Physiology Flashcards

1
Q

What is the study of respiratory physiology?

A

the study of how oxygen is brought into the lungs and delivered to the tissue and how carbon dioxide is removed

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2
Q

What are 6 functions of the respiratory system?

A

1) Provide oxygen and eliminate carbon dioxide (homeostatic/stable regulation of blood gases)
2) protects against microbial infection (filtering toxins that are inhaled)
3) regulates blood pH (in coordination with the kidneys)- through CO2
4) contributes to phonation (passage of air through the vocal cords/larynx allowing speech formation)
5) contributes to olfaction (sense of smell when air passes through the epithelium in the nasal cavity)
6) is a reservoir for blood

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3
Q

What are the structures that are apart of the upper airways

A

the nasal and oral cavities, pharynx, larynx (vocal cords)

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4
Q

How does air pass through?

A

starts at nasal and oral cavities then pharynx then larynx then trachea and then lungs

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5
Q

What do the muscles of respiration do?

A

allow for continuous change in pressure and volume in lungs

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6
Q

Structure of the trachea and the primary bronchi?

A

they have C-shaped cartilage in the front (anteriorly) and smooth muscle at the back (posteriorly)

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7
Q

What is the purpose of the structure that the trachea and primary bronchi have?

A

to provide protection and elasticity

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8
Q

Structure of the bronchi

A

they have plates of cartilage (no longer C-shaped) and smooth muscle

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9
Q

Structures of bronchioles

A

smooth muscle only no cartilage

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10
Q

Beyond the larynx what are the 2 zones that the airways can be divided into?

A

conducting zone and respiratory zone

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11
Q

What structures are a part of the conducting zone

A

the trachea, bronchi, bronchioles and terminal bronchioles

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12
Q

Conducting zone

A

no gas exchange occurs here since no alveoli

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13
Q

Which zone is called the anatomical dead space

A

conducting zone

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14
Q

What structures are a part of the respiratory zone

A

the respiratory bronchioles, alveolar ducts and alveolar sacs

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15
Q

respiratory zone

A

where gas exchange happens (bc alveoli are here)

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16
Q

Terminal bronchioles

A

the smallest airway without alveoli

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17
Q

What are the alveoli

A

tiny, thin-walled capillary rich sac in the lungs where the exchange of oxygen and carbon dioxide takes place

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18
Q

What are the alveoli surrounded by

A

capillaries

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19
Q

What do the type I alveolar cells do

A

they are involved in the process of gas exchange between alveoli and capillaries, squamous (flattened) in shape and thin, unable to replicate/divide so are more susceptible to toxins

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20
Q

What do type ii alveolar cells do?

A

they are responsible for the secretion of pulmonary surfactants, only comprise a fraction of the alveolar surface ~7% but are numerous ~60% of total cells, and can act as progenitor cells

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21
Q

What is surfactant and what does it do?

A

a detergent-like substance made of lipoproteins; reduces the surface tension of the alveolar fluid

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22
Q

What does it mean that the type II alveolar cells act as progenitor cells?

A

that when there is an injury to type I cells, type II cells can multiply and eventually differentiate into type I cells

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23
Q

Alveolar wall structure

A

contains a dense network of capillaries and a small interstitial space (connective tissue and interstitial fluids)

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24
Q

Size of capillaries

A

they are small just enough space for a RBC to pass

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25
Q

How does oxygen and carbon dioxide pass through the respiratory membrane?

A

this occurs through diffusion

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26
Q

The direction that oxygen diffuses

A

oxygen diffuses from the alveoli to the bloodstream

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27
Q

The direction that carbon dioxide diffuses?

A

it diffuses from the bloodstream to alveoli

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28
Q

Properties of the respiratory membrane

A

it is extremely thin and can be easily damaged

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29
Q

What does the respiratory membrane include

A

the alveolar fluid (with surfactant), alveolar epithelium, basement membrane of the alveolar epithelium, interstitial space, basement membrane of capillary endothelium, capillary endothelium

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30
Q

What are the 3 steps of respiration

A

1) ventilation: exchange of air between atmosphere and alveoli by bulk flow
2) exchange of oxygen and CO2 between alveolar air and blood in lung capillaries by diffusion (oxygen leaves alveoli entering the capillaries to heart and CO2 leaves capillary into alveoli to get oxygenated)
3) exchange of O2 and CO2 between blood in tissue capillaries and cells in tissues by diffusion (oxygen gets dumped into the cells and CO2 gets picked up by the capillaries to go back to the lungs)

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31
Q

How is respiratory airflow (ventilation) produced?

A

1) CNS sends rhythmic excitatory (respiratory) drive to respiratory muscles
2) respiratory muscles contract rhythmically and in a very organized pattern
3) changes in volume and pressures at the level of the chest and lung occur
4) air flows in and out

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32
Q

Inspiratory pump muscles

A

diaphragm, external intercostals, parasternal intercostals

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33
Q

Expiratory pump muscles

A

internal intercostals, abdominals

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34
Q

inspiratory airway muscles

A

tongue protruders (genioglossus), alae nasi, muscles around airways (pharynx and larynx)

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35
Q

expiratory airway muscles

A

pharynx and larynx

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36
Q

inspiratory accessory muscles

A

sternocleidomastoid, scalene

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37
Q

What do the accessory muscles do

A

facilitate respiration when increased metabolic drive

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38
Q

5 muscles of inspiration

A

1) sternocleidomastoid
2) scalenes
3) external intercostals
4) parasternal intercostals
5) diaphragm

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39
Q

5 muscles of expiration

A

1) Internal intercostals
2) external abdominal oblique
3) internal abdominal oblique
4) transversus abdominis
5) rectus abdominis

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40
Q

What is the diaphragm?

A

a dome-shaped muscle

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41
Q

What else happens when the diaphragm contracts?

