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Molecular Animals > Kidneys!! > Flashcards

Kidneys!! Flashcards

(71 cards)

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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
shrinkage compensatory effect
WNK phosphorylates PASK/OSR1 to phosphorylate NKCC to bring salts and water into the cell
26
PASK and channels..
phosphorylates to ACTIVATE NKCC and NCC and INACTIVATE KCC.
27
cell bursting short term compensation
KCC pumps potassium and Cl out of the cell if its gonna burst. activated when dephosphorylated by PP1 in absence of WNK activation
28
renal pelvis
connects to bladder
29
medulla
part of kidney closer to pelvis, has loops and salt conc
30
cortex
part of the kidney w glomeruli and tubules
31
renal papilla
amount of kidney within the pelvis (inc.with loop length and conc it can make)
32
salt gland structure
blind ended tube, salt is secreted in
33
ADH
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
single effect
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
who can make more conc urine
some birds and mammals
36
glomerulus
ball of capillaries that filter at Bomans capsule
37
why does the kidney filter
allows us to excrete many toxins without having a spec mechanism for each one
38
podocytes
cells that straddle glomerulus and help filter only small molecules
39
size for free glomerular filtration
less than 10 kDa
40
GFR calculation
give a freely filtered, not absorbed substance, calculate urine level/plasma level = filtration rate vol/urine volume
41
reabsorbed things from kidney move to...
peritubular capillaries > vasa recta >system
42
aldosterone
made in adrenals, cued by AT2. inc salt reabsorption in DCT by controlling NCC
43
furosemide
diuretic, inhibits NKCC2 in the ascending limb
44
thiazide
inhibits NCC in DCT (bp control)
45
RAAS system
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
angiotensigen
prohormone made in the liver
47
KLHL3
ubiquitin ligase, gets rid of WNK when not needed and reduces activation of salt reabsorption
48
egestion
emptying digestive tract
49
excretion
non digestive waste
50
proximal tubule
bulk reabsorption, 80% absorbed but osmolarity is maintained throughout (water and solvents removed)
51
what can move through tight junctions
ions, sometimes..
52
mellitus
sweet urine...
53
distal tubule
refines pH and salt conc, regulated by hormones (low H2O permeability)
54
who has loop of Henle
birds and mammals
55
ACE is made in..
blood vessels
56
loop of Henle limbs
descending = thin, ascending - thick
57
ADH aka..
arginine vasopressin(AVP)
58
diuresis
high urine flow, low conc, low ECF conc
59
antidiuresis
low urine flow, high conc, high ECF conc
60
how to inc medullary osmotic gradient
use urea as well!doubles max conc.
61
where is urea made
liver
62
NHE
(Na+ in, H+ out) - apical in proximal tubule
63
SGLT
brings Na and Glucose in, apical in proximal tubule
64
NKCC2
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
NCC
brings Na and Cl in apical, regulated by WNK/PASK OSR1 in DCT.
66
NBC
(Na/bicarbonate sym out basolateral) in proximal tubule
67
transporters in proximal tubule
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
what drives secondary transporters in the DCT
it's still basolateral Na/K ATPase!
69
long term response to change in osmolarity
organic osmolytes synthesized to keep conc up without disrupting proteins/cell
70
when does RAAS activate ADH
extreme blood loss. preserve volume by losing osmolarity
71
AT2 purpose in transporters
ACTIVATE NHE and Na/K atpase in PCT

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