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Medicine Year 1 Semester 1 > CB Quiz 4 > Flashcards

CB Quiz 4 Flashcards

1
Q

What are the two processes referred to as respiration?

A

External respiration

Internal or cellular respiration

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2
Q

What is cellular respiration

A

Intracellular metabolic process that uses oxygen to produce ATP and CO2. It can also perform anaerobic respiration.

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3
Q

What are the 4 steps of respiration and indicate which are internal and which are external

A
  1. Ventilation or gas exchange between the atmosphere and air sacks in the lungs (external)
  2. Exchange of O2 and CO2 between air in alveoli and blood in pulmonary capillaries (external)
  3. Transport of O2 and CO2 by the blood between the lungs and tissues
  4. Exchange of O2 and CO2 between the blood in the systemic capillaries and the tissue cells (Cellular respiration => internal)
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4
Q

What are the two main parts of the basic anatomy of the respiratory system?

A

Extra-thoracic and Intra-thoracic

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5
Q

What components of the respiratory system are located in the extra-thoracic portion?

A

Nasal passages
Mouth
Pharynx
Larynx

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6
Q

What components of the respiratory system are located in the intra-thoracic portion

A

Trachea
Bronchus
Bronchioles
Alveoli

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7
Q

Does gas exchange use ATP? Why or Why not?

A

No ATP is used in gas exchange as gas exchange is driven by diffusion along the concentration gradient => Passive

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8
Q

What is ventilation driven by? how does air move in and out of lungs?

A

Mechanical forces where air is moved into and out of the lungs across pressure gradients

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9
Q

How are pressure and volume related at constant temperature?

A

They are inversely proportional

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10
Q

Where does a pressure differential exist in the respiratory system? How do they compare?

A

Between the lungs and pleural cavity.

Pleural pressure < Pulmonary pressure

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11
Q

Why is Pleural pressure < Pulmonary pressure?

A

Lungs are normally stretched and pull inwards => the decreased pleural pressure allows the lungs to remain stretched

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12
Q

When is the pressure equilibrium in lungs disrupted?

A

Inspiration and exhalation

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13
Q

How does the pressure change during inspiration and expiration?

A

The pressure difference between the pleural cavity and lungs remain the same. These values decrease during inspiration to allow for air to flow in and increase during expiration to force air out.

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14
Q

List the events that occur during inspiration

A
  1. Inspiratory muscles contract
  2. Diameter of thoracic cage increases
  3. Intrapleural pressure becomes more negative
  4. Transmural pressure increases and causes alveoli to swell or open

(Due to pleural pressure decreasing, air particles come from the environment into the alveoli increasing its pressure and causing it to swell)

  1. Intra-alveolar pressure falls relative to atmospheric pressure
  2. Air flows down pressure gradient from atmosphere to alveoli
  3. At the end of inspiration - No airflow and intra-alveolar pressure = atmospheric pressure
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15
Q

How does the diameter or volume of the thoracic cage change as a result of inspiration

A

Increases in diameter => increase in volume

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16
Q

What are the primary muscles involved in inspiration? Briefly state their involvement

A

Diaphragm: Flattens upon contraction
External intercostales: Lifts ribs upwards and outwards
Both of these motions expand the volume of the thoracic cavity allowing for more air to flow in

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17
Q

What are the accessory muscles involved in inspiration and briefly state their function

A

Scalenes: Raise first 2 ribs
Sternomastoid: Raise the Sternum
They are used during exercise and respiratory disease

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18
Q

What are some diseases that require the use of accessory muscle activity? State 2

A 
Chronic bronchitis
Asthma
Chronic obstructive pulmonary disease
Emphysema
Bronchiolitis
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19
Q

What are the airway muscles and what’re their overall function during inspiration?

A

Laryngeal
Pharyngeal
Genioglossus

They enlarge the airway reducing flow and resistance as well as maintaining stabilisation of the airways preventing collapse

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20
Q

What are the two types of expiration and describe each briefly

A

Passive expiration: Passive process and occurs when at rest. The relaxation of inspiratory muscles are sufficient for expiration.

Active expiration: Contraction of abdominal muscles which involve pushing up the diaphragm as well as internal intercostal muscles

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21
Q

What device is used to obtain a Spirogram

A

Spirometer

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22
Q

An increased RV (Residual volume) is an indication of?

A

Obstructive Disease

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23
Q

What are 3 signs of restrictive lung disease?

A

Decreased TV or total volume

FEV1 decreased

FEV1/FVC is normal or increased

RV normal

Decreased compliance in lungs

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24
Q

What are 3 signs of obstructive lung disease and give 3 examples

A

FEV 1 and FEV1/FVC reduced
Airflow rate reduces
Airway obstruction
Higher RV

Examples include;
Asthma
COPD
Chronic bronchitis
Emphysema
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25
Q

What cannot be measured by a spirometer? What method can be used to fix that?

A

A spirometer cannot measure RV, FRC, TLC

The Helium Dilution Technique can be used to calculate FRC which involved a helium/oxygen mixture in spirometer. Review the physics behind it on the slides

FRC can also be calculated by Body Plethysmography.

