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Anatomy > Final Exam Babyyy > Flashcards

Final Exam Babyyy Flashcards

1
Q

What does the CV system transport?

A
  • nutrients to tissue
  • waste products away from tissues
  • hormones
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2
Q

What is velocity?

A

Distance / time

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3
Q

What is blood flow?

A

Volume / time

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4
Q

How does high vascular resistance affect blood flow? & how does low vascular resistance affect blood flow?

A

High resistance – less blood flow
Low resistance – greater blood flow

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5
Q

If we had something causing high resistance in a vessel, what would the pressure measure upstream of the resistance? & what would it measure downstream?

A

Upstream – pressure would be high
Downstream – pressure would be low

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6
Q

What controls blood pressure?

A

Vascular resistance

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7
Q

What does the brain use to drive blood flow?

A

Cerebral perfusion pressure

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8
Q

What is the inverse of vascular resistance?

A

Vascular conductance
- how easy it is to drive blood flow

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9
Q

If vascular resistance is high what is vascular conductance is what?
If vascular resistance is low what is vascular conductance?

A

High resistance – low conductance
Low resistance – high conductance

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10
Q

Where is vast majority of blood stored?

A

veins
- (84%)

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11
Q

What percentage of blood is stored in the high pressure system of CV ?

A

17%
- heart, arteries, & arterioles/capillaries

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12
Q

What is the kidney in control of?

A

How much fluid we have in our body

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13
Q

Describe a system in series

A

Connecting 2 tubes together along with their resistance – over all resistance is now doubled as there is only one pathway

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14
Q

Describe a system in parallel

A

Connecting different tubes – not end to end – gives blood options on different pathways to take – decreases over resistance

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15
Q

Which organ contains both system in series & system in parallel?

A

Kidney

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16
Q

What blood vessel is a single tube with a cross sectional area of 2.5?

A

Aorta

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17
Q

The more total cross sectional area the less __ blood flow will have & vice versa

A

velocity

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18
Q

Why is the velocity in the Aorta greater than in the capillaries?

A

The aorta is one tube with a smaller cross sectional area than all the capillaries combined

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19
Q

What blood vessels in the circulatory system are the high resistance vessels?

A

Small arteries & arterioles

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20
Q

What blood vessels does phenylephrine work on?

A

small arteries & arterioles

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21
Q

blood flow to a tissue is determined by what?

A

its metabolic rate
- high metabolic rate – more blood flow
- low metabolic rate – less blood flow

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22
Q

Describe Laminal flow

A

organized blood flow, efficient & non problem causing
- blood in the middle of the vessel will travel the furthest
- walls of the vessel act as resistance causes blood near the wall not to travel as far

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23
Q

Describe Turbulent flow

A

Inefficient & disorderly
- blood is pushed against walls of vessels & causes remodeling & cause things to get stuck such as cholesterol & calcium
- Clots/blockage can cause turbulent flow

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24
Q

What percentage of CO per minute do kidneys get?

A

20% (1 Liter)

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25
Q

What is Ohm’s law>

A

Voltage = current x resistance

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26
Q

Movement out of the capillaries is called?

A

Filtration

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27
Q

Movement into the capillaries is called?

A

Reabsorption

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28
Q

Where is nutrient & gas exchange taken place?

A

Capillaries

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29
Q

When we are measuring blood pressure, which vessels are we measuring?

A

Large arteries

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30
Q

The large drop in blood pressure between large arteries & capillaries is due to what?

A

High Vascular resistance in the arterioles & small arteries – mast majority is arterioles

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31
Q

Blood flow to the capillaries is controlled by what?

A

Arterioles

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32
Q

Relaxation of arterioles has what affect on blood flow to capillaries?

A

increased blood flow

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33
Q

Constriction of arterioles has what affect on blood flow to capillaries?

A

reduced blood flow

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34
Q

about how much surface area in square meters do we have if we combine all the capillaries together?

A

500 - 700 square meters

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35
Q

How many layers do the capillaries have & what composes the capillaries?

A

1 layer & composed of endothelium cells

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36
Q

Do the capillaries contain smooth muscle?

A

No
- this is good as there is nothing to hinder nutrient/gas exchange

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37
Q

The typical MAP at the arterial end of a capillary is?

A

30mmHg

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38
Q

The typical MAP at the venous end of a capillary is?

A

10mmHg

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39
Q

What is the normal arterial MAP we are using for class?

A

100mmHg

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40
Q

Which end of the capillary favors filtration?

A

Arterial end

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41
Q

Which end of the capillary favors reabsorption?

A

Venous end

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42
Q

What are the 4 Capillary Starling forces?

A
  • Hydrostatic pressure in capillaries
  • Hydrostatic pressure in ISF
  • Capillary Colloid osmotic pressure (oncotic pressure
  • Interstitial fluid colloid osmotic pressure
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43
Q

What is Hydrostatic pressure in capillaries?

A

The blood pressure in the capillaries – also called the hydrostatic pressure – physical fluid pressure of the blood in the capillaries

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44
Q

What is Hydrostatic pressure in ISF? Why is it negative?

A

The blood pressure outside the capillaries & outside cells - ISF
- negative pressure d/t lymphatics pulling extra fluid

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45
Q

What is Capillary colloid osmotic pressure? (plasma osmotic pressure)

A

Proteins dissolved in blood in capillaries – creates a pulling force keeping fluid in CV
- normal capillary oncotic pressure is 28 mmHg

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46
Q

What is Interstitial fluid colloid osmotic pressure?

A

Proteins in the ISF – creates a pulling force into ISF

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47
Q

What can cause the Capillary plasmic oncotic pressure to decrease?

A

Hemorrhage, liver failure, sepsis & trauma

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48
Q

What happens to the osmotic pressure when the semi-permeable membrane becomes permeable?

A

Not only can proteins escape into ISF but the proteins in the capillaries lose their osmotic pressure – this is because osmotic pressure is based on a semi-permeable membrane where fluid can move but a dissolved substance cant

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49
Q

What kind of proteins can we find in the ISF & how much osmotic pressure do they produce in the ISF?

A

Proteoglycan filaments, Hyaluronic acid, & collagen
- osmotic pressure of 8mmHg

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50
Q

Which one has more proteins producing osmotic pressure the CV or the ISF?

A

CV
- osmotic pressure produced is 28mmHg

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51
Q

What happens to extra proteins that leak into ISF by sepsis? & what can affect the rate of this?

A

Lymphatic slowly removes extra proteins this takes time – this process is slowed even more in bedridden patients

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52
Q

What does the lymphatic system rely on for passive movement?

A

The contraction/relaxation of skeletal muscle – lymphatic uses this to move fluid forward

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53
Q

What is the capillary filtration coefficient?

A

How permeable the capillary is & how much surface area
- the more porous to water the more water will move
- the more surface area the more movement
(this is secondary to the other forces)

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54
Q

What are the three main proteins that make up the total oncotic pressure in the CV?

A

Albumin (Primary), Globulins (2nd most important – Abx) & Fibrinogen (clotting factor)
- total plasma oncotic pressure is 28mmHg

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55
Q

Where do the lymph vessels tie in?

A

Around capillaries

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56
Q

What is the purpose of lymph

A

Retrieving extra fluid from around the interstitial fluid around capillaries and returning it to the CV system

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57
Q

Where does the lymphatic system dump contents back into the CV system?

A

Lymphatic ducts at the top of the thorax dump into “very large veins.”

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58
Q

Do lymph vessels have valves? How goes blood return to the CV system?

A

Yes; one way valves, similar to veins. Need muscle contraction for lymph return. This is why bed bound people get swollen.

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59
Q

Lymph flow can be described as a

A

Passive one way pumping system

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60
Q

At rest, how fast is lymph flow?

A

Relatively slow

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61
Q

If we increase our activity, how much can we increase lymphatic flow?

A

20x; maybe even higher if our activity is enough

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62
Q

What is used in the hospital to prevent fluid backup in patients who are bed bound?

A

Sequential compression devices; helps get venous/lymphatic system moving, possibly more so for lymph

*requires intact path to top of thorax

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63
Q

What are capillaries most permeable to?

A

Water

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64
Q

What electrolyte is highly permeable in capillaries? Why?

A

NaCl - small

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65
Q

In regard to permeability to capillaries, the larger the electrolyte, the ___

A

less permeability we will have

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66
Q

On the arterial side of a capillary, the pressure is

A

30mmHg

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67
Q

On the venous side of a capillary, the pressure is

A

10mmHg

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68
Q

Oncotic pressure throughout the NON-RENAL capillary according the Schmidtty is

A

28mmHg

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69
Q

Interstitial fluid hydrostatic pressure around the capillaries in a healthy adult is typically ____. What does this create?

A

-3mmHg

A vacuum; favorable condition for filtration on the arterial side

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70
Q

Osmotic pressure of proteins in the interstitial fluid outside capillaries is typically

A

8mmHg

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71
Q

Oncotic pressure ______ filtration

A

Opposes

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72
Q

Capillary pressure, interstitial hydrostatic pressure, and interstitial protein oncotic pressure _____ filtration

A

Favor

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73
Q

In a healthy person, the total mmHg favoring filtration is

A

41mmHg

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74
Q

In a healthy person, the total mmHg opposing filtration is

A

28mmHg

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75
Q

In a healthy person, the net filtration pressure for filtration is

A

13mmHg

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76
Q

In a healthy person, the total pressure favoring reabsorption is

A

21mmHg

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77
Q

In a healthy person, the total pressure opposing reabsorption is

A

28mmHg

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78
Q

The a healthy person, the net filtration pressure for absorption is ____. Why is this important?

A

-7mmHg

Not completely favorable for reabsorption. Some fluid is left behind. This requires an intact lymph system to scavenge the remainder of fluid to prevent buildup provided there is not an extreme excess of fluid.

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79
Q

In the systemic system, the capillary is

A

short

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80
Q

What is the average capillary blood pressure in systemic circulation? (delta P between the arterial and venous side of capillary).

A

17.3mmHg

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81
Q

Why is delta P of the capillary not 30-10=20mmHg?

A

It is 17.3mmHg because capillaries get larger as we go from the arterial side to the venous side, which increases cross sectional area and decreases pressure.

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82
Q

What is the net filtration pressure on average PER capillary?

A

0.3mmHg

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83
Q

What specialized capillary bed does NaCl have trouble getting through?

A

Blood Brain Barrier

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84
Q

The opening between endothelial cells at the capillary don’t have much barrier for what?

A

Water

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85
Q

The blood brain barrier requires what for transport of glucose?

A

….glucose transporters

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86
Q

When blood comes into the kidney from the renal artery, it has a MAP of what?

A

100mmHg

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87
Q

When blood exits the kidney via the renal vein, it has a MAP of what? Why?

A

0mmHg

BP drops as it moves through areas of high resistance within the kidney. Energy is removed, so pressure drops

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88
Q

What is delta P between the renal artery and renal vein?

A

100mmHg

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89
Q

What blood vessel supplies the glomerulus capillary bed?

A

Afferent arteriole

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90
Q

What defines blood pressure of the glomerulus capillary bed?

A

Systemic BP (pressure coming in from renal artery)

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91
Q

Why does the pressure drop between the afferent arteriole and the glomerular capillary bed?

A

High resistance within the afferent arteriole

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92
Q

What is the typical pressure within the glomerulus capillary bed? How does this relate to the systemic capillary?

A

60mmHg

2x greater than systemic capillary, allowing for high filtration

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93
Q

What should we not be filtering out in the kidneys in a healthy individual?

A

RBC/Large proteins

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94
Q

If someone has proteinuria or RBC in the urine, what disease state could they have?

A

DM, lifetime HTN

It is okay to have a very low number filtered out per daddy

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95
Q

How many capillary beds does the nephron have?

A

2

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96
Q

The glomerulus capillary bed is the ____ renal capillary bed.

A

1st

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97
Q

In front of the afferent arteriole, what happens?

A

The renal artery splits into a bunch of smaller arteries, which eventually become the afferent arteriole for a given nephron.

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98
Q

What defines filtration in the glomerular capillaries?

A

Pressure

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99
Q

What is GFR?

A

Glomerular Filtration Rate - Amount of filtration sent into a compartment to process what has been filtered

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100
Q

Is increased or decreased GFR what we want?

