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Physiology > Exam 12: April 10-14 > Flashcards

Exam 12: April 10-14 Flashcards

1
Q

what are the types of hypotension?

A

hemorrhage and shock

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2
Q

what is hemmorrhage?

A

loss of plasma fluids

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3
Q

what is shock?

A

visceral bleeding

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4
Q

is hypertension chronic?

A

yes

patients are consistently higher than steady state

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5
Q

what is hypertension caused by?

A

usually due to increased peripheral resistance

somewhere out in the circulatory system we have increased resistance

resistance means we have something preventing flow from happening

we have lots of tubing in our body and the resistance can be anywhere out in the system and if have a problem at any point then the heart will have to work harder to push past it

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6
Q

do we know specifically what causes hypertension?

A

no, the cause is often unknown

most of the time we can’t find where in the system that problem is

the small vessels are hard to pinpoint so we never actually try to resolve the underlying cause, we just treat the symptoms and try to lower BP so you can’t stop treatment or else the symptoms will come back

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7
Q

what organ is often associated hypertension?

A

kidneys

the blood gets filtered in the kidneys so if there’s a problem there, it can raise the blood pressure

kidneys make erythropoietin, EPO. EPO binds to recpetors in the bone marrow which makes RBC’s. However if too much EPO is produced by the kidneys, we will have too many RBC’s being produced. If we increase the RBC level above 45%, the plasma component of the blood will have to decrease and the blood will become more viscous. Viscosity is the resistance of flow, so the more viscous the blood, the more it resists the convective flow of the cardiovascular system (increases peripheral resistance) , and the heart has to work harder to pump the blood throughout the body, creating hypertension.

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8
Q

what does hypertension lead to?

A

ventricular hypertrophy

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9
Q

what is ventricular hypertrophy?

A

hypertension often leads to ventricular hypertrophy

you can get a quick response to raise BP through sympathetic but there isn’t an equivalent parasympathetic response to drop it back down

we don’t want our heart to sustain high BP because we need a bigger muscle with bigger volume and bigger pressure sustained

bigger heart creates 2 problems:

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10
Q

what two problems does ventricular hypertrophy lead to?

A

1) imposing on the lungs

2) heart binds on itself

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11
Q

how does ventricular hypertrophy impose on the lungs?

A

if you expand your heart, it’s not in an area that can be expanded

if you double your heart, it’s limited by your rib cage and you’ll be imposing on your lungs

individuals with heart conditions first go to their doctors thinking they have a pulmonary condition because their lungs can’t expand as far since their heart has taken over the space; shortness of breath is a common symptom

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12
Q

how does ventricular hypertrophy cause the heart to bind on itself?

A

when we try to squeeze in 3D, having too much tissue there can start binding on itself

for most people, making a bigger bicep isn’t a problem but ask some of the people at the Arnold to scratch their opposite shoulder and they can’t because their muscle is too big and it gets bound up; same thing goes for our heart

getting a bigger heart is good for a little but then problems start happening

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13
Q

what are the three components of the blood?

A

1) plasma
2) hematocrit
3) erythrocytes

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14
Q

how much of the blood is plasma?

A

55%

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15
Q

is plasma liquid of non-cellular?

A

plasma is he liquid part of the blood

our endocrines move through the plasma

plasma is 90% water which is what the endocrines move through

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16
Q

what happens if plasma levels drop?

A

plasma is the liquid portion of the blood used to transport endocrines and other things

if the amount of plasma drops then it’ll be harder to transport cellular components

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17
Q

what if there is too much plasma in the blood?

A

if you get too watery then you lose cellular function of components traveling through plasma

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18
Q

what are the components of plasma?

A

1) albumin
2) immunoglobulin
3) fibrinogen

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19
Q

what is albumin?