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26
Q

What is required to fully characterize lung volumes and capacities?

A

Helium dilution technique/ Plethsymography + Spirometry

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27
Q

What is dead space and what are the three different types?

A

Dead space is the volume occupied by gas in the lungs which does not participate in gas exchange

  1. Anatomical dead space
  2. Alveolar dead space
  3. Physiological dead space
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28
Q

What is anatomical dead space?

A

Is its the components of the respiratory system that are filled with air but dont have any pulmonary capillaries such as Trachea and bronchus

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29
Q

Is dead space included in total volume or tidal volume?

A

Yes

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30
Q

What is alveolar dead space?

A

Alveolar dead space represents the air in the alveoli that are surrounded by pulmonary capillaries without blood flow.

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31
Q

What is average amount of alveolar dead space present within a healthy individual? What increases it?

A

Usually negligible in healthy people

Can increase in disease such as pulmonary embolism

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32
Q

What is the physiological dead space

A

It is the total dead space found within an individual

=> Anatomical dead space + Alveolar dead space

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33
Q

How is anatomical dead space measured?

A

Fowler’s method: Nitrogen washout

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34
Q

What does the slope in the graph obtained by Fowler’s method represent? Explain briefly

A

Mixture of dead space and alveolar air

Patients take in 100% O2 after an initial inhalation. When exhalation beings, the first part of the air exhaled will be 100% O2 => no N2. The next part of the air will be alveolar air which is N2-rich

=> Volume of N2-free air represents the anatomical dead space

The line that bisects the exponential increase of expired N2 represents the anatomical deadspace

This is due to mixture of deadspace and alveolar air

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35
Q

What method is used to calculate physiological and Alveolar dead space? Explain briefly

A

Bohr’s method

Detects expired CO2 concentration. Atmospheric CO2 is neglected. Partial pressure of CO2 in the alveoli is the same as that of the arterial blood (PaCO2). The alveolar dead space, or non-functioning alveoli due to no blood supply, will represent a difference between PaCO2 and PeCO2 (Exhaled air). The more dead space present, the less PeCO2 is present and the more PaCO2 is present. => we look at PeCO2/PaCO2.
VD/VT = 1 - (PeCO2/PaCO2)

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36
Q

Define the work of breathing

A

It is the work required to move the lung and chest wall (W = P x DeltaV)

It is the energy necessary to perform tidal ventilation over a set unit of time

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37
Q

What muscles are involved in quiet breathing?

A

Inspiratory muscles as expiration is passive

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38
Q

What are the two types of work present during breathing and what percentage does each contribute?

A

Elastic work 70%

Non-elastic work 30%

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39
Q

Do respiratory muscles consume much oxygen? If so, approximately how much?

A

Respiratory muscles consume only 2-3% of total oxygen consumption

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40
Q

What are two conditions that involve increased energy expenditure on breathing?

A

Exercise which increases minute volumes

Disease which limits exercise tolerance

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41
Q

What are the components of minute ventilation/volume?

A

Tidal volume and rate

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42
Q

What is the relationship between?

Tidal volume and Respiratory rate
Tidal volume and Elastic Work
Rate of Respiration and Flow
Rate of Respiration and resistive work
Resistive work and elastic work
Elastic Work and Non-elastic work
Tidal volume and Flow
Respiratory rate and elastic work
A

Inversely proportional =NP
Proportional = P

NP
P
P
P
NP
NP
NP
NP
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43
Q

Define Compliance/Elastic Work

A

Force required to expand lung against its elastic properties

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44
Q

Define Frictional/Resistive Work

Non-elastic

A

Force to overcome air-flow resistance (force to move air through airways)
Force to overcome viscosity resistance

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45
Q

Define Compliance

A

Measure off the ease with which the lungs can be stretched or inflated

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46
Q

Define how each of the following are measured

Static Compliance

Dynamic Compliance

Specific Compliance

A

Static compliance is compliance measured when there is no airflow

Dynamic Compliance is compliance measured during airflow

Specific Compliance measures elastic properties correcting for lung volume

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47
Q

In terms of the pressure-volume relationship, what do the following represent?

Slope

Steep slope

Area within inspiration and expiration curves

Large area

A

Slope measures the compliance

Steep slope indicates more compliance

Area represents the work

A large area indicates greater work required

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48
Q

What does specific compliance measure and how is it calculated?

A

Specific compliance measures the intrinsic elastic properties of the lung tissue

Calculated as: Compliance/FRC (Lung volume)

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49
Q

How does a disease alter compliance?

