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Renal Module > Loop, DT, CD, CCM > Flashcards

Loop, DT, CD, CCM Flashcards

1
Q

Where do most urine osmolarity regulatory mechanisms target? Why?

A

The Distal tubular segments; bc the DT is specialized to form urine with variable osmolarity

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2
Q

Massive reabsorption in the PT is________ but the final urine excreted is not ________.

A

iso-osmotic; iso-osmotic

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3
Q

What three structures are distal to the PT?

A
  1. Loop of Henle (Thin descending limb,tAL, TAL)
  2. DCT
  3. Collecting Ducts
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4
Q

What is the function of these three structures distal to the PT? How?

A

This is where tubular fluid is converted to urine; specialized and tightly regulated transport characteristics

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5
Q

What ions maintain the pH of the urine at 4.5-8?

A

PO4 and H+

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6
Q

What percent of the filtered load of Na+ ends up in the urine?

A

0-2%

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7
Q

What are some structural characteristics of the tDL of L of H?

A

a. Starts at distal end of PST (it’s length varies)
b. Runs from cortex to the outer medulla
c. Consists of thin epithelial cells with few mitochondria

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8
Q

Describe the interstitial environment around the tDL:

A

It is hyperosmotic to plasma; it’s osmolarity increases progressively between the cortex and the medulla

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9
Q

What is the maximum osmolarity of interstitial environment of the tDL? What contributes to this osmolarity?

A

Reached maximum of 1200 mOsm; 600mOsm urea and 600mOsm NaCl

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10
Q

What is the function of the tDL of L of H? How?

A

It concentrates the tubular fluid

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11
Q

What are the transport properties of the tDL?

A

No active transepithelial transport; highly permeable to water due to high levels of Aquaporins; minimal permeability to NaCl and urea

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12
Q

What is the driving force of water reabsorption thru AQP’s? How does this affect the osmolarity in the tDL?

A

The driving force is the osmotic gradient (water reabsorbed into hyperosmotic ISF): osmolarity increases from 280 to 1200 mOsm in the tubular fluid as water moves out into the ISF along the length of the tDL.

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13
Q

How does the structure of the tAL compare to that of the tDL? How do their transport properties compare?

A

They have similar structures, but their transport properties are dramatically different.

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14
Q

What are the transport properties of the tAL?

A

Extremely impermeable to water bc it has no AQP’s; impermeable to urea; Permeable to NaCl (this is the only thing that can alter osmolarity in the tAL)

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15
Q

Describe the reabsorption of NaCl in the tAL? What is the driving force?

A

Strong reabsorption of NaCl→20-25% of NaCl fitered load or greater than 2/3 of the volume it receives are reabsorbed.
The driving force is the osmotic gradient

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16
Q

What is the gradient of urea from tubular fluid to ISF?

A

50mOsm in TF and 600mOsm in ISF, but impermeable.

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17
Q

What happens to the osmolarity of the tubular fluid as it passes along the length of the tAL? Why?

A

The tubular fluid osmolarity drops and becomes hypo-osmotic by the time is reaches the Thick AL because of NaCl diffusion into the ISF and the impermeabilty to tubular fluid.

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18
Q

Where is the TAL located? What type of cells does it consist of?

A

Located between the medulla and the cortex; composed of thick epithelial cells with many mitochondria

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19
Q

What are the transport properties of the TAL?

A

Impermeable to water; strong NaCl reabsorption via an active transport mechanism

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20
Q

What are the two main transporters in the TAL? (hint both involve Na+)

A

Na-K-2Cl (NK2C) transporter on the apical membrane; Na-K-ATPase on the basolateral membrane

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21
Q

How do the NKA and NK2C work together in the TAL?

A

NKA activity on BL membrane creates electrochemical gradient. NK2C transporter binds luminal Na, K, and 2Cl and transports them into the cell down the electrochemical gradient (driving force) created by the NKA. This is a net ACTIVE process

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22
Q

What are the other channels in the TAL and where are they located? (3)

A

BL Membrane: 1. Cl- channel (electrogenic) 2. K-Cl Cotransporter (electroneutral
Apical: 1. K+ channel

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23
Q

How is NK2C is regulated?

A
  1. Loop diuretic agents (furosemide, bumetanide)
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24
Q

How do diuretic agents regulate NK2C?

