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A&P Final > 11/20 > Flashcards

11/20 Flashcards

1
Q

Where in the kidney do we secrete the compounds that the body needs to get rid of like organic compound transporters?

A

in the PCT

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2
Q

Why does the PCT have a really high metabolic rate?

A

It needs energy to reabsorb and secrete everything that it does

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3
Q

Which part of the loop of Henle do we have 20% of our water that was originally filtered be reabsorbed?

A

Thin descending limb

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4
Q

By the time the water that was filtered at the glomerular capillaries makes it to the end of the thin descending limb of Henle, what percent of it is reabsorbed?

A

~85%

2/3 + 20% = ~85

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5
Q

the ascending limb of the loop of Henle is relatively ______ to water

A

impermeable

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6
Q

The regulation of exactly how much water we hold on to happens where in the kidney?

A

The collecting duct and distal tubule

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7
Q

The Thick Ascending Limb is where we reabsorb what? (vague)

A

lots of stuff, primarily ions

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8
Q

What percent of the ions or electrolytes that are filtered get reabsorbed in the Thick ascending limb?

A

25%

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9
Q

2/3 of the ions/electrolytes that are filtered get reabsorbed in the PCT + 25% get reabsorbed in thick ascending limb.
Which cells decide what happens to the rest of it?

A

principal cells in the last part of the tubule

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10
Q

Where are principal cells found?

A

late part of distal tubule and pretty much all of the collecting duct

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11
Q

Water regulation in the late part of the tubular system is dependent on

A

How much Vasopressin/ADH floating around

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12
Q

Vasopressin/ADH allows us to

A

fine tune the amount of water we are reabsorbing

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13
Q

Which two portions of the tubule have a high metabolic rate?

A

PCT and thick ascending limb

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14
Q

In the distal tubule, which transporter does the heavy lifting in regards to getting Ca++ reabsorbed from the tubular lumen?

A

Na+/Ca++ exchanger

The secondary pumps are the Ca++ ATPase pumps

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15
Q

The electrochemical gradient that the Na+/Ca++ pump depends on is formed from the

A

Na+/K+ pump

This keeps Na+ concentrations low in the cell and bc of that Na+ wants to come into the cell from the interstitium

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16
Q

One of the things we can do to make the Na+/Ca++ pump spin faster is to

A

block Na+ entry from the tubular fluid from entering the cell

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17
Q

How does sodium get into the distal tubule cell?

A

Though a simple Na+/Cl- pump on the luminal side of the cell, then it is pumped out by the Na+/K+ pump and then brought back into the cell via the Na+/Ca++ exchanger.

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18
Q

If we block the Na+/Cl- pump in the distal tubule with a ________ (drug) then

A

thiazide diuretic

Then it should speed up the cycling of the Na+/Ca++ exchanger which would increase the amount of Ca++ that gets reabsorbed.

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19
Q

What kidney drug is prescribed for osteoporosis and why?

A

thiazide diuretic

It speeds up the Na+/Ca++ exchanger which helps them reabsorb more Ca++

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20
Q

if you are on a thiazide diuretic, then which supplement do you have to be mindful of?

A

Ca++ supplements

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21
Q

Prevention of kidney stones can include ____(drug). why

A

thiazide diuretics.

Stones are made from crystalized Ca++.

This drug is not good for removing stones that are already formed but can be good for prevention

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22
Q

When you think of principal cells think of

A

Aldosterone

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23
Q

The more aldosterone we have the more ____ we reabsorb

A

Na+

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24
Q

Aldosterone is a

A

mineralocorticoid. It helps us manage and maintain our electrolyte balance

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25
Q

What makes aldosterone levels rise?

A

low blood pressure or low sodium

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26
Q

Having a lot of aldosterone has what effect on K+?

A

It decreases K+

works by:

aldosterone binding to intracellular aldosterone receptors which speeds up the Na+/K+ pump on the ISF side of the cell. Na+ goes into the ISF and K+ goes into the cell.

We have channels on the tubule side of the cell that is going to allow K+ out into the tubule and Na+ into the cell.

