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Renal Final > Physiology > Flashcards

Physiology Flashcards

1
Q

What is normal serum K level?

A

3.5-5.0 mEq/L

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2
Q

What percentage of K is located in ICF vs ECF? What accounts for the difference?

A
  • 98% intracellularly (80% muscle cells); 2% extracellularly

- mainly due to Na/K ATPase and NKCC2 channels

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3
Q

What is hypokalemia and what causes it?

Effect on resting membrane potential?

A
  • Plasma K < 3.7 mEq/L
  • due to vomiting/diarrhea, insulin excess, K deficiency, and alkalosis
  • hyperpolarizes membrane -> RMP more negative -> harder to excite
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4
Q

What is hyperkalemia and what causes it?

Effect on resting membrane potential?

A
  • plasma K > 5.2 mEq/L
  • due to excessive intake, tissue release/damage, acidosis, insulin deficiency
  • hypopolarizes membrane -> RMP less negative -> easier to excite
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5
Q

What is pseudohyperkalemia?

A

artificially high plasma K due to lysis of RBCs during blood draw

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6
Q

What effect do hyper and hypokalemia have on the heart?

A
  • opposite other tissues
  • hypokalemia: tachycardia
  • hyperkalemia: bradycardia
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7
Q

What effect do Epi have on K? Why does this make sense?

A
  • lowers serum K by uptake into extrarenal tissues and stimulating K excretion by kidneys
  • hypokalemia causes tachycardia (Epi has a sympathetic effect on HR)
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8
Q

What effect does insulin have on serum K?

A

lower serum K by stimulating Na/K ATPase to bring K into cells and release Na

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9
Q

What effect does aldosterone have on K?

A

Renal: increases K excretion
Extrarenal: increase K secretion into intestinal fluid and saliva

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10
Q

What effect does acidosis have on serum K?

A

increases serum K through inhibition of Na/K ATPase (cells will intake H+ to increase pH and remove K)

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11
Q

What effect does alkalosis have on serum K?

A

lowers serum K (cells will release H+ to decrease pH and intake K)

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12
Q

What effect does hyperosmolarity have on serum K?

A

increases serum K due to contraction of ICF volume -> fluid enters ECF and K follows

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13
Q

How do you calculate GFR? How do you calculate Puf?

A 
GFR = (Kf)(Puf)
Puf = Pgc - Pbc - Pigc
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14
Q

How do you calculate renal clearance? In what circumstances is this equal to GFR?

A

Renal Clearance = (Ux)(V)/(Px)

equal to GFR when substance is freely filtered (inulin and creatine)

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15
Q

How do you calculate filtered load?

A

Filtered load = (Px)(GFR)(% filterability)

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16
Q

What is reabsorbed in the PCT?

A

water, Na, K, Cl, HCO3, Ca, Pi, and all glucose and AA

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17
Q

What is the major mechanism of the PCT?

A

Na/K ATPase in basolateral membrane

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18
Q

What drives K reabsorption in the late PT?

A

lumen-positive transepithelial difference (TEPD) -> build up of positive charge in lumen -> like repels like -> K is pushed out

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19
Q

How do you develop a positive TEPD in the PCT?

A

Na reabsorbed in early PT (Na/K ATPase) -> Cl left behind -> negative TEPD builds up -> Cl repelled and reabsorbed -> positive TEPD builds up -> K repelled and reabsorbed

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20
Q

What secretes and reabsorbs K in the LoH and collecting ducts?

A
  • K reabsorbed by medullary collecting duct
  • K secreted into late PT and descending thin limb of LoH
  • K secreted into cortical collecting duct
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21
Q

What is the goal of K medullary recycling?

A
  • increase presence of medullary K which decreases NKCC2 reabsorption in thick ascending limb -> increased Na to distal tubule -> stimulates Na reabsorption and K secretion
  • overall goal is to excrete more K
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22
Q

What do principal cells and B-intercalated cells do w/ K? How does each do it?

A
  • secrete K
  • principal cells through ROMK (renal outer medullary K channels) and BK channels
  • B-intercalated cells through K/H exchanger on basolateral membrane (brings K inside cell from blood and flows down concentration gradient)
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23
Q

What factors stimulate K secretion in the collecting duct?

A
  • increased ECF K concentration
  • aldosterone
  • increased tubular flow rate
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24
Q

What do A-intercalated cells do w/ K? How?

A

reabsorb K through K/H exchanger on apical membrane (brings K into cell from lumen)

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25
Q

What factors stimulate K reabsorption in the collecting duct?

