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Medicine > COPD, Asthma, Bronchiectasis > Flashcards

COPD, Asthma, Bronchiectasis Flashcards

1
Q

RF for COPD

A

Cigarette smoking

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2
Q

Pack years

A

Ave. no. of packs of cigarettes/day x total no. of years of smoking

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3
Q

Early onset COPD

genetic consideration

A

alpha 1 antitrypsin deficiency

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4
Q

Abnormal permanent enlargement of air spaces distal to the terminal bronchiole accompanied by destruction of walls of airways

A

Emphysema

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5
Q

Gene associated with COPD

A

HHIP Hedge hog interacting protein ch4

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6
Q

2 most important pathologic types of emphysema

A

Centriacinar emphysema

Panacinar emphysema

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7
Q

Central or proximal parts of the acini
Distal alveoli are spared

Consequence of cigarette smoking

Most common type

A

Centriacinar Centrilobular/Focal Emphysema

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8
Q

The acini are uniformly enlarged, from the level of respiratory bronchiole to the terminal blind alveoli

More common: lower lung zone

More common: a-1 antitrypsin deficiency

A

Panacinar (Panlobular) Emphysema

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9
Q

3 most common symptoms of COPD

A

Cough
Sputum production
Exertional dyspnea - increased effort to breathe, heaviness, air hunger or gasping

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10
Q

COPD PE

A 
Prolonged expiratory wheeze
Expiratory wheezing
Signs of hyperinflation: barrel chest
Use of accessory muscles
Sitting in tripod position 
Cyanosis - lack of cyanosis in emphysema
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11
Q

Significant weight loss
Bitemporal wasting
Diffuse loss of subcutaneous adipose tissue
Hoover sign

A

Advance COPD

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12
Q

Independent poor prognostic factor in COPD

A

Bitemporal muscle wasting

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13
Q

Paradoxical inward movement of the rib cage with inspiration

A

Hoover sign

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14
Q

COPD Diagnostic

A

Pulmonary function testing
shows airflow obstruction with

dec FEV1
dec FEV1/FVC ratio

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15
Q

Hallmark of COPD

A

Airflow obstruction

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16
Q

Emphysema

A

Pinf puffer

Not cyanotic

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17
Q

Blue bloater

A

Chronic bronchitis

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18
Q

Persistent cough with sputum production for:

at least 3 months in
at least 2 consecutive years

A

Chronic bronchitis

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19
Q

Increased size of bronchial mucous glands (Reid index)
Squamous metaplasia of bronchial epithelium
Bronchiolar narrowing from mucous plugging
Inflammation and fibrosis

A

Chronic bronchitis

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20
Q

Increased size of bronchial mucous glands

A

Reid index

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21
Q

Ratio of thickness of mucous gland layer to the thickness of bronchial wall

A

Reid index

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22
Q

Current definitive test for establishing presence or absence of emphysema in living subjects

A

CT scan

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23
Q

Most important intervention in chronic bronchitis

A

Smoking cessation

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24
Q

Has been demonstrated to have a significant impact on mortality rate

A

Oxygen supplementation

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25
Q

In general, used for symptomatic benefit

B2 agonists

A

Bronchodilators

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26
Q

Improves symptoms and produces acute improvement in FEV

Decreases mucous secretions

A

Anticholinergics

Ipratropium bromide

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27
Q

Pharmacotherapy Emphysema

A

Beta agonist
Oral glucocorticoids
Antibiotics

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28
Q

GOLD Criteria for Severity of Airflow Obstruction

GOLD I

A

Mild
FEV1/FVC <0.7
FEV1 >/= 80% predicted

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29
Q

GOLD II

A

Moderate (50-80)
FEV1/FVC <0.7
FEV1 >/= 50% but <80% predicted

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30
Q

GOLD III

A

Severe (30-50%)
FEV1/FVC <0.7
FEV1 >/= 30% but <50% predicted

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31
Q

GOLD IV

A

Very severe
FEV1/FVC <0.7
FEV1 <30% predicted

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32
Q

Stable COPD Tx

A

Smoking cessation (Buproprion antidepressant, nicotine replacement therapy, varenicline)