A

a component of plasma

helps us maintain oncotic blood pressure

volume is set by amount of water that’s there; the amount of albumin in the blood, draws water into the blood vessels via osmolarity

to change the amount of water in this area use osmolarity

albumin sets the right osmolarity so that the movement of water in our blood isn’t too much or too little

since the albumin controls the oncotic pressure (how much water goes into the blood & how much water goes out of the blood), the albumin can control BP. If a lot of water goes into the blood, the n in our PV = nRT equation will go up. Assuming that the V (size of our vessel) remains the same, this will increase the pressure and since the albumin controls this movement of water, it in turn controls the BP.

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20
Q

what is immunoglobulin?

A

a components of plasma

aka antibodies

also help maintain oncotic pressure = osmotic pressure in the circulatory system specifically

hyperthyroidism is caused by an antibody!

they are why we get shots to avoid diseases so that our immune system creates the immunoglobulin necessary

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21
Q

what is fibrinogen?

A

a component of plasma

fibrous protein that is inactive (“ogen”)

we want it moving around inactive so that when we need it, it’s there and accessible and we can activate it at the time and place needed

this is key for preventing blood loss

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22
Q

what are the functions of plasma?

A

1) transport
2) maintain BP
3) maintain pH
4) immunity
5) clotting

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23
Q

how does plasma help with transport?

A

transporting ions, oxygen, cellular components, and heat

this is why individuals that have pale skin and you can tell what’s going on with their temperature; if someone is cold they get pastier but if they’re warm, blood goes to the surface and they become more pink in the skin

in our extremes, when we’re too warm or cold, we raise HR to cool or heat areas of our body

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24
Q

what happens when people have pale skin?

A

plasma helps with transport

individuals that have pale skin and you can tell what’s going on with their temperature; if someone is cold they get pastier but if they’re warm, blood goes to the surface and they become more pink in the skin

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25
Q

how does plasma maintain blood pressure?

A

albumin helps us make sure we don’t overload amount of water

our V plays into pressure

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26
Q

how does plasma maintain pH?

A

albumin is critical for this process

immunoglobins play a distant second role in this process

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27
Q

how does plasma help with clotting?

A

it prevents blood from exiting blood vessels thorough fibrinogen

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28
Q

what is hematocrit?

A

the part of the blood made of red blood cells but it also includes the buffy white coat = leucocytes and platelets

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29
Q

what percentage of the blood of erythrocytes?

A

45%

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30
Q

how much of the blood is the white layer? what is in the white layer?

A

<1%

leucocytes = WBC and platelets

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31
Q

what are leucocytes?

A

WBC

it’s really just a catch-all category for anything that’s not RBC

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32
Q

what are platelets?

A

they work with fibrinogens to prevent blood loss

if you damage a blood vessel, platelets limit how much blood exits the system

platelets are highly derives cells that are often referred to as not being cellular because they’re lost so much of their cellular activity

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33
Q

what are the components of the hematocrit?

A

1) erythrocytes
2) leucocytes
3) platelets

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34
Q

when do people need blood transfusion?

A

if you don’t have the right amount of RBC, that is why we give people a whole blood transfusion rather than just an IV drip

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35
Q

how big are RBC?

A

they’re small

5-7 micrometers

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36
Q

why do you want RBC to be small?

A

RBC go through capillaries one at a time so the bigger the RBC are, the bigger the capillaries are and the bigger the capillaries, the slower diffusion is

you want RBC to be as small as possibly

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37
Q

how are RBC so small?

A

RBC have no nucleus or organelles to keep them as small as possible

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38
Q

what do RBC sacrifice because they’re so small?

A

they don’t have organelles so they lose mitochondria!

this limits ATP production so they’ll be making ATP only with anaerobic glycolysis (aerobic glycolysis would make NADH and there’s no TCA/ETC to use it because those are only in the mitochondria)

however, they don’t really have a need for ATP because they aren’t making new proteins since they don’t have a nucleus

they also don’t have to move on their own because they’re getting moved by convective flow of the heart

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39
Q

what is the shape of RBC?