A

Increased GFR is typically better

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101
Q

The total filtration of all glomerular capillaries is ____ mL/min; assuming they are all healthy and functional.

A

125mL/min

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102
Q

If renal blood flow is low, what will the afferent arteriole do?

A

It will relax (dilate) to increase blood flow to glomerulus

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103
Q

If renal blood flow is high, what will the afferent arteriole do?

A

It will constrict to decrease blood flow to glomerulus

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104
Q

What is the plasmic oncotic pressure at the end of the glomerular capillary?

A

36 mmHg

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105
Q

What is the plasmic oncotic pressure in the middle of the glomerular capillar?

A

32 mmHg

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106
Q

Why does the plasmic oncotic pressure increase from the beginning to the end of the glomerular capillary?

A

we lose a lot of fluid due to filtration leading to an increase in concentration in the plasma

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107
Q

What is the hydrostatic pressure in the tubule?

A

18 mmHg

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108
Q

What creates the hydrostatic pressure in the tubule?

A

The fluid filling up in the tubule generates a physical pressure

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109
Q

What is the protein osmotic pressure in the early part of the tubule?

A

0
- if we are healthy we should not be filtering proteins

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110
Q

What is the net filtration pressure in glomerulus?

A

10 mmHg
(60 mmHg - 32 mmHg- 18 mmHg)

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111
Q

How can we determine the filtration rate? What is the normal filtration rate?

A

Filtration rate = Kf x NFP
125ml/min = 12.5 x 10 mmHg

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112
Q

What is Kf?

A

Filtration coefficient
- normal is 12.5

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113
Q

Where does the efferent arteriole sit?

A

Behind the glomerular capillaries
- post glomerulus capillary

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114
Q

How does the kidney fine tune the GFR?

A

constricts or dilates efferent arteriole

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115
Q

What happens to GFR if the efferent arterioles constricts?

A

Upstream pressure increases –> increases blood pressure –> GFR is increased

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116
Q

What happens to GFR if the efferent arteriole dilates?

A

Upstream pressure decreases –> decreases blood pressure –> GFR is decreased

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117
Q

What is the blood pressure at the end of the efferent arteriole?

A

18 mmHg
(blood pressure drops from 60 to 18 – 42 mmHg difference)

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118
Q

Which arteriole has a greater vascular resistance in the kidney?

A

The efferent arteriole has the highest vascular resistance
- efferent drops BP from 60 to 18 – 42 mmHg difference
- afferent drops BP from 100 to 60 – 40 mmHg difference

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119
Q

Where does reabsorption happen? What is it?

A

Reabsorb 98-99% of stuff that was filtered at the peritubular capillary

i.e., afferent arteriole –> Glomerular capillary –> Bowmans capsule –> PCT –> reabsorbed at peritubular capillary

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120
Q

What is tubular secretion?

A

Cells in peritubular capillaries pump stuff out to the proximal convoluted tubule to be excreted

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121
Q

What is excretion?

A

Urine; about 1-2% of what goes through the renal capillaries

Filtration - absorption + secretion = excretion

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122
Q

What happens if stuff is filtered at the glomerular capillaries, but we have no specialized transport to reabsorb? (filtration only)

A

What is filtered is lost as urine, and some stays within the renal vein.

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123
Q

What happens with filtration; partial reabsorption? What electrolyte mentioned in class follows this pathway?

A

Some filtrate is sent as urine, some stays in the renal vein, and some of the filtrate is reabsorbed back into the peritubular capillaries

Sodium; we eat way more than we need, the body chooses to not reabsorb all of this sodium

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124
Q

What happens with filtration with complete reabsorption? What follows this pathway?

A

Will not go to urine - what is filtered gets completely reabsorbed at the peritubular capillaries from the PCT.

Glucose in a non-diabetic patient. If glucose is controlled and in normal limits, all glucose is reabsorbed by the PCT.

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125
Q

What does it mean if glucose is found in the urine?

A

Elevated glucose (transporters can’t reabsorb fast enough; spill over)

Something may be wrong with the transport system for glucose reabsorption

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126
Q

What happens with filtration with complete secretion?

A

A small portion is filtered at the glomerulus (near afferent arteriole), but then is secreted from peritubular capillaries to the PCT. None shows up in the urine.

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127
Q

How much renal flood flow is filtered at the glomerulus?

A

1/5 or 20% of renal blood flow

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128
Q

After filtration at the glomerulus, how much of the renal blood flow makes it to the efferent arteriole?

A

4/5, or 80%

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129
Q

What is Para-aminohippuric acid (PAH)?

A

Diagnostic compound to estimate renal blood flow; removal from kidney is dependent on how much blood is moving through kidney. If we know how much of this we gave the patient, we can use it to estimate renal blood flow.

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130
Q

How does Para-aminohippuric acid (PAH) work?

A

Assume all of the blood in the renal artery has Para-aminohippuric acid (PAH)

The more removed by the time it gets to the renal vein = higher renal blood flow

The less removed by the time it gets to the renal vein = lower renal blood flow

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131
Q

Under normal circumstances, what is GFR rate in ml/min?
Reabsorption rate?
How about excretion rate?

A

GFR - 125ml/min
Reabsorption - 124mL/min
Excretion - 1ml/min

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132
Q

What is normal renal plasma flow in ml/min?

A

660ml/min

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133
Q

Why do we not factor in protein osmotic pressures within the PCT?

A

We don’t really filter proteins normally

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134
Q

What are the layers of the glomerular capillaries?

A

Inner - endothelial cells
Middle - connective tissue called the basement membrane
Outside - epithelial cells

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135
Q

What’s special about the inner layer of the glomerular capillaries?

A

Much more permeable than generic systemic capillaries

Have openings in wall called fenestrations

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136
Q

What’s special about the middle layer of the glomerular capillaries?

A

Connective tissue called the basement membrane

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137
Q

What’s special about the outside layer of the glomerular capillaries? What is the other name for these cells?

A

Specialized to provide structural support to the capillary bed

Podacytes

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138
Q

What can podacytes be compared to in function?

A

Astrocytes within the blood brain barrier (support the capillaries of the brain)

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139
Q

Why are podacytes important?

A

Pressure is very high within glomerular capillaries - provides structural support and prevents swelling. They also keep the surface area of the capillaries in check.

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140
Q

What happens to the podacytes/glomerular capillaries if someone has longstanding HTN? (i.e. pressure is 200 instead of 100)

A

Glomerular capillaries swell, fall apart, and lose function

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141
Q

Podacytes has processes on them. What are the spaces between these processes called? What is special about the processes?

A

Silt pores

Processes are negatively charged and help repel proteins, which are also usually negatively charged. Proteins can’t make it through fenestrations because of the charge.

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142
Q

Which layer of the glomerular capillaries is negatively charged?

A

Epithelium (where podacytes are located; silt pores are here)

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143
Q

What is the pressure within bowman’s capsule?

A

0mmHg per daddy

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144
Q

What arteriole is in charge of auto regulation of blood flow through the kidneys?

A

Afferent arteriole

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145
Q

What arteriole is in charge of autoregularion of fine tuning GFR?

A

Efferent arteriole

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146
Q

What happens to downstream pressure when increasing resistance at the afferent arteriole? What happens to GFR?

A

Lower pressure; lower GFR

Renal blood flow DROPS

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147
Q

What happens if you constrict the efferent capillary?

A

Pressure inside of the glomerular capillaries rise, GFR rises

Renal blood flow DROPS

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148
Q

No matter if the afferent or efferent renal arteriole constricts, what is the similarity?

A

Renal blood flow DROPS

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149
Q

If the afferent or efferent arteriole relax, what happens to renal blood flow?

A

Increases renal blood flow

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150
Q

What happens if you relax the afferent arteriole?

A

Increase GFR, increase glomerular pressure

Increase renal blood flow

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151
Q

What happens if you relax the efferent arteriole?

A

Decrease GFR, decrease glomerular pressure

Increase renal blood flow

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152
Q

What is dextran? Is a positive or negative dextran more likely to be filtered?

A

A synthetic sugar; can be larger or smaller based on how many chains are linked together. Used to test filterability in the kidney

A positive dextran is more permeable than a negative dextran due to the negative charge of the epithelial layer or the glomerular capillaries.

Larger + negative charge = less filterable

Smaller + positive charge = more filterable

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153
Q

What percentage of everything that is filtered is reabsorbed?

A

99%

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154
Q

What is the filterability of water, sodium, and glucose?

A

1.0 - very filterable because they are all small

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155
Q

What is inulin? What is its filterability?

A

Can be used to figure out GFR - synthetic, more sensitive than creatinine. Can inject into the patient to determine clearance. Creatinine clearance is variable, and doesn’t follow the same kinetics as inulin.

Filterability is 1.0, just as filterable as water, sodium, and glucose.

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156
Q

Is inulin better than creatinine clearance to determine GFR?

A

Yes; but we’re lazy and use creatinine clearance

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157
Q

Should myoglobin normally be floating around in our blood? What is the filterability of it?

A

no

Filterability 0.75

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158
Q

What is the filterability of albumin? Why don’t we want to filter it?

A

0.005
Very large
If we filter it, it adds to oncotic pressure which changes tendency for reabsorption

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159
Q

What pressures can the kidney autoregulate well with in a healthy person? What about someone unhealthy i.e. in the ICU?

A

50mmHg-150mmHg

ICU patients will not fare well with a map of 50mmHg in terms of autoregulation

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160
Q

The ability to autoregulate is dependent on what?

A

Afferent arterioles ability to dilate

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161
Q

What disease process(s) might lead the afferent arterioles to not be able to dilate as well? How can these patients autoregulate?

A

HTN for years
Uncontrolled DM

Need a higher BP to autoregulate for kidneys to be happy

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162
Q

Autoregulation prevents ______ which gives us a relatively constant ____.

A

Over/underperfusion; GFR

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163
Q

What percentage of everything that is filtered is excreted?

A

1%

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164
Q

How is autoregulation past 150mmHg between renal blood flow and glomerular filtration rate?

A

GFR fares well - line stays pretty flat, the GFR stays more or less the same with a slight rise.

Renal blood flow increases sharply past 150mmHg

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165
Q

What is the process reabsorption in the kidney from the tubule back to the per-tubular capillaries?

A

Reabsorption goes through the cells or in between the cells that make up the lining of the tubule –> through the renal interstitium–> then cross the wall of the peri-tubular capillaries

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166
Q

If BP is above 150mmHg and renal blood flow is increasing, do we produce a lot more urine?

A

In a healthy person, no. GFR is able to hold onto fluid and not let too much go.

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167
Q

If BP is above 150mmHg in someone who did not have good autoregulation, who was unhealthy, what happens to urine output?

A

Someone without good GFR autoregulation at high BP will have a dramatically increased urine output which could be problematic.

Example: CVA resulting in high BP –> Don’t want to lose a liter of fluid per hour, this would be bad

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168
Q

What is a normal urine output for a perfectly healthy patient?

A

1ml/min

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169
Q

While near autoregulation was a straight line, what is different in the kidneys? What does this mean?

A

Autoregulation in the kidneys is more of a slanted line.

As BP goes up, UOP increases
As BP goes down, UOP decreases

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170
Q

Does autoregulation of the kidneys require aldosterone, vasopressin, transporters, etc?

A

No - completely independent. Autoregulation is based on pressure. If pressure goes up, favors fluid reduction and reduced pressures.

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171
Q

What is filtration fraction? What is the normal amount for filtration fraction? How is it calculated?

A

How much is filtered vs how much makes it through the kidney

20% is normal

GFR (125ml/min) divided by renal plasma flow (660ml plasma/min)
125/660 = 0.19

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172
Q

In the middle of the peritubular capillaries, what is the plasmic oncotic pressure?

A

32 mmHg
- plasma gets diluted which drops pressure from 36 to 32

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173
Q

For our class, what is the normal renal blood flow?

A

1100ml/min

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174
Q

How is RBC volume calculated in relation to renal blood flow?

A

Renal blood flow is 1100ml/min
If hct is 0.4, take 40% of 1100ml/min. That will give you RBC volume.

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175
Q

How do you find renal plasma flow if given renal blood flow?

A

Assuming hct is 0.4.

