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Physiology > Exam 3 Resp, Immune, and Endo > Flashcards

Exam 3 Resp, Immune, and Endo Flashcards

1
Q

what is the Whipp and washerman model

A

when you have muscle and circulation and ventilation working together to take in O2 and remove CO2

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2
Q

where is the visceral pleura and can it feel pain

A

right against the lung.. the serous lining against the lung, insensitive to pain.

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3
Q

what does the parietal layer cover

A

the internal wall of the thoracic cavity

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4
Q

si the pleural space opened or closed

A

closed

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5
Q

what does the fluid int he pleural space do

A

lubricates and facilitates movement

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6
Q

what happens when air gets into the pleural space

A

the lungs collapse

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7
Q

the pleural chambers sit at ___ mmHg, which is slightly positive/negative to the air

A

755, negative

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8
Q

the upper airway is anything proximal to the

A

bifurcation at the angle of Louis

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9
Q

what is the purpose of the upper airway

A

to filter and humidify the air before it goes to the lungs

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10
Q

does phonation happen in the lower or upper away. why is it hard for people with pulmonary problems to talk

A

upper. they cannot get enough air going past the vocal cords

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11
Q

lower tract is defined as the space below the

A

trocheal bifurcation

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12
Q

difference between conducting airways and the acing airways

A

the conducting airways is where gas travels, so ventilation. the acing airways is where respiration happens

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13
Q

how many lobes are there, and where are they broader and shorter

A

the right has 3 lobes and is shorter because of the liver and the left has 2 lobes, broader because of the heart

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14
Q

both lobes have a ___ fissure, and the right lung also has a ___ fissure

A

both have oblique, the right also has the horizontal

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15
Q

difference between type 1 and type 2 alveolar cells

A

the type 1 cells allow for gas exchange, so these are on most of the alveolar wall
type 2 cells stretch (when we breath in) and make surfactant, which breaks the surface tension (which could make the alveoli collapse). this allows the alveoli to stay open

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16
Q

what is so special about type 2 alveolar cells

A

they make surfactant

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17
Q

Mucocilliary Escalator

A

the goblet cells make mucus, and the cilia will transport the mucus and debris up and out of the airways DOESN’T WORK WITH PNEUMONIA

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18
Q

what removes debris that travels to the alveoli. when these are overtaxed, and rupture, what disease is that

A

the macrophages, and COPD

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19
Q

PNS and CNS on bronchioles

A

the PNS causes bronchoconstriction and the CNS causes bronchodilation

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20
Q

what are two local factors released by mast cells that cause bronchoconstriction

A

histamine and leukotrienes

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21
Q

hat do the muscles of the ventilatory pump work against, if it is not gravity

A

the airway resistance and the elastic recoil

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22
Q

inspiration is primary done via the…

A

diaphragm

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23
Q

what other muscles are used during inspiration

A

the external intercostals, and the scalenes, SCM, and pec minor

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24
Q

what muscles are used during expiration

A

this is passive, but we can get forced expiration with abdominals and internal intercostals

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25
Q

what happens during inspiration

A

the diaphragm contracts and descends, which increases the volume of the thoracic cavity. this is turn will decrease the pleural pressure and pull on the lungs, which then expand. upon this expansion, they fill with gas and the intrapulmonary volume increases too. this ends when the thoracic volume is no longer increasing

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26
Q

how is thoracic volume increased during deep inspiration

A

accessory muscles

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27
Q

what happens during expiration

A

the disparage relaxes and ascends and the rib cage descends which decreases the thoracic volume and the lungs recoil to push air out

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28
Q

coughing is heavily reliant on…

A

abdominal tone. so in clinic, this is often an issue with SCI, stroke or impaired abdominal tone.

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29
Q

what happens during coughing

A

inspiratory phase, the air is brought in
compression, at the larynx closes and the chest wall and everything contracts to increase inter-thoracic pressure, a
expiratory phase: the glottis opens and the air is pushed out

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30
Q

total lung capacity

A

TLC is the total amount of air in the lungs (usually 5-7L)

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31
Q

residual volume

A

the amount of air that cannot be removed after expiration

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32
Q

vital capacity

A

the ability to maximally breathe in and then forcibly breathe out (men is 5L and women is 3.8L)

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33
Q

tidal volume

A

the amount of air you breathe in and out normally.