A

the abdominal contents are forced down and forward and the rib cage is widened also there is an increase in the volume of the thorax

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42
Q

movement of the external intercostal muscles during inspiration

A

contract and pull ribs upward increasing the lateral volume of the thorax

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43
Q

movement of the diaphragm during inspiration

A

it flattens

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44
Q

What is lung compliance

A

a measure of the elastic properties of the lungs and a measure of how easily the lungs can expand; the magnitude of the change in lung volume (V) produced by a given change in the transpulmonary pressure (PTP)

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45
Q

Why do the small airways play a greater role in determining airflow resistance in disease conditions than larger airways?

A

because they are easily occluded by smooth muscle contraction in their walls, edema occurring in the walls of the alveoli and bronchioles, mucus collecting in the lumens of bronchioles

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46
Q

Which sized airway in diseased conditions will play a greater role in determining airflow resistance?

A

the small airways

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47
Q

Resistance is highest in the ___(large/medium/small)sized conducting airways and lower in the (small/large/medium) airways because of their (…)

A

medium, large, larger diameters

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48
Q

how does having a smaller radius/ small airway radius affect the resistance and the airflow ?

A

resistance will increase and the airflow will decrease

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49
Q

Where is turbulent airflow found?

A

in the large airways like the trachea, larynx, pharynx

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50
Q

What kind of airflow results in the greatest resistance

A

turbulent

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51
Q

Where is the airflow transitional

A

throughout most of the bronchial tree

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52
Q

amount of airflow resistance in transitional airflow

A

higher because it takes more energy to produce the vortices (whirlpools inside the tubes)

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53
Q

What kind of airways is laminar airflow characteristic to?

A

small airways that are distal (so starting at bronchi) to terminal bronchioles

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54
Q

Amount of airflow resistance in a laminar flow

A

there is little airflow resistance

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55
Q

When is airflow resistance even more sensitive to changes in radius?

A

when the flow is not laminar

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56
Q

A way to reduce the friction created by the lung and chest wall gliding past each other

A

the intrapleural fluid in between the 2 pleura cavities

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57
Q

Types of frictions that act as resistive forces to airflow

A

1) lung tissue past itself during expansion
2) lung and chest wall tissue surfaces gliding past each other
3) frictional resistance to flow of air through the airways (the majority of resistance comes from here)

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58
Q

Resistive forces to air flow

A

1) Inertia of the respiratory system - the lungs and chest wall have a nonzero mass, which like all matter resists(inertia- wants to stay in dormant position) being accelerated. Inertia and its contribution is difficult to estimate though so its said to be negligible
2) friction

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59
Q

What is airway resistance?

A

the change in transpulmonary pressure (the pressure difference between the mouth and the alveoli) needed to produce a unit flow of gas through the airways of the lung

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60
Q

movement of parasternal intercostal muscles during inspiration

A

contract and pull sternum forward, increasing anterior posterior dimension of the rib cage

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61
Q

movement of abdominals during expiration (at rest)

A

relaxed and involved in other physiological functions (coughing, vomiting, defecation, posture)

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62
Q

movement of abdominals during expiration (deep fast breathing)

A

contracting to return the lung to its resting position

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63
Q

movement of internal intercostal muscles during inspiration (at rest)

A

relaxed

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64
Q

movement of internal intercostal muscles during expiration (during exercise)

A

pull rib cage down, reducing thoracic volume

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65
Q

movement of scalenes during inspiration

A

elevate upper ribs

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66
Q

movement of sternocleidomastoids during inspiration

A

raise the sternum

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67
Q

When do scalenes and sternocleidomastoids contribute most

A

when there is exercise or forced respiration is when they will contract. They contribute little to quiet breathing ( at rest)

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68
Q

Inspiration at rest

A
  • diaphragm contracts (moves down)

- external intercostal muscles pull ribs up and out

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69
Q

Inspiration during forced respiration

A
  • sternocleidomastoid elevates sternum
  • pectoralis minor elevate ribs
  • diaphragm contracts more (goes down)
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70
Q

expiration at rest

A
  • diaphragm relaxed (up)

- abdominal organs recoil and press the diaphragm upward

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71
Q

expiration during forced respiration

A
  • posterior internal intercostal muscles pull ribs down and inward
  • abdominal organs force diaphragm higher
  • abdominal wall muscles contract and compress abdominal organs
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72
Q

What is obstructive sleep apnea

A

reduction in upper airway patency (openness) during sleep causing snoring, sleep disturbances, lower levels of oxygen in the blood, daytime sleepiness, cognitive impairments etc.

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73
Q

What causes sleep apnea

A

reduction in muscle tone and anatomical defects i.e. fat

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74
Q

What are the conducting airways lined with?

A

a superficial layer of epithelial cells which comprise of mucus-producing (goblet) cells and ciliated cells

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75
Q

What is the “mucociliary escalator”

A

the mucus producing goblet cells and ciliated cells work together to entrap inhaled biological and inert particulates and remove them from the airways

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76
Q

What do the ciliated cells do

A

they produce a periciliary fluid (sol layer) that has low viscosity optimal for ciliary activity ( the ciliary rest on top of the epithelial cells and are surrounded by sol layer which lets them move freely)

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77
Q

What do goblet cells do

A

they produce mucus (gel layer) that will trap inhaled materials

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78
Q

What direction do cilia move in

A

downward from the nasopharynx, and upward from trachea

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79
Q

What does smoking do to the cilia and goblet cells

A

it reduces the activity of the cilia and increases the number of goblet cells which makes for more mucus

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80
Q

What acts as a last defense to inhaled particles if the goblet and cilia cells did not catch it

A

the macrophages in the alveoli. The particulates will attract macrophages and will be rapidly phagocytosed

