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A&P Fall 24 Final > FINAL. > Flashcards

FINAL. Flashcards

1
Q

What are the 3 main functions of the CV system?

A
  1. transport nutrients to tissues
  2. transport waste products away from tissues
  3. transporting hormones: signaling (ex. endocrine system)
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2
Q

vascular conductance is the _____ of vascular resistance

A

inverse

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3
Q

High conductance = ______ flow
Low conductance = ______ flow

A

high = high
low = low

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4
Q

How much blood is found in our veins?

A

64%

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5
Q

a system in series will have _____ resistance while a system in parallel will have _____ resistance

A

Series = High
Parallel = Low

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6
Q

The greater the cross sectional area, the ______ the velocity of blood flow

A

lower

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7
Q

the smaller the cross sectional area, the ___ the velocity of blood flow

A

higher

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8
Q

What are the high resistance vessels in the systemic circulation

A

Small arteries and arterioles (mainly arterioles)

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9
Q

When measuring blood pressure:
Proximal to the choke point the BP would be _____.
Distal to the choke point the BP would be ______.

A

Proximal: higher
Distal: lower

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10
Q

What is it called when we have nice orderly blood flow?

A

laminar flow

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11
Q

What is it called when we have disorderly flow..maybe due to a plaque build up.

A

turbulent flow

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12
Q

When looking at laminar blood flow, why does the blood in the middle of the tube flow faster?

A

the blood on the outside edges are making contact with the wall which is where the high resistance is

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13
Q

How much of our CO goes to the kidneys to be filtered?

A

~22%

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14
Q

How can we rearrange ohms law to figure out flow?

A

Flow = delta P / Resistance

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15
Q

True/false: If we constrict a vessel to half of its original diameter, we decrease flow by 16 fold

A

true

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16
Q

How can we arrange ohms law to solve for resistance?

A

Resistance = Delta P / flow

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17
Q

The drop in blood pressure that occurs between large arteries and capillaries is due to what?

A

mainly due to the increase in resistance and NOT due to the face that it has multiple paths to take.

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18
Q

if we have decreased total cross sectional area that would cause an _______ in velocity.

A

increase (think aorta)

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19
Q

what are capillaries responsible for?

A

exchange of nutrients and waste products

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20
Q

blood flow through capillaries is controlled by ______

A

arterioles

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21
Q

Why are arterioles good at managing blood flow?

A

bc they have a layer of smooth muscle associated with them

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22
Q

true/false: arterioles have two laters of smooth muscle fibers

A

false, roughly four

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23
Q

how many capillaries do we have in our body?

A

10+ billion

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24
Q

What is the total surface area of all our capillaries combined?

A

500-700 sq meters

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25
Q

The blood pressure associated with the arteriole end of the capillaries is _______.

A

30mmHg

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26
Q

The blood pressure associated with the venous end of the capillaries is _______.

A

10mmHg

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27
Q

The average blood pressure associated with the capillaries is _______.

A

17.3 mmHg

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28
Q

Why is the avg blood pressure in the capillaries 17.3 and not 20?

A

bc it starts small and gets bigger in diameter as it moves towards the venous end

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29
Q

Pcap in:
Art end
Avg
Vein end

A

Art end: 30 mmHg
Avg: 17.3 mmHg
Vein end: 10mmHg

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30
Q

Pisf

A

-3 mmHg

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31
Q

Cap oncotic pressure

A

28 mmHg

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32
Q

Isf oncotic pressure

A

8 mmHg

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33
Q

What are the proteins associated with the Cap oncotic pressure

A
  1. Albumin
  2. Globulin
  3. Fibrinogen
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34
Q

What are the proteins associated with the Isf oncotic pressure?

A
  1. proteoglycan filaments
  2. Hyaluronic acid
  3. collagen
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35
Q

The lymphatic system can increase activity by ____

A

20-40X

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36
Q

True/false: If your capillaries become swiss cheese, the lymphatic system will rapidly reuptake the lost proteins.

A

false. its slow af

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37
Q

Kf is the capillary filtration coefficient. What does this look at?

A
  1. permeability
  2. surface area
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38
Q

In a normal 70 kg patient. How much intracellular fluid do we have?

