Lecture 6 Final Flashcards

1
Q

How much PAH can the kidneys remove

A

90%

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2
Q

Does Angiotensin II only work on the efferent arteriole?

A

No, it works on both but mainly on the efferent arteriole.

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3
Q

What does the Macula Densa release to make the afferent arteriole dilate?

A

Nitrous Oxide

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4
Q

Can the Macula Densa also relax the efferent arteriole with the use of NO?

A

Yes, it can work on both arteriole as well but mainly work on the afferent arteriole.

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5
Q

What does the angiotensin 2 type 1 receptors do?

A

Located in proximal tubule, when bound, it speeds up the Na/K pump located next to it as well as the secondary transporters (NHE) within that area.

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6
Q

What transporters also get sped up after the Na/K pump is sped up in the PCT?

Na to interstitium; K influx (cell)

A

NHE (secondary)
1 Na influx, 1 H+ to the lumen

Na/bicarb secondary active
1 Na;1 bicarb to the interstitium

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7
Q

T/F: When H+ is transported into the lumen, bicarb is transported into the interstitium as well.

A

True

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8
Q

Where else does reabsorption occur?

A

“Tight junctions”
Paracellular pathways (in between cells) mainly water but CL- is also dragged here.

Trancellular pathway (through a channel in the cell wall)

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9
Q

Which ion mainly is involved within our primary and secondary transporters in the renal system?

A

Na+

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10
Q

T/F: Normally where Na goes, Cl- follows through the paracellular pathways.

A

True

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11
Q

Aquaporins are normally called…

A

Transcellular route/pathway

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12
Q

What is bulk flow? where does this occur?

A
  • Tons and tons of reabsorption/filtration
  • In the peritubular capillaries and glomerular capillaries
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13
Q

Which transport system does water go through in the renal system?

A

There isn’t one, it only travels through tight junctions or through osmosis.

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14
Q

What is the main solute does water follow in the renal system?

A

Urea

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15
Q

What drives transcellular pathways?

A

Some primary active transporter within the cell

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16
Q

On the lumen side of the proximal tubular cells, there’s a rush/rough border made up of?

A

Lining of proximal tubular cells (20 fold). Lots of surface area for multiple transporters.

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17
Q

Why is the cell wall of the PCT on the lumen side not flat?

A

It would be too crowded with the amount of transporters it uses. Having the rush/rough border allows for more transporters to be planted and used for reabsorption.

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18
Q

What is the typical membrane potential in the kidney?

A

-70 mV

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19
Q

The ions that are left inside the lumen creates a charge of?

A

-3mV

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20
Q

Does Na ever get concentrated in the PCT?

A

No, water follows it to keep it controlled. But Cl- does.

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21
Q

T/F:
Large negatively charged compounds like proteins are filtered through the capillaries?

A

False, but sometimes some albumin gets filtered (ex. 0.001 = 1.8g/day)

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22
Q

If 1.8g of protein are filtered/day, and 1.7g are reabsorbed, how much is excreted?

A

100mg of protein in urine. (Should not make it look cloudy)

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23
Q

What’s the purpose of the proximal tubular cell?

A

It will pull the protein from the peritubular capillaries and pull it apart to turn it into amino acids. (aka endocytosis; pinocytosis)

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24
Q

What do you call a string of at least 10 amino acids?

A

Peptide

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25
Q

Acid and base regulation at the PCT is helped with the use of…

A

Carbonic anhydrase and the NHE with N/K pump

26
Q

How is the bicarb reabsorbed in the PCT?

A

Bicarb in the urine is converted into H2CO3 by carbonic anhydrase by combining it with H+. It then gets broken down to CO2 and H2O. CO2 diffuses into the PCT and again gets remade into H2CO3 by combining it with H2O by the Carbonic anhydrase before it gets broken down to H+ and HCO3. HCO3 is then sent into the interstitium via Na+/HCO3 pump while H+ is sent into the urine via NHE.

27
Q

How is carbonic anhydrase attached to the PCT?

A

Tethered, wedged in the cell wall and some are located inside the PCT.

28
Q

What is the side effects of using Carbonic anhydrase inhibitors?

A

Acidosis

29
Q

Does the PCT produce HCO3?

A

Yes, it’s able to produce new HCO3.

30
Q

How is new bicarb produced in the PCT?