Oxygen supplementation

Long acting beta 2 agonist
the only interventions proven to influence natural history of COPD

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33
Q

Syndrome characterized by airflow obstruction that varies markedly both spontaneously and with treatment

A

Asthma

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34
Q

Acute narrowing of bronchioles due to bronchospasm which causes obstruction to airflow maximal in expiration

A

Asthma

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35
Q

Risk factors in Asthma

A

Endogenous
Environmental
Triggers

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36
Q 
Genetic predisposition
Atopy
Airway hyperresponsiveness
Gender
Ethnicity
Obesity
Early viral infections
A

Endogenous factors

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37
Q 
Indoor allergens
Outdoor allergens
Occupational sensitizers
Passive smoking
Respiratory infections
Diet
Acetaminophen (paracetamol)
A

Environmental factors

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38
Q 
Allergens
Upper respiratory tract viral infections
Exercise and hyperventilation
Cold air
Sulfur dioxide and irritant gases
Beta blockers, Aspirin
Stress
Irritants (household sprays, paint, fumes)
A

Triggers

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39
Q

Single largest risk factor of Asthma

A

Atopy 40-50%

80% asthmatics have allergic rhinitis

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40
Q

Central to the disease pathophysiology and causes airway dysfunction through

inflammatory mediators
airway wall remodelling

A

Airway inflammation

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41
Q

asthma sputum cytology

A

Curschmann spirals
Eosinophils
Charcot-leyden crystals

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42
Q

Twisted mucous plugs admixed with sloughed epithelium

Results from extrusion of mucous plugs from subepithelial mucous gland ducts or bronchioles

A

Curschmann spirals

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43
Q

Eosinophil membrane proteins in asthma

A

Charcot-leyden crystals

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44
Q

Most striking gross finding in asthma

A

Occlusion of bronchi and bronchioles by thick, tenacious mucus plugs which often shed epithelium

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45
Q

Ciliated columnar cells sloughed from the bronchial linings

A

Creola bodies

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46
Q

Cough
Wheeze
Dyspnea

Inspiratory and expiratory rhonchi

A

Asthma

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47
Q

Most common stimuli that evoke asthma exacerbations

A

Infection

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48
Q

The only stimuli that can produce constant symptoms of asthma for weeks

A

Respiratory viruses

Young children: RVS, parainfluenza
Older children and adults: Rhinovirus, influenza

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49
Q

Abnormal and irreversible dilatation of the bronchial tree proximal to the terminal bronchioles

A

Bronchiectasis

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50
Q

Causes can be infectious or noninfectious

May be focal (bronchiectatic changes in a localized area of the lung)
or
Diffused (widespread bronchiectatic changes throughout the lung)
A

Bronchiectasis

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51
Q

Most common clinical presentation of bronchiectasis

A

Persistent, productive cough with

thick, tenacious sputum

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52
Q

Bronchiectasis hallmark

A

Honeycomb lung

Cystic spaces

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53
Q

Modality of choice for diagnosis of Bronchiectasis

Displays tram tracks
Bronchial wall thickening

A

Chest computed tomography (CT)

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54
Q

Bronchiectasis Tx

A

Treatment directed at control of
active infection
improvement in secretion clearance
bronchial hygiene

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55
Q

Bacterial infection implicated in severe asthma

A

Mycoplasma

Chlamydophila

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56
Q

Hypothesis proposes that lack of infection in early childhood preserves the TH2 cell bias at birth, whereas exposure to infections and endotoxin results in a shift towards a predominant protective TH1 immune response

A

Hygiene hypothesis

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57
Q

More severe persistent asthma
Later onset of disease
Nasa polyps
Aspirin-sensitive

A

Intrinsic or Non-atopic asthma

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58
Q

Most common allergen to trigger asthma

A

Dermatophagoides species

Dust mite

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59
Q

Exercise induced asthma is triggered by

A

Hyperventilation

Increased osmolality in airway lining fluid and triggers mast cell mediator release resulting in Bronchoconstriction.