A

They have high affinity for Cl- binding site on NK2C→ blocks NaCl reabsorption→increased NaCl load delivered to distal nephron→interferes with urine concentration→Diuresis (increased water loss in urine)

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25
Q

Which diuretics are most effective? Why?

A

Loop diuretics are most efficient due to high NaCl reabsorption in ascending limb

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26
Q

How does ADH affect diuresis? What inhibits ADH?

A

It reduced diuresis by stimulating NaCl reabsorption which inhibits diuresis. This causes ISF osmolarity to increase, which ulitmately downregulates ADH levels.

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27
Q

What does the TAL flow into?

A

DCT

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28
Q

How many DCT’s join together to form a CD?

A

6-8

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29
Q

Where are collecting ducts located?

A

they start in the cortex and run down to the medulla

30
Q

How is Duct of Bellini formed?

A

CD’s join together in the medulla to form a duct of Bellini

31
Q

How do the cell types and cellular functions in DCT and CD compare?

A

They are composed of distinct different cell types, but the functions are similar

32
Q

How much of the filtered load of water is received in the DCT? NaCl and KCl? Urea?

A

DCT receives ~10% of the filtered load of water; s filtered load

33
Q

What ion is actively reabsorbed in DCT? What ion is secreted?

A

Na+; K+

34
Q

Why is Cl- reabsorbed in DCT?

A

because Na+ reabsorption is greater than K+ secretion

35
Q

What is the net result of tubular fluid processing in the DCT?

A

Dilution of tubular fluid (if impermeable to water)

36
Q

In water diuresis, urine becomes progressively what? Why?

A

urine becomes progressively dilute because DCT/CD is impermeable to water

37
Q

In dehydration, urine is what? Why?

A

urine is hyperosmotic because DCT/CD is highly permeable to water which equilibriates with ISF

38
Q

What two distinct transport mechanisms for Na+ occur in the distal nephron? Where specifically are they located? Electrogenic or electroneutral transport?

A
  1. Electrically conductive Na+ channels (electrogenic transport)→ located in both DCT and CD
  2. Na-Cl Co-transporter (electroneutral transport) present only in DCT.
39
Q

What drives entry of Na+ into DCT and CD cells thru electrically conductive Na+ channels?

A

The electrochemical gradient created by NKA activity, allows Na to move down its gradient and into cells

40
Q

Which diuretics block Na+ channels? So, where do they work?

A

Amiloride and Triamterene; work in both DCT and CD

41
Q

Which diuretics inhibit Na-Cl co-transporters? So, where do they work?

A

Thiazide diuretics; work ONLY in DCT

42
Q

Why does there a lumen-negative transepithelial voltage?

A

Lumen is more negative due to electrically conductive Na+ transport thru its channel, resulting in depolarized membrane (like an action potential)

43
Q

Is the Lumen more electronegative in the DCT or CD? Why?

A

Lume is more electronegative in the CD; this is because CD only has Na+ channels, while DCT also has Na-Cl co-transporter

44
Q

What happens to potassium in DCT and CD?

A

It is secreted, moved from cell to tubular lumen via specific K+ channel

45
Q

What are the two driving forces of K+ secretion in DCT and CD?

A
  1. High intracellular concentration of K+ caused by NKA activity
  2. Lumen-negative transepithelial voltage
46
Q

What are three regulatory factors of K+ secretion in DT/CD? What effect do they have on K+ secretion?

A
  1. Fluid/Urine flow rate: increased flow by diuretics increases K+ secretion
  2. Delivery of Na+ to distal tubule→ changes in Na+ reabsorption alter the lumen-negative transepithelial voltage????
  3. As aldosterone increases, K+ secretion increases
47
Q

How do the following diuretics affect K+ balance: a) Loop diuretics b) Thiazides c) Amilorides

A

a) LDs increase flow and Na+ output (greater membrane depolarization) into DT, which increases K+ secretion.
b) TZD’s block electroneutral Na+ transport without affecting membrane depolarization→ so no change in transport (???)
c) Amilorides prevent membrane depolarization→ no increase in K+ secretion

48
Q

Where is aldosterone produced and where does it act?

A

It is a mineralocorticoid secreted by adrenal cortex and it acts exclusively on DCT and CD

49
Q

What are the net effects of aldosterone?

A

Increased Na+ reabsorption and K+ secretion

50
Q

What is the general mechanism of aldosterone?

