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Physiology > Exam 13: April 17-24 > Flashcards

Exam 13: April 17-24 Flashcards

1
Q

what is inside alveoli?

A

air that diffuses out into the circulatory system

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2
Q

what are alveoli?

A

alveoli are chambers within the lungs surrounded by the circulatory system capillaries to do exchange

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3
Q

what are the characteristics of alveoli?

A

they create lots of surface area and have very thin walls because of diffusion

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4
Q

what are the types of alveoli cells?

A

type I and type II

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5
Q

what are type I alveolar cells?

A

gas exchange

thin cells that reduce distance for diffusion and also have big surface area

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6
Q

what are type II alveolar cells?

A

surfactant

they look like regular cells, don’t have extra surface area or decreased distance

they keep alveoli open

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7
Q

why do we need type II alveolar cells?

A

water from your body is pushing on air so not much hydrostatic pressure is needed to take out Type I cells since they won’t be able to withstand water inside your body

so you somehow need to keep air bubbles from collapsing on themselves from push of water which is what Type II cells do

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8
Q

what do type II cells produce?

A

a blue film aka surfactant which allows air bubbles to withstand hydrostatic pressure

helps out the type I cells by decreasing surface tension

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9
Q

what is surfactant?

A

it’s a soapy solution secreted by type II cells to ensure that alveoli don’t collapse

it’s reduces surface tension and allows air bubbles to last

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10
Q

what cells in babies respiratory systems are not developed?

A

immature babies don’t have developed Type II cells so they would breath in air and their alveoli would collapse

so to help them, they gave them a soapy solution until their Type II cells develop to maximize surface area

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11
Q

what is the effect of having undeveloped type II cells?

A

reduced surface area of alveoli because they are collapsing

reduced surface area means not enough oxygen exchange so the body isn’t making enough ATP

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12
Q

what are the limits of the thoracic cavity?

A

ribs on the sides and the top

diaphragm on the bottom of the thoracic cavity

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13
Q

what are the contents of the thoracic cavity?

A

the lungs and heart

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14
Q

what controls the size of the thoracic cavity?

A

intercostal muscles and diaphragm

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15
Q

what do the intercostal muscles do?

A

they control the position of your ribs

they don’t move your lungs, they move your skeleton! aka the ribs

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16
Q

what does Bronson want to open when she retires?

A

an intercostal restaurant

when you’re eating ribs you’re actually eating intercostal muscle!

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17
Q

what type of muscle are the intercostal muscle and diaphragm?

A

skeletal!!

we have control over our breathing aka it’s under somatic control

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18
Q

how come we don’t have to think about breathing even though our intercostal and diaphragm aren’t under autonomic control?

A

we can control skeletal muscles with reflexed!

so we don’t always have to control these muscles through the motor cortex, we can do it through the spine

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19
Q

what is the pleural sac?

A

it’s a water-filled balloon around the lungs

it’s a super thin film

it has two walls: one associated with the thoracic cavity and another wall associated with the lungs

in between the two walls is fluid

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20
Q

what are the parts of the pleural sac?

A

the parietal pleura and the visceral pleura

in between the parietal and visceral pleura is pleural fluid that serves to prevent friction between the two layers

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21
Q

what is the parietal pleura?

A

it’s the outside wall of the pleural sac connected to the thoracic cavity

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22
Q

what is the visceral pleura?

A

it’s the inside wall of the pleural cavity connected to the lungs

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23
Q

what are the lungs attached to?

A

the visceral and parietal pleural are layers/lining around the lungs so the lungs themselves aren’t attached to the ribs

the lungs are indirectly attached to the bones since your bones are connected to the parietal pleural

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24
Q

what is the purpose of the pleural fluid?

A

water is polar so the hydrogen bonds make water cohesive and fluid which allows for movement transfer

when you move the parietal pleural (since it’s attached to your ribs) the pleural fluid transferred the movement and passed it along to the visceral pleura

if you put too much water or you put in the pleural cavity then the two walls will move separately

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25
Q

what happens to a cold bottle and coaster on a hot day?

A

to drink something cold in the nice weather, your drink probably sweated and stuck to the coaster so you pick up both the bottle and the coaster because you created a thin film of water and the cohesiveness of the water was strong enough to pick up the coaster

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26
Q

what happens if you rupture the pleural sac?

A

if one of the walls is damaged, you can get air coming in which means the two walls will move separately from each other

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27
Q

what is a pneumothorax?

A

it’s a collapsed lung

this means a disconnect from our ability to move both walls of the pleural cavity at the same time

someone with pneumothorax will have a ribcage that’s moving fine but there won’t be convection because lungs wont be moving with the rib cage

no convection

this is not the same as collapsed alveoli

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28
Q

what happens if there’s collapsed alveoli?

A

pneumothorax and collapsed alveoli are not the same

you can still have convection with collapsed alveoli because your lungs are still moving

collapsed alveoli just means lost surface area

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29
Q

what does air pressure depend on?

A

1) temperature

2) gases present

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30
Q

how does air pressure depend on temperature?

A

we change the temperature of the air and by the time it gets to alveoli, it’s down to body temperature

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31
Q

how does air pressure depend on the gases present?