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81
Q

What is a result if silica dust and asbestos is inhaled

A

pulmonary fibrosis

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82
Q

What is spirometry

A

a pulmonary function test where the patient breathes into a tube to determine the amount and rate of inspired and expired air

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83
Q

What kind of lung volume cannot be measured by means of simple spirometry test

A

residual volume (max. air that remains in lung after max. respiration )

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84
Q

What is Atelectasis and how does it develop

A

complete or partial collapse of a lung or lobe of a lung; it develops when alveoli become deflated/collapse

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85
Q

Tidal volume (TV)

A

the volume of air moved in or out of the respiratory tract (breathed) during each ventilatory cycle

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86
Q

Inspiratory reserve volume (IRV)

A

the additional volume of air that can be forcibly inhaled followed a normal inspiration. It can be accessed simply by inspiring maximally to the maximum possible inspiration

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87
Q

Expiratory reserve volume (ERV)

A

the additional volume of air that can be forcibly exhaled following a normal expiration. It can be accessed simply by expiring maximally to the maximum voluntary expiration

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88
Q

Residual Volume (RV)

A

the volume of air remaining in the lungs after a maximal expiration. It cannot be expired no matter how vigorous or long the effort

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89
Q

What are lung capacities

A

the sum of 2 or more lung volumes

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90
Q

Vital capacity (VC)

A

the maximal volume of air that can be forcibly exhaled after a maximal inspiration VC=TV + IRV + ERV

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91
Q

Inspiratory capacity (IC)

A

the maximal volume of air that can be forcibly inhaled IC= TV+IRV

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92
Q

Functional Residual Capacity (FRC)

A

the volume of air remaining in the lungs at the end of a normal expiration FRC=RV+ERV

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93
Q

Total lung capacity (TLC)

A

the volume of air in the lungs at the end of a maximal inspiration (Total)
TLC= FRC+ TV+ IRV+ VC+RV

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94
Q

Total/minute ventilation

A

total amount of air moved into the respiratory system per minute = tidal volume (volume of inspired air at each breath) x respiratory frequency (breaths per minute bpm)

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95
Q

Alveolar ventilation VA

A

amount of air moved into the alveoli per minute (VA= (TV or tidal volume - VD or dead space volume) x frequency ))

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96
Q

What does the alveolar ventilation depend on

A

the anatomical dead space (volume of air contained in conducting zone)

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97
Q

around how much of our normal breath is not available for gas exchange

A

~1/3

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98
Q

increased depth of breathing is more effective in increasing…

A

alveolar ventilation than an equivalent increase in breathing rate (minute ventilation )

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99
Q

FEV1

A

Forced Expiratory Volume in 1 second ( a healthy person can normally blow out most of the air from their lungs within 1 second)

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100
Q

FVC

A

forced vital capacity, the total amount of air that is blown out in one breath after max inspiration as fast as possible (FEV1+FEV1+FEV3 etc.)

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101
Q

FEV1/FVC

A

proportion of the amount of air that is blown out in 1 second

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102
Q

What are the 3 main patterns that the spirometry test shows?

A

1) Normal (age, gender, weight, height)
2) An obstructive pattern
3) A restrictive pattern

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103
Q

What happens to patients with obstructive lung disease (shows the obstructive pattern in spirometry )

A

they have shortness of breath due to difficult in exhaling all the air from their lungs (the exhaled air comes out more slowly than normal)

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104
Q

FEV1 and FVC and FEV1/FVC in obstructive pattern

A

FEV1 is significantly reduced (slower to expire air)
FVC is normal/reduced
FEV1/FVC is reduced (<0.7)

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105
Q

Way to help asthma caused by obstructive lung disease

A

beta2 adrenergic agonists to reduce bronchospasm (which makes it difficult to breath)

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106
Q

What happens to patients who have been affected by restrictive lung disease seen by the restrictive pattern on spirometer?

A

they cannot fully fill their lungs with air. Their lungs are “restricted” from fully expanding

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107
Q

What does restrictive lung disease result from?

A

a condition causing stiffness in the lungs themselves. In other cases, stiffness of the chest wall, weak muscles or damaged nerves may cause the restriction in lung expansion

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108
Q

FEV1, FVC and FEV1/FVC in restrictive pattern

A

FEV1 is reduced
FVC is reduced
FEV1/FVC almost normal

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109
Q

What is the Helium Dilution Method (Gas Dilution Technique)

A

a method of measuring the FRC (functional residual capacity) of the lungs which is RV+ ERV

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110
Q

How is the helium dilution technique conducted

A

a spirometer is filled with a mixture of helium and oxygen. The patient is asked to breathe in the mixture starting from FRC (gas volume in the lung after a normal breath out). The spirometer measures helium concentration V2 (FRC+volume of spirometer)=V1 (volume of gas in spirometer) (C1(initial helium concentration )-C2)/C2 (final helium concentration measured)

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111
Q

Static properties of the lung

A

mechanical properties when no air is flowing (necessary to maintain lung and chest wall at a certain volume)

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112
Q

Dynamic properties of the lung

A

mechanical properties when the lungs are changing volume and air is flowing in and out (necessary to permit airflow)

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113
Q

Bulk flow

A

gas moves from high pressure to low

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114
Q

Boyle’s law

A

for a fixed amount of an ideal gas kept at a fixed temperature (constant T) P1V1=P2V2 (where if pressure increases volume decreases and if pressure decreases volume increases)

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115
Q

What happens if the alveoli has low volume but high pressure

A

it will cause expiration

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116
Q

What happens if the alveoli has high volume but low pressure

A

it will cause inspiration

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117
Q

What are the 2 pressures in ventilation

A

Palv (P alveoli) and Patm (P atmosphere)

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118
Q

What happens if Palv< Patm

A

air will enter from the atmosphere (following bulk flow H to L) and increase the thoracic volume, lung volume and decrease alveolar pressure