A

K deficiency, hypokalemia, loss of K through severe diarrhea

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26
Q

How does tubular flow rate effect K secretion by principal cells in the collecting duct?

A
  • increased flow rate enhances K secretion -> dilutes K in lumen -> larger concentration gradient -> principal cells secrete more K
  • decreased flow rate slows K secretion -> K concentration builds up earlier -> concentration gradient decreases -> principal cells secrete less K
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27
Q

How do high Na intake and high tubular flow rates counterbalance each other?

A
  • high Na -> low aldosterone (want to reabsorb less salt) -> inhibits secretion of K
  • high Na -> increased GFR and decreased Na reabsorption in PT -> increased DT flow rate -> increased K secretion
  • allows person to eat lots of Na w/o becoming hypokalemic
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28
Q

How does chronic acidosis differ from acute acidosis on K?

A
  • Acute acidosis decreases Na/K ATP activity and decreases K secretion (hyperkalemia)
  • Chronic acidosis stimulates K secretion b/c over time, decreased K secretion leads to increased K concentration -> increased aldosterone -> increased Na/K ATPase and increased secretion
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29
Q

What effect does ADH have on K secretion?

A

increased K secretion via Na reabsorption

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30
Q

What effect do diuretics have on K secretion?

A

Diuretics that inhibit Na reabsorption will promote K secretion (except K-sparing) -> increased Na to distal tubule which promotes K secretion

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31
Q

How much Ca is adequate per day? How is the majority of ingested Ca lost?

A

1000mg/day; majority is lost through feces

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32
Q

What is total plasma Ca levels? Where is 99% of Ca stored?

A
  • 5.0 mEq/L

- in bones

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33
Q

What causes hypocalcemia and what effect does it have on neuromuscular excitability?

A
  • caused by hypoparathyroidism, renal disease, and vitamin D deficiency
  • shifts membrane potential to a less positive value -> increases excitability
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34
Q

What causes hypercalcemia and what effect does it have on neuromuscular excitability?

A
  • caused by primary hyperparathyroidism or malignancy

- shifts membrane potential to a more positive value -> depresses excitability

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35
Q

What are 3 regulators of Ca levels?

A

PTH, calcitonin, and calcitriol

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36
Q

What percentage of serum Ca is diffusible through the glomerulus (non-protein bound)?

A

60%

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37
Q

What do Ca and H compete for?

A

binding sites on plasma albumin

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38
Q

How do hypoalbuminemia and hyperalbuminemia affect plasma Ca levels?

A
  • hypoalbuminemia increases plasma Ca -> less albumin to bind to
  • hyperalbuminemia lower plasma Ca -> more albumin to bind to
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39
Q

How do acidosis and alkalosis affect free Ca in circulation?

A
  • Acidosis increases free Ca -> hydrogen beats Ca in binding to albumin
  • alkalosis decreases free Ca -> more Ca bound to albumin
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40
Q

What is another name for calcitriol? What is its function and overall effect?

A

Vitamin D; works w/ PTH to resorb bone (stimulates osteoclasts)
Overall effect: increases serum Ca and Pi

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41
Q

What effect does calcitriol have on bone, intestine, and kidney?

A
  • Bone: promotes bone resorption
  • Intestine: increases Ca and Pi absorption
  • Kidney: increases Pi and Ca reabsorption
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42
Q

What stimulates calcitonin? What is its overall effect?

A
  • stimulated by hypercalcemia

- Overall effect: decrease serum Ca and Pi concentrations

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43
Q

What effect does calcitonin have on bone and kidneys?

A
  • Bone: inhibits resorption (decreases activity and # of osteoclasts)
  • Kidney: promotes Pi and Ca excretion
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44
Q

What is the overall effect of PTH?

A

Increases serum Ca and decreases serum Pi

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45
Q

What effect does PTH have on bone, intestine,and kidney?

A
  • Bone: increases resorption
  • Intestine: increases Ca/Pi absorption via calcitriol production
  • Kidney: increase Ca reabsorption in DCT; decrease Pi reabsorption in PCT
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46
Q

What is the function of the calcium sensing receptor (CaSR)?

A

monitors Ca levels in the blood and inhibits Ca reabsorption in the thick ascending limb when plasma Ca is high (activated on basolateral membrane and inhibits NKCC2 receptor on apical membrane)

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47
Q

How much is Ca reabsorbed in the PT and how?

