Respirology Flashcards

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1
Q

Length of “Acute cough”

A

• Acute cough <3 weeks

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2
Q

Length of “chronic cough”

A

• Chronic cough >4-8 weeks

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3
Q

How long can a cough last after a viral infection?

A

Persistenceofcough after viral infection:
– 10 days: 50%
– 16 days: 25%
– 25 days: 10%

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4
Q

How often is there a choking history with aspiration?

A

Clinical choking history in ~40-85% of cases

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5
Q

How old are most kids with FBA?

A

• Majority of cases <3 years of age

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6
Q

Symptoms of FBA?

A
• Symptoms of presentation
– Cough
– Wheeze/stridor
– Dyspnea/Respiratory distress 
– Asymptomatic
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7
Q

CXR findings for FBA?

A
Radiologic findings
– Localized emphysema
– Pneumonia
– Atelectasis
– Normal

if you have a foreign body in a mainstem bronchi you can breathe air IN but it is hard to breathe out/ Hyperinflation of affected lung

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8
Q

Consequences of missed foreign body:

A

– Recurrent pneumonia
– Bronchiectasis
- Cardiac Arrest

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9
Q

Investigations if cough >4 weeks

A

CXR

PFTs

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10
Q

Differential for chronic cough

A

Healthy Children
• Frequent viral respiratory tract infections
• Postviral cough
• Pertussis/Pertussis like cough

Chronic Cough
• Cough variant Asthma
• Chronic Rhinitis
• Persistent Bronchitis
• GERD
• Psychogenic Cough
• Non-specific Isolated Chronic Cough
Potentially Serious Lung Disorder
• Cystic Fibrosis
• Immunodeficiency
• Primary Ciliary Dyskenesia
• Foreign Body Aspiration
• Recurrent Pulmonary Aspirations
• Tuberculosis
• Anatomic Disorder
• Interstitial Lung Diseases
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11
Q

What is a honking cough that disappears with sleep?

A

psychogenic cough

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12
Q

What has a Dry cough, dyspnea, restrictive spirometry

A

Interstitial Lung Disease

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13
Q

What has Progressive cough, weight loss, fevers,

A

TB, Malignancy

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14
Q

Red flag symptoms for chronic wet cough

A
Concerning features 
– Year round
– Starting at early age
– Not responsive to therapies
– Specific pointers to other illnesses
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15
Q

Chronic Wet Cough differential

A
  • Cystic Fibrosis
  • Primary Ciliary Dyskinesia
  • Immunodeficiency
  • Bronchiectasis
  • Persistent Bacterial Bronchitis
  • Missed Foreign body
  • Chronic Infections
  • Asthma+/- AllergicRhinitis
  • Recurrent Viral Infections
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16
Q

How does CF present in infancy

A
Infancy
• Failure to thrive
• Meconium ileus
• Recurrent respiratory symptoms
– Wheeze, cough, bronchiolitis
• Hyponatremic, hypochloremic metabolic alkalsosis
• Prolonged Jaundice
• Severe pneumonia
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17
Q

How does CF present in childhood/adolescence

A

• Recurrent respiratory symptoms
– Cough, pneumonia, wheeze poorly controlled asthma etc..
• Failure to thrive
• Recurrent rectal prolapse
• Clubbing
• Bronchiectasis
• Nasal polyps/sinus disease nasal polyps in children are CF until proven otherwise
• Chronic Pseudomonas aeroginosa colonization

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18
Q

Diagnosis of CF

A

Prenatal: CVS with DNA analysis/ amnio

Postnatal:
– Newborn Screening: IRT (immunoreactive trypsinogen level)

• Sweat Chloride – ≥60mEq/L
– Normal:
• <30 1st 6 months
• >40 after 6 months
• CFTR analysis may be misleading should not do without first having SCT
– >1900 associated mutations 
– >160 disease causing mutations
• Newborn Screen programs may miss up to 5% of classic CF

Diagnostic criteria —
Both of the following criteria must be met to diagnose CF:
1) Clinical symptoms consistent with CF in at least one organ system
OR
Positive newborn screen
OR
Having a sibling with CF

AND

Evidence of cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction (any of the following):
Elevated sweat chloride ≥60 mmol/L
OR
Presence of two disease-causing mutations in the CFTR gene, one from each parental allele
OR
Abnormal NPD (nasal potential difference)

