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Block 2; Week 4 > Keef 3 > Flashcards

Keef 3 Flashcards

1
Q

T/F @ the level of the peritubular capillaries filtration happens & substances move from the capillaries to the PCT.

A

False. This is not filtration. This is secretion. Filtration specifically refers to the stuff that happens @ the level of the glomerulus.

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2
Q

What do the terms reabsorption, secretion, & excretion refer to?

A

Reabsorption: movement of fluid from the tubule to the capillaries
Secretion: movement of fluid from the capillaries (not glomerulus) into the tubules
Excretion: movement of fluid out of the body in the form of urine.

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3
Q

What are the 2 ways that you can transport substances thru the epithelium of the tubules?

A

Paracellular: b/w the epithelial cells
Transcellular: thru the cells

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4
Q

What are the 2 names of the membranes of the epithelial cells that are in the tubules?

A

Apical: this is the side of the epithelium that is facing the lumen
Basolateral: this is the side of the epithelium that is facing the interstitial space

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5
Q

What transport category does the symport & anti port fall into?

A

Secondary Active Transport. They thrive off of a gradient that was already established by primary transport.

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6
Q

What transport category does uniport fall into?

A

Passive Transport–Facilitated Diffusion

Ex: in the kidney–transport of urea

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7
Q

In the PCT…what transporters are there that get molecules into the epithelial cells of the border? What gets them out of the epithelial cells into the peritubular space?

A

Into the epithelium:
Sodium Gradient–
symport w/ sodium & glucose or amino acids
antiport w/ hydrogen ions (acidifies urine)
Out of the epithelium:
sodium potassium pump

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8
Q

In the thick ascending limb of the loop of Henle what transporters bring molecules into & out of the epithelial cells?

A 
Into the epithelium:
Sodium gradient--
moves sodium, potassium, chloride into the cells.
Out of the epithelium: 
sodium potassium pump
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9
Q

In the DCT what transporters bring molecules into & out of the epithelial cells?

A 
Into the epithelium:
Sodium gradient--
sodium & chloride are brought into the cells
Out of the epithelium:
sodium potassium pump
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10
Q

In the collecting duct what transporter bring molecules into & out of the epithelial cells?

A 
Into the epithelium:
important sodium channels
**these are affected by aldosterone. Increases sodium reabsorption
Out of the epithelium:
sodium potassium pump
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11
Q

What class of diuretics blocks the sodium chloride symport on the distal convoluted tubule?

A

Thiazide.

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12
Q

About how much of the sodium that is originally filtered thru the glomerulus is excreted in your urine?

A

0.5%

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13
Q

Where is the sodium reabsorbed w/i the uriniferous tubule?

A

67% is reabsorbed in the PCT
25% is reabsorbed in the loop of Henle
5% is reabsorbed in the DCT
4.5% is reabsorbed in the collecting duct

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14
Q

What are the percentages of water reabsorption w/i the nephron?

A

The same as those for the sodium. B/c rule: water always follows sodium.

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15
Q

What does it mean if you have less than 0.5% of your original sodium filtration in your urine?

A

It is a sign of dehydration.

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16
Q

Movement of sodium into the epithelial cells is up/down its gradient.
Movement of chloride into the epithelial cells is up/down the gradient.

A

Sodium is down its gradient.

Chloride is up its gradient.

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17
Q

In the PCT…how is chloride moved into & out of the epithelial cells?

A

Into: anti port w/ the electrochemical gradient of X-.
Out: chloride channel

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18
Q

In the Thick ascending limb of the loop of Henle…how is chloride moved into & out of the epithelial cells?

A

Into: symport w/ sodium, potassium, chloride moving in–>w/ the power of the sodium gradient
Out: chloride channel

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19
Q

In the DCT…how is chloride moved into & out of the epithelial cells?

A

Into: symport w/ sodium & chloride…w/ the power of the sodium gradient
Out: chloride channel

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20
Q

T/F There is no passive reabsorption of chloride.

A

False. About 50% of chloride is absorbed by paracellular (b/w cells) transport. This is accomplished by a gradient that is created…electrical gradient by loss of sodium ions (gets more negative–>repels the chloride). Conc’n gradient by getting rid of water…higher conc’n of chloride ions.

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21
Q

How does sodium reabsorption & water reabsorption make urea passive reabsorption possible?

A

As water leaves there is a higher conc’n of urea in the lumen. This creates a conc’n gradient for its passive diffusion.

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22
Q

When you are looking @ a graph of y axis: TF/P & x -axis: % proximal tubule length:
What does a value of one mean? This is the case w/ sodium & potassium.

