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Molecular Animals > Kidneys!! > Flashcards

Kidneys!! Flashcards

1
Q

Inside vs outside cell conditions

A

inside: lots of proteins, - charge, more k+. outside: no proteins, higher na+ and cl-

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2
Q

diffusion

A

high to low conc (or electrochemical gradient

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3
Q

diffusion and distance

A

diffusion slows exponentially as distance increases

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4
Q

fick eq flux covaries with..

A

SA, permeability, 1/path length, and concentration difference

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5
Q

molecules with simple diffusion

A

water, CO2, O2, steroid hormones

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6
Q

channel diffusion

A

selective, passive, does not saturate. tightly regulated by ligands, voltage, or touch

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7
Q

capacitance

A

ability to store electrical charge

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8
Q

facilitated diffusion

A

proteins act like enzymes, saturate. but are always passive. usually for polar organics

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9
Q

primary active transporters

A

ATPases, require ATP

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10
Q

Na/K atpase

A

keeps separation of Na and K in cells, primary active transporter. basolateral surface, brings in 2K and removes 3 Na for charge

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11
Q

vmax for transport proteins

A

called tmax

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12
Q

Ca ATPase

A

in sarcoplasmic reticulum (and ER), keeps Ca conc in the ER

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13
Q

secondary active transport

A

at least 1 thing must move toward eq as gradient helps something actively transport

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14
Q

secondary transporter examples

A

NHE (Na+ in, H+ out), SGLT (Na and glu in), NKCC (Na/K/2Cl sym), NCC (Na/Cl sym), NBC (Na/bicarbonate sym out basolateral)

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15
Q

water is only transported..

A

PASSIVELY

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16
Q

1 Osm difference =

A

22 atm pressure

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17
Q

aquaporins

A

water channels

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18
Q

tonicity

A

ability of a soln to change a cells volume

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19
Q

hypotonic soln causes..

A

cell bursting, brain swelling, enzymes inhibited

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20
Q

hypertonic soln causes…

A

proteins crammed together, DNA breaks, enzyme activity inhibited

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21
Q

aggregation

A

unfolded proteins stack and can form massive useless proteins that cannot be destroyed,eventually wreck membranes.

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22
Q

ions disrupt..

A

H bonds and hydrophobic effect

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23
Q

ultimate causes of aggregation

A

aging or hypertonicity

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24
Q

comet assay

A

shows broken DNA strands using gel electrophoresis

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25
Q

shrinkage compensatory effect

A

WNK phosphorylates PASK/OSR1 to phosphorylate NKCC to bring salts and water into the cell

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26
Q

PASK and channels..

A

phosphorylates to ACTIVATE NKCC and NCC and INACTIVATE KCC.

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27
Q

cell bursting short term compensation

A

KCC pumps potassium and Cl out of the cell if its gonna burst. activated when dephosphorylated by PP1 in absence of WNK activation

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28
Q

renal pelvis

A

connects to bladder

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29
Q

medulla

A

part of kidney closer to pelvis, has loops and salt conc

30
Q

cortex

A

part of the kidney w glomeruli and tubules

31
Q

renal papilla

A

amount of kidney within the pelvis (inc.with loop length and conc it can make)

32
Q

salt gland structure

A

blind ended tube, salt is secreted in

33
Q

ADH

A

antidiuretic hormone, controls insertion of aquaporins at collecting duct by activating a GCPR in basolateral membrane > G protein > adenyl cyclase > cAMP > kinase> aquaporins go in

34
Q

single effect

A

horizontally, sections of the ascending and descending loops get a 200 mOsm diff by the descending absorbing some Na and the ascending actively pumping it out. NKCC in ascending

35
Q

who can make more conc urine

A

some birds and mammals

36
Q

glomerulus

A

ball of capillaries that filter at Bomans capsule

37
Q

why does the kidney filter

A

allows us to excrete many toxins without having a spec mechanism for each one

38
Q

podocytes

A

cells that straddle glomerulus and help filter only small molecules

39
Q

size for free glomerular filtration

A

less than 10 kDa

40
Q

GFR calculation

A

give a freely filtered, not absorbed substance, calculate urine level/plasma level = filtration rate vol/urine volume

41
Q

reabsorbed things from kidney move to…

A

peritubular capillaries > vasa recta >system

42
Q

aldosterone

A

made in adrenals, cued by AT2. inc salt reabsorption in DCT by controlling NCC

43
Q

furosemide

A

diuretic, inhibits NKCC2 in the ascending limb

44
Q

thiazide

A

inhibits NCC in DCT (bp control)

45
Q

RAAS system

A

renin - angiotensin - aldosterone system. increases bp. renin cleaves angiotensigen to angiotensin 1, ace cleaves AT1 into AT2 which signals vasoconstriction, ADH, thirst, and WNK/PASK/OR1/channels via aldosterone. AT2 also activates NHE3 and Na/K ATPase

46
Q

angiotensigen

A

prohormone made in the liver

47
Q

KLHL3

A

ubiquitin ligase, gets rid of WNK when not needed and reduces activation of salt reabsorption

48
Q

egestion

A

emptying digestive tract

49
Q

excretion

A

non digestive waste

50
Q

proximal tubule

A

bulk reabsorption, 80% absorbed but osmolarity is maintained throughout (water and solvents removed)

51
Q

what can move through tight junctions

A

ions, sometimes..

52
Q

mellitus

A

sweet urine…

53
Q

distal tubule

A

refines pH and salt conc, regulated by hormones (low H2O permeability)

54
Q

who has loop of Henle

A

birds and mammals

55
Q

ACE is made in..

A

blood vessels

56
Q

loop of Henle limbs

A

descending = thin, ascending - thick

57
Q

ADH aka..

A

arginine vasopressin(AVP)

58
Q

diuresis

A

high urine flow, low conc, low ECF conc

59
Q

antidiuresis

A

low urine flow, high conc, high ECF conc

60
Q

how to inc medullary osmotic gradient

A

use urea as well!doubles max conc.

61
Q

where is urea made

A

liver

62
Q

NHE

A

(Na+ in, H+ out) - apical in proximal tubule

63
Q

SGLT

A

brings Na and Glucose in, apical in proximal tubule

64
Q

NKCC2

A

Na/K/2Cl sym into cell via apical. useful for if cell is shrinking, and used in TAL (absorption into the medulla instead of the blood)

65
Q

NCC

A

brings Na and Cl in apical, regulated by WNK/PASK OSR1 in DCT.

66
Q

NBC

A

(Na/bicarbonate sym out basolateral) in proximal tubule

67
Q

transporters in proximal tubule

A

water diffuses, follows solutes. SGLT and NHE in apical bring solutes in, K+ channels in both membranes leak it out, Cl- goes out of lumen via junctions, all fueled by Na/K ATPase in basolateral. NBC and glucose facilitated diffusion are also in basolateral.

68
Q

what drives secondary transporters in the DCT

A

it’s still basolateral Na/K ATPase!

69
Q

long term response to change in osmolarity

A

organic osmolytes synthesized to keep conc up without disrupting proteins/cell

70
Q

when does RAAS activate ADH

A

extreme blood loss. preserve volume by losing osmolarity

71
Q

AT2 purpose in transporters

A

ACTIVATE NHE and Na/K atpase in PCT

Molecular Animals (4 decks)

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