COPD Flashcards

1
Q

What is a major respiratory disease in Canada that is often preventable and can be treated, but remains underdiagnosed?

A

COPD

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2
Q

It is the thought that the prevalence of COPD is underestimated because those with earlier symptoms of COPD are not recognized and/or do not seek treatment.

True or False?

A

True

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3
Q

COPD affects at least 700,000 adults, approximately 4.4% of Canadians aged 35 years or older.

In this age group, is there a higher prevalence in males or females?

A

Females

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4
Q

Which group in Canada does COPD affects a much higher percentage of?

A

off reserve Aboriginal people (at 7.9%)

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5
Q

COPD is the 5th leading cause of death in females and 4th in males.

True or False?

A

False (COPD is the 4th leading cause of death in females and 5th in males.)

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6
Q

There is a higher prevalence for COPD, in women, except for the aged 75 years and older group.

True or False?

A

true

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7
Q

There is a higher prevalence for COPD, in women, except for the aged 75 years and older group.

True or False?

A

true

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8
Q

Mortality rates from COPD are higher in males (4.5/100,000) than females (2.8/100,000) and may actually be higher than reported because two complications of COPD, pneumonia and congestive heart failure, may be listed as the cause of death, instead of COPD.

True or False?

A

True

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9
Q

COPD is ranked what in the leading cause of death in the US and is the what rank of death in the worldwide?

A

US has COPD ranked 4th leading cause of death

6th cause of death worldwide

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10
Q

What is the condition of being ill, diseased, or unhealthy called?

A

Morbidity

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11
Q

What is the condition of being dead called?

A

Mortality

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12
Q

Morbidities always eventually lead to mortality.

True or False?

A

False

Morbidities may or may not lead to mortality.

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13
Q

The burden of COPD from a health, economical, and societal cost is not enough too cause an impact.

True or False?

A

False

Burden of COPD from a health, economical, and societal cost is significant.

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14
Q

Among major chronic illnesses in Canada, what now accounts for the highest rate of hospital admissions?

A

COPD (AECOPD)

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15
Q

How long, on average, is a hospitalization for AECOPD and how much does it cost?

A

10 days and $10,000

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16
Q

What is the leading cause of COPD and is the most important etiologic factor?

A

Cigarette smoking

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17
Q

15-25% of smokers will be diagnosed with COPD?

True or False?

A

true

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18
Q

An average smoker loses lung function at twice the rate of a nonsmoker; this means that smoking adults lose lung function at a more rapid rate as they age, in comparison to nonsmokers.

True or False?

A

True

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19
Q

Smoking is common in people with COPD, as 40-50% of them have a history of smoking.

True or False?

A

False (80-90%)

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20
Q

Smoking is toxic to cells in the lungs and also impairs the mechanisms responsible for _________ ____________ __________.

A

lung tissue repair

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21
Q

Other than smoking, what also play a contributing factor to developing COPD?

A

Genetics

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22
Q

Genetics susceptibilities have been identified for developing COPD.

Polymorphisms of genes that code for TNF, surfactant, proteases, and antiproteases are examples.

True or False?

A

True

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23
Q

A hereditary deficiency (mutation) in which gene may result in early onset and severe COPD?

A

Alpha-1 Antitrypsin (AAT Deficiency)

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24
Q

Alpha-1 antitrypsin gene may result in early onset and severe COPD (AAT deficiency)

The onset and severity is worsened by what?

A

Smoking

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25
Q

The heterogeneous nature of COPD can be attributed to multiple genetic and environmental factors as well as gene-gene & gene-environmental interactions, known as what?

A

epigenetics

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26
Q

Genetics have a role in how these phenotypes are expressed and how gene-environment interactions contribute to disease manifestations such as what?

A

exacerbations

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27
Q

What are environmental risk factors that could lead to COPD from inhalational exposure?

A

occupational dusts or chemicals, indoor pollution (from heating and cooking with biomass fuels), and outdoor pollution

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28
Q

What are some other risk factors, other than environmental risk factors, that could lead to COPD?

A

Severe childhood respiratory infections, asthma, airway hyper responsiveness, nutritional compromise, impairment of fetal development resulting in low birth weight, infants who develop bronchopulmonary dysplasia

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29
Q

COPD can be considered a SINGLE disorder.

True or False?

A

False

It is a group of disorders that are characterized by airflow

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30
Q

The different phenotypes of COPD may overlap and include what three?

A

chronic bronchitis, emphysema, and bronchiectasis

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31
Q

Which COPD phenotype is characterized by airway inflammation & obstruction of the major and small airways?

A

chronic bronchitis

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32
Q

Which COPD phenotype includes history of a chronic, productive cough for at least 3 consecutive months, over 2 consecutive years, and is required for clinical diagnosis?

A

chronic bronchitis

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33
Q

Which COPD phenotype is characterized by a loss of lung elasticity & abnormal enlargement of the airspaces distal to the terminal bronchioles, with destruction of the alveolar walls & capillary beds?

A

Emphysema

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34
Q

Which COPD phenotype is an uncommon form of COPD characterized by a permanent dilation of the bronchi and bronchioles?

  • It is caused by destruction of the muscle and elastic supporting tissue due to vicious cycles of infection & inflammation.
A

Bronchiectasis

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35
Q

Although, asthma is a chronic inflammatory airway disorder, why is it not the same?

A

lung function is often normalized in the absence of triggers (especially early on in the disease, prior to significant airway remodeling)

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36
Q

Asthma is usually not classified as COPD, but together, asthma and COPD can be called obstructive airway diseases

True or False?