A

65-70%; mostly passive (follows Na and water reabsorption) and paracellular

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48
Q

What drives Ca reabsorption in the thick ascending limb? What stimulates and inhibits Ca reabsorption?

A
  • driven by positive lumen voltage (TEPD)
  • promoted by ADH
  • inhibited by CaSR
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49
Q

How much is Ca reabsorbed in the DT and how?

A

8%; active transport

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50
Q

What channels are used to reabsorb Ca in the DT?

A

renal epithelial Ca channel (TRPV5) brings Ca into cell from tubular lumen; Ca crosses basolateral membrane via Na-Ca exchanger (NCE)

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51
Q

What stimulates Ca reabsorption in the DT?

A

PTH and calcitriol

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52
Q

What is the purpose of calbindin?

A

Ca binding protein when Ca is intracellular b/c excessive intracellular Ca would cause apoptosis

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53
Q

What effect does academia have on Ca excretion? Why does this make sense?

A

increases Ca excretion (inhibits TPRV5); less Ca bound to albumin (hypercalcemia)

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54
Q

What effect does alkalemia have on Ca excretion? Why does this make sense?

A

decreases Ca excretion (stimulates TPRV5); more Ca bound to albumin (hypocalcemia)

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55
Q

What is recommended daily intake of Pi? How much is actually absorbed?

A

1500mg/ day; only about 900mg would be absorbed

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56
Q

What are the 4 regulators of Pi Metabolism?

A

dietary phosphate intake, calcitriol, PTH, and renal tubular reabsorption of Pi

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57
Q

Is Pi freely filtered at the glomerulus?

A

Yes; filterability is 1.0

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58
Q

How is Pi reabsorbed in the early and late PT?

A

through the Na-Pi symporter (moreso in the late PT); Pi crosses basolateral membrane by an unknown transporter

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59
Q

How does FGF-23 affect Pi reabsorption

A

decreases it

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60
Q

Where is Vitamin D converted from its inactive form to active form? What enzyme is involved?

A

converted in the the PT by renal 1a-hydroxylase

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61
Q

What upregulates and inhibits renal 1a-hydroxylase?

A
  • unregulated by low Ca, low phosphate and high PTH

- inhibited by high Ca (more specifically by CaSR)

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62
Q

What effect does PTH have on serum Pi? How does it do this?

A
  • lowers it by increasing renal excretion

- inhibits Na-Pi symporter and Na-H antiporter in apical membrane of PT cells

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63
Q

What effect does insulin have on serum Pi?

A

lower serum levels by shifting Pi into cells

64
Q

What effect do chronic acidosis and chronic alkalosis have on Pi excretion?

A

acidosis increases Pi excretion

alkalosis decreases Pi excretion

65
Q

How does PTH differ from the PT to the DT?

A

inhibits Pi reabsorption in the PT; stimulates Ca reabsorption in the DT

66
Q

What are the normal values of total serum Mg and free serum Mg (non-protein bound)?

A

Total serum Mg = 1.8-2.2 mg/dL

Free serum Mg = 0.8-1.0 mg/dL

67
Q

How is Mg reabsorbed in the PT?

A

paracellularly; follows Na and water reabsorption

68
Q

What is the major site of Mg reabsorption? How is it reabsorbed?

A

thick ascending limb; reabsorbed paracellularly and depends on the uptake and Na and K through the NKCC2 (inhibited by CaSR)

69
Q

What is the primary driver of Mg in the DT?

A

electrical potential since Mg concentration is about the same on both sides; reabsorbed through active transport

70
Q

What effect does PTH have on Mg reabsorption?

A

increases

71
Q

How do acidosis and alkalosis effect Mg reabsorption?

A

acidosis decreases reabsorption

alkalosis increases reabsorption

72
Q

How do ECF volume contraction and expansion effect Mg reabsorption?

A

contraction increases reabsorption

expansion decreases reabsorption

73
Q

What is normal pH for the following: arterial blood, venous blood, ICF, and urine?

A

arterial blood: 7.40
venous blood: 7.35
ICF: 6.0 to 7.4 (usually 7.1)
Urine: 4.5 to 8.0 (allows you to excrete acids and alkaloids as needed)

74
Q

What is the major buffer system in mammals?

A 
Carbonic acid (weak acid)
H20 + CO2  H2CO3  HCO3 + H+
75
Q

How are CO2 and H2O produced and removed?

A

produced by aerobic metabolism; blown off by lungs

76
Q

How are HCO3 and H+ produced and removed?