This means we have a bunch of Na+ moving towards the renal ISF (reabsorption) and a bunch of K+ moving towards the tubule (secretion)

Aldosterone (probably) increases the number of K+ channels and (definitely) increases the number of Na+ channels found on the tubule side of the cell. The more channels we have the more/faster the ion movement is going to be.

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27
Q

How does K+ get into the tubule from the tubular cells in the distal tubule?

A

Through a channel that stays open NOT A PUMP.
Despite this, this process is still called secretion because it is relying on the Na+/K+ pump

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28
Q

Lots of aldosterone = lots of K+ ______ in the distal tubule

A

secretion

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29
Q

What does the aldosterone do directly in the distal tubule?

A
  1. speeds up Na+/K+ pump
  2. Enhances the number of Na+ channels in the cell wall
  3. Likely also plays a role in how many open potassium channels we have in the tubule side of the wall as well. (not as well ironed out)
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30
Q

What are the two types of K+ channels that operate in the principal cells?

A

ROMK (renal outer medullary K+ Channel)
BK (Big K+ channels)

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31
Q

How do the ROMK and BK channels work?

A

If we don’t need to get rid of a lot of K+ then the channels are sequestered inside the cell, waiting to be needed.

If we need to pick up K+ secretion then the ROMK channels get put in the cell wall to be used as extra pathways for K+ to move out of the cell. This is aldosterone mediated

If we have really high K+ excretion the BK channels also open up. This is aldosterone mediated

Those are in the cell wall all the time, it’s just a matter of if they’re open or closed. If we don’t need them they’re closed and if we have a ton of K+ we need to secrete they open.

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32
Q

POTASSIUM maintenance think

A

PRINCIPAL cells

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33
Q

What is another name of the Na+ channel that is found on the tubule side of the tubular cell in the Distal tubule?

A

Epithelial Na+ channel
ENaC

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34
Q

What do Amiloride and Triamterene do?

A

Block the ENaC pump in the distal tubule which indirectly slows down the K+ secretion by slowing down the Na+/K+ pump. This might be useful if you wanted to hang on to K+.

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35
Q

aldosterone receptor antagonist example:

A

spironolactone

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36
Q

spironolactone

A

Blocks the aldosterone receptor in the distal tubule which slows down the Na+/K+ pump which slows down K+ secretion and Na+ reabsorption

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37
Q

What are the K+ sparing diuretics?

A

Amiloride
Triamterene
spironolactone

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38
Q

A loop diuretic slows down reabsorption where in the kidney?

A

Thich Ascending Limb in the loop of Henle

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39
Q

Thiazide diuretics work in what part of the kidney?

A

just upstream of principal cells

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40
Q

Osmotic diuretics reabsorb water in which part of the kidney?

A

the early parts of the tubule

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41
Q

Anything that reduces NaCl reabsorbed upstream of principal cells have what effect on water reabsorption?

A

indirectly decreases water reabsorption or increases water leaving the body

K+ wasting diuretic.

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42
Q

Anything that reduces NaCl reabsorption before the principal cells leads to what effect in the later part of the tubule?

A

Means more will be reabsorbed in the later parts where there are principal cells which would increase K+ secretion

K+ wasting diuretic

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43
Q

Smidt says if you are on a K+ wasting diuretic but you want to conserve K+ then

A

you might be put on a small dose of a K+ sparing diuretic too to increase volume excretion but limit K+ wasting.

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44
Q

what is the most commonly prescribed diuretic combination?

A

Triamterene with Hydrochlorothiazide

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45
Q

Where does aldosterone come from?

A

zona glomerulosa- the most outside part of the adrenal gland

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46
Q

Layers of the adrenal cortex outside to inside:

A

zona glomerulosa
zona fasciculata
zona reticularis
Medulla

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47
Q

What do the zona fasciculata and zone reticularis produce?

A
  • most of our cortisol (helps us even things out when we are under stress)
    and androgens including androstenedione (an anabolic steroid that converts to sex hormones)
    a small amount of estrogen from the zona fasciculata specifically.
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48
Q

If you have a crazy on the tumor zona fasciculata you would produce a lot of

A

estrogen

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49
Q

Where do catecholamines(epi/norepi) come from?

A

The deep inner part of the adrenal cortex called the Adrenal Medulla.