A

True

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37
Q

Comparing Asthma and COPD

When is the age of onset for asthma?

A

Anytime in childhood

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38
Q

Comparing Asthma and COPD

When is the age of onset for COPD?

A

midlife

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39
Q

Comparing Asthma and COPD

What is the smoking history for one with asthma?

A

Usually nonsmokers

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40
Q

Comparing Asthma and COPD

What is the smoking history for one with COPD?

A

Usually smokers

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41
Q

Comparing Asthma and COPD

What is the usual etiology (cause of the disease) for one with asthma?

A

Immunologic stimuli and family history

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42
Q

Comparing Asthma and COPD

What is the usual etiology (cause of the disease) for one with COPD?

A

Tobacco smoke or other air pollution

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43
Q

Comparing Asthma and COPD

Is the airflow limitation reversible or not fully reversible for one with asthma?

A

usually reversible

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44
Q

Comparing Asthma and COPD

Is the airflow limitation reversible or not fully reversible for one with COPD?

A

Not fully reversible

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45
Q

Comparing Asthma and COPD

What does the past medical history look life for one with asthma?

A

Allergies, sinusitis, respiratory infections and nasal polyps

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46
Q

Comparing Asthma and COPD

What does the past medical history look life for one with COPD?

A

Respiratory Infections (Allergies and sinusitis rare)

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47
Q

Comparing Asthma and COPD

What do clinical features look like for those with asthma?

A

Episodic wheeze with chest tightness, cough and dyspnea

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48
Q

Comparing Asthma and COPD

What do clinical features look like for those with COPD?

A

Persistent (or worsening) dyspnea and chronic cough

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49
Q

Comparing Asthma and COPD

What do inflammation features do those with asthma have?

A

Acute eosinophilic inflammation

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50
Q

Comparing Asthma and COPD

What do inflammation features do those with COPD have?

A

Neutrophil and macrophage induced inflammation

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51
Q

Comparing Asthma and COPD

The following are pathologic changes for COPD.

Fragile epithelium, thickening of basement membrane, mucus gland metaplasia and enlargement

True or False?

A

False

The following are pathologic changes for asthma

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52
Q

Comparing Asthma and COPD

The following are pathologic changes for asthma.

squamous metaplasia of epithelium, parenchymal destruction, mucus gland metaplasia and enlargement

True or False?

A

False

The following are pathologic changes for COPD

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53
Q

What is a respiratory disorder largely caused by smoking, characterized by progressive, partially reversible airway obstruction and lung hyperinflation, systemic manifestations, and increasing frequency and severity of exacerbations?

A

COPD

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54
Q

What is COPD is characterized by?

A

persistent inflammation of airways, lung parenchyma and its vasculature

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55
Q

What is the pathophysiological hallmark of COPD?

A

Expiratory flow limitation

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56
Q

What are the four most important mechanisms for airflow limitation (these can occur for asthma or COPD)?

A

Loss of lung elastic recoil, peribronchiolar fibrosis, increased airway secretions, airway smooth muscle

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57
Q

Which of the four most important mechanisms for airflow limitation occurs with emphysema due to protease mediated degradation of connective tissue elements in the lungs?

A

Loss of elastic recoil

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58
Q

Which of the four most important mechanisms for airflow limitation occurs due to an imbalance between the lung’s repair and defense mechanisms?

A

Peribronchiolar fibrosis

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59
Q

____________ of small airways contribute to airway remodeling, which is a key factor in the development of the irreversible airflow limitation seen in COPD.

A

Fibrosis

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60
Q

What is the persistent changes that occur within the structural components of the airways in response to inflammation?

A

Airway remodeling

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61
Q

Which of the four most important mechanisms for airflow limitation occurs in COPD and there is mucus hyperplasia and increased expression of mucin genes?

A

Increased airway secretions

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62
Q

What two things play a role in mucus hypersecretion?

A

Inflammation and oxidant injury

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63
Q

Which of the four most important mechanisms for airflow limitation includes an increased tone in airway smooth muscle due to hyperreactivity of the bronchi with bronchoconstriction, due to persistent inflammation?

A

Airway smooth muscle

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64
Q

Even if tone is not increased in airway smooth muscle in persons with COPD, their airways are narrower, resulting in an increase in what?

A

airway resistance

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65
Q

Airway smooth muscle - increased tone in airway smooth muscle due to hyperreactivity of the bronchi with bronchoconstriction, due to persistent inflammation.

Even if tone is not increased in persons with COPD, their airways are narrower, resulting in an increase in airway resistance

Relaxing airway smooth muscle with bronchodilators will have a detrimental effect on airflow no matter what.

True or False?

A

False

(Relaxing airway smooth muscle with bronchodilators will have a beneficial effect on airflow whether there is increased tone or not.)

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66
Q

People diagnosed with COPD usually have some degree of which two phenotypes of COPD?

A

emphysema and chronic bronchitis

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67
Q

What COPD phenotype is the result of inflammation of the airway epithelium and mucus hypersecretion, due to inspired irritants like tobacco smoke or air pollution?

A

chronic bronchitis

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68
Q

What is the first feature of chronic bronchitis?

A

Mucus Hypersecretion in the large airways

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69
Q

Mucus Hypersecretion in the large airways is the first feature of chronic bronchitis

There is an increase in the size and the number of ___________ __________ and ___________ ___________ in airway epithelium

A

Mucous glands and goblet cells

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70
Q

Mucus Hypersecretion in the large airways is the first feature of chronic bronchitis

There is an increase in the size and the number of mucous glands & goblet cells in airway epithelium.

