286 - Chronic Obstructive pulmonary disease

Harrisons chapter 286 - Chronic Obstructive pulmonary disease
Study online at https://quizlet.com/_7udb43
1. What is chronic It is defined as a disease state characterized by persistent

obstructive pul- respiratory symptoms and airflow limitation that is not fully
monary disease reversible.
2. COPD includes Emphysema = anatomically defined condition character-

three diseases ized by destruction of the lung alveoli with air space
what are they enlargement
Chronic bronchitis = clinically defined condition with

chronic cough and phlegm
3. What is the Cigarette smoking

most common-
ly noxious envi-
ronmental expo-
sure that causes
COPD
4. COPD hold what Third leading cause of death

place as the lead-
ing cause of
death and affects
>10 million per-
sons in the Unit-
ed States
5. Statement Airflow limitation is a major physiologic change involved

in COPD and can result from small airway disease and or
emphysema.
So chronic bronchitis cannot cause airflow limitation?
6. What is con- Small airways may become narrowed by cells (hyperpla-

sidered a hall- sia and accumulation), mucus, and fibrosis, and extensive
mark of ad- small airway destruction which as been demonstrated to
vanced COPD be a hallmark of advanced COPD
7. What are the (1) Chronic exposure to cigarette smoke in genetically

four interrelated susceptible individuals triggers inflammatory and immune
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events that lead cell recruitment within large and small airways and in the
to emphysema terminal air spaces of the lung.
(the pathogene-
sis)
(2) Inflammatory cells release proteinases that damage
the extracellular matrix supporting airways, vasculature,
and gas exchange surfaces of the lung.
(3) Structural cell death occurs through oxidant-induced

damage, cellular senescence, and proteolytic loss of
cellular-matrix attachments leading to extensive loss of
smaller airways, vascular pruning, and alveolar destruc-
tion.
(4) Disordered repair of elastin and other extracellular

matrix components contributes to air space enlargement
and emphysema.
8. What protein is Elastin, which is the principal component of elastic fibers,

critical to the is a highly stable component of the ECM that is critical to
integrity of the the integrity of the lung.
lung
9. What is the elas- It was based on the observation that patients with genetic
tase : antielas- deficiency in ± 1antitrypsin (±1AT), the inhibitor of the serine
tase hypothesis proteinase neutrophil elastase, were at increased risk of
of emphysema emphysema, and that instillation of elastases, including
neutrophil elastase, into experimental animals, results in
emphysema.
10. What transcrip- NRF2 = major regulator of oxidant and antioxidant bal-
tion factor is ance
a major reg-
ulator of OXI- SOD3 = potent antioxidant
DANt and antiOX-
IDANT balance
2 / 25
What transcrip-
tion factor is
a potent antioxi-
dant
11. Is interleukin It is a pro inflammatory cytokines

a pro-inflamma-
tory or anti-in-
flammatory cy-
tokine
12. Statement Upon exposure to oxidants from cigarette smoke, lung

macrophages and epithelial cells become activated, pro-
ducing proteinases and chemokines that attract other
inflammatory and immune cells.
Oxidative stress is a key component of COPD pathobiol-

ogy; the transcription factor NRF2, a major regulator of
oxidant-antioxidant balance, and SOD3, a potent antioxi-
dant, have been implicated in emphysema pathogenesis
by animal models.
Mitochondrial dysfunction in COPD may worsen oxidative

stress. One mechanism of macrophage activation occurs
via oxidant-induced inactivation of histone deacetylase-2
(HDAC2), shifting the balance toward acetylated or loose
chromatin, exposing nuclear factor-kappaB sites, and re-
sulting in transcription of matrix metalloproteinases and
proinflammatory cytokines such as interleukin 8 (IL-8)
and tumor necrosis factor ±TNF-±);
( this leads to neutrophil
recruitment.
CD8+ T cells are also recruited in response to cigarette