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50
Q

What is the ratio of epi to norepi that is released at the adrenal gland?

A

4epi : 1norepi

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51
Q

aldosterone secretion is sensitive to

A

K+ levels.
High potassium= high aldosterone
Low potassium = low aldosterone

angiotensin II binding to at1 receptors at the zona glomerulosa

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52
Q

What is the enzyme that produces aldosterone? Where in the body is this found?

A

aldosterone synthase

Found in the zona glomerulosa

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53
Q

aldosterone, cortisol and estrogen are derivatives of

A

cholesterol

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54
Q

What is the difference in the shape of aldosterone, cortisol and estrogen?

A

1 chemical modification to differentiate them from each other.

However they all look very similar to cholesterol and each other

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55
Q

If you have a buttload of extra cortisol, sometimes it interacts with aldosterone receptors. Why?

A

It structurally looks very similar to aldosterone

56
Q

If you have someone with an ACTH lung tumor what would you expect to see?

A

increases cortisol levels that overwhelm the 11 beta hydroxy steroid dehydrogenase type 2 enzyme. Cortisol looks like aldosterone= cortisol binding to aldosterone receptors= HTN & hypokalemia

57
Q

why don’t people like steroids?

A

they drive up bp by increasing cortisol which interacts with aldosterone receptors

58
Q

cortisol is a

A

glucocorticoid. It helps provide glucose to the brain to help us make good decisions when we are under stress

59
Q

The body tends to have more cortisol in the principal cells than aldosterone receptors in normal circumstance, much less when we are stressed and secreting extra cortisol. How does the body regulate cortisol interacting with aldosterone receptors and not have really high bp all the time?

A

Inside of the principal cell is an enzyme called 11β- HSD type 2 that floats around and degrades/destroys cortisol within the cell.

59
Q

Can cortisol cross through the cell wall easily?

A

Yes, it is a steroid compound so it has no problem.

60
Q

What does 11β- HSD type 2 stand for?

A

11 beta hydroxy steroid dehydrogenase type 2

61
Q

What is the one natural inhibitor of 11 beta hydroxy steroid dehydrogenase type 2?

A

Natural Chinese licorice

62
Q

Can you use licorice candy to inhibit 11 beta hydroxy steroid dehydrogenase type 2?

A

No, that’s fake.

63
Q

Where are people exposed to real Chinese licorice?

A

Flavoring in tobacco compounds, like smokeless tobacco

64
Q

what is one reason why people who smoke have HTN?

A

A flavoring compound in tobacco is made of Chinese licorice which is a natural inhibitor of 11β- HSD type 2

65
Q

Where are Angiotensin 1 receptors found?

A

blood vessels
kidneys
adrenal cortex

66
Q

PIcture slide 37

A

The effect of plasma K+ concentration on how much aldosterone we are going to have around, and how much K+ excretion we are going to have as aldosterone levels increase.

picture slide 27 the blue chart at the bottom left.

67
Q

aldosterone influences ______ secretion

A

K+

68
Q

The more K+ we secrete in the distal tubule the more we

A

excrete

69
Q

What is a great controller of blood potassium in the body?

A

Aldosterone level from the adrenal cortex working with the kidneys.

70
Q

If you have healthy kidneys and adrenal glands it is almost impossible to have

A

hyperkalemia

71
Q

What are the two types of cells found in the Distal tubule?

A

principal cells=potassium
intercalated cells= acid/base

72
Q

What role do intercalated cells play in acid base regulation?

A

They secrete protons/hydrogen or reabsorb protons and secrete bicarb

73
Q

The cells that secrete protons in the distal tubule are called

A

Type A intercalated cells
manage acid

74
Q

The cells that reabsorb protons and secrete bicarb are called

A

Type B intercalated cells
manage base

75
Q

Generally, which cells do people think about when you mention intercalated cells, and why?

A

type A
acidosis is way more common than alkalosis so the type a intercalated cells are usually the cells working to get rid of protons/H+

76
Q

What are the two ways Type A intercalated cells secrete protons/H+? Which pump is stronger?

A

Strongest: H+ ATPase pump- burns 1 ATP to pump H+ into the tubule. This can move a lot of H+ compared to the second pump.

