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A&P II > Week 10: Urinary > Flashcards

Week 10: Urinary Flashcards

1
Q

I have blood inside the capillary, what’s that doing?

A

pushing out

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2
Q

I have particles inside capillaries, whats that doing?

A

sucking in

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3
Q

I have fluid outside capillary, whats that doing?

A

pushing in

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4
Q

I have particles outside, whats that doing?

A

sucking out

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5
Q

It’s the same thing as starling but the difference is?

A

all same pressures in the same direction but all we did is there is a capsule around it and draw it like it’s a knot and rather than a straight capillary like we do in systemic capillaries

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6
Q

whats gonna be different about this?

A

this system is not built to have filtration at one part of glomerulus and reabsorption at another part glomerulus.

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7
Q

what is it built for?

A

only allow filtration

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8
Q

how do we do that?

A

by having the glomerular capillary pressure higher than systemic capillary pressure

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9
Q

CHP in the glomerulus, instead of being 35, its?

A

60 mmHg

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10
Q

COP and IFOP is gonna be 0 because?

A

we’re not leaving the capillary/particles

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11
Q

a lot of the things that contribute to the osmotic concentration of blood (RBC, WBC, Platelets, plasma proteins) are too big to?

A

get filtered
- they’re not getting in the interstitial fluid space

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12
Q

, so the osmotic concentration of interstitial fluid is going to be higher or lower?

A

much lower than you expect in a systemic capillary

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13
Q

the COP is gonna be relatively high because?

A

we’re not reabsorbing

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14
Q

mostly what is leaving?

A

mostly water is leaving and a whole bunch or particles that are too big to get filtered.

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15
Q

the interstitial pressure (pressure in the capsilar space) is going to be higher but the whole thing is rigged to have?

A

the net filtration pressure throughout the glomerulus be positive
- if it gets to 0, we have a problem

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16
Q

the net filtration pressure is?

A

10 mmHg
- bc that’s gonna give us glomerular filtration rate (how much am i filtering collectively at all my glomeruli in a period of time)

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17
Q

glomerular filtration rate is?

A

directly proportional to net filtration pressure

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18
Q

net filtration pressure goes up the glomerular filtration rate should go up or down

A

up

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19
Q

net filtration pressure goes down, glomerular filtration rate goes? up or down

A

down

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20
Q

with a net filtration pressure of 10 mmHg, in a healthy person, what is the glomerular filtration rate?

A

180 liters a day
- 60x a normal plasma volume

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21
Q

what is the daily urine output?

A

a liter and a half a day
- 99% of what you filter gets reabsorbed

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22
Q

what problems would affect the capillary hydrostatic pressure in the glomeruli?

A

hemorrhage, dehydrated, and medication problems

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23
Q

that affects what?

A

whether or not your patients kidneys are working effectively or not

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24
Q

what’s gonna determine CHP in a glomerulus is?

A

how much blood you have in the glomerulus

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25
Q

anything that makes it easier for blood to get into glomerulus or harder for blood to get out is going to?

A

increase net filtration pressure which will increase glomerular filtration rate

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26
Q

anything that makes it harder for blood to get in or easier to get out is?

A

lower the amount of blood in glomerulus and lower glomerular filtration rate

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27
Q

i have an entrance to glomerulus which is the afferent arteriole, and i have an exit from glomerulus which is the efferent arteriole.
If i dilate my afferent arteriole, and this particular nephron, it makes it easier for?

A

blood to get into the glomerulus.
- it increases glomerular blood volume

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28
Q

what’s that gonna do to net filtration pressure?

A

increase it
- if net filtration pressure goes up, glomerular filtration rate goes up

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29
Q

if i leave my afferent arteriole alone in its normal resting state but i constrict my efferent arteriole, now it’s harder to?

A

let blood out and then bringing blood in at the same rate i have before that’s also gonna increase volume of blood in glomerulus and ultimately increase GFR

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30
Q

if i dilate efferent arteriole, its easier for?

A

blood to get out

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31
Q

if i constrict my afferent arteriole and make it harder for blood to get in,

A

it has the same affect

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32
Q

if i want to really want to screw things up, i can dilate my afferent arteriole and constrict efferent arteriole,

A

make a huge jump in glomerulus filtration rate

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33
Q

or i can constrict my afferent and dilate my efferent..

A

harder to get in and easier to get out and it will drop a lot

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34
Q

the sympathetic nervous system is going to?