A

A disease can either increase compliance or decrease it:

Increased compliance is due to the loss of elastin fibres which are the elastic tissue found in lung tissue

Decreased compliance affects chest wall compliance causing scoliosis and pulmonary fibrosis

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50
Q

Define Elastance. How are compliance and elastance related? How are they affected by Emphysema and Fibrosis

A

Elastance is the measure of the “Snap back” or elastic recoil force of the lungs

Elastance is inversely related to compliance

Emphysema causes increased compliance and decreased elastance

Fibrosis causes decreased compliance and increased elastance

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51
Q

What are the two main contributors to Elastic work and explain each briefly

A

The two main contributors to this phenomenon are Tissue elasticity due to the presence of elastin fibers in connective tissue as well as surface tension of the film of fluid that lines the alveoli called Pulmonary Surfactant

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52
Q

Describe tissue elasticity during inhalation and exhalation

A

Inhalation: Energy is required to stretch lungs open such as diaphragm and intercostals

Exhalation: Elastic recoil of the stretched lung occurs

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53
Q

What is the film of fluid that lines the alveoli?

A

Pulmonary Surfactant

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54
Q

Learning Outcome: Explain the role of surfactant in elastic work

A

The pulmonary surfactant is a complex mais true of proteins (10%) and lipids (90%).

It is synthesized by type II pneumocystis and stored in cytoplasmic lamellar bodies until released to surface of alveolus at the air-liquid interface.

It’s main function is to reduce surface tension by interfering with water molecule interactions increasing compliance of the lung

Another important role is the stabilisation of alveoli of different sizes. Usually alveoli with small radius => volume causes it to have a high pressure which would empty the air into larger alveoli causing its collapse. The surfactant will position itself with its hydrophilic end on the lining of the alveoli and it’s hydrophobic fatty acid chain projecting into the alveolar air which causes repulsion due to lipid.

It also contributes to defense mechanisms in the lung enhancing macrophage activity

Overall, the surfactant differentials reduces surface tension in alveoli, more at lower volumes and less at higher volumes leading to alveolar stability and co-existence of large and small alveoli

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55
Q

Briefly explain the Newborn Respiratory Distress Syndrome

A

Developing fetal lungs to not normally synthesis surfactant until late in pregnancy => premature infants may not have enough pulmonary surfactant and struggle to breath

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56
Q

Briefly describe Alveolar Interdependence

A

Where an alveolus in a group of interconnected alveoli begin to collapse, the surrounding alveoli are stretched. Neighboring alveoli, in response, pull outwards on the collapsing alveoli and keep it open

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57
Q

Define Airway Resistance

Is it present during Inspiration and expiration?

A

Airway resistance is the impedance of air flow through the tracheobronchial tree as a result of friction of gas molecules

Yes

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58
Q

Describe Airway resistance at rest and the effects of increased resistance on the maintenance of tidal volume

A

At rest, airway resistance is low. Normal pressure difference between mouth and alveoli is sufficient to give normal resting tidal volume. Increased resistance requires greater pressure gradients to drive airflow in order to maintain the same tidal volume.

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59
Q

What is the typical tidal volume?

A

500 ml

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60
Q

What are the components that determine airway resistance

A

Diameter of airway (cross sectional area)
Distance air needs to travel
Flow type/pattern (laminar vs. Turbulent)

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61
Q

What is the relationship between airway radius and flow rate

A

Radius has a strong influence (r^4) on Flow rate where an increase in the radius also increases flow rate

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62
Q

What is the relationship between resistance and airway radius

A

There is a strong influence of airway radius on resistance (r^4). Radius is inversely proportional to resistance

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63
Q

Is resistance greater in the trachea or bronchioles? Explain

A

An individual bronchiole has a far smaller radius than the trachea but has a lower resistance. Although the radius is smaller, the large number of bronchioles means that overall the airway widens => resistance in the trachea and bronchus is greater than in the bronchioles.

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64
Q

Is airway resistance greater at high lung volume (inspiration) or low lung volume (expiration)? Give reasoning

A

Resistance to airflow decreases during inspiration where lung volume increases due to airways expanding

Resistance to airflow increases during exhalation where lung volume decreases due to airways contracting

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65
Q

What prevents the trachea and main bronchi from collapsing?

A

Cartilage

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66
Q

Although bronchioles offer little resistance, what is the effect of disease on airway resistance?

A

Resistance in bronchioles are significant in disease as they are subject to physical, neural, and humoral factors

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67
Q

What are the determinants of airway diameter? Give an example of each

A

Outside the airway: Radial traction of elastic tissue and pressure from lymph nodes

In the wall: Smooth muscle tone and thickness of mucosa/submucosa

In the lumen: Mucus

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68
Q

What the extrinsic factors (Neural and hormonal control) involved in the control of smooth muscle tone with regards to bronchioles?

A

Circulating Catecholamines such as adrenaline cause bronchodilation via Beta 2 receptors

The peripheral nervous system causes bronchoconstriction via acetylcholine release and muscarinic receptors.

Non-adrenergic non-cholinergic (NANC) autonomic systems releasing dilators (nitric oxide) or constrictors (neurokinin A)

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69
Q

What the Intrinsic factors (chemical mediators) involved in the control of smooth muscle tone with regards to bronchioles?

A

Mast cell degranulation (release of histamine) and inflammatory mediators cause bronchoconstriction.

