tubule transport Flashcards

1
Q

what is primary effect of angiotensin 2 binding to AT1 receptors

A

increasing speed of Na/K ATPase

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2
Q

paracellular reabsorption help together by _____ ______

A

tight junctions

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3
Q

transcellular reabsorption is ______ transport via _____ or ______

A

active transport (primary or secondary)

via channels or transporters

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4
Q

tight junctions at the proximal tubule are _____ than other tight junctions in the tubule

A

looser

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5
Q

what gets dragged or reabsorbed via the paracellular pathway?

A

chloride

lots of Na via transporters… and Cl typically wants to follow Na

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6
Q

aquaporins are a _____ route

A

transcellular

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7
Q

places in the kidney that are impermeable to water, have _____ tight junctions and typically lack aquaporins too

A

tighter

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8
Q

reabsorption occurring at the proximal tubule as a result of starling forces in the peritubular capillaries creates a NRP _____. This is also called _____ ______.

A

NRP 100 mmHg
Bulk Flow

combines both paracellular and transcellular reabsorption

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9
Q

in absence of aquaporins, water reabsorption occurs following solutes. This is called _____.

A

osmosis

both transcellular and paracellular

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10
Q

______ is in abundance in the interstium and provides and osmotic gradient for water to follow

A

*urea

also proteins and filaments

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11
Q

______ _____ is really evident in the proximal tubule (on luminar side). It increases the surface area x20 to promote greater reabsorption. Also allows MORE ion channels/transporters.

A

brush boarder

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12
Q

proximal tubular epithelial cell membrane potential is ______ vs. tubular lumen membrane potential is ______.

A

-70 mV
secondary to Na/K APTase pumps creating electrochemical gradient which are activating secondary active transporters

-3 mV
Na, K, Cl… if more Cl -> more (-) charge

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13
Q

first half of proximal tubule ____ Cl reabsorption vs the second half of the proximal tubule.

A

less

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14
Q

in healthy kidneys, how much protein get filtered per day?

How much is reabsorbed?

how mu excreted in urine?

A

1.8 g
1.7 g
100 mg

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15
Q

reabsorption of protein in the proximal cells is via _____ or ______.

A

endocytosis or pinocytosis
*PT cells grab protein from inside tubular brush boarder, bring it inside, destroy them into amino acids… then reabsorb them

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16
Q

2 condition for proteinuria

A

sepsis, DM

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17
Q

whats a big protein that gets filtered?

what are 2 small proteins that get filtered?

A
  • protein
  • growth hormones
  • peptides: signaling compounds in blood that have micro proteins…. small string of 10-20 amino acids
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18
Q

what transporter is the primary reabsorption of Na in the PT?

A

sodium hydrogen exchanger

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19
Q

3 places in tubule where carbonic anhydrase is found

A
  • implanted in epithelial cell membrane
  • tethered to cell membrane
  • suspended in the tubule
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20
Q

carbonic anhydrase takes a water out of carbonic acid, this is called a _______ process

A

anhydrase

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21
Q

H+ gets put back into the lumen via ______ exchanger. H+ can then form with bicarb, or get excreted if no bicarb available, or attach to a larger compound forming ________.

A

sodium hydrogen exchanger

ammonium
*buffers the acidity of our urine

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22
Q

H+ + ammonia -> ______

A

ammonium

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23
Q

effects of carbonic anhydrase inhibitor

A
  • bicarbonate not reabsorbed via Na bicarbonate symporter -> wasting bicarbonate in UO -> acidosis***
  • decrease Na hydrogen exchanger -> more Na and H2O in tubule -> increase UO (weak diuretic)
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24
Q

what is glutamine, where is it produced, what effect on kidney?

A

glutamine is an amino acid produced in the liver

used in epithelial cells of PT to produce bicarb

glutamine + 1 glucose molecule -> 2 HCO3- + 2NH4+ (ammonium)

25
Q

why do liver failure patients have a hard time balancing acid base balance?

A

their liver can’t produce enough glutamine

glutamine can be supplemented through another source

26
Q

2 urinary buffers

A

ammonium NH4+
phosphate PO4-3

27
Q

phosphate concentration is ______ inside the cell vs outside the cell

A

higher
- lots of phosphorylation inside cells BUT also found outside cells (tubular lumen)

28
Q

calcium reabsorption in the tubules occurs where?

