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Pulmonology
Advanced A and P
| Term | Definition |
|---|---|
| Asthma | Obstructive, chronic pulmonary disease characterized by: chronic inflammation and bronchial hyperresponsiveness |
| Incidence | One of the most common noncommunicable chronic illnesses globally and in children in the US |
| Age | Most asthma cases 50% diagnosed in childhood, with peak at age 3. Adults (about 33%) are diagnosed by age 40 typically |
| Male vs. Female | Women more likely than men, but boys are more likely than girls. |
| Ethnicity | People with multiple races/ethnicities and black adults and kids are more likely to be diagnosed |
| Obesity | 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. |
| Asthma and Atopy | type 1 hypersensitivity reaction (childhood asthma is usually from this) |
| Atopy | Atopy=genetic predisposition to produce exaggerated IgE response to allergens and irritants. Not all people with Atopy get asthma. They share genetic alterations that give genetic immune dysregulation. |
| Dysregulation factors (not atopy) | Other factors: smoking, pollen, and other environmental factors lead to the dysregulation. |
| Key Characteristics | chronic airway inflammation and bronchial hyperresponsiveness with intermittent, reversible airway obstruction |
| Early Phase | 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 |
| Early part 2 | 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). |
| Early part 3 | 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. |
| Early Part 4 | Cytokine and/or specific interleukins cause tissue injury, release of toxic chemicals, enhanced inflammatory response, impaired mucociliary response, increased fibroblasts, and airway remodeling |
| Late Phase | few hours after acute event, a late response can happen. Neutrophils, lymphocytes and eosinophils can further release same ones from acute phase. Late response peaks within 6 hours of symptom onset. |
| Late part 2 | This phase is caused by airway edema and mucous production. Leukotrienes are synthesized, which causes smooth muscle contraction. Air trapping occurs due to alveolar hyperinflation. |
| Late part 3 | 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. |
| Late part 4 | Leaky broncihial vessels release plasma proteins, help develop mucous plugs. W/out treatment, changes develop, are not reversible, can include fibrosis under epithelial layer and hypertrophy of smooth muscle/mucous glands. Changes called airway remodeling |
| Atopic | most common phenotype. Different people can have different genes and have one type of asthma expression. Severity is constant with the individual. Mild asthma will continue mild and so on. |
| nonatopic | eosinophilic asthma, aspirin-induced asthma, and occupational asthma. Nonatopic is more common in adults. |
| Eosinophilic | high eosinophil levels. Even though it is related to eosinophils, which trigger IgE due to allergic reaction, these individuals do not necessarily have allergies. |
| Aspirin-exacerbated respiratory disease | chronic rhinosinusitis and nasal polyposis. Aspirin and NSAIDs block enzymes called cyclooxygenase, leading to arachidonic acid conversion to prostaglandins, which stimulates leukotriene release (bronchoconstrictor). |
| ASA resp. disease part 2 | Consequently, arachidonic dysregulation and an overproduction of leukotrienes causes subsequent bronchoconstriction and promotion of airway inflammation in cases of aspirin sensitivity. |
| Occupational Asthma | 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 |
| Intermittent | Daytime and nighttime sx - <2 times per week |
| Mild Persistent | Daytime> 2 x per week, but <daily; nighttime > 2 nights/month |
| Moderate persistent | daytime - daily; nighttime >1 night/week, but < daily |
| Severe persistent | daytime is continual and nighttime is frequent |
| Manifestations | Expiratory wheezing, dyspnea, chest tightness, cough, anxiety, tachypnea, and tachycardia |
| More manifestations | Work of breathing increases (wheezing may be heard during inspiration but is commonly heard on expiration); accessory muscle use if not treated or not responding to treatment; increased work of breathing leads to hypoxemia |
| Exercise-induced | mast cell changes during exercise leads to bronchoconstriction. Usually, 10-15 mins after activity ends and symptoms can linger for an hour. |
| Exercise part 2 | 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 |
| Exercise part 3 | right then, little or no bronchospasm can occur, even if the person is re-challenged with vigorous exercise. Athletes often take advantage of this: a refractory period prior to competition. Weather changes can trigger asthma symptoms in the same manner. |
| Make symptoms/asthma worse | premenstrual worsening; stress through a cholinergic reflex pathway; beta blocker medication; nocturnal worsening |
| Nocturnal Worsening | usually between 0300 to 0700 and is thought to be related to circadian rhythms. At night, cortisol and epinephrine levels decrease while histamine levels increase, these changes in the substances leads to bronchoconstriction |
| Status asthmaticus | life-threatening, prolonged asthma attack, does not respond to usual treatment. Patent airway is critical, intubation may be needed. |
| Status part 2 | 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 |
| PFT (pulmonary Function test | Spirometry - typically, FEV1 decreases, which is reversible. |
| Diagnosis | CXR, ABG, CBC, challenge testing (bronchoprovacation) and allergen testing. Some people can develop irreversible airflow limitations |
Created by:
jhudblue
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