CO2 exerts direct effect on smooth muscle:

  • When levels are raised, bronchodilation
  • When levels are low, bronchoconstriction
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70
Q

what are the factors influencing secretions of seromucous glands and goblet cells in the respiratory system?

A

These secretions are controlled by parasympathetic nervous system reflexes and by local chemical stimulation. Secretions are decreased by atropine and increased in bronchitis

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71
Q

What effect does increased mucus production have on the work of breathing? Why?

A

It increases non-elastic/ flow-resistive work. Mucus decreases the diameter of the airway hence increasing air resistance which increases non-elastic work

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72
Q

What are the two types or patterns of flow?

A

Laminar flow and turbulent flow

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73
Q

Define laminar flow

A

Streamline, well ordered flow

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74
Q

Define turbulent flow and it’s effects on air flow

A

Chaotic, non-streamline flow. Turbulent flow is very inefficient and consumes energy due to an increase in airflow resistance

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75
Q

According to Reynold’s number, what is considered as turbulent flow?

A

R>2000

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76
Q 
\_\_\_\_\_\_ velocities and \_\_\_\_\_\_\_ diameters promote turbulent flow.
Answers can be:
High
Low
Large
Small
Increased 
Decreased
A

High/increased

Large/Increased

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77
Q

Under what conditions is turbulent flow exhibited in:
Upper airways
Bronchioles

A

Upper airways: During exercise

Bronchioles: No turbulence

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78
Q

Explain why turbulent flow is not exhibited in bronchioles

A

They have low velocities due to their small radii

79
Q

Around 80% of resistance in airways is located in the trachea and main bronchi and around 20% is located in bronchioles
True or False?

A

True

80
Q

What is the effect of exercise on alveolar and inter pleural pressure?

A

Both increase

81
Q

During maximal forced expiration, there is a great increase in both intra pleural pressure and intra-alveolar pressure. As a result of maximal forced expiration, what occurs with regards to small airways?

A

Compression occurs in small airways as pressure gradient decreases

82
Q

In a patient with obstructive lung disease, what is expected to occur in their small airways? Why (2 reasons)? Give an example for each reason.

A

In a patient with obstructive lung disease, collapse occurs for two reasons:

  1. Pressure drop decreases as resistance increases (Chronic bronchitis)
  2. Transmural pressure gradient less than normal due to loss of elastic recoil (Emphysema)
83
Q

For an airway structure to collapse does intrapleural pressure have to be greater, less, or equal to intra-airway pressure?

A

Greater

84
Q

What is asthma (briefly) and how is it treated?

A

Asthma is a respiratory disease characterized by lung inflammation.
It is treated with bronchodilators and corticosteroids

85
Q

Give two examples of COPD (chronic obstructive pulmonary diseases)

A

Chronic Bronchitis

Emphysema

86
Q

Briefly define what chronic bronchitis is

A

It is the excess production of mucus which results in cough and production of sputum

87
Q

Briefly define what emphysema is

A

Loss of elastic tissue due to uncontrolled action of proteolytic enzymes where lung elastase is normally inhibited by antiproteases.

88
Q

Briefly define what pulmonary fibrosis is. What type of lung disease is it?

A

It is the formation of excess fibrous tissue in the lung causing reduced compliance.

It is a restrictive lung disease

89
Q

What are the two types of respiratory diseases? Give an example for each. Then, give 2 (or more) differences that classify each.

A

Obstructive respiratory diseases (COPD, emphysema, chronic bronchitis, asthma):

  • Interferes with the movement of air through airways
  • Increases flow-resistive work
  • No effect on elastic work
  • Decreases FEV1 but not FVC (or only slightly) (ratio decreases)

Restrictive respiratory diseases (pulmonary fibrosis):

  • Interferes with the lung’s ability to expand (=>compliance is decreased)
  • Increased elastic work
  • No effect on flow-resistive work
  • Decreases FEV1 and FVC (Ratio remains normal)

Restrictive

90
Q

What are the effects of obstructive respiratory diseases and restrictive respiratory diseases on FEV 1, FVC, and their ratio

A

Obstructive respiratory diseases decrease FEV1 but not FVC (or only slightly) decreasing the ratio

Restrictive respiratory diseases decrease FEV1 and FVC. Ratio remains normal

91
Q

List the major cell types in lungs

A 
Smooth muscle cells 
Lung macrophages
Mast cells
Goblet cells and Submucosal glands
Endothelial cells
Large alveolar Cells (Type II Pneumocytes)
Flat Alveolar Cells (Type I Pneumocytes)
92
Q

State the role of smooth muscle cells in the lungs and how asthma affects smooth muscle content

A

Smooth muscle cells control the diameter and tension of the bronchi

In patients with chronic asthma, they can have increased bronchial smooth muscle content

93
Q

Briefly explain the role of lung macrophages.

A

Lung macrophages are found along the length of the respiratory tract. They are important for immune defense in respiratory bronchioles and function through phagocytosis. They also produce potent anti microbial and antiviral agents.

94
Q

Explain the role of Mast Cells in the lungs along with the effects of their degradation.