The mucus produced is _________ and more ____________ (tending to keep a firm hold of something; clinging or adhering closely.)

A

thicker and tenacious

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71
Q

Within chronic bronchitis, what causes the reduction in mucus clearing?

A

impaired ciliary function

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72
Q

When the lung’s defense mechanisms are compromised (like in chronic bronchitis), there is an increased risk of what?

A

pulmonary infection and injury (there may be bacterial colonization occurring)

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73
Q

Bacteria such as Haemophilus influenza and streptococcus pneumoniae can become embedded in the what?

A

airway secretions

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74
Q

Infection and injury cause further mucus production and inflammation

True or False?

A

true

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75
Q

Recurrent infections and persistent inflammation result in what two things?

A

bronchospasm and eventual permanent narrowing of the airways

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76
Q

Organize the steps in chronic Bronchitis.

A ) Eventually, if not reversed, hypoxemia will lead to pulmonary hypertension and Cor pulmonale (which is enlargement of the right ventricle)

B ) Airway obstruction causes ventilation-perfusion mismatch, hypercapnia and hypoxemia

C ) Pulmonary hypertension and Cor pulmonale can then cause right heart failure

D ) Significant Hypoxemia will lead to polycythemia (which is the over production of RBCs) and cyanosis.

E ) Thick mucus & hypertrophied bronchial smooth muscle leads to airway obstruction.
- Air trapping can result as the airways collapse early in expiration, when the airways are narrows, trapping gas in the distal portion of the lungs.

A

E, B, D, A, C

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77
Q

What COPD phenotype is characterized by the breakdown of elastin in the alveolar septa and bronchial walls (as well as breakdown of alveolar and bronchial wall components) by proteases?

(What are proteases?)

A

Emphsyema

Proteases are enzymes that digest proteins

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78
Q

Emphysema occurs due to imbalance between proteases and antiproteases as a result of increased protease activity and inhibition of what?

A

normal endogenous antiprotease activity (in the lungs)

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79
Q

The leading cause of the imbalance between proteases and antiproteases as a result of increased protease activity and inhibition of normal endogenous antiprotease activity in the lungs, is airway epithelial inflammation, from toxins in what two things?

A

Tobacco smoke or air pollution

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80
Q

Where are proteases released from?

A

inflammatory cells

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81
Q

What are three examples of the most important proteases activated in emphysema?

A

elastases, cathepsins and matrix metalloprotease

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82
Q

Normally antiproteases (such as alpha1-antitrypsin) inhibit _____________ in the lungs; however, antiprotease production and release is inadequate in smokers with COPD.

A

proteases

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83
Q

What type of emphysema is commonly linked to an inherited deficiency of alpha1-antitrypsin and accounts for approximately 1-3% cases.

A

Primary emphysema

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84
Q

Primary emphysema is commonly linked to an inherited deficiency of ________-_______________ and accounts for approximately 1-3% cases.

A

alpha1-antitrypsin

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85
Q

Primary emphysema often develops in individuals who develop the disease before age 40 or in their early 40s and do not have a smoking history.

True or False?

A

true

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86
Q

Primary emphysema often develops in individuals who develop the disease before age 40 or in their early 40s and do not have a smoking history.

True or False?

A

true

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87
Q

Persons with inherited alpha1-antitrypsin deficiency with a history of smoking are even more susceptible to developing emphysema.

True or False?

A

True

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88
Q

Septal destruction destroys portions of the pulmonary capillary bed causing what?

A

ventilation-perfusion mismatch (and eventually hypoxemia)

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89
Q

Within emphysema, decreased elastic recoil in ______________ ___________ contributes to air trapping

A

bronchial walls

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90
Q

Within emphysema, there is an abnormal enlargement of gas exchange airways (called acin) due to what?

A

air trapping

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91
Q

Within emphysema, due to the air trapping, what two things are inevitable?

A

An increase in Residual Volume (RV) and Total Lung Capacity (TLC)

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92
Q

Within emphysema, persistent inflammation of the airways can result in what?

A

hyperreactivity of the bronchi with bronchoconstriction

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93
Q

Within emphysema, when smoking or air pollution initiates an inflammatory response, which inflammatory cells release elastin?

A

neutrophils and alveolar macrophages

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94
Q

Within Emphysema:

Smoking or air pollution initiates an inflammatory response.

Inflammatory cells, specifically neutrophils and alveolar macrophages release elastin.

The action of elastin is normally inhibited by what?

A

alpha1-antitrypsin

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95
Q

Within Emphysema:

Smoking or air pollution initiates an inflammatory response.

Inflammatory cells, specifically neutrophils and alveolar macrophages release elastin.

The action of elastin is normally inhibited by alpha1-antitrypsin; however, as inflammation persists, there is a _______________ in alpha1-antitrypsin activity.

A

decrease

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96
Q

Within Emphysema:

Smoking or air pollution initiates an inflammatory response.

Inflammatory cells, specifically neutrophils and alveolar macrophages release elastin.

The action of elastin is normally inhibited by alpha1-antitrypsin; however, as inflammation persists, there is a decrease in alpha1-antitrypsin activity.

In turn, there is destruction of which part of the lung?

A

elastic fibres in the lung (resulting in emphysema)

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97
Q

Within Emphysema:

In the case of inherited alpha1-antitrypsin deficiency, there is a limited amount of alpha1-antitrypsin to counteract elastase released.

True or False?

A

True

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98
Q

Within Emphysema:

The amount of alpha1-antitrypsin is determined by a pair of codominant genes named what?

