| What is asthma? | common disease increasing over years, heterogenous disease with multiple etiologies, so different management options, characterized by chronic airway inflammation.
Two key features: Respiratory symptoms (Wheeze, SoB, tight chest, cough) and variable expiratory airflow limitation |
| How is the epidemiology of asthma? | Common and increasing, highest in vulnerable populations , 5-10% world wide, 2/3 are under 18, 50% are dx under aged 6 |
| What is the burden of asthma? | It is the most common cause if hospitalization of children, and most common chronic disease, consequences on lung growth and obstructive diseases, poor control is costly.
Dramatic increase in mortality in the 60s (with use of b-agonist) |
| What are the factors affecting asthma susceptibility? | Genetics (development of disease) and environment (onset of symptoms)
but complex (all interact with each others)
Host factors : genes of atopy and hyperresponsiveness of airway
Environmental: indoor dust, furred animal, cockroaches, fung.
outdoor: pollen, molds...
infectious: viral (RSV increases it 4 folds), occupational , tobacco/pollution..
Allergies: strongest risk factor of asthma (increases 3 folds)
Hygiene hypothesis: caused increased allergies (no desensitisation due to increased hygiene) |
| How is the pathogenesis of asthma? | Despite various etiologies, same chronic inflammation of airway.
activated mast cells, eosinophils, NK cells and Th2 lymphocytes, released mediators causing inflammation
We see airway smooth muscle contraction, hypertrophy and hyperplasia, microvascular leakage, mucus secretion, laying collagen in basal lamina |
| What is remodeling done in asthma? | increased collagen in basal lamina, thickening, produced by epithelia and myofibroblasts, this would cause irreversible airway obstruction and remodeling, and we might see exaggerated narrowing if we see bronchoconstricting agent |
| How is the histology and cytokines in asthma? | Infiltrates of mast cells, eosinophils, T cells and neutrophils.
if severe eosinophils we may see eosinophilic infiltrates in alveolar septae and arteries.
cytokines seen are chemokines (recruitment by epithelia), LT (bronchoconstrictors and pro inflammatory by mast cells and eosinophils, inhibition of them can improve lungs)
Histamines (bronchoconstrictor by mast cells), NO (bronchodilator, useful to monitor asthma and inflammation exhaled level), PG D2 (bronchoconstrictor by mast cells, recruits Th2 cell) |
| What are the pathophysiologic changes in asthma? | Bronchial hyperresponsiveness (BHR): exaggerated bronchoconstriction due to stimuli, can be determined by PFT, tested also by delivering nebulized methacholine in doubling concentrations till FEV1>20% falls, we see the degree by PC20 (dose to get this fall, if no asthma doesn't reach 16 mg/ml, mild asthma 4-16, modetare 1-4, severe <1)
Airway limitation (bronchoconstriction, mucus plugging, wall edema, inflammatory infiltrates, fibrosis, smooth-muscle hypertrophy, elastic recoil uncoupling. |
| How is pulmonary function in an asthmatic attack? | airway resistance increases and limited airflow
reversible after admin of bronchodilators (increase FVC/FEV1), air trapping and hyperinflation of lungs (increased TLC and RV)
During remission, may all be normal |
| What are the clinical manifestations of asthma? | Typical: wheeze, SoB, chest tight, cough
Variable symptoms (time and intensity, triggered by exercise/allergen/laugh..., can worsen with infection)
can be confused with acute viral tracheobronchitis (resolves after 6 weeks), or COPD.
hypersensitivity has 2 phases, immediate one with allergen , and late one after 6 hours for example
10% don't have SoB (more tolerant).
Symptoms more episodic than COPD and prolonged remission period typically, more in children (COPD in elderly), seasonal (Unlike COPD)
Some pt have overlap syndrome (smokers with asthma) |
| What is the differential diagnosis in asthma symptoms? | COPD, vocal cord dysfunction, CF/ bronchiectasis, Congestive HF, sleep apnea, pneumonia, sarcoidosis, psychosomatic. |
| What is cough variant asthma? | Asthmatic with isolated cough, dry cough for years before full triad, caused by stimulation of sensory nerves by inflammatory mediators and triggered by irritants.
One cough triggers a series of violent coughing paroxysms (exhausting lasts for minutes).
May have PFTs, so imp to use bronchoprovocation test (methacholine) to rule out asthma |
| List some Hx taking exams for asthma? | Do you have an attack or recurrent attack of wheezing?
Are you bothered by a cough at night?
Do you cough or wheeze after an exercise?
Do you cough, wheeze, or feel chest tightness after exposure to certain allergens or pollutants?
Do feel your colds go “chesty” & take longer to clear?
Are your symptoms relieved by asthma treatments? |
| What are PE findings in asthma? | Tachypnea (25-30), tachycardia (100-120) [universal]
diffuse wheezes (but don't show severity)
if wheeze with inspiration and expiration, loud or high-pitched this indicates large airway obstruction, and in very severe cases it may be absent -->poor air movement and respiratory failure.
Prolonged expiration (due to obstruction), chest hyperinflation (trapped air), accessory muscle use and pulsus paradoxus (severe airflow obstruction), cyanosis and mental obtundation (acute hypercarbic acidosis in extreme cases) |
| What is pulsus paradoxus? | During inspiration, increased thoracic negative pressure so venous return, so right ventricle distention and thus septum buldges to left ventricle reducing its size so we get decreased SV of left ventricle during inspiration
Paradox is that we can hear heart sound over percordium during inspiration without radial pulse felt |
| What occurs for gas exchange in asthma? | Ventilation/perfusion mismatch caused by bronchospasm, mucus plugging and swelling.
hypoxemia, hypocarbia and respiratory alkalosis present in 75% of acute asthma pt
When obstruction worsens FEV1 approaches 20%, PCO2 normalizes, and then respiratory acidosis may occur when FEV1 reaches 10% due to retention of CO2 |
| What are goals of asthma control? | No daytime symptoms, no limitation of activity, no nocturnal symptoms, no need for rescue medication (minimal twice per week), normal lung function and no exacerbation |
| How is the measure of asthma control? | Asthma control test (ACT) five question health survey measure asthma control
score <20 poor control, 20-24 control, >25 good control
Each question can get from 1-5 points, see asthma in last 4 weeks, ask about life functioning, symptoms, inhaler use and self rating |