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60
Q

Typically begins after exercise has ended
Recovers spontaneously within about 30 mins
Worse in cold, dry climates than in hot, humid conditions
More common in crosscountry running in cold weather, overland skiing and ice hockey
M

A

Exercise-induced asthma

61
Q

Exercise-induced asthma is best prevented by

A

regular treatment with ICS (reduced mast cell)

prior administration if B2 agonist and antileukotriene

62
Q

Asthma occurs more frequently in obese peopel with this value of BMI

more difficult to control

63
Q

A food additive and preservative that may trigger asthma through release of sulfur dioxide gas in the stomach

A

Metabisulfite

64
Q

Physiologic abnormality of asthma

A

Airway hyperresponsiveness

65
Q

Process allergen into peptides and migrate into lymph nodes and project these allergens into T cells to program allergen-specific T cells

A

Dendritic cells

66
Q

Inflammatory cell linked to the development of airway hyperresponsiveness due to release of basic proteins and oxygen-deprived free radicals

A

Eosinophils

67
Q

Which cytokine is deficient in asthma

A

IL 10 and 12 (antiinflammatory)

Mediate allergic inflammation: IL 4,5,9,13

68
Q

Proinflammatory cytokines that amplify inflammatory response and play a role in more severe disease

A

TNF-a

IL-1B

69
Q

Lung function test that demonstrates reversibilirt of airflow limitation

A

> 12% AND 200 mL increase in FEV1 15 mins after inhaled SABA (inhaled albuterol 400ug)

Or

2-4 week trial of oral corticosteroids (Prednisone or Prednisolone 30-40mg daily)

70
Q

Confirms diurnal variation in airflow obstruction in asthma

A

PEF twice daily measurement

71
Q

Flow-volume loop of asthma show

A

Reduced peak flow

Reduced maximum expiratory flow

72
Q

Increased airway hyperresponsiveness in asthma with calculation of the provocative concentration that reduces FEV1 by 20%

A

Metacholine or histamine challenge

73
Q

Chest Xray in asthmatics

A

Normal (in severe cases, hyperinflated lung)

Blood test not helpful
Skin prick test are positive in allergic asthma

74
Q

Now being used as noninvasive test to measure eosinophilic airway inflammation

May be a test for compliance with therapy

A

Exhaled NO

75
Q

Aims of asthma therapy

A

Minimal or no chronic symptom including nocturnal
Minimal infrequent exacerbation
No emergency visits
Minimally (ideally no) use of a required B2 agonist
No limitations on acitvities including exercise
Peak expiratory flow circadian variation <20%
Near normal PEF
Minimal or no adverse effect from medication

76
Q

Drugs for asthma

A

Relievers - B2 agonist, anticholinergics, theophylline

Controllers -inhaled steroids, systemic steroids, leukotrienes, steroid sparing therapies, anti-IgE, Anti-IL5, immunotherapy

77
Q

Activate Beta 2 adrenergic receptors in airways
Inc cAMP
Smooth muscle relaxation
Inhibits mast cell

Potential problem: tolerance

A

B2 agonists

78
Q

SABA example

Duration: 3-6 hours

A

Albuterol

Terbutaline

79
Q

LABA example

Should be given with ICS therapy

A

Salmeterol
Formoterol
Indacaterol
Olodaterol

80
Q

Most common side effect of b2 agonist

A

Muscle tremor
palpitations

elderly
small fall in plasma sodium due to increasef uptake of skeletal muscle

81
Q

Urinary retention from 10 year asthma medication use is caused by

A

Ipatropium

Anticholinergic

82
Q

Prevent cholinergic nerve-induced bronchoconstriction and mucus secretion

Less effective than B2 agonist

A

Anticholinergics

83
Q

SAMA example

A

Ipratropium

84
Q

LAMA example

A

Tiotropium

Glycopyrronium

85
Q

Most common SE of anticholinergic use

In the elderly

A

Dry mouth

Urinary retention and glaucoma

86
Q

Inhibition of phosphodiesterase in airway smooth muscle cell

Inc cAMP causing smooth muscle relaxation

Anti-inflammatory effect

A

Theophylline

87
Q

Key nuclear enzyme activated by theophylline that is a critical mechanism for switching off activated inflammatory genes and may reduce steroid insensitivity in severe asthma