A

It is permeable to cell membrane, enters the cell and binds to nuclear and cytoplasmic receptors, these complexes act as transcription factors and alter gene expression

51
Q

What is the result of aldosterone regulation of gene expression on transporters in the DCT and CD? What do these cause? (4)

A
  1. Increased open Na+ channels and Na-Cl cotransporters in apical membrane→increased Na+ reabs and transepith voltage
  2. Increased NKA and BL surface area→increased Na reabs and K secr.
  3. Increased CAC enzymes→increased ATP for NKA
  4. Increased number and activity of apical membrane K channels→secretion
52
Q

What is Addison’s Disease?

A

Complete absence of aldosterone

53
Q

How does Addison’s disease affect urinary NaCl? What does this tell us?

A

There is increased urinary excretion of NaCl: it reaches a max of 500meq/L (2% of FL)
Therefore, Na reabs and K secr do not entirey depend on aldosterone.

54
Q

What is Conn’s syndrome? What effect does it have?

A

Aldosterone secreting tumor (excessive aldosterone); increased Na reabs and K secretion

55
Q

In Conn’s Syndrome, how much Na+ is excreted? What are symptoms/effects?

A

Excretes<0.2% of filtered load of Na+;

Symptoms: Hypokalemia, Hypernatremia, Hypertension

56
Q

What percentage of Na excretion is aldosterone-dependent? (based on Add’s disease and Conn Syndrome #’s)

A

0.1-2.0% of filtered load of Na excretion is aldosterone-dependent

57
Q

What is LIddle’s Syndrome?

A

Pseudohyperaldosteronism: same effects as Conn’s syndrome but do to a mutation making Na channel constitutively active

58
Q

How is Liddle’s distinguished from Conn’s?

A

In Liddle’s, the aldosterone level is normal or slightly decreased.

59
Q

What factors increase aldosterone secretion (feedback regulation)? (5)

A
  1. Reduced ECFV and CO 2. Decreased plasma Na 3. Increased plasma K 4. High plasma Ang-II 5. Trauma, Stress
60
Q

What factors cause decreased aldosterone secretion? (5)

A
  1. Increased ECFV 2. Increased plasma Na 3.Decreased plasma K 4. Low plasma Ang-II 5. Low plasma ACTH levels
61
Q

Where does the final acidification of urine occur? How?

A

In DCT and CD; bicarbonate is reabsorbed in exchange for H+ secreted (proton secretion)

62
Q

What two cell types are involved in urine acidification in DCT and CD? What do they do?

A
  1. Principal cells→ Na reabs and K secr

2. Intercalated cells→ proton secretion; some secrete bicarbonate

63
Q

How do intercalated cells secrete protons?

A

Pretty similar to H+ secretion in PT; cellular CA generated H+ which is secreted into lumen by active transport process (H+ATPase proton pump)

64
Q

Why is active transport required to secrete protons in DCT and CD, but not in proton secretion in PT?

A

H+ is being secreted against its electrochemical gradient in DCT/CD (from cytoplasm pH 7.4 to luminal pH 4.5) and this is not the case in the PT.

65
Q

What else is different about H+ secretion in DCT/CD compared to PT?

A

In DCT/CD epithelium is impermeant to diffusion

66
Q

What is the transporter involved in proton secretion in both DCT and CD? What happens to the HCO3- that results from H+ production by CA in CD and DCT?

A

Proton-ATPase in apical membrane; HCO3- intracellular concentration increases and drives its reabsorption into ISF via HCO3-Cl exchanger

67
Q

Under high acidosis conditions what new transporter is expressed in DT/CD?

A

H+-K+ATPase on apical membrane to further increase H+ secretion and try to reduce the acidosis

68
Q

What happens in the DCT and CD under alkalosis conditions?

A

Bicarbonate secretion→Simplification: H+ATPase and HCO3-Cl exchanger switch directionality

69
Q

How is this switch of directionality accomplished?

A

The presence of two different intercalated cell types that are activated by different conditions:

  1. In acidosis, alpha-cells: proton pumps in lumenal membrane with HCO3-Cl exchanger in BL membrane
  2. In alkalosis, beta-cells: HCO3-Cl exchanger in luminal membrane with proton pump on BL membrane
70
Q

What effect does parathyroid hormone have on distal nephron?

A

PTH stimulates reabsorption of calcium in distal nephron

Renal Module (13 decks)

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