A

This means that along the length of the PCT…the conc’n of the molecule in the tubular fluid is the same as the plasma fluid.
Flat line: is an iso-osmotic process

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23
Q

When you are looking @ a graph of y axis: TF/P & x -axis: % proximal tubule length:
Why is it that you see chloride conc’n increasing & then flat lining?

A

B/c as water & sodium are reabsorbed…the conc’n of chloride increases until a sufficient electrochemical gradient is created for its passive diffusion paracellularly.
This is shown in the line…once flat lining: paracellular passive transport.

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24
Q

When you are looking @ a graph of y axis: TF/P & x -axis: % proximal tubule length:
Why is it that the lines for PAH & inulin are consistently rising?

A

B/c as water is reabsorbed the conc’n of inulin keeps increasing. However, inulin (unlike chloride) can’t move freely once it reaches a certain conc’n.
PAH is tricky: is both freely filtered/reabsorbed & secreted.

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25
Q

What percentage of the potassium that we take in is excreted each day?

A

ideally: 100%.

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26
Q

Is there a higher conc’n of potassium inside the cell or outside the cell?

A

INSIDE THE CELL! This is super duper important for RMP & AP.

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27
Q

Why do ppl freak out about keeping ECF K+ conc’n low?

A

B/c if it gets too high…you will mess w/ RMP & AP. Potassium is a huge determinant of RMP. This could mess w/ heart, smooth muscle, nerves.

28
Q

What is the target conc’n of potassium in the ECF?

A

~4.2mmol/L

29
Q

You eat a banana. Insulin is released. Does insulin cause a shift of potassium into or out of the cell? How?

A 
Shift into the cell. 
Insulin stimulates directly the sodium hydrogen ion anti porter. 
This indirectly (thru the extra sodium ions inside the cells) stimulates the sodium potassium pump. 
Thus, potassium ions are shuffled into the cell.
30
Q

When you exercise, what naturally happens to the potassium?

If you are seriously exercising…fight or flight…what happens to potassium?

A

Naturally, w/ exercise… a lot of AP & a lot of potassium leaving cells.
Epinephrine is released…or beta agonists…sodium potassium pump will be directly stimulated.

31
Q

When aldosterone levels increase…does potassium move more into or out of the cell? By what mechanism?

A

Into the cell.

Aldosterone stimulates the sodium potassium pump.

32
Q

If the ECF is in a state of alkalosis…does that indirectly cause more potassium to shift into the cell or out of the cell? By what mechanism?

A

Into the cell.
Not many H+ in the ECF…they need more.
Sodium hydrogen ion antiport…get more H_ there.
Extra sodium inside the cell will indirectly stimulate the sodium potassium pump.
Essentially: the movement of more H+ out of the cell will be balanced by the movement of more K+ inside the cell.

33
Q

If cell lysis occurs…the cell just breaks apart…what essentially happens: the movement of potassium inside the cell or outside the cell?

A

Outside the cell.

34
Q

In a case of the cell being in a hyper osmotic solution…what would happen to the movement of potassium…inside or outside of the cell? By what mechanism?

A

In a hyperosmotic solution…the water inside of the cell would flow out to the ECF. This would cause the cell to shrink.
As the water moves out, the conc’n of potassium inside the cell will increase.
Thus, potassium will move out.

35
Q

What are 4 factors that can cause potassium to shift inside the cell?

A

Insulin
Beta-agonists
Aldosterone
Alkalosis

36
Q

What are 3 factors that can cause potassium to move outside of the cell?

A

Hyperosmolarity
Exercise
Cell Lysis

37
Q

What does hyperkalemia refer to?

A

Too much potassium on the outside of the cell.

38
Q

Will epinephrine shift potassium inside the cell?

A

YES!

39
Q

Will a state of acidosis shift potassium inside the cell?

A

NO!

40
Q

Will exercise shift potassium inside the cell?

A

NO!

41
Q

What are the 2 mechanisms by which potassium can enter the peritubular space from the PCT? Which mechanism is most important?

A

Most important: passive reabsorption. paracellular transport.
Other mechanism: Potassium moving into the epithelial cells. Requires a potassium ATPase b/c it is moving UP its conc’n gradient.
To get out of the cells: passive potassium ion channels.

42
Q

Remember in the DCT & collecting tubules there are 2 important cells? 65% ____ & 35% ____. The dominant cells is important for the secretion of _____.

A

65% principal cells–secrete potassium back into the tubular lumen
35% intercalated cells.

43
Q

How do the principal cells secrete potassium back into the tubular lumen? What are some things that stimulate & inhibit this process?

A

Goes thru a potassium channel & leaks back into the tubular lumen.
Looks like it leaks out when sodium goes into the cell.
This process is promoted by aldosterone.
This process is inhibited by K+ sparing diuretics.