A

biconcave ellipse shape

to get a RBC through a vessel better, you want a small diameter and to do that you can compress it into a cylinder so RBC are actually biconcave ellipse shaped

you don’t want RBC to be round

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40
Q

why do RBC have the shape that they do?

A

they are biconcave so that we can maximize surface area in the smallest space and depressions increase SA while maintaining minimum width = helps with diffusion

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41
Q

what are RBC packed with?

A

RBC are packed with hemoglobin!

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42
Q

what does hemoglobin do?

A

Hb does primary function of RBC which is transport

plasma does transport but that transport is an issue in terms of endocrines because it’s polar and some of the things we need to transport are non polar

well we need to transport oxygen which is a nonpolar components! The amount of oxygen that can be free in plasma is super low so you need to give it a plasma binding protein that is in a cell aka Hb

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43
Q

what is the function of RBC?

A

transport of O2, CO2, H+ and CO

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44
Q

what does Hb carry?

A

it carries CO2 waste and helps move H+ so it impacts pH levels

Hb also binds CO and binds at the same spot on Hb as O2

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45
Q

what’s the lifespan of an RBC?

A

120 days!! fast turnover rate

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46
Q

why do RBC have a short life span?

A

in order to have these super high levels of Hb in RBC, they had to lose their nucleus and organelles = no ATP or protein production

when Hb breaks down, we don’t get any more because we don’t have protein production

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47
Q

what is erythropoiesis?

A

the making of RBC

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48
Q

where does erythropoiesis occur?

A

in the bone marrow

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49
Q

what is the rate of RBC production?

A

you make 2-3 million RBC per second

you need lots of supplies or else that rate drops of

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50
Q

what does erythropoiesis need?

A

1) Fe
2) vitamin B12
3) folic acid
4) erythropoietin

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51
Q

why does erythropoiesis need iron?

A

Fe is necessary for Hb

you need 4 Fe per Hb

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52
Q

why does erythropoiesis need erythropoietin? (EPO)

A

EPO is made by the kidney and goes and binds to receptors in the bone marrow and causes bone marrow to make RBC

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53
Q

what makes erythropoietin?

A

it’s a protein made by the kidneys and it’s an endocrine

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54
Q

what do high EPO levels mean?

A

high EPO levels means bone marrow will make more RBC

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55
Q

what was the blood doping scandal associated with?

A

artificial EPO means more RBC which means more oxygen carrying capacity which means they stay aerobic longer and are better at their event

kidneys have chemoreceptors for oxygen so if O2 levels drop, kidneys will put out more EPO so we can get more RBC and more O2 into the system

56
Q

when do the kidneys produce more EPO?

A

kidneys have chemoreceptors for oxygen so if O2 levels drop, kidneys will put out more EPO so we can get more RBC and more O2 into the system

57
Q

where does erythrocyte removal occur?

A

in the spleen and liver

both locations look at RBC that come through and if one is damaged, they catabolize it

after you breakdown the parts, you can reuse them

58
Q

what is the consequence of erythrocyte breakdown?

A

bilirubin

59
Q

what is the problem with bilirubin?

A

it’s produced during erythrocyte removal

bilirubin can’t be used in our body and if you can’t clear bilirubin after you’ve made it through the breakdown via liver to feces or liver to urine you have a problem

too high of levels of bilirubin causes us to appear yellow which is why your urine is yellow

if liver isn’t clearing things properly, bilirubin levels rise and your eyes will get yellow and skin, etc.

60
Q

what is measured when you pee in a cup?

A

bilirubin levels to see if your rate of removing RBC is good

endocrines are also being measured

61
Q

what is anemia?

A

decreased oxygen carrying capacity in the blood

62
Q

what causes anemia?

A

could be caused by not having enough RBC or not having enough functioning Hb in those RBC

overall, anemia is a decreased oxygen carrying capacity in the blood

63
Q

what are the types of anemia?

A

1) nutritional
2) pernicious
3) folic acid
4) aplastic
5) hemorrhagic
6) hemolytic
7) sickle cell
8) renal

64
Q

what is nutritional anemia?