smoke and release interferon-inducible protein-10 (IP-10,
CXCL-7), which in turn leads to macrophage production
of macrophage elastase (matrix metalloproteinase-12
[MMP-12]).
13.
3 / 25
What are thought Elastin degradation and disordered repair
to be prima-
ry mechanisms
in the develope- Matrix metalloproteinases and serine proteinases, most
ment of emphy- notably neutrophil elastase, work together by degrad-
sema ing the inhibitor of the other, leading to lung destruc-
tion. Proteolytic cleavage products of elastin serve as
a macrophage chemokine, and proline-glycine-proline
(generated by proteolytic cleavage of collagen) is a neu-
trophil chemokinefueling this destructive positive feed-
back loop.
14. What factors Cigarette smoke induced loss of cilia in the airway epithe-
caused by lium and impaired macrophage phagocytosis predispose
smoke will lead to bacterial infection with neutrophilia
the patient to
a predisposition
to bacterial in-
fection with neu-
trophils
15. Statement In end-stage lung disease, long after smoking cessation,

there remains an exuberant inflammatory response, sug-
gesting that cigarette smoke-induced inflammation both
initiates the disease and, in susceptible individuals, es-
tablishes a chronic process that can continue disease
progression even after smoking cessation
16. What are the 1. Excessive ceramide production

different mecha-
nisms on how 2. RTP801 inhibition of mammalian target or rapamycin
cigarette smoke (MTOR)
oxidant mediat-
ed structural cell These two lead to cell death as well as inflammation and
death occurs proteOlysis
Involvement of mTOR and other senescence markers led

to the concept that emphysema resembles premature
aging of hte lung .
4 / 25
17. Does cigarette Cigartte smoking will IMPAIR the macrophage uptake of
smoking im- apoptotic cells therefore limiting repair
pair or enhance
macrophage up- This is because uptake of apoptotic cells by macrophages
take of apoptotic normally results in production of growth factors and
cells dampens inflammation which promote lung repair
18. Cigarette smoker The large airways, small airways d2 mm diameter, and
affect what part alveoli
of the lungs
19. What causes Changes in LARGE airways = cough and sputum produc-
cough and spu- tion
tum production?
Changes in small airways and alveoli = responsible for
What are respon- physiologic alterations
sible for changes
in the physiolog- Airway inflammation , destruction and the developement
ic alterations of emphysema are present in most persons with COPD
20. The early stages Primarily associated with medium and small airway dis-
of COPD appear ease with the majority of GOLD 1 and GOLD2 subjects
to be caused by demonstrating little or NO emphysema
what part of the
lung
21. What drives the It is driven by small airway disease

early develope-
ment of chronic
air flow obstruc-
tion
22. What are the typ- Extensive emphysema, although there are a small num-
ical characteris- ber of subjects with very severe (GOLD 4) obstruction
tics of GOLD 3 with virtually no emphysema
and GOLD 4 pa-
tients
23. What imaging Chest CT

modality can you
5 / 25
find emphysema
in
24. The subjects at Aggressive airway disease and emphysema

greatest risk of
progression in Thus finding of emphysema (by chest CT) either early or
COPD are those late in the disease process suggests enhanced risk for
subjects with disease progression
what findings
25. In the large air- Smooth muscle hypertrophy and bronchial hyperreactivity
ways what leads leads to airflow limitation
to airflow limita-
tion Cigarette smoking often results in mucus gland enlarge-
ment and goblet cell hyperplasia leading to cough and
mucus production that define chronic bronchitis, but these
abnormalities are not related to airflow limitation
26. What type of Squamous metaplasia which predisposes to carcinogen-

metaplasia oc- esis and disrupts the mucociliary clearance
curs in the
bronchi of ciga-
rette smokers
27. What has been Neutrophil elastase.

identified as one
of the most Neutrophil influx has been associated with purulent spu-
potent secreta- tum during respiratory tract infections
gogue in a pa-
tient with COPD
28.
29. Where is the Airways d2 in diameter

major site of
increased resis-
tance in most
individuals with
COPD
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30. What cells are The surfactant secreting CLUB cells are replaced with
replaced in the GOBLET CELL METAPLASIA
small airways
31. What causes Respiratory bronchiolitis with mononuclear inflammatory

proteolytic de- cells collecting in the distal airway tissue
struction of elas-
tic fibers in
the repspiratory
bronchioles and
alveolar ducts
32. Statement Narrowing and DROP out of small airways PRECEDE

