Advanced A and P
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| show | Obstructive, chronic pulmonary disease characterized by: chronic inflammation and bronchial hyperresponsiveness
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| Incidence | show 🗑
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| show | Most asthma cases 50% diagnosed in childhood, with peak at age 3. Adults (about 33%) are diagnosed by age 40 typically
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| show | Women more likely than men, but boys are more likely than girls.
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| Ethnicity | show 🗑
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| show | Obesity has a higher incidence of asthma, increased risk is possibly related to fat stores having adipokines (cytokines secreted by adipose tissues) -proinflammatory, have less anti-inflammatory capacity. Roles of obesity and asthma still not clear.
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| show | type 1 hypersensitivity reaction (childhood asthma is usually from this)
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| Atopy | show 🗑
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| Dysregulation factors (not atopy) | show 🗑
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| show | chronic airway inflammation and bronchial hyperresponsiveness with intermittent, reversible airway obstruction
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| show | related to bronchospasm and bronchoconstriction, usually shown with cough. Peak=30 mins, resolves 3 hours. Inflamm. mediators released by mast cell degen. include leukotrienes ,histamine, prostaglandins, tumor necrosis factor, begin inflamm. recruitment
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| show | Dendritic cells present the antigen, and Th2 (T helper) lymphocytes release multiple cytokines (interleukins 3, 4, 5, 8, 13, 17, and 22 as well as granulocyte macrophage-stimulating factor).
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| show | cytokines cause B-cell activation, mast cell proliferation, eosinophil production and survival, neutrophil release, basophil survival, and T-cell recruitment and differentiation into Th2 cells.
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| Early Part 4 | show 🗑
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| Late Phase | show 🗑
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| Late part 2 | show 🗑
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| show | Airways begin to scar and bronchial hyperresponsiveness continues, which leads to impaired clearing of mucous and therefore, mucous plugs (glycoproteins) form. Mucous plugs secreted by goblet cells in the airways.
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| Late part 4 | show 🗑
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| Atopic | show 🗑
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| nonatopic | show 🗑
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| show | high eosinophil levels. Even though it is related to eosinophils, which trigger IgE due to allergic reaction, these individuals do not necessarily have allergies.
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| Aspirin-exacerbated respiratory disease | show 🗑
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| ASA resp. disease part 2 | show 🗑
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| show | work-related, happens during exposure to occupational allergens like plant proteins or animal proteins or other chemicals. This develops instead of atopic asthma. Symptoms develop over time and get worse with each exposure, improving when away from work
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| Intermittent | show 🗑
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| show | Daytime> 2 x per week, but <daily; nighttime > 2 nights/month
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| show | daytime - daily; nighttime >1 night/week, but < daily
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| Severe persistent | show 🗑
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| Manifestations | show 🗑
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| More manifestations | show 🗑
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| Exercise-induced | show 🗑
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| show | airways can become cool/dry during exercise, asthmatic symptoms may be a compensatory mechanism to warm and moisten the airways. Following each episode of exercise-induced asthma, a refractory (symptom-free) period begins within 30 minutes up to 90
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| Exercise part 3 | show 🗑
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| Make symptoms/asthma worse | show 🗑
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| Nocturnal Worsening | show 🗑
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| show | life-threatening, prolonged asthma attack, does not respond to usual treatment. Patent airway is critical, intubation may be needed.
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| show | Respiratory alkalosis from exhaling too much carbon dioxide because of tachypnea and hypoxemia can happen early in the attack. Eventually muscles fatigue and CO2 retained and causes acidosis
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| show | Spirometry - typically, FEV1 decreases, which is reversible.
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| show | CXR, ABG, CBC, challenge testing (bronchoprovacation) and allergen testing. Some people can develop irreversible airflow limitations
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