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119
Q

What happens if Palv>Patm

A

air will leave so because the gas molecules are being compressed the alveolar pressure increases

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120
Q

The pleurae

A

thin double-layered envelope that includes the visceral pleura and parietal pleura

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121
Q

Visceral pleura

A

covers the external surface of the lung

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122
Q

Parietal pleura

A

covers thoracic wall (against the ribs) and superior face of the diaphragm (on bottom of lungs but covering top of diaphragm)

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123
Q

Intrapleural fluid

A

reduces friction of lung against thoracic wall during breathing (in between the two pleural tissues allowing them to slide around with each inspiratory effort)

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124
Q

Elastic recoil

A

Tendency for the lungs to collapse or reduce in volume and the chest wall to expand and pull the thoracic cage outward after being stretched or expanded

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125
Q

The 3 pressures involved in the movement of air in and out of the lungs

A

1) Intrapleural pressure PIP
2) Alveolar pressure PALV
3) Transpulmonary pressure PTP

126
Q

What is intrapleural pressure

A

pressure in the pleural cavity that acts as a relative vacuum, it fluctuates with breathing but is always subatmospheric (lower than atmosphere) due to the opposing directions of the elastic recoil of lungs and thoracic cage

127
Q

What would happen if PIP equals PALV

A

the lungs would collapse (collapsed lung)

128
Q

Alveolar Pressure (PALV)

A

pressure of the air inside the alveoli that is involved in producing air flow

129
Q

What happens when the glottis is open and no air flows into or out of the lungs

A

the pressure in all parts of the respiratory tree including the alveoli PALV are equal to atmospheric pressure PATM

130
Q

Transpulmonary pressure PTP

A

the force responsible for keeping the alveoli open, expressed as the pressure gradient across the alveolar wall

131
Q

in order to maintain the lungs expanded in the thorax PALV

A

should alway be > PIP

132
Q

PTP is a static parameter which does not cause airflow, but determines

A

lung volume (VL)

133
Q

PALV unlike PTP is a static or dynamic component

A

dynamic because it determines air flow

134
Q

Summary of how inspiration works

A

1) CNS
2) Diaphragm and inspiratory intercostals contract
3) thorax expand
4) PIP becomes subatmospheric
5) increase in transpulmonary pressure (PALV- PIP)
6) lungs expand
7) PALV becomes subatmospheric
8) air flows into alveoli (following high to low pressure)

135
Q

Summary of how expiration works

A

1) Diaphragm and inspiratory intercostals STOP contracting
2) Chest wall recoils inwards/ going back to resting state
3) PIP moves back toward pre-inspiration value
4) Transpulmonary pressure moves back toward pre-inspiration value (negative)
5) lungs recoil toward pre-inspiration size
6) air in alveoli becomes compressed
7) PALV becomes greater than PATM (high to low- our alveoli is the high and the atmosphere is low)
8) air flows out of lungs

136
Q

Resistive forces to air flow

A

1) Inertia of the respiratory system - the lungs and chest wall have a nonzero mass, which like all matter resists(inertia- wants to stay in dormant position) being accelerated. Inertia and its contribution is difficult to estimate though so its said to be negligible
2) friction

137
Q

Static compliance of the lung

A

represents lung compliance (elasticity) measured during period of no gas flow e.g. during an inspiratory/expiratory pause ; determined by P(transpulmonary pressure which is between lung and pleural cavity)/V (lung volume) slope when measured at the end of an expiratory event

138
Q

What does high compliance mean

A

floppy lungs because of the lost of alveolar tissue which makes for less surface area available for gas exchange

139
Q

What is an example of high compliance

A

emphysema- lung condition that causes shortness of breath because the air sacs in the lungs (alveoli) are damaged. Over time, the inner walls of the air sacs weaken and rupture creating larger air spaces instead of many small ones

140
Q

What is an example of low compliance?

A

pulmonary fibrosis- chronic damage to lungs due to inhalation of asbestos or silica dust which kills macrophages that are present in the lungs. This will then promote accumulation of the asbestos or silica dust since they cannot be killed by macrophages, leading also to an overproduction of collagen. Collagen makes lungs stiff and that means that there will be a big effort to expand the chest wall to increase transpulmonary pressure that is responsible for changing lung volume

141
Q

Dynamic compliance

A

represents pulmonary compliance during periods of gas flow e.g. inspiration or when transpulmonary pressure continuously changes; reflects not only lung stiffness but also airway resistance

142
Q

What happens to the dynamic compliance when there is an increase in lung stiffness or airway resistance

A

dynamic compliance will decrease/fall

143
Q

At high lung volume the compliance will

A

decrease

144
Q

What is hysteresis

A

difference between the inflation and deflation compliance paths

145
Q

Why does hysteresis exist?

A

because a greater pressure difference is required to open a previously close (or narrowed) airway than to keep an open airway from closing

146
Q

What are 2 factors that determine lung compliance

A

1) elastic components of the lungs and airway tissue (elastin, collagen)
2) surface tension at the air-water interface within the alveoli

147
Q

Elastin vs collagen

A

Elastin- is like a weak spring , low tensile strength(can easily break if stretched too far), extensible (stretchable)

Collagen- like a strong twine, high tensile strength(stronger), inextensible (not stretchable)

148
Q

With aging elastin and collagen levels will (increase/decrease) and so lung compliance will (increase/decrease)

A

decrease… increase (floppy lungs)

149
Q

an increase in surface tension will (increase/decrease) lung compliance

A

decrease

150
Q

What is surface tension

A

the cohesive force by hydrogen bonding that makes the water molecules at the surface of a liquid-gas interface (air-water) attracted to each other

151
Q

What is the purpose of surface tension?

A

to “cause” the surface to maintain as small an area as possible

152
Q

What is the air-liquid interface in relation to the respiratory system?