A

“n” matters

air is a mixture of gases and it’s not just oxygen so we have to pay attention to which gases are present and at what level

we can add pressures of individual gases to get total pressure so each gas has a partial pressure

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32
Q

what gases are present in the air and at what partial pressures?

A

N2 = 79%

very little CO2 and H2O

P(O2) = 21% or 160 mmHg

P(CO2) = 0.3 mmHg

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33
Q

how do gases diffuse?

A

gases diffuse from high to low partial pressure

gases can also diffuse into and out of liquids

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34
Q

how do we do gas exchange between alveoli and the circulatory system?

A

exchange between alveoli and circulatory system is based on partial pressure of blood entering the lungs and the partial pressure of the air in the alveoli

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35
Q

what is the partial pressure of gases in the blood entering the lungs? how about the air in the alveoli? what will happen?

A

blood entering lungs:
PCO2 = 46 mmHg
PO2 = 40 mmHg

blood coming to the lungs is deoxygenated

air in alveoli:
PCO2 = 40 mmHg
PO2 = 105 mmHg

CO2 will diffuse out of the blood and into the lungs while the O2 will diffuse out of the alveoli and into the lungs due to the partial pressure gradients

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36
Q

is the partial pressure of gases in the alveoli the same as the composition of air?

A

no

when you squeeze air out of the lungs, we can never have zero air in the lungs

we take the air that we did the exchange with and pushed most of it out and then brought in fresh air so the numbers are an average

numbers will drop for oxygen and rise for CO2 because we’re mixing remnants of old air with new air

the only time the numbers will match is your very first breath

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37
Q

what is the source of the control of ventilation?

A

skeletal muscles so that we can control our breathing via our cerebral cortex

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38
Q

what part of your brain is devoted to breathing?

A

respiratory rhythm generator (RRG)

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39
Q

where is the respiratory rhythm generator located?

A

the medulla oblongata in your brainstem

your brainstem controls all the keys to life like setting up a base heart rate and breathing and digestion

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40
Q

what are the inputs to the respiratory rhythm generator?

A

1) pacemaker potentials
2) chemoreceptors
3) pulmonary stretch receptors

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41
Q

what input to the RRG do pacemaker potentials give?

A

if everything stayed as is, you would keep at a steady pace in breathing and the pacemaker potentials set this rate however, things usually change and you have to breath faster or slower sometimes

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42
Q

what input to the RRG do chemoreceptors give?

A

they register O2, CO2 and H+ levels that tell you if you need to breath more or less to get to the right levels in your blood

this is afferent input

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43
Q

what input to the RRG do pulmonary stretch receptors give?

A

further afferent input because you can’t overstretch your lungs or else they’ll pop because you can’t overinflate

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44
Q

what is the chain of events when you breath in?

A

stimulate –> contract –> expansion –> inspiration

Shortening of intercostals moves ribs to create more space

the diaphragm runs from one side of the rib cage to the other so the diaphragm drops down to make the thoracic cavity bigger

so now we’ve made lung volume bigger because your pleural sac changed the size of the lungs in the process of intercostal contraction

increased lung volume means the pressure inside your lungs drops compared to the outside of your body so air comes into your lungs = follows pressure gradient from high to low

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45
Q

what is the chain of events when you breath out?

A

no stimulation –> relax –> rebound –> expiration

you stop sending stimulation to muscles to contract so that they relax which causes rebound which gets space to become smaller

if volume goes down then pressure goes up relative to the outside of your body so air goes out and you exhale

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46
Q

how can you change the amount of air in your lungs?

A

we can change the amount of air coming in by changing pressure gradient by changing volumes that we create

we can inhale more by stimulating longer or we can exhale more by stopping stimulation

duration of stimulation or non stimulation sets size/amount of air

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47
Q

what is the limit of how much you can inhale?

A

if you try to inhale too much you’ll inhale then get a quick exhale

you’ve activated stretch receptors and they tell you to stop because you don’t want to blow out the lungs

the stretch receptors cause inhibition on motor neurons that control the diaphragm and intercostal muscles and cut the stimulation so your muscles relax and you get expiration

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48
Q

what happens if you raise the pressure outside your body so that your lungs get a lot of stimulation from outside rather than yourself?

A

pulmonary stretch receptors will go off if there’s a very large inhale and inhibit motor neurons that control intercostal/diaphragm usuallyyy

but if the pressure outside your body is so big that your lungs are being stimulated to expand from something other than your body….air will come in because it’s not ht lungs controlling it

the pulmonary stretch receptors will go off and tell you to exhale but the pressure outside is telling you to inhale

this is why in an explosion, the purpose of the bomb was to create high enough pressure area that it actually blew the people’s lungs out from the inside: you should close your nose and not breath in

another situation is using an adult bag on a little kid during CPR but you could blow out their lungs because you’ve created a pneumothorax

GO LISTEN TO LECTURE

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49
Q

what is the tidal volume?

A

how much air you move in one breath

analogous to stroke volume

tidal volume varies from resting to vital capacity

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50
Q

what are the limits of tidal volume?

A

minimum TV = resting (500 mL)

maximum TV = vital capacity (5 L)

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51
Q

what is the vital capacity?