1-0.4 = 0.6
or
60%

Renal blood flow is 1100ml/min
60% of 1100ml/min = 660ml/min renal plasma flow

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176
Q

As filtration fraction was increased, what would happen to blood colloid osmotic pressure? When does this usually occur?

A

Proteins would be more concentrated, which would lead to a higher blood colloid osmotic pressure at the end of the glomerulus.

Normally occurs if the efferent arteriole constricts. When it constricts, more fluid is filtered.

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177
Q

What is the blood pressure at the beginning of the Peri-tubular capillaries?

A

18 mmHg

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178
Q

What is the average blood pressure in the peri-tubular capillaries?

A

13 mmHg

(end of the peri-tubular capillaries should be lower – he didnt give a number)

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179
Q

If we were filtering less fluid, what would happen to the blood colloid osmotic pressure at the end of the glomerulus? When does this normally happen?

A

Would not be as high as normal.

Normally occurs if the efferent arteriole relaxes, which makes it easier for blood to get by. This decreases the amount of fluid filtered.

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180
Q
A
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181
Q

What is the oncotic pressure in the renal intersitium?

A

15 mmHg

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182
Q

What is the hydrostatic pressure in the renal interstitium?

A

6 mmHg

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183
Q

What is the Net filtration pressure or the Net reabsorption pressure?

A

Net filtration pressure = - 10mmHg
Net reabsorption pressure = 10 mmHg

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184
Q

What percentage of the blood plasma gets filtered?

A

10% or 1/5th

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185
Q

where does the tubule empty into?

A

Ureters & fills into bladder

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186
Q

What is the process by which we remove things from the body via urine?

A

Excretion?

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187
Q

How can we determine excretion?

A

Excretion = filtration - reabsorption + secretion

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188
Q

How does secretion work into the tubule?

A

The body can actively pump things it doesn’t want into the tubule – works the opposite of reabsorption – things are pumped out of the peri-tubular capillaries into the renal intersitium –> then cross the cells that make up the walls of the tubule & gets dumped into tubule

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189
Q

Excretion can be thought of in terms of in units of ___ or ___

A

Volume or Quantities (quantity of substance dissolved in a volume)

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190
Q

What are the several roles of the kidney discussed in lecture?

A
  • long term BP regulator
  • long term pH regulator
  • Long term RBC regulator
  • long term electrolyte regulator
  • long term vitamin D regulator
  • long term glucose regulator
  • Drug clearance
  • long term metabolic waste disposal
  • Osmolarity regulator
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191
Q

How does the kidney manage BP?

A

Determines how much volume we have in the CV system

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192
Q

How does the kidney manage pH?

A

Regulates acid/base balance
- dictates how much bicarb we reabsorb & can produce its own bicarb
- gets rid of excess protons

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193
Q

What is the short term regulator of pH & what is the long term regulator?

A

short term - lungs – can get rid of excess CO2 but not protons
Long term - kidneys – through getting rid of protons & keeping/producing bicarb

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194
Q

How does the kidney control RBCs?

A

In the deep medullary kidney, there are sensors that measure blood oxygen levels – if oxygen is low the kidney releases erythropoietin which stimulates the bone marrow to produce more RBCs

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195
Q

How does the kidney regulate calcium levels?

A

determines how much we reabsorb & can determine how much we absorb through Vitamin D
– Activation of Vitamin D is controlled by kidney –

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196
Q

How does the kidney regulate glucose levels?

A

Normally the more we filter the more we reabsorb
- once reabsorption max is reached glucose will be excreted via in high blood glucose levels (blow off valve)

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197
Q

How can kidneys clear drugs?

A

it can transport drugs from the blood stream to the tubule to be excreted via urine (secretory process)

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198
Q

How does the kidney control blood osmolarity?

A

Determines how much water we reabsorb second to salt reabsorption – kidney can choose to get rid of salts or be selective of how much water we reabsorb –> the kidney can differentiate between the two & choose what to keep or get rid of

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199
Q

How is water retention accomplished in the kidney?

A

ADH
(by osmoreceptors in brain)

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200
Q

How does the kidney control most of its roles?

A

Maintaining GFR - auto regulation is important

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201
Q

What is the pathway blood flows through starting from the renal artery out to the renal vein?

A

Renal artery –> Segmental arteries –> Interlobar arteries –> arcuate arteries –> interlobular arteries –> afferent arterioles –> Glomerular capillaries –> efferent arterioles –> Peri-tubular capillaries –> interlobular veins –> arcuate veins –> interlobar veins –> segmental veins –> renal veins

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202
Q

What is a nephron & what makes up a nephron?

A

The basic functional unit of the kidney
- a nephron consists of the Afferent/efferent arteriole, the glomerular/peri-tubular capillary, & the tubule/collecting duct

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203
Q

How many nephrons do we have at birth & when do we begin to lose nephrons?

A

1 million per kidney (2 milli total)
- at age 40

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204
Q

What are the two types of nephrons? & what percentage do each take up?

A

Superficial cortical - make up 90-95% of nephrons
Deep medullary nephrons – make up 5-10%

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205
Q

A descending splits into more ascending blood vessels, why does this happen & what does this aid in?

A

This slows blood velocity going up the ascending limb
- this helps prevent the washing out of the renal interstitium by maintaining a normal level of solutes in the deep medulla

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206
Q

what is the term used to describe the deep peri-tubular capillaries?

A

Vesa Recta

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207
Q

Which nephrons are the most sensitive to hypotension/inadequate perfusion?

A

The deep medullary nephrons as there are so few (5-10%) ischemia would most affect here

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208
Q

The kidneys are housed underneath what muscle?

A

Diaphragm

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209
Q

The renal artery/vein sit beneath what major artery?

A

Mesenteric artery

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210
Q

What sits right on top of the kidneys?

A

Adrenal glands

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211
Q

The upper part of the right kidney comes into contact with what organ?

A

Liver

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212
Q

The middle lateral part of the right kidney come into contact with what?

A

Colon

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213
Q

The upper proximal part of the left kidney comes into contact with what organ?

A

Gastric surface (stomach)

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214
Q

The upper distal part of the left kidney comes into contact with what organ?

A

Spleen

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215
Q

The middle part of the left kidney comes into contact with what organ?

A

Pancreas

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216
Q

The lower lateral part of the left kidney comes into contact with what organ?

A

Colon

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217
Q

Why is know what comes into what part of the kidney important?

A

Cancer spreading
- Cancer of the kidney itself is very rare as it doesnt really generate new nephrons – most cancer of kidney is due to infiltration

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218
Q

Where is kidney stone pain referred to ?

A

Back

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219
Q

As men age the prostate gland enlarges, what issue does this cause?

A

The larger the prostate the more is squeezes the urethra & makes it difficult to empty the bladder
(us men have it so difficult :( )

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220
Q

What controls emptying of the bladder?

A

SNS & PNS
- example – if we are nervous we may lose control of bladder or have inability to empty bladder

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221
Q

Which nerve is in control of the bladder & solid waste? & what does it come off from?

A

Pudendal nerve
- comes from S2,S3, & S4

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222
Q

What is the pudendal nerve also in charge of?

A

ERECTIONS

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223
Q

What is the pathway from the beginning of the tubule to the end

A

Bowman’s capsule (Corpuscle) –> Proximal tubule –> proximal straight tubule –> Descending thin limb –> Ascending thin limb –> Ascending thick limb –> Distal convoluted tubule –> Cortical collecting duct –> Medullary collecting duct –> empties into papillary duct

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224
Q

What makes up the Loop of Henle?

A

Descending thin limb, Ascending thin limb & Ascending thick limb

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225
Q

Where are the Macula Densa found per lecture?

A

Thick Ascending limb

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226
Q

What is the role of the Macula Densa? & what does it come into contact with?

A

Tells the kidney how much is being filtered - monitors filtration rate by acting like a speedometer
- is in contact with Afferent & Efferent Arterioles

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227
Q

If the Macula Densa senses flow is low, what happens?

A

The Juxtaglomerular cells connected to the afferent/efferent arterioles release renin –> renin eventually gets converted to Angiotensin II –> this constricts the Efferent Arteriole –> increases pressure in glomerulus –> filtration is increased

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228
Q

If Macula Densa senses flow is too low what happens?

A

Renin production is reduced –> leads to dilation of efferent arterioles

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229
Q

Who was Linus Pauline? Why was he important?

A

Chemist who had prostate cancer for 25years

  • there is a correlation between cancer and antioxidants, such as vitamin C

-Antioxidants help prevent free radical oxidative stress

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230
Q

What does renal clearance describe?

A

Quantity of plasma that is cleared of a substance per time (ml fluid/min)

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231
Q

If the kidney reabsorbs lots of fluid, but not the substance that is in the fluid, clearance is what?

A

High

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232
Q

If the kidney reabsorbs all of the fluid and substance that it is filtering, clearance is what

A

Low

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233
Q

in regard to clearance, what unit does the following use?

Plasma
Time

A

ml

Minute

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234
Q

Will clearance ever be L/min?

A

No - it will only ever be mL/min

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235
Q

Where can clearance be something other than mL/min?

A

Hepatic clearance

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236
Q

If our body wants to keep a substance in the body and reabsorbs a lot of it, clearance is what?

A

Low

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237
Q

How is excretion rate calculated?

A

Urinary flow rate (1ml/min) x urinary concentration of the compound = excretion rate

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238
Q

How do you calculate renal clearance?

A

(Urinary flow rate x concentration of the compound)/Plasma = Renal clearance

239
Q

How many nephrons do we have per kidney in a healthy person?

A

1,000,000 (one million PER kidney)

240
Q

How many nephrons collectively filter 125mL/min?

A

2,000,000 (two million)

241
Q

How much do we reabsorb at the peritubular capillaries per minute?

A

124ml/min (99% of what is filtered, leaving 1ml/min of urine)

242
Q

What is the symbol in equations for urine output?

A

v̇

Note: can also be v̇u̇, but not commonly

243
Q

What does the dot mean with v̇?

A

volume per unit of time

244
Q

If something is small and positively charged, would it be hard or easy to filter? Would this fluid have the same or different composition in Bowmans capsule vs the glomerulus?

A

Easy

Roughly the same composition EARLY in Bowmans capsule

245
Q

How much stuff is reabsorbed at the proximal convoluted tubule?

A

2/3 of everything

246
Q

If we have normal glucose levels, how much is reabsorbed at the proximal tubule?

A

All of it

247
Q

Does glucose have a low or high clearance normally?

A

No clearance at all at normal glucose levels

248
Q

If glucose is 900, will our clearance be zero?

A

No - will have some spill over into the urine which would result in a non-zero clearance.

249
Q

If you have a compound that is freely filtered, does not have reabsorption pump/process, how much plasma would be reabsorbed?

A

124ml, and none of the compound.

250
Q

If you have a compound that is freely filtered, does not have reabsorption pump/process, where would the compound be?

A

It would stay within the proximal convoluted tubule and make its way to the bladder.

251
Q

If you have a compound that is freely filtered, does not have reabsorption pump/process, how would the concentration of said substance change throughout the tubule system?

A

Early on in the PCT the concentration would be the same as it was in the glomerulus.

Later in the PCT, after 124ml plasma is reabsorbed at the peritubular capillaries, the 1ml of urine will become more concentrated with the substance as it flows to the bladder.

252
Q

What should clearance be close to? What is the typical number we use?

A

GFR; 124ml/min

253
Q

What happens to concentration of fluid within the peritubular capillaries?

A

It becomes dilute as it heads to the renal vein. This is due to reabsorption of 124ml/min of fluid. The fluid dilutes what fluid is there.

254
Q

Is the renal vein more concentrated than the peritubular capillaries?

A

No

Peritubular capillaries are more concentrated than the renal vein.

255
Q

If you are dividing two fractions, how can you make it easier?

A

Multiply by the reciprocal of the denominator

256
Q

How many ml are in one dL?

A

100

257
Q

How many dL are in 500ml?

A

5

258
Q

If something is freely filtered, how does it compare to what is sent to the urine if it doesn’t reabsorb?

A

The amount filtered is the same amount that goes to the urine.

259
Q

How is concentration in plasma typically described?