(Comes before) the onset of emphysema thus destruc-
tion.
Smooth muscle hypertrophy may be present as well as

luminal narrowing can occur by fibrosis, excess mucus,
edema or cellular infiltration
33. Advanced COPD Loss of many of the smaller airways and a similar signifi-
has been asso- cant loss of the lung microvasculature
ciated with what
findings
34. What is emphy- It is characterized by destruction of gas exchanging air

sema spaces (the respiraotry bronchioles, alveolar ducts and
alveoli)
35. What cells ac- Large number of macrophages roughly 5x as many as

cumulate in the macrophages from non smokers.
respiraotry bron-
chiles of essen- Neutrophils and T lymphocytes (CD8+ cells) are also
tially all smokers increased in the alveolar space of smokers.
36. What are the 1. Cetrilobular

three distinct 2. Panlobular
pathologic types 3. Paraseptal
of emphysema
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37. What is the most Centrilobular emphysema is the most frequently type
frequent patho-
logic type of em- It is characterized by enlarged air spaces found initially in
physema associ- association with respiraotry bronchioles.
ated with cig-
arette smoking Usually is most prominent in the upper lobes and superior
and what is its segments of lower lobes and is quite focal
characterisation
38. What is panlobu- Refers to abnormally large air spaces evenly distributed
lar emphysema within and across acinar units.
39. What deficiency a1AT deficiency which has a predilection for the LOWER
is commonly ob- lobes
served in pa-
tients with pan-
lobular emphy-
sema
40. What is parasep- Occurs in 10-15% of cases and is distributed along the
tal emphysema pleural margins with relative SPARING of the lung core
or central regions
Commonly associated with significant airway inflamma-

tion and with centrilobular emphysema
41. Wjhat is that is Persistent reduction in forced expiratory flow rates

the most typi-
cal finding in pa-
tients with COPD
42. What is the Key parameters obtained from spirometry include the
FEV1/ FVC ratio volume of air exhaled within the first second of the forced
expiratory maneuver (FEV1 ) and the total volume of air
exhaled during the entire spirometric maneuver (forced
vital capacity [FVC])
43. Patients with Patients with airflow obstruction related to COPD have a
COPD have a chronically reduced ratio of FEV1 /FVC.
reduced or in-
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creased ratio of
FEV1/FVC
44. How do you dif- in contrast to asthma, the reduced FEV 1in COPD sel-
ferentiate the air- dom shows large responses to inhaled bronchodilators,
flow obstruction although improvements up to 15% are common.
in asthma vs
COPD
45. Is there hyperin- There is hyperinflation because of "air trapping" and pro-
flation or hypoin- gressive hyperinflation (increased total lung capacity) in
flation in patients the disease.
with COPD
46. What is hyperin- It preserves maximum EXPIRATORY airflow because as

flations effect on the lung volume increases, elastic recoil pressure in-
tidal breathing creases and airways enlarge so that airway resistance
decreases
47. What happens to Push the diaphragm into a flattened position

the diaphragm in
a patient with hy-
perinflation
48. What are the First, by DECREASING the zone of apposition between
adverse effects the diaphragm and the abdominal wall, positive abdomi-
of a flatted di- nal pressure during inspiration is not applied as effectively
aphragm to the chest wall, hindering rib cage movement and im-
pairing inspiration.
Second, because the muscle fibers of the flattened di-

aphragm are shorter than those of a more normally
curved diaphragm, they are less capable of generating
inspiratory pressures than normal.
Third, the flattened diaphragm must generate greater ten-

sion to develop the transpulmonary pressure required to
produce tidal breathing.
Fourth, the thoracic cage is distended beyond its normal