A

protein inhibitor genes

There are more than 75 mutations of the gene, which are inherited as an autosomal recessive disorder.

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99
Q

Within Emphysema:

The most serious alpha1-antitrypsin deficiency is caused by the ______-____________, which is found in 5% of the population.

A

PIZ variant

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100
Q

Within Emphysema:

Homozygous individuals who carry 2 PIZ genes, only have 15-20% of the normal plasma concentration of alpha1-antitrypsi and have a 70-80% likelihood of developing emphysema.

True or False?

A

true

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101
Q

The sites of involvement for emphysema determine whether it is called _______________ or __________________ emphysema.

A

centriacinar or panacinar

102
Q

What is the most common form of emphysema?

A

centriacinar emphysema

103
Q

What kind of emphysema has the destruction confined to terminal and respiratory bronchioles and often involves the upper parts of lung?

A

Centriacinar Emphysema

104
Q

What kind of emphysema has involvement of the peripheral alveoli, and later, the more central bronchioles?

This more common in individuals with inherited alpha1-antitrypsin deficiency and often involves the lower parts of lung?

A

Panacinar Emphysema

105
Q

What kind of emphysema has involvement of the peripheral alveoli, and later, the more central bronchioles?

This more common in individuals with inherited alpha1-antitrypsin deficiency and often involves the lower parts of lung?

A

Panacinar Emphysema

106
Q

When air trapping occurs, airways are pulled open during inspiration, allowing gas to flow past obstruction, caused by narrowed airways and mucus plugs.

However, during expiration what prevents normal expiratory flow?

A

decreased elastic recoil of bronchial walls (causes the airways to collapse)

107
Q

When air trapping occurs, airways are pulled open during inspiration, allowing gas to flow past obstruction, caused by narrowed airways and mucus plugs.

However, during expiration, decreased elastic recoil of bronchial walls causes the airways to collapse, preventing normal expiratory flow.

On the physical exam, the person with hyperinflated lungs due to air trapping, will have the appearance of what?

A

barrel chest

108
Q

During air trapping, an expanded thorax, puts the respiratory muscles at what type of disadvantage? What does this result in?

A

mechanical disadvantage and decreased tidal volume, hypoventilation and hypercapnia

109
Q

Although both chronic bronchitis and emphysema contribute to air trapping, air trapping is usually more associated with what?

A

Emphysema

110
Q

Why is air trapping usually more associated with emphysema?

A

There is a loss of elastic recoil due to destruction of lung tissue significantly prevents normal expiratory flow

111
Q

Why is air trapping usually more associated with emphysema?

A

There is a loss of elastic recoil due to destruction of lung tissue significantly prevents normal expiratory flow

112
Q

What is a central feature of COPD that leads to damage & remodeling of the lung parenchyma and airflow limitation?

A

Inflammation

113
Q

What type of immunity is activated at all stages of COPD?

A

Innate Immunity

114
Q

What type of immunity is activated in more severe diseases?

A

adaptive immunity

115
Q

Innate Immunity is activated at all stages of COPD and Adaptive Immunity is activated in more severe disease.

What mediates both types of immunity?

What cells link innate and adaptive immunity in COPD?

A

Cytokines and dendritic cells

116
Q

Since inflammation is a central feature of COPD, there is an increase in what type of cells?

A

lymphocytes

117
Q

What are thought to be the most important inflammatory cells in COPD?

A

Neutrophils, macrophages, CD8+ lymphocytes

118
Q

Since inflammation is a central feature of COPD, there is also an increase in what two immune cells?

A

CD4+ T lymphocytes and B cell

119
Q

Neutrophils, macrophages, CD8+ lymphocytes are thought to be the most important inflammatory cells in COPD.

Neutrophils release proteases, specifically neutrophil elastase cathepsin G, proteinase-3, matrix metalloproteinase 8 and 9.

True or False?

A

True

120
Q

Neutrophils, macrophages, CD8+ lymphocytes are thought to be the most important inflammatory cells in COPD.

What type of cells secrete inflammatory meditators that activate neutrophils and CD8+ T Lymphocytes?

A

Macrophages

121
Q

Neutrophils, macrophages, CD8+ lymphocytes are thought to be the most important inflammatory cells in COPD.

Macrophages secrete inflammatory meditators that activate neutrophils and CD8+ T Lymphocytes.

Macrophages also release ________________, specifically cathepsins and matrix metalloproteases.

A

proteases

122
Q

Neutrophils, macrophages, CD8+ lymphocytes are thought to be the most important inflammatory cells in COPD.

CD4+ T lymphocytes activate B cells, and B cells are involved in what?

A

antibody production

123
Q

Within COPD, there is an increase in the following pro-inflammatory cytokines: TNF-alpha, IL-1B, IL-6, IL-32, thymic stromal lymphopoietin (TSLP), T cell cytokines.

True or False?

A

True

124
Q

Which Pro-Inflammatory Cytokine increases expression of adhesion molecules on leukocytes and endothelial cells, upregulates other pro-inflammatory cytokines like IL-1 and IL-6?

A

TNF-alpha

125
Q

Which Pro-Inflammatory Cytokine is especially increased during COPD exacerbations and associated weight loss?

A

TNF-alpha

126
Q

Which Pro-Inflammatory Cytokine activates macrophages to secrete inflammatory cytokines, chemokines, and matrix metalloproteinase?

A

IL-1B

127
Q

Which Pro-Inflammatory Cytokine is a link between innate and acquired immunity and stimulates C-reactive protein release from the liver?