A

adjust what’s going on with the afferent and efferent arteriole.
- there are gonna be some other things here that are going to be into play to help determine glomerular filtration rate

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35
Q

what if inward pressures equal outward pressures and NFP is 0?

A

nothing happens cuz NFP is 0

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36
Q

if you give a patient medication that doubles their mean arterial pressure, their GFR would not go up about?

A

15%
- why? your body autoregulates glomerular filtration rate. it is a way of protecting the size of filtration slits.

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37
Q

if you give patient medication that doubles their mean arterial pressure and the glomeruli have no defense mechanisms, what will happed?

A

im going to blow out their kidneys

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38
Q

we don’t need much protection against ?

A

effects of bp lowering too much
- it may kill you but it wont cause permanent damage to kidneys
- really high bp at the glomeruli will

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39
Q

what is the myogenic mechanism?

A

has to do with what’s going on in the afferent arteriole. if bp to this particular nephron goes up, it stretches smooth muscle which causes a reflex vasoconstriction. im protecting glomerulus from that big jump in bp, im not damaging filtration slits, im letting plasma proteins and RBC and stuf wind up in filtrate

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40
Q

this is something that is happening at each individual?

A

nephron

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41
Q

if you have 50 nephrons where bp is higher than it should be, theyll all?

A

stretch and vasoconstrict

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42
Q

if your other nephrons aren’t seeing that, theyre not going to?

A

respond as a group
- this is going to be evaluated one nephron at a time based on what the pressure is in the afferent arteriole and whether we’re stretching that smooth muscle

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43
Q

once we get to glomerulus, what are the 2 problems?

A
  1. there is no way to constrict it
  2. once it gets to glomerulus, we’re already doing damage
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44
Q

we have hormones that will affect GFR which include? RASS especially renin will be?

A

adjusted by bp

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45
Q

if bp is low, what happens to renin release?

A

it will go up

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46
Q

if bp is high and it happens to be coupled with high blood volume, then we get release of?

A

atrial natriuretic hormone

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47
Q

when you have too much blood volume, and that is causing the high bp, ANH will help to ?

A

increase my GFR so i can get rid of the excess fluid`

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48
Q

if bp is low, and renin secretion has gone up, renin will?

A

decrease my GFR so i lose less water

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49
Q

if we increase GFR, more filtrate is produced. most of that filtrate is water. so if i have a high blood volume and i need to get rid of more water, high blood volume stimulates ANH release, and the ANH will act as?

A

on a nephron to increase GFR. filter more, got more water in filtrate, and now i will leave it there and go out of the body.

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50
Q

when i have low bp at my nephron, renin release goes up. low blood pressure may be an indicatory of?

A

low blood volume
- not always but it might be

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51
Q

the renin, among the other things it does, is going to decrease GFR. less fluid goes into the filtrate meaning?

A

there’s less time of losing that fluid so if my bp problem was bc i have low blood volume, i dont want my blood volume to keep dropping, so im going to filter less and decrease the chance of losing ?? 1:29

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52
Q

if bp goes up, that is detected by the JG cells, what happens to renin release?

A

it will go down

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53
Q

if bp goes up bc blood volume goes up, you’re going to stretch the?

A

atria of heart and get ANH released into the blood.

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54
Q

not having as much renin, will help increase?

A

GFR

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55
Q

the hormone affects the?

A

GFR

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56
Q

we’re also going to have some sympathetic system innervation in our?

A

afferent arterioles

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57
Q

if patient is having baroreceptor response bc their bp is too low, what does that crank up?

A

your sympathetic nervous system
- HR goes up
- you’re vasoconstricting
- in systemic arterioles is also vasoconstricting
- and afferent arterioles 1:31 to decrease GFR

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58
Q

what else affects this?

A

autonomic activity

59
Q

what and how is getting reabsorbed is going to depend on?

A

what part of the tubular system we’re in

60
Q

the proximal convoluted tubule is gonna be responsible for?

A

absorbing lots of things
- sodium 1:33
- organic things we’re trying to keep (glucose, galactose, etc)
- water

61
Q

all of this is dependent on?

A

the ability we have to generate three different types of gradients in the prop between the fluid in the proximal convoluted tubule and the cell in the blood

62
Q

this filtrate came from?

A

the blood

63
Q

the filtrate from blood has a sodium concentration that looks like ?

A

the sodium concentration of blood

64
Q

the first thing to do is?

A

have sodium cotransport with all those organic things

65
Q

its facilitated diffusion co-transport, the two things are both bound to ?

