14. Renal Tubular Transport Flashcards

1
Q

what is reabs-ed in the PCT

A

NaHCO3 - initatied by Na/H exhanger (85%)

NaCl - 65% total Na

K+ - via paracellular path 65%

glucose, AA - 100%

h2o - 65% total reabs passively

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2
Q

what is the purpose of the Na/K ATPase in the basement membrane

A

reabs Na into interstitum to maintain low intracell Na

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3
Q

what occurs in the straight segment of the proximal tubule

A

acid secretory system secrete organic acids into luminal fluid

(uric acid, NSAIDs, diuretics, antiobiotics)

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4
Q

what are carbonic anhydrase inhibitors used for

A

decrease H formation inside PCT

decrease Na/H antiport

increase Na & HCO3 in lumen

increase diuresis

increase urine pH (decrease body pH)

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5
Q

where is water reabs in the loop of henle

A

thin descending limb

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6
Q

what occurs at the thin ascending limb of LoH

A

almost nothing

relatively impermeable to h2o & other ions/solutes

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7
Q

what occurs at the thick ascending limb of LoH

A

25% reabs Na

(impermeable to h2o)

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8
Q

how is NaCl reabs-ed into interstitial space in thick ascending limb

A
  1. luminal side - Na/K/2Cl cotransporter (NKCC2) - establish ion concentration gradient in interstitium
  2. increase [K] in cells –> back diffusion of K into tubular lumen –>
  3. allow lumen-positive electrical potential to drive cation (Mg, Ca) reabs via paracellular pathways
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9
Q

what is reabsed at the DCT and how

A

10% NaCl via thiazide-senstive Na-Cl co transporter

Ca2+ -passively via Ca channels

==> results in d_ilute tubular fluid_

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10
Q

what do you get if you inhibit Na/K/2Cl ccotransporter

A

(do so w/ loop diuretics)

decrease intracel Na, K, Cl in TAL

decrease K back diffusion & positive potential

decreased reabs of Ca & Mg

increased diuresis - decrease urine pH (increases body pH)

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11
Q

what happens with use of thiazide diuretics

A

inhibit Na/Cl cotransporter (NCC)

inhibit NaCl reabs in DCT –>

increase luminal Na & Cl & increase diuresis (decrease urine pH)

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12
Q

How is NaCl reabs in collecting tubule

A

2-5% NaCl reabs thru epithelial Na channel (ENaC)

aldosterone increase expression of ENaC–>

basolateral Na/K ATPase lead to increase Na reabs & K secretion –>

retain h2o –> increase blood vol & BP

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13
Q

what is the most important site of K+ secretion

A

collecting tubule (CCT)

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14
Q

what do you get when a diuretic acts upstream to CCT

A

increase Na delivery

enhance K secretion

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15
Q

How is H+ secreted in the CCT

A

by proton pump (H-ATPase) into lumen @ alpha intercalating cells & increase urine acidity

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16
Q

what does ADH do at the CCT

A

control permeability of CCT to h2o

control expression of aquaporin-2 into apical membrane

regulated by serum osmolality and volume status

17
Q

what happens with absence of ADH

A

impermeable to h2o –> make dilute urine

(ADH can be decreased by alc –> lead to increase urine production)

18
Q

what are the two mechanisms for K sparing diuretics

A
  1. inhibit aldosterone receptor - decrease ENaC
  2. inhibit ENaC

==> - increase Na excretion - increase diuresis - decrease K excretion -increase urine pH

19
Q

what stimulates Na reabs

A
  1. hyponatremia, low Na diet
  2. Na loss thru severe diarrhea
  3. angiotensin II
  4. aldosterone
20
Q

what stimulates Na secretion

A

increased [Na] in ECF

increased tubular flow rate

21
Q

what stimulates K reabs

A

hypokalemia (low K diet)

K loss thru severe diarrhea

22
Q

what stimulates K secretion

A
  1. increased [K] ECF
  2. aldosterone
  3. increased tubular flow rate
  4. Na delivery to cortical CD
23
Q

what is the urea permeability in inner medullary collecting duct (IMCD)

A

during anti-diuresis - h2o reabs in CCT

urea flows thru the duct & is concentrated in IMCD

high [urea] promotes passive reabs down [] from IMCD into interstitium

  • go to LoH where [urea] is low –> flow down gradient into LoH
24
Q

what does ADH do to NKCC2 channels in TAL

A

increase presence of NKCC2 channels – increase permeability of NaCl at apical mem of TAL

increase reabs –> increased osm

IMCD gets very concentrated bc Na & urea –> greater urine concentrating abliity

25
Q

describe the blood osm as it moves thru the LoH

A
  1. filtrate enter PCT = 300
  2. go down descendng LoH –> h2o leave tubule @ end concentration = 1200
  3. fluid goes up ascending LoH - solute pumped out –> become dilute
  4. get to DCT & =100
26
Q

what is the path blood takes after entering the peritubular cap system (PTC)

& what happens to blood

A
  1. head down next to ascending LoH (= countercurrent) - pick up solute
  2. at bottom of hair pin = 1200
  3. then vessel turns to go up beside descending LoH (= countercurrent) - h2o into blood vessel
  4. return to 300 mOsm/L
27
Q

how do you calculate free water clearance

A

negative = h2o conservation

positive = h2o excess

28
Q

what is osmolar clearance

A

total clearance of solute from blood

29
Q

what is obligatory urine volume (OUV)

A

= minimal vol of urine required to excrete waste solutes needing to be excreted from the body

30
Q

what is natriuresis

A

excretion of excessive Na in urine

could be drug or hormone (ANP) or elevated perfusion induced

31
Q

what is diuresis

A

large urine output

could be water or solute diuresis

32
Q

what is antiduresis

A

plasma ADH is high

& small vol of concentrated urine is excreted

33
Q

high BP is associated with

A

increased risk of MI, heart failure, stroke & kidney disease

34
Q

what are the possible mechanisms for antihypertensive agents

A
  1. diuretics
  2. agents that block production/action of angiotensin
  3. direct vasodilators
  4. sympathoplegic agents –> alter sym fxn
35
Q

what is the fxn of the nephron

A

separate h2o, ions & small molecules from blood

filter our wastes/toxins

facilitates [urine]

36
Q

what is the relationship of the glomerulus and bowman’s capsule

A

glomeular caps (=glomerulus) filter fluid into bowmans capsule

fluid then goes into proximal tubule

37
Q

what is the concentration of tubular fluid in the descending & ascending limb

A

concentrated in descending limb

dilute in ascending limb

38
Q

what do diuretics target

A
  1. specific mem transport proteins -NKCC2 (loop), Na-Cl cotransporter (thiazides) & Na channels (K-sparring)
  2. enzymes: carbonic anhydrase inhibitors
  3. hormone receptors: mineralocorticoid receptor (K sparring)