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34
Q

inspiratory reserve volume

A

how much you can take in on top of the normal amount

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35
Q

expiratory reserve volume

A

how much you can breath out forcibly

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36
Q

forced expired in 1 sec (FEV1)

A

the amount of air you can push out in 1 sec

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37
Q

minute ventilation

A

amount of air per minute

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38
Q

DLCO (diffusion capacity )

A

ability to diffuse at the alveoli, about 80%

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39
Q

forced expiratory volume is normally ___ of the forced vital capacity

A

80%

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40
Q

obstructive vs restrictive lung diseases on FEV 1/FVC

A

obstructive, decreased

restrictive, increased

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41
Q

the blood volume in the lungs is about ___ of the total blood volume. what amount of this blood volume is in the capillaries

A

9% (450 ml)

70ml in the capillaries

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42
Q

blood volume in the systemic circulation is ___x that of the pulmonary system. what does this mean to a shift in blood from one system to another

A

9x

this means that a shift in blood will affect the pulmonary circulation greatly.

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43
Q

in what kind of situations can blood be shifted from the reservoir of volume I the pulmonary blood to the systemic circulation

A

when blowing a trumpet (high thoracic and pulmonary pressure)
or when bleeding in systemic circulation, the blood flow is automatically shifted to the systemic vessels

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44
Q

which pressure is higher, the pulmonary or the systemic

A

systemic

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45
Q 
Pulmonary Artery Pressures
systolic
diastolic
mean
capillaries
A

systolic: 25
diastolic: 8
mean: 15
capillaries: 7 mmHg

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46
Q

what happens if you increase the pump nary artery pressures

A

you can cause an increase in afterload or workload or possibly even a right sided heart failure

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47
Q

pulmonary blood flow is equal to…

A

cardiac output

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48
Q

pulmonary vessels are passive. this means…

A

they enlarge with an increase in pressure, and they narrow with a decrease in pressure

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49
Q

what is the pressure difference across the lung, and what is the difference above and below the heart. what does this mean in standing

A

23mmHg difference, 15 above the heart and 8 below

this means that while standing, the uppermost part of the lungs are 15mmHg less then the arteries at the level of the heart. additionally, int he lower part of the lung, the pressure is 8mmHg more then the arteries at the level of the heart

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50
Q

describe blood flow to the parts of the heart (top bottom) during standing

A

at the top, there is little blood flow, and 5x more blood flow in the lower parts

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51
Q

describe zone 1 and 2 and 3

A

1: no blood flow because the pressure in the alveoli is much higher then the pressure in the capillary. no part of the lung is zone 1
2: this is dependent on the changes in systolic and diastolic pressures. in the systolic phase, the pressure in the vessel is higher then the alveoli, so there is flow. during diastolic, it is closed. so there is no flow. this is usually at the top of the lungs
3: is continuous. capillaries P is always higher then alveolar. in supine, all of the lung is zone 3

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52
Q

in the clinic what do you do if someone is having a hard time breathing? why?

A

you put them in supine to unload the diaphragm, make all zones zone 3 and make the lungs have an easier time recruiting air for respiration .

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53
Q

what happens during hypoxia

A

in the lungs, low O2 makes the alveolar capillaries constrict to redirect blood flow to areas with better ventilation. this is the opposite of hypoxia to systemic vessels (which will dilate to increase blood flow).

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54
Q

how does that constriction of vessels help in terms of shunting

A

shunting would cause a decrease in systemic O2 levels, so by constricting capillaries int eh lungs and redistributing to areas with better ventilation, there is less of a decrease in the O2 of systemic?

