phys -renal II Flashcards

1
Q
  1. in the proximal convoluted tubule, what % of what is filtered is reabsorbed?
  2. how is this accomplished (what type junctions and what membranes)?
A
  1. 65% of what is filtered is reabsorbed back into the blood by the PCT
  2. tight leaky junctions which separate the apical and basolateral membranes
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2
Q
  1. how is the surface area of the apical membrane increased?
  2. what is on the surface of these
  3. what is this “border” called, why?
A
  1. fingerlike microvilli increase surface area
  2. on the surface of these is a sugar group called glycocalyx
  3. called a brush border, because it looks like shrubbery
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3
Q

what is the function of the brush border

A

enzymes become trapped in the bursh border (ex. apical carbonic anhydrase)

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4
Q

there are alot of folds in the BL membrane, what is contained in the basolateral membrane folds

A

tons of mitochondria

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5
Q

what is the difference in surface area between the proximal convoluted tubule and the loop of henle?

A

there are no or less folds in the loop of henle because it doesnt need the extra surface area.

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6
Q

how much of the filtering does the DCT (distal convoluted tubule) do?

A

10-15%

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7
Q

how much filtrate does the kidneys filter daily (in liters)?

  1. how much of that becomes urine?
  2. so ___ liters is reabsorbed
A
  1. the kidneys filter 180 liters of filtrate daily
  2. 2.5 liters becomes urine
  3. 177.5 liters of filtrate is reabsorbed
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8
Q
  1. what does the PCT have on its membranes?

2. what does that do to the lytes and charges inside?

A
  1. has alot on Na+/K+ pumps so

2. there is low sodium inside along with negatively charged protein

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9
Q
  1. in the apical region the sodium uses what to get in?

2. however what happens to it at the basolateral membrane?

A
  1. in the apical membrane sodium is pumped in with a co-transporter (glucose or amino acid).
  2. it is pumped out the back using Na+/K+ pumps (basolateram membrane)
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10
Q

what is reabsorbed in the early PCT

A

glucose, amino acids, bicarb, (by moving sodium with co-transporters)

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11
Q

what is “the load”

A

the load is when all glucose/ sodium co-transporters are occupied

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12
Q
  1. what is the maximum rate that somthing can be extracted by the body
  2. what happens if this is exceeded
A
  1. transport max or V-max

2. if v-max is exceeded, there is overflow

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13
Q

what is the normal rate of glucose extraction?

A

125 mg/min

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14
Q
  1. what happens if your body were to have glucose coming down at 200 mg/min?
  2. what is this rate of 200 mg/min called ?
A
  1. your body could get most of it, but there would be there would start to be spillage of glucose into the urine
  2. “threshold”
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15
Q

what is 375 mg/min and why is there such a big range?

A

375 mg/min is transport max, the range is large because some nephrons are new, some old, some large and some small.

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16
Q
  1. what hormones can increase your glucose?

2. what is Dawn syndrome?

A
  1. cortisol and growth hormone can increase blood glucose

2. Dawn syndrome is when your body releases growth hormone into your blood and your glucose shoots up

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17
Q

At what point does reabsorption of glucose and amino acids cease?

A

once into the late proximal convoluted tubule

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18
Q
  1. what happens if glucose gets past the early PCT

2. how is this manifest in diabetics?

A
  1. it becomes osmotically active

2. you see polyuria and polydipsia

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19
Q

once all the solutes leave the filtrate, what follows (through what does it move), where does it go? and what are you left with?

A

once the solute leaves, water follows (thru the leaky junctions into the interstitial space) leaving urea behind.

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20
Q

since the concentration gradient is against the filtrate once everything leaves and the urea is left, what does the urea do? what transport method?

A

the urea leaves the filtrate via passive transport

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21
Q

how is active transport set up

A

via sodium/ potassium pumps

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22
Q

how is secondary active transport done

A

via sodium/ glucose pumps (co-transporters)

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23
Q

what are factors that change the effecicacy of passive reabsorption?

A
  1. the concentration gradient
  2. premeability of the substance thru the membrane or tight leaky junctions
  3. residual time in the tubule (the longer it stays, the more time it has to move thru).
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24
Q

how many strands on a tight leaky junction?

A

2

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25
Q
  1. what are the two types of carbonic anhydrase?