A

PT, TAL, DT

29
Q

calcium reabsorption in PT occurs _____ and _____ pathways.

A

transcellular and paracellular
- gets drug along with everything else

30
Q

what drives Ca++ reabsorption in the PT?

A

negative charges inside the tubular cells and low Ca+ levels

31
Q

calcium bound to albumin in the plasma _____ get filtered

32
Q

in acidosis there is ____ ionized Calcium that will get freely _______.

A

more
filtered

33
Q

in alkalosis there is _____ ionized calcium that will be freely filtered.

34
Q

_______ gland monitors calcium levels in the extracellular fluid

A

parathyroid
- located on the sides of the thyroid gland

35
Q

low calcium in the blood, leads to release of _____

A

parathyroid hormone

36
Q

increase in PTH leads to what 3 things

A
  • increase vit D action -> increase intestinal Ca+ reabsorption
  • increase renal Ca+ reabsorption -> increase number of apical membrane Ca channels in PT and DT
  • increase Ca release from bones -> increase osteoclast and reduce osteoblast activity
37
Q

osteoclasts work by…

A

breaking calcium phosphate bonds (bone) to release Ca into bloodstream -> osteoporosis

38
Q

osteoblast work by….

A

binding calcium and phosphate to build stronger bones

39
Q

long term vs short term storage places in the body

A

short term = SR
long term = bone

40
Q

what year did first person take PNC

41
Q

who discovered in WW2 that hippurates added to PNC was competative secretion via using the same transporters -> PNC lasting longer in circulation

A

Alexander fleming

42
Q

most powerful diuretic class and where they act on tubule

A

loop diuretics
- furosemide
- ethacrynic acid
- butetanide

they GREATLY reduce the renal interstitium conc. -> reducing water reabsorption via osmosis

43
Q

highest conc that the renal insterstitium can have

A

1200 mOsm

reabsorbs most water at this mOsm

also urine conc would be 1200 mOsm

44
Q

what 2 things account for the renal interstium conc.

A

KCL and urea

45
Q

how conc. can lizards make their renal interstitum

46
Q

electrolyte reabsorption in tubule

A
  • PT: 2/3
  • Thin AT: 25%
  • late DT and Collecting duct via principle cells: determines remaining electrolytes for reabsorption or not
47
Q

principle cells location and what they are sensitive to

A

late DT and collecting duct

ALDO

48
Q

principle cells and intercalated cells are sensitive to ______

A

ADH: water reabsorption

49
Q

what two parts of the tubule have a high metabolic rate

A

proximal tubule and thick ascending limb

50
Q

where do thiazide diuretics work and how?

A

apical distal tubule blocking the Na/Cl co-transporter

*speeds up the Na/Ca exchanger on basolateral side -> increase Ca reabsorption (tx osteoporosis or prevent kidney stones)

51
Q

careful not to take _____ supplements while taking thiazide diuretics

A

calcium

could get hypercalcemic

52
Q

aldersterone is a ________ and increases ______ reabsorption and increases ________ excretion

A

mineralocorticoid
Na+
K+

53
Q

ALDO is a _______ derivative, thats why the receptor is inside the distal tubule. It has no issue getting through the cell wall

A

cholesterol

54
Q

3 primary effects of ALDO in order

A

1: increase pumping of Na/K/ATPase
2. plants addiction ENAC on apical surface
3. increases K channel opening on apical membrane, increasing K secretion (both opening of ROMK and BK)

55
Q

what are the 2 potassium channels called in principle cells

A

ROMK (renal outer medullary K) channel

BK (big K) channel

56
Q

osmotic diuretics MOA

A

conserve water in early parts of tubule?

57
Q

Inhibition of Na reabsorption from ANYWHERE upstream from the principle cells will have ______ Na conc. reaching the principle cells (DCT and collecting duct) -> more _____ reabsorption at principle cells and more ______ excretion from ______ activity of the Na/K/ATPase pump

A

increased
Na+
K+
increased

***K+ wasting diuretics

58
Q

what diuretic is commonly given with Triamterene to inhibit K+ wasting

A

hydrochlorothiazide