A

when air entering the lungs is humidified and saturated with water vapor at body temperature

153
Q

What does surface tension in the alveoli cause?

A

an inward recoil which leads to alveolar collapse (it is reducing the alveolis volume and increasing its pressure)

154
Q

What happens to the alveolar surface tension at equilibrium?

A

the tendency of increased pressure to expand the alveolus will balance with the tendency of surface tension to want to collapse the alveolus

155
Q

The smaller the alveoli’s radius the (smaller/greater) needed to keep it inflated

A

greater

156
Q

But if the pressure to keep the small alveoli’s open is greater than the larger ones then what could hypothetically happen?

A

the small alveoli will collapse into the larger one because gas moves high to low pressure

157
Q

Why is it not physiologically possible for the small alveoli to collapse into the larger one despite having greater pressure?

A

because of surfactant

158
Q

What does surfactant do to the surface tension?

A

it will decrease it so we can breathe without too much effort as well as making the alveoli stable against collapse

159
Q

What are the most important components of the pulmonary surfactant?

A

phospholipids dipalmitoyl-phosphatidylcholine (DPPC), phosphatidyl-choline, surfactant apoproteins and calcium ions … it is made of 90% lipids and 10% proteins

160
Q

How does the surfactant get into the air-water interface to decrease the density of the water molecules/ decrease surface tension between them?

A

because it has hydrophobic and hydrophilic properties (as 90% lipid)

161
Q

surfactant (reduces/increases) the surface tension of water which will (increase/decrease) the lung compliance making it (harder to expand lungs/easier to expand lungs)

A

reduces…increase…easier to expand lungs

162
Q

the relationship between the thickness of surfactant and the surface area

A

low SA= thick surfactant

high SA= thin surfactant

163
Q

Surface tension with high-quality surfactant and the consequences of that interaction?

A

surface tension will fall as the radius of the alveoli gets smaller because the surfactant molecules become crowded. And will increase with an increasing alveolar radius. When the radius is very small, the surface tension falls almost to zero, and the pressure required to keep the smaller bubble open is negligible, and thus it does not collapse.

164
Q

The dynamic properties of surfactant permit the alveolar surface tension to?

A

change with inflation and deflation; keeping the small alveoli from total collapse (atelectasis) and larger ones from hyperinflation

165
Q

2 purposes of surfactant

A

1) to improve compliance (by reducing surface tension of alveolar fluid)
2) to stabilize the alveolar size

166
Q

surfactant in premature infants

A

they lack surfactant which will decrease their lung compliance making it more difficult for them to breath -resulting in IRDS (infant respiratory distress)

167
Q

How can a baby be able to breath easier if they have IRDS?

A

by being administered artificial surfactant

168
Q

How to measure the regional differences in ventilation?

A

using an inhalation test where the person is inhales radioactive xenon which will penetrate the chest wall and be able to be measure in counters. The amount of radioactivity is an indication of how much air is inhaled in different regions of the lung

169
Q

Ventilation vs respiration

A

ventilation- mechanical action of bringing in air

respiration- involves the exchange of gases

170
Q

radioactivity measured in a person lying flat

A

large amount of radioactivity found at the back of the lungs (towards back)- more air is inhaled in back(b/c of gravity)

171
Q

Which zone of the lungs is lower ventilation found

A

upper zone

172
Q

Which zone of the lungs has the greatest ventilation

A

lowest zone

173
Q

Why do the bottom regions of the lung receive a larger portion of the inspired air than the top regions?

A

because of the weight of fluid in the pleural cavity which will increase the PIP to a less negative value allowing for the alveoli to have higher compliance/ able to expand more now at the base. Thus, bottom regions of lung receive a larger portion of the inspired air

174
Q

Why is inhalation a negative pressure ventilation?

A

because when you inhale the diaphragm and muscles between your ribs will contract (ribs expand and go up and diaphragm moves down), creating negative pressure -or vacuum- inside your chest cavity . This negative pressure will draw in the air

175
Q

motion/movement and pressure

A

pressure will increase with increasing movement

176
Q

Dalton’s Law

A

in a mixture of gases (e.g. air) each gas operates independently i.e. has its own specific pressure . Total pressure will be the sum of these individual pressures (partial pressures)

177
Q

% of gases in air

A

78% nitrogen
21% oxygen
1% water (in inhaled air)
0.04% carbon dioxide

178
Q

How do you measure the partial pressures of gases in the atmosphere at sea level?

A

Partial pressure of gas x 760mmHg (atmosphere pressure)

179
Q

Diffusion constant (D)

A

the amount of gas transferred between the alveoli and the blood by diffusion , proportional to the gas solubility (Sol) in fluids or in tissue

180
Q

Which has higher solubility oxygen or carbon dioxide and as a result diffuses faster?

A

carbon dioxide has a much higher solubility than oxygen , because it is more polar

181
Q

Henry’s law

A

the amount of gas dissolved in a liquid is directly proportional to the partial pressure of gas in which the liquid is in equilibrium(lining up against e.g. in the alveoli and in the resp membrane)

182
Q

Partial pressures in gas vs liquid

A

they are the same except if their solubility differs

183
Q

How to determine the concentration of a gas (in liquid)

A

total pressure x solubility

184
Q

if oxygen is bound to hemoglobin does it contribute to partial pressure

A

no because only gas that is dissolved in the solution will contribute

185
Q

total pressure in the inspired air vs alveolar air

A

equal , both are at 760 mmHg

186
Q

why is PO2 in air (160mmHg) > than PO2 in alveoli (105mmHg)

A

1) warming and humidification of air in respiratory tract (has gone through cycles of “Washing” out the concentration)
2) loss of oxygen to blood diffusion (alveoli dumps oxygen into capillaries to go to heart)
3) mixing of inspired air with functional residual volume

187
Q

Perfusion

A

circulation of blood through tissues (capillaries meeting with alveoli)

188
Q

Effect of alveolar ventilation on alveolar PO2 and alveolar CO2

A

When ventilation is sufficient, oxygen enters the alveoli at a high rate, and the partial pressure of oxygen in the alveoli remains high as the PCO2 is decreased

189
Q

Effect of metabolic rate on alveolar gas pressures

A

increasing metabolic rate will increase oxygen consumption and carbon dioxide production, this will decrease alveolar PO2 since its O2 diffuses to capillaries and increase PCO2 because carbon dioxide will enter to become oxygen

190
Q

What does the partial pressure of gas in alveoli determine?

A

the arterial levels (PO2 and PCO2 in the lung capillaries)

191
Q

Cardiac output (CO)

A

the volume of blood pumped by the heart per minute (mL blood/min)

192
Q

Flow of the systemic circulation(in tissue cells) is equal to?

A

the flow of the pulmonary circulation (in the lungs)

193
Q

Is systemic circulation a high or low pressure system?

A

high pressure system

194
Q

Why is systemic circulation a high pressure system

A

because it delivers blood to the peripheral tissue (brain) and has to overcome high resistance and gravity

195
Q

Is pulmonary circulation a high or low pressure system?

A

low pressure system

196
Q

Why is pulmonary circulation a low pressure system?

A

because it just has to deliver blood to lungs of which high pressures are risky since the respiratory membrane is fragile

197
Q

The pulmonary circulatory system is also a low resistance system because?

A

it has shorter and wider vessels than in systemic circulation

198
Q

What does it mean by the pulmonary circulatory system has high compliance vessels?

A

means that they can expand easily (low resting tone- floppy), due to the thin walls and smooth muscle it can accept large amounts of blood, it can also dilate in response to modest increases in arterial pressure

199
Q

how much mL is the pulmonary blood volume?

A

450mL

200
Q

The pulmonary capillary blood volume at rest and during exercise

A
rest= 70 mL
exercise= up to 200mL
201
Q

Why does it mean by the alveolar capillaries are collapsible?

A

if the capillary pressure is below alveolar pressure, the capillaries will close off (collapse), diverting blood to other pulmonary capillary beds with higher pressures

202
Q

Ventilation/perfusion ratio (V/Q)

A

balance between the ventilation (bringing O2 in to/removing CO2 from the alveoli) and the perfusion (removing O2 from the alveoli and adding CO2)

203
Q

What happens to PO2 and PCO2 of the alveoli when there is an increase in ventilation

A

their values (mmHg) will be closer to the inspired air

204
Q

What happens to the composition of local alveolar air when there is more perfusion?

A

it will more closely approach the value of the mixed venous blood

205
Q

What does a high V/Q ratio mean?

A

occurs when there is decreased perfusion in the lungs, can be due to disease or blockage of the blood vessels in the lungs

206
Q

What does a low V/Q ratio mean?

A

the ventilation is more severely affected than the perfusion (low ventilation with nearly perfect perfusion). blockage to airway going to alveoli (shunt)

207
Q

Alveolar VD or dead volume

A

regions of lung with high V/Q ratios. Regions that are relatively over ventilated (under perfused) so that a portion of the fresh air reaching these alveoli can not be taken up by the blood

208
Q

Shunt

A

a portion of the venous blood does not get oxygenated and goes back to arterial blood (goes on being deoxygenated)

209
Q

PO2 and PCO2 levels in a alveoli with high V/Q

A

high PO2- because the alveoli cannot pass it to the capillary
low PCO2- because the alveoli cannot get receive it from the capillary

210
Q

PO2 and PCO2 levels in a alveoli with low V/Q ratio

A

low PO2- cannot get it from the airway

high PCO2

211
Q

Hemoglobin structure

A

protein composed of 4 amino acid subunits called globins (2 alpha and 2 beta) and 4 heme groups (to bind to 1 oxygen each)

212
Q

How does oxygen bind to a heme group?

A

by attaching to the iron (Fe2+) found in the porphyrin ring structure in the heme

213
Q

Deoxyhemoglobin

A

not bound to oxygen = Hb

214
Q

Oxyhemoglobin

A

bound to oxygen = HbO2

215
Q

What is O2 capacity?

A

the max amount of oxygen that can be combined with Hb

216
Q

Hb saturation

A

percentage of the available Hb binding sites that have oxygen attached (the Hbs that oxygen)

217
Q

What are ways to determine the Hb saturation

A
  • arterial PO2 (most important)

- cooperative binding seen in a sigmoidal dissociation curve

218
Q

Cooperative binding

A

when oxygen binds to a heme group, it deforms the shape of the heme group which changes the shape of its associated globin chain from tense(T) to relaxed (R) state. The change in the shape of a globin chain will deform the others exposing the iron and letting it bind with oxygen molecules

219
Q

What produces the characteristic sigmoidal (S) shaped oxygen binding curve of Hb

A

cooperative binding

220
Q

Anemia

A

a reduction in the amount of Hb in the blood (makes for a smaller curve)

221
Q

Polycythemia

A

increase of Hb amount in the blood or reduction of blood volume that increases Hb concentration (make for a tall curve)

222
Q

Effect of Carbon Monoxide Poisoning on O2-Hb dissociation curve

A

carbon monoxide has 200x affinity for Hb compared to oxygen so it reduces the binding sites on Hb that oxygen can bind onto

223
Q

Curve for carbon monoxide on a O2-Hb Dissociation curve

A

shifted to the left because there is a decrease in unloading of oxygen to tissues (due to there not being many oxygen available)

224
Q

The O2 dissociation curve shifts to the right which means

A

oxygen affinity of Hb is reduced, more unloading (removal of oxygen from oxyhemoglobin)

225
Q

The O2 dissociation curve shifts to the left which means

A

that oxygen affinity of Hb is increased, less unloading

226
Q

What is 2,3-diphosphoglycerate (DPG)

A

the end product of RBC metabolism

227
Q

DPG results in the O2 dissociation curve to shift to the?

A

right (because there is a decrease in affinity for oxygen, thus oxygen will unload)

228
Q

What does 2,3-DPG do?

A

it is bound to hemoglobin and will stabilize the T-state conformation and decrease hemoglobins affinity for oxygen

229
Q

Carbon dioxide movement in the peripheral tissue

A

CO2 exit cells, is dissolved in interstitial fluid and diffuses to blood (from tissue to tissue capillary) CO2 will then either remain in the plasma of capillary as PCO2, enter RBC and remain dissolved as CO2 or bind to deoxyHB or react with water to produce HCO3- and H+ (HCO3- will exit RBC, H+ will interact with Hb)

230
Q

Respiratory acidosis

A

hypoventilation(not breathing enough air)

when CO2 production > CO2 elimination which increases PCO2 and also H+ concentration

231
Q

Respiratory alkalosis

A

hyperventilation (rapid breathing)

CO2 production < CO2 elimination which will decrease PCO2 and decrease H+ concentration

232
Q

Metabolic Acidosis

A

increase in blood H+ concentration- increasing acidity (no changes in PCO2)

233
Q

Metabolic Alkalosis

A

decreases blood H+ concentration (no changes in PCO2)

234
Q

How is the rhythm of breathing established

A

by the CNS with the help of central/peripheral chemoreceptors and mechanoreceptors in the lung and chest wall

235
Q

What are the 3 groups within the brainstem that are important for breathing?

A

1) Pontine respiratory group(in pons)
- phase transition between inspiration and expiration

2) Dorsal respiratory group (in medulla)
- generates inspiratory movements

3) Ventral respiratory group
- controls voluntary forced exhalation and acts to increase the force of inspiration

236
Q

PreBotzinger complex (PreBotC)

A

a group of neurons in the ventral respiratory group that will generate excitatory inspiratory rhythmic activity that excites inspiratory muscles (via polysynaptic pathway)

237
Q

Parafacial respiratory group (pFRG)

A

group of neurons in the ventral respiratory group that is important for generating rhythmic excitatory activity that excites expiratory muscles (via polysynaptic pathway)

238
Q

Why must the rhythm of breathing change

A

to accommodate changes in metabolic demands (PO2, PCO2, pH), varying mechanical conditions (e.g. changing posture), non-ventilatory behaviors (e.g. speaking, sniffing, eating), pulmonary and non-pulmonary diseases

239
Q

Neuro-respiratory pathway: Inspiration (How are your diaphragm and external intercostals activated)

A

(1) preBotC activates inspiratory premotorneurons (rostral ventral root ganglion)
(2) which will activate phrenic and thoracic motoneurons found in the cervical and thoracic part of the spinal cord
(3) which will ultimately activate the diaphragm and external intercostal muscles

240
Q

Neuro-respiratory pathway: Inspiration (How are your tongue and upper airway muscles activated)

A

(1) preBotC will activate a premotoneuron (found in the rostral (towards front of head like nose) part of the ventral root ganglia and in the parahypoglossal region)
(2) this will activate the cranial motor neurons in the medulla
(3) which will ultimately activate the tongue and upper airway muscles

241
Q

Neuro-respiratory pathway: Expiration (how are the internal intercostals and abdominals activated)

A

(1) pFRG will activate expiratory premotorneurons in the caudal (close to the tail/back of self) ventral root ganglia
(2) they will activate thoracic and lumbar motorneurons (in the spinal cord
(3) which will ultimately activate the internal intercostals and abdominals

242
Q

Are tidal volume and respiratory rate values fixed?

A

no, they can increase and decrease depending on the activity of the respiratory networks (if they are stimulated or inhibited)

243
Q

What is hypercapnia

A

high PCO2

244
Q

What are some things that can increase ventilation?

A

hypoxia (low PO2), hypercapnia (high PCO2), and acidosis (low pH in blood)

245
Q

Chemoreceptors

A

specialized structures that sense changes in PO2, PCO2, and pH

246
Q

What are the 2 types of chemoreceptors?

A

peripheral chemoreceptors and central chemoreceptors

247
Q

What is it that carotid and aortic bodies primarily sense?

A

hypoxia (low arterial PO2) but they are also sensitive to pH

248
Q

Characteristics of carotid bodies

A

they are extremely small, chemo sensitive, are highly vascularized (receive lots of blood flow)and have a high metabolic rate

249
Q

What are the 2 types of carotid bodies?

A

Type I (Glomus cells): the chemo sensitive cells (the ones that will respond to changes and act)

Type II (sustentacular cells): supporting cells

250
Q

What do glomus cells do when there is low arterial PO2?

A

they will display an increase in firing rate which will generate action potentials that cause a release of neurotransmitters which interact with terminals in glossopharyngeal nerve endings stimulating respiratory centers in brain

251
Q

How low does the arterial PO2 have to be for peripheral chemoreceptors to be stimulated

A

<60mmHg

252
Q

What do peripheral chemoreceptors do?

A

they will activate the dorsal and ventral respiratory group neurons in the medulla which will control centrally the activity of the respiratory muscles via increasing the respiratory rate and tidal volume

253
Q

central chemoreceptors

A

specialized neurons located close to ventral surface of the medulla (close contact with blood vessels and CSF)- so if PCO2 increases at level of capillaries the CO2 can diffuse easily into the extracellular tissue of the brain

254
Q

are peripheral or central chemoreceptors responsible for hypercapnia?

