertion of Na+ channel in luminal side

48
Q

What is the effect of ADH on the collecting duct?

A
  • Acts at V2 receptor –>insertion of aquaporin H2O channels on luminal side
  • Promotes reabsorption of urea
49
Q

How much Na+ is reabsorbed in the collecting duct?

A

3-5%

50
Q

What are some substances reabsorbed less quickly than water?

A

PAH, creatinine, inulin, urea, Cl-, K+

51
Q

What are some substances reabsorbed at the same rate as water?

A

Na+

52
Q

What are some substances reabsorbed more quickly than water?

A

Pi, HCO3-, AAs, glucose

53
Q

What are three causes of increased renin production?

A

Decreased blood pressure (JG cells)
Decreased Na+ delivery (MD cells)
Increased sympathetic tone (B1 receptors on JG cells)

54
Q

What are the effects of ANGII on vascular smooth muscle

A

Causes vasoconstriction –>increased BP

55
Q

What are the effects of ANGII on the glomerulus?

A

Causes constriction of efferent arteriole –>increased FF to preserve renal function in low-volume states

56
Q

What are the effects of aldosterone?

A

Increased Na+ channel and Na+/K+ pump insertion in principal cells –>increased K+ and H+ excretion to crease favorable Na+ gradient for reabsorption

57
Q

What is the effect of ADH?

A 
Increases H2O channel insertion in principal cells -->increased H2O reabsorption
Regulates osmolarity (volume more important than osmolarity)
58
Q

What is the effect of ANGII on proximal tubule Na+/H+ activity?

A

Na+, HCO3-, and H2O reabsorption (can permit contraction alkalosis)

59
Q

What is the effect of ANGII on the hypothalamus?

A

Stimulates hypothalamus –>increases thirst

60
Q

What is the effect of ANGII on the baroreceptors?

A

Limits reflex bradycardia

61
Q

What is the effect of ANP?

A

Released from atria in response to increased volume; may act as a check on RAAS
Relaxes VSMC via cGMP –>increased GFR, decreased renin production

62
Q

What is the juxtaglomerular apparatus?

A

Modified smooth muscle of the afferent arteriole (JG) and distal convoluted tubule (MD); defends GFR via RAAS

63
Q

What is the effect of beta blockers on the JGA?

A

Inhibits B1 receptors –> decreased renin release –>decreased BP

64
Q

What are causes of high renin/high aldo in pt. with HTN and hypokalemia?

A

Secondary hyperaldosteronism: renovascular HTN, malignant HTN, renin-secreting tumor, diuretic use

65
Q

What are causes of low renin/high aldo in pt. with HTN and hypokalemia?

A

Primary hyperaldosteronism (Conn’s): aldo-secreting tumor, bilateral adrenal hyperplasia

66
Q

What are causes of low renin/low aldo in pt. with HTN and hypokalemia?

A

Non aldo related causes: CAH, deoxycorticosterone producing adrenal tumor, Cushing syndrome, exogenous mineralocorticoid

67
Q

What is the function of erythropoietin?

A

Released by interstitial cells in the peritubular capillary bed in response to hypoxia –>increased RBC production

68
Q

What is the action of the kidney on 25-OH vitamin D?

A

Proximal tubules convert it to 1,25-(OH)2 vitamin D (active form) using 1a-hydroxylase (regulated by PTH)

69
Q

What is the effect of ANP on kidney?

A

Causes inc GFR and inc Na+ filtration with NO COMPENSATORY Na+ reabsorption –>Na+ and volume loss

70
Q

What is the effect of PTH on the kidney?

A

Causes inc. Ca++ reabsorption in DCT, dec. phosphate reabsorption in PCT, and increased 1,25(OH)2 vit D production

71
Q

What is the effect of Digitalis on K+?

A

Shifts out of the cell –>hyperkalemia

72
Q

What is the effect of Hyperosmolarity on K+?

A

Shifts out of the cell –>hyperkalemia

73
Q

What is the effect of Insulin deficiency on K+?

A

Shifts out of the cell –>hyperkalemia

74
Q

What is the effect of cell lysis on K+?

A

Shifts out of the cell –>hyperkalemia

75
Q

What is the effect of acidosis on K+?

A

Shifts out of the cell –>hyperkalemia

76
Q

What is the effect of beta-adrenergic antagonist on K+?

A

Shifts out of the cell –>hyperkalemia

77
Q

What is the effect of hypoosmolarity on K?

A

Shifts into the cell –>hypokalemia

78
Q

What is the effect of insulin on K+?