A

maximum TV

this is the maximum that you can accomplish aerobically

if you need more than this you’re in trouble

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52
Q

what is the equation for vital capacity?

A

VC = IRV + TV + ERV

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53
Q

what is the expiratory reserve volume?

A

ERV

maximal volume of air, usually about 1000 milliliters, that can be expelled from the lungs after normal expiration

if we exhale more, we’re using the reserve

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54
Q

what happens as you increase your tidal volume?

A

as we increase TV towards our vital capacity, we’ll end up using one or more of our reserve; we either have to inhale or exhale more

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55
Q

what happens at the vital capacity?

A

IRV and ERV are being used and their size at their maximum

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56
Q

What happens if tidal volume = vital capacity?

A

then IRV and ERV are at zero because you’ve used them all up

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57
Q

what is the inspiratory reserve volume?

A

IRV

the maximal amount of additional air that can be drawn into the lungs by determined effort after normal inspiration

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58
Q

can you change your vital capacity short term?

A

no

between today and tumor you can’t change it

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59
Q

can you change your vital capacity long term?

A

yes

how much you inhale/exhale depends on skeletal muscles

you can also stop training and decrease vital capacity by letting muscles atrophy

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60
Q

what is residual volume?

A

this is the minimum amount of air that we can never get out of the lungs

we can’t put all the air out of our lungs, we’ll always have air left in the lungs

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61
Q

why do always have air left in your lungs? aka why do you have a residual volume?

A

bronchioles that are part of conducting part of respiratory system that have low resistance to air flow and you can’t close your bronchioles so you have space there

your alveoli have paper thin walls but you don’t want walls to mush against each other because they’ll stick and rip so you can get alveoli smaller but not completely collapsed which is why you have air left in the lungs

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62
Q

can you change residual volume?

A

?

probably

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63
Q

is O2 dissolved in the blood?

A

dissolved, but poorly

oxygen is small and nonpolar but your blood is polar

the measurement that the doctor takes is only measuring the 1% of oxygen in your blood that is free, the 99% isn’t being detected

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64
Q

what oxygen level does your doctor measure?

A

the 1% free oxygen in your blood

99% isn’t being measured because it’s reversibly bound to Hb in RBC

this is the reason we can have a polar environment moving our key nonpolar gas because we effectively give it a plasma binding protein

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65
Q

what is the structure of hemoglobin?

A

4 identical subunits that all have heme which needs Fe to share electrons with oxygen and allow it to bind

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66
Q

how does Hb carry oxygen?

A

each Hb carries 4 oxygens

the oxygen reversibly binds with Fe and shares electrons

it doesn’t give up electrons because covalent bonds are a lot harder to break and we need oxygen to pop off Hb once it gets to tissues

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67
Q

how is cooperativity expressed in Hb?

A

oxygen is binding at each subunit and binding is dependent on shape and charge; each subunit has specificity for oxygen

once one oxygen binds, the affinity for oxygen increases at the other subunits

we bind and change the shape of one subunit, it will change the shape of all the other 3 subunits and increase affinity for oxygen and make it more likely for oxygen to bind

then once an oxygen binds to the second subunit, the affinity in the remaining two, again increases

then, if one oxygen comes off, it lowers the affinity in the other three spots and they’re more likely to come off so both loading and unloading happen quickly

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68
Q

how does hemoglobin increase the amount of O2 transferred to tissues?

A

Hb helps increase amount of O2 transferred by aiding diffusion by maintaining a large diffusion gradient

there’s 8 oxygens in the blood and the in the air so the gradient is gone; if we put Hb in the blood, 6 oxygen will be attached to Hb so now the gradient is reformed since we’re only looking at the free oxygen

there’s 8 oxygen in the lungs but 2 in the blood so we’ve recreated the gradient = oxygen will move into the blood and Hb will continue to grab oxygen due to cooperatively and you end up being able to move 14/16 oxygen into the blood!

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69
Q

what factors affect Hb affinity for O2?

A

1) CO2
2) H+
3) DPG
4) CO
5) temperature

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70
Q

how does CO2 affect Hb affinity for O2?

A

binding of CO2 causes decreased affinity for O2

changes affinity by changing shape of Hb so that it can’t hold on to oxygen but doesn’t actually interfere at the site

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71
Q

how does H+ affect Hb affinity for O2?

A

binds and shape changes and decreases affinity for O2

changes affinity by changing shape of Hb so that it can’t hold on to oxygen but doesn’t actually interfere at the site

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72
Q

how does temperature affect Hb affinity for O2?

A

T changes shape of proteins

heating Hb decreases O2 affinity

changes affinity by changing shape of Hb so that it can’t hold on to oxygen but doesn’t actually interfere at the site

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73
Q

how does DPG affect Hb affinity for O2?

A

key component in glycolysis

if glycolysis is occurring, there’s DPG in the system

DPG binds to Hb and decreases O2 affinity

changes affinity by changing shape of Hb so that it can’t hold on to oxygen but doesn’t actually interfere at the site

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74
Q

how does CO affect Hb affinity for O2?

A

this one does interfere at the actual site

it has the appropriate shape and size to bind at oxygen’s binding site so it’s a competitor

it’s an antagonist because it replaces oxygen

CO has a higher affinity than O2 which starts dropping 99% number

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75
Q

does CO or O2 have a higher affinity for Hb?