A

carrier proteins and they’re moving in the same direction

66
Q

if all carriers are active, we are reabsorbing?

A

lots and lots of sodium along with lots of organic stuff

67
Q

every time i take a sodium out of filtrate, it’s what in the cell and filtrate?

A

a little more positive in the cell and little bit more negative in the filtrate

68
Q

gradient #1 is the sodium gradient, we have to have that bc no sodium gradient, what happens?

A

no sodium gradient we can’t get the other two

69
Q

as i reabsorb more sodium than amino acids, more sodium than glucose, etc.. i start to build what?

A

an electrical gradient

70
Q

inside the cell is going to become?

A

more positive than the filtrate

71
Q

that electrical gradient is going to drive what?

A

the reabsorption of negatively charged ions
- fluoride
- a little bit of bicarb

72
Q

all of those that are neagtively charged are going to follow?

A

an electrical gradient

73
Q

as we get these things into the cell, in various mechanisms that you don’t need to worry about, they will?

A

make their way to the blood

74
Q

the one you do have to worry about is?

A

we’re actively transporting sodium out from the tubular cell into blood

75
Q

the osmotic concentration of the filtrate it getting?

A

lower and lower

76
Q

the osmotic concentration inside the cell is getting?

A

higher and higher bc im adding particles and not water

77
Q

what is gradient number 3?

A

osmotic gradient
- drives water reabsorption in the proximal convoluted tubule

78
Q

what are the three gradients you need?

A
  • sodium
  • electrical that we get from moving sodium out
  • osmotic that you get from moving all the particles you have moved out from the tubular lumen and into the cell and into the blood
79
Q

proximal convoluted tubule is the only place in a nephron that?

A

could reabsorb glucose

80
Q

if concentration of glucose in the filtrate is higher than the concentration that the sodium glucose transporter can handle (300mg of glucose per 100ml of fluid), what will happen?

A

you’re gonna start to see glucose actually making it out of the proximal convoluted tubule, thats a problem

81
Q

what are the two problems?

A
  1. every one that makes it out of the proximal convoluted tubule is 36 ATP that is not in the toilet
  2. glucose that made it past the proximal convoluted tubule, is now contributing to the osmotic concentration of the fluid of the filtrate
82
Q

the more glucose that got out of the proximal convoluted tubule, the more?

A

water its gonna hold in the filtrate
- stuff that stays in the filtrate is leaving the body

83
Q

in a diabetic, why is lots of urine production a problem?

A

lots of urine production bc the glucose that should be reabsorbed isnt getting reabsorbed bc their concentration of glucose is so high and so that glucose is holding water in the tubule and it’s going to stay in the tubule and leave the body, out in the urine

84
Q

why is thirst a problem you’re gonna see in a diabetic?

A

they’re losing water that they shouldn’t be losing
- they’re not in fluid balance and they just keep adding water to try to get back into balance

85
Q

which one causes which? the glucose staying in the filtrate causes the loss of water, the thirst comes from losing water they shouldn’t have, theyre not peeing more bc theyre drinking more, theyre drinking mroe bc they have a higher urine volume than they should have and they are essentially dehydrated

A
86
Q

the third problem you’re gonna see has nothing to do with kidney function but?

A

has something to do w the face that you can’t get glucose into cells to metabolize it so we’re using an alternate metabolic pathway that just uses lipids winding up with acidosis

87
Q

what is it called when you have this glucose holding water in the urine?

A

osmotic diuresis

88
Q

what we see in someone with poorly controlled type I diabetes is ?

A

the osmotic part is the glucose acting as a particle holding water in the tubular system and not letting any get reabsorbed

89
Q

the diuresis is that that causes a lot of?

A

urine production

90
Q

the reason why glucose is not getting reabsorbed is bc?

A

carriers are saturated

91
Q

the proximal convoluted tubule is supposed to reabsorb?

A

70% of what got filtered
- it goes out and boom getting it back

92
Q

the loop of henle is not built to handle?

A

a large volume of filtering

93
Q

if we have too much filtrate coming forward from the proximal convoluted tubule and going into the loop of henle, what will happen?

A

its going to mess up what we can reabsorb

94
Q

we have filtrate moving down and up in?

A

moving down in descending limb and moving up in the ascending limb
- vasa recta, if talking about juxtamedullary nephron, that part of vasa recta that runs next to descending limb, the blood is moving down next to that part and the part thats next to the ascending limb, the blood is going to be moving up. so the the filtrate and the blood of juxtamedullary nephron is moving in the same direction

95
Q

what is that called?