A

1/3 of TBW
~14L

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39
Q

In a normal 70 kg patient. How much plasma do we have?

A

1/4-1/5 of the ECF
~3L

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40
Q

In a normal 70 kg patient. How much ISF do we have?

A

3/4-4/5 of the ECF
~11L

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41
Q

In a normal 70kg patient. How much Intracellular fluid do we have?

A

2/3 of TBW
~28L

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42
Q

What kind of valves are in the lymphatic system?

A

one way valves

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43
Q

Where do the lymphatics empty?

A

into the subclavian veins on either side; R lymphatic duct, thoracic duct

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44
Q

What is the NFP in a capillary on the arteriole end?

A

13 mmHg

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45
Q

What is the NFP in a capillary on the venous end?

A

-7 mmHg (net reabsorption pressure = 7 mmHg)

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46
Q

What is the NFP in a capillary using the average bp in a cap?

A

0.3 mmHg (using 17.3)

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47
Q

True/false: NaCl is generally small enough to diffuse paracellularly

A

true

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48
Q

MAP in the renal artery

A

100 mmHg

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49
Q

Glomerular capillary pressure

A

60 mmHg

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50
Q

The afferent arteriole is important for

A

regulating renal blood flow

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51
Q

the efferent arteriole is important for

A

fine tuning GFR

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52
Q

If we have an increase in BP what will happen to the afferent arteriole? What will happen to the pressures and GFR?

A

It will constrict.
-decrease RBF
-decrease Pcap
-decrease GFR

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53
Q

If we have a decrease in BP what will happen to the afferent arteriole? what will happen to the pressures and GFR?

A

It will dilate
-increase RBF
-increase Pcap
-increase GFR

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54
Q

Normal GFR

A

125 mL/min

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55
Q

Autoregulation in the nephrons is meant to control what two things?

A
  1. Blood flow
  2. Filtration
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56
Q

True/False: Autoregulation in the kidney is just as tight as it is in the brain

A

False

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57
Q

If we have constriction of the efferent arteriole, what would that cause?

A

-decrease RBF
-increase Pcap
-increase GFR

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58
Q

If we have dilation of the efferent arteriole what would that cause?

A

-increase RBF
-decrease Pcap
-decrease GFR

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59
Q

What is the oncotic pressure in the afferent art?

A

28 mmHg

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60
Q

what is the oncotic pressure in the efferent art right after glomerular caps?

A

36 mmHg

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61
Q

What is the oncotic pressure in the glomerulus

A

32 mmHg

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62
Q

What is the Ptubule

A

18 mmHg

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63
Q

What is the oncotic pressure in the tubule

A

0

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64
Q

What is the NFP in glomerulus? what favors/opposes filtration?

A

10 mmHg
favor (Pcap: 60 mmHg)
oppose (Onc Cap: 32 mmHg & Ptubule 18mmHg).
60-18-32= 10

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65
Q

How do we find the filtration coefficient

A

Kf = filtration rate/NFP
Kf = 125mL/min / 10mmHg
Kf = 12.5

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66
Q

what is the Pcap at the end of the efferent art?

A

18mmHg

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67
Q

What blood vessel segment has the highest amt of resistance in the kidney?

A

efferent art

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68
Q

How do we know the efferent art has a greater resistance compared to the afferent art

A

It has a drop in Pcap of 42 mmHg.

afferent art: bp goes from 100 in renal art to 60 in glomerulus (drop of 40)
efferent art: bp goes from 60 in glomerulus to 18 at end of efferent art (drop of 42)

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69
Q

Approx ______% of what is filtered gets reabsorbed

A

99%

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70
Q

Oncotic pressure in peritubular caps

A

32 mmHg

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71
Q

Pcap (peritubular cap)

A

13 mmHg

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72
Q

Oncotic ISF (peritubular cap)

A

15 mmHg

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73
Q

Pisf (preitubular cap)

A

6 mmHg

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74
Q

what is the NFP at the peritubular cap? what opposes/favors filtration

A

-10 mmHg
favor: Pcap 13 mmHg, Onc ISF 15 mmHg
Oppose: Onc CAP 32 mmHg, Pisf 6 mmHg
13 + 15 - 32 - 6 = -10

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75
Q

Excretion = what

A

filtration - reabsorption + secretion

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76
Q

If the kidneys decide to filter more fluid at the glomerulus, how would it achieve that?