A

CO

it binds to Hb better

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76
Q

what is on the axis of the Hb saturation curve?

A

% saturation of Hb vs. P(O2)

direct relationship

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77
Q

what relationship is there between the % saturation of Hb and the partial pressure of O2?

A

direct relationship

increasing partial pressure of oxygen increases % saturation of Hb

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78
Q

what % saturation of Hb is there in the lungs?

A

the partial pressure is around 100 so we’ll have fully saturated in Hb since [O2] is so high

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79
Q

what % saturation of Hb is there coming back to our lungs?

A

partial pressure is around 40 mmHg so we’re at about 80% saturation since our tissues are taking oxygen

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80
Q

what is the venous reserve?

A

it’s the amount of oxygen associated with Hb returning to the heart and going to return to the lungs (it can be tapped into)

our pick up location is around 100% but drop off location is lower than 100% which means that oxygen got dropped off at tissues = partial pressure of free oxygen is lower

but nearly 80% of Hb is still loaded with oxygen from the last pass around!

there’s oxygen coming back to the heart and out to the pulmonary system that is from the last cycle = venous reserve

Lots of Hb take the whole loop and never offload their oxygen – this is referred to as the venous reserve

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81
Q

what’s the point of hands only CPR?

A

to tap into the venous reserve!

we just need to get convection going and we’ll get venous reserve activated and we don’t need any new oxygen to be transferred over, we just need the oxygen already on the Hb to get transferred to the tissues

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82
Q

can P(O2) = 0?

A

you cells can have a partial pressure of zero but your blood cannot

if our blood has zero free oxygen in it and your cells have any oxygen in them, then the oxygen will follow gradient and go from cells to the blood

so the only time your blood has a partial pressure of zero is if you cells have zero oxygen and if that’s true, you’re dead because neither your cells or blood have oxygen

so your blood can’t have zero P(O2) but your cells can have P(O2) of zero like during anaerobic conditions which run off of glycolysis

so the cells for a little while can have P(O2) =0 which will help us drive oxygen towards those cells because of the gradient

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83
Q

is CO2 soluble in the blood?

A

it’s a little more soluble than O2 because it’s not as non polar

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84
Q

how much free CO2 is there in the blood?

A

about 10%

compared to only 1% free O2 in the blood

85
Q

how much CO2 is carried on Hb?

A

CO2 can bind to Hb so 30% of CO2 is carried on Hb

when CO2 binds it lowers Hb affinity for oxygen

86
Q

where is the rest of the CO2 in the body?

A

we convert it to HCO3-!

CO2 is waste so we don’t care if we change it and we don’t need it to do anything so it’s okay if we do a chemical reaction with it

CO2 + H2O ←→ HCO3- + H+ (equation 3)

87
Q

why do we want HCO3- in our blood?

A

we want bicarbonate in our blood because HCO3- is polar so it’s soluble in the plasma which can be transported a lot more easily

88
Q

what kind of system is plasma?

A

plasma is a buffered system

buffered system means that if you pour acid or base into it and measure it’s pH, it doesn’t really change

if the blood wasn’t buffered we wouldn’t be able to have 60% transport of CO2

89
Q

what help to make plasma a buffered system?

A

Hb and albumin help make plasma a buffered system by binding H+ so then the reaction will shift right towards bicarbonate

because we keep pulling out H+ we make high levels of HCO3- possible

90
Q

do veins or arteries have higher pH?

A

venous pH < arterial pH

veins are more acidic than arteries

we’re still going to be having some H+ created when our tissues make CO2 waste from glycolysis so the blood associated with our venous side will decrease in pH as H+ increases

equation 3 happens in the tissues

so we’ll see a slightly more acidic pH in venous side than arterial side

91
Q

why do arteries have a higher pH?

A

we’re offloading CO2 at the lungs

this means we need to run the equation towards the left

CO2 is moving out of our plasma and into lungs so it’ll shift the equilibrium to the left which turns more HCO3- into CO2

H+ levels decrease which increases pH

92
Q

what factors influence the ventilation rate?

A

pacemakers and chemoreceptors

93
Q

do oxygen levels impact ventilation rate?

A

there’s no change in ventilation rate regardless of oxygen levels as long as it’s above 60 mmHg = intensive above 60 mmHg

when O2 levels drop below 60 mmHg then you see increased ventilation rate

60 mmHg is where you start to see a significant drop in saturation on the Hb binding curve

94
Q

what type of O2 do chemoreceptors measure?

A

they aren’t responsive to bound O2, they just measure free O2**

CO binds and replaces O2 so the free doesn’t change so the ventilation doesn’t change

HOW IS THIS POSSIBLE

95
Q

what is the sensitivity of chemoreceptors to CO2?

A

they’re sensitive to small changes in CO2 levels in blood will have immediate changes in respiration rate

increased CO2 levels in blood = increased respiration rate

96
Q

what happens to the respiratory rate at super super high levels of CO2?

A

you drop to zero respiration rate because the CO2 that is not really high in the blood has now impacted and killed our neurons of which some control our respiratory rhythm generators so we can no longer control our respiration and we stop breathing

no ventilation rate at very high levels of CO2 like killing mice in lab

97
Q

what do chemoreceptors in the respiratory system respond to?