A

Mast cells are found along the length of the respiratory tract and is rich in heparin and histamine. Their role is to speed up immune response.

Mast cell degranulation leads to the release of histamine, prostaglandin-D2, and Leukotriene C4&D4. This release causes bronchoconstriction and increased mucous production.

95
Q

Explain the function Goblet cells and submucosal glands in lungs. What are the effects of cystic fibrosis on goblet cells?

A

Present from bronchioles and up, in the epithelium. They function in secreting mucous.

Cystic fibrosis increases the density of goblet cells

96
Q

Explain the role of Pulmonary endothelial cells.

A

Pulmonary endothelial cells shape the environment for alveolar capillaries. They produce vasoactive peptides that control blood flow, fluidity, pressure, and viscosity

97
Q

Explain the function of Type I pneumocytes.

A

They make up 95% of the epithelial lining of the respiratory zone. They fuse with epithelial cells to enhance gas exchange. This fusion results in a once-cell-thick layer that is perfect for diffusion.

98
Q

Can Type-1 pneumocytes replicate? If so, how?

A

They do not replicate

99
Q

Explain the structure and role of type 2 pneumocytes

A

Type II pneumocytes. They have large nuclei, microvilli, and extensive mitochondria.

They are the site of synthesis, storage, and secretion of surfactant.

They are also stem cells. They can replace themselves or other pulmonary cell types after injuries including replacing damaged type 1 cells.

100
Q

Compare volumes obtained during deflation and inflation. What is this difference called? And what is the cause behind this difference?

A

Volumes obtained during deflation exceed those during inflation, at a given pressure.

The difference in volumes is called Hysteresis. This is due to the air-water surface tension that occurs at the beginning of inflation.

This is governed by the law of Laplace where Pressure = 2xSurface tension/r. Surfactant decreases the alveolar surface tension. At the end of expiration, compressed surfactant phospholipid molecules decrease the surface tension to near zero levels and hence increasing compliance allowing the lung to inflate much more easily.

101
Q

List the components of surfactant.

A

40% dipalmitoyl-phosphatidylcholine (DPPC)

40% other phospholipids (PC)

5% surfactant-associated proteins (SP-A,B,C, and D)

Cholesterol

Traces of other substances

102
Q

What is the active component of surfactant? What allows it to perform its role?

A

DPPC Dipalmitoyl-phosphatidylcholine

It has a higher compaction capacity than the other phospholipids due to it having an a polar tail that is less bent.

103
Q

What makes DPPC (dipalmitoyl-phosphatidylcholine)

A

DPPC is made and secreted by Type II pneumocytes

104
Q

Outline the structure of dipalmitoylphosphatidylcholine

A

It is composed of a choline head, a phosphate neck connected to position 3 of the glycerol, and positions 1 and 2 are occupied by palmitate

105
Q

Discuss the synthesis of surfactant

A

Glycerophospholipid synthesis involves 2 possible pathways
A) Donation of the phosphatic acid from cyditine diphoshate (CDP) in CDP-diacylglycerol to an alcohol
OR
B) Donation of the CDP from the alcohol to 1,2 diacylglycerol

Both form phosphatidylcholine

This CDP-bound structure is the active intermediate and cytosine monophosphate (CMP) is released as a side product

This reaction is catalyzed by phosphatidic acid phosphatase.

Then, Phosphatidylcholine gains palmitate at positions 1 and 2 of glycerol to form DPPC. DPPC then joins to apolipoproteins to form a unique lipoprotein found only in lung alveoli as surfactant.

106
Q

What are the 4 surfactant apolipoproteins and outline their roles

A

SPA,B,C,and D

A and D are hydrophilic and play a crucial role in pulmonary immunity (major surfactant associated proteins)

B and C are hydrophobic and are closely linked to alveolar surface tension.

107
Q

How is used surfactant disposed of?

A

Used surfactant is either recycles of degraded by type II pneumocytes and alveolar macrophages

108
Q

Discuss Neonatal Respiratory Distress Syndrome (NRDS) with reference to testing and treatment

A

NRDS is the rapid, labored breathing in newborns due to insufficient surfactant. It is correlated with the degree of prematurity of the newborn.

Testing is done by sampling the amount of surfactant in the amniotic fluid through amniocentesis. It is commonly done by testing the Lectithin-sphingomyelin ratio which is recommended to be over 2:1

Treatment involves treating the mother with corticosteroids to increase surfactant lipid synthesis which speeds up fetal lung development. Alternatively treating with exogenous surfactant or positive pressure mechanical breathing could also be used.

109
Q 
State the effect of Decreased Alpha 1-anti trypsin on:
Elastase concentration
Elastin concentration
Elasticity of the lung 
Incidence of emphysema
A

Increase
Decrease
Decrease
Increase

110
Q

What is the main role of alpha 1-anti trypsin in the lung and where is it synthesized? Is it found in high or low concentrations in the lung?

A

In the lung, it inhibits the activity of leukocyte elastase.

It is synthesized in the liver

Found at high concentrations in the lung

111
Q

Briefly describe the inheritance of alpha 1-anti trypsin disorders.