A

1mg/dL

260
Q

If the concentration of a substance is 1mg/dL, and we freely filtered 125ml/min, how much of the substance are we filtering per minute?

A

125mL –> 1.25dL
1.25dL/min x 1mg = 1.25mg/min

261
Q

If the concentration of a substance is 1mg/dL, and we freely filtered 125ml/min, we are clearing 1.25mg/min of the substance. What would the concentration be? How about the excretion rate?

A

1.25mg/ml of urine

Excretion is 1.25mg/min

262
Q

What is excretion rate?

A

Quantity of stuff lost in the urine over a minute

263
Q

What is the gold standard for finding GFR? How many readings to we take?

A

Inulin

Two (measure two minutes after administration, then another time after another two minutes)

264
Q

What are the renal characteristics of inulin?

A

Freely filtered, not reabsorbed or secreted. Great to find GFR. Exogenous.

265
Q

What is typically used to measure GFR? Why is this variable?

A

Creatinine clearance.

Creatinine is endogenously produced, some is released continuously as it is a byproduct of skeletal muscle. This leads to artificially high GFR readings.

266
Q

Would a frail person have a high or low creatinine level? How does this relate to GFR/creatinine clearance?

A

Low

GFR/creatinine clearance would be low due to lack of creatinine. Use inulin to get accurate measure of kidney function.

267
Q

If we have a compound that is fully secreted/pumped into the PCT, what is the clearance rate? What would this be equal to? Would any of the substance be in the renal vein?

A

Very high

Renal plasma flow

None in the renal vein

268
Q

How does the kidney get rid of Para-aminohippuric acid (PAH)? What does this mean for clearance rate and renal plasma flow?

A

It has massive amounts of transporters at the peritubular capillaries that secrete it back into the PCT. The clearance rate is very high, and the renal plasma flow is equal to the clearance rate.

269
Q

Does Para-aminohippuric acid (PAH) make it to the renal vein?

A

No; heavily/totally secreted into the PCT.

270
Q

Review renal formulas in Guyton chapter 28

A

Daddy said please

271
Q

How can we use Para-aminohippuric acid (PAH) to calculate renal blood flow?

A

Clearance rate of Para-aminohippuric acid (PAH) is equal to the renal plasma flow.

Divide renal plasma flow (RPF) by (1 minus HCT level) –> will give renal blood flow

272
Q

The Guyton textbook makes an adjustment to the % of Para-aminohippuric acid (PAH) removed from the kidney. How much is actually removed from the kidney?

A

90% of Para-aminohippuric acid (PAH) is removed from the kidney.

273
Q

According to Guyton, how much Para-aminohippuric acid (PAH) did Daddy say makes it into the renal vein?

A

10%

274
Q

Formula for excretion rate is

A

Concentration x amount (how long we took the urine sample were direct words)

***review the book please

275
Q

What is the formula for secretion rate?

A

Excretion rate - filtered load

276
Q

What is the formula for reabsorption rate?

A

Filtered load - excretion rate

277
Q

What should we know how to do with all of the formulas?

A

Rearrange them to solve for each part of the equation; keep your eyes on units

278
Q

If renal artery pressure is extremely high, the afferent artery will constrict, but it can only constrict so much, as a result what will increase?

A

Glomerulus capillary blood pressure –> which will increase Net filtration pressure

279
Q

If our GFR increased up to 500mL/min & we only reabsorbed 124mL/min, what would happen to the excess fluid?

A

It would be excreted as urine

280
Q

In the case of Hypotension, how does, this affect GFR & urine output?

A

Low renal arterial pressure would lead to a low GFR –> low GFR would lead to low filtration rate –> increased reabsorption –> low urine output

281
Q

What is low renal blood pressure offset by in the glomerulus capillaries?

A

How well the afferent arterioles dilate

282
Q

How does long term uncontrolled HTN or diabetes affect the Afferent arteriole, & how does this affect the afferent arterioles capabilities in hypotension?

A

The afferent arteriole will get used to constricting & in the case of hypotension will have difficulty dilating

283
Q

Constant high pressure in the glomerulus can have what affect on the podocytes?

A

Podocytes can lose ability to reinforce capillary bed, fenestrations can widen & scarring can develop

284
Q

Angiotensin II affects which arteriole more than the other?

A

Efferent arteriole is affected more than afferent

285
Q

All meds/pressors will have a greater affect on what arteriole?

A

Afferent arteriole compared to efferent

286
Q

If high pressure lead to high filtration rate, what would the Macula densa do to compensate?

A

Macula dense would sense extra fluid –> leading to reduction in angiotensin II –> which would dilate the efferent arteriole & reduce filtration rate

287
Q

How much water is reabsorbed at the proximal tubule?

A

2/3rds
(power points has 65% written)

288
Q

A higher filtration rate of Na at the glomerulus but a normal reabsorption rate would lead to what at the Macula Densa?

A

A higher amount of Na reaching Macula densa –> kidney would interpret this as having a high GFR

289
Q

A lower filtration rate of Na at the glomerulus but a normal reabsorption rate would lead to what at the Macula Densa?

A

A lower amount of Na reaching Macula Densa –> kidney would interpret this as having a low GFR

290
Q

Explain what would happen if something were to cause an increase in the amount of Na reabsorbed in the proximal tubule

A

This would cause a deficit in the amount of Na that reaches the Macula Densa –> kidney would interpret this as having a low GFR & in response the kidney will increase the amount of Angiotensin II

291
Q

Explain what would happen long term if unwanted Angiotensin II is increased in scenarios where Na reabsorption in the proximal tubule is increased

A

Angiotensin II in normal glomerulus pressures will increase glomerulus pressures & long term this can increase the wear & tear tear of the capillary beds

292
Q

What are good medications to combat the effects of Angiotensin II?

A

ACE inhibitors, ARBs, & renin inhibitors
- mostly ACE inhibitors

293
Q

Where is all of the glucose that is filtered reabsorbed?

A

The proximal tubule

294
Q

What is the normal concentration of Sodium in the proximal tubule? What is it in the Tubular cells?

A

Proximal Tubule – 142
Tubular cells – 14
(10:1 gradient)

295
Q

In the early part of the proximal tubule, for every 1 glucose that is reabsorbed 1 __ is also reabsorbed

A

Na
- 1:1 ratio

296
Q

In cases where we have very high blood glucose, the kidneys will filter more & reabsorb more glucose, what affect will this have on the kidney?

A

The more glucose that is reabsorbed the more Na is also reabsorbed –> this will reduce the amount of Na that reaches Macula Densa –> kidney will think GFR is low & try to increase GFR –> more Angiotensin II release

297
Q

What is the actual problem
in uncontrolled blood sugar & its affects on the kidney?

A

Hyperfiltration – kidneys will always be trying to increase GFR –> which will increase the wear & tear of the nephrons
- Sugar is also very sticky & will stick to things & elicit & immune response to destroy it
- for every nephron that dies the remaining nephrons must increase their workload - increasing their wear & tear

298
Q

For every 1 Amino acid reabsorbed, what else is also reabsorbed? (in proximal tubule)

A

1 Na
(1:1 ratio)

299
Q

If we have increased amino acid levels in our blood, how will this affect the kidneys?

A

(Same as high blood glucose)
more amino acids –> more is filtered –> more is reabsorbed & along with Na –> less Na makes it to Macula densa –> kidney thinks GFR is low –> Angiotensin II is released

300
Q

Should glucose or amino acids be in the PCT?

A

not normally

301
Q

What is the pathophysiology behind the side effect of SGLT inhibitors?

A

Reduced reabsorption of glucose –> downstream urine has higher glucose level –> urethra has high glucose –> increased UTI risk

Glucose also makes the tubule sticky, leading to immune system response. The immune system can attack the tubule/urethra.

302
Q

What is the problem with GLP-1 agonists? How can weight loss be achieved better?

A

Can reduce glucagon - we need this. Most of the weight loss comes from muscle loss; not a great way to lose weight.

Stop eating so much

303
Q

Where is glucose reabsorbed? Is it reabsorbed anywhere else?

A

Glucose is only reabsorbed in the PCT. If it makes it through the PCT, it will not be reabsorbed.

304
Q

What is the name for the part of the kidney tubular cell that makes up the cell wall of the tubular lumen?

A

Apical side of the cell

305
Q

What is the name for the part of the kidney tubular cell that makes up the cell wall of the interstitial fluid?

A

Basolateral side

306
Q

What transporter does the tubular cell use in the kidney to reabsorb glucose? What is it dependent on?

A

SGLT

Dependent on the sodium electrochemical gradient to help pull glucose along with it into the cell.

307
Q

Concentration of glucose early in the PCT would be different or the same as in the glomerulus? How about as we go further down through the tubule?

A

Roughly the same; freely filtered, small, uncharged

As we go further in the PCT, more and more is reabsorbed into the peritubular capillaries. This would mean we have a smaller amount of glucose in the distal areas of the PCT. Eventually, this number should be zero.

308
Q

What transporter brings glucose from the tubular cells into the interstitial fluid? Is energy required? Why or why not?

A

GLUT; No energy required. SGLT packs glucose into the cell, increasing glucose concentration in the tubular cell. If the concentration of glucose within the tubular cell is greater than the interstitial fluid, glucose flows through the basolateral side of the tubular cell passively.

309
Q

What are the three segments of the PCT?

A

S1 (early, S2/3 (late)

310
Q

Where is most of the glucose that flows through the PCT absorbed? How much is absorbed here? What is the name of the transporter?

A

S1 (early part of the PCT). 90% of all glucose is absorbed here. The transporter is the SGLT2 transporter.

311
Q

How does the SGLT2 transporter work? What transporter is it paired with on the opposite side of the cell wall of the tubular cell?

A

SGLT2 - works through concentration gradient of Na. It takes 1 Na and 1 glucose into the apical side of the tubular cells.
-These are high through-put, or high efficiency transporters. However, they are low affinity compared to the later segments***

The basolateral side of the cell uses GLUT2 transporters to bring glucose into the interstitial fluid.

312
Q

What transporters are within S2/3 of the PCT? What do they do, where are they located, and how do they work? What % of glucose is transported through these?

A

SGLT1 - “first isoform of the transporter”
Located on the apical side of the tubular cell
Requires 2 Na per each 1 glucose to reabsorb via concentration gradient of Na
-High affinity, lower capacity than SGLT2**
10% of reabsorption of glucose is here

GLUT-1 is on the basolateral side of the tubular cell

There are very few SGLT1/GLUT1 transporters here

313
Q

Why does the SGLT1 transporter require more Na than the SGLT2 transporter?

A

As fluid goes through the PCT, less and less glucose is present. This makes it more dilute. It is harder for glucose transporters to move glucose when it’s dilute, so we use 2 Na to help move things along.

314
Q

In a perfect world, which SGLT transporter would we rather use? Why?

A

SGLT2 - only use 1 Na

SGLT1 should be used to SCAVENGE**

315
Q

What is the amount of glucose filtered (filtered load) determined by?

A

Plasma concentration (assume normal GFR)

Normal GFR + normal glucose = normal glucose filtered (filtered load)

316
Q

If GFR is 125mL/min, and normal glucose is 100mg/dL, what is the normal filtered load?

A

Convert mL to dL
1.25dL/min GFR
100mg/dL
Multiply those two
dL cancels out
- 125mg/min of normal glucose filtered load**

317
Q

What is the normal amount of glucose filtered load? (mg/min)

A

150mg/min

Note: he gave us this number but did an example (last flash card) that gave us 125mg/dL. He just said “it’s in the general ballpark.”

318
Q

What is a normal glucose? Would it ever be lower?

A

100mg/dL

Yes - healthy and fasting would be lower

319
Q

What is filtered load?

A

How much stuff that is dissolved in plasma that is being filtered.

320
Q

If something is freely filtered, how do you calculate filtered load?

A

Stuff filtered x quantity filtered = filtered load

321
Q

What is the threshold that we would see glucose in the urine?

A

200mg/dL - know the term “threshold,” he made a deal about it

Note: He also said 200mg/dL might be a bit high, and typically between 100-200mg/dL you would see glucose in the urine.

322
Q

After threshold of plasma glucose concentration is met, what happens?

A

Shortly after threshold, Excretion increases at a linear, 1:1 rate because our SGLT1-2 transporters cannot transport any faster (they are saturated). This is called “transport maximum.”