A

iron deficiency

65
Q

what is pernicious anemia?

A

we need vitamin B12 as a key factor in RBC

vitamin B12 absorption can be problematic in digestive tract

so it’s a digestive problem that you can bypass by injecting patients with B12

66
Q

what is folic acid anemia?

A

only a problem for pregnant woman because they’re making RBC for two individuals

67
Q

what is aplastic anemia?

A

if the bone marrow can’t produce RBC

68
Q

what is renal anemia?

A

kidney’s filter blood and check oxygen level and if it’s too low they increase RBC production by releasing erythropoietin endocrine

chemoreceptors or ability to produce EPO is damaged

69
Q

what is hemorrhagic anemia?

A

RBC loss

rate of production stays the same but rate of destruction goes up

individual has BP problem so you give them fluids but if they’ve lost too much blood you give them a blood transfusion

there’s been damage to the closed vessel system and you’ve lost a significant number of RBC so fluid will help BP but not the anemia

70
Q

what is hemolytic anemia?

A

RBC destruction

removal organs, liver and spleen, are too job at their job

one or both is doing their job too well and destroying too many RBC so removal rate is too high compared to production rate so overall you’re losing RBC

71
Q

what is sickle cell anemia?

A

RBC are not biconcave ellipse RBC which is critical for RBC to move through the system

instead they’re sickle shaped

if Hb can’t do it’s job that’s bad because it can’t cary oxygen but what causes more problems is actually the shape because it can’t fit through the capillaries and they clog the system and creating resistance = hypertension and eventually you’ll have hypertrophy and an enlarged heart and capillaries

if capillaries are wider we’ll have a hard time with diffusion so the oxygen, even in the good RBC, will have a hard time getting to tissues

72
Q

what causes sickle cell anemia?

A

sickle cell is created by the miscreation of the Hb within there that creates an internal problem that messed up the shape

it’s a one AA difference that leads to Hb not being able to do it’s job and a weird shape

73
Q

what is polycythemia?

A

having too many RBC, over 45% of the blood

74
Q

what happens if you have polycythemia?

A

if RBC is over 45% then fluid drops below 55%

the fluid is moving the cells and creating convective flow so if there’s too many cells compared to the fluid it becomes hard to move them

this is like a good milkshake: if the milkshake is thick then it’s really hard to get it to move up the straw

75
Q

what is the level of red/yellow in anemia patients?

A

20-80 red/yellow

normal is 45-55 red/yellow

too low of red

76
Q

what is the level of red/yellow in polycythemia patients?

A

80-20 red/yellow

normal is 45-55 red/yellow

77
Q

what are the physiological effects of polycythemia?

A

you get increased oxygen carrying capacity because increased RBC but the tradeoff is the huge increase in viscosity of your blood

you get an enlarged heart and capillaries increase in size or you’ll have to increase the number of capillaries

78
Q

what are the causes of polycythemia?

A

1) increased EPO
2) hyper-responsiveness to EPO
3) chronic low level of oxygen

79
Q

how does increased EPO cause polycythemia?

A

there’s too much erythropoiesis so too much RBC being produced so increased viscosity

80
Q

how does hyper-responsiveness to EPO cause polycythemia?

A

you can change receptors in bone marrow and make them more responsive to the EPO that’s already there

81
Q

how does chronically low levels of oxygen cause polycythemia?

A

if we keep oxygen level low in the plasma then the kidney’s will naturally raise EPO levels

so individuals in constantly low oxygen environments are polycythemic like individuals that live on mountains; as you go higher up, you have lower levels of oxygen

if we put individuals in high altitude situations you’ll cause them to naturally become polycythemic; hello the main Olympic training center’s are in Colorado! You can also do it at normal altitudes in chambers that have lower oxygen levels

you have to make sure their heart and vascular system can compensate for polycythemia and can handle an enlarged heart

82
Q

what is hemostasis? how often does it occur?

