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Unit 6: LGS > Week 4 > Flashcards

Week 4 Flashcards

1
Q

5 Models of Osteopathic Patient Care impact on pulmonary function

  • Biomechanical
  • Respiratory-Circulatory
  • Neurological
  • Metabolic
  • Behavioral
A
  • Structure of the rib cage can affect the viscera underneath and vice versa
  • The lungs act as a pump that creates an area of low/negative pressure which encourages venous return to the right atrium of the heart. Similarly, this pump facilitates movement of lymphatic fluid up towards lymphatic trunks and ducts.
  • Lungs are controlled extrinsically by sympathetic and parasympathetic inervation
  • Lungs participate in Oxygen and carbon dioxide exchange, which allows for Bicarbonate buffering
  • Breathing helps with adequate sleep, speaking -> expressing yourself/verbal expression, exercise, smoking habits, birth (birth delivery depends on ability to control pressures.
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2
Q

Muscles for breathing

  • Primary
  • Secondary (accessory)
A
  • diaphragm,

- scalene, SCM, external intercostal mm.

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3
Q

Examples of biomechanical problems for pulmonary

  • Viscera affecting lungs
  • Lungs affecting viscera
A
  • an example is obesity/increased abdominal volume can push up on the diaphragm, decreasing respiratory function
  • an example is the Valsalva maneuver where increased thoracic pressure can increase abdominal pressure
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4
Q

How do lungs create pump for return of blood and lympathics?

A

As pressure changes in the thoracic cavity, other pressure changes occur as a consequence. As the diaphragm contracts during inhalation and moves downward toward the abdomen, volume of the thoracic cavity decreases and abdominal pressure increases. As the diaphragm relaxed during exhalation, lung pressure increases and the abdominal pressure decreases.

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5
Q

CNS innervation of lungs

  • Sympathetic: come from? causes?
  • Parasympathetic : come from? causes?
A
  • Sympathetic
  • Innervation comes from levels T3-5; Bronchodilation and decreased mucus secretion
  • Comes from branches of the vagus nerve; Increases bronchoconstriction and mucus secretion
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6
Q

Immunologic purposes of lungs

A

Catch debris and pathogens in mucus and expel with mucociliary escalator. Also contains macrophages that will help protect against infection

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7
Q

Diaphragm

  • borders
  • movements
  • type of inspiration
  • how much does it move during inspiration?
A
  • Originates at xiphoid process, the lower 6 intercostal cartilages & L1-L3. And inserts onto the central tendon.
  • As it contracts it flattens, which increases the space of the thoracic cavity
  • Quiet
  • Moves down 1-2 spinal levels
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8
Q

Scalenes

- importance in movement

A
  • Supports the cage vertically to support the movement of the diaphragm
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9
Q

latissimus

- importance in breathing

A
  • Attaches at inferior ribs

- help to brace the lower ribs outwards in support, even if you don’t move your arms

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10
Q

Expiratory mm

  • normally
  • forced
A
  • During normal there are no real drivers of exhalation–in a passive sense when you’re just breathing normally
  • Forced expiration: Innermost intercostals, internal intercostal and Abdominal mm (rectus abdominus, obliques, transversus abdominus) ->
    Encourage exhalation by increasing intra abdominal pressure, which pressures back up onto the thoracic cage
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11
Q

Compliance in the lungs

A

The ability to stretch

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12
Q

Elastic recoil

  • lungs
  • chest wall
A
  • Ability to come back to its shape
  • lungs want to naturally pull in so their recoil is inward
  • chest wall wants to naturally go out so it has outward elactic recoil
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13
Q

Do the alveoli change their volume bc they’re being filled up with air or bc they’re being pulled open?

  • what does this?
  • what is alveoli affect on it?
A
  • Bc they’re being pulled open
  • Your chest wall wants to go out & as it goes out to its natural state it pulls the alveoli open
  • As your brain ceases the inspiratory command & your mm relax then change of pressures & alveoli pull in everything & pull in chest wall
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14
Q

Differences in elastic recoil in inspiration and expiration for lungs and chest wall?

  • Inspiration
  • Expiration
A
  • Lungs: increase in elastic recoil, Chest: decrease in elastic recoil
  • Lungs: decrease in elastic recoil, Chest: increase in elastic recoil
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15
Q

Compare and contrast amount of different elastic recoils?