A

1) unbound O2
2) CO2
3) H+

98
Q

what happens is there’s high levels of H+?

A

ventilation rate will increase

99
Q

what happens during anaerobic conditions to ventilation rate?

A

under anaerobic conditions we only run glycolysis which makes lactic acid which moves out of muscles and into blood so we’re acidifying blood and raising H+ concentration when we’re doing anaerobic activity

this is why we breathe harder when we’re exercising hard

you get rid of CO2 so the equilibrium shifts left to get rid of H+

100
Q

what is metabolic acidosis?

A

anaerobic exercise

the metabolism has created an acidity problem in our blood via anaerobic glycolysis (lactic acid build up in the blood)

we need to correct this by decreasing H+ by breathing off CO2 and increasing VR

101
Q

what is metabolic acidosis? what causes it?

A

vomiting is bringing up stomach content

the stomach is acidic so we’re bringing out all the acid

we need to replace this acid after you vomit and this acid comes from the blood

so after you vomit, your blood pH increased = metabolic alkalosis

102
Q

what happens if you anaerobically exercise too much?

A

if you stay anaerobic for a long time you’ll start to feel nauseous like during a super hard practice

your body is getting put into metabolic acidosis and telling the individual to slow down

the body’s only recourse is to vomit to try to get rid of acid since breathing harder isn’t doing enough to remove H+

103
Q

what are ventilation rate issues attributed to?

A

CO2 issues make you have either too high or low of a rate a problem

104
Q

what is hypoventilation? what condition does it lead to?

A

Individual isn’t breathing off enough CO2 so CO2 goes through the heart and back into the system so CO2 goes into arteries

now due to equilibrium shift you’ll have increased H+ and decreased pH

you’re sending your tissues a higher H+ concentration of blood

since it’s a respiratory cause for this acidosis problem it’s referred to as respiratory acidosis*

105
Q

why is respiratory acidosis a problem?

A

arterial pH is lower since CO2 levels are high and shifting equilibrium to the right

decreased pH is a problem because proteins work best and physiological pH so low pH means they can’t do they’re job

Hb is impacted by H+ and will kick off O2 when it binds H+ which is bad because you’re trying to deliver O2 to tissues in the arteries

106
Q

what is hyperventilation? what condition does it lead to?

A

too much CO2 is being taken out of the system

arterial P(CO2) is decreased so there’s an increase in pH

respiratory alkalosis

107
Q

why is respiratory alkalosis a problem?

A

causes protein issues because again, you’re out of physiological pH range

increased O2 on Hb which can be bad because then delivery rate is lower since Hb is holding onto oxygen too well and won’t deliver it when it gets to the tissues

108
Q

what is hypoxia?

A

O2 deficiency in tissues

every single person will die of some type of hypoxia essentially

109
Q

what is hypoxic hypoxia?

A

insufficient O2 intake

you’re not getting enough O2 from in front of you into alveoli

could be that you’re in a low oxygen environment like high altitudes or it could be that you’re having a problem with convection (you have a pneumothorax or you’re choking

if you don’t get enough to alveoli, you don’t have enough O2 to arteries to our tissues

110
Q

what is anemic hypoxia?

A

you get oxygen to blood just fine but there’s something wrong with your RBC

normal partial pressure of free O2 in the blood

all the anemia types you learned about contribute to anemic hypoxia because the O2 amount bound to Hb is not where it’s supposed to be so tissues aren’t getting enough O2

111
Q

what is ischemic hypoxia?

A

insufficient blood flow to deliver O2

individuals that have heart attacks or strokes actually died because of ischemic hypoxia

112
Q

what is histotoxic hypoxia?

A

cell toxic hypoxia

cells are unable to use O2

we get the oxygen to the tissues but there’s something wrong with the mitochondria that they can’t use the oxygen

113
Q

what kind of hypoxia do spies in movies experience when they pop a cyanide pill?

A

if spies don’t want to give up information they take a cyanide pill and die of histotoxic hypoxia since cyanide actually prevents ETC from finishing the process and takes all mitochondria off line and your whole body can’t run on glycolysis alone

114
Q

what is the primary function of the renal system?

A

regulate water and ions in the blood

115
Q

what is the secondary function of the renal system?

A

1) get rid of wastes and toxins in the blood
2) endocrine and enzyme production (RBC, Ca, Na)

kidney makes EPO which helps with RBC production, kidney makes enzymes that help with Ca regulation etc.

116
Q

what’s the problem with your kidneys filtering out toxins and wastes in the blood?

A

your kidney’s don’t recognize most drugs as something that should stay in your so your kidneys filter them right out and they end up in your urine

this is how drug tests works

117
Q

what kind of filtration does your kidney do?

A

size filtration, period, there’s no other kind

it doesn’t matter what it is;
if it’s smaller than a protein, it will go out into the kidneys and get filtered out

uh this is a problem because water, AA, Na, K, Ca, glucose are all smaller than a protein

but not to fear the kidney has reabsorption techniques to bring them back into the body

urea is smaller than a protein but that’s fine, we usually don’t want it

118
Q

what stuff gets reabsorbed into the kidney?

