Loop of Henle, DT, and CD (Rao) Flashcards

1
Q

What is the function of the DT?

A

to form urine w/ variable osmolarity

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2
Q

According to physiologist, where does the DT start?

A

at loop of henle, contains distal convoluted tubule, and collecting duct

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3
Q

What maintains the pH of urine from 4.5-8?

A

PO4 and H+

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4
Q

What is the loop of Henle thin?

A

lack of mitochondria or few of them since no active transport occurs here

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5
Q

What happens to the ISF environment of the thin descending LOH?

A
  1. hyperosomotic to plasma
  2. increases progressively b/w cortex and medulla
  3. reaches max of 1200 mOsm
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6
Q

What is the function of the thin descending LOH?

A
  1. concentrates tubular fluid
  2. no active transepithelial transport
  3. highly permeable to water - due to lots of AQP
  4. minimal permeability to NaCl and Urea
  5. osmotic gradient is the driving forces
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7
Q

What are the transport properties of the thin ascending LOH?

A
  1. extremely water IMPERMEABLE
  2. Impermeable to urea
  3. permeable to NaCl – strong NaCl reabsorption
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8
Q

What happens to the osmolarity in the thin ascending LOH?

A

it drops b/c of NaCl diffusion and impermeable to tubular fluid

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9
Q

What is the structure of the Thick Ascending LOH?

A
  1. b/w medulla and cortex

2. thick epithelial cells w/ many mitochondria

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10
Q

What are the transport properties of the thick ascending LOH?

A
  1. serves in STRONG reabsorption of NaCl

2. impermeable to water

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11
Q

What transporters are found at the thick ascending LOH?

A
  1. NaK2Cl - electroneutral, apical side
  2. NaKATPase at basolateral side
  3. Cl channel - BL side
  4. K/Cl cotransporter - BL side
  5. Apical K Channel
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12
Q

What can inhibit the NK2Cl channel?

A

furosemide, bumetanide – have a high affinity for Cl site on channel –> block NaCl reabsoprtion –> leads to diuresis

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13
Q

What is diuresis?

A

increased water loss in urine

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14
Q

How does one form a collecting duct?

A

joining 6-8 DT together

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15
Q

What do CDs do in the medulla?

A

join to form duct of Bellini

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16
Q

What happens to the tubular fluid at the DT and CD?

A
  1. Na is actively reabsorbed
  2. K is secreted
  3. Na reabsorption is greater than K secretion so Cl is reabsorbed
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17
Q

how much filtrate is received at the DT and CD?

A

10% of filtered load of water, <10% filtered load of NaCl and KCl, and 50% urea

18
Q

What is the net result of DT and CD?

A

dilution of tubular fluid

19
Q

What are the 2 distinct transport mechanism at DT and CD?

A
  1. electrically conductive Na channels (in both)

2. NaCl co-transporter (only in DT)

20
Q

What does amiloride and tramterene do?

A

block Na channels at DT and CD

- amiloride prevents membrane depolarization and has no increase on K secretion

21
Q

What do thiazide diuretics do?

A

inhibit NaCl cotransporters in DT –> doesn’t affect membrane potential though

22
Q

Which diuretic is more efficient?

A

loop –> increase K secretion

23
Q

What happens to the lumen voltage when all the Na is reabsorbed?

A

more negative so membrane if depolarized and K is secreted

24
Q

What is the driving fore for K secretion?

A
  1. high IC [K] caused by NKA

2. lumen-negative transepithelial voltage

25
Q

What effect does fluid flow have on K secretion?

A

if increased by diuretics –> increased K secretion

26
Q

How does aldosterone function?

A
  • acts only on DCT and CD
  • increases Na reabsorption
  • increases K secretion
27
Q

What is the MOA of aldosterone?

A

enters cell and binds to cytoplasmic and nuclear receptors to induce gene expression

28
Q

What effect does aldosterone have on the cell?

A
  1. increases Na channels (apical)
  2. increases NaCl cotransporter
  3. increases NKA
  4. increased basolateral surface ara
  5. increase synthesis of Krebs Cycle enzymes to make ATP
  6. increase activity of apical K channel
29
Q

What is Addison’s disease?

A
  • complete absence of aldosterone

- increased urinary excretion of NaCl

30
Q

What is Conn’s syndrome?

A
  • aldosterone secreting tumor
  • increased Na reabsorption and K secretion
  • hypokalemia, hypernatremia, HTN
31
Q

What is Liddle’s Syndrome?

A

pseudo hyperaldosteronism

32
Q

What do principal cells do?

A

Na reabsoprtion and K secretion

33
Q

What do intercalated cells do?

A

alpha cells - proton channel in luminal membrane

beta cells - bicarb channel in luminal membrane

34
Q

Why is proton secretion different in DT/CD than PT?

A
  • H+ secreted against electrochemical gradient so needs high E active transport and epithelium is impermeant to diffusion
35
Q

What transporter is used for H+ secretion?

A

Proton activated ATPase – ATP hydrolysis drives transport of H from cell to lumen via apical channel

36
Q

What drives HCO3- diffusion from cell to renal ISF?

A

increase in IC [HCO3-], diffused via HCO3-/Cl exchanger

37
Q

What happens during a high acidosis condition?

A

cells express a new H transporter –> H/K ATPase or proton pump

38
Q

What happens during Alkalosis?

A

H-ATPase and HCO3-/Cl exchange channels switch directionality

39
Q

How is the directional switch of the channels activated?

A

by alpha and beta intercalated cells

40
Q

What stimulates distal nephron Ca reabsorption?

A

PTH