A

produced by anaerobic metabolism; regulated by kidneys

77
Q

How is the majority of CO2 transported in the blood? How?

A

transported as HCO3; CO2 dissolves into RBCs -> in presence of H2O becomes HCO3 and H+ -> released into the blood through the HCO3/Cl transporter

78
Q

What is the Henderson-Hasselbalch equation?

A
  • pH = 6.1 + log ([HCO3]/[H2CO3])

- H2CO3 equivalent to 0.03 x PCO2

79
Q

What effect does hyperventilating and holding your breath have on blood pH?

A
  • hyperventilating increases pH -> removes CO2 -> less H+

- holding breath decreases pH -> build up of CO2 -> more H+

80
Q

Describe how HCO3 is reabsorbed in the PCT?

A

Na/H antiporter pumps H into tubular fluid -> binds to HCO3 and becomes H2O and CO2 through carbonic anhydrase -> diffuse into cell and converted to HCO3 and H+ through carbonic anhydrase again -> HCO3 flows into blood and H transported back to tubular fluid

81
Q

Name 6 factors that increase H+ secretion?

A
  • decrease in plasma HCO3
  • increased PCO2
  • decrease in ECF
  • increase in Ang II
  • increase in aldosterone
  • hypokalemia
82
Q

What do the kidneys metabolize for energy? What is cleaved off this molecule and secreted into PCT?

A

glutamine -> 2 ammonia groups cleaved and secreted as ammonium (NH4+)

83
Q

Describe the path of ammonium in the nephron?

A

can substitute for K in NKCC2 in thick ascending limb -> trapped in interstitium due to + charge -> spontaneously transform into NH3 and diffuses back into tubular fluid in collecting duct -> H+ added to NH3 to make NH4+ (trapped in urine)

84
Q

How do alpha and beta intercalated cells handle H+ and HCO3

A
  • Alpha secrete H+ and reabsorb HCO3 (through same process as PCT)
  • Beta reabsorb H+ and secrete HCO3
85
Q

What is metabolic acidosis? What is the compensation?

A

loss of base or addition of acid; hyperventilation as respiratory compensation

86
Q

What are some causes of metabolic acidosis? How would a pt present?

A
  • DKA, lactic acidosis, EtOH poisoning, renal tubular acidosis
  • if pH < 7.10: N/V and malaise; pt will have long deep breaths w/ no dyspnea
87
Q

Describe renal tubular acidosis (RTA) - 3 types?

A

Type I: intercalated cells can’t secrete H+
Type II: lose HCO3 in PCT
Type IV: high plasma K due to deficiency of aldosterone

88
Q

What is metabolic alkalosis? What is the compensation?

A

addition of base or loss of acid -> hypoventilation as respiratory compensation

89
Q

What are some causes of metabolic alkalosis?

A

vomiting (loss of H); antacid tablets (gain of HCO3), diuretics (volume contraction

90
Q

What is respiratory acidosis? What is the compensation?

A

decreased ventilation -> CO2 goes up -> kidneys increase HCO3 regeneration and acid excretion

91
Q

What are some causes of respiratory acidosis?

A

CNS depression, airway obstruction, pneumonia, embolism, COPD

92
Q

What is respiratory alkalosis? What is the compensation?

A

increased ventilation -> CO2 decreases -> kidneys decrease acid excretion

93
Q

What are some causes of respiratory alkalosis?

A

hypoxia, anxiety, mechanical ventilators, progesterone, salicylates/sepsis

94
Q

What is responsible for creating a 200 mOsm difference between the thin ascending limb and medullary interstitium?

A

NKCC2 transporter

95
Q

How does the descending limb respond to the increased osmolarity of the medullary interstitium?

A

Water passively flows into interstium to lower osmolarity -> LoH becomes more concentrated the further into the medulla it goes

96
Q

What is the max concentration that can be reached at the bottom of the LoH?

A

1200-1400 mOsm

97
Q

What is the osmolarity of tubular fluid leaving the ascending limb and entering the DCT?

A

hypotonic after pumping out ions but not water (can be as low as 100 mOsm)

98
Q

What is the purpose of the vasa recta?

A

supply blood (very slowly) to the medulla -> supplies O2 and nutrients and removes water and solutes

99
Q

What is medullary washout? What effect does it have on the nephron’s ability to concentrate urine?

A

increase in vasa recta blood flow literally washes solutes out of the medulla -> reduces the concentration gradient and reduces the ability to concentrate urine

100
Q

What transporters move urea from the medullary collecting duct to the medullary interstitium?