323
Q

Is transport maximum of glucose at threshold?

A

No - it is shortly after threshold.

324
Q

What is happening between threshold and transport maximum with glucose reabsorption?

A

Glucose is making it past S1, S2, and S3. S2/3 transporters aren’t necessarily maxed out, glucose is just starting to make it past the transporters.

Transport maximum is when all SGLT transporters are saturated.

325
Q

Why is there a transport maximum of glucose? Why can’t we just transport it into the cell?

A

There is a set time for conformation/release/reset of SGLT transporters. When transporters reach saturation, they can’t physically go any faster.

326
Q

All filtered load of glucose is being reabsorbed until what amount of glucose? What is this called?

A

200mg/dL

Threshold

327
Q

Transport maximum occurs at around what level of glucose?

A

300mg/dL

328
Q

Where is the macula densa located? What does it come into contact with?

A

Thick ascending limb of the loop of henle, ALMOST at the start of the DCT but not quite. Comes into contact with the efferent and afferent arterioles.

329
Q

Why is the Macula Densa nicknamed our “speedometer?” What does it look at? Is it more specific to any electrolytes?

A

It counts the # of Na and Cl flowing past it to help manage GFR. It is more sensitive to Na.

330
Q

Where are the Juxtaglomerular cells? What do they release?

A

Cells within the macula densa that come into contact the the efferent and afferent arterioles.

They release renin when the macula densa thinks that GFR is too low.

331
Q

What is the rate limiting step in the process of forming Angiotensin II?

A

Renin

332
Q

What does Renin convert?

A

Angiotensinogen is converted to Angiotensin I by Renin.

333
Q

Where is Angiotensinogen produced?

A

Liver

334
Q

Where is Angiotensin Converting Enzyme (ACE) found largely?

A

Lungs

335
Q

What converts Angiotensin I to Angiotensin II?

A

Angiotensin Converting Enzyme (ACE)

336
Q

What is the primary signaling arm of the RAAS?

A

Angiotensin II

337
Q

If we take ACE inhibitors, why do we get “wonky congestion?”

A

ACE found primarily in the lungs

338
Q

What does Angiotensin II act on? What does this result in?

A

Constricts the efferent arteriole –> Reduced renal blood flow, BUT increased glomerular pressure, which should increase GFR.

339
Q

When the macula densa releases renin, leading to AG II constricting the efferent arteriole, how is the afferent arteriole dilated in the process? Is it clear how this happens? What is the result?

A

While research is currently unclear, it is thought that the afferent arteriole dilates in response to nitric oxide release from the macula densa.

The efferent arterioles constricting decreases renal flow while increasing glomerular pressure and GFR.
The afferent arteriole dilating makes up for the loss of renal blood flow from the efferent arteriole , and also raises glomerular pressures further, leading to even higher GFR.
Clarification: afferent arteriole dilation causes INCREASE in renal blood flow.

340
Q

If we have low BP, what is the physiology between the glomerulus and the macula densa that results in increased GFR?

A

Low BP –> Decrease in glomerular hydrostatic pressure –> Less NaCl flowing past the macula densa –> Juxtoglomerular cells release renin –> Renin converts angiotensinogen to AG I –> ACE converts AG I to AG II –> AG II constricts the efferent arteriole, while nitric oxide dilates the efferent arteriole –> Increase in glomerular hydrostatic pressure –> Increase in GFR

341
Q

What arteriole does Angiotensin II selectively constrict?

A

Efferent arteriole

342
Q

Aside from constricting the efferent arteriole, what else can angiotensin II do in the kidney?

A

Increase NaCl and H2O reabsorption.

This helps conserve volume, hopefully increasing BP, which will directly result in increased renal blood flow. (Expands blood volume)

343
Q

What does Angiotensin II bind to in the proximal tubule?

A

Angiotensin I receptors

344
Q

What is a result Angiotensin II binding to AT1 receptors?

A

Na/K pump is sped up – this decreases the amount of intracellular Na & increases & increases secondary active transporter/exchangers that depend on Na/k pump

345
Q

Which pumps are affected by the increase in the Na/K pump?

A

NHE – Na/H exchanger is most heavily affected as the more Na is removed intracellularly, the more Na will move down its concentration gradient into the cell in exchange for a H
The reabsorption of bicarb is also sped up – this is secondary active transporter Na/HCO3 – as bicarb is being reabsorbed into the renal interstitium it brings along a Na – this is Bicarb driven & the Na/H exchanger also aids in this

346
Q

What are the two routes things can get reabsorbed from the lumen to the peri-tubular capillaries?

A

Paracellular route – in between cells (Cl is mostly reabsorbed through this route)
Trans-cellular route – through cells via channels or transporters

347
Q

What drives Cl to cross via paracellular route into interstitium?

A

All the Na pumps that push Na into the renal interstitium makes the renal interstitium more positive given Cl motive to cross

348
Q

Another name for the heavy reabsorption process at the peri-tubular capillaries is called?

A

Bulk flow

349
Q

Are there water pumps on cells?

A

NO, most water reabsorption is due to being pulled via osmosis

350
Q

What is a waste product that is found in the renal interstitium? & why is it there & not excreted?

A

Urea
- it is stored in the renal interstitium to help reabsorb water via osmosis

351
Q

What is found on the tubular cells on the lumen side that increases surfaces area?

A

Brush border – increases surface area & is prevalent in the proximal tubule – this allows more room to place transporters by up to x20

352
Q

What is the Vrm of Tubular epithelial cells in the kidney

A
  • 70
353
Q

What is the charge tubular lumen in the proximal tubule & what causes this charge?

A

-3 mV
The charge is a product of the left over ions in the proximal tubule – more so Cl

354
Q

How many proteins are filtered a day?

A

1.8 grams a day

355
Q

How many proteins are reabsorbed in the proximal tubule? how many are not reabsorbed?

A

1.7 grams a day are reabsorbed
100 mgs are not reabsorbed?

356
Q

What happens to the proteins that were not reabsorbed at the proximal tubule? Are proteins absorbed anywhere else in the kidney?

A

They are excreted via urine
Proteins are not absorbed anywhere else, only in proximal tubule

357
Q

How are proteins reabsorbed in the proximal tubule? What happens once the proteins are reabsorbed?

A

Proteins are reabsorbed via endocytosis or Pinocytosis
- once the proteins are reabsorbed they are degraded into amino acids that can be absorbed

358
Q

Regulation of acid/base management in the kidney is dependent on the enzymatic activity of which enzyme?

A

Carbonic Anhydrase

359
Q

The function of carbonic anhydrase is linked to which pump?

A

NHE

360
Q

Why is the NHE considered a form of secretion?

A

A compound is being actively pumped into the tubule

361
Q

Describe how Carbonic anhydrase works in the lumen

A

Once H binds to HCO3 to form H2CO3, Carbonic anhydrase speeds up the process of H2CO3 dissociating into CO2 & H2O which can easily diffuse across into tubular cells

362
Q

Describe how Carbonic anhydrase works in the Tubular cells

A

Carbonic anhydrase speeds up the combining of CO2 & H2O to form carbonic acid (H2CO3) which then dissociates into HCO3 & H2O

363
Q

When H is excreted via urine what is it usually paired with to buffer the acidity?

A

H is paired with NH3 to form NH4

364
Q

What is the affect of a Carbonic anhydrase inhibitor?

A

Bicarb would be absorbed & the NHE pump would slow down leading to acidosis
- if the NHE pump is slowed Na reabsorption will be reduced, water will follow Na which would lead to less water reabsorption as well – increased urine output

365
Q

Where is majority of new bicarb produced?

A

Proximal tubule

366
Q

How is new bicarb produced?

A

Glutamine will be used to produce 2 bicarbs (HCO3) & 2 ammoniums (NH4)
- this occurs via stoichiometry by taking 1 glucose & converting it to produce 2 HCO3 & 2NH4

367
Q

Where is most of the Glutamine produced?

A

Liver
- pts with liver failure have difficulty producing glutamine which then interferes with Acid/base balance

368
Q

What is the relationship of concentration between ICF/ECF of Phosphate? Why?

A

Greater inside the cell than outside the cell.

Lots of cellular functions use phosphate.

369
Q

Aside from phosphate, name another urinary buffer

A

Ammonium

370
Q

Is calcium only reabsorbed in the PCT?

A

No - a number of places

371
Q

Within the PCT, what pathway does Ca follow to be reabsorbed?

A

Paracellular (between cells)
Transcellular (Through cells)

A lot of Ca reabsorbed is dragged along with water and other stuff being reabsorbed

372
Q

Is the calcium channel within the PCT cells a pump?

A

No: Just a channel selective for Ca

373
Q

What is the relationship between concentration inside vs outside the PCT cells? What does this mean?

A

High outside the cell, inside the cell - calcium is motivated to come into the cell

374
Q

Other than the chemical gradient of calcium, what else makes calcium want to come into the PCT cells?

A

Electro-gradient - the cell is negative, calcium is positive

375
Q

Once calcium is within the PCT cell, how is it reabsorbed to the renal interstitial space?

A

Ca ATPase pump directly moves 1 Ca for 1 ATP.

We also use the Na/Ca exchanger (3Na/1Ca), which is the same channel we have in the rest of the body

376
Q

What is filtered in glomerular capillaries? (what does it depend on)

A

Variable: Depends on acid/base status

377
Q

Acid/base status affects free flow of calcium within the plasma. How does this affect filtration?

A

Harder to filter calcium if it is not free floating.

i.e. calcium likes to hang around albumin (which is negatively charged, larger protein). Not all calcium in the plasma is filtered since it’s following this larger negatively charged protein around

378
Q

What is the controller of Calcium levels in our body?

A

Parathyroid gland - monitors for levels of Ca in the ECF. This should mirror/relate to Ca levels in our blood

379
Q

What does para mean?

A

Sides

380
Q

Where is the parathyroid gland?

A

Little nodules on the SIDE (Para) of your thyroid

381
Q

What happens when the parathyroid gland thinks Calcium is low?

A

Parathyroid hormone (PTH) is released

382
Q

What four things does parathyroid hormone (PTH) do?

A
  • Encourages vitamin D3 activation
  • Increases the Ca reabsorption system in the kidney
  • Stimulates bone breakdown
  • Decreases activity of osteoblasts
383
Q

How does Parathyroid Hormone (PTH) encourage vitamin D3 activation?

A
  • Increases amount of calcium we absorb from our diet
384
Q

How does calcium get absorbed from our diet if we take a supplement?

A
  • If we take calcium supplements, we need to take it with activated vitamin D3 so it absorbs
385
Q

How does parathyroid hormone (PTH) increase the calcium reabsorption system in the kidney?

A

-Increases numbers of calcium channels in the kidney. Not in Guyton, but daddy said so

386
Q

How does parathyroid hormone (PTH) stimulate bone breakdown?

A

-Increases osteoclast activity

387
Q

What are osteoclasts?

A

Cells that break down bones - break bonds between calcium and phosphate which liberates them.

Note: he said phosphate is broken by a different system, but that we shouldn’t worry about that for now.. just know the above

388
Q

What is bone made of?

A

Hardened calcium salt (Calcium and phosphate fused together)

389
Q

Where is the main calcium storage site in our body?

A

Bones

390
Q

Parathyroid hormone (PTH) decreases activity of osteoblasts. What does that mean?

A

Osteoblasts take calcium and phosphate, stick it together to form more bone

Osteo = bone
Blasts = build
(if you see osteoB- just think B for build, makes it easy)

391
Q

If you’re chronically hypocalcemic, what medical condition might you have? Why?

A

Osteoporosis

High PTH –>increased osteoclast activity –> decreased bone mass –> used up stores of calcium –> Swiss cheese bones –> MORE LIKELY TO FRACTURE

392
Q

Where is our long term calcium storage?

A

Bones

393
Q

Where is our short term calcium storage?

A

Sarcoplasmic reticulum

394
Q

If we have calcium levels, our Parathyroid hormone (PTH) levels should be ___. What does this mean with osteoclast/blasts?

A

Low

Osteoclast - activity reduced
Osteoblast - activity increased

Emphasis from Schmidt - if we want to build bone, take calcium w/ activated vitamin D supplements. It reinforces bones and makes them stronger

395
Q

What endogenous organic cations did Schmidt mention in class?