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55
Q

during exercise, how does flow to the lungs increase 4-7 fold

A

by increasing the number of open capillaries (decreases pulmonary vascular resistance), by dilating all the capillaries and increasing the rate of flow through each (decreases pulmonary vascular resistance), and by increasing pulmonary arterial pressure ( increases very little because of the decrease in resistance)

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56
Q

exercise does what to the capillaries

A

increase in recruitment and increase in distention

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57
Q

during exercise the blood flow to the lung is increased. to what portion of the lung is the flow increased the most

A

the upper part by 700-800%

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58
Q

what happens in terms of zones during exercise

A

since the vascular pressure increases, the apices of the lungs go from zone 2-3

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59
Q

how do they figure that the pulmonary capillaries are about 7 mmHg of pressure

A

the left atrial P is about 2 mmHg and the mean arterial pulmonary pressure is about 15, so the 7 mark was right in the middle

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60
Q

what happens to transit time with an increase in CO

A

normally, it transit time (or the time for a RBC to pass through the capillary system) would be 0.8sec. when the CO is increased, the transit time goes to about 0.3 seconds.

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61
Q

how often is the volume of alveolar air replaced. what does this mean in terms of breathing

A

it is replaced only 1/7th of the new breath taken, so to completely recycle the air you need multiple breaths. even after 16 breaths, not all excess air is removed.

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62
Q

why is it important to take such a long tie in recycling air

A

this prevents and increase or a decrease in the tissue O2, and CO2 and pH when breathing is interrupted like during eating or swimming

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63
Q

which diffuse coefficient is higher, that of CO2 or O2. what does this mean

A

CO2. it diffuses faster

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64
Q

what is the V/Q ratio, and what is normal

A

that is the V= ventilation and the Q is blood flow/CO (which is higher at the base of the lungs). normal is 0.8

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65
Q

what does it mean when V/Q is higher than 0.8

A

ventilation exceeds perfusion

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66
Q

give an example of a shunt (when V/Q = 0)

A

this would be like pneumonia because there is no ventilation happening due to the blockage because of fluid

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67
Q

what is dead space

A

the volume of air that is inhaled but not part of gas exchange (either what is remaining in the conducting airways or that that reaches the poorly perfused alveoli)

68
Q

what happens if transit time is too fast

A

there is not enough time for gas exchange, the RBC travels way to fast

69
Q

how do the lungs adapt to a decreased transit time

A

the capillary will increase its blood volume

70
Q

78% of the air we breathe in is nitrogen. why is this important

A

to keep the airways patent

71
Q

what percentage of the air we breath in is oxygen

A

20%

72
Q

if O2 is absorbed rapidly, what happens to its concentration

A

its concentration decreases

73
Q

what does exercise do to pulmonary blood flow, ventilation and diffusion

A

it increases them all

74
Q

how does the diffusion capacity increase during exercise

A

by opening the diameter of the vessels, this increases the SA for diffusion

75
Q

what happens to the zones of the lungs with exercise

A

they become all 3, which helps match the V/Q ratio, and allows more recruitment

76
Q

what happens to pulmonary capillaries during exercise

A

they recruit more and dilate more

77
Q

how far into the capillary does the blood become saturated with O2

A

along the first 1.3

78
Q

what does the quick saturation of O2 in the capillary mean with a decreased transit time

A

means that the blood stays in longer to be oxygenated

79
Q

there are two areas from which blood enters the L atrium, what are they

A

the 98% that went through the pulmonary capillaries and the 2% that went through the lung tissue, that did not go through respiration

80
Q

what happens when the blood from the two places (lung tissue and pulmonary capillaries) mix

A

there is a slight drop off

81
Q

if there is a PO2 of 95mmHg in the capillaries and a PO2 of 40mmHg in the ISF surrounding a vessel, what will happen

A

there will be rapid diffusion from the capillary into the tissue

82
Q

why is it that there is way more diffusion of CO2

A

there is a small pressure difference (5mmHg) which can lead to a rapid exchange.

