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Renal system > pumps and ATPases > Flashcards

pumps and ATPases Flashcards

1
Q

what are the 2 methods of transport across the membrane?

A

diffusion or active transport

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2
Q

types of diffusion

A

simple and facilitated

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3
Q

why do things get transported by facilitated transport?

A

ionic
hydrophilic
polar
too large

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4
Q

active transport

A

moving against a concentration or electrochemical gradient

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5
Q

what is kidney important for?

A 
regulating 
fluid
waste
vitamins
minerals
hormones
electrolytes
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6
Q

where is the Na+/K+ pump/ ATPase

A

every epithelial of the kidney
only on the interstitial side of cell (basolateral membrane)
most cells do

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7
Q

what does the Na+/K+ pump do?

A

3 sodium bind
phosphorylating it
releasing sodium to other side and allows binding of 2 potassiums against the concentration gradient

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8
Q

secondary active transport

A

allowed by the Na+/K+ pump by passive entry, anti-porter and co-transport

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9
Q

anti-porter

A

diffuses sodium into cell and exchanges for H+

no energy used

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10
Q

co-tranport

A

Na+ and another solute diffuse into cell

e.g. glucose simporter

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11
Q

nephron can

A

dissociate the reabsorption of water and sodium

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12
Q

where is most sodium reabsorbed?

A

PCT
50%
nitrogen/ hydrogen exchanger

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13
Q

sodium reabsorption in ascending loop of Henle

A

sodium/ potassium/ chloride transporter

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14
Q

water in loop of henle

A 
ascending = water impermeable
descending = water permeable
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15
Q

sodium reabsorption in DCT

A

fine-tuning
by Na+/Cl- transporter
ENaC

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16
Q

what happens if K+ levels increase

A

aldosterone released by RAAS
affects principal cells in collecting duct
causes production of more sodium potassium pumps and ENaCs

17
Q

regulation of transporters

A

transporters are continuously recycled
transporter synthesis can be up-regulated or
degradation inhibited degradation can be up-regulated
to adjust electrolyte concentrations

18
Q

daily recommendation for K+

A

3500mg

19
Q

what amount of K+ causes adverse effects?

A

6000mg, but no upper limit

20
Q

Liddle’s syndrome

A

gain of function due to impaired degradation of ENaC in collecting duct
pseudohyperaldosteronism
low renin and low aldosterone (only looks like aldosterone is up)
Na+ retention
increased ECF volume and BP
decreased K+

21
Q

how to treat Liddle’s syndrome

A

low sodium diet

diuretic

22
Q

Gitelman’s syndrome

A

Na+/Cl- transporter loss of function

23
Q

Bartter’s syndrome

A

sodium/potassium/ 2 chloride transporter loss of function

24
Q

Pseudohypoaldosteronism

A

loss of function of ENaC
low sodium
serum osmolality is high because another solute replaces sodium

25
Q

primary polydipsia

A

drinking in excess causing hyponatraemia

low serum sodium, serum osmolality and urine osmolality

26
Q

what decreases aldosterone

A

increased water

27
Q

where does reabsorption of water by ADH take place?

A

collecting duct

28
Q

ADH

A

increases the permeability of the collecting ducts to water

29
Q

different types of aquaporins are there in the nephron?

A

1,2,3,4,6,7,8,11

allows dissociation of water and sodium transport

30
Q

what do aquaporins do?

A

control osmolality

31
Q

how does ADH increase permeability of the collecting duct?

A

binds to receptors on interstitial side of epithelial cells
GPCR activates adenyl cyclase to convert ATP to cAMP which activates PK A causing vesicle containing AQP2 to move and insert into the membrane on the luminal side

32
Q

AQP3&4

A

ready in cytosol to be expressed on interstitial side

open channels for reabsorption of water

33
Q

what transporter reabsorbs glucose?

A

GLUT2 on PCT

facilitated by Na+/K+ pump

34
Q

loop diuretic

A

blocks NKCC
loss of NaCl and K+
reabsorb less K+ so decreases osmotic gradient
less water can be reabsorbed due to reduced osmolality in interstitial fluid
increases Na+ in collecting duct, so absorbed by ENaC causing more K+ lost
changes membrane potential so Ca2+ and Mg2+ lost
loss of fluid activates aldosterone via RAAS increasing ENaC activity

35
Q

NKCC

A

sodium/ potassium/ 2 chloride cotransporter

36
Q

end result of loop diuretics

A

loss of Na+ and water
hypokalemic metabolic acidosis
increased Ca2+ loss

Renal system (17 decks)

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