A
  • Acetylcholine
  • Creatine
  • Dopamine
  • Epinephrine
  • Choline
  • Histamine
  • Serotonin
  • Norepinephrine
396
Q

What endogenous organic cations did Schmidt mention in class?

A
  • Atropine
  • Isoprel
  • Morphine
  • Procaine
  • Quinine
  • Tetraethylammonium
397
Q

Regarding the antiporter system, organic cations are ____ dependent.

A

Proton

398
Q

Regarding the antiporter system, organic anions are _____ dependent.

A

Sodium

399
Q

What does “antiporter” mean?

A

Two things headed the opposite direction (i.e. 1 of A comes into the cell, 1 of B leaves the cell etc.).

400
Q

What should you do?

A

Look at the figures in the kidney book. He used them in class a lot

401
Q

What are the steps in getting rid of organic cations?

A
  • Cation goes into PCT via secretion from renal interstitial space (got there by being leaked out of the peritubular capilaries. The peritubular capillaries reabsorb plenty of things, but they are porous*). [know this, pathway below)

-Leaked from peritubular capillaries to the renal interstitial space
- From renal interstitial space, transporters move the cation into the PCT cells
- from PCT cells, removed from cell and placed into tubular lumen via proton cation antiporter (One proton comes into the cell, the organic cation leaves the cell and goes into the tubular lumen)

402
Q

How was the organic cation/anion antiporter system discovered?

A

WWII, there was an interest in keeping injured military personnel alive.

  • was really the only antibiotic
  • Mold in petrie dish was making PCN producing mold/fungus
  • Used PCN in people (in 1942 for the first time), but did not stay in the blood for long
  • They found that synthetic hippurate made the PCN last a lot longer in the bloodstream, through competitive inhibition of antiporters (PCN and Hippurate use the same antiporter)
403
Q

Can the secretory system be used for creatine? If so, how is filtration/secretion?

What else does the secretory system secrete that is important for transporting organic anions into the tubular lumen?

A

It can be used to secrete a little creatine. It’s a larger compound that is also easily filtered/secreted

Paraaminohippurate (sorry spelling)

404
Q

What endogenous organic anions did Schmidt mention in class?

A
  • Bile salts
  • Hippurates
  • Prostaglandins
  • Urate/Uric acid
  • Oxalate acid
405
Q

Is PAH (Paraaminohippurate) an endogenous anion?

A

No. PAH is exogenous, however we do have other hippurates that ARE considered endogenous organic anions.

406
Q

What exogenous organic anions did Schmidt mention?

A
  • Lots of drugs
  • Furosemide
  • Penicillin (super important; he stressed about kidney removing this easily without synthetic hippurate)
  • Salicylates
  • Sulfonamide
  • Acetazolamide
  • Chlorothiazide
407
Q

What common Salicylate did Schmidt mention in class? Is this an organic anion or cation? Endogenous or exogenous?

A

Aspirin; Exogenous organic anion

408
Q

What mediator does the body use to assist in getting rid of organic anions?

A

aKG (Alpha Ketogluterate)

409
Q

Where is aKG (alpha-ketogluterate) found?

A

Freely floating around the cells normally in our body

410
Q

How does the body remove organic anions?

A
  • Within PCT, aKG (alpha-ketogluterate) is taken into the PCT cell alongside 3 Na. (from interstitial space; verify this)
  • Increased aKG (alpha-ketogluterate) concentration is tied to moving anion from renal interstitial space into the PCT in exchange for moving aKG back out to the interstitial space.
  • Facilitated transport allows anion to be moved into the proximal tubule for elimination
411
Q

Look at the vanders book page 72 & 75, he said he may get to this. Shows how protonated vs non protonated things are handled differently by the kidney

A

Not covered yet, but if you have extra time just look at it

412
Q
A
413
Q

How much water is reabsorbed by the Proximal tubule?

A

2/3rds or 65%

414
Q

How much water is reabsorbed at the descending thin loop of henle?

A

20%

415
Q

How much water is reabsorbed at the distal convoluted tubule & collecting duct?

A

15%

416
Q

What percentage of ions get reabsorbed at the thick ascending loop of henle?

A

25%

417
Q

What percentage of ions get reabsorbed at the Proximal tubule?

A

2/3rds or 65%

418
Q

The remaining percentage of solutes that were filtered get reabsorbed where?

A

The remaining percentage of solutes that were filtered is about 10% & the determination of whether or not these ions get reabsorbed is taken place in the later portions of the distal convoluted tubule & the collecting duct

419
Q

What are the types of cells located in the distal convoluted tubule & Collecting duct that determine which ions we hang on to?

A

Principle cells

420
Q

Water regulation also occurs in the Principle cells, what does water regulation in the Principle cells depend on?

A

Depends on how much ADH we have
- ADH allows us to fine tune water reabsorption

421
Q

What is the main way calcium is reabsorbed into the renal interstitium from the Tubular cells in the distule tubule?

A

Via the Na/Ca exchanger
- Ca/ATPase pump also found here but majority of the work is done by Na/Ca exchanger

422
Q

What is the Na/Ca exchanger dependent on?

A

Na/K pump - it keeps the Na concentration intracellularly low by forcing Na into the renal interstitium – this drives Na to want to come into the cell via Na/Ca exchanger

423
Q

If we want to increase the Na/Ca pump, what medication can be given? & how does it work?

A

Thiazides
- it inhibits the Na/Cl pump that allows entry of Na & Cl from the tubule into the Distal Tubular cells, this lowers the intracellular concentration of Na even more which in turn increases the motive of Na to want to come into the cell & place a Ca in the renal interstitium via Na/Ca exchanger

424
Q

Who might benefit from thiazides aside from its diuretic affects?

A
  • Pts with osteoporosis as it increases calcium reabsorption
  • pts with history of kidney stones as it increases Ca reabsorption & kidney stones are crystalized calcium
425
Q

Aldosterone is what type of steroid?

A

Mineral Corticosteroid

426
Q

How does Aldosterone manage electrolyte balance?

A

it manages the amount of Na we hang on to

427
Q

Where can aldosterone receptors be found?

A

Principle cells

428
Q

If we have low BP or low Na, what does the release of aldosterone do?

A

It binds to aldosterone receptors in the principle cells which increases the absorption of Na & H2O

429
Q

While Aldo increases Na absorption, what does it do to K?

A

Increases rate of secretion into lumen

430
Q

Why is K secretion in the distal tubule considered a secretory process even though K moves through a channel into the lumen not a pump?

A

K leaving via these K channels is driven by the Na/K pump therefore is still considered a secretory process

431
Q

Aldo receptors have a direct effect on 3 things within the principle cell, what are they?

A
  • speed of Na/K pump
  • the number Na channels on tubular lumen side
  • the number of open K channels on the tubular lumen side (Although daddy did say the details on the k channels are uncertain but he believes it is)
432
Q

What are the 2 types of K channels found with the Principle cells & when are they activated?

A
  • ROMK – these K channels are sequestered in the cell until K secretion is needed, then they will be placed on the cell wall (Aldo mediated)
  • BK channels (Big K) – these are always found on the cell wall & do not move, these remain closed until ALOT of K secretion is needed (Aldo mediated - but details not certain)
433
Q

When you think of principle cells, Jimbo said to think of 2 things, what are they?

A

Aldo & Potassium maintenance

434
Q

What is another name for the Na channels found in principle cells on the lumen side?

A

ENaC - epithelial Na channels, these are Aldo mediated
- tubule is made up of epithelial cells

435
Q

What meds can block the ENaC? & why might these be beneficial?

A

Amiloride & Triamterene
- useful if we want retain K

436
Q

What meds are Aldosterone receptors blockers?

A

Spironolactone & Eplerenone

437
Q

Why are Aldosterone antagonists & ENaC blockers potassium sparring? how do they work?

A
  • ENaC Blockers –> prevent influx of Na from tubule –> this slows Na/K pump –> reduces the amount of K being secreted
  • Aldosterone antagonists –> prevent aldosterone from binding –> this slows Na/K pump & slows the amount of Na we reabsorb –> in turn reduces the amount of K we secrete
438
Q

Anything that prevents reabsorption of Na upstream of the principle cells will directly increase & indirectly increase what at the principle cells?

A

Directly increase the reabsorption of Na & indirectly increase the secretion of K

439
Q

Where does aldo come from?

A

Zona glomerulosa – outermost part of the adrenal gland

440
Q

What produces most of the cortisol & androgens in the adrenal gland?

A

Zona fasciculata & Zona Reticularis
- both are deeper in the adrenal cortex but Zona Reticularis is deeper than Zona fasciculata (so basically below it)

441
Q

What zone produces a small amount of estrogen?

A

Zona fasciculata

442
Q

Where are Catecholamines produced in the adrenal gland?

A

Medulla – the inner part of the adrenal gland

443
Q

What is the ratio of Epi to Norepi production in the adrenal gland

A

Epi is produced more by a 4:1 ratio

444
Q

What is the Zona Glomerulosa sensitive to? & what happens as a result?

A

Sensitive to K levels
- High levels of K –> more aldo released to reduce K
- Low levels of K –> less aldo released to preserve K

445
Q

Aldosterone, Cortisol & androgens are all cholesterol derivatives & look similar, as a result of their similarity what can excess cortisol result in?

A

Excess cortisol can bind to aldosterone receptors & release aldosterone which leads to increase reabsorption of Na & H2O & ultimately HTN & hypokalemia

446
Q

What can also stimulate the release of aldosterone?

A

Angiotensin II by binding to AT1 receptors found in the Zona Glomerulosa

447
Q

What is the enzyme found in the principle cell that is specific for cortisol that prevents it from binding to aldosterone receptors?

A

11Beta-HSD Type 2

448
Q

What natural product inhibits 11Beta-HSD Type 2?

A

Licorice

449
Q

What is the cell found in the distal tubule what deals with Acid/base regulation? & what are the types?

A

Intercalated cells
- 2 types –> Type A & Type B

450
Q

What do Type A intercalated cells have the ability to do?

A

Secrete protons (H)
- deals with acidosis

451
Q

What do Type B intercalated cells have the ability to do?

A

Reabsorb protons & secrete bicarb
- deals with Alkalosis

452
Q

What are the secretory processes for protons in Type A intercalated cells? Which one has the ability to pump a lot of H if needed?

A
  • Hydrogen ATPase pump - takes 1 H & burns an ATP to dump it in the lumen – this pumps givens type A cells the ability to pump ALOT of H if needed
  • H/K ATPase Pump - takes 1K in & pumps 1H out into lumen
453
Q

What are both principle & intercalated cells sensitive to?

A

Vasopressin (AVP) or ADH

454
Q

What are the receptors vasopressin binds to in the Distal tubule/collecting duct?

A

V2 receptors

455
Q

When ADH binds to V2 receptors what happens?

A

cAMP is increased which leads to activation of enzymes –> Protein Kinase A –> phosphorylates Aquaporin channels (AQP-2) which leads to more aquaporin channels being placed on the lumenar side of the principle cell –> leads to increased water reabsorption

456
Q

What type of Aquaporin channels are located on the Renal interstitium side of the principle cell that do not require ADH for activation?

A

AQP-3 & AQP-4

457
Q

A problem with the kidney & how it responds to ADH/AVP is called?

A

Nephrogenic Diabetes insipidus

458
Q

A problem with the release of ADH/AVP is called?

A

Central Diabetes Insipidus

459
Q

what can cause Nephrogenic Diabetes insipidus?

A

Lithium

460
Q

What is the lower limit that urine osmolarity can be?

A

50 mOsm

461
Q

What is another name for the Thick ascending limb?

A

Diluting segment – called this because we reabsorb electrolytes here & not water

462
Q

What affect does alcohol have on ADH?

A

Alcohol reduces the amount of ADH released from the brain & reduces kidneys response to ADH

463
Q

What is the osmolarity of the tubular fluid post proximal tubule?

A

300 mOsm
- same as plasma as both water & Na were reabsorbed

464
Q

What is the osmolarity of the tubular fluid at the bottom of the descending loop of henle?