A

it’s the stopping of the flow of blood

our circulatory system doesn’t want leaks or else we can have hemorrhagic anemia so you circulatory system fixed these holes

1000 of times a day you rip open your cardiovascular system usually in a capillary and blood leaks out but you resolve the issue because you have any issues and lose a significant number of RBC

83
Q

where does hemostasis work best?

A

works best in small vessels: aka capillaries and arterioles so it does NOT work in arteries or veins

84
Q

why does hemostasis happen best in small vessels?

A

hydrostatic pressure in arteries is the highest and is returning to a high level in the veins

the highest BP is in the arteries as well – BP in the veins is the lowest in the system

if hydrostatic pressure is pushing against the wall then it’ll blow away any kind of fixing your body tries to do

kind of like red rover because if so and so is an offensive lineman, you’re not going to be very successful in preventing them from coming over aka high hydrostatic pressure and they’ll break through

85
Q

what are the primary players in hemostasis?

A

endothelial cells

the vessels are lined with endothelial cells

86
Q

what is hemostasis?

A

it’s a way to seal vessel damage: by using our own system without medical assistance to make sure pressure and RBC count aren’t effected and you prevent blood loss

uses hemorrhagic anemia

87
Q

what is the progression of the stages of hemostasis?

A

stage 1 gets started the quickest so it gets started first

once you get things started, all of them can be happening at the same time

it just takes 3 longer to get started than 1

88
Q

what are the stages of hemostasis?

A

1) vascular spasm
2) platelet plug
3) clot formation

89
Q

what happens during the vascular spasm stage of hemostasis?

A

the vessel itself is creating this process

1) vasoconstriction: as soon as an endothelial cell gets damaged, it causes vasoconstriction in the area – vasoconstriction brings sides of the opening together so it’s possible that vasoconstriction on a small opening can close it all by itself – there are often times where vasoconstriction can solve the problem so you only need the first stage
2) collagen reconnecting: ECM holds our cells in place and a key components of ECM is fibrous protein collagen – when you damage collagen, the ends are sticky and will link up to reseal

90
Q

what happens during the platelet plug stage of hemostasis?

A

platelet are another key component of fluffy coat with the WBC

platelets moving around in our blood are flowing with blood so when we have an opening in a vessel, they’ll go out of the opening just like the plasma, RBC and everything else in the blood

when this happens, we know that the collagen is sticky and the platelets can get stuck on collagen as they go by

collagen while they’re moving doing really do much but when they stop moving, that’s the indicator that says it’s time to do their job; they change shape when they become activated and go from round to star shape just like how microglial cells go from spiky to round to do phagocytosis and movement so in this case, we don’t want platelets to move so we make them spiky

they also release chemicals that cause further vasoconstriction on top of the vasoconstriction that happened during the vascular spam

91
Q

what do active platelets do during the platelet plug stage of hemostasis?

A

they release chemicals that start activating other platelets so that they don’t have to get stuck in the collagen and instead they’ll stick to each other and starts to get some of the platelets not even stuck to start changing shape

this is positive feedback since activated platelets start activating platelets around them

you have to limit positive feedback and isolate platelet clot only to the area of damage; when you get to healthy endothelial cell it doesn’t need a platelet plug covering it

92
Q

what limits the platelet plug stage of hemostasis?

A

lmited by healthy endothelials

healthy endothelial cells cause vasodilation via nitric oxide (NO) so we get squeezing at the opening but right outside of it, we get relaxation

93
Q

what is also happening during platelet plug stage of hemostasis?

A

we have recruitment happening since other platelets are being activated so instead prostacyclin tells the other platelets to keep on moving, nothing to see here

prostacyclin works against recruitment while vasoconstricution is countered by NO

the stickiness is caused by activation

94
Q

what happens during the clot formation stage of hemostasis?