A

countercurrent
- moving in opposite directions

96
Q

what is the reason for the loop to get progressively darker?

A

countercurrent mechanism, what we’re reabsorbing, what’s getting picked up by vasa recta or not, all that is leading to us building an osmotic concentration gradient in the tissue around the loop of henle

97
Q

as we work our way down the descending limb, the number are?

A

getting higher

98
Q

all the descending limb is permeable to water NOT?

A

solutes

99
Q

solutes can’t?

A

move or move the tubule

100
Q

as we’re moving our way down the descending limb, water can?

A

move out and make the osmotic concentration of the filtrate to match the concentration of the fluid outside the tube.

101
Q

physiology of that:

A

if bc the descending limb is permeable to water not solutes, nature needs a gradient and need to equal things out. if you have a concentration diff and you can’t move the solute, you move water to change concentration. tubule is traveling through osmotic conc gradient, as you get further into descending limb and closer to the bottom of loop, more water is getting reabsorbed and the solute can’t follow so we wind up at each region with filtrate in tubule at equilibrium of osmotic concentration of that level of the renal medulla. what we’re doing as we work down is concentration the filtrate. then the getting to the bottom of the loop, you swing down here and the permeability has changed.

102
Q

the thick ascending limb of the loop of henle is NEVERR EVERRR !!

A

permeable to water

103
Q

as the filtrate goes up into the thick ascending limb, now we are reabsorbing?

A

solute and the water cant follow

104
Q

we’re actually reabsorbing sodium and chloride which is going to contribute to ?

A

this osmotic concentration gradient in the renal medulla but

105
Q

i’m going to reabsorb so much of it that by the time i get to the top of the thick ascending limb and im ready to let that filtrate in the distal convoluted tubule, the osmotic concentration is ?

A

lower than the osmotic concentration of blood
- rn i have dilute filtrate

106
Q

what happens with this loop of henle is what makes it possible to do two diff things depending on the hormonal situation..

A
  1. is to make concentrating urine, something that has an osmotic concentration HIGHER than blood
  2. to make dilute urine. something that has osmotic concentration LOWER than blood
107
Q

importance of vasa recta:

A

blood in vasa recta is moving in the same direction as the blood in whichever side of the loop you’re on and the blood is moving SLOWLY

108
Q

what happens if the blood in the vasa recta moved really quickly?

A

it would suck up all of our osmotic particles in the renal medulla

109
Q

blood in vasa recta moving slowly makes it possible for us to ?

A

keep this osmotic gradient and the osmotic gradient is the key to our ability to make concentrated urine

110
Q

when am i gonna wanna make urine that has a higher osmotic concentration than blood?

A

when dehydrated, don’t have enough water and don’t want to lose much more

111
Q

this counter current is gonna get us a couple of things?

A
  • lets us get a lot of water out of the tubule before we go to the part where we need to reabsorb more sodium chloride
  • helps us maintain the osmotic gradient
112
Q

without osmotic gradient in the renal medulla, what happens?

A

we can’t make concentrated urine bc what’s gonna happen: we’re gonna go in distal convoluted tubule and down into collecting duct which has to pass through the osmotic concentration gradient and if we have ADH present, more water can get sucked out as we move down the renal medulla

113
Q

if we don’t have ADH present, what happens?

A

nothing after thick ascending limb is gonna be permeable to water so we will be stuck with dilute urine

114
Q

now we have distal convoluted tubule and collecting duct. in this particular situation where ADH is present, I know this bc ?

A

water is coming out of tubule, no ADH= collecting duct is not permeable to water

115
Q

urea is one of those break down products for?

A

metabolizing proteins and yanking amino groups off things. its a small non-polar molecule. it can go wherever it wants as long as its following concentration gradient

116
Q

as we move down to the collecting duct and reabsorb water, urea concentration is going to?

A

increase
- as it gets higher, it’s gonna move out and some of its gonna wind up here and we’re gonna use urea to help make the concentration of our renal medulla higher to it makes it possible to retain more water
- also help us get rid of protein biproducts

117
Q

distal convoluted tubule and collecting ducts are the places where we will?

A

-secrete and reabsorb under the control of hormones
- antidiuretic hormone and aldosterone do their thing

118
Q

when talking about aldosterone, vocab is changing to?

A

sodium reabsorption and potassium secretion

119
Q

i have under control aldosterone bc?

A

aldosterone is what stimulate the production at the luminal end of tubular cell

120
Q

i have Na and K exchanger thats gonna?