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resting volume and during tidal breathing the inspiratory
muscles must do work to overcome the resistance of the
thoracic cage to further inflation instead of gaining the
normal assistance from the chest wall recoiling outward
toward its resting volume.
49. The partial pres- Around 50% of predicated and even much lower FEV1
sure of oxy- values can be associated with a normal PAo2 at least at
gen in arteri- rest ...
al blood PAO2
usually remains
near normal un-
til the FEV1 is de-
creased to how
much
50. At what FEV1 ra- Until FEV1 is <25% of predicted

tio is an elevation
of arterial level of So around 50% = PAo2 change
CARBON dioxide <25% = increased in CO2
expected
51. statement Pulmonary hypertension severe enough to cause cor pul-

monale and right ventricular failure due to COPD typically
occurs in individuals who have marked decreases in FEV
1 (<25% of predicted) and chronic hypoxemia (Pao <55
mmHg);
52. What is the Ventilation perfusion mismatching accounts for essential-

cause of the re- ly all the reduction in PAo2
duction in PAo2
that occurs in Shunting is only minimal
COPD
This explains the effectiveness of modest elevation of
inspired oxygen in treating hypoxemia due to COPD and
therefore the need to consider problems other than COPD
when hypoxemia is d cult to correct with modest levels of
supplemental oxygen.
53. Male gender due to them smoking more

10 / 25
What gender has
a higher preva-
lence of COPD
54. What is the Pack years of cigarette smoking

most highly sig-
nificant predictor But only 15% of variability in FEV1 is explained by pack
of FEV1 years
This finding suggests that additional environmental or

genetic factors contribute to the impact of smoking on the
development of chronic airflow obstruction
55. Is the airway It is hyper responsive

of patients with
COPD hyper re- There is a tendency for increased bronchoconstriction
sponsive or hy- in response to a variety of exogenous stimuli including
poresponsive methacoline and histamine
This is also one of the defining features of asthma and

COPD as well
56. Is there sig- No it is not typically seen in an individual after an acute

nificant long episode of bronchitis or pneumonia
term reductions
in pulmonary However respiraotry infections are important causes of
function follow- COPD exacerbations
ing an individ-
ual episode of
acute bronchitis
or pneumonia
57. Increased respi- Coal mining, gold mining, and cotton textile dust.
ratory symptoms
and airflow ob-
struction have
been suggested
to result from ex-
posure to dust
and fumes at
11 / 25
work. What oc-
cupations have
been implicated
as risk factors
for chronic air-
flow obstruction
58. Statement Among coal miners, coal mine dust exposure was a sig-
nificant risk factor for emphysema in both smokers and
non smokers
59. There are in- Urban

creased respi-
raotry symptoms
in those living in
urban or rural ar-
eas
60. What genetic A1AT deficiency

risk factor pre-
disposes a pa-
tient to de-
veloping airflow
obstruction in
smokers
61. What allele is M allele = normal ±1 AT levels

associated with
normal, slight- S allele = slightly reduced ±1 AT levels
ly reduced and
markedly re- Z allele = markedly reduced ±1 AT levels
duced ±1AT levels
Null allele = absence of ±1 AT
62. What is the most PiZ is the most common form of severe a1AT deficiency
common form of
severe ±1
AT defi- Individuals with two Z alleles or one Z and one null allele
ciency get PiZ
63. Approximately 1%
12 / 25
What % of pa-
tients with COPD
are found to have
severe a1AT defi-
ciency as a con-
tributing cause
of COPD
64. What laborato- measurement of the immunologic level of ± 1AT in serum

ry test is used
most frequently
to screen for
a1AT deficiency
65. What is the treat- Specific treatment in the form of ± 1AT augmentation
ment for a1AT de- therapy is available for severe ± 1AT deficiency as a weekly
ficiency IV infusion
66. Statement Cigarette smokers with severe a1AT deficiency are more
likely to develop COPD at early ages.
67. Effects of ciga- 1. Intensity of smoking exposure

rette smoking on
pulmonary func- 2. Timing of smoking exposure during growth
tion appear to
depend on what 3. Baseline lung function of the individual
factors
68. In an individ- Individuals follow a steady trajectory of increasing pul-

uals life when monary function with growth during childhood and adoles-
does his pul- cence followed by a plateau in early adulthood and then
monary function gradual decline with aging
grow and decline
69. Statement Death or disability from COPD can result from a normal
rate of decline after a reduced growth phase , an early ini-
tiation of pulmonary function decline after normal growth
, or an accelerated decline after normal growth
13 / 25
Subjects had reduced growth but normal rates of lung
function decline. (So basically reduced growth)
70. FEV1 annual loss Absolute annual loss in FEV1 tends to be highest in mild
tends to be high- COPD and lowest in very severe COPD
est in mild or se-
vere COPD?
71. What are the 1. Cough