A

IL-6

128
Q

Which Pro-Inflammatory Cytokine is a newly described pro inflammatory cytokine and is correlated with disease severity?

A

IL-32

129
Q

Which Pro-Inflammatory Cytokine belongs to the IL-7 family and plays a key role in dendritic cell programming by stimulating specific chemokines, which attract T helper lymphocytes and cytotoxic T lymphocytes?

A

TSLP (thymic stromal lymphopoietin)

130
Q

T-cell cytokines secrete pro-inflammatory cytokines sometimes called what?

A

lymphokines

131
Q

What can induce leukocyte chemotaxis, specifically promoting neutrophil activation and migration?

A

Chemokines

132
Q

What can also contribute to airway remodeling?

A

Growth factors

133
Q

Cytokines can only have anti-inflammatory effects.

True or False?

A

False

(Cytokines can also have inhibitory or anti-inflammatory effects.
An example is IL-10, which is reduced in the sputum of persons with COPD
IL-10 inhibits TNF-alpha, IL-1Beta, granulocyte-macrophage colony-stimulating factor (GM-CSF), chemokines and matrix metalloproteinase, all of which are increased in COPD)

134
Q

There is a ___________ _________________ to COPD in terms of systemic inflammation, systemic manifestations and co-morbidities.

A

systemic component

135
Q

The airflow obstruction characteristic of COPD has significant effects on what two things, with systemic consequences.

A

cardiac function and gas exchange

136
Q

There are two schools of thought related to COPD and systemic involvement

  1. Systemic manifestations are co-morbidities are the result of a systemic “spill over” of the inflammatory and respiratory events in the lungs
    - In this type of view, therapies should be directed primarily towards ____________
  2. COPD systemic inflammatory disease in which lungs are one form of expression (to explain, the pulmonary manifestations are simply one form of expression of a “systemic” inflammatory state where there is multiple organ compromise)
    - In this type of view, therapies should be shifted to the ______________ _____________ ___________
A

the lungs and systemic inflammatory state

137
Q

Although there are two schools of thought related to COPD and systemic involvement and research is underway in both of these views, most treatments are directed where?

A

to the lungs

138
Q

Systemic Inflammation appears to relate to an accelerated decline in lung function and is increased during what?

A

exacerbations

139
Q

Cytokines have been linked to either muscle weakness, skeletal muscle atrophy or cachexia:

IL-6, TNF-a, IL-1B, chemokines (specifically CXCL8 or IL-8).

All of these except IL-1B have increased plasma concentrations

True or False?

A

True

140
Q

What is an adipokine which is a cytokine derived from fat cells, plays an important role in regulating energy and is decreased in COPD.

A

Leptin

141
Q

What four acute phase proteins can be linked to COPD, particularly during exacerbations?

A

CRP, fibrinogen, serum amyloid A, and surfactant protein D

142
Q

Which of the four acute phase proteins has been linked to health and exercise capacity and appears to be a significant predictor of BMI?

A

Increased CRP

IF CRP remains high 2 weeks after an exacerbation, there is likelihood of recurrent exacerbation

143
Q

Which of the four acute phase proteins is increased with frequent exacerbations?

A

Increased Fibrinogen plasma

Worse FEV1 and increased risk of hospitalization for COPD was linked to elevated plasma fibrogen

144
Q

occurs during exacerbations; correlated with severity of exacerbations?

A

Elevated serum amyloid A

145
Q

Which of the four acute phase proteins is better related disease severity and symptoms than CRP

(Both CRP and fibrinogen have been associated with increased cardiac co-morbidity)

A

Surfactant protein D

146
Q

Systemic inflammation can contribute to the following systemic manifestations and comorbidities of COPD:

o Skeletal muscle weakness
o Cachexia
o Lung cancer
o Schizophrenia
o Pulmonary hypertension
o Cardiac failure
o Osteoporosis
o Normocytic anemia
o Diabetes
o Seizures
o Obstructive sleep apnea
o Depression

All these are true but what two?

A

Schizophrenia and seizures

147
Q

Airway remodeling causes ___________ around small airway which is thought to be a major mechanism to progressive, irreversible airway narrowing.

A

fibrosis

148
Q

Protease mediated degradation of connective tissue elements, specifically elastin, leads to ______________ and the destruction of alveolar septa and loss of elastic recoil of bronchial walls.

A

emphysema

149
Q

Clinically, the person with COPD complains of dyspnea or shortness of breath and a productive or non-productive cough?

A

productive cough

150
Q

What three things are often manifested as the disease progresses?

A

Hypoxemia, hypercapnia and cor pulmonale

151
Q

COPD is not one singular disease process clinical features often differ between patients.

True or False?

A

True

152
Q

The role of Oxidative Stress occurs as a direct result from cigarette smoke which contains numerous oxidants as well as from inflammatory cells which release what?

A

reactive oxygen species

153
Q

What is considered to be the cause of corticosteroid resistance in COPD?

A

oxidative stress

154
Q

Oxidative stress contributes to the damage that occurs where?

A

in the lungs

155
Q

Muscle dysfunction in COPD has been strongly associated with enhanced what?

A

oxidative stress

156
Q

What are acute changes in symptoms (such as cough, dyspnea & sputum production)?

A

AECOPD (Acute Exacerbations of COPD)

157
Q

HALF of Acute Exacerbations of COPD are infectious.

True or False?

A

True

158
Q

When it comes to AECOPD, what is considered to be more common, viral or bacterial infections?

A

viral infections

159
Q

HALF of Acute Exacerbations of COPD are infectious.