Hydrogen potassium ATPase- Exchanges H+ into the tubule for K+ into the cell

77
Q

How do the kidney’s manage pH?

A

By getting rid of acid through type A intercalated cells, mostly from the proton ATPase but some through the H+/K+ATPase exchanger

78
Q

Both intercalated and principal cells are sensitive to

A

vasopressin/ADH

79
Q

Where are intercalated and principal cells found?

A

At the end of the distal tubule called the Distal convoluted tubule and the collecting duct

80
Q

Besides K+ and acid/base management, intercalated and principal cells do what?

A

Help manage water balance

81
Q

What is the receptor called that Vasopressin/ADH binds to in the distal tubule?

A

V2 receptor

82
Q

If you have an agent that can selectively activate V2 receptors, where in the body would you see an effect?

A

The kidney, specifically the late distal tubule and collecting ducts

83
Q

Where are V1 receptors found?

A

Out in the periphery on blood vessels that produce lots of squeeze and vascular resistance

84
Q

When Vasopressin/ADH binds to receptors in the DCT/collecting tubule, what happens?

A
  1. cAMP increases
  2. which activates PKA
  3. PKA phosphorylates aquaporin-2 vesicles where aquaporin channels are built and ready to go.
  4. Aquaporin-2 channels are then moved to the tubule side of the cell where they allow water entry on the tubular side of the cell
85
Q

Which isoform of aquaporin channels are completely dependent on vasopressin/ADH?

A

AQP-2

86
Q

Where are AQP-3 and AQP-4 found? Are they dependent on vasopressin/ADH?

A

The renal ISF side of the distal convoluted and collecting duct

They are not dependent on vasopressin/ADH, they are in the cell wall at all times

87
Q

if you have a problem at the kidney and/or how it responds to vasopressin/ADH(like maybe something is wrong with the PKA gene), then what will be the result?

A

you are going to have a problem getting the AQP-2 channels to the cell wall on the tubular side where they can be used for water reabsorption. This is called nephrogenic DI

88
Q

What is keeping us from having to go to the bathroom every 45 minutes?

A

A constituent level of vasopressin/ADH binding to V2 channels in the DCT and collecting duct that are increasing cAMP which are activating PKA which are moving AQP-2 channels to the tubular side of the cell wall to help us reabsorb water.

89
Q

If you have a problem with the secretion of Vasopressin/ADH this disorder is called

A

Diabetes insipidus

90
Q

What is an example of something that causes nephrogenic DI?

A

High Lithium doses.

91
Q

If your pt. is on lithium they will have what kind of urine?

A

producing about 20L a day and drinking a ton to try and replace it.

Very dilute, about 50mOsm

92
Q

What is the lower limit of renal osmolarity?

A

50mOsm

93
Q

What is the diluting segment of the kidney? Why is it called that?

A

The thick ascending limb of the loop of Henle

We are reabsorbing a lot of electrolytes but not reabsorbing water

94
Q

Why is it that you have to urinate a lot and frequently after drinking alcohol?

A

Alcohol takes your vasopressin/ADH system offline.

It reduces the amount of Vasopressin/ADH that is released from brain and impairs the kidney from being able to respond to the little ADH that was there

95
Q

Water levels in the body are controlled via

A

vasopressin/ADH

If we need to get rid of water we drop our vasopressin/ADH levels

If we are in a desert and need to conserve water our vasopressin/ADH levels are going to be very high

96
Q

If someone has a head injury and they start dumping a lot of urine, what do you suspect is the cause?

A

They have damaged their hypothalamus and are not releasing vasopressin/ADH anymore.

This would be a bad cause of Diabetes Insipidus

97
Q

What are the sensors in the body that trigger Vasopressin/ADH release or no release?

A
  • Primary: Osmolarity- salty blood triggers more release of Vasopressin/ADH to dilute out the blood
  • Arterial bp- low arterial bp triggers more release of Vasopressin/ADH to help increase blood volume and therefore blood pressure.
  • Blood volume- low blood volume triggers more release of Vasopressin/ADH to help increase blood volume
98
Q

Where are our blood volume sensors?

A

Low pressure side of the circulation: large veins, atria of heart

99
Q

Where are our blood pressure sensors?