three most com-
mon symptoms 2. Sputum production
in COPD
3. Exertional dyspnea
72. What type of ac- Difficult = involving significant arm work , particularly at or
tivities are dif- above shoulder level
ficult and what
type of activities Better tolerated = activities that allow the patient to brace
are better toler- the arms and use accessory muscles of respiration are
ated in patients better tolerated
with COPD
73. As COPD ad- Worsening dyspnea on exertion with increasing intrusion

vances what is on the ability to perform vocational or avocational activi-
the principal fea- ties
ture
74. in the physical Prolonged expiratory phase and may include expiratory
examination of wheezing.
the lungs for pa-
tients that are Signs of hyperinflation include a barrel chest and en-
smokers what larged lung volumes with poor diaphragmatic excursion
can be seen as assessed by percussion
75. What position do They use the characteristic "tripod" position and it is used
the patients with to facilitate the actions of the sternocleidomastoid, sca-
severe airflow lene, and intercostal muscles .
obstruction use
and why do they
use this
14 / 25
76. Differentiate pink Pink puffers = emphysema , thin and noncyanotic at rest
puffers from blue and have prominent use of accessory muscles
bloaters
Blue bloaters = chronic bronchitis , lively to be heavy and
cyanosis
77. What is the The paradoxical inward movement of the rib cage with
Hoovers sign inspiration
78. Is clubbing of the No it is not a sign of COPD and it should alert the clinician
digits a sign of to investigate reasons for the clubbing
COPD
79. In this popula- Lung cancer

tion what is the
most likely expla-
nation for newly
developed club-
bing of the nails
80. What is the hall- Airflow obstruction

mark of COPD
81. What is reduced The diffusing capacity is reduced , reflecting the lung
in patients with parenchyma destruction characteristic of the disease
emphysema
82. Arterial blood Acutely = 0.08 units / 10mmHG acutely

gases and
oximetry may Chronic state = 0.03 units / 10mmHG in the chronic state
demonstrate
resting or
exertional
hypoxemia.
Arterial blood
gases provide
additional
information
about alveolar
15 / 25
ventilation and
acid-base status
by measuring
arterial Pco and
pH. The change
in pH with PCO2
is how much
acutely and
chronicle
83. Knowledge of ar- Ventilatory failure, defined as PCO2 > 45mmHG into
terial pH allows acute or chronic conditions
the classification
of of ventilatory
failure defined as
what
84. What is as- Acute respiratory failure = acidemia

sociated with
acidemia? Acute
or chronic respi-
ratory failure
85. What findings Elevated hematocrit as well as right ventricular hypertro-

suggests the phy
presence of
chronic hypox-
emia
86. On X-ray what Obvious Bullae, paucity of parenchymal markings, hyper-

findings sug- lucency on chest X-ray
gests emphyse-
ma
87. What is the CT scan

current definitive
test for estab- Also enables discovery of coexisting interstitial lung dis-
lishing the pres- ease and bronchiectasis which are common complica-
ence of emphy- tions in COPD
sema, pattern of
16 / 25
emphysema and
presence of sig-
nificant disease
involving medi-
um and large air-
ways
88. What are the two Provide symptomatic relief and reduce future risk
main goals fo
therapy in pa-
tients with COPD
89. What are the 1. Smoking cessation

three known in-
terventions that 2. Oxygen therapy in chronically hypoxemic patients
have been
demonstrated to 3. Lung volume reduction surgery
improve survival
in patients with
COPD There is suggestive, but not definitive, evidence that the
use of inhaled corticosteroids (ICS) and muscarinic an-
tagonists may reduce the mortality rate.
90. Statement Current recommendations from the U.S. Surgeon General

are that all adult, nonpregnant smokers considering quit-
ting be offered pharmacotherapy, in the absence of any
contraindication to treatment.
91.
92.
93. What are the pri- Bronchodilators