83
Q

what causes a right shift int he oxygen hemoglobin dissociation curve. what does the right shift mean

A

the right shift means that there is a lower affinity for O2 by hemoglobin. (it is more readily available for tissues)
caused by an increase in H ions (a lower, more acidic pH), more CO2 in the area, and a higher temperature or a higher 2-3DPG concentration

84
Q

why would it be useful to have a right shift in the OHD Curve

A

this means that it will be more useful in delivering oxygen to the tissues

85
Q

what happens and what causes a left shift curve in the oxygen hemoglobin dissociation curve

A

a left shift means that there is a higher affinity for O2 by hemoglobin, and that decreases the availably to tissues. This is a result of less H ion (more alkaline, higher pH), a decrease in temp and a decrease in the amount of 2-3 DPG concentration

86
Q

what is the Haldane effect

A

this is when the deoxygenated (right shifted) hemoglobin has a higher affinity for CO2, which brings it to the lungs faster, and gets rid of it easier.

87
Q

where is breathing controlled

A

in the brainstem with conscious input from the cortex.

88
Q

what kind of receptors play a role in the regulation of breathing

A

the chemoreceptors in the brainstem and carotid and aortic bodies that sent pH, CO2
metaboreceptors in the
mechanoreceptors in the lungs

89
Q

what is the Hering-Breur Reflex

A

when you take in a breath and hold it, you trick the mechanoreceptors in the lungs that they are full, and you do not feel like you need to inspire again. This is overridden by the need to remove CO2

90
Q

chemoreceptors pick up many things. One of its chemicals is ___ which is responsible for normal breathing rate

A

CO2 in the atrial and CSF

91
Q

true or false: changes in PO2 have virtually no direct effect on respiratory drive

A

TRUE

92
Q

what gas controls respiration

A

CO2

93
Q

what are rCPG’s and where are they found

A

respiratory central pattern generator. found in the medulla and pons

94
Q

describe how rCPG’s work

A

afferent signals from chemo and mechano receptors enter the medulla. Rhythms are released, which drive the nerves that innervate the muscles of inspiration (Botzinger complex)

95
Q

decrease the neural signals to the diaphragm

A

its not just one AP, it is the summation of signals, and the ramping up of signals. the ramping will stop after 3 seconds, which will cause an elastic recoil until the next inspiratory signal

96
Q

why is it important to ramp up the signals to the diaphragm

A

to allow for a steady increase in the volume of the lungs, keeps airflow consistent and also prevents gasping)

97
Q

pain and emotions can have an effect on the breathing rate, which is situated by what system

A

the limbic

98
Q

what can pain and exercise do to the HR and breathing rate

A

increase them

99
Q

what happens to oxygen consumption and CO2 production and tidal volume when you exercise

A

they all increase

100
Q

if exercise stimulates the liberation of H ions, what will this do to the chemoreceptors

A

will stimulate them and increase the breathing rate

101
Q

what are the most common cells in the blood

A

RBC

102
Q

what are the three main types of blood cells. where are they made

A

RBC, WBC and platelets. they are made from a common stem cell int he bone marrow

103
Q

three main types of WBC and their subcategories

A
  1. granulocytes (neutrophils, basophils and eosinophils)
  2. monocytes
  3. lymphocytes (b and t)
104
Q

which of the following can squeeze out of the blood vessel, red or white blood cells

A

white

105
Q

what is the lifespan of erythrocytes

A

120 days

106
Q

what happens when a RBC becomes worn out

A

it is phagocytksed and destroyed by macrophages

107
Q

what are three ways CO2 is transported with the RBC

A
  1. dissolved (7%)
  2. Hgb-CO2 (bound to hemoglobin- 23%)
  3. HCO3 (70%)
108
Q

what does carbonic anhydrase do

A

it takes carbon dioxide and water and turns it into carbonic acid and a bicarbonate. this is what allows the CO2 to be transported to the lungs. when it is back at the lungs, it is reverted to CO2 and released/expired.

109
Q

what organ filters old dying RBC

A

the spleen

110
Q

what is the amount of RBC in a man and women

A

men: 5.2 million
women: 4.7 million

111
Q

with age, RBC production will..