2. how are they different?

A
  1. apical carbonic anhydrase (which is at the apical membrane’s brush border) and cytoplasmic carbonic anhydrase
    2a) apical joins bircarb and hydrogen to form carbonic acid to get it into the tubule. once inside, it breaks into H+ and Hco3-
    2b) cytoplasmic carbonic anhydrase re-joins the co2 and H20 to form carbonic acid which breaks down again retaining the bicarb and expelling the H+
26
Q

once the carbonic acid breaks down into HCO3- and H+, how do the convoluted tubules get rid of it and what happens to the bicarb (ahd what part of the PCT does this happen)?

A

the hydrogen is pumped out via H+ pumps

bicarb is exchanged (like in the bohr effect) for Cl- ion (in the late PCT)

27
Q

how is chloride pumped out of the filtrate?

A

via sodium/ chloride pumps (dual pumps) and chloride also follows the concentration gradient thru the tight leaky junctions (between cells)

28
Q

how does the body deal with calcium?

A

whatever happens to Na+, happens to Ca++

29
Q

osmolarity in the early PCT is 300 mOsm, what is it in the late PCT?

A

because even when solute is pulled out in a portion (65%), water will follow in a portion (65%); therefore, the osmolarity will remain 300 mOsm.

30
Q

what factors increase the absorption percentage (65%) in the PCT/

A

vasopressors such as angiotensin II, epi and nor epi

31
Q

what kind of cells are in the descending loop of henle?

A

simple squamous cells

32
Q

what kind of cells are in the thick ascending loop of henle?

A

cuboidal

33
Q

1.what is special about the space between the cells in the early PCT?

A
  1. the space between the cells has concentrated solute
34
Q
  1. how much of the urea is absorbed at the early PCT?

2. what is urea used for in humans?

A
  1. 30%

2. it is used for osmolarity to keep serum osmo between 270-300

35
Q

what is different about the thick ascending limb and the descending limb (of the loop of henle)?

discuss the gradient that one creates and the osmolarity changes of the other

A

the descending limb has a high mOsm, it goes from 300 mOsm to 1200 mOsm at the bottom (becase you have lost alot of water).

the ascending limb is permeable to solutes (but not to water. solutes will leak out, creating a gradient that will pull water out of the descending limb (seems backward, but it creates a gradient for the next fluids)

36
Q

what is the NAME of the system that is created by solutes (sodium) being leaked out of the thick ascending limb of the loop of henle and the descending loop of henle losing water because of it?

A

counter current system

37
Q

what happens to the water that is pulled from the descending loop of henle?

A

the vasa recta absorbs it

38
Q
  1. how much of the filtrate water is pulled out at the descending loop of henle?
  2. that means ___% of salt/solutes is secreted from the thicck ascending loop of henle
A
  1. 25%

2. 25%

39
Q
  1. where in the loop of henle is urea reabsorbed?

2. how much is kept over by the body for osmolyte?

A
  1. at the end of the descending and the beginning of the ascending (the thin ascending limb).
  2. 50%
40
Q
  1. how does lasix (a loop diuretic) work?

2. how does that make you diruese?

A
  1. it blocks the Na+/K+/Cl- triple pump located in the thick loop of henle.
  2. if you prevent the pumps from putting solute (Na+, K+, Cl-)out into the space to be picked up (absorbed) by the vasa recta, you will pee it out.
41
Q

what is special about the Na+/K+/Cl- (triple pump)?

A

it is a triple pump (thats different!!) and it prevents Ca++ from doing what sodium does (which calcium usually does what sodium does).

42
Q

there is alot of K+ inside the ascending loop of henle d/t potassium being pumped in, so what happens to the K+

A

the K+ drives all of the divalent (2++) ions out of the ascending loop …i.e. mag++, ca++

43
Q

what hormone controls the process of electrolyte exchange in the proximal and loop of henle?

A

parathyroid hormone

44
Q

as the vasa recta flows across the loop of henle, does it become hyper or hypo osmotic?