A

UT-A1 and UT-A3

101
Q

How is urea recycled back into the nephron?

A

Some diffuses into the thin ascending and descending limbs and the rest is added back to the LoH through the UT-A2 transporter

102
Q

What hormone plays a role in the recycling process of urea?

A

ADH

103
Q

What can you assume about the DCT and collecting duct if ADH is not present?

A

they are impermeable to water

104
Q

What is another name for ADH?

A

Arginine Vasopressin -> AVP

105
Q

Where is ADH synthesized? What stimulates these regions to release ADH?

A

supraoptic and paraventricular nuclei of the hypothalamus; stimulated by increased osmolarity

106
Q

What 2 things will osmoreceptors cause? Which comes first?

A

cause release of ADH and stimulate thirst -> ADH will be released first generally

107
Q

On what cell type does ADH stimulate the reabsorption of water? How does it do this?

A

principal cells in the late distal tubule and collecting duct; increases the # of AQP-2 channels in the apical membrane (water reabsorbed)

108
Q

How does increased plasma osmolarity affect K secretion?

A

It increases K secretion

109
Q

How does aldosterone affect intercalated cells?

A

increases H secretion by stimulating H ATPase

110
Q

Describe the RAAS system?

A

decreased renal perfusion -> renin secreted -> Ang II -> ADH (water reabsorption) and Aldosterone (salt reabsorption) -> increased blood volume

111
Q

What releases aldosterone? What stimulates the release?

A

released from the adrenal cortex in response to Ang II or directly in response to increased plasma K

112
Q

What channel does aldosterone increase the # of and what is the result?

A

ENaC (epithelial Na channels) which increases the amount of Na being reabsorbed in exchange for secreting K simultaneously

113
Q

What effect does a decrease in plasma Na have on aldosterone?

A

stimulates aldosterone secretion through the RAAS system

114
Q

What effect does a decrease in plasma osmolarity have on osmoreceptors?

A

reduces osmoreceptor signaling -> ADH not secreted -> collecting duct not permeable to water -> water excreted in urine

115
Q

What happens to ADH when a person is overhydrated? Dehydrated?

A 
Overhydrated = ADH inhibited
Dehydrated = ADH stimulated
116
Q

What is normal blood osmolarity?

A

275 - 295 mOsm/kg

117
Q

What is central neurogenic DI? What can cause it?

A

failure to produce or release ADH from the posterior pituitary; may be caused by head injuries, infections, or congenital

118
Q

What is the treatment of central neurogenic DI?

A

desmopressin -> synthetic analog of ADH that increases permeability of DCT and collecting duct to water

119
Q

What is nephrogenic DI?

A

inability of the kidneys to respond to ADH -> failure of countercurrent multiplier to create hyperosmotic medullary interstitium or failure of DCT and collecting duct to respond to ADH

120
Q

What is one thing that can impair the LoH to concentrate urine? What are 2 things that can impair the distal nephron to respond to ADH?

A

LoH: diuretics that inhibit electrolyte reabsorption

Distal nephron: lithium and tetracyclines

121
Q

How do you differentiate between nephrogenic and neurogenic DI?

A

neurogenic will respond to desmopressin; nephrogenic won’t

122
Q

What is SIADH?

A

syndrome of inappropriate ADH secretion -> excessive release of ADH

123
Q

What does SIADH lead to?

A

excessive water retention which leads to reduced plasma osmolarity, hyponatremia, water intoxication, and elevated GFR

124
Q

How do you distinguish between DI and SIADH?

A

DI: high urinary output, low levels of ADH, hypernatremia, dehydrated

SIADH: low urinary output, high levels of ADH, hyponatremia, overhydrated

125
Q

Dilution of urine is dependent on what part of the nephron and what transporter?

A

Thick ascending limb; NKCC2 transporter

126
Q

What is the highest and lowest osmolarity final urine can be? What hormones are involved?

A

50 mOsm when ADH not secreted

1200 mOsm when max ADH is secreted

127
Q

What is hyponatremia (water to solute)? What will serum Na and serum osmolarity be?

A
  • excess water relative to solutes in the body
  • serum Na < 135 mEq/L
  • serum osmolarity < 280 mEq/L
128
Q

What is hypernatremia (water to solute)? What will these pt’s generally also have?

A
  • deficient free water relative to solute

- most pt’s will also have volume depletion

129
Q

What is normal urine volume?

A

1-2 L/day

130
Q

Define polyuria. What are some causes?