A

decrease

112
Q

what is the name of the stem cell that gives rise to all kinds of blood cells

A

multipotent hemopoietic stem cells

113
Q

the multipotent hemopoietic stem cells can become either one of two kinds of cells what are they

A

a lymphoid or a common myeloid

114
Q

there is only one blood cell that is not made in the marrow. what is it and where is it mad

A

T cells are made in the thymus

115
Q

what stimulates the production of RBCs

A

erythropoietin (EPO)

116
Q

what is hypoxia and what is stimulated to correct this

A

hypoxia is a decrease in RBC, decrease in Hgb synthesis, a decrease in blood flow, or hemorrhaging or even increased oxygen consumption. EPO will be stimulated

117
Q

what organ secretes EPO

A

KIDNEYS

118
Q

why is it that when a person has damaged or removed kidneys they become anemic

A

no more EPO is being produced.

119
Q

what is HIP (hypoxia inducing factor) and when is it activated. what will it do

A

activated with decreased O2 levels and a subsequent increase in EPO. This will secrete VEGF (vascular endothelial growth factor) which stimulates blood cells to stimulate angiogenesis and secretion of more capillaries which will spread the blood out better

120
Q

exercise does what to plasma and blood volume? this eventually causes RBC count to …

A

increases

increases

121
Q

what is the danger of blood doping. w

A

whether an athlete is injected just their RBC back in, or training for two weeks and getting the Increased RBC count (and eventual decrease in plasma V), the increase in RBC increases viscosity, and can lead to MI or stroke

122
Q

what vitamins are needed for the maturation or RBCs and DNA synthesis

A

you need vitamin B12 and folic acid otherwise the RBC will become too large and irregularly shaped and even fragile which will decrease their life span which is normally 120 days

123
Q

what is pernicious anemia

A

this is w B12 deficiency. B12 needs IF (intrinsic factor) to bind to it so it is not digested. Then it will bind to the mucosal walls for absorption. When there is no B12 being absorbed, you get he abnormal RBC and macrocytotic anemia

124
Q

describe where iron is and why is it so important to blood cells

A

67% iron is bound to heme in RBCs and myoglobin
30% are in macrophages and hepatic parachymal cells
3% is lost in sweat and urine and bile and blood

you need iron for erythropoiesis

125
Q

how much iron do you need a day? from what sources and in what amount?

A

you need 25 mg iron a day, only 1-2 mg comes from the diet, the rest should come from recycled RBCs

126
Q

what does bilirubin cause

A

jaundice

127
Q

what leads to bilirubin causing jaundice

A

when RBC are broken down, bilirubin increases. if its not excreted, then there is a buildup in the blood and jaundice. if this buildup is because there was a blockage in the drainage of bilirubin, then it is obstructive jaundice

128
Q

what is hemolytic jaundice

A

its in infants. they have a lot of RBCs from the mothers that need to be recycled and can become jaundiced.

129
Q

microcytic hypochromic anemia

  • causes
  • presentations
  • characteristics
A

most common
when you are iron deficient (nutritional or blood loss)
the RBCs are too small and there is less Hgb
can be from issues with iron metabolism (heme needs iron) or can be from a global synthesis issue

130
Q 
Normocyotic Normochormic Anemia 
-causes
-presentations
-characteristics 
what are some types of this
A 
normal RBC size and Hgb count. 
just not enough of them 
types:
-aplastic: loss of marrow functioning
-post-hemorrhage 
- immune destruction of RBCs
-sickle cell
131
Q

what is polycythemia

A

too many RBCs. can be an overproduction or relative (meaning that fluid loss but the number of RBC remains the same)

132
Q

what is absolute polycythemia (primary and secondary)

A

primary: the stem cells in the marrow just keep overproducing. the JAK2 gene is affected
secondary: there is an increase in EPO (with supplementation, tumor or even chronic hypoxia- high altitude)

133
Q

what are some of the effects of anemia

A

the heart rate will increase, as will the SV and the CO, there will be an increased O2 demand, and increased EPO and an increase in the RAAS system