A

a clot is when you’re trying to turn the blood from a fluid to a gel because a gel doesn’t allow fluid to go through it since a gel has high viscosity which is bad for convection but that’s good because we’re trying to avoid fluid from moving

we get clot formation to happen because it’s a cascade of multiple events – this cascade of events is big because there’s around 12 processes

95
Q

what are the key players in clot formation?

A

fibrinogen and thrombin

96
Q

what does fibrinogen do during clot formation?

A

fibrinogen is a plasma protein that helps with clotting

it’s constantly moving through our blood so when we have a situation where we want a clot to form, we activate it so that it starts creating net like structure called fibrin and turning it into a more viscous situation

97
Q

what does thrombin do during clot formation?

A

it activates fibrinogen into fibrin

98
Q

how are platelet plug and color formation related?

A

platelet plug is not the same at clot formation!

99
Q

what kind of process is anti-clotting?

A

positive feedback

100
Q

what is anti-clotting?

A

it limits the clot to the area of injury

101
Q

why do we need anti-clotting?

A

we also want anti-clotting mechanisms because eventually we’re going to need to break down clot because we’ve sealed the hole and don’t need to the clot any more

this is just like forming a scab because eventually the skin heals and the scab can get peeled off

102
Q

how does anti-clotting eliminate unneeded clots?

A

clots are more than one cell held together by fibrin

if we take multiple cells help together by fibrin and move it off of our opening and let it move through our system, it’ll end up down stream and eventually it’ll go through a capillary which only have capacity for one RBC so we’ll effectively cause a blockage

103
Q

what techniques are used in anti-clotting/clot breakdown?

A

plasmin protein that moves through our blood regularly dissolves fibrin

prostacyclin prevents further recruitment of platelets

104
Q

what is plasminogen? what activates it?

A

the inactive form of plasmin which dissolves fibrin

when we need a clot broken down, the newly healthy cells behind the scab release a compound that turn plasminogen into plasmin which then dissolves fibrin into individual cells in an orderly way

105
Q

which drugs impact hemostasis?

A

1) aspirin
2) oral anticoagulants
3) plasminogen activators

106
Q

what does aspirin do?

A

first came into play as pain reliever but it was then realized that in those patients that took aspirin bruised a lot more easily

so if we have a patient that has too much platelet formation, too much hemostasis, we can limit it by giving them aspirin

aspirin effectively acts like prostacyclin to limit recruitment of platelets

when people have problems with their cardiovascular system and there’s not enough convection, platelets can stop; preventing recruitment slows down hemostasis process

someone on aspirin bleeds and bruises a lot more easily – goes after second stage

107
Q

what are oral anticoagulants?

A

we give them and they enter digestive system and they go against coagulation (3rd stage)

effectively decrease vitamin K

dropping vitamin K is a key component in making thrombin so without vitamin K we can’t make thrombin and thrombin activates fibrinogen into fibrin aka without thrombin we don’t have web creator so we don’t get gel and we don’t get cloth = anticoagulant

108
Q

what are plasminogen activators?

A

when put into system, the plasminogen in the body gets activated

now if we have a clot that’s creating a blockage, we just put plasmin into the system and the clot will get dissolved into individual cells and moved through so it’s no longer a problem = blood flow retained

109
Q

what is a disease that’s caused by clots in the wrong area?

A

strokes

110
Q

how can strokes be helped?

A

plasminogen activators

a disease caused by clots in the wrong area is strokes

a stroke is a clot in the brain and downstream of that clot all the neurons are without oxygen and are dying so whatever function they had ceases

if we can break down the clot within a short time frame, the cells won’t die and they’ll recover so people who get to ER in time with stroke symptoms can get plasminogen activators and return to regular function

111
Q

what is a negative tradeoff of plasminogen activators?

A

hemostasis is a common event in your circulatory system so plasminogen activators activates all plasmin so every single clot in the body gets broken down and you could potentially bleed out if some of the clots are in critical spots

some individuals don’t get plasminogen activators if they have other cardiovascular damage that they could bleed out

also if they’re been experiencing symptoms of a stroke for a long time plasminogen activators won’t help because neurons are probably already dead

112
Q

what are the functions of the respiratory system?