A
  • excessive urine production (> 2.5 L/day)

- DM, DI, excess caffeine, diuretics, excessive water intake

131
Q

Define oliguria. What are some causes?

A
  • urine output below minimum volume (300-500 mL/day)

- dehydration, blood loss, diarrhea, or kidney disease

132
Q

Define anuria. What are some causes?

A
  • virtual absence of urine production (< 50 mL/day)

- kidney failure, obstruction, enlarged prostate

133
Q

What is polydipsia? What is it usually associated w/?

A

water intake of more than 6 L/day; usually associated w/ polyuria

134
Q

Water diuresis vs solute (osmotic) diuresis

A
  • water diuresis is increased water excretion w/o increased salt excretion
  • solute (osmotic) diuresis is increased water excretion along w/ increased salt excretion
135
Q

How do you calculate urine volume?

A

solutes excreted per day/max urine concentration ability; less than 0.5 L/day is oliguria

136
Q

What is free water clearance? What do positive and negative results mean?

A
  • rate at which solute-free water is excreted by the kidneys
  • positive = excess water is being excreted
  • negative = excess solutes are being excreted and water is being conserved
137
Q

What will free water clearance be when urine osmolarity is greater than plasma osmolarity?

A

negative -> water is being conserved

138
Q

What will free water clearance be when urine osmolarity is less than plasma osmolarity?

A

positive -> excess water loss

139
Q

How do you calculate free water clearance?

A

CH2O = V – Cosm = V – [(Uosm x V)/(Posm)]

140
Q

What does a Uosm:Posm greater than 1 mean?

A

kidneys can concentrate urine

141
Q

What does a Uosm:Posm of 1 indicate?

A

water and solutes are being excreted in a state that is isosmotic w/ plasma

142
Q

What does a Uosm:Posm less than 1 mean?

A

kidneys are able to dilute urine

143
Q

What does regulating ECF volume do? How is it maintained?

A

helps regulate BP through maintaining salt balance

144
Q

What does regulating ECF osmolarity do? How is it maintained?

A

prevents swelling or shrinking of cells by maintaining water balance

145
Q

What is effective circulating volume (ECV) and what is special about it?

A

portion of ECF volume that is effectively perfusing tissues; it is not measurable

146
Q

Explain how pt’s w/ CHF have a low ECV and what effect this has

A

pt’s have low ECV due to decreased CO; they will have Na and fluid retention (edema) which will increase ECF volume w/o correcting ECV

147
Q

How are decreases in EVC counteracted (4)?

A
  • activating RAAS system
  • stimulator of sympathetic nervous system through baroreceptors
  • increase ADH secretion
  • increased renal fluid retention
148
Q

What 2 receptors control ADH secretion? What does each sense and which is more sensitive?

A
  • osmoreceptors (changes in body fluid osmolarity) -> more sensitive
  • baroreceptors (changes in blood volume)
149
Q

What effect does decreased BV and BP have on ADH?

A

increases ADH secretion

150
Q

Name 3 types of baroreceptors and what each senses?

A

Arterial: sense pressures in aorta and carotid arteries
Cardiopulmonary: sense pressures in atria and pulmonary arteries
Intrarenal: sense renal blood flow (major role in RAAS)

151
Q

What effect does increases sympathetic activity have on GFR, renin secretion, and NaCl excretion

A

increased sympathetics decreases GFR, increased renin, NaCl excretion (more Na reabsorption)

152
Q

What effect does increased activation of RAAS have on NaCl excretion?

A

increased RAAS decreases NaCl excretion

153
Q

What effect does increased natriuretic peptides (ANP, BNP, and urodilantin) have on NaCl excretion, GFR, and renin secretion?

A

increased natriuretic peptides increases NaCl excretion, increases GFR, and decreases renin

154
Q

What effect does increased ADH/AVP have on H2O excretion? Where in the nephron does this take place?

A

increased ADH/AVP decreases H2O excretion in the DCT and collecting duct

155
Q

What 3 factors result in the release of renin by cells of the JG apparatus?

A
  • low perfusion of afferent arterioles
  • activation of sympathetics
  • less NaCl delivery to the macula densa
156
Q

What cells produce ANP and in response to what?

A

atrial cardiac cells produce ANP in response to being mechanically stretched (increased ECF, increased BP, increased Na and H2O retention)

157
Q

What hormone is responsible for increasing permeability of the medullary collecting duct to urea?

A

ADH

Renal Final (2 decks)

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