A

Disorders of alpha 1 antitrypsin involve alpha 1 antitrypsin deficiency.

Carriers produce lower than normal levels of the protein but they still have enough to protect their lungs. Having both alleles will cause a massive deficiency but will still produce a low amount. In both cases reduced AAT activity in the lung increases the activity of elastase making the lungs less elastic.

112
Q

What are the effects of smoking on the action of breathing?

A

Cigarette smoke can lead to the oxidation of methionine 358 of alpha1-antitrypsin. This residue is issential for binding elastase.

113
Q

What are the common mutations of alpha 1 antitrypsin

A

Z mutation (ZAAT) where glutamate is changed into Lysine resulting in the deficiency of AAT in the lung

S mutation involved Glutamate changing into valine which results in reduced serpin activity

114
Q

What is the % O2 in the atmosphere

A

21

115
Q

What is the % O2 in expired air

A

16

116
Q

What is the % O2 in alveolar air

A

14

117
Q

What is the % CO2 in inspired air

A

0

118
Q

What is the % CO2 in expired air

A

4

119
Q

What is the % CO2 in alveolar air

A

6

120
Q

What is PO2 in mmHg in inspired air

A

150

121
Q

What is PO2 in mmHg in expired air

A

120

122
Q

What is the PO2 in alveolar air

A

100

123
Q

What is PCO2 in mmHg in inspired air

A

0

124
Q

What is the PCO2 in mmHg in expired air

A

30

125
Q

What is the PCO2 in mmHg in alveolar air?

A

40

126
Q

When it is said that % O2 in alveolar air is 14, is that dry gas or water vapor? How much saturation?

A

Water vapor of 100% saturation

127
Q

How is arterial blood gas pressure measured?

A

Using arterial blood samples and a blood gas analyser

128
Q

How are alveolar PCO2 values measured?

A

They are approximately measured through end-tidal values

129
Q

What is the relationship between exchange and the pressure gradient in terms of gas diffusion across the alveolar surface?

A

Directly proportional

130
Q

What is the relationship between exchange and distance in terms of gas diffusion across the alveolar membrane

A

Inversely proportional

131
Q

What is the relationship between exchange and surface area in terms of gas diffusion across the alveolar membrane

A

Directly proportional

132
Q

Define Diffusing Capacity

A

It is the ability of the alveolar-capillary membrane to allow for gaseous exchange

133
Q

What is the Anatomical shunt in the respiratory system

A

It is the venous mixture with oxygenated blood and blood coming from the bronchial and thebesian veins.

134
Q

In one word, describe the mismatch, if any, between ventilation and perfusion in the lungs

A

Slight

135
Q

The mismatch between ventilation and perfusion in the lungs is due to…

A

It is due to the position of the heart compared to the lung and gravity

136
Q

With regards to ventilation and perfusion, answer the following questions:
Which is greater at the base?
Which is greater at the apex?
Which gradient is steeper? Why?
As we move from the base of the lung to the apex, what happens to the V(alveolar)/Q?

A

Perfusion
Ventilation
Perfusion (Q) is steeper since it is more affected by gravity (and position of the heart)
Increases

137
Q

Is pleural space more negative at the apex or at the base

A

Apex

138
Q

Would you consider the alveoli at the apex to be overventilated or under ventilated? Why?

Where is Tuberculosis more likely to be present

A

The alveoli at the apex are overventilated as there is less blood (due to gravity) and more air.
TB is more likely in the apex where there is a higher PO2

139
Q

When discussing the Fowler’s method (or single-breath N2 curve), go through the main phases briefly explaining them.

A

Initially, there is a very slow increase of N2 due to the 100% O2 inhaled earlier being left in the deadspace and not mixing

Then there is a sharp increase in N2 since here O2 was diffused into the blood. N2 is mixed with CO2 and O2 and hence creates this steep increase.

There is then an alveolar plateau where there is almost no increase in % N2

At the end, when reaching residual volume and forced exhalation, there is another increase(not as steep as the first) due to apex having more N2 and less ventilation when compared to the base.

140
Q

During forced exhalation, what are the first alveoli to collapse?

A

Alveoli located at the base

141
Q

What are the effects of respiratory disease on the V/Q ratio? Explain

A

In respiratory disease, the V/Q ratio may be increased (due to over ventilation/underperfusion) or decreased (under ventilation/overperfusion)

An increase V/Q ratio means that there is an increase in alveolar deadspace due to lack of perfusion.

A decreased V/Q (more dangerous) indicates shunting where deoxygenated venous blood will bypass the exchange area and enters the left heart with deoxygenated blood.

142
Q

A decreased V/Q ratio can cause…

A

Hypoxemia

143
Q

What is a true shunt? Give an example.

A

A true shunt is where blood flows through a region with zero ventilation. An example would be abnormal right-left shunts in the heart where blood goes directly from the right ventricle to the left ventricle => bypassing the lungs

144
Q

With regards to a shunt and a true shunt, how would oxygen therapy improve each?