A

Increases Na+/K+ ATPase –>shifts into the cell –>hypokalemia

79
Q

What is the effect of alkalosis on K+?

A

Shifts into the cell –>hypokalemia

80
Q

What is the effect of a beta-adrenergic agonist on K+?

A

Increases Na+/K+ ATPase –>shifts into the cell –>hypokalemia

81
Q

What is the effect of low serum Na+?

A

Nausea and malaise, stupor and coma

82
Q

What is the effect of high serum Na+?

A

Irritability, stupor, coma

83
Q

What is the effect of low serum K+?

A

U waves on ECG, flattened T waves, arrhythmias, muscle weakness

84
Q

What is the effect of high serum K+?

A

Wide QRS and peaked T waves on ECG, arrhythmias, muscle weakness

85
Q

What is the effect of low Ca++?

A

Tetany, seizures

86
Q

What is the effect of high Ca++?

A

Renal STONES, pain in the BONES, abdominal pain (GROANS), and psychiatric disturbances (MOANS)

87
Q

What is the effect of high Mg++?

A

Tetany, arrhythmias

88
Q

What is the effect of low Mg++?

A

Decreased DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

89
Q

What is the effect of low phosphate?

A

Bone loss, osteomalacia

90
Q

What is the effect of high phosphate?

A

Renal stones, metastatic calcifications, hypocalcemia

91
Q

What is the pH, PCO2, and HCO3- in metabolic acidosis?

A

Low pH, decreased PCO2 (immediate hyperventilation) and decreased HCO3-

92
Q

How is compensated metabolic acidosis assessed?

A

Winter’s formula: PCO2= 1.5[HCO3-] +8 +/-2

93
Q

What is the estimated PCO2 compensation in metabolic acidosis?

A

1:1

94
Q

What is the pH, PCO2, and HCO3- in metabolic alkalosis?

A

High pH, increased PCO2 (immediate hypoventilation) and increased HCO3-

95
Q

What is the estimated PCO2 compensation in metabolic alkalosis?

A

1:2 (i.e. half the increase in bicarb)

96
Q

What is the pH, PCO2, and HCO3- in respiratory acidosis?

A

Low pH, increased PCO2, and increased HCO3-

97
Q

What is the estimated HCO3- compensation in respiratory acidosis?

A

1 pt in acute condition (i.e. 25 mEq/L)

3 pts in chronic (i.e. 27 mEq/L)

98
Q

What is the pH, PCO2, and HCO3- in respiratory alkalosis?

A

High pH, decreased PCO2, decreased HCO3-

99
Q

What is the estimated HCO3- compensation in respiratory alkalosis?

A

2 pts in acute condition (i.e. 22 mEq/L)

5 pts in chronic condition (i.e. 19 mEq/L)

100
Q

What are the PCO2 and the HCO3- in a mixed resp/met acidosis?

A

Inc PCO2, decreased HCO3-

101
Q

What are the PCO2 and HCO3- in a mixed resp/met alkalosis?

A

Dec PCO2, increased HCO3-

102
Q

What is the Henderson-Hasselbach equation?

A

pH=6.1 + log [HCO3-]/(0.03*PCO2)

103
Q

What are respiratory causes of acidemia?

A

Hypoventilation due to: airway obstruction, acute lung dz, chronic lung dz (COPD), opioids, sedatives, resp. muscle fatigue, structural

104
Q

What are metabolic causes of acidemia?

A

Anion gap: MUDPILES

Non anion gap: hyperalimentation, Addison’s, RTA, Diarrhea, acetazolamide, spironolactone, saline infusion (HARDASS)

105
Q

What are respiratory causes of alkalemia?

A

Hyperventilation due to: early high altitude exposure, early salicylate toxicity, PE, PNA, CHF

106
Q

What are metabolic causes of alkalemia?

A

Vomiting, antacid use, volume contraction (usu. with loop diuretic), mineralocorticoid/high GC

107
Q

What defines type I RTA?

A

Defect in collecting duct (DISTAL) excretion of H+ leading to urine pH >5.5
Associated with hypokalemia and formation of Ca+ phosphate kidney stones

108
Q

What defines type II RTA?

A

Defect in PROXIMAL tubule reabsorption of HCO3- leading to urine pH <5.5
May be seen with Fanconi syndrome
Associated with hypokalemia and increased risk for hypophosphatemic rickets

109
Q

What defines type IV RTA?

A

Hypoaldosteronism or lack of collecting tubule response to aldo causes HYPERKALEMIA –>impaired ammoniagenesis and decreased H+ buffering capacity
Low urine pH

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