44
Q

What is the fractional excretion of sodium? What is the fractional excretion of potassium normally?

A

Sodium: 0.5%
Potassium (normally): 10-20%
**can range from 1-100%

45
Q

Where is the potassium reabsorbed/secreted as it moves on its journey toward excretion?

A

PCT reabsorption: 50% thru paracellular passive route.
Descending limb of the loop of Henle; a little potassium secretion
Ascending limb of the loop of Henle; huge potassium reabsorption.
Net: 42% reabsorbed.
Cortical CT: avid K+ secretion based on body’s needs…brings the 8% to 1% or all the way to 100% for excretion.

46
Q

How does aldosterone affect potassium secretion in the cortical CT?

A

It increases the reabsorption of sodium & thereby causes the increased secretion of potassium. Essentially: aldosterone increases sodium conductance & kind of causes depolarization of the membrane.

47
Q

If you have increased intracellular conc’n of potassium in your cells (maybe b/c of insulin)…what will this do to secretion in the cortical CT?

A

It will increase it! You want to dump the extra into the urine.

48
Q

What is an approximate GFR value?

A

125 ml/min

49
Q

What are the 2 ways that you can stimulate the adrenal gland to release aldosterone?

A 
Angiotensin II (pressure changes--RAAS)
High extracellular potassium levels (very disregulated w/o the aldosterone system)
50
Q

What are some examples of potassium losing diuretics?

A

Furosemide

Thiazide

51
Q

What are some examples of potassium sparing diuretics?

A

Amiloride

52
Q

Why are patients often given potassium supplements along w/ their diuretic (furosemide, thiazide)?

A

B/c they are potassium losing diuretics. You need to replenish.

53
Q

What does furosemide target? Why is it a potassium losing diuretic?

A

It blocks the sodium, chloride, potassium transporter that causes reabsorption of these substances in the thick ascending limb of the loop of Henle. This means that these substances will be excreted.
In the Cortical CT… you then have a higher water & sodium flow…depolarization of the membrane & flow of potassium ions into the tubule.
Thus, a potassium losing diuretic.

54
Q

What does thiazide target? Why is it a potassium losing diuretic?

A

It blocks the reabsorption of sodium & chloride in the DCT.

This will cause a greater flow of sodium & water @ the cortical CT…thus, depolarization & excretion of potassium.

55
Q

What does amiloride target? Why is it a potassium sparing diuretic?

A

It blocks sodium reabsorption in the cortical CT/late DCT.
This doesn’t cause the increase in potassium excretion, but does cause increased sodium excretion.
It is less effective as a diuretic, however.

56
Q

Which diuretic is the “anti-aldosteron” in that it blocks sodium conductance in the cortical collecting ducts?

A

Amiloride

57
Q

What transporter is messed up w/ Bartter’s Syndrome? What diuretic is this analogous to?

A

Na+/K+/Cl- transported is blocked in the thick ascending limb of the loop of Henle.
Similar to furosemide.

58
Q

What transporter is messed up w/ Gitelman’s syndrome? What diuretic is this analogous to?

A

Na/Cl transporter in the DCT is blocked.

Similar to thiazide.

59
Q

What is changed w/ Liddle’s syndrome? What is this analogous to?

A

Increased sodium conductance in the cortical collecting ducts.
Pseudohyperaldosteronemia

60
Q 
Will the follow changes occur w/ Bartter's Syndrome? 
Low potassium levels
Alkalosis
Polydipsia
Polyuria
HTN
Normal to low BP
A 
Low potassium levels YES
Alkalosis YES
Polydipsia YES (b/c diuretic-losing water)
Polyuria YES (b/c diuretic)
HTN NO 
Normal to low BP YES
61
Q 
Will the follow changes occur w/ Gitelman's Syndrome? 
Low potassium levels
Alkalosis
Polydipsia
Polyuria
HTN
Normal to low BP
A 
Low potassium levels YES
Alkalosis YES
Polydipsia YES (b/c diuretic--losing water)
Polyuria YES (b/c diuretic)
HTN NO
Normal to low BP YES
62
Q 
Will the follow changes occur w/ Liddle's Synrome? 
Low potassium levels
Alkalosis
Polydipsia
Polyuria
HTN
Normal to low BP
A 
Low potassium levels YES
Alkalosis YES
Polydipsia NO (b/c not losing water)
Polyuria NO (not making a lot of urine)
HTN YES
Normal to low BP NO
63
Q

Low potassium levels causes acidosis/alkalosis?

A

Alkalosis.

64
Q

What is polydipsia?

A

Drinking a bunch of water.

65
Q

What is polyuria?

A

Excessive passage of urine.

Block 2; Week 4 (6 decks)

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