A

Histone deacetylase 2 (HDAC2)

88
Q

Increases blood concentration if theophylline

A 
Erythromycin 
(inhibitor) 
Cimetidine
Ciprofloxacin
Allopurinol
Zafirlukast

CHF, liver disease, pneumonia
Viral infection, vaccination
High carbohydrate diet
Old age

89
Q

Increases clearance of theophylline

A

Inducers
Rifampicin
Phenobarbitone
Ethanol

High protein, low carbohydrate diet
Barbecued meat
Childhood

90
Q

Most effective anti-inflammatory agent used in asthma therapy

Reduce eosinophils in the airways and sputum and activated T cells and mast cells in airway mucosa

First line therapy for patients with persistent asthma

A

Inhaled corticosteroids

91
Q

Inhaled corticosteroid SE

A

Hoarseness

Oral candidiasis

92
Q

Block cys-LT1 receptors by mast cells thereby causing bronchorelaxation

Modest clinical benefit in asthma

Given once or twice daily orally

A

Montelukast
Zafirlukast
Leukotriene inhibitors

93
Q

Inhibit mast cell and sensory nerve activation
Effective in blocking trigger-Induced asthma such as EIA and allergen and sulfur dioxide-induced symptoms

Little benefit in long term control due to short duration of action

A

Cromones
Cromolyn sodium
Nedocromil sodium

94
Q

Antibody that neutralized circulating IgE without binding to cell-bound IgE

Reduce the number of exacerbations in severe asthma

Very expensive

Only suitable for highly selected patients who are not controlled on maximal doses of inhaler therapy

A

Omalizumab

95
Q

Reduce blood and tissue eosinophils and reduce exacerbations in patients with persistently increased sputum eosinophils despite maximal ICS therapy

96
Q 
Daytime symptoms: None or = 2/week 
No limitation in activity
No nocturnal symptom/awakening
No or =2/week need for reliever/rescue treatment
Normal lung function (PEF or FEV1)
A

Controlled

97
Q

Daytime symptoms >2/week
Any limitation of activities
Any nocturnal symptom/awakening
Need for reliever/rescue treatment >2/week
Lung function (PEF1 or FEV1) <80% predicted or personal best if known

A

Partly controlled

98
Q

> /= 3

Daytime symptoms >2/week
Any limitation of activities
Any nocturnal symptom/awakening
Need for reliever/rescue treatment >2/week
Lung function (PEF or FEV1)
A

Uncontrolled

99
Q

ABG picture consistent with impending respiratory failure

A

ph 7.4, pCO2 40, PaO2 80, HCO3 35

Hpoxemia and PCO2 usually low due to hyperventilation

But a normal or rising PCO2 is an INDICATION OF IMPENDING RESPIRATORY FAILURE and requires immediate monitoring and therapy.

100
Q

Laboratory test to confirm compliance to asthma therapy

A

Fractional NO may identify adherence to ICS

101
Q

Type of asthma that presents with chaotic variations in lung function despite appropriate therapy and may have precipitous, unpredictable falls in lung function which may result in death

Generally normal of near-normal lung function but precipitous, unpredictable falls may result in death

Difficult to manage

A

Type 2 brittle asthma

102
Q

Chaotic variations in lung function despite taking appropriate therapy. Persistent pattern of variability and may require OCS or at times, continuous infusion of B2 agonist