A

constriction of efferent art

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77
Q

If we have increased filtration at the glomerulus what would happen to the oncotic pressure in glomerulus?

A

it would increase (become more concentrated)

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78
Q

What is normal GFR?

A

125 mL/min

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79
Q

Normal RBF

A

1100 mL/min

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80
Q

normal RPF

A

660 mL/min

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81
Q

normal FF (filtration fraction)

A

19%

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82
Q

How do we find filtration fraction?

A

FF = GFR/RPF
FF = 125mL/min / 660mL/min
FF = 0.19 (19%)

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83
Q

How to we find RBF

A

its just ~22% of our CO (1100 mL/min)

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84
Q

How do we find RPF?

A

RPF = Plasma % * RBF
RPF = 0.6 * 1100mL/min
RPF = 660 mL/min
(if HCT is 0.4)

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85
Q

in response to increased hydrostatic pressure the afferent art will ______

A

constrict

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86
Q

in response to decreased hydrostatic pressure the efferent art will _____

A

dilate

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87
Q

Constriction of either afferent/efferent art will do what to RBF

A

decrease

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88
Q

normal UOP

A

1mL/min

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89
Q

What is an example of something that is filtered and partially reabsorbed

A

Na

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90
Q

Example of something that is filtered and completely reabsorbed

A

glucose

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91
Q

example of something that is filtered and the completely secreted (nothing reabsorbed)

A

PHA (para aminohippuric acid)

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92
Q

what is the innermost layer of the glomerular caps? what is special about this layer

A

endothelium
has fenestrations

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93
Q

what layer in the glomerular caps comes after the endothelium? what is special about this layer

A

connective tissue called basement membrane. has neg charges to repel things that we dont want to filter like proteins

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94
Q

what is the outermost layer in the glomerular caps

A

epithelium. made up of podocytes used for support due to the high pressure and has slit pores

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95
Q

How are podocytes helpful particularly with chronic HTN

A

prevents swelling of glomerulus

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96
Q

how does the kidney handle LT regulation of BP

A

through RAAS and fluid retention/secretion

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97
Q

how does kidney regulate LT pH

A

short term pH regulator is lungs.
Kidney produces and reabsorbes HCO3 and can also excrete excess protons (H+)

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98
Q

LT regulation of RBC by the kidneys

A

O2 sensor deep in medullary renal interstitum. if pO2 is low erythropoietin is released

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99
Q

LT vit D regulation by the kidneys

A

Vit D is activated by the kidneys, vit d is important for ca reabsorption

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100
Q

Drug clearance in kidneys

A

drugs metabolized in liver and the filtered/secreted by kidneys

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101
Q

What do the kidneys have to do with the removal of metabolic waste products

A

gets rid of them. like nitrogenous compounds (urea)

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102
Q

All of the regulatory roles of the kidney is primarily carried out by what?

A

GFR

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103
Q

What are the more superficial nephrons

A

cortical nephrons

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104
Q

what % makes up the cortical nephrons

A

90-95%

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105
Q

what are the deep nephrons

A

medullary nephrons

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106
Q

what % make up the medullary nephrons

A

5-10%

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107
Q

What is the capillary bed that surrounds the tubules of the medullary nephrons?

A

vasa recta

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108
Q

what is special about the vasa recta

A

has more ascending compared to descending

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109
Q

with more split points that exist in the ascending vasa recta, flow velocity will be ______

A

decreased

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110
Q

why is a decrease in velocity in ascending vasa recta helpful?

A

maintain normal concentration of solutes in the deep medullary interstitum

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111
Q

what happens if the velocity in the ascending vasa recta is increased?

A

ends up washing out the interstitum and then that affects reabsorption

112
Q

True/false: the deep medullary is sensitive to low BP and has limited O2 delivery

A

true

113
Q

Where do the kidneys sit?

A

slightly below diaphragm

114
Q

What sits on top of each of the kidneys

A

adrenal glands

115
Q

The superior lateral side of the right kidney comes into contact with what organ?