Viral infections seem to be more common than bacterial; however it is difficult to establish what bacterial pathogen has caused the exacerbation as chronic ______________ ________________ of the airways is common in COPD.

A

bacterial colonization

160
Q

Most of the time the etiology for 1/3 of AECOPD (the cause), is well known.

True or False?

A

False

The etiology for 1/3 of AECOPD (the cause) is unknown

161
Q

What are some triggers for AECOPD?

A

Congestive Heart Failure, Pulmonary Embolis, exposure to allergens and, irritants

162
Q

The most frequently involved respiratory viruses in AECOPD are which two?

A

rhinoviruseses and RSV (respiratory syncytial virus)

163
Q

The following are probable bacterial pathogens to cause AECOPD:

haemophilus influenza and other haemophilus species, moraxella catarrhalis & streptococcus pneumoniae

True or False?

A

True

164
Q

What are these all common signs and symptoms of?

breathlessness wheezing, chest tightness, increase cough and sputum production, change in colour and tenacity of sputum and fever

tachycardia, tachypnea, malaise, insomnia, fatigue, depression and confusion

Exercise intolerance and fever may present prior.

A

AECOPD

165
Q

What are these examples of?

  • Initiate or increase bronchodilator therapy
  • If no improvement, admit to hospital
  • Administer oxygen; combination therapy of Beta 2-agonists & anticholinergics; and oral, IV, inhaled corticosteroids
  • Intravenous methylxanthines, antibiotics, NIPPV may be considered considered
  • It is important to treat comorbidities as needed
A

Management Techniques for AECOPD

166
Q

What are the best two ways to prevent AECOPD?

A

Smoking cessation and vaccinations (annual influenza vaccine and pneumococcal vaccine every 5 to 10 years)

167
Q

Vaccinations - specifically annual influenza vaccine and pneumococcal vaccine every 5 to 10 years

This reduces morbidity and mortality for the disease by as much as 50% in elderly patients and hospitalization rate by 39% in persons with chronic lung disease.

True or False?

A

True

168
Q

What two medications may be prescribed as combination therapy, in moderate to severe COPD with 1 or more AECOPD/year?

A

Regular Inhaled Corticosteroid and long acting beta 2 agonist

169
Q

What type of symptom can be identified as the subjective sensation of being unable to get enough air?

A

Dyspnea (shortness of breath)

170
Q

Dyspnea/Shortness of Breath: subjective sensation of being unable to get enough air.

Dyspnea may be caused by disturbances in ventilation, gas exchange or ventilation-perfusion relationships, as well as increased work of breathing or diseases that damage the lung parenchyma.

True or False?.

A

true

171
Q

What type of symptom can be identified as it occurs as breathing with effort depletes energy stores?

A

Fatigue and Exercise Intolerance

172
Q

What type of symptom is a reflex stimulated in COPD by excessive secretions of irritants?

A

Cough

173
Q

What type of symptom is caused by inflammation in the airways?

A

Sputum production

174
Q

What type of symptom is caused by air passing through narrowed airways?

A

Wheezing

175
Q

What may be present during AECOPD or COPD to indicate an infection?

A

fever

176
Q

What abnormal finding would occur due to prolonged expiratory phase?

A

Hypoventilation

177
Q

What abnormal finding may be present and related to several mechanisms (including fever, use of a Beta-2 agonist, hypovolemia)?

A

Tachycardia

178
Q

What abnormal finding shouldn’t be affected and if you do, consider hypovolemia or sepsis for hypotension and a history of high blood pressure for hypertension?

A

Blood Pressure

179
Q

What abnormal finding may be present related to inadequate gas exchange in COPD?

A

Hypoxemia

180
Q

Although a person with COPD warrants a head to toe assessment, one may argue that the most important system to asses is what?

A

the respiratory system

181
Q

What is a COPD patient often doing to help to prevent expiratory airway collapse?

A

Pursed lip breathing (in tripod position)

182
Q

What three accessory muscles are usually used in COPD?

A

sternocleidomastoid, scalene and intercostals muscles

183
Q

What can be a result of hypoxemia?

A

Cyanosis

184
Q

When percussing someone with COPD, there may be air trapping. What is the common sound found when percussing?

A

Hyperresonant sound

185
Q

When auscultating someone with COPD, what sound is caused by abnormal secretions, mucus or fluid in the airways?

A

Crackles

186
Q

When auscultating someone with COPD, what sound occurs as air passes through narrowed airways?

A

Wheezing

187
Q

When auscultating someone with COPD, Inspiratory wheeze is associated with what type of obstruction?

A

Upper airway obstruction

188
Q

When auscultating someone with COPD, Expiratory wheeze is associated with what type of obstruction?

A

Lower airway obstruction

189
Q

What other abnormal findings may be common when assessing someone with COPD?

A

muscle weakness (and muscle wasting), cachexia, and finger clubbing

190
Q

What abnormal laboratory findings may be found when testing ABGs in a COPD patient?

A

Hypoxemia, hypercapnia, and acidosis

191
Q

When there is inadequate gas exchange for a prolonged period of time, what is the ultimate risk?

A

respiratory failure

192
Q

What abnormal laboratory findings may be found when testing CBC in a COPD patient?

A

elevated leukocytes, anemia, elevated cytokines and acute phase proteins

193
Q

When reviewing a chest x-ray, hyperinflation can indicate what?

A

air trapping

194
Q

When reviewing a chest x-ray, flattening of the hemidiaphragms can indicate what?