134
Q

anemia on the circulation

A

decreased viscosity and decreased resistance which will lead to increased blood flow and CO. also there will be decreased oxygen transport and and increase in hypoxia, which will cause vasodilation and increase blood flow and CO

A BIG INCREASE iN CO

135
Q

what does the exercise capacity of an anemic person look like

A

very decreased because they cannot adapt to the exercise

136
Q

how does polycythemia affect circulation

A

increased viscosity and resistance decrease in the flow, but the increase in the number of cells increases the resistance, so that balances each other out and CO remains normal

137
Q

what are the different types of granulocytes

A

neutrophils (plymorphonucelar leucocytes)
basophils
eosinophils

138
Q

monocytes life span in the circulation versus in the tissue

A

in the circulation, they are goo for about 10 to 20 hours, in the tissues can live for weeks or months or years

139
Q

what is the role of a neutrophil

A

the phagocytosis in early inflammation and ingest and destroy bacteria and particles

140
Q

what do eosinophils do

what induces them

A

they ingest antigen-antibody complexes. they are induced by IgE hypersensitivity and are increased with parasitic infection. they kill the parasites that neutrophils cannot

141
Q

what are basophils like

A

mast cells

142
Q

where are granulocytes and monocytes made and stored

A

in the bone marrow and stay there until needed.

143
Q

where are lymphocytes made

A

in the peripheral lymphoid organs (thymus, spleen, tonsils, lymph nodes and peyer patches)

144
Q

megakaryocytes are made in the _____ and fragment into _____

A

marrow

platelets

145
Q

what do monocytes do

A

they mature in the tissues to become macrophages

146
Q

both neutrophils and monocytes exhibit ___

A

motility

147
Q

diapedesis

A

squeeze through endothelial cells

148
Q

chemotaxis

A

the cell movement controlled by a gradient of diffused chemical
neutrophils can sense a super small change and respond quickly

149
Q

how do cells move with chemotaxis

A

with actin. they move like a treadmill, depolymerize and repolymerize to move towards the chemical

150
Q

what is phagocytosis

what cells do this

A

the ingestion of particles.

neutrophils and macrophages

151
Q

how can neutrophils and macrophages distinguish between what is foreign and what is not

A

rough surfaces, lack of protective protein coats, immunicologically marked by antibodies

152
Q

how many bacteria can a neutrophil and macrophage ingest

A

neutrophil can ingest about 3-20. macrophages can ingest upwards of 100 when activated.

153
Q

what makes macrophages better and different from neutrophils

A

they can digest and extrude what they digested and still live. they can also digest RBCs and even parasites

154
Q

what does a neutrophil do when a pathogen is too large

what does this do to the neutrophil

A

it ejects large parts of chromatin (spiderwebs) to entrap the nearby bacteria until other neutrophils or macrophages can come over and finish the job
this kills the neutrophil because the chromatin is their DNA

155
Q

what are phagolysosomes

A

they are the combination of neutrophils and macrophages fusing the phagosomes and lysosomes to create a beast that becomes a digestive vesicle

156
Q

what are bactericidal agents

A

these are chemicals that will kill bacteria, even if they are not destroyed. they are biological reactive oxygen species

157
Q

monocyte-macrophage cell system

A

monocytes enter a tissue and become macrophages where they become fixed and stay until they are called away to an infection.

158
Q

what are the mechanisms to prevent blood loss

A

vascular constriction, formation of a platelet plug, blood coagulation and fibrous organization of a blood clot

159
Q

does vasoconstriction or vasodilation happen after a trauma

A

constriction

160
Q

do platelets have contractile capabilities

A

yes

161
Q

describe the membrane of a platelet

A

they adhere only to injured and exposed collagen and repels intact endothelium

162
Q

how does a platelet plug form

A

platelets travel to the injured wall and build up and develop an immobilizing mesh

163
Q

blood clot formation beings within

A

15-20 seconds

164
Q

in how many minutes does an occlusion clot stop the bleeding

A

in a few minuets

165
Q

when is there a tight clot

A

in about 20-60 min

Physiology (7 decks)

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