A

liver

116
Q

the right kidney comes into contact with what organs

A

liver and colon

117
Q

the left kidney comes into contact with what organs

A

stomach, spleen, pancreas, and descending colon

118
Q

The top lateral side of the left kidney comes into contact with what organ

A

spleen

119
Q

green

A

zona glomerulosa

120
Q

where is aldosterone released?

A

from the zona glomerulosa

121
Q

blue

A

zona fasciculata

122
Q

pink

A

zona reticularis

123
Q

yellow

A

medulla

124
Q

what is released from the adrenal medulla

A

catecholamines

125
Q

what is released from zona fasciculata and zona reticularis

A

Glucocorticoids: cortisol and a little bit of estrogen

126
Q

what is the ratio of epi:norepi

A

4:1

127
Q

blue

A

minor calyx

128
Q

pink

A

major calyx

129
Q

contact with liver:
red

A

liver (hepatic surface)

130
Q

contact with liver:
yellow

A

colon (right colic flexure surface)

131
Q

contact with liver:
blue

A

duodenal surface

132
Q

contact with liver:
orange

A

stomach (gastric surface)

133
Q

contact with liver:
purple

A

spleen (splenic surface)

134
Q

contact with liver:
pink

A

pancreas (pancreatic surface)

135
Q

contact with liver:
green

A

descending colon (descending colic surface)

136
Q

artery & veins:
light blue

A

interlobular

137
Q

artery and veins:
Green

A

segmental

138
Q

artery and veins:
purple

A

arcuate

139
Q

artery and veins:
orange

A

interlobar

140
Q

pink

A

renal artery. obvi

141
Q

dark blue

A

renal vein

(wow you’re literally so smart)

142
Q

Name the renal arteries in sequential order starting with the renal artery.

A
  1. renal art
  2. segmental art
  3. interlobar art
  4. arcuate art
  5. interlobular art
143
Q

what are the layers of the adrenal cortex. starting from outermost moving inward

A
  1. zona glomerulosa
  2. zona fasciculata
  3. zona reticularis
144
Q

when the macula densa senses a decrease in Na, _____ is released from the juxtaglomerular cells

A

renin

145
Q

describe how renin gets converted to Ang II

A

renin leads to increased angiotensinogen (produced in liver) this leads to angiotensin 1, ang 1 is converted to ang 2 via ACE (angiotensin converting enzyme) that is found in large amounts in the lungs

146
Q

angiotensin 2 primarily constricts the ______ arteriole

A

efferent

147
Q

what happens as a result of constriction of the efferent arteriole following ang 2 release

A

increased Pcap in glomerulus
increased filtration

148
Q

what nerve controls the bladder?

A

Pudendal nerve. coming from S 2, 3 and 4

149
Q

what is renal clearance

A

the quantity of plasma that is cleared of a substance per measured time (mL/min)

150
Q

what is the normal rate of filtration and rate of reabsorption?

A

filtration: 125mL/min
reabsorption: 124mL/min

151
Q

Approximately _____ of everything that is filtered is reabsorbed at the PCT

A

2/3 or 66%

152
Q

When thinking about glucose in a normal healthy individual (without glucose issues) the clearance should equal what?

A

zero. we aren’t clearing the plasma of any glucose

153
Q

if we have a BP of 200, what happens to the afferent art? why would this happen?

A

it constricts due to autoregulation

154
Q

Kf = what

A

12.5

155
Q

If we have chronic hypertension and then have a period of super low bp (like 50) what is going to happen

A

the afferent art will try to dilate to bring glomerular pressure up but if it has been constricting for a long time due to chronic HTN, it might not be able to relax

156
Q

If we have a decrease in GFR we are going to have a ______ in reabsorption

A

increase. This is because we have slower filtration so its staying in the tubule longer, which would increase absorption.

157
Q

______ affects the efferent constricting/dilating more so than the afferent art

A

ang 2

158
Q

solutes that are freely filtered but reabsorbed primarily in the PCT will have a ____ concentration in the tubule distal the the PCT

A

low

159
Q

the PCT can be split into ____ segments. what are they

A

3.
S1
S2
S3

160
Q

How is glucose reabsorbed in the S1 segment of the proximal tubule. what %.

