OPD Flashcards
obstruction
worsen expiration
cause increased WOB (use accessory muscles), emptying of lungs slows (dereased FEV1)
cause v/q mismatch and hypoxemia
air trapping -> hypovent and hypercap
dyspnea and wheezing always
air trