Asthma Flashcards
1
Q
Asthma definition
A
- Airway narrowing
- Hyperreactivity
- Reversibility: at least 15% improvement w/ bronchodilators (distinguishes it from other obstructive diseases)
- Inflammation-> remodeling
2
Q
Risk factors for asthma
A
- African americans, young, elderly, poor
- Favoring Th2 phenotype: urban environment, early use of antibiotics
- Genetics: heterogeneity, influences atopy (IgE), specifically polymorphisms of the B2 receptor gene (16 arg/arg have more severe disease- won’t respond as well)
- Prior hospitalization, nocturnal exacerbations, multiple drugs for Rx (all indicate more severe disease)
3
Q
Physiology of asthma
A
- Process of airway hyper reactivity -> acute infl -> chronic infl -> remodeling
- Epithelial cells are first contact w/ Ag via TLR, dendritic cells stimulated then T cells
- T cells release IL 4, 5, 13 which stimulate eosinophils
- Active B cells release IgE
- IgE causes mast cell degranulation, which releases PGE, leukotrienes, and histamine (all cause inflammation)
4
Q
Signs and Sx of asthma
A
- Signs: wheezing, diminished breath sounds, prolonged expiration, accessory muscle use, tachypnea and tachycardia, pulses paradoxus
- Sx: persistent cough, SOB, sputa, chest tightness
- PFTs: reduction in flow rates, reduced ability to exhale-> increased lung volumes/hyperinflation (looks like emphysema but is reversible w/ bronchodilators)
5
Q
Other diagnostic findings in asthma
A
- CXR usually normal, eosinophilia on CBC and in sputum
- Increased IgE levels
- Curschmann’s spirals: mucus plugs in shape of distal bronchiolar lumen (spirals)
- Charcot-leyden crystals: crystallized breakdown products of basophils and eosinophils
- eNO elevation
- ASA sensitivity (blocking COX shunts more arachidonic acid to LOX) and nasal polyps (classic triad)
6
Q
Triggers of asthma
A
- Environmental allergens
- ASA sensitivity (nasal polyps triad)
- Exercise induced
- URI (viral)
- GERD
- Emotional stressors
7
Q
Asthma classification
A
- Intermittent: Sx ≤2 days/wk, nocturnal Sx ≤2x/mo, SABA use ≤2 days/wk, ASx under normal activity, lung function normal
- Mild persistent: Sx ≥2 days/wk (but not daily), minor limitation on activity, nocturnal Sx 3-4x/mo, FEV 1x/wk (but not nightly)
- Moderate: SABA use daily, some limitations to activity, FEV 60-80%
- Severe persistent: continuous Sx, activity extremely limited, nightly nocturnal Sx, SABA used multiple times/day, FEV <60%
8
Q
Types of asthma meds
A
- Relievers: inhaled short acting B2 agonists, inhaled cholinergic
- Controllers: inhaled or systemic glucocorticoids, leukotriene modifiers, long acting B2 agonists, theophylline, oral antiallergic
- Never use LABA alone (MUST pair it w/ corticosteroid)
- Can step down management levels if asthma is controlled for 3 mo
9
Q
Management guidelines
A
- Intermittent (step 1): only SABA prn (should always have a SABA no matter what severity)
- Persistent: once at persistent stage MUST add controller
- Mild (step 2): low dose ICS (inhaled corticosteroid)
- Moderate (step 3): low dose ICS + LABA or medium dose ICS + LABA (step 4)
- Severe (step 5): high dose ICS plus LABA plus omalizumab (anti-IgE Ab)
- Severe (step 6): high dose ICS + LABA + oral corticosteroid + omalizumab
10
Q
Risk factors for poorly controlled asthma
A
- Poor adherence, poor technique
- Exposure to allergens/irritants
- GERD
- Drugs
- Obesity
11
Q
Asthmatic remodeling
A
- Airway wall thickening: sub epithelial fibrosis, increase of airway smooth muscle
- Mucus metaplasia (goblet cell hyperplasia) and mucus plugs
- Angiogenesis, inflammatory cell infiltrate
- Overall lumen narrowing
12
Q
Overlap syndrome
A
- Share features of asthma and COPD (fixed airflow obstruction w/ reversibility to SABA)
- DLCO is important to distinguish (DLCO is normal or elevated in asthma, often reduced in COPD- emphysema)
- ABGs in asthma normal (btwn exacerbations), ABGs in COPD usually abnormal
- Airway hyper responsiveness usually not helpful (should be higher in asthma but not always)
- eNO may be higher in asthma