A

Oxygen therapy will improve PaO2 (arterial) when there is a shunt since there is a low V/Q ratio but when there is a true shunt, there is no ventilation whatsoever and hence no benefit.

145
Q

Explain the effects of V/Q ratio on vasoconstriction in the lungs. Give the names of the two conditions

A

Hypoxia Pulmonary Vasoconstriction (low V/Q): Blockage in the airway (such as in COPD, Asthma, and Bronchitis) decreases alveolar PO2 and increases PCO2. This leads to the relaxation of respiratory smooth muscles and the constriction of vascular smooth muscles.

Hypoxia pulmonary vasoconstriction causes the diversion of blood away from poorly ventilated/overperfused alveoli and therefore limits shunting

Hyperoxia pulmonary vasodilation (large V/Q): Blockage in the vessels (such as in embolus and emphysema) increases alveolar PO2 and decreases PCO2. This leads to the contraction of respiratory smooth muscles and the relaxation of vascular smooth muscles.

146
Q

How is oxygen transported in the blood?

A

O2 is carried either physically dissolved in plasma (minor) or combined with hemoglobin (major)

147
Q

How does O2 bind with hemoglobin

A

O2 binds loosely and reversibility with iron

148
Q

What is hemoglobin rich with O2 called?

A

Oxyhemoglobin

149
Q

How is the %O2 saturation in the blood measured? (2 ways) incdicate which is invasive and non-invasive

A
  1. Can be measured non-invasively using a pulse oximeter

Can be measured invasively using arterial blood samples and a blood gas analyser

150
Q

What is the typical O2 capacity of hemoglobin?

A

20ml%

151
Q

The sigmoid also shape of the curve has 2 significant phases being the steep and the plateau. What is the significance of each?
Give a limitation of the plateau phase

A

At the plateau, where % saturation is almost 100%, the PO2 can fall without much of a fall in % saturation. This is a protection mechanism against altitude and respiratory disease.

The limitation, however, is that the plateau reduces the usefulness of hyperventilation and O2 therapy

The steep portion allows for quick O2 unloading in tissues once there is a gradient

152
Q

What is the crucial PO2 and saturation?

A

PO2 = 8kPa=60mmHg

90% saturation

They are the at the same coordinate

153
Q

What is the effect of HbF on the oxygen-hemoglobin dissociation curve?

A

Shifts the curve to the left

154
Q

Discuss the effect of 2,3-DPG on the the oxygen-hemoglobin dissociation curve

A

2,3-DPG is formed in the RBC and binds to the beta chains of hemoglobin causing O2 release.

2,3-DPG is increased in exercise, altitude, anemia, and respiratory disease.

2,3-DPG causes the curve to shift to the right

155
Q

Why does HbF bind to O2 better than HbA?

A

2,3-DPG binds poorly to the gamma chains of HbF

156
Q

Where is myoglobin found and compare its O2 affinity to that of Hb.

A

Myoglobin is found in skeletal and cardiac muscle. It has a higher O2 affinity than Hb and acts as a tissue store of O2

157
Q

What is the effect of anemia on the transport of oxygen?

A

In anemia, hemoglobin concentration is reduced so the PaO2 (arterial) is normal but the O2 content is reduced.

158
Q

What are the effects of chemicals and drugs such as nitrates and local anesthetics on the transport of oxygen

A

Fe2+ can be oxidized into Fe3+ to form Methemoglobin which does not bind to O2

159
Q

What is the effect of carbon monoxide on O2 transport?

A

Hemoglobin binds to carbon monoxide 240 times more than O2 forming carboxyhemoglobin. This prevents O2 from binding and is not reversible.

160
Q

What is the effect of sickle cell anemia on O2 transport?

A

In sickle cell anemia, the abnormal Hb causes deformation of the RBC so blood flow is impaired

161
Q

Discuss Cyanosis (peripheral and central)

A

Cyanosis is a blue coloration of the skin and mucous membranes especially the tongue, mouth, lips, and nail beds.

It occurs when the arterial blood is 85% saturated or when the capillary blood is 70% saturated

Peripheral cyanosis is due to reduced tissue blood flow due to vasoconstriction, vascular obstruction, or decreased cardiac output

Central cyanosis is due to arterial blood desaturation

162
Q

How is CO2 carried in the blood? Indicate which is the majority

A 
Physically dissolved (3%)
Carboamino compounds (3%)
Bicarbonate (42%)
163
Q

CO2 carried in the form of bicarbonate is catalyzed by which enzyme

A

Carbonic Anhydrase catalyzes this reaction.

164
Q

What is the Haldane Effect

A

The deoxynation of blood increases its ability to carry CO2.

165
Q

Define Eupnoea

A

Normal quiet breathing

166
Q

Define Hyperpnea

A

Increased ventilation

167
Q

Define Tachypnea

A

Increased respiratory rate

168
Q

Define Hyperventilation

A

Over ventilation (PaCO2 less than normal)

169
Q

Define Hypocapnia

A

PCO2 less than normal

170
Q

Define Hypercapnia

A

PCO2 greater than normal

171
Q

Define Hypoxia

A

PO2 less than normal

172
Q

Define Hyperoxia

A

PO2 greater than normal

173
Q

Define Hypoxemia

A

PO2 less than normal in the blood

Note: It is associated with hypoventilation

174
Q

Define Asphyxia

A

Hypoxia and hypercapnia

175
Q

Define Dyspnea. Does it necessarily mean the presence of disease?