A

90% via SGLT 2 pumping 1Na and 1 Glucose. then out the basolateral side via GLUT 2.

Low affinity

161
Q

How is glucose reabsorbed in S2 segment of proximal tubule? what %

A

10% via SGLT1 requiring 2Na for every 1 glucose. then out basolateral side via GLUT 1

high affinity

162
Q

At what point would we reach a transport maximum for glucose

A

a serum glucose level of 300 mg/dL

163
Q

we have a low BP resulting in a reduction in Pcap in glomerulus resulting in a decrease in GFR which means there will be decreased NaCl making it to macula densa.

What is the primary response to this?

A

Increased renin release from JG cells. leading to increased Angiotensin 2.

ultimately constricting the EFFERENT art

164
Q

we have a low BP resulting in a reduction in Pcap in glomerulus resulting in a decrease in GFR which means there will be decreased NaCl making it to macula densa.

What is the secondary response to this?

A

dilation of the AFFERENT art (likely due to NO release)

165
Q

we have a low BP resulting in a reduction in Pcap in glomerulus resulting in a decrease in GFR which means there will be decreased NaCl making it to macula densa.

What is the tertiary response to this?

A

Angiotensin 2…when all is said and done and all is right in the world, it will increase the reabsorption of NaCl and the macula densa will be happy again.

166
Q

where is the macula densa

A

thicky thick ascending limb of the loop of hennessy.

167
Q

almost all drugs will affect the ______ arteriole

A

afferent.

168
Q

what is the angiotensin receptor that is found in the PCT. where are they located

A

AT1. on BOTH the basolateral and apical sides

169
Q

on the basolateral membrane, AT1 receptors will do what?

A

Speed up the rate of the Na/K/ATPase, thereby decreasing intracellular Na

170
Q

What is the most important effect of angiotensin 2 binding to AT1 receptors in the PCT

A

the increase in speed of the Na/K/ATPase

171
Q

What transporter is affected first as a result of the Na/K/ATPase increasing cycling speed after Ang 2 binds to the AT1 receptor in the PCT on the basolateral membrane

A

the intracellular Na will be lower therefore the NHE pump would be pumping faster. pumping Na in and H out (into lumen)

172
Q

What transporter is affected second as a result of the Na/K/ATPase increasing cycling speed after Ang 2 binds to the AT1 receptor in the PCT on the basolateral membrane

A

the Na/HCO3 pump on the basolateral membrane. pumps BOTH Na and HCO3 out into renal interstitum

173
Q

what is transcellular reabsorption

A

reabsorption via channels within the cell membrane

174
Q

what is paracellular reabsorption

A

between cells

175
Q

the paracellular space is held together by ______

A

tight junctions

176
Q

at the PCT, Cl is reabsorbed primarily via _____

A

paracellular route

177
Q

In the PCT, when does Cl reabsorption happen?

A

later on. there is little to no Cl reabsorbed in the first half bc its besties with Na so once Na starts to leave, it follows.

178
Q

Urea is found in abundance in the _____

A

interstitum.

179
Q

what helps promote greater reabsorption in the tubule?

A

brush border.

180
Q

Brush border increases the surface area by _____

A

20X

181
Q

In the PCT, the tubular epithelial cells have a membrane potential of _____.

A

-70mV

182
Q

in the PCT the tubular lumen has a membrane potential of _____

A

-3mV

183
Q

On average _____ proteins are filtered. Of those, _____ are reabsorbed and ______ are excreted in the urine

A

1.8g
1.7g
100mg

184
Q

what is the primary reabsorption process for Na in the PCT?

A

the NHE transporter

185
Q

How is acid base managed in the PCT

A

the whole ass process with CA.
H binds to HCO3
forming H2CO3
carbonic acid breaks this down to
H20 and CO2

186
Q

Glutamine is an ______ produced in the ______. It is used in the tubular epithelial cells of the PCT to produce _______

A

amino acid.
liver.
bicarb

187
Q

glutamine is converted stoichiometrically into two compounds, what are they

A

2 HCO3
2 NH4

188
Q

the 2 NH4 that are produced via the breakdown of glutamine serve what purpose?

