Gene models + nephron function (2) Flashcards

Semester 1 year 1

1
Q

What is reabsorbed in the loop of Henle?

A

-sodium
-chloride
-water
-calcium
-magnesium

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2
Q

How does fluid move through the loop of Henle?

A

-arrives from proximal tubule
-moves down thin descending limb
-then moves up thin ascending limb
-then up thick ascending limb

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3
Q

What is the water permeability of the the thin descending limb and what is reabsorbed here?

A

-very water permeable
-water moves out
-nothing reabsorbed

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4
Q

What is the water permeability of the the thin ascending limb and what is reabsorbed here?

A

-not very water permeable
-permeable to sodium + chloride
-they move out

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5
Q

What is the water permeability of the the thick ascending limb and what is reabsorbed here?

A

-water impermeable
-permeable to sodium + chloride
-they move out

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6
Q

What protein channels are on which membranes of the cells of the thick ascending limb (TAL)?

A

On apical membrane:
-NKCC2
-ROMK (Kir1.1)
On basolateral membrane:
-ATPase
-Kir1.1
-CLCK
-Barttin

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7
Q

How does the protein NKCC2 work?

A

-1 Na+, 2 Cl-, 1 K+ bind to the protein
-causes conformational change
-ions released into intracellular fluid environment
-works due to Na+ grad. from ATPase

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8
Q

How does the sodium that enters via NKCC2 leave?

A

-via ATPase
-net Na+ reabsorption

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9
Q

How does the chloride that enters via NKCC2 leave?

A

-via CLCK on basolateral membrane
-net Cl- reabsorption

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10
Q

What is Barttin?

A

-a beta subunit (accessory protein)
-regulated CLCK channel
-in absence of Barttin, CLCK doesn’t work

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11
Q

How does the potassium that enters via NKCC2 leave?

A

By Kir1.1

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11
Q

Why does NKCC2 not work if potassium isn’t recycled by Kir1.1?

A

-potassium isn’t recycled
-results in low K+ conc. on apical membrane side
-wouldn’t be able to reabsorb Na+ or K+

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12
Q

How are calcium and magnesium reabsorbed?

A

Paracellular transport

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13
Q

Is Bartter’s syndrome recessive or dominant?

A

Recessive

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14
Q

What are the symptoms of Bartter’s syndrome?

A

-salt wasting (losing sodium + chlorine in urine)
-polyuria (excreting higher urine vol.)

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15
Q

What do individuals with Bartter’s syndrome have?

A

-hypotension (due to excreting water that would remain in blood)
-hypokalaemia
-metabolic alkalosis
-hypercalciuria (high Ca2+)

16
Q

How many types of Bertter’s syndrome are there?

A

5 types

17
Q

What do loop diuretics do?

A

-increase water loss in urine
-treatment for high blood pressure

18
Q

What reabsorption occurs in the early distal tubule?

A

-sodium
-chloride
-magnesium

19
Q

How does reabsorption occur across early distal tubule cells?

A

-sodium potassium ATPase on basolateral membrane decreases intracellular sodium
-sodium + chloride move in using NCC proteins on apical membrane
-potassium recycled using protein on basolateral membrane
-Mg2+ + Ca2+ ion enter via proteins on apical membrane + lost via proteins on basolateral membrane

20
Q

How do thiazide diuretics work on the NCC protein?

A

-block sodium + chloride co-transporter, preventing their reabsorption
-reduces water reabsorption

21
Q

What are thiazide diuretics used to treat?

A

High blood pressure

21
Q

Is Gitelman’s syndrome dominant or recessive?

A

Recessive

22
Q

What are the symptoms of Gitelman’s syndrome?

A

-salt wasting + polyuria
-hypotension
-hypokalaemia
-metabolic alkalosis
-hypocalciuria