A

central chemoreceptors

255
Q

Respiratory response to metabolic acidosis

A

high H+ (what makes things acidic) will stimulate the peripheral chemoreceptors since they cannot easily cross the blood brain barrier

256
Q

PCO2 stimulates the peripheral or central chemoreceptors?

A

central chemoreceptors

257
Q

pH and PO2 stimulates the peripheral or central chemoreceptors?

A

peripheral chemoreceptors

258
Q

The 2 purposes of motility

A

1) Moves contents from the mouth to the anus

2) Mixes contents to facilitate digestion and absorption

259
Q

Digestion

A

process of breaking down large particles of food and high-molecular-weight substances into small molecules

260
Q

Absorption

A

movement of the products of digestion across the intestinal epithelium into the body

261
Q

Secretion

A

release of substances into the lumen of the GI tract, which facilitate digestion, absorption and motility

262
Q

Epithelium

A

“Barrier” of cells that nutrients must traverse to be absorbed into the body

263
Q

Circular and longitudinal layers of smooth muscle function

A

allow motile contractions of the intestine

264
Q

Myenteric plexus function

A

controls multiple aspects of motility and secretion

265
Q

Endocrine cells function

A

secrete hormones into blood that regulate digestion and appetite

266
Q

Exocrine cells function

A

secrete substances into lumen that aid digestion (e.g. acid, enzymes, water, ions,…)

267
Q

What are sphincters

A

rings of muscle creating a constriction point in the tube

268
Q

How do sphincters work?

A

opening and closing of them regulates flow through the tract

269
Q

Purpose of sphincters

A

prevents backflow

270
Q

3 roles the mouth has in the digestive system

A

1) Mechanical breakdown of food
2) Preparation for swallowing
3) Onset of digestion

271
Q

What is the mechanical breakdown of food called?

A

mastication (chewing)

272
Q

How is the food prepared to be swallowed?

A

by being moistened by the saliva

273
Q

How does the onset of digestion occur?

A

through the enzymatic breakdown of carbohydrates by salivary amylase

274
Q

Oral phase of swallowing

A

initiated by voluntary collection of food bolus into the pharynx by the tongue

275
Q

Pharyngeal phase of swallowing

A

triggers involuntary contraction of pharyngeal muscles, pushing bolus into esophagus

276
Q

Esophageal phase of swallowing

A

bolus driven down esophagus by peristaltic contraction

277
Q

4 steps of swallowing

A

1) tongue pushes food to bolus to back of mouth
2) soft palate elevates to prevent food entering the nasal passage
3) epiglottis covers the glottis, preventing bolus entry into the trachea, upper esophageal sphincter relaxes
4) food descends the esophagus

278
Q

Functions of the stomach

A

stores ingested material, continues digestion (dissolves and breakdowns), regulates emptying into small intestine

279
Q

How mechanical digestion is done?

A

it is facilitated by the stomach’s folded surface (rugae)

280
Q

How is chemical digestion done?

A

by HCI and pepsin

281
Q

HCl role in chemical digestion

A

its acidity denatures proteins (more soluble), cleaves pepsinogen into pepsin

282
Q

Pepsin role in chemical digestion

A

it is an enzyme that breaks down proteins

283
Q

How does ingested food leave the stomach as?

A

as chyme

284
Q

the 3 sections that the small intestine is split into

A

1) Duodenum
2) Jejunum
3) Ileum

285
Q

Function of small intestine

A

primary site of digestion and absorption

286
Q

What is the small intestine

A

a highly specialized structure, evolved to maximize food absorption

287
Q

How does the small intestine absorb?

A

absorption across intestinal epithelia is facilitated by a large surface area

288
Q

Increased surface area

A

maximized contact between intestinal contents and epithelium, facilitating digestion and absorption

289
Q

What is the function of the large intestine?

A

to store and concentrate undigested material, prior to its excretion

290
Q

Cecum

A

“first part”, where cellulose digestion in herbivores occurs

291
Q

Appendix

A

thought to be vestigial, may act as a “haven” for gut bacteria

292
Q

Function the colon has

A

absorption of ions, water; bacterial metabolism

293
Q

Rectum

A

holds feces; its contraction expels feces (defecation)

294
Q

The 3 salivary glands

A

parotid, sublingual and submandibular

295
Q

Secretions of salivary glands

A

water, mucus and amylase

296
Q

Function of the water and mucus that are secreted by the salivary glands

A

moisten and lubricate food bolus

297
Q

Function of amylase in salivary glands?

A

begins digestion of large carbohydrates into small units

298
Q

Where do the liver and gallbladder empty into?

A

into the small intestine via the common bile duct

299
Q

What does the liver secrete?

A

bile salts, bicarbonate and organic waste products, and trace metals

300
Q

Function of bile salts

A

facilitate fat digestion

301
Q

Function of bicarbonate

A

neutralizes acidic chyme coming from stomach

302
Q

Where do organic waste products and trace metals go?

A

they are eliminated in feces

303
Q

Acinar cells

A

secrete into the small intestine via the pancreatic duct

304
Q

What do islets of Langerhans do?

A

they secrete hormones into the bloodstream

305
Q

Peristalsis

A

reflex response, triggered by luminal contents stretching the intestinal wall. This stretch initiates circular contraction behind the stimulant and relaxation in front of it

306
Q

Purpose of peristalsis

A

to propel food along the length of the intestine from the esophagus to the rectum

307
Q

Difference between segmentation and peristalsis

A

Segmentation does not propel luminal contents along the intestine like peristalsis does

308
Q

Where does segmentation occur?

A

primarily in the small intestine

309
Q

What is the purpose of segmentation?

A

To mix contents in situ, facilitate digestion and absorption

310
Q

Steps of segmentation

A

1) local contractions separate intestine into pockets
2) subsequent contractions divide pockets centrally (side by side)
3) rhythmic contractions continue to subdivide pockets, mixing their contents