Gene models + nephron function (3) Flashcards

Semester 1 year 1

1
Q

What 2 types of cell are the late distal tubule and cortical collecting duct made up of?

A

-principal
-intercalated

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2
Q

What are the principal cells involved in?

A

-Na+ and H2O absorption
-K+ and H+ secretion

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3
Q

What are the 2 types of intercalated cell?

A

-alpha intercalated cell
-beta intercalated cell

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4
Q

What do the alpha and beta intercalated cells do?

A

-alpha - H+ secretion and HCO3- reabsorption
-beta - H+ reabsorption + HCO3- secretion

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5
Q

How does transport occur across the principal cell?

A

-Na+ moves out + K+ in via ATPase on basolateral membrane
-Na+ moves in via ENaC protein on apical membrane
-K+ moves out via ROML on apical membrane (stays in urine) + via Kir2.3 on basolateral membrane
-H2O moves in via aquaporin 2 on apical membrane + out via aquaporins 3 + 4 on basolateral membrane

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6
Q

What diuretic works on cells in the late distal tube + CCD and how?

A

-amiloride
-blocks ENaC to prevent sodium reabsorption, inhibiting water reabsorption
-excrete more sodium + water, decreasing blood volume
-treatment for high blood pressure

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7
Q

What are diseases that affect the principal cells of the late distal tubule and CCD?

A

-diabetes insipidus
-Liddle’s syndrome

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8
Q

What is diabetes insipidus?

A

When you struggle to concentrate the urine

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9
Q

Describe Liddle’s syndrome

A

-affects ENaC inheritance
-dominant inheritance
-retain too much sodium, so reabsorb more water, leading to hypertension
-hypokalaemia

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10
Q

Where do mutations occur to cause Liddle’s syndrome?

A

-in COOH tail of beta or gamma subunits
-deletes proline rich motifs

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11
Q

What does excessive sodium transport as a result of Liddle’s syndrome do to water reabsorption?

A

-more ENaC channels causes more sodium transport
-driving force for water reabsorption increased
-expansion of extracellular fluid volume + cardiac output
-mean arterial pressure = cardiac output x heart rate

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12
Q

What does excessive sodium transport as a result of Liddle’s syndrome do to potassium secretion ?

A

-more ENaC channels causes more sodium transport
-driving force for potassium secretion increased
-lose potassium in urine - hypokalaemia

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13
Q

What is treatment for Liddle’s syndrome?

A

-amiloride
-inhibitor of ENaC

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14
Q

How does transport across alpha intercalated cells work?

A

-H+ pumped across apical membrane using proton ATPase + is lost in urine
-AE1 protein on basolateral membrane - HCO3^- out + Cl- in
-bicarbonate made in cell absorbed using AE1 + chloride enters cell
-Cl- recycled out of cell using Cl- protein

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15
Q

How does transport across beta intercalated cells work?

A

-AE1 on apical membrane, Cl- transporter + proton ATPase on basolateral membrane
-Cl- moves into cell to allow HCO3^- to be secreted from cell + lost in urine
-net reabsorption of Cl-
-removal of H+ by proton ATPase into interstitial fluid then peritubular capillaries

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16
Q

What determines whether the alpha or beta intercalated cells dominate?

A

H+ levels

17
Q

Describe the permeability of the medullary collecting duct to sodium, water and urea

A

-low Na+ permeability
-high H2O + urea permeability in presence of ADH

18
Q

What are the symptoms of acute renal failure?

A

-fall in glomerular filtration rate over hrs/days
-hypervolaemia - oliguria (low urine flow rate) due to low GFR
-hyperkalaemia - lack of K+ secretion
-acidosis - depression of central nervous system
-high urea/creatinine - impaired mental function, nausea, vomiting

19
Q

What is rhabdomyolysis?

A

-release of myoglobin from damaged muscle
-toxic effect on kidney tubules

20
Q

What happens as a result of the acidosis?

A

Low HCO3^- to compensate

21
Q

What happens as a result of the hyperkalaemia?

A

-tachycardia
-high K+ due to lack of secretion + release from damage cells

22
Q

What is the treatment for acute renal failure?

A

-dialysis
-IV saline to treat hyperkalaemia + hypotension
-add HCO3^- to bring level back to normal