A

Baroreceptors look at the high pressure side of the circulation

100
Q

What are osmoreceptors? Where are they found?

A

specialized cells in the hypothalamus that sense changes in osmolarity

101
Q

Osmoreceptor send information to

A

2 nuclei in the brain:
1. supraoptic nucleus (above the eye)
2. paraventricular nuclei (on the sides of the 3rd ventricle)

102
Q

If we have a bad bacterial infection what does the hypothalamus do?

A

Increases body temp to try and kill the bacteria

103
Q

If we have really salty blood the hypothalamus releases

A

vasopressin/ADH

104
Q

What are collections of cell bodies in the CNS called?

A

Nuclei

105
Q

How much vasopressin/ADH is released by the supraoptic nuclei?

A

5/6 or 83.33%

106
Q

How much vasopressin/ADH is released by the paraventricular nuclei?

A

1/6 or 16.67%

107
Q

Para means

A

to the side of

108
Q

Which ventricle is the paraventricular nuclei situated next to?

A

3rd ventricle

109
Q

How does vasopressin/ADH get into the bloodstream?

A

Produced in the hypothalamus
sent through “pathways” to the posterior pituitary gland aka neurohypophysis which is surrounded by a lot of blood vessels.

110
Q

What is another name for the posterior lobe of the pituitary gland?

A

neurohypophysis

111
Q

What is another name for the anterior lobe of the pituitary gland?

A

adenohypophysis

112
Q

How does the body handle changes in osmolarity: think of the cell as an osmoreceptor and the solution as our blood.

  1. If you put a cell in a solution that the has same osmolarity(isotonic), what happens?
  2. If you put a cell in a hypertonic solution what happens?
  3. If you put a cell in a hypotonic solution what happens?
A
  1. The volume of the cell isn’t going to change
  2. Water is going to move into the cell until the osmolarity is equal to the solution. This slows the rate of action potentials that are being sent to the 2 vasopressin/ADH production areas which reduces Vasopressin/ADH in the pituitary gland and therefore reduces it in the body to get rid of water
  3. Water is going to leave the cell until the concentration is equal to the solution. Increase Vasopressin/ADH in the pituitary gland This increases the rate of action potentials that are being sent to the 2 vasopressin/ADH production areas which increases Vasopressin/ADH in the pituitary gland and therefore increases it in the body to retain water
113
Q

Explain the effect of vasopressin/ADH

picture

A

Vasopressin/ADH produces a wide variation of osmolarity of urine

In the proximal tubule we are reabsorbing 2/3 of EVERYTHING- not picky on electrolytes besides making sure to keep most of the amino acids and glucose, and it is really porous to water. So here the osmolarity of the urine should be isotonic with the blood

In the loop of Henle-deep parts are concentrated with urea and electrolytes so as the blood moves deeper into the kidney and water leaves the tubule, the solutes left behind in the urine are concentrated. When the tubule is permeable to water(descending limb), the urine will have the same osmolarity as the environment in the ISF of the kidney, as the urine moves into the ascending limb and early part of the distal tubule the renal ISF becomes more dilute and we are now impermeable to water but permeable to NaCl. Therefore NaCl leaves the urine and is reabsorbed into the ISF making the urine more dilute. this is the diluting segment

Late part of distal tubule: completely dependent on ADH.
Lots of ADH= lots of water is reabsorbed so very concentrated urine. 1200mOsm

Really low levels of ADH: the urine is already dilute from the diluting segment. If we are reabsorbing electrolytes still but not reabsorbing any water d/t no ADH moving APQ-2 channels to the cell wall then the urine is very dilute. 50mOsm

114
Q

What role does Vasopressin/ADH play in the loop of Henle?

A

It plays a role in how much urea we reabsorb from the tubular fluid.

Urea is small and freely filterable at the glomerular capillaries.

As it moves down the PCT some urea is reabsorbed d/t it being dragged out of the tubule with water.

Half is left in the tubule about midway down the thin descending limb

This half follows the path of the tubule until the collecting duct.

If there is a lot of vasopressin/ADH the collecting duct it has a lots of AQP channels and urea transporters in the cell wall that help us to reabsorb urea. If we reabsorb urea and water then we increase blood volume and are left with concentrated urine.