A

The liver produces Glutamine and it’s converted by proximal tubular cells into bicarbonate (HCO3-) and ammonium (NH4+). NH4+ is then sent into the urine via Na+/NH4+ exchanger causing the urine to be very acidic with multiple H+ floating around.

1 glucose is turned into 2 molecules of bicarbonate and 2 molecules of ammonium

31
Q

Why do people with liver failure have trouble with acid/base balance?

A

They are unable to produce glutamine.

32
Q

Where is bicarb mainly made?

A

It can be made anywhere in the tubule but mainly in the proximal tubule.

33
Q

What else serves as a urinary buffer?

A

Phosphate. NaHPO4- serves as a good buffer for H+

34
Q

Where is Ca++ reabsorbed in the proximal tubule(PCT)?

A

Via trancellular (through the cells via ca channels gradient) and paracellular (in between cells).

35
Q

Does Ca++ just gets dragged along with everything else?

A

Yes

36
Q

How does Ca++ get put inside the cell and into the interstitium?

A

From the lumen (urine), it goes through Ca channels and then through a Ca++ atp’ase pump into the blood and Na/Ca exchanger.

37
Q

Where does PTH work?

A

PCT and DCT

38
Q

T/F: Vit D3 activation, renal Calcium reabsorption and bone breakdown is increased by the parathyroid hormone.

A

True

39
Q

What do you call the cells that breakdown bone?

A

Osteoclasts

40
Q

What do you call cells that build bones? What does PTH do with those?

A

Osteoblasts; decrease

41
Q

What 2 things make up the bones?

A

Really tightly packed calcium and phosphate

42
Q

What do you see in bones if you have osteoporosis?

A

Really porous bones with low calcium levels.

43
Q

Where is our long term calcium stores located? Short term?

A

Bones; SR

44
Q

What does osteoblasts do?

A

Build bones by packing phosphate and calcium together.

45
Q

What are signs of low PTH?
High PTH?

A
  • Low osteoclasts; High osteoblast
  • High osteoclast; Low osteoblast
46
Q

What organic cations are secreted into the tubule?

H+ dependent transporters

A

Endogenous:
Ach, Choline, creatine, serotonin, histamine, epinephrine, NE, Dopa

Exogenous:
Isoprene, atropine, morphine, procaine

47
Q

What organic anions are secreted into the tubule?

Na+ dependent transporters

Fact check (aKG)?

A

Endogenous:
Bile salts, hippurates, PG’s, urates, oxalate

Exogenous:
Furosemide, PCN, salicylates (ASA), sulfonamides, chlorothiazides

48
Q

How was PCN discovered?

A

By accident in 1942 during WWII

49
Q

If you wanted to prevent something like, (PCN) from getting removed out of your renal system, what can you do?

A

Ex.
You can overwhelm the transporter by providing more hippurates in the system which will prevent the removal of PCN. It will still remove some PCN but not as much.

50
Q

What is the rule of thumb if you don’t know how much of something is reabsorbed in the kidneys?

A

2/3

51
Q

Which part of the nephron is water permeable?

A

Thin descending loop of henle and collecting duct

52
Q

What is the only transport system in the thin ascending loop?

A

NaCl- atp-ase (Thin AL)

53
Q

In the TAL, what gets absorbed through the paracellular route?

A

cations (Mg+, Na+, K+, Ca++) driven by K+ channels causing a positive charge of +8mV in the TAL lumen.

54
Q

What transporters are there in the TAL?

A

N/K pump

(2nd)
Na/H pump (NA+ in; H+ out), and NKCL2 influx

55
Q

Where does loop diuretics work?

A

in the TAL and it’s the most potent diuretic. It stops the NKCL2 pump, and more water stays in the lumen to be excreted.

56
Q

How does PTH work in the DCT?

A

It activates the NA/CL channel and Ca channel from lumen into the DCT

57
Q

Where does the thiazide diuretics work?

A

In the DCT shutting down the NaCl channel.

58
Q

ADH and aldosterone works on what part of the kidney?

A

Distal tubule

59
Q

What do you call the aldosterone/ADH sensitive cells?

A

Principal cells and intercalated cells

60
Q

T/F:
Aldosterone is a type of protein.

A

False, it’s a cholesterol.

61
Q

How does aldosterone work? Angiotensin II? in the DCT

A
  • It speeds up the tubular side K channel to efflux and Na channel to influx.
  • It speeds up the N/K pump causing the tubular side channels to speed up as well.