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19
Q

Treatment of CF

A

• Multidisciplinary Clinic
– Nurse,Physiotherapy, Dietician, Social Worker, Psychologist
• Aggressive treatment of infections, airway secretion clearance, nutrition
• Novel therapies aimed at underlying CFTR mutations
– $$$$$

Maintain normal lung function

  • Regular chest physiotherapy
  • Treat chronic infections with oral or inhaled Abx
  • Treat acute infections with oral or IV Abx
  • Use mucolytics

Maintain normal nutrition & growth

  • High fat/high energy diet
  • Pancreatic enzymes, vitamin supplements
  • Supplements/g-tube feeds

Regular follow-up with multi-D team
Educate patient and family about CF

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20
Q

Why do we do genetic testing in CF?

A

To help with various treatment options

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21
Q

Median survival age for CF?

A

Median survival age: 50.9

– Median age of death: 34

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22
Q

Prognostic factors for CF?

A
Male > female 
– Lung disease 
• FEV1
• Burkohlderia Cepacia
• Pneumothorax
– Nutritional status*** 
• Weight/height
• Diabetes
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23
Q

Clinical Presentation of PCD?

A
Clinical
– Year round daily wet cough
– Year round nasal congestion
– Recurrent Otitis media
– Neonatal Respiratory distress
- male infertility
– Laterality defects (situs inverses totalis)
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24
Q

Diagnosis of PCD?

A

Electron Microscopy
Nasal nitric oxide
Genetic testing

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25
Q

What is protracted bacterial bronchitis?

A

• Emerging (controversial) diagnosis
– >3-4 weeks of chronic wet cough
– Resolution of cough with antibiotic treatment
– Associated with significant pus and neutrophils on bronchoscopy

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26
Q

How old are kids who get protracted bacterial bronchitis?

A

Most common in children <5 years of age

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27
Q

Most common pathogens in protracted bacterial bronchitis

A

H influenza
S. Pneumo
S. Aureus
M Catarrhalis

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28
Q

When should you consider a diagnosis of laryngeal cleft?

A
• Associated with direct aspiration on swallowing (recurrent aspirations)
• Videoflouroscopy
• Rigid bronchoscopy required to rule out
– Grade1-4
• Consider with syndromes 
– VACTRL
– CHARGE
– OpitzFrias
– MidlineDefects
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29
Q

What conditions pre dispose you to recurrent aspirations?

A

– Choking/coughing with feeds, especially liquids
– Neurologic abnormalities
– Previous intubations
– Syndromes associated with anatomic malformations (VACTRL)

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30
Q

How to diagnose a H type fistula?

A

Rigid Bronchocopy is gold standard

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31
Q

Characteristics of psychogenic cough?

A

usually do not look distressed
more often in the daytime, goes away at night
often starts with viral infection + cough —> turns into psychogenic cough can be successful to get them to drink water every time they need to cough can last years in some children

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32
Q

Treatment of Non specific chronic cough?

A

• Medium dose Inhaled corticosteroids
– Especially if positive family or atopic history, wheezing or other signs of asthma

• Intranasal corticosteroids +/- anti-histamines
– Especially if other signs and symptoms of chronic
rhinitis and/or upper airway symptoms
• Always look for red flags and give a time defined treatment trial

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33
Q

Chronic Wet cough should have what investigations?

A

Strong consideration for children with a chronic wet cough should include:

  • CXR
  • PFT with bronchodilator
  • sweat chloride

• Further investigations based on above +/- trial of treatment

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34
Q

What is asthma

A
  • paroxysmal or persistent symptoms such as dyspnea, chest tightness, wheezing, sputum production, and cough
  • associated with variable airflow limitation and airway hyperresponsiveness to endogenous and exogenous stimuli.
  • Inflammation and it’s resultant effects on airway structure are considered the main mechanisms leading to the development and persistence of asthma.
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35
Q

What are the symptoms of good asthma control?

A
Daytime Symptoms: <4 days/week
Nighttime Symptoms: <1 night/week
Physical Activity: Normal
Exacerbations: Mild, Infrequent
Absence from work/school: None
Fast acting B-agonist use: <4 doses/week*
FEV1 or PEF: ≥90% personal best
PEF diurnal variation: <10-15%
Sputum eosinophils (adults): <2-3%
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36
Q

Diagnosis of Asthma

A
Clinical symptoms
\+
Diagnosis of Asthma
• Objective evidence
– Spirometry: obstruction (↓FEV1/FVC) + bronchodilator
response (↑FEV1 by ≥12%)
– Peak Flow: increase by ≥20% following bronchodilator
– Methacholine Challenge:
• +ve: <4 mg/mL
• Borderline: 4-16 mg/mL 
• Negative: >16mg/mL
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37
Q

What ages should use an aerohamber?