A

1200 mOsm
- renal interstitium is heavy concentrated leading to reabsorption of water

465
Q

What is the osmolarity of the tubular fluid post Ascending thick limb & early distal convoluted tubule?

A

100 mOsm
- solutes were reabsorbed but water was not diluting tubular fluid

466
Q

What is the osmolarity of tubular fluid at the beginning of the collecting duct?

A

300 mOsm
- renal interstitium osmolarity begins to increase & water follows

467
Q

What is the highest osmolarity the tubular fluid can get at the end of the collecting duct?

A

1200 mOsm
- this is in conservation mode where renal interstitium is heavy concentrated leading to a lot of water reabsorption

468
Q

If were in a state where we had excess water & ADH was reduced, how would this affect the tubular osmolarity?

A
  • the renal interstitium will be reduced 1200 leading to less water reabsorption in the loop & collecting duct
  • as the tubular fluid makes its way down the collecting duct Ions will still be absorbed however water will not as there is no ADH to activate aquaporin channels & urea transporters leading to an even lower urine osmolarity
469
Q

What is the lowest urine osmolarity can get to?

A

50 mOsm

470
Q

What compartment does most of the fluid that is excreted via diuretic therapy come from? & where does the rest come from?

A

ECF - 4/5ths
Plasma - 1/5th

471
Q

What affect does a high salt intake have on the ANGII?

A

High Na intakes –> ANGII is reduced –> Aldo is reduced –> Reduced amount of salt that is reabsorbed as well as water

472
Q

What affect does high salt intake have in someone who has chronically high ANGII? What is a non-pharmacologic therapy that be used to combat this affect?

A

High salt intake will lead to an increase in BP as more Na is being reabsorbed d/t high ANGII levels and water follows Na leading to increased blood volume
- Decrease Na intake

473
Q

If there is an ANGII blockade, how will this affect Na & BP? what is a non-pharmacologic method to combat this affect?

A

Less ANGII –> less Aldo –> less Na & water being reabsorbed –> low BP
- increase Na intake

474
Q

What affect do ACE inhibitors have on BP short term?

A

ACE inhibitors block ANGII & affects body’s ability to deal with hypotension as ANGII plays a crucial role in dealing with low BP

475
Q

How does a high Na diet affect ANGII long term?

A

High Na –> decreases ANGII to get rid of excess salt –> long term levels of low ANGII will lead to poor management of hypotensive states

476
Q

If we have a stenotic kidney, how will this affect the kidney? & what will the kidney do to compensate?

A

The BP in the stenotic kidney will be low –> low BP leads to low pressures in the glomerulus capillaries & Low GFR –> less Na/Cl will reach the macula densa –> Kidney will think GFR is low & secrete renin which converts to ANGII –> ANGII will work on efferent arteriole to increase GFR & increase Na reabsorption –> this will lead to increased MAP

477
Q

If we have two Kidneys, one is healthy & one is stenotic releasing ANGII, what affect will ANGII have on the healthy kidney? & what will the healthy kidney do to compensate?

A

ANGII will increase pressure in the healthy kidney, the healthy kidney will try to compensate by reducing its amount of renin –> however this will only have slight effect on the overall pressure

478
Q

What drugs can be given to combat the affects of High BP due to ANGII?

A

ACE inhibitors, ARBS, & Renin inhibitors

479
Q

How does excess Na influence a taste bud?

A

Taste bud is an electronically excitable cell – it has both Na & K channels (No Cl channels) – the more Na we have around the cell the taste bud the more excitable/positive it becomes making our food easier to taste

480
Q
A
481
Q

If you don’t know how much of something is reabsorbed at the PCT, odds are ____ of it is reabsorbed at the PCT

A

2/3rds

i.e, 2/3rds of calcium is reabsorbed at the PCT.

482
Q

What is the segment after the straight proximal tubule? What’s special about this area? (i.e. what is absorbed and why)

A

Thin descending loop of henle

As the tubule goes from the cortical area to medullary area of the kidney, the interstitial space is highly osmotic. This segment is permeable to water, so water reabsorption occurs.

Not many ion transporters here - primary thing is water reabsorption.

483
Q

Where does water reabsorption happen throughout the tubule, and in what amount?

A

2/3 PCT
“A bunch more” in the descending loop of henle
Fine tune adjustment in the later parts of the tubule

484
Q

What is reabsorbed in the thin ascending loop of henle? What single transporter are we to know here?

A

Coming from medullary to cortical area of the kidney - interstitial space is less osmotic.

This area is relatively impermeable to water, so there is not much reabsorption here.

NaCl transporter - Uses active transport via ATP/primary active transport to reabsorb relatively small amounts of NaCl from tubular fluid.

485
Q

What does the thick ascending loop of henle reabsorb? What is this driven by?

A

Important place for reabsorption of cation electrolytes of the tubular fluid. Driven by a system that allows K to leak back into the tubular fluid (or interstitial fluid if we need to not reabsorb as much mg/ca) via K leak channels on either end of the tubular cell.

Mg, Ca - come though the paracellular route

486
Q

What is the charge of the tubular fluid at the thick ascending loop of henle? Why? What does this do?

A

+8mV (note, other areas of tubule were +3)

Increased amount of K in the tubular fluid makes the charge this way.

This charge helps push Mg/Ca (as they have a double positive charge) back into the tubular cells to be reabsorbed.

487
Q

What pump do tubular cells have in common with all other cells?

A

Na/K/ATPase pumps

488
Q

What other channel exists in the thick ascending loop of henle that helps with acid base balance?

A

Na/H (one H into the tubule, one Na in the tubular cell)

489
Q

What area of the nephron is responsible for concentrating the renal interstitium? What channel/pump is responsible for this? Why?

A

Thick ascending limb of henle is responsible for concentrating the renal interstitium.

NKCC pump (Transports 1 Na, 1K, and 2 Cl into the tubular cell from the tubular lumen) is responsible for concentration of the renal interstitium. The concentration settles into the deeper areas (1200mOsm is the highest concentration)

Note: K leaks back out of the cell to help Mg/Ca move via the paracellular route to be reabsorbed.

490
Q

What is the most powerful diuretic class? What does it shut down, and what happens as a result?

A

Diuretics shut down the NKCC (1 Na, 1Ka, 2Cl into the tubular cell) pump.

This decreases concentration of the renal interstitium, which inhibits the ability to reabsorb water. We depend on the concentration of the renal interstitium to reabsorb water.

Result: More water shows up in urine.

491
Q

In someone who is trying to conserve water, what is the osmolarity of the tubule at the PCT, deepest part of the interstitium, and between the thick ascending loop of henle/DCT?

A

300mOsm
1200mOsm
100mOsm

492
Q

What is the most concentrated the renal interstitium can get in humans?

A

1200mOsm

493
Q

If the osmolarity of the deep renal interstitium is 1200, what will be the osmolarity of the tubule (urine) assuming there is not excessive velocity of fluid?

A

1200

Note: He hinted that if there was higher flow, the osmolarity may not be the same.. Something to think about with high BP or poor autoregulation with hyperfiltration

494
Q

What dictates water permeability/reabsorption in the collecting ducts?

A

ADH

495
Q

How does a lizard nephron compare to a Human nephron?

A

Lizards live in arid environments and need to conserve water for extended time frames.

Lizard osmolarity is significantly more concentrated, so they are able to reabsorb much more water.

496
Q

What is the DCT sensitive to? What does this do?

A

Parathyroid hormone (PTH)

Increases Ca reabsorption

497
Q

What channels in the DCT help with Ca reabsorption?

A

Na/Ca exchanger

Ca/ATPase pump

^These two are usually found together.

498
Q

How do we get sodium reabsorption in the DCT?

A

NaCl channel (1Na in, 1 Cl in as well)

499
Q

Where is the site of action for Thiazide diuretics?

A

Na/Cl channel in the DCT

500
Q

Thick ascending limb of loop of henle is reabsorbing how much of our ions?

A

A quarter

Called the diluting segment sometimes; diluting electrolytes but no water from the tubule.

501
Q

What hormone is the water control system of the body?

A

Vasopressin

502
Q

What is another name for vasopressin?

A

Antidiuretic hormone (ADH)

503
Q

What would happen to vasopressin levels if we needed to hang on to water? How about get rid of water?

A

Hang on to water - high vasopressin levels

Get rid of water - low vasopressin levels

504
Q

What could happen to urine output in the event of a head injury? Why?

A

Central Diabetes Insipidus (dumping large amounts of urine)

Brain stops producing ADH

505
Q

What are two controllers in the body that control how much vasopressin is released?

A

Osmolarity of blood (i.e., salty blood from dehydration would cause high vasopressin levels so we can hang on to more water)

BP - if the arterial BP is low (or blood volume), Vasopressin is released to hold onto volume to raise BP.

506
Q

If you have no blood volume, you have __ _____.

A

No pressure

507
Q

Which areas of the body have sensors that look for volume changes?

A

Large veins, atria

508
Q

What areas of the body have sensors that look for higher BP?

A

Baroreceptors

509
Q

What is the PRIMARY controller of vasopressin (ADH) release?

A

Osmolarity of blood

510
Q

What are osmoreceptors? What do they do?

A

Cells that specialize in sensing osmolarity.

They send information to two nuclei in the brain (within hypothalamus/posterior pituitary)

511
Q

What area of the brain can sense bacteria, and then turn up the temperature to kill off said bacteria?

A

Hypothalamus

512
Q

Where is vasopressin produced? Where are these production centers located?

A

Two production centers

Supraoptic neuron - nuclei (collection of cell bodies) in front of the hypothalamus, but above the optic nerve

Paraventricular nucleus - located on each side of the 3rd ventricle

513
Q

How much of our vasopressin (ADH) is produced at the supraoptic neuron?

A

5/6th of our ADH - major production area

514
Q

How much of out vasopressin (ADH) is produced at the paraventricular nucleus?

A

1/6th

515
Q

Where does the paraventricular nucleus/supraoptic neuron send the vasopressin that is produced?

From there, how does it go systemic?

A

Posterior pituitary

From there, it is dumped into a rich network of blood vessels surrounding the posterior pituitary to be distributed around the body

516
Q

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

A

Neurohypophysis

517
Q

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

A

Adenohypophysis

518
Q

If a RBC was placed into an isotonic solution, what would happen to the osmolarity? Why?

A

Volume wouldn’t change much - same osmolarity inside vs outside the cell

519
Q

What is the main thing that determines our osmolarity?

A

NaCl

520
Q

If we put a RBC into a hypotonic solution (Less osmolarity), what would happen to the cell & the osmolarity? Why?

What would be the result of this in regard to vasopressin?

A

The cell would swell. The osmolarity in the cell is greater than the solution, so water would move from the solution into the cell to balance the osmolarity.

Reduce the amount of vasopressin (ADH) production - if we get rid of water, we can get closer to a normal osmolarity.

521
Q

What would happen to a RBC dropped into a hypertonic (higher osmolarity than cell) solution? Why?

What would happen to vasopressin production?

A

Cellular dehydration - water would leave the cell to attempt to balance the osmolarity between the cell and solution.

Vasopressin (ADH) production would increase - we want to conserve free water to dilute the osmolarity, thus bringing it closer to normal.

522
Q

What did Schmidt say to think of cells as when dropped into hypotonic/hypertonic solution? Give examples.

A

Think of the cell as an osmoreceptor.

With swelling osmoreceptors (cell), the rate of production of action potentials to the vasopressin production are is decreased.

With shrinkage of osmoreceptors (cell), the rate of action potentials sent to the vasopressin production area is increased. Vasopressin production is increased.

Note: He compared this to the neuro stretch receptors; these work opposite to those.

523
Q

What is the highest and lowest osmolarity vasopressin can produce in urine?

A

Low: 50mOsm
High: 1200mOsm

524
Q

After the DCT, what is osmolarity dependent on?

A

Vasopressin (ADH)

525
Q

High vasopressin levels would result in a ___ osmolarity of urine.

A

High

526
Q

Low vasopressin levels would result in a ____ osmolarity of urine.

A

Low

527
Q

Other than water reabsorption at the collecting ducts, what else does vasopressin control?

A

Urea reabsorption from tubular fluid

528
Q

What is urea, what is it useful for, and how is it filtered? Finally, where is it reabsorbed?