mary treatment
for almost all pa-
tients with COPD
and are used
for symptomatic
benefit and to
17 / 25
reduce exacerba-
tions
94. Are bronchodila- Inhaled route is preferred for medication delivery because
tors proffered as side effects are LESS than with systemic medication de-
inhaled or IV livery
95. Differentiate Short acting ipratropium bromide improves symptoms

short acting with acute improvements in FEV1
from long acting
muscarinic Long acting muscarinic antagonists improve symptoms
antagonists and reduce exacerbations
96. What is the most Dry mouth (antimuscarinic antagonists)

frequent side ef-
fect of anti-
cholinergic mus-
carinic antago-
nists
97. What is the main Tremor and tachycardia

side effect of
beta agonists
Long-acting agents (LABA) provide symptomatic benefit
and reduce exacerbations, though to a lesser extent than
a LAMA
98. What is the main Reduce exacerbations

role of corticos-
teroids in the
management of
COPD
99. Why are corti- That is because their use has been associated with in-
costeroids only creased rates of oropharyngeal candidiasis and pneumo-
used to reduce nia and in some studies increased rate of loss of bone
exacerbations density
100. The corticos- Inhaled

teroids above are
18 / 25
taken in or given
how
101. Are the use It is not recommended because of an unfavorable benefit

of glucocorti- / risk ratio.
coids recom-
mended for treat- The side effects include osteoporosis, weight gain,
ment of COPD cataracts, glucose intolerance, and increased risk of in-
fection
102. What are the ef- It produces modest improvements in airflow and vital ca-
fects of theo- pacity but is NOT FIRST LINE therapy due to side effects
phylline in pa-
tients with COPD
103. What are the side Nausea is common but tachycardia and tremors have
effects of theo- been reported.
phylline
104. Are PDE4 in- PDE4 is a selective phosphodiesterase 4 inhibitor and

hibitors given has been demonstrated to reduce exacerbation frequen-
to patients with cy in patients with severe COPD , chronic bronchitis and
COPD a prior history of exacerbations
So basically PDE4 are also given if exacerbation...
105. What is the ex- Roflumilast

ample for a PDE4
inhibitor
106. Do you give pa- Yes because exacerbations (a substantial portion of

tients with COPD which) are caused by bacterial infection
antibiotics
107. What antibiotic (Not sure)

is given for pa-
tients with COPD A randomised trial of azithromycin administered daily to
exacerbation subjects with a history of exacerbation in the past 6
months demonstrated a reduced exacerbation frequency
and longer time to first exacerbation
19 / 25
108. What is the Supplemental oxygen

only pharmaco-
logical therapy
demonstrated to
unequivocal yde-
crease mortality
rates in patients
with COPD
109. What is resting resting O 2saturation d88% in any patient or

hypoxemia
d89% with signs of pulmonary hypertension or right heart
failure),
For patients with resting hypoxemia (resting O 2 satura-

tion d88% in any patient or d89% with signs of pulmonary
hypertension or right heart failure), the use of O 2 has
been demonstrated to have a significant impact on mor-
tality
110. Prior to start- Hepatitis B vaccination prior to starting augmentation

ing IV a1AT Aug- therapy
mentation Thera-
py for patients
with this genet-
ic defect what
should be done
111. What is required It requires a serum ±1

AT level <11 ¼
M (~50 mg/dL).
to be eligible for
a1AT augmenta-
tion therapy
112. Is a1AT aug- No it is not. Only those with COPD should get it and even
mentation thera- then it is controversial
py recommend-
ed for severe-
ly a1AT de-
20 / 25
ficient persons
with normal pul-
monary function
and a normal
chest CT to pre-
vent COPD
113. What vaccines Influenza vaccine annually

are recommend- Pneumococcal vaccines and vaccination for Bordatella
ed for patients pertussis are recommended
with COPD
114. Statement Pulmonary rehabilitation is a comprehensive treatment