A

The magnitude for the 2 recoil factors for chest wall and lungs increase and decrease equally and opposite, so inward recoil to outward recoil is equal

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16
Q

How does inspiration occur?

A

Brain initiates inspiratory command, muscles of inspiration contract, outward elastic recoil starts to decrease and inward elastic recoil starts to increase, allows for passive distension of alveoli and volume increases

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17
Q

Interpleural pressure, what is it?

A

Pressure between the chest wall and the lungs

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18
Q

What happens to interpleural pressure as you expand alveoli volume during inspiration?

A

Interpleural pressure becomes more negative. So your volume is increasing, you start to distend, your interpleural pressure becomes more negative, bc you’re distension your transmural pressure increases and becomes more positive

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19
Q

What’s transmural pressure?

A

Pressure across the alveolar wall

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20
Q

Why does transmural pressure become more positive?

A

bc alveoli are expanding, and at the same time alveolar pressure is becoming more negative, so by process of pressure gradients, air moves passively down its pressure gradient (remember atmospheric pressure=0) and air flows in

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21
Q

Overall walk through of inspiration

A

Brain starts inspiratory command, inspiratory muscles contract, volume increases, interpleural pressure becomes more negative, alveoli expands, transmural pressure is increased, and alveolar pressure on the inside becomes negative, so air flows into the alveoli bc atmospheric pressure higher than alveolar pressure at this point

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22
Q

Expiration pathway

A
  • Brain signals inspiratory command to stop -> muscles relax -> volume decreases -> inward elastic recoil increases and outward elastic recoil decreases -> intrapleural pressure becomes alveolar pressure become more positive -> transmural pressure less positive than that of inspiration (this happens bc alveolar distension is decreasing, volumes are decreasing, pressure in alveoli increasing and become more positive), so now air flow goes out bc pressure gradient
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23
Q

If lung has decreased compliance, what happens to work of breathing?

A

Increases

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24
Q

negative pressure breathing

- difference in alveoli pressure

A
  • normal breathing
  • you have a greater distension in alveoli that are closer to chest wall than those farther away from the chest wall. So every one of them helps pull each other one open
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25
Q

positive pressure ventilation

A
  • ventilator that’s inducing movement

- greater distension in alveoli further away from wall than those closer to wall.

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26
Q

Mechanical interdependence

A
  • If alveoli in middle collapses, it increases stress on adjacent walls and other alveoli pull and hold it open to try to prevent collapsing of that alveoli
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27
Q

Pulmonary surfactant

  • how it relates to lungs
  • if you didnt have it?? why?
  • what does this do to elastic recoil?
  • If you didn’t have surfactant, what would happen to elastic recoil?
A
  • reduce surface tension, this is important for small alveoli
  • small alveoli would collapse; reducing the surface tension keeps the surface tension on the different sides of the alveoli a little bit altered, reducing surface tension on those smaller ones, and prevents them from collapsing into the larger ones so that you get air flow going into all of them
  • reduces it even at very high lung volumes
  • It would increase
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28
Q

If you have an increase in elastic recoil, what happens to compliance?

A

It decreases

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29
Q

FRC

  • stands for?
  • what is it?
  • usually?
A
  • functional residual capacity
  • amount of volume left in lungs at end of expiration
  • 0
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30
Q

What happens to FRC in a patient with restrictive disease?

A

Decreases. And compliance decreases bc elastic recoil increases

31
Q

What happens to FRC in a patient with obstructive disease

A

increases

32
Q

What affects FRC physiologically?

- example?

A
  • body position

- In supine position, FRC decreases, sitting up increases FRC

33
Q

Four components of pulmonary function

A

• Mechanical breathing, alveolar ventilation, pulmonary perfusion, and gas exchange

34
Q

Mechanics of breathing

  • what is it?
  • what affects it?
A
  • mechanics that’s getting air in and out of the lungs, depending upon the pressure gradient
  • atmospheric pressure versus alveolar pressure, resistance of the airways and then inward and outward elastic recoil.
35
Q

Alveolar ventilation

  • what is it?
  • what does it have to deal with?
A
  • gas exchange between the external environment and the alveolar space.
  • lung volumes and your capacity
36
Q

Pulmonary perfusion:

- what is it?

A
  • The blood flow and vascular resistance.
37
Q

V/Q matches

  • what is it?
  • what happens when it is changed?
A
  • ventilation to perfusion ratios.