A

All!!

But can switch to mouth piece at 5 years of age

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38
Q

Management pathway for asthma for kids 6-11 years of age

A
Low Dose Inhaled Corticosteroid 
Low-Medium Dose Inhaled Corticosteroid
 THEN
Medium Dose Inhaled Corticosteroids (201-400 mcg/day)
  THEN
Add a LABA  or Add a LTRA
THEN
add the other
THEN
Medium Dose Inhaled Corticosteroids + LABA + LTRA
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39
Q

Management pathway for asthma for kids >12

A

Low Dose Inhaled Corticosteroid (≤250 mcg/day)

THEN

Low Dose Inhaled Corticosteroid + LABA

THEN

Increase ICS to Medium Dose OR Add LTRA

THEN

Add the other

THEN

Low-Medium Dose Inhaled Corticosteroids + LABA + LTRA

40
Q

Low/Med/High dose for fluticasone in kids 6-11

A

Fluticasone
Low Dose: ≤200
Med Dose:201- 400
High Dose: >400

41
Q

Low/Med/High dose for fluticasone in kids >12

A

Fluticasone
Low Dose: ≤250
Med Dose: 251-500
High Dose: >500

42
Q

A clinical diagnosis of asthma in preschool children is:

A

A clinical diagnosis of asthma can be made in preschool children with a combination of:
– Documentation of airflow obstruction
– Documentation of reversibility of airflow obstruction
– No clinical evidence of alternative diagnosis

Preferred when these are done by healthcare professionals
– Convincing parental reports

43
Q

Low/Med/High dose for fluticasone in kids <5

A

Fluticasone
Low:100-125
Med: 200-250

44
Q

Management pathway for asthma is kids less than 5

A
Low Dose Inhaled Corticosteroid
THEN
Increase ICS to Medium Dose
THEN 
Medium Dose Inhaled Corticosteroid + Leukotriene Receptor Antagonist
45
Q

What is the definition of recurrent pneumonia

A

– ≥2 pneumonias in 1 year or ≥3 lifetime

• Radiologic clearing in between episodes

46
Q

Differential diagnosis for recurrent pneumonia that is always in the same location?

A
• Anatomic abnormality
– External airway compression (ie – lymphadenopathy, vascular abnormality)
– Intrinsic airway abnormality
• Congenital malformation
– CPAM
– Pulmonary sequestration
– Bronchogenic Cyst
• Foreign Body
• Right Middle Lobe syndrome
• Bronchiectasis
• Persistent Infection (ie TB)
47
Q

Differential diagnosis for recurrent pneumonia that is in different locations?

A
Multiple locations
• Immune deficiency
• Cystic Fibrosis
• Primary Ciliary Dyskinesia
• Recurrent aspirations – Anatomical
– Swallowingdisorder
– Neurologicimpairment
48
Q

Congenital Pulmonary Malformations Diagnosis?

A

Majority today are diagnosed prenatally
– All symptomatic lesions require surgical resection
• Increased risk of pneumonia
• Increased risk of malignancy

49
Q

Congenital Pulmonary Malformations Imaging?

A

CT chest WITH CONTRAST

50
Q

What are the clinical symptoms of OSA?

A
Neurocognitive
– Behavioral,attention,school
performance, development
• Cardiovascular
– Hypertension,CorPulmonale
• Failure to Thrive
• Inflammatory
• Quality of Life
  • Behavioral problems
  • “ADHD” symptoms
  • Poor School Performance
  • Developmental delay
  • Shyness
  • Difficulty waking up in AM
  • Failure to thrive
  • Enuresis
  • Daytime fatigue
51
Q

OSA Diagnosis

A
1) Polysomnography
Benefits
– Gold Standard for diagnosis of OSA
– Best differentiation of severity
• Limitations
– Poor accessibility in Canada
– Does not always correlate with sequalae
2) Overnight Oximetry
• Benefits
– “Positive”test in context of symptoms can be diagnostic
– Easily available
• Limitations
– Poor sensitivity
– Does not differentiate causes of desaturations
– Technical limitations`
52
Q

OSA treatment

A

Non-Pharmacologic
– Nasal hygiene saline rinses
– Sleep hygiene

• Pharmacologic
– Intranasal Corticosteroids
– Montelukast

• Surgical
– Adenoidectomy • +/- Tonsilectomy

If obesity related:
• Weight Loss
• ContinuousPositive Airway Pressure (CPAP

53
Q

Side effects of ventolin

A

↑HR, tremors, hypokalemia

54
Q

When is ipatropium bromide most effective?