A

act as a urine buffer the avoid free H from floating around in the urine

189
Q

What is another buffer for the urine aside from NH4?

A

NaHPO4. protons can bind to become NaH2PO4

190
Q

How is Ca reabsorbed in the PCT

A

via transcellular AND paracellular.

191
Q

what is the apical membrane transcellular route Ca takes in the PCT to be reabsorbed?

A

just a good old Ca channel. It wants to flow in that bitch due to the charge and the concentration gradient

192
Q

what is the basolateral membrane transcellular route Ca takes in PCT to be reabsorbed

A

Ca/ATPase
Na/Ca exchanger (3Na for 1Ca)

193
Q

what monitors the Ca level in the ECF?

A

PTH (parathyroid hormone)

194
Q

if we have low Ca what will 3 things will follow

A

the PTH will
1. increase Vitamin D3 activation (increasing Ca reabsorption)
2. Increase Ca reabsorption by increasing apical Ca channels
3. Increase osteoclast activity (decrease osteoblast activity)

195
Q

what is the short term and long term storage of Ca

A

short: SR
long: bones

196
Q

Organic cations are secreted in the PCT via ____

A

H dependent antiporters.
Cation gets into cell on basolateral side allllll by itself. on apical side the cation is exchanged for 1 H.

197
Q

what are some of the endogenous cations (6)

A
  1. creatinine
  2. ACh
  3. Choline
  4. Histamine
  5. Serotonin
  6. Epi/norepi
198
Q

what are the organic exogenous cations? (6)

A
  1. atropine
  2. isoproterenol
  3. morphine
  4. procaine
  5. quinine
  6. tetraethylammonium (thats a mouthful)
199
Q

How are the organic anions secreted in the PCT?

A

Na-dependent antiporters.
to get into the cell on the basolateral membrane it needs its hand held, unlike the cation.
FIRST. there is a pump on the basolateral membrane that pumps 3Na and 1 aKG into the cell.
THEN the anion can be pumped into the cell (on basolateral membrane) with one of the aKG.
FINALLY it can cross to the tubular lumen all by itself.

200
Q

what is the intermediary that helps anions get tf out?

A

aKG. alpha ketoglutarate

201
Q

what are some of the organic endogenous anions (6)

A
  1. hippurates
  2. bile salts
  3. PGE
  4. uric acid
  5. oxalate
202
Q

what are the organic exogenous anions (4)

A
  1. Furosemide
  2. PCN
  3. ASA
  4. sulfonamides
203
Q

during WW2 alexander fleming found that hippurates added to PCN compound did what?

A

“competitive secretion”. basically if you overwhelm the secretion mechanism with hippurates then you have PCN floating around for longer

204
Q

how much water is reabsorbed in the thin descending loop

A

20%

205
Q

how much water is reabsorbed in PCT

A

65%

206
Q

what transporter is in the thin ascending limb

A

Na/Cl/ATP

207
Q

in the thick ascending limb, Mg and Ca are reabsorbed via paracellular diffusion. this is driven by what?

A

K has leak channels on both the apical and basolateral sides. the increase in K causes the membrane potential to increase. which will drive those big bitches out.

208
Q

what is the membrane potential for the thick ascending limb

A

8mV

209
Q

% of ion reabsorption in:
PCT ____
TAL ____

A

PCT: 65%
TAL: 25%

210
Q

what transporters are in the TAL

A

Na/K/2Cl (1Na/1K/2Cl)
NHE (1Na/1H)
Na/K/ATPase
(Cl and K channels)

211
Q

what is the highest our osmolarity goes? lowest?

A

1200.
50.

212
Q

How is Ca reabsorbed in the DCT

A

apical: Ca channel
basolateral: 3Na/1Ca pump

213
Q

what can influence the rate of reabsorption of Ca on the apical side

A

PTH

214
Q

thiazides block what?

A

the Na/Cl symporter in the DCT

215
Q

what happens if we block the Na/Cl symporter in the DCT?

A

the Na concentration gradient will further be reduced which will increase the Na/Ca exchanger which will increase the rate of reabsorption of Ca

216
Q

How can thiazide diuretics be helpful for patients with osteoporosis?