- Changes in that ventilation profusion ratio can alter gas exchange.

38
Q

gas exchange

A

dealing with Fick’s law of diffusion and transport of oxygen and co2

39
Q

Pathway for mechanics of breathing

  • How to get air in? What does this to chest cavity? what does that do to outward and inward recoil? what happens to alveoli?
  • how does this affect atmospheric air?
  • How do you get expiration?
A
  • brain sends an impulse that’s going to lead to contraction of your inspiratory muscles (diaphragm and external intercostal muscles) –> The thoracic cavity increases which decreases outward elastic recoil of the chest wall and increases inward elastic recoil of the lungs –>since chest wall and your alveoli are connected and as the chest wall increases there is an increase in intrapleural pressure between the alveoli and chest wall (more negative) –> alveoli distend out.
  • on inspiration the volume inside the lungs increases –> alveolar pressure decreases and becomes more negative –> And so compared to atmospheric pressure, which is zero, where does the air go? Air flows in
  • The inward elastic recoil of the lungs, pulls everything back in. So what happens to the inward elastic recoil as it pulls it back in?
40
Q

So what happens to the inward elastic recoil as it pulls it back in?

A

It starts to decrease, while the outward elastic recoil is going to start to increase –> your volume decreases –> your alveolar pressure starts to increase more positive than that of atmospheric pressure –> you exhale out

41
Q

Alveolar ventilation

- what does i depend on? how can you change it?

A
  • Your tidal volume – if you increase your tidal volume, you can increase your alveolar ventilation
          ▪ This is where structure indicates function – When we're talking about anatomical, we all have anatomical dead space in the conducting zone. What's unique about the conducting zone that's different than the respiratory zone?
  • alveolar ventilation is also dependent upon the amount of anatomical dead space that you have.
42
Q

Dead space

  • types
  • where does it occur
A
  • anatomical and alveolar, and physiological is the combination of the two
  • Dead Space is where there is no gas exchange. Anatomically, that’s the conducting zone.
43
Q

Alveolar dead space

  • what is it?
  • how can you increase it?
  • PE
  • how to measure?
  • how does this effect ventilation
A
  • areas where there is no perfusion, but you may have ventilation.
  • Pathologies: Emphysema and embolisms
  • Pulmonary embolism is a great example of that, because you have blockages in the in the capillaries. And so those alveoli may be ventilated, but they are not perfused, so that leads to alveolar dead space.
  • If you measure alveolar CO2 versus arterial co2 ->
    If arterial co2 in the blood is greater than alveolar co2, meaning there’s more co2 left in your blood than you are expiring out, are you getting that co2 out?
  • You don’t have perfusion, there is no gas exchange, and so it means your physiological dead space is greater than the anatomical dead space because physiological dead space is anatomical + alveolar. So, if your physiological dead space is greater than that means if you have a significant amount of alveolar dead space.
44
Q

How does gas diffuse?

A

from high partial pressure to low partial pressure

45
Q

how the environment measures the partial pressure gradient in the alveoli, is dependent upon

A

how much oxygen is present in the atmosphere and the barometric pressure.

46
Q

How much oxygen is the atmosphere?

  • is this dependent on location
  • how can you change this?
A
  • 21%
  • No
  • by giving the patient 100% oxygen
47
Q

Importance of barometric pressure?

- does this change with location?

A
  • it impacts the partial pressure in the alveoli

- YES

48
Q

How alveolar ventilation and levels of O2 and CO2 coorelate

A

as you start to increase alveolar ventilation, your partial pressure of oxygen in your alveoli starts to increase, and as you increase alveolar ventilation, your partial pressure of co2 in your alveoli start to decrease

49
Q

Explain how alveolar ventilation is altered during exercise

  • why is this important?
  • what happens to inspiratory reserve volume?
  • what happens to inspiration and expiration?
  • kind of expiration?
  • pathway
A
  • It’s increasing, because you’re increasing your tidal volume and your breathing frequency also increases
  • You have increased metabolic demand, you’re producing more co2, you’re trying to blow it off as well as get more oxygen in.
  • slight decrease
  • You have very big inspiratory volumes and expiratory volume is decreased
  • forced, having to use muscles
  • have very big volume inspired and so the area is bigger than normal and you have to contract the muscles during expiration –> Your thoracic cavity decreases in size by a lot due to the use of the muscles –> lower volume in the lungs –> greater increase in outward elastic recoil than normal –> have to work harder to inspire –> when you inspire and get bigger than normal volume then the outward elastic recoil is over stretched which makes the chest wall want to come back in and makes expiration easier.
50
Q

Why does tidal volume increase in exercise?