A

Anticholinergic-BD by antagonizing Ach at receptor
↑ FEV1 by 10% if added to β2 agonist

Works best in 1st four hours

55
Q

Main side effect of LABA?

A

Tachyphylaxis

  • lasts ~12 hrs
    • Add to IHS if inadequate control with optimal dose
    • Must be used with inhaled steroid (combo inhaler)
56
Q

Side effects of ICS?

A

oral thrush
hoarseness
↓ linear growth with high dose

57
Q

What is Omalizumab and when/who is it used in?

A

Recombinant DNA-derived humanized IgG monoclonal antibody
• Selectively binds to human IgE
• Subcutaneous injection q 2 – 4 weeks
• For moderate to severe persistant allergic asthma,
not controlled on IHS
• For >12 years of age
• Risk of anaphylactic reaction – done in MD office

58
Q

How do steroids help with asthma exacerbations?

A

They help increase the responsiveness of B2 agonists

59
Q

Typical Age of Epiglottitis?

A

2-6

60
Q

Bugs causing epiglottitis?

A

Bacterial: H. influen- zae type B (+++), B-hemolytic strep (+)

61
Q

How does epiglottitis present clinically?

A
Toxic
Severe airway obstruction 
Drooling, sitting forward
Stridor
Sternal recession
62
Q

Age of croup?

A

6 months - 4 years

63
Q

Bugs causing croup?

A

parainfluenza 1
RSV
Influenza

64
Q

Clinical Presentation of Croup

A
Not toxic
Not drooling
Stridor common
Sternal recession common
Barking cough 
hoarseness
coryza
65
Q

Common age for bacterial tracheitis

A

any age

66
Q

Bugs causing tracheitis

A

S. Aureus
pneumococcus
H.influenzae

67
Q

Clinical Presentation of tracheitis

A

Toxic; croup-like cough Stridor

68
Q

Inheritance of CF

A

Autosomal Recessive
• CFTR is abnormal- Cystic Fibrosis Transmembrane
Regulator Protein

69
Q

PFT findings for CF

A

PFTs:
– Early disease - peripheral airway disease - results in airway obstruction, gas trapping, ↓FEF25-75
– Late disease - chronic inflammation- ↑lung destruction and fibrosis- late: restrictive pattern with persistent gas trapping

70
Q

Causes of elevated sweat chloride test

A
Cystic fibrosis
• Untreated adrenal insufficiency 
• Glycogen storage disease, type I 
• Fucosidosis
• Hypothyroidism
• Nephrogenic diabetes insipidus 
• Ectodermal dysplasia
• Malnutrition
• Mucopolysaccharidosis
• Panhypopituitarism

(skin and things that make you salty)

71
Q

CF bugs

A
Bugs:
• S Aureus
• H Influenza
• Psuedomonas Aeruginosa 
• Burkholderia Cepacia
• Aspergillus fumigatus
72
Q

What is ABPA?

A

Allergic bronchopulmonary aspergillosis (ABPA)

  • Hypersensitivity reaction in response to colonization of the airways with Aspergillus fumigatus
  • Occurs almost exclusively in patients with asthma or CF
  • In chronic cases, repeated episodes of bronchial obstruction, inflammation, and mucoid impaction can lead to bronchiectasis, fibrosis, and respiratory compromise.
73
Q

Clinical Presentation of ABPA?

A

Wheezing
Increased cough
Rust colored sputum or “brown plug”

Have high suspicion in patients >6 years of age, screen yearly with IgE levels

74
Q

Labs suggestive of ABPA?

A

Decreased PFTs
Peripheral eosinophilia
Increased IgE
Specific precipitants to aspergillus

75
Q

Diagnosis of ABPA?

A

Skin test for aspergillus

And IgE level

76
Q

Treatment of ABPA?

