Obstructive disease Flashcards
7 types of asthma:
Extrinsic asthma
Intrinsic asthma
Exercise induced asthma
Triad asthma
Cough-variant asthma
Occupational asthma
Refractory asthma
When does extrinsic asthma usually onset and what are its triggers?
Usually in childhood, triggered by exposure to inhaled allergen
When does intrinsic asthma usually onset and what are its triggers?
Usually in adulthood, triggered by viral infections or other nonspecific irritants
What is a strong risk factor for intrinsic asthma?
Obesity, particularly in women
What is the triad of “triad asthma?”
Asthma
Nasal polyps
Aspirin sensitivity
Temporal pattern of occupational asthma:
“Monday morning” symptoms as sx’s abate over weekend.
Better in AM, worse in PM
6 causes of refractory asthma:
Chronic allergen exposure
Beta-blockers
ASA-containing drugs
Mucocutaneous fungal infections
Allergic bronchopulmonary aspergillosis
Churg-strauss vasculitis
Frequency cut-off for “persistent” or “intermittent”asthma:
> 2 episodes per week
Stepwise therapy for mild intermittent asthma:
Short-acting bronchodilator as needed
Stepwise therapy for mild persistent asthma:
low/medium inhaled corticosteroids + SABA
Stepwise therapy for moderate persistent asthma:
High inhaled corticosteroid, LABA, SABA
When to consider step-down therapy for asthma:
If well-controlled symptoms for 3 months
Acute asthma attack treatment:
Nebs q20minutes x3 doses
60 - 120 mg steroids q6h if no relief
Indications for hospitalization for asthma attack:
- Peak flow < 40% of baseline after 4-6 hrs of treatment
- Persistent hypoxemia
- Hypercapnia
- Altered sensorium
- Hx of prior near fatal asthma attacks
Definition of chronic bronchitis:
Daily sputum production for >3 months/year for 2 consecutive years
Four risk factors for developing COPD in smokers:
- Airway reactivity
- Family history of COPD
- Childhood lung dz
- Occupational dust exposures
What is the BODE index?
Body mass index (low is bad)
Obstructive defect (severe is bad)
Dyspnea (severe is bad)
Exercise tolerance (on 6 MWT)
What is the earliest abnormality seen on spirometry for COPD?
Decreased maximal flow at low lung volumes seen on flow-volume loops
Stepwise approach for COPD treatment:
Mild - Short acting bronchodilators
Moderate - Long acting bronchodilators, ICS
Severe - long-term oxygen + above
Very severe - LVRS, transplant
Benefit of exercise rehab in COPD:
Improves exercise function, no effect on lung function
Benefit of oxygen for hypoxemic patients with COPD:
Improves long-term survival in pts with hypoxemia
Indications for chronic oxygen in COPD:
PaO2 < 55 or SpO2 < 89% in usual health
OR
PaO2 < 60 or SpO2 < 90% if cor pulmonale or neurocognitive impairment
Bullectomy indications:
For single bulla occupying 1/2 of hemithorax
Lung transplant candidate criteria for COPD:
FEV1 < 20%
Age younger than 60-65 yo
Good social support
Maximum beneficial steroid course length in COPD exacerbation:
2 weeks
Inheritance pattern of A1AT deficiency
Autosomal recessive
3 most common alleles of A1AT deficiency
M: normal
S: intermediate
Z: marked decrease
Null: absent
Phenotypes and associated problems with A1AT mutations:
M, MS, MZ: No increased risk
SZ: mildly increased risk
ZZ: increased risk of emphysema, 10% also liver disease
Causes of bronchiolitis obliterans:
Connective tissue diseases, e.g. RA
Organ transplantation
Inhalation of toxic fumes
Viral infections
Neuroendocrine cell hyperplasia
Idiopathic
Treatment for bronchiolitis obliterans:
Immunosuppressive drugs but often not useful
Macrolides if post-transplant
Radiographic features of ABPA:
“Gloved finger” on CT or CXR from dilated central airways
Recurrent pulmonary infiltrates
Perihilar evanescent oval shadows on CXR from mucoid impactions