that incorporates exercise, education, and psychosocial
and nutritional counseling
115. What is lung vol- It is a surgery to remove the most emphysematous por-
ume reduction tions of lung , improves exercise, lung function and sur-
surgery vival
116. What type of Upper lobe predominant emphysema and a LOW post
patients benefit rehabilitation exercise capacity are most likely to benefit
most from lung
volume reduc-
tion surgery
117. What type of pa- Patients with an FEV 1 <20% of predicted and either
tients are NOT diffusely distributed emphysema on CT scan or diffusing
candidates for capacity of lung for carbon monoxide (DLCO ) <20% of
lung volume re- predicted have increased mortality after the procedure,
duction surgery and thus are not candidates for LVRS.
118. Fill in the blank 2nd leading.
COP is current-
ly the ____ lead-
ing indication for
lung transplanta-
tion
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119. Current recom- very severe airflow limitation,
mendations are
than can- severe disability despite maximal medical therapy,
didates for
lung transplanta- and be free of significant comorbid conditions such as
tion should have liver, renal, or cardiac disease.
what factors
120. What is the A history of a previous exacerbation

strongest single
predictor of ex-
acerbations The frequency of exacerbations increases as airflow ob-
struction worsens; patients with severe (FEV 1 <50%
predicted) or very severe airflow obstruction (FEV 1 <30%
predicted) on average have 1-3 episodes per year.
121. What is the major Bacterial infection / infection in general involved in >50%
cause of exac- of exacerbations
erbations in pa-
tients with COPD Viral respiratory infections are present in approximately
one third of COPD exacerbations (so out of >50 , viral is
33% )
20-35% no specific precipitant can be identified
122. What is the sin- History of previous hospitalisation

gle greatest risk
factor for hospi-
talisation with an
exacerbation
123. 25% of xrays in Be abnormal with the most frequent findings being pneu-
exacerbations of monia and congestive heart failure
COPD will show
what So this is only in 25% of patients
124. What is hyper- Defined as PCO2 > 45mmHG

carbia
Patients with advanced COPD have a history of hyper-
22 / 25
carbina, mental status changes (confusion and sleepi-
ness) or those in significant distress should have an ABG
125. Are pul- In contrast to its utility in the management of EXACERBA-

monary func- TOIN of astham
tion test need-
ed for EXACER- Measurement of pulmonary function has not been
BATION COPD demonstrated to be helpful in the diagnosis or manage-
ment of EXACERBATIONS of COPD
126. Statement Pulmonary embolus (PE) should also be considered, as

the incidence of PE is increased in COPD exacerbations.
127. What are the Bronchodilators

four things men-
tioned in the Antibiotics
book for the
treatment of Oxygen
acute exacerba-
tion Mechnical ventilatory support
128. What bron- Inaheld B- AGONISTS and

chodilators are
given to these Muscarinic ANTAGONISTS
patients with ex-
acerbations If theophylline are given it should be monitored to min-
imise toxicity
129. Bacteria fre- include Streptococcus pneumoniae,

quently implicat-
ed in COPD ex- Haemophilus influenzae, and
acerbations in-
clude what Moraxella catarrhalis.
In addition, Mycoplasma pneumoniae or Chlamydia

pneumoniae are found in 5-10% of exacerbations.
130. What is the In patients admitted to the hospital, the use of systemic
role of glucocor- glucocorticoids reduces the length of stay, hastens recov-
ticoids in pa- ery, and reduces the chance of subsequent exacerbation
23 / 25
tients with acute or relapse.
exacerbations of
COPD
Current recommendations suggest 30-40 mg of oral pred-
nisolone or its equivalent typically for a period of 5-10
days in outpatients.
131. What is the Hyperglycaemia

most frequent-
ly reported acute
complication of
glucocorticoids
132. Supplemental O2 e90%.

should be sup-
plied to main- Studies have demonstrated that in patients with both
tain oxygen satu- acute and chronic hypercarbia, the administration of sup-
ration above how plemental O 2does not reduce minute ventilation.
much %
133. What are con- Contraindications to NIPPV include cardiovascular insta-

traindications to bility, impaired mental status, inability to cooperate, copi-
noninvasive pos- ous secretions or the inability to clear secretions, cranio-
itive pressure facial abnormalities or trauma precluding effective fitting
ventilation of mask, extreme obesity, or significant burns.
The initiation of noninvasive positive-pressure ventilation