A

you’re trying to get to very high volumes of oxygen in your lungs and very low volumes on expiration to blow off that co2.

51
Q

Why does airway resistance increase in exercise?

A

During exercise the bronchioles dilate -> so the radius of the bronchioles are bigger, so you have a bigger tube -> more airflow –> more turbulent airflow and that increases resistance

52
Q

What happens to your smaller airways when you have more and more forced expiration?
- explain dynamic compression

A
  • They start collapsing because when you have forced expiration, your inner pleural pressure becomes positive. Your alveolar pressure as well as the elastic recoil pressure becomes very positive.
  • There is a point where the intrapleural pressure and the pressure inside the airway will equalize and then the intrapleural pressure becomes greater than the pressure inside the airway so if you’re not in an area that has a lot of cartilage the airway will collapse because you have greater pressure on the outside than you do on the inside.
53
Q

How to manage airways?

A

Sympathetics and parasympathetics

54
Q

Sympathetics

  • Effect on bronchioles
  • Acting on?
  • Receptor
A

○ Dilate
- Smooth muscle– myosin light chain kinase and phosphatase
- Beta 2 adrenergic receptor
G alpha s protein because it increase cAMP which inhibits myosin light chain kinase -> relaxes smooth muscle

55
Q

Parasympathetics

  • Effect on bronchioles
  • Working on?
  • Receptor?
A
  • Constrict
  • Smooth muscle
  • Muscarinic (M3)
    G q protein: increases IP3 -> increase in Ca -> Ca binds to calmodulin -> activates myosin light chain kinase -> stimulates contraction
56
Q

Overview of smooth muscle

  • dependent on?
  • contraction?
  • relaxation?
  • B2
  • M3
A
  • myosin light chain kinase and phosphatase
  • you activate the kinase
  • you activate the phosphatase/ inhibit the kinase
  • B2 -> inhibits the kinase; Nitric Oxide (NO) in vasculature activates the phosphatase
  • M3 activates IP3 -> will cause increase in Ca -> activate the kinase
57
Q

For bronchial dilation, what is something that increases adnelyl cyclase?

  • how does this work?
  • examples of short acting?
A
  • Beta 2 agonists
  • Activated adenylyl cyclase through G alpha s which increases cAMP which then inhibits myosin light chain kinase which causes relaxation
  • Short: albuterol and salbutamol
58
Q

For bronchial constriction med you can use?

  • name?
  • type?
A
  • Acetylcholine
    ○ Inhibitor: muscarinic antagonists
    ○ Short acting and long acting
59
Q

If a drug binds to a receptor, does it stay there?

- The probability of binding the receptor will change depending on …?

A
  • It can, but most bind reversibly, so it binds off and on

- the concentration of drug in the serum

60
Q

What things can alter ligands ability to occupy receptor?

- how to measure drug occupancy?

A
  • Pharmacokinetics: Absorbed
    ( Bio-availability: Can it get into serum?); Metabolism (is the drug degraded and no longer active or a Prodrug: needs to be metabolized before it can be active?); Clearance rate; Chemical properties of drug
    (Lipophilicity: Can alter volume of drugs distribution and affects concentration in the serum)
  • Pharmacodynamics: Drug Occupancy (drugs ability to bind the receptor)
  • To measure: use Dissociation constant (KD)- looks at relative association and disassociation rates of a drug and drug receptor pair
61
Q

Tiotrpoium

  • What do we know about duration? why?
  • how?
  • is it just because it has high affinity?
  • why is this an advantage?
  • short acting version?
A
  • anti-muscarinic broncho dilator
  • Long acting; Low KD
  • Based on biochemistry and the type of bond and functional groups in the binding domain -> They tell the receptor whether it is going to bind tightly or not
  • no, more about how quickly it dissociates from the different receptors; it disassociated from M3 receptors more slowly but rapidly disassociates from M2s
  • Because it allows it to be more selective for the lungs –> It disassociates from M2 receptors so quickly that it has no effect on them.
  • indotropium
62
Q