A

reabsorb Na and put K in filtrate

121
Q

at the other end of the cell, i have a similar protein that is not gonna move?

A

Na towards blood and K into the cell from the blood

122
Q

when we’re adjusting Na and K concentration in body, we’re using what to do it?

A

aldosterone
- its a 1 for 1 exchange

123
Q

we are also gonna be reabsorbing?

A

bicarb in diff mechanisms

124
Q

Na hydrogen ion exchanger that gives u?

A

Na reabsorption for hydrogen ion secretion
REALL IMPORTANT

125
Q

Na and K exchanger has a lower affinity for sodium than?

A

Na hydrogen ion exchanger
- body way of telling us that too many hydrogen ion are more of a risk to K ions

126
Q

if i have a limited amount of Na to reabsorb, im gonna use?

A

all i need for hydrogen ion secretion and put that in filtrate to get out of the body and then wtvr i have left, ill use to secrete K

127
Q

one of the problems you see in patients who are acidotic?

A

high K levels bc their body is dealing with H+ problem and not with K+

128
Q

if drinking lots of water, you end up with dilute urine bc?

A

all that water that enters the tubule, we’re gonna reabsorb some of it in the descending limb but after the descending limb, no water gets reabsorbed

129
Q

if i have ADH present then im reabsorbing water from the ?

A

distal convoluted tubule and im reabsorbing water out of the collecting duct to reach equilibrium with the osmotic concentration of where i am in the renal medulla, so as i move down further, ive reabsorbed more water and i wind up with a small volume of concentrated urine. im getting rid of the stuff i need to get rid of, in as little water as i can

130
Q

regulating urine volume is how we regulate?

A

blood volume

131
Q

if blood volume is too higher, what do the hormones do?

A

hormones that affect my cardiovascular system will also affect kidneys to make me produce more urine

132
Q

if i dont have aldosterone, what happens?

A

water follows sodium

133
Q

if im not reabsorbing sodium, what happens?

A

another way of losing water that i could be reabsorbing

134
Q

blocking aldosterone and ADH release is gonna cause?

A

me to lose more water and more Na from body decreasing blood volume

135
Q

if im not greatly hydrated and i have ADH present, im also not gonna have ANH. taking ANH away is gonna lower?

A

GFR and let me release aldosterone and ADH

136
Q

if im reabsorbing more Na, im putting more solute in?

A

renal medulla for water to follow

137
Q

reabsorbing Na and having a bigger osmotic gradient in renal medulla will cause me to?

A

reabsorb more water
- lose more water and produce a small volume of concentrated urine and have a much smaller decrease of blood volume
- we have to sacrifice some water to get some stuff out of our body

138
Q

the only time you will see someone stop producing urine is?

A

if they don’t have enough blood to give you a positive net filtration pressure

139
Q

urine volume goes up, what happens to blood volume?

A

goes down
- urine volume goes down, blood volume goes up or doesn’t drop as quicky

140
Q

if im losing more water, where did i take it from?

A

the blood

141
Q

what do we expect to see in urine of healthy person?

A
  • lots of water (95%)
  • other 5% is solutes (waste products like urea and ammonia, creatinine)
  • ions that wind up
  • Na and K (we can absorb a lot of Na in filtrate but not all in normal circumstances)
  • NH4+ (help us get rid of 2:11)
  • chloride
  • some bicarb
  • phosphate and sulfate
  • toxins (we remove toxins from blood. more water you drink, more urine you produce and the more of those things given by bacteria will leave the blood and leave body through urine)
  • pigments (urochrome also part of hemoglobin recycling that tend to give urine the yellow color. asparagus turns urine green)
  • hormones (kidneys take some hormones out of blood. OTC pregnancy/ovulation tests look for hormones taken from blood and put into urine)
142
Q

the percentage all depends on the amount of things that you will lose such as?

A
  • what the hormonal status is in respect to aldosterone and ADH
  • what your diet is
  • level of metabolic activity
143
Q

things that should NOT be in urine?

A
  • blood (blood cells are bigger than filtration slits so blood in urine indicate infection in urinary tract or damage to filtration apparatus in kidney)
  • glucose (we work very hard to absorb it all. its a main player in pathways to make our fav energy molecule, ATP)
  • albumin (tells u that filtration slits is damaged. too big to get through filtration slits. big molecule in physiological)
  • protein in urine of any type indicates damage of kidneys
  • calculi (stones)
  • epithelial cells (if present, indication of not reading directions before providing urine sample)

A&P II (17 decks)

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