A

hypo-osmotic because it is absorbing all of the fluid that the descending loop of henle is releasing

45
Q
  1. why is the thick loop of henle called the “diluting limb”?
  2. what is the mOsm of the thick loop of henle?
A
  1. because the ascending (thick) loop of henle is getting rid of all of the solutes that will create the salt gradient that will pull the fluid out of the descending loop of henle.
  2. 150 mOsm
46
Q

what happens if there is too much acid in the cells of the kidneys

A

you can exchange H+ with a Na+/H+ exchanger that brings sodium into the cell and pushes H+ out of the cell.

47
Q

the JGA connects to what 2 structures?

A

JGA connectes between the afferent arteriole and the distal convoluted tubele

48
Q
  1. where is the Macula Densa?

2. what does it do?

A
  1. on the section of the distal convoluted tubule facing the Afferent Arteriole.
  2. it samples the salt content of the filtrate and tells the grandular cells when to secrete renin (which will eventually constrict and change sodium flow).
49
Q

what happens if the macula densa samples the filtrate and the sodium is low

A

the macula densa “takes the brakes off” the granular cells and they secrete renin

50
Q
  1. grandular cells are what type of intervention?

2. what other hormones do the grandular cells respond to (and under what circumstances)?

A
  1. Grandular cells are beta 1
  2. they respond to:
    a) epinephrine from the ardrenal cortex and to
    b) nor epi in the blood from post ganglionic sympathetic release
51
Q
  1. what is the path of renin?

2. What vessel does Angiotensin II work on?

A
  1. renin turns angiotensinogen(from liver) into angiotensin I. Angiotensin I goes to the lungs and is converted by Angiotensin converting Enzyme (ACE) into Angiotensin II …
  2. which is the potent vasoconstrictor on the Efferent arteriole
52
Q
  1. angiotensin works of the efferent arteriole to do what?

2. what hapens if that doesnt fix your sodium deficet?

A
  1. angiotensin II constricts the efferent arteriole which increases GFR (reabsorption of Na+ in the PCT).
  2. the adrenal cortex will secrete Aldosterone which to cause more reabsorption of sodium
53
Q

where does aldosterone work

A

on the late DCT

54
Q
  1. what are the 2 cells in the late DCT and cortical collecting ducts?
  2. what hormone affects them?
A

1a) principle cells (called principle because they make up 90%)
1b) intercalated cells
2. aldosterone works on these cells

55
Q
  1. what does aldosterone cause to be exchanged or secreted?

2. what conditions cause aldosterone release?

A
  1. aldosterone can cause an exchange between sodium and hydrogen or sodium and potassium
  2. hyperkalemia can cause aldosterone secretion
56
Q

what do the primary cells do with aldosterone and what do the intercalating cells do with aldosterone

A

primary cells exchange sodium for H+ or K+ (pulls sodium in and kicks the others out)
intercalating cells get rid of H+ ions (deal only with acidosis and proton pumps)

57
Q

how do intercalating cells deal with H+

A

they have carbonic anhydrase in its cells which turns co2 and h20 int h2co3 which turns into HCO3- and H+.
the H+ is pumped out and the bicarb is exchanged for Cl-

58
Q

what is special about the medullary collectind ducts

A

they have aquaporins which react to ADH and move together to form water permeable tubules (because the protein coats cant cover the space between each tubule) which will leak water out of the collecting duct and back into the body.
without ADH, they stay far apart and a protein coat seals each individual tubule no water leaks out of collecting ducts and you urinate it out

59
Q

if you are dehydrated, your body will reabsorb water. what mOsm will your urine be?

A

1200 mOsm

60
Q
  1. ADH aka___?
  2. what kind of chemical/ hormone is it?
  3. what kind of cell is it released from? where are they?
  4. whak kind of cells do ADH work on?
A
  1. ADH aka vasopressin
  2. it is a neuropeptide (a protein released from neural tissue)-NOT A NEUROTRANSMITTER!!!
  3. it is released from neuro-endocrine cells
  4. made in hypothalamus and stored in posterior pituitary
61
Q
  1. if you eat salty food , your body will reabsorb water. What does that have to do with ADH?
  2. If you drink too much water, your body will want to get rid of water, what does ADH do with that?
  3. what does ETOH do to ADH secretion?
A
  1. if you have too much salt, you want to keep water so you secrete ADH
  2. if you drink too much water, you need to get rid of water, so you dont secrete ADH
    3 etoh blocks ADH secretion so you pee
62
Q

when is filtrate considered urine?

A

at the end of the collecting duct.