A

Steroids
Remember – allergic! Decrease systemic response to aspergillus
Tx for months
Antifungals can be added but that is to decrease the aspergillus load so steroids can work

77
Q

How do you monitor ABPA?

A

Monitoring

IgE levels to trend

78
Q

What electrolyte disturbances present with CF?

A

Hyponatremic, hypochloremic dehydation

79
Q

Treatment of PCD?

A

Treatment
– no cure available
– Regular chest physiotherapy
– Aggressive antibiotic treatment
– Routine and other vaccinations, flu shot
– Surgical intervention • Tympanostomytubes • Sinus drainage

80
Q

Causes of Pneumothorax

A
Causes:
􏰀 idiopathic/spontaneous
􏰀 thoracic trauma
􏰀RDS/ meconium aspiration 􏰀CF with pleural blebs
􏰀 Asthma
􏰀 Marfans
􏰀+/- mechanical ventilation
81
Q

Treatment of pneumothorax

A
Treatment
􏰀conservative, +/- 100% oxygen
􏰀chest tube
􏰀+/- surgery
􏰀pleurodesis for recurrent pneumothorax

PTX has nitrogen in it (just like regular air, 80%)
theoretically want to wash out the nitrogen - replace it by O2 - which then reabsorbs

82
Q

Treatment of tension pneumothorax

A

Tension Pneumothorax
􏰀 Intrapleural pressure> atmospheric pressure
􏰀 Ipsilateral lung collapses
􏰀 Mediastinal shift
􏰀 ↓venous return
􏰀 Management – needle aspiration, chest tube

83
Q

What is a transudate?

A

Transudates occur secondary to conditions which cause an increase in the pulmonary capillary hydrostatic pressure or a decrease in the capillary oncotic pressure

Leads to accumulation of protein poor pleural fluid

Common causes include: CHF, nephrotic syndrome, cirrhosis, hypoalbuminemia, pulmonary embolism

LOW PROTEIN

84
Q

What is an exudate?

A

Exudates occur secondary to conditions which cause inflammation or increased pleural vascular permeability

Leads to accumulation of protein rich pleural fluid and cells

Common causes include: pneumonia, cancer, tuberculosis, pulmonary embolism

HIGH PROTEIN

85
Q

What is bronchiectasis?

A

Bronchiectasis

  • irreversible dilatation of the airways
  • inflamed and easily collapsible airways
  • obstruction to airflow

Diagnosis is established clinically on the basis of cough on most days with tenacious sputum production
- often one or more exacerbations/year,

86
Q

Imaging modality to diagnose bronchiectasis?

A

CT:

  • presence of bronchial wall thickening and airway dilatation
  • “tramlines” railroad tracks that should taper but dont
  • signet ring - airways diameter is bigger than neurovascular or vascular bundle beside it
87
Q

Clinical presentation of OSA?

A

Night: paradoxical chest and abdo motion, snoring, apnea, sweating, cyanosis

Day: Mouth breathing, difficulty waking up, moodiness, daytime sleepiness, hyperactivity, cognitive problems

88
Q

What is OSA?

A

Repeated events of partial or complete U/A obstruction during sleep, disrupting normal gas exchange and sleep patterns

89
Q

AHI for moderate OSA?

A

> 5

90
Q

AHI for severe OSA?

A

> 10

91
Q

Investigations for OSA?

A
Investigations
• Lateral Neck Xray
• overnight oximetry
• early morning capillary blood gas 
• polysomnography
92
Q

Treatment of OSA?

A

Treatment
• T&A (if severe and clinical signs of tonsillar hypertrophy)
• NIPPV-CPAP

93
Q

D/Dx for central apnea/hypoventilation

A
Insufficient resp drive 
– CCHS (10)
– Arnold-Chiari malformation (10) 
– Asphyxia (20)
– Tumour (20)
– Central System Infarct (20)
– Medications (20)
– Decreased muscle strength (e.g SMA) (20) 

Rx: Depends on etiology

94
Q

Pattern of restricted PFT?

A

Small…lower lung volumes. Small loop

Ddx

  • pulmonary fibrosis (eg post radiation)
  • chest wall deformity
  • ??neuromuscular
95
Q

Pattern of obstructed PFT?

A

SCOOP

  • asthma for sure
    CF - would be obstructive but no increase in FEV1 post bronchodilator
  • if no response to bronchodilators THINK BRONCHIECT ASIS
  • CF
    -PCD -Bronciolitis obliterans -asthma still