A

air trapping

195
Q

What is the standard assessment tool for diagnosing, staging and monitoring COPD?

A

Spirometry

196
Q

Current COPD guidelines recommend that spirometry be performed on any patient who has a history of exposure to risk factors for COPD, a history of a chronic respiratory illness or chronic symptoms of cough, sputum production or dyspnea.

True or False?

A

True

197
Q

What is the volume of air forcibly exhaled during the first second of expiration after maximal inspiration.

What value of FEV1 causes a concern?

A

Forced Expiratory Volume in 1 Second (FEV1) and LESS than 80% indicates more advance disease

198
Q

What is the maximum volume of air exhaled until the lungs are emptied?

A

Forced Vital Capacity (FVC)

Note: FVC is not always reduced in early stages of COPD

199
Q

In spirometry, what ratio is used to assess lung function?

A

FEV1/FVC (less than 70% confirms airflow limitation)

200
Q

What stage of COPD is oxygen therapy typically used in?

A

Stage IV (4)

201
Q

What are three ways oxygen therapy can be delivered?

A

Long-term continuous therapy, during exercise or as needed (to relieve episodes of acute dyspnea)

202
Q

How many hours per day does long term therapy oxygen look like? What is the the goal of oxygen saturation

A

15 hours or more and 90% or greater

203
Q

Oxygen therapy has NOT been shown to improve pulmonary hypertension, increases exercise capacity & lung function, improves mental and emotional states, increases survival on persons with chronic respiratory failure

True or False?

A

False

(Oxygen therapy has been shown to improve pulmonary hypertension, increases exercise capacity & lung function, improves mental and emotional states, increases survival on persons with chronic respiratory failure)

204
Q

What can be considered during severe exacerbations or in persons with chronic hypercapnic respiratory failure (although it is not considered standard of care for persons with COPD)?

A

NIPPV (noninvasive positive pressure ventilation)

205
Q

What are the main pharmacological therapy for COPD?

A

Bronchodilators (short and long acting)

206
Q

What type of pharmacological therapy decreases bronchoconstriction by reducing muscle tone and glandular mucus.

They act by inhibiting Ach from interacting with cholinergic M1 and M3 receptors in the airway smooth muscle that control bronchoconstriction and secondary the glands that produce mucus secretion

A

Inhaled anticholinergics

207
Q

Inhaled anticholinergics are generally well tolerated but used with caution in persons with what conditions?

A

glaucoma or prostate symptoms

208
Q

What is the most common side effects for people taking inhaled anticholinergics?

A

Dry mouth (10-14% of people)

209
Q

What type of pharmacological therapy cause bronchodilation by acting on B2 adrenergic receptors in the smooth muscle of the airways?

A

Inhaled B2-adrenergic receptor agonists

210
Q

When B2-adrenergic receptors are stimulated, there is an increase in CAMP (cyclic adenosine monophosphate), which inhibits what?

A

bronchoconstriction

211
Q

Long acting beta 2 adrenergic receptor agonists such as formoterol and salmeterol are recommended as maintenance therapies for the long term-prevention and reductions of COPD related symptoms.

True or False?

A

True

212
Q

What type of pharmacological therapy include a combination of inhaled anticholinergics or Beta 2 agonists with corticosteroids?

Note: The trade names do not provide information about what is in the inhalation

  • It is important to identify the generic name and what they are prior to administering a combination inhalation therapy
A

Combination inhalations

213
Q

What type of pharmacological therapy as monotherapy are usually not effective in COPD due to _______________ resistance caused by effects of oxidative stress in COPD lungs?

A

corticosteroid

214
Q

When are oral pharmacological methods used?

A

severe exacerbations

215
Q

What type of pharmacological therapy are used as a third line of treatment after inhaled anticholinergics or inhaled B2 agonists when treating exacerbations?

A

Methylxanthines (i.e. aminophylline & theophylline)

216
Q

What type of pharmacological therapy can also be used especially in patients with significant mucus hypersecretion?

A

Mucolytics

217
Q

All persons with COPD should maintain what type of lifestyle?

A

active lifestyle

218
Q

Pulmonary rehabilitation should not be offered, nor encouraged for those who continue to have dyspnea and exercise limitation despite optimal pharmacotherapy.

True or False?

A

False?

(Pulmonary rehabilitation should be offered and encouraged for those who continue to have dyspnea and exercise limitation despite optimal pharmacotherapy.)

219
Q

What can reduce COPD symptoms and has been shown to significantly improve dyspnea, exercise endurance and improves quality of life?

A

Pulmonary Rehabilitation

220
Q

What is the goal of pulmonary rehabilitation?

A

To restore a patient to the fullest medical, emotional, social and vocational status possible

221
Q

What are the three components of pulmonary rehabilitation?

A

Exercise training (aerobic and resistance exercises - all pts with COPD should maintain an active lifestyle), Nutritional counselling, and Patient education

222
Q

Peripheral muscle dysfunction is extensively studied, but the mechanisms for decreased exercise capacity; skeletal muscle weakness and cachexia are still what?

A

poorly understood

223
Q

Both inactivity and inflammation play a role in what?

A

peripheral muscle dysfunction

224
Q

What is the only intervention shown to slow the rate of lung function decline?

A

Smoking cessation

225
Q

Along with smoking cessation, what has been shown to reduce health resources utilization related to management of acute exacerbations?

A

Self-management programs

226
Q

Effective inhaler technique is not very important in very severe cases, as long as the medication is taken.

True or False?

A

False

Effective inhaler technique is important as it ensures adequate drug delivery

227
Q

Early recognition and treatment of acute exacerbations is important because it avoids what?