115
Q

What is one of the major components of the renal interstitium?

A

Urea. This is what makes the renal ISF as concentrated as it is

-also has-
proteins
electrolytes

116
Q

What are the urea transporter isoforms that get placed in the cell wall d/t an increase in ADH

A

UT-A1
UT-A3
“urea transporter”

117
Q

If we are in a state of antidiuresis what kind of transporters will we have in the collecting duct?

A

We would need to hanging on to as much electrolytes and water as possible so lots of UT-A3, UT-A1 and AQP-2

118
Q

What is the primary controller of
blood plasma osmolarity?

A

vasopressin/ADH

119
Q

What is the only signaling compound able to influence water reabsorption without simultaneously influencing salt reabsorption?

A

vasopressin/ADH

120
Q

picture slide 44

A

It doesn’t matter if we have a low sodium intake (30mEq/day) to high sodium intake(180mEq/day), it doesn’t mess with osmolarity that much if you have normal Vasopressin/ADH present.

121
Q

Why does caffeine make you urinate?

A

It decreases vasopressin/ADH release

122
Q

If you remove vasopressin/ADH and have a wide variety of salt intake 30mEq/day-180mEq/day, what would you expect your blood osmolarity to look like?

A

Picture slide 44

It would have a huge range from ~137mEq/L-151mEq/L

123
Q

What are the thirst controllers related to decreased thirst?

A

Decreased plasma osmolarity
(overhydrated, Na+ levels drop)

Increase in blood volume (sensed from atria)

Increased BP (sensed from high pressure baroreceptors)

Decreased in angiotensin II

Gastric distention (full belly)

124
Q

What are the thirst controllers related to increased thirst?

A

Increased plasma osmolarity (dehydrated, Na+ levels are high)

Low blood volume or low blood pressure (sensed from high and low pressure sensors)

Increase in angiotensin II

Dryness in the mouth or lips

125
Q

What are the vasopressin/ADH controllers related to decreased vasopressin/ADH?

A

Decreased plasma osmolarity
Increased blood volume
Increased blood pressure

drugs:
Alcohol
Clonidine
Haloperidol (common)

126
Q

What are the vasopressin/ADH controllers related to increased vasopressin/ADH?

A

Increase blood osmolarity
Decreased blood volume
Increased blood pressure
Nausea(losing fluid or anticipating losing fluids)

drugs:
Morphine
Nicotine

127
Q

picture slide 47

A

When we have changes in potassium intake, as long as we have a functional aldosterone system the body regulates potassium very well.
However, when you block the aldosterone system you can have a wide range of K+ levels.

128
Q

What meds block the aldosterone system?

A

Spironolactone
Triamterene

129
Q

picture slide 56

A

The subject drinks 1 liter of distilled water.
It takes a bit to absorb but when it does, it produces a small reduction in blood osmolarity that is going to decrease vasopressin/ADH levels.

This makes urinary flow rate go way up. It should be 1mL/min but in this scenario, 30 mins later, urine production rate increases as a function of getting rid of the excess water. It doesn’t really do anything with the body’s electrolytes (there might be a small increase in excretion as a function of water pulling a few electrolytes out with it but the majority of what is lost is just water). The flow rate stays high until balance is restored .

Though we only see a small change in the blood osmolarity, we would see massive amount of change in the urine osmolarity as it becomes very dilute to get rid of the excess water.

130
Q

What is the only scenario Smidt can think of that makes the body have a hard time regulating K+ levels?

A

renal failure

131
Q

How long does it take for the healthy body to get rid of 1 liter of distilled water we drank?

A

a couple of hours.

132
Q

urine osmolarity under ideal conditions

A

600mOsml

133
Q

what percent of water and electrolytes that get filtered get reabsorbed in the PCT?

A

65%

134
Q

The last 15% of water that is left after it goes through the thin descending limb must be dealt with where in the kidney?

A

Distal tubule and collecting duct

135
Q

The thick ascending limb reabsorbs what percent of the electrolytes that were filtered?

A

25%

136
Q

As water reabsorption decreases, what happens to urine osmolarity?

A

urine osmolarity drops

A&P Final (8 decks)

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