(NIPPV) in patients with respiratory failure, defined as
Paco >45 mmHg, results in a significant reduction in mor-
tality rate, need for intubation, complications of therapy,
and hospital length of stay.
134. When is in- indicated for patients with severe respiratory distress de-
vasive (conven- spite initial therapy, life-threatening hypoxemia, severe
tional) mechnical hypercarbia and/or acidosis, markedly impaired mental
ventilation indi- status, respiratory arrest, hemodynamic instability, or oth-
cated er complications
135.
24 / 25
What is the prog- The mortality rate of patients requiring mechanical ven-
nosis of patients tilatory support is 17-30% for that particular hospitaliza-
with mechanical tion.
ventilatory sup-
port For patients aged >65 admitted to the intensive care unit
for treatment, the mortality rate doubles over the next year
to 60%, regardless of whether mechanical ventilation was
required.
Following a hospitalization for COPD, about 20% of pa-

tients are re-hospitalized in the subsequent 30 days and
45% are hospitalized in the next year. Mortality following
hospital discharge is about 20% in the following year.
25 / 25

286 - Chronic Obstructive pulmonary disease

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286 - Chronic Obstructive pulmonary disease

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Harrisons chapter 286 - Chronic Obstructive pulmonary disease

Study online at https://quizlet.com/_7udb43

1. What is chronic It is defined as a disease state characterized by persistent

2. COPD includes Emphysema = anatomically defined condition character-

Chronic bronchitis = clinically defined condition with

3. What is the Cigarette smoking

4. COPD hold what Third leading cause of death

5. Statement Airflow limitation is a major physiologic change involved

So chronic bronchitis cannot cause airflow limitation?

6. What is con- Small airways may become narrowed by cells (hyperpla-

7. What are the (1) Chronic exposure to cigarette smoke in genetically

(3) Structural cell death occurs through oxidant-induced

(4) Disordered repair of elastin and other extracellular

8. What protein is Elastin, which is the principal component of elastic fibers,

11. Is interleukin It is a pro inflammatory cytokines

12. Statement Upon exposure to oxidants from cigarette smoke, lung

Oxidative stress is a key component of COPD pathobiol-

Mitochondrial dysfunction in COPD may worsen oxidative

CD8+ T cells are also recruited in response to cigarette

15. Statement In end-stage lung disease, long after smoking cessation,

16. What are the 1. Excessive ceramide production

Involvement of mTOR and other senescence markers led

21. What drives the It is driven by small airway disease

23. What imaging Chest CT

24. The subjects at Aggressive airway disease and emphysema

26. What type of Squamous metaplasia which predisposes to carcinogen-

27. What has been Neutrophil elastase.

29. Where is the Airways d2 in diameter

31. What causes Respiratory bronchiolitis with mononuclear inflammatory

32. Statement Narrowing and DROP out of small airways PRECEDE

Smooth muscle hypertrophy may be present as well as

34. What is emphy- It is characterized by destruction of gas exchanging air

35. What cells ac- Large number of macrophages roughly 5x as many as

36. What are the 1. Cetrilobular

Commonly associated with significant airway inflamma-

41. Wjhat is that is Persistent reduction in forced expiratory flow rates

46. What is hyperin- It preserves maximum EXPIRATORY airflow because as

47. What happens to Push the diaphragm into a flattened position

Second, because the muscle fibers of the flattened di-

Third, the flattened diaphragm must generate greater ten-

Fourth, the thoracic cage is distended beyond its normal

50. At what FEV1 ra- Until FEV1 is <25% of predicted

51. statement Pulmonary hypertension severe enough to cause cor pul-

52. What is the Ventilation perfusion mismatching accounts for essential-

53. Male gender due to them smoking more

54. What is the Pack years of cigarette smoking

This finding suggests that additional environmental or

55. Is the airway It is hyper responsive

This is also one of the defining features of asthma and

56. Is there sig- No it is not typically seen in an individual after an acute

59. There are in- Urban

60. What genetic A1AT deficiency

61. What allele is M allele = normal ±1 AT levels

64. What laborato- measurement of the immunologic level of ± 1AT in serum

67. Effects of ciga- 1. Intensity of smoking exposure

68. In an individ- Individuals follow a steady trajectory of increasing pul-

71. What are the 1. Cough

73. As COPD ad- Worsening dyspnea on exertion with increasing intrusion

79. In this popula- Lung cancer