A

Type I Brittle asthma

103
Q

Brittle asthma Tx

A

Subcutaneous Epinephrine

localized airway anaphylactic reaction with edema

104
Q

1/3 improve during the course of pregnancy
1/3 deteriorate
1/3 remain unchanged

Drugs that are safe and without teratogenic potential

A

Asthma and pregnancy

105
Q

Drugs that are safe and without teratogenic potential in pregnants with asthma

A

SABA, ICS and theophylline

Prednisone&raquo_space; Prednisolone

106
Q

Mosy common form of bronchiectasis

A

Cylindrical/tubular

Varicose/cystic

107
Q

Bronchiectatic changes in a localized area of the lung and can be consequence of obstruction of the airway - either extrinsic (lymphadenopathy, parenchymal tumor) or intrinsic (airway tumor, aspirated body, stenotic airway)

A

Focal bronchiectasis

108
Q

Widespread bronchiectatic changes throughout the lung and often rises from an underlying systemic or infectious disease process

A

Diffuse bronchiectasis

109
Q

Upper lung field bronchiectasis may be due to

More common

A

Cystic fibrosis

Post radiation fibrosis

110
Q

Lower lung field bronchiectasis may come from

A

Chronic recurrent aspiration
End-stage fibrotic lung disease
Recurrent immunodeficiency association

111
Q

Causes bronchiectasis in midlung fields

A

Mycobacterium avium intracellulare complex

Dyskinetic/immotile cilia syndrome (Kartegener)

112
Q

Bronchiectasis of central aways is due to

A

Allergic bronchopulmonary aspergillosis
Tracheobronchomegaly
(Mounier-Kuhn Syndrome and Williams-Campbell syndrome)

113
Q

Most widely cited mechanism of infectious bronchiectasis that states that susceptibility to infection and poor mucociliary clearance result in microbial colonization of the bronchial tree

A

Vicious cycle hypothesis

114
Q

Dilated airways arising from parenchymal distortion as a result of lung fibrosis (eg. postradiation fibrosis or idiopathic pulmonary fibrosis)

A

Traction bronchiectasis

115
Q

Crackles and wheezing
Clubbing of digits
PFT: mild to moderate airflow obstruction

Acute exacerbation: Changes in the nature of sputum production with increased volume and purulence

A

Bronchiectasis

116
Q

Bronchiectasis Xray reveal

A

Tram tracks indicating dilated airways

117
Q

Cross sectional area of the airway with a diameter of at least 1.5 times that of the adjacent vessel in CT

Bronchiectasis

A

Signet ring sign

118
Q

Inspissated secretions on CT of a bronchiectatic lung

A

Tree-in-bud appearance

Cyst eminating in a bronchial wall in cystic bronchiectasis

119
Q

Diagnosis of a true non-tuberculous mycobacterial infection in a patient with bronchiectasis is seen in

A

One bronchioalveolar lavage sample positive on culture

Diagnostic criteria for true clinical infection with NTM should be considered in patients with symptoms and radiographic findings of lung disease who have at least 2 sputum samples positive on culture.

At least one BAL fluid sample postive on culture

A biopsy sample displaying histopathologic features of NTM infection (granuloma, positive stain for acid-fast bacilli) along with one positive sputum culture

Pleural fluid sample (or a sample from another sterike extrapulmonary site) positive

120
Q

Most common nontuberculous mycobacterial pathogens implicated in bronchiectasis

A

M avium-intracellulare

Tx:
HIV negative - Macrolide + Rifamin + Ethambutol
Check macrolide susceptibility testing

121
Q

Bronchiectasis Tx

A

Antibiotic treatment
Bronchial hygiene (Pulmonary rehabilitation)
Anti-inflammatory therapy (OCS/systemic steroids)
Surgical interventions for refractory cases

122
Q

Prevention of bronchiectasis

A

Reversal of an underlying immunodeficient state - IVIg

Vaccination -influenza, pneumococcal

Smoking cessation

123
Q

Complications of bronchiectasis

A

Microbial resistance to antibiotics
Injury to superficial mucosal vessels with bleeding -> life threatening hemoptysis

Endotracheal intubation
Identification of source of bleeding
Control of bleeding - bronchial artery embolization, surgery