A

the “good” stuff is returned

what’s good depends on your current status

are you in a good range?

daily loss = daily intake

ex. if your BP is really high then you want to lose H20
ex. if Na levels are really high you want to get rid of Na

119
Q

what does your kidney adjust for?

A

your kidney is the biggest player in making sure intake = loss!!

your kidney makes adjustments for diet, environment, activity to make sure you have a proper daily output

ex. if you bring in more water than you pee out, you’re overhydrated and vice versa if you lose more water than you bring in = dehydrated

120
Q

what is the functional unit of the kidney?

A

nephron

121
Q

what is the renal pelvis?

A

part of the kidney that collects urine so that it can be sent out via one vessel, the ureter

all the nephrons empty urine into the renal pelvis

122
Q

what are the parts of the renal system?

A

1) kidney (2)
2) ureter (2)
3) bladder (1)
4) urethra (1)
5) sphincter muscles (2)

123
Q

what are the components of the urethra?

A

1) internal urethral sphincter

2) external urethral sphincter

124
Q

what is the internal urethral sphincter? what controls it?

A

part of the urethra

a ring of muscle that we can squeeze closed and cut off all flow from the vessel

under sympathetic control

the SNS is always keeping IUS closed because even though you’re kidney is making urine right now, you’re not peeing on the chair in class

you don’t have to think about not peeing because you’re under sympathetic control in the autonomic nervous system

125
Q

what is the external urethral sphincter? what controls it?

A

part of the urethra

skeletal muscle (somatic control) because you have control to when you urinate aka you’re potty trained

you don’t go just because the autonomic tells you to go, it’s under somatic control

126
Q

what happens in the bladder when you have to pee?

A

bladder fills because you’re constantly making urine but the sphincters are kept closed so you don’t leak urine at all times

you have stretch receptors (mechanoreceptors) that register a larger “n” so there’s also an increase P and an increased stretch on the muscle which tells you need to empty bladder and decrease V = empty bladder

mechanoreceptors provide this information

127
Q

what happens in an unpotty trained individual?

A

the bladder starts contracting under PNS control

this means decreased volume and increased pressure and they just pee when their body tells them it’s time

they can’t hold it

128
Q

what are the parts of the kidney?

A

cortex = outside; above the blood vessels

medulla = inside; below the blood vessels

129
Q

what is the ureter?

A

each kidney has a ureter

each kidney has a renal pelvis which collects urine and send it out via the ureter vessel

the ureter then sends urine to the bladder

130
Q

what is the bladder?

A

it’s smooth muscle controlled by the parasympathetic nervous system

receives urine from the ureter

131
Q

are the sphincters in the urethra open or closed?

A

the sphincters are kept closed

sympathetic keeps internal closed

somatic keeps external closed

132
Q

what is micturition?

A

urine exiting the body

133
Q

what are the components of the nephron?

A

1) renal corpuscle

2) tubules

134
Q

what does the renal corpuscle do?

A

it’s part of the nephron in the kidney where we actually do the filtering of the blood

135
Q

what are the components of the renal corpuscle?

A

1) glomerulus

2) bowman’s capsule

136
Q

what does the glomerulus do?

A

it’s part of the renal corpuscle in the nephron

it’s the part of the vascular system that is associated with the nephrons that allows for filtering of the blood to happen

137
Q

how does the glomerulus filter flood?

A

via fenestration

spaces between endothelial cells that is size dependent*

it has openings/holes in the endothelial layer rather than tight connections

138
Q

does everything that get filtered in the blood get excreted?

A

no

GFR = 180 L/day exiting your blood and going into your kidney

urine production = 1.8 L/day

aka the kidney’s bring back a lot of stuff that doesn’t go into the collecting duct

we need to reabsorb a lot of stuff

139
Q

what is the bowman’s capsule?

A

part of the renal corpuscle in the nephron of the kidney

it’s the “catch” component that has tubules coming off of it that runs through the rest of the nephron

once you’ve left the blood, you’ve actually left the body: the original kidney was just the blood vessels on the surface but we realized it was better if we brought the kidney back in

so the tubule walls are actually made of epithelial cells because we can actually take a device and put it through your urethra all the way up without breaking a single cell

140
Q

what are tubules?

A

a component of the nephron

141
Q

what types of tubules are there in the nephron?

A

1) PCT
2) loop of henle
3) DCT
4) CD

142
Q

what is the PCT?

A

proximal convoluted tubule in the nephron

it’s the first tubule after the Bowman’s capsule

whatever came out of the Bowman’s capsule was whatever was able to fit out via size filtration so we lost some good things

active transporters bring back glucose, AA, Na, and water

143
Q

why don’t we urinate 180 L a day even though that’s how much the kidney is filtering each day?

A

the proximal convoluted tubule has active transporters that bring back glucose, AA, Na and other “good” stuff

as we create gradients by bringing things back, we also bring water with them and this is why we don’t urinate 180 L a day

144
Q

where is the PCT located?

A

in the cortex of the kidney

145
Q

what happens if the transporters in the PCT are saturated?

A

the PCT reabsorbs good things that were filtered out in the bowman’s capsule via active transporters

if the transporters are saturated aka we have too much sugar in our system, you see too sugar in the urine because it wasn’t pulled back in

146
Q

where is the loop of henle located?