A

thiazides block the Na/Cl symporter in DCT. with less Na coming into cell, the Na/Ca exchanger will pick up pace because that Na wants to move down its concentration gradient. this will lead to increased reabsorption of Ca.

217
Q

When I say principal, you say _____

A

ALDO

218
Q

Aldosterone increases the reabsorption of ______

A

Na

219
Q

what happens in response to the increased Na reabsorption from aldosterone

A

it will indirectly increase the reabsorption of H2O.
AND it will result in excess K excretion

220
Q

Aldosterone is released from the adrenal glands, the primary effect is ____. The secondary effect is ______. The third effect is _____.

A
  1. increasing Na/K/ATPase
  2. planting additional ENAC (Na coming in)
  3. increasing K channels (K leaving)
221
Q

what two drugs inhibit the ENaC channels

A

triamterene and amiloride

222
Q

_____ is commonly given with triamterene to inhibit K wasting

A

HCTZ

223
Q

aldosterone R antagonists

A
  1. spironolactone
  2. eplerenone
224
Q

Low K excretion:
ROMK is ____
BK is ____

A

ROMK: sequestered
BK: closed

225
Q

Normal K excretion:
ROMK is ____
BK is _____

A

ROMK: open
BK: closed

226
Q

High K excretion:
ROMK is ____
BK is _____

A

ROMK: open
BK: open

227
Q

opening of both ROMK and BK and likely _____ mediated

A

aldosterone

228
Q

Why does K wasting happen?

A

inhibit Na reabsorption anywhere upstream to principal cells = increased Na concentration at principal cells.

this leads to increased Na reabsorption which leads to more K excretion due to the Na/K/ATPase working in overdrive

229
Q

Aldosterone is secreted from the zona glomerulosa in response to ______

A

increased extracellular K

230
Q

How can ang 2 affect aldo release?

A

there are AT1-R on the adrenal glands and when Ang 2 binds, it induces aldosterone secretion.

231
Q

what is RAAA

A

renin angiotensin aldosterone axis

232
Q

what is the enzyme in the principal cells that prevent cortisol from binding to the aldo receptors

A

11 B-HSD Type 2

11 beta-Hydroxysteroid Dehydrogenase type 2

233
Q

What can happen as a result of excess cortisol from a ACTH secreting tumor

A

the 11 B-HSD type 2 becomes overwhelmed, cortisol binds to the aldo receptors, increasing Na and H2O retention and leading to Hypokalemia

234
Q

How can REAL licorice cause hypokalemia

A

11 B-HSD is inhibited. cortisol can bind to the aldo receptors, increasing Na and H2O retention and leading to Hypokalemia

235
Q

Aldo effects on high K.

A

increased aldo release.
increased K secretion

236
Q

Aldo effects on low K.

A

decreased aldo release
decreased K secretion

237
Q

Type A intercalated cells secrete ____ via _____

A

Protons (H+).
H/ATP pump AND K/H/ATP

238
Q

Type B intercalated cells secrete ____

A

HCO3

239
Q

walk through H2O reabsorption in the intercalated cells starting the vaso binding to receptor

A

AVP (arginine vasopressin) binds to V2. they are Gs. ATP —–>cAMP—->activates PKA—-> phosphorylation of AQP2. AQP2 placed on apical membrane allowing H2O to flow in. On basolateral membrane we have AQP3 and 4 that are always open

240
Q

What happens in nephrogenic DI

A

lack of response to AVP. no AQP2 moving to apical membrane for H2O reabsorption

241
Q

Lithium effects on urine

A

reduces expression of AQP2. urinate ~20L/day. urine osmolarity can go down to 50 mOsm

242
Q

affects of alcohol regarding ADH.

A

impairs ADH release from pituitary gland. as well as AVP response by the intercalated cells. thats why we have to pee all the time when we are getting litty for schmidty at Joes

243
Q

High osmolarity will _____ ADH

A

stimulate ADH release

244
Q

osmoreceptors stimulate two areas within the hypothalamus. what are they

A
  1. supraoptic nucleus
  2. periventricular nucleus
245
Q

supraoptic nucleus is located ______. It is responsible for ______ of our ADH release

A

above the optic nerve.
5/6

246
Q

Periventricular nucleus is located _____. It is responsible for _____ of our ADH release

A

either side of the 3rd ventricle.
1/6

247
Q

both the supraoptic nucleus and the periventricular nucleus delivery ADH to the _____

A

posterior part of the ballsack. neurohypophysis

248
Q

osmoreceptors have _____ membranes.