A

1) interact with environment
2) convection
3) regulation of blood pH
4) enable speech
5) microbe defense

113
Q

how does the respiratory system interact with the environment?

A

bring air in via our respiratory system to get O2 in and CO2 out (more important to get CO2 out)

114
Q

how does the respiratory system play a role in convection?

A

convection is done to get air from lungs to tissues

115
Q

how do the lungs help diffusion be successful?

A

diffusion is dependent on SA and has problems with distance

lungs have huge SA and are very thin so there’s small distance between endothelial cells of lungs and the capillaries to give them oxygen

116
Q

how does the respiratory system regulate blood pH?

A

through equation 3, we regulate pH of blood

Protein functions: proteins work best at a certain pH so we need to regulate blood pH

117
Q

how does the respiratory system enable speech?

A

it creates convective flow that we use with our vocal cords to cause them to vibrate, to change the waves of pressure going to other people that listeners pick up with their ears

118
Q

how does your respiratory system play a role in microbe defense?

A

lungs can be used to expel foreign matter; this is the point of coughing to clear airways for better convection and clear things out of your lungs and out of your system

trade off with our sympathetic response that opens up the lungs to more microbes

119
Q

what do cilia in our respiratory system do?

A

cilia that move along our respiratory tract catch and move pathogens out of our system

120
Q

what does mucus in your respiratory system do?

A

mucus is there to trap components so that it can’t get into us but then we have to move mucus out of us

kids that have eat their own snot, helps their immune system be able to fight antigens so later on they’re healthier

121
Q

what do macrophages in the respiratory system do?

A

macrophages are present in respiratory system as a first line of defense to try and attack foreign things trying to come in

122
Q

what are the parts of the respiratory system?

A

1) conducting zone

2) respiratory zone

123
Q

what happens in the conducting zone?

A

it’s about conducting, creating the movement convectively of the air so that you can go from mouth to tissues so that you can do diffusion

124
Q

what are the components of the conducting zone?

A

1) larynx
2) trachea
3) bronchi

125
Q

what does the trachea do?

A

part of the conducting zone

tube that you don’t want food to go down, this is your air tube

126
Q

what do bronchi do?

A

part of the conducting zone

main two connectors to our lungs, we have two bronchi

it’s a network system so the bronchi get branched into smaller tubes called bronchioles

127
Q

what kind of air resistance is in the conducting zone?

A

components of the conducting zone need to have low air resistance aka need to allow as much air to flow as possible

we want as little friction as possible so that we can have the best convection and conduction as possible

128
Q

is there diffusion in the conducting zone?

A

no!

We will not see exchange of oxygen or CO2, we just see bulk movement of oxygen and CO2

129
Q

what does the smooth muscle in the conducting zone do?

A

we can change the size of these tubes because we have smooth muscle

when we want tubes to be bigger we relax muscles to get more flow

constricting the tubes gives us less flow because we don’t need as much flow so we avoid the tradeoff of having less pathogens in our body

130
Q

what happens in the respiratory zone?

A

where respiration and exchange happens

131
Q

what are the components of the respiratory zone?

A

1) respiratory/terminal bronchioles
2) alveolar ducts
3) alveoli

132
Q

what are respiratory bronchioles?

A

part of the respiratory zone

the final bronchioles at the very end of the system can act in the respiratory zone

133
Q

what are alveolar ducts?

A

part of the respiratory zone

the hallways in between the rooms of the alveoli

134
Q

what are alveoli?

A

part of the respiratory zone

the rooms in your lungs that give you increase SA

135
Q

what are the characteristics of the respiratory zone?

A

all about maximizing diffusion

increase SA and decrease distance

thin walled: one cell thick epithelial cell walls

highly vascularized: want a big blood supply to the alveli, lots of capillaries surrounding alveli so we can do exchange

136
Q

what is hemostasis?

A

stopping the flow of blood

Physiology (15 decks)

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