A

the medulla of the kidney

147
Q

what are the parts of the loop of henle?

A

ascending and descending limb

148
Q

what does the descending limb of the loop of henle do?

A

has aquaporins that allows water to move out of descending limb and come back into us

reabsorbs water via aquaporins

149
Q

what does the ascending limb of the loop of henle do?

A

has transporters that allow Na to come back in and be kept

150
Q

what is the DCT?

A

distal convoluted tubule of the nephron

it fine tunes what we have in the filtrate

don’t need to know anything else for this class

it comes up right next to the renal corpuscle, right next to the glomerulus side

151
Q

what’s special about the collecting duct?

A

part of multiple nephrons because it collect from multiple nephrons

everything else we’ve seen is only part of one nephron

152
Q

where is the collecting duct located?

A

both the medulla and the cortex

everything else has been only part of one

CD collects in the cortex and then moves through the medulla

153
Q

what impacts the collecting duct?

A

ADH impacts kidney in the CD

if ADH is present, CD will allow water to be reabsorbed

if there’s no ADH then water will stay in collecting duct and we’ll produce more urine

154
Q

under what conditions would be reabsorb urea?

A

sometimes we reabsorb urea in the CD sometimes because the only way we can get water to come back is to pull something else back so that it follows the osmolarity gradient

155
Q

when do you get rid of H+?

A

in the collecting duct

another way to get rid of H+ other than the lungs is dumping it into the urine

but you don’t want to do it too early in the system because low pH can damage proteins like the transporters and aquaporins so you dump the H+ as late as possible to limit damage to the other tubules

156
Q

what symptoms will a person with acidosis have?

A

they will breath more to get rid of CO2 and shift the equation left = decrease H+

they will also have more acidic urine

157
Q

where can water exit the kidney?

A

the descending limb of the loop of henle

water cannot exit the ascending limb

158
Q

where can Na exit the kidney?

A

in the ascending limb of the loop of henle

Na cannot exit in the descending limb

159
Q

where is the countercurrent multiplier?

A

the loop of henle in the kidney

160
Q

what happens in the countercurrent multiplier?

A

1) flow from the PCT comes down descending limb - osmolarity is 300 inside and outside the tubule so lumen osmolarity = IF osmolarity and there’s no driving force for diffusion
2) flow reaches ascending limb and NaCl is pumped into IF so IF increases in osmolarity and lumen osmolarity decreases
3) new flow enters descending limb at 300 osmolarity and water will move out of the tubule via aquaporins since you’ve created a gradient and IF has increased osmolarity
4) continual new flow allows the process to repeat so that the osmolarity in the IF in the medulla increases more and more

161
Q

what is lumen osmolarity?

A

osmolarity inside the tubule

162
Q

when do you first see changes in the osmolarity of the lumen?

A

the ascending limb

NaCl can be pumped out of the tubule into IF

163
Q

when does the lumen osmolarity change?

A

lumen osmolarity:

increases in the descending limb

decreases in the ascending limb

164
Q

where is the IF in reference to the loop of henle?

A

the IF is in the medulla

165
Q

what would increase the osmotic gradient created by the loop of henle?

A

a longer loop of henle

166
Q

how would you make more concentrated urine?

A

that means you’re trying to reabsorb more water into the IF

you would have to increase the osmolarity of the IF even more

167
Q

what controls the movement of the collecting duct?

A

a gradient

168
Q

what happens in the collecting duct if ADH is present?

A

if ADH present: aquaporins in CD will let water follow gradient so that the IF in the medulla and what’s in the CD will have the same osmolarity

169
Q

what happens in the collecting duct if ADH isn not present?

A

with no ADH: the aquaporins will go away and water can’t exit so we will see a low concentration of urine; dilute urine with low osmolarity

170
Q

what is the fast way to regulate Na+ and H2O levels?

A

changing GFR via smooth muscle

glomerulus is our vessel that has smooth muscle around it and can change size of vessel = change flow of blood

171
Q

how do you decrease GFR quickly?

A

1) contract smooth muscle around afferent arteriole
2) dilate smooth muscle around efferent arteriole
result: increases Na+/H2O

to decrease GFR we want less to go through fenestrations so contract afferent smooth muscle that’s incoming –> so if less comes in, less will go through the holes aka contract the afferent

also if we dilate the efferent smooth muscle and make it easier to exit then less will go through the holes so we’ll also decrease GFR

if we get the kidney less to do, the kidney will be able to do its job better

decreasing GFR means we can reabsorb more sodium and water

172
Q

how do we increase GFR quickly?

A

1) dilate afferent smooth muscle
2) contract efferent smooth muscle
result: decrease Na/H2O

to have a bigger GFR we want to dilate the afferent smooth muscle so more comes in means more goes in both directions

or we want to close off the exit by contracting efferent smooth muscle

bigger GFR means we overloaded kidney and we lose more sodium and water and don’t reabsorb as much because it’s harder for the kidney to do its job

173
Q

how do you slowly regulate Na and water levels?

A

endocrines via reabsorption

174
Q

what endocrines will slowly alter Na/H2O levels?