A

severe exacerbations

228
Q

Nutritional counseling can part of pulmonary rehabilitation.

True or False?

A

True

229
Q

There is no cure for COPD, so when appropriate what should be discussed?

A

end of life care

230
Q

There is no cure for COPD, so when appropriate what should be discussed?

A

end of life care

231
Q

What is the main cause of AECOPD?

A

Infection

232
Q

Tutorial

COPD is best defined as:

a) An inflammatory airway disease characterized by eosinophilic infiltration and smooth muscle hyperplasia
b) A respiratory disorder largely caused by allergies, resulting in episodic airway flow limitation
c) A group of disorders characterized by airway flow limitation
d) An obstructive airway disease characterized by declining Total Lung Capacity (TLC)

A

C

233
Q

Tutorial

What is emphysema typically known as? Pink Puffer or Blue Bloater?

A

Pink Puffer

234
Q

Tutorial

What is Chronic Bronchitis typically known as? Pink Puffer or Blue Bloater?

A

Blue Bloater

235
Q

Tutorial

Which feature is common to both Asthma and COPD?

a) History of respiratory infections
b) History of smoking (active)
c) Reversible airway flow limitation
d) Neutrophilic inflammation
e) Disease manifests earlier in life

A

a

236
Q

Tutorial

How does Cor Pulmonale occur?? Put it In order:

A . Dilation and/or hypertrophy of right ventricle causing right sided heart failure due to problem with the lungs

B . Chronic Bronchitis

C . Why was the RV failing?

  • Resistance to flow to the lungs due to low oxygen. If alveoli is not well ventilated, it contracts and sends the blood somewhere else.
  • A person with COPD can’t send the blood anywhere so blood backs up, causing pulmonary hypertension
A

B, A, C

237
Q

Tutorial

If a patient develops emphysema earlier in life (30 to 40 years of age), what genetic defect is usually the cause?

a) Leukocyte chemotaxic factor
b) Alpha-1 antitrypsin
c) Matrix metalloproteinase
d) Fibroblast growth factor

A

B

238
Q

Tutorial

What does a loss of alpha-1 antitrypsin results in imbalance between?

A

protease (elastase) and anti-protease

239
Q

Tutorial

Loss of alpha-1 antitrypsin results in imbalance between protease (elastase) and anti-protease.

What does a Damaged alveolar septa cause?

A

emphysema

240
Q

Tutorial

What is anti-protease production impaired by?

A

cigarette smoke

241
Q

Tutorial

Put the pathophysiology of emphysema in order:

A. Attraction of Inflammatory Cells
B. Destruction of elastic fibres in lung
C. Decreased alpha1-antrypsin activity (by inheritance or smoking)
D. Release of Elastase
E. Smoking
F. Emphysema
A

E, A, D, C, B, F

242
Q

Tutorial

Which of the following is an anti-inflammatory cytokine that is often reduced in COPD?

a) TNF-alpha
b) IL-1
c) C-reactive protein
d) IL-10

A

d

243
Q

Tutorial

What are two PRO-inflammatory cytokines? What innate immune cells release them?

A

TNF-alpha and IL-1 and macrophages and neutrophils

244
Q

Tutorial

What are the following cytokines examples of: interleukin (IL)-1 receptor antagonist, IL-4, IL-6, IL-10, IL-11, and IL-13.

A

Anti-inflammatory cytokines

245
Q

Tutorial

What is an acute phase protein released by the liver; it is also a marker of inflammation?

A

C-reactive protein

246
Q

Tutorial

The hyperinflation often observed in emphysema is problematic because:

a) It results in hyperventilation causing respiratory alkalosis
b) It places the respiratory muscles at a mechanical disadvantage
c) It reduces total lung capacity (TLC) resulting in hypoxemia and hypercapnia
d) It causes collapse of distal airways leading to gas trapping

A

B

247
Q

Tutorial

Breathing out against __________ ________ increases the resistance to airflow (creates back pressure) which prevents distal airways from collapsing (reduces trapping of air)

A

pursed lips

248
Q

Tutorial

True Or False (T or F)

Cigarette smoke:
o Induces airway epithelial cell inflammation with recruitment of innate immune cells
o Impairs mucocilliary function and induces mucus hypersecretion
o Is the 2nd leading cause of COPD; occupational dust/chemical exposure is 1st leading cause
o Causes mutations in the alpha-1 antitrypsin gene resulting in loss of lung elastic tissue

A

F,T,F,F

249
Q

Tutorial

What is the BEST measure to assess lung function in COPD?

a) FEV1
b) FVC
c) FEV1/FVC
d) Peak Expiratory Flow

A

C

250
Q

Tutorial

Which of the following represents a comorbidity in COPD?

a) Cachexia
b) Depression
c) Diabetes
d) Osteoporosis
e) All of the above

A

E

251
Q

Tutorial

Which intervention should be employed first when treating a patient suffering from an AECOPD?

a) Begin O2 therapy and continuous O2 saturation monitoring
b) Administer intravenous antibiotics and anticholinergics STAT
c) Knock down inflammation with oral corticosteroid mono-Th
d) Initiate or increase bronchodilator therapy
e) Utilize IV methylxanthines in combination with NIPPV

A

D

252
Q

Tutorial

Which of the following is NOT a benefit observed with O2 therapy?

a) Reduction in pulmonary hypertension
b) Improvement in patient mental and emotional state
c) Increase in survival for those with severe COPD
d) Reduction in the decline of lung function associated with COPD

A

D