A

semipermeable

249
Q

If the osmoreceptors are exposed to hypotonic conditions what happens

A

ADH inhibited.
AP’s slow down

250
Q

If osmoreceptors are exposed to hypertonic conditions, what happens

A

ADH released.
AP’s pick up speed

251
Q

How would the baroreceptors stimulate ADH release

A

if they have slow signaling (d/t low BP)

252
Q

urea is reabsorbed in the collecting duct via

A

UT-A1 and UT-A3

253
Q

Urea is secreted via ____ back into the tubule in the thin loop of henle

A

UT-A2

254
Q

Why is ADH the primary controller of osmolarity

A

it is the only hormone that controls water reabsorption and water reabsorption ONLY.

255
Q

Caffeine can take ADH offline causing _____

A

increased Na concentrations

256
Q

what can decrease thirst (5)

A
  1. decreased plasma osmolarity
  2. increased blood volume
  3. increased BP
  4. decreased Ang 2
  5. gastric distention
257
Q

what can increase thirst (5)

A
  1. increased plasma osmolarity
  2. decreased blood volume
  3. decreased BP
  4. increased Ang 2
  5. dryness of mouth
258
Q

what can decrease ADH (4)

A
  1. decreased plasma osmolarity
  2. increased blood volume
  3. increased blood pressure
  4. Drugs (alcohol, clonidine, haloperidol)
259
Q

what can increase ADH (6)

A
  1. increased plasma osmolarity
  2. decreased blood volume
  3. decreased blood pressure
  4. nausea
  5. hypoxia
  6. drugs (morphine, nicotine)
260
Q

if we chug 1L of water, what happens in regard to:
1. ADH
2. Urine osmolarity
3. plasma osmolarity
4. urine flow rate
5. urinary solute secretion

A
  1. ADH secretion is reduced
  2. urine osmolarity drops (becomes more dilute)
  3. plasma osmolarity stays nearly the same
  4. urine flow rate increases
  5. solute secretion remains nearly constant
261
Q
A
262
Q

In regard to potassium:
Insulin causes____

A

Hypokalemia

263
Q

In regard to potassium:
Aldosterone causes _____

A

Hypokalemia

264
Q

In regard to potassium:
Beta-adrenergic stimulation causes _______

A

Hypokalemia

265
Q

In regard to potassium:
Alkalosis =

A

Hypokalemia

266
Q

In regard to potassium:
Insulin deficiency (DM) =

A

Hyperkalemia

267
Q

In regard to potassium:
Aldosterone deficiency =

A

Hyperkalemia

268
Q

Addisons diseases causes

A

Aldo deficiency——>hyperkalemia

269
Q

In regard to potassium:
Beta-adrenergic blockade =

A

Hyperkalemia

270
Q

In regard to potassium:
Acidosis =

A

Hyperkalemia

271
Q

In regard to potassium:
Cell lysis =

A

Hyperkalemia

272
Q

In regard to potassium:
Strenuous exercise =

A

Hyperkalemia

273
Q

In regard to potassium:
Increased ECF osmolarity =

A

Hyperkalemia

274
Q

ACUTE metabolic alkalosis causes _____ k secretion (increased/decreased)

A

Increase. Only with acute. Once the body figures out that it’s turning into a basic bitch (bc of the alkalosis) it’s gonna keep the K around.

275
Q

Excretion rate formula

A

Concentration of substance in urine * urine flow rate

276
Q

Reabsorption rate formula

A

Filtered load - excretion rate

(Filtered load = GFR * plasma concentration)
(Excretion rate = concentration in urine * urine output)

277
Q

Secretion rate formula

A

Excretion rate - filtered load

(Filtered load= GFR * plasma concentration)
(Excretion rate = urine concentration * UOP)

A&P Fall 24 Final (1 decks)

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