A

1) renin-angiotensin-aldersterone system (RAAS)
2) pulmonary capillaries
3) aldosterone
4) atrial natriuretic peptide (ANP)

175
Q

what kicks the RAAS system into place?

A

what kicks this system into play is:

1) decreased NaCl
2) decreased BP
3) decreased ECF volume

176
Q

how does the RAAS regulate Na and H2O levels? what does the RAAS system do?

A

RAAS helps us keep water on board by keeping NaCl on board aka increase BP

juxtaglomerular cells release renin if any indicators are registered by chemoreceptors

the cells right by the glomerulus on the afferent and efferent tubules will put renin into the system

when renin is in the system, it converts inactive angiotensinogen from the liver into angiotensin I

177
Q

what does angiotensin I do?

A

once activated by renin, ATI will end up in the pulmonary capillaries

angiotensin-converting enzyme (ACE) in the pulmonary capillaries will finish the conversion of ATI to angiotensin II

ATII is a vasoconstrictor

178
Q

what are ACE inhibitors?

A

ACE converts angiotensin I to angiotensin II which is a vasoconstrictor

people with high BP get put on ACE inhibitors so that they can’t make AT II which is a vasoconstrictor among other things

ACE inhibitors help lower BP

179
Q

what does angiotensin II do?

A
  • it’s a vasoconstrictor
  • it makes sure we get more vasopressin into the system which is another vasoconstrictor
  • helps hold water in collecting duct (increases BP)
  • makes you more thirsty = brings in more water
  • increases aldosterone levels
180
Q

where does aldosterone come from?

A

adrenal cortex which is above the kidney releases aldosterone

181
Q

what stimulates release of aldosterone?

A

angiotensin II binds adrenal cortex receptors to stimulate release of aldosterone

182
Q

what does aldosterone do?

A

impacts kidney and increases Na transporters

transporters bring back Na which brings back water with it

however, transporters that bring Na back cause us to lose K

183
Q

what causes atrial natriuretic peptide (ANP) to be released?

A

1) high NaCl
2) high BP
3) high ECF volume

184
Q

what does ANP do?

A

it comes from the heart and decreases BP

inhibits secretion of other things to decrease water volume by decreasing osmolarity

inhibits release of renin, aldosterone, vasopressin

you want to be losing water, you want a diuretic

185
Q

what is the effect of ANP on GFR?

A

ANP increases GFR by impacting the smooth muscle

increased GFR overwhelms the kidney so you lose more water and sodium

186
Q

why does ANP come from the heart?

A

we don’t want to much volume in the heart because if EDV gets too big, we’ll get congestive heart failure

we don’t want our heart to get too big

ANP is analogous to pulmonary stretch receptors in the lungs in that it makes sure we don’t overinflated the heart

lowering levels of water and sodium

187
Q

what’s the pathway of the reproductive system?

A

GnRH –> FSH and LH –> gonads

188
Q

what are the gonads?

A

testis or ovary

189
Q

what do gonads do?

A

1) release sex endocrines

2) create gametes

190
Q

what are gametes?

A

egg and sperm

191
Q

what is the creation of egg and sperm?

A

gametogenesis

creation of gametes

192
Q

what type of cells are gametes?

A

haploid cells

aka they only have 1/2 of the DNA so that when you combine with another gamete you have a full set

haploid = 23 chromosomes

diploid = 46 chromosomes

193
Q

via what process are gametes created?

A

meiosis

meiosis creates haploids via 2 divisions

194
Q

how many gametes do males make?

A

males are always making gametes

constantly putting cells through meiosis

males have billions of true haploid cells

195
Q

when do females make their gametes?

A

females make all of their gametes in utero

all eggs get stopped before the 1st meiotic division at birth

196
Q

when does the first meiotic division of female gametes happen?

A

ovulation

197
Q

when does the second meiotic division of female gametes happen?

A

fertilization

when egg meats sperm

198
Q

how many true haploid cells do females have?

A

the number of true haploid cells in a girl is the number of times she’s pregnant

199
Q

how long is the overian cycle?

A

28 days

200
Q

what are the phases of the ovarian cycle?

A

folliclar phase (12-14 days)

luteal phase (about 14 days)

201
Q

what happens during the follicular phase?

A

controlled by follicle

starts with loss of the uterine wall

estrogen released from follicle which causes a build up of the uterine wall

202
Q

what controls the luteal phase?

A

controlled by the corpus luteum

203
Q

what is the corpus luteum?

A

the remanence of the follicle after the egg is released from it

204
Q

what is the luteal phase?

A

post ovulation

maintain the uterine wall: more blood supply and glucose

estrogen and progesterone secreted from corpus luteum

205
Q

when does the corpus luteum die?

A

10 days after ovulation if there’s no intervention

it takes with it the estrogen and progesterone levels so they drop = signal to deteriorate wall because you don’t need it

if there’s a pregnancy the corpus luteum survives

206
Q

what are the steps of the ovarian cycle?

A

1) loss of wall
2) follicular phase
3) ovulation
4) luteal phase

207
Q

what is the GFR?

A

the amount exiting your blood and going into your kidney

208
Q

how are ANP and RAAS related?

A

they do the opposite things

ANP decreases BP

RAAS increases BP

Physiology (15 decks)

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