Solbuterol

  • what is it?
  • What factors influence the duration of action? (2)
A
  • Long acting beta agonsist
  • Highly lipophilic: goes into the plasma membrane very rapidly and diffuses out very slowly. Keeps pocket of drug near receptor and diffuses out as needed. Can also be tethered to the membrane by a chain (chemist comes up with interesting formulations). So if drug cannot be degraded it will increase the probability of it binding.
63
Q

Emphysema

  • how can you tell histologically?
  • effect on surface area?
  • why is decrease in tissue so important?
  • what does decrease in tissue leave? what does this do to the vol of the lungs?
  • flow volume curve?
A
  • Damage alveolar septal wall
  • Decreases
  • If you loose tissue then you start having trouble keeping the alveoli open and then they collapse creating pockets of air
  • air pockets– increases
  • has concave portion on curve during expiration - effort dependent and independent parts
64
Q

What is difference between emphysema and bronchitis

  • Type of disease process -> effects?
  • elastic recoil and compliance
A
  • Emphysema is destructive process; Damages lung tissue -> decreases elastic recoil -> Compliance increases
  • Bronchitis is inflammatory process -> Produces excess mucus -> Decrease in radius because of inflammation; thickening of bronchi
65
Q

What is big over arching name for bronchitis and emphysema?

- what condition is this?

A
  • COPD
  • Obstructive
  • Decrease in septal tissue -> loss of radial traction -> leads to air trapping
66
Q

How would obstructive disease alter spirometry?

  • FVC
  • FEV (forced expiration volume) /FVC (forced vital capacity)
  • Residual volume?
  • FEV1
  • TLC
  • FRC
  • FEF
A
  • Forced Vital Capacity? Decreased -> The airways collapse as you force air out of them because of dynamic compression; In this case during expiration your airways are going to close pre-maturely at a higher lung volume than normal
  • FEV/FVC -> decreased ; Because it is an obstructive condition
  • Residual volume? There is air trapping so residual volume increases.
  • FEV1: amount you can expire in 1 sec- Decrease
  • TLC: increased
  • FRC: increased because it is made up of residual volume and expiratory reserve
  • FEF in smaller airways? Depends on severity; The more severe -> the greater the obstruction in the smaller airways -> lower the number
67
Q

Why is residual volume increased in obstructive disorder?

A

Loss alveolar septal tissue that is tethered to the airways -> Lose radial traction that helps to keep the airways open -> When air is forced out then you get greater dynamic compression at a higher lung volume which contributes to increased residual volume.

68
Q

Flow/Volume Curve in obstructive disorders

  • what happens during expiration?
  • effect on loop?
  • what happens to loop during inspiration?
A
  • Less traction on airways so they are collapsing
  • Concave and shifted to left
    because TLC and RV are increasing
  • What happens to inspiration? Nothing -> loop will be close to normal
69
Q

Differentiate Emphysema and bronchitis

  • dyspnea
  • cough
  • chest expansion
  • cyanosis
  • breath sounds
  • JVP
  • edema
  • Arterial P02
  • Arterial PCO2
A
  • both increase over years
  • E: little/ no; B: frequent w/ sputum
  • E: yes, A LOT; B: no or moderate
  • E: no, B: yes
  • E: quiet; B: rales and rhonchi
  • E: normal; B: raised
  • E: none; B: yes
  • E: moderatley depressed, B: low
  • E: normal, B: low
70
Q

what’s the difference between asthma and COPD

- difference in curves?

A

Asthma is a reversible disease process

- would still have shift tot the right but would not be concave

71
Q

Asthma

  • type of disease
  • how is it reversible?
A
  • obstructive lung disease

- FEV and FVC can improve once medications are given

72
Q

Emphysema vs asthma

A
  • emphysema is actually destroying that septal issue.

where with asthma, you’re not damaging the alveoli it’s the inflammation of your bronchioles.

73
Q

Restrictive conditions

  • what happens?
  • why?
  • what happens to FRC?
  • what happens to flow volume curve?
  • what happens to alveolar ventilation during exercise
A
  • You lose compliance, you have an increase in elastic recoil
  • Fibrosis
  • decreases because inward ER creates a greater elastic recoil of the lungs so FRC must decrease to match the new elastic recoil
  • Shifted to the right and small.
  • decreased and would not be able to meet metabolic demand because unable to increase tidal volume due to inability to be compliant

Unit 6: LGS (10 decks)

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