124
Q

Decline rate of FEV1 among patients with non-CF bronchiectasis

A

50-55 ml per year

125
Q

Worse outcomes in bronchiectasis are associated with this infection

A

P aeruginosa colonization

126
Q

Disease state characterized by persistent respiratory symptoms and airflow limitation that is not fully reversible

127
Q

Noxious environmental exposures by spirometry in setting of noxious exposure eg cigarette smoking

Chronic airflow obstruction

128
Q

Subset of COPD

A

Emphysema
Chronic bronchitis
Small airway disease

129
Q

A condition characterized by destruction of the lung alveoli with airspace enlargement

130
Q

A clinically defined condition with chronic cough and phlegm

A

Chronic bronchitis

131
Q

Condition in which small bronchioles are narrowed and reduced in number

A

Small airway disease

132
Q

Hallmark of advanced COPD

A

Extensive small airway destruction

Small airways may be narrowed by cells (hyperplasia and accumulation), mucus, and fibrosis

133
Q

The elastase:antielastase hypothesis was based on the clinical observation that patients with genetic deficiency of this substance were at increased risk of emphysema

A

a-1 anti trypsin

Elastase > Anti-elastase (a1 antitrypsin)

134
Q

Major site of increased resistance in most individuals with COPD

A

Small airways <2mm diameter

135
Q

Associated with significant airway inflammation and with centrilobular emphysema

Along the pleural margins with relative sparing of the lung core or central regions

A

Paraseptal emphysema

136
Q

Lung hyperinflation among patients with COPD indicate

A

Increase in lung volume (inc RV, inc RV/TLC)
Increase in elastic recoil pressure (inc TLC)
Decrease airway resistance

137
Q

Hypoxemia in COPD is caused by

A

ventilation-perfusion mismatch

reflects heterogenous nature of disease process
multiple parenchymal regions with different v/q
Dec PO2
Shunting at minimal rate

138
Q

Most highly significant predictor of FEV1 among COPD patients

A

Pack-years of cigarette smoking

But only 15% of the variability in FEV1 is explained by pack-years

139
Q

70/Male
Ex smoker

FEV1/FVC <0.7
FEV >80% predicted

GOLD Criteria?

A

GOLD stage I

140
Q

Only 3 interventions demonstrated to improve survivals of patients with COPD

A

Smoking cessation
Oxygen therapy
Lung volume reduction surgery

141
Q

Only pharmacologic therapy demonstrated to unequivocally decrease mortality rates in patients with COPD

A

Supplemental O2

142
Q

Patient with resting hypoxemia

A

Resting O2 saturation =88% in any patient

= 89% with signs of pulmonary hypertension or right heart failure

143
Q

Type of infection most associated with COPD exacerbation

A

Bacterial

Hib

144
Q

Antibiotic that has demonstrated a reduced exacerbation of frequency and longer time to first exacerbation

A

Azithromycin

145
Q

COPD patients most likely to benefit from lung volume reduction surgery

A

Those with upper lobe-predominant emphysema and a low post-rehabilitation exercise capacity

Most emphysematous portion of lung

146
Q

Reduce the length of hospital stay, hasten recovery, and reduce the chance of subsequent exacerbation or relapse among admitted COPD patients

A

Systemic corticosteroids

147
Q

70/F
Known smoker, COPD
Dyspnea at rest
Productive cough with yellowish sputum

What makes her unfit for noninvasive positive pressure ventilation

a able to expectorate secretion
b being obtunded
c able to cooperate
d normotensive SBP 120 mmHg

A

Being obtunded

148
Q

Contraindications for Non invasive Positive-Pressure Ventilation (NIPPV)

A

Cardiovascular instability
Impaired mental status
Inability to cooperate
Copious secretions or inability to clear secretions
Craniofacial abnormalities or trauma precluding effective fitting of mask
Extreme obesity
Significant burns

149
Q

Indications for Invasive Mechanical Ventilation

A 
Severe respiratory distress despite therapy
Life-threatening hypoxemia
Severe hypercarbia and/or acidosis
Markedly impaired mental status
Respiratory arrest
Hemodynamic instability

Medicine (29 decks)

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