A

Stressful breathing

No

176
Q

Define Apnea

A

Absence of breathing

177
Q

a respiratory sensor senses an abnormality. How is this abnormality dealt with? Trace the general steps beginning with the sensor.

Any loss of function in this system can lead to…

A

The sensor (chemoreceptors, lung receptors…) senses an abnormality. It will then input this information to the control center in the medulla which would then output the command onto the effector. Once the abnormality is solved, the sensor will input the normality back to the medulla where it will stabilize.

Any loss of function in this system can lead to hypoventilation and hypoxemia

178
Q

What are the most important inputs to the respiratory center and what is each classified into?

A

Airways and lung receptors are classified into stretch receptors, irritant receptors, and J receptors

Chemoreceptors are classified into peripheral and central receptors

179
Q

Describe the role of stretch receptors

A

These are nerve endings in the airway smooth muscle which are stimulated by stretch during inspiration.

The nerve impulses travel in the vagus nerve to inhibit the inspiratory center in the medulla

180
Q

The inhibition of the inspiratory center goes through which nerve? What is this inhibition called?

A

Vagus nerve

Hering-Breuer inflation reflex

181
Q

Describe the role of irritant receptors

A

They are nerve endings near the airway epithelial cells which are stimulated by noxious gases, cigarette smoke, dust, and cold air

The nerve impulses travel in the vagus nerve causing reflex bronchoconstriction or coughing.

182
Q

Describe the role of J receptors

A

They are nerve endings near capillaries in the alveoli called juxtacapillary (next to capillary) receptors which are stimulated by pulmonary congestion and edema.

The nerve impulses travel in the vagus nerve causing reflex apnea or rapid shallow breathing.

183
Q

What bodies are involved in peripheral chemoreceptors?

A

Aortic and carotid bodies

184
Q

Describe the role of peripheral chemoreceptors

A

Peripheral chemoreceptors are stimulated by a decrease in PaO2 (arterial) and an increase in PaCO2 and H+. This stimulates the respiratory center causing an increase in breathing.
The increase in breathing causes an increase in PaO2 and a decrease in PaCO2 and H+ so there is negative feedback control of blood gasses

185
Q

Where are the peripheral chemoreceptors located?

A

Aortic bodies on the aorta

Carotid bodies on the common carotid arteries (right and left)

186
Q

Describe the role of central chemoreceptors

A

Located in the medulla, separate from the respiratory centers. They are stimulated by an increase in brain extracellular fluid PCO2 and H+ but not by a decrease in PO2. They are responsible for 80% of the ventilators response to increased PaCO2 as they are more sensitive.
They do, however, have poor response to arterial blood H+ because of the blood brain barrier

187
Q

What are the differences between central and peripheral chemoreceptors

A
  1. Location
  2. Central are more sensitive
  3. Central are only stimulated by an increase in PCO2 and H+
188
Q

Answer the following with Central chemoreceptors or Peripheral chemoreceptors

All ventilatory responses to decreased PaO2 are due to the

Most of the ventilatory response to increased arterial blood H+ is due to the

Most of the ventilatory response to increased PaCO2 is due to the

A

Peripheral

Peripheral

Central

189
Q

Although both peripheral and central chemoreceptors are sensors for PaCO2 and H+,

Why do the central chemoreceptors account for 80% of the ventilatory response?

Why do the peripheral chemoreceptors account for most of the arterial blood H+?

A

Because they are more sensitive

Because of the blood brain barrier, H+ cannot be transported in

190
Q

Compare the O2 and CO2 response curved

A

The Ventilatory response to hypoxia (low O2) is not so sensitive with little response until PaO2 falls below 60 mmHg where it is critical

The CO2 response line is steep indicating that ventilation is sensitive to a very small change in PaCO2

191
Q

What is the effect of hypocapnia on the body?

A

Hypocapnia causes increased neuromuscular excitability and tetany.

192
Q

What is the effect of hypercapnia on the body

A

Hypercapnia causes depression of the nervous system and coma

193
Q

What are the classifications of Hypoxia. Briefly define each

A

Hypoxia Hypoxia: PaO2 is less than normal

Anemic Hypoxia: PaO2 is normal but the O2 content is less than normal

Stagnant Hypoxia: PaO2 and O2 content are normal but O2 delivery to the tissues is reduced due to decreased blood flow

Histotoxic Hypoxia: PaO2, O2 content, and delivery are normal but the tissues cannot use the O2 due to metabolic poisoning.

194
Q

Give 3 causes of respiratory disorders

A

Decreased ventilation
Decreased alveolocapillary diffusion
Decreased transport

Medicine Year 1 Semester 1 (23 decks)

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