A

Waste product of metabolism

Useful for water reabsorption (raises osmolarity of interstitium)* major component of the concentrated renal interstitium**

Filtered freely due to being small. No specific channel, just dragged along with everything else.

Reabsorbed in the late PCT and loop of henle.

529
Q

What kind of channel does water come through in the collecting duct? (hint: controlled by vasopressin)

A

Aquaporin channels

530
Q

If we have lots of vasopressin, we have ____ of aquaporin channels.

A

a lot

531
Q

Where are urea transporters located?

A

Cell wall of the collecting duct (prevents some urea from being removed from the body)

532
Q

What is an important thing to have within the interstitium to hang onto water via osmosis through aquaporin water channels in the collecting tubule?

A

Urea

533
Q

What are the two urea transporters mentioned in class?

A

UT-a1
UT-a3

534
Q

What is the primary controller of plasma osmolarity? What’s special about this vs other things that influence water reabsorption?

A

Vasopressin (ADH); the only thing in our body that influences water reabsorption WITHOUT affecting salt reabsorption.

Aldosterone/AGII both influence water reabsorption, but also affect salt reabsorption.

535
Q

If a healthy person had a lot of salt, or lack thereof, would it impact blood pressure much?

A

not really - kidney does a good job managing osmolarity (But NOT perfect, slight slant on autoregulation graph)

536
Q

What happens with a significant dose of caffeine?

A

The vasopressin system is knocked out, which then knocks out control of osmolarity.

This would result in significant swings in plasma osmolarity.

537
Q

If Na levels drop, what does that mean with fluid status?

A

Probably have too much fluid - decrease in vasopressin to fix it

538
Q

What does having a full belly do for thirst?

A

Gastric distention decreases thirst

539
Q

In the ICU, patients are often on fluid restrictions. How can we help them avoid being thirsty?

A

Keep lips moist. Dry lips lead to increased signaling to drink water/thirst.

540
Q

What three drugs mentioned in class decrease vasopressin levels?

A

Alcohol
Clonidine
Haloperidol

541
Q

How does nausea affect vasopressin levels?

A

Body anticipates vomiting. When we vomit, we lose fluids. When we lose fluids, the brain produces more vasopressin to conserve/replace lost fluid.

542
Q

What two drugs mentioned in class increase vasopressin release?

A

Morphine
Nicotine

543
Q

If we change our potassium intake, what happens to the plasma concentration?

A

Not much - it is controlled (but slanted graph) as long as we have a functional aldosterone system.

544
Q

What disease, and what two drugs can impact our aldosterone system? Why is this important?

A

Renal failure

High dose of spironolactone or triamterene

If we take the control system offline, we have to be careful about K intake, as levels could change dramatically.

545
Q

If we are given 1L of distilled water (no electrolytes), what happens?

A

Blood osmolarity is reduced slightly.
Vasopressin levels are reduced.
Urinary flow rate goes up within around half a hour.
Urinary flow rate goes up until blood osmolarity is balanced once again, taking just a few hours.

Urinary osmolarity will have massive decrease during time that water reabsorption decreases. (more water, no extra electrolytes).

546
Q

Vasopressin regulation can help get rid of extra fluid. What is special about this?

A

Doesn’t affect electrolytes - only water.

547
Q

A healthy person with an ideal diet would have a urine osmolarity of ____. Do we all have this?

A

600mOsm

We see wide ranges between person to person, as we all consume vastly different diets (often times too much salty pizza)

548
Q

When a normotensive person ingests a lot of fluid and salt, what happens to their BP?

A

Might have a small increase in BP, but the kidney is able to take care of most of it with no long term BP effects.

549
Q

When a person with essential HTN ingests a lot of fluid and salt, what happens to their BP?

A

They have a higher baseline BP than a normotensive person.
The kidneys are capable of maintaining BP/fluid status without long term BP effects even with HTN.

Note: The kidneys are slightly less capable of managing fluid/salt status in patients with essential HTN than someone who is normotensive.

550
Q

What is salt sensitive HTN?

A

Renalvascular HTN - Usually because of a stenotic renal artery, which creates salt sensitivity. The kidneys have a lard time getting rid of extra electrolytes and fluid because of this. The higher our salt intake, the higher our BP in this case.

Note: Anything that over expresses the RASS system will create some salt sensitivity.

551
Q

Who tends to be predisposed to salt sensitive HTN? When might this not be the case?

A

African American people tend to have salt sensitive HTN, as well as some parts of Asia.

African Africans don’t have salt sensitive HTN.

African Americans who have recent ties to African Africans usually do not have salt sensitive HTN.

552
Q

Why is salt sensitive HTN odd? What is the treatment?

A

We expect to see over expression of RASS, but instead we see LOW RASS activity.

Despite this, ACE inhibitors are still useful even through there’s not much to inhibit.

553
Q

Is HTN genetic, or based on diet?

A

Diet can play a role in HTN, but HTN is usually genetic.

554
Q

How do osmotic diuretics work? Give some examples.

A

Every molecule of an osmotic diuretic = one less water molecule reabsorbed.
An osmotic diuretic is filtered, but not reabsorbed.

Manitol is an osmotic diuretic.
Glucose can be an osmotic diuretic if it stays in the tubule.
5000iU of vitamin C is filtered but not reabsorbed well - can be an osmotic diuretic.

555
Q

Na/Electrolyte reabsorption in the PCT is dependent on what?

A

Angiotensin I

556
Q

How can we reduce Na reabsorption in the tubule with -sartan or ACE drugs?

A

Na/electrolyte reabsorption is dependent on ATI receptors.

If we block AGII, AGI receptors are not activated. Less AGI activity = less Na reabsorption in the tubule.

557
Q

What hormone mention in class is technically considered a pressor?

A

AGII - will talk about this more next semester; can constrict blood vessels

558
Q

What kind of diuretic affects aldosterone portions of the principle cells?

A

K sparing diuretics

559
Q

What kind of diuretic affects varying parts of the nephron other than the aldosterone portion of principle cells?

A

K wasting diuretics

560
Q

How old are we when we start to lose nephrons?

A

40

561
Q

How does taste work? Why does salty food taste better?

A

There is a taste receptor. This receptor is activated when the cell fires an action potential. Action potentials are driven by Na/K channels. Salt increases excitability of the cell, leading to increased action potentials, and more tasty food.

562
Q

What is the common ingredient in salt substitute?

A

Potassium - a little goes a long way, and it tastes bad.

563
Q

If you have renal failure and are put on a Na restriction, how does that impact thirst?

A

Less thirst; won’t drink as much, fluid volume will decrease

564
Q

If you are cooking with expensive ingredients, how can you avoid using a lot of it?

A

Add more salt

565
Q

If drugs and other procedures can’t help unilateral renal artery stenosis, why would you remove the kidney?

A

To save the other kidney from damage.

If a kidney is stenotic, there is less flow –> less NaCl past the macula densa –> more renin –> more AGII –> elevated BP –> raises glomerular pressures of healthy kidney an can cause harm

566
Q

What is used to find renal clearance? How does this change if you’re rich?

A

Broke - creatinine
Rich - Inulin

567
Q

What is the normal amount of creatinine filtered?

A

1.25mg/min (125mL/min)

1mg/dL x 1.25dL/min = 1.25mg/min

568
Q

What is the normal concentration of creatinine in our blood?

A

1mg/dL

569
Q

How much creatinine is secreted?

A

0.15mg/min; small amount compared to what is filtered (1.25mg/min)

He said don’t worry about this.. but just in case

570
Q

How much creatinine is excreted normally? What does this mean for creatinine production?

A

1.40mg/min creatinine excreted.

Excretion = production normally, so 1.40mg/min creatinine is produced.

Excretion = production
Will not build up in our blood under normal circumstances

571
Q

What is the primary way to get creatinine in the tubule? What about the rest of it?

A

Filtration

Small amount is secreted into the tubule from peritubular capillaries

572
Q

How do you calculate excretion?

A

Filtered load + secretion into tubule - absorption = excretion

573
Q

What is creatinine?

A

Byproduct of skeletal muscle metabolism

574
Q

Creatinine is excreted at 1.25mg/min. Is this per nephron?

A

No: split between 2,000,000 nephrons if we’re under 40, healthy, with both kidneys.

575
Q

How does losing a kidney suddenly (i.e. unilateral nephrectomy) affect filtration/excretion if we only have 1,000,000 nephrons left? What about creatinine level?

A

Filtration will now be 0.625dL/min (62.5mL/min). This is half as much as before. We are filtering less fluid, so we will also excrete less. We still produce the same amount (1.40mg/min). If we lose half of our nephrons, we must find a new normal balance of production/excretion. Creatinine levels double if half of the nephrons are lost. Each halving of nephrons doubles creatinine level again and again, as we need more and more creatinine to filter the same amount as before (increases workload of remaining nephrons).

Sorry wordy

576
Q

We talked about losing a kidney and how it affects filtration/excretion/creatinine levels.

How is COPD the same physiology wise?

A

When we lose a kidney, we double the workload of the remaining nephrons. We also double concentration of creatinine.

When we have COPD, the body has trouble getting rid of extra CO2, so over time the blood CO2 levels rise till it finds a new equilibrium. (breathe off as much as we are producing).
More concentration of CO2 = easier it will be to get rid of CO2

577
Q

What will make us lose nephrons faster than normal?

A

Sicker, worse blood sugar, higher BP (Nephrons take a harder beating over time)

As we lose nephrons, filtration is reduced, workload is increased, and creatinine is increased.

578
Q

In patients with a unilateral nephrectomy, what is special about their other kidney?

A

There is physiologic hypertrophy. The GFR is able to increase by as much as 50%, so looking at these patients a year later would not have the GFR we expect - they would have higher. The kidney would not have much overwork injury.

This is similar to the heart with exercise.

579
Q

Physiologic hypertrophy is good with the heart or kidney in cases of unilateral nephrectomy. When is it bad?

A

Diabetes induced hypertrophy of the kidney - likely will get worse, not better.

580
Q

In patients with physiologic hypertrophy of the kidney, will glomerular pressures be elevated?

A

No - somehow the kidney can filter 50% more than usual while keeping the glomerular pressure at 60mmHg

581
Q

In cases of unilateral nephrectomy, do we need hormone replacement?

A

No - the remaining adrenal gland can pickup the workload similar to the kidney.

582
Q

What is the single nephron GFR with a fully functioning kidney?

A

62.5nl/min (nanoliter)

583
Q

What is the volume excreted per nephron?

A

0.75nl/min

584
Q

What is the volume excreted for all nephrons?

A

1mL/min

585
Q

If you have renal failure, do you need to be careful with your diet? Why or why not?

A

Yes

Decreased ability to do work.
Can’t eat as much salt, K, proteins (break into amino acids)
Takes a lot of work to filter/excrete/secrete this stuff - takes a toll on the nephrons

586
Q

How is acid base balance impacted by renal failure?

A

Acid-base balance is toast

Can’t get rid of protons as well - results in metabolic acidosis.

587
Q

If you have a cell with an osmolarity of 300mOsm, ECF of 300mOsm, and drop it into a fluid with 250mOsm (hypotonic), what will the new osmolarity be?

A

275mOsm

588
Q

What organ controls osmolarity?

A

Kidney

589
Q

What is the normal osmolarity?

A

300mOsm

590
Q

How much of total body fluid is ICF? How about ECF?

A

2/3rds ICF
1/3rd ECF

591
Q

If you give 0.9% NS (isotonic), what happens to the fluid compartments?

A

Same osmolarity roughly.
Not much water movement - no need for osmolarity to change.
Fluid stays in ECF

592
Q

If you give 0.45% NS (Hypotonic), what happens to the fluid compartments?

A

Fluid has more water than salt than we do in our bodies.

Lowers osmolarity in all compartments.

Water stays in ECF, but some moves over to the ICF to help balance osmolarity.

593
Q

If you give 3% NS (hypertonic), what happens to the fluid compartments?

A

Fluid has a larger portion of salt than water than our bodies.

Osmolarity of body will be elevated.

Extra salts from ECF will pull water from ICF into the ECF to balance osmolarity. This can cause cellular dehydration.

594
Q

Can this be over now

A

It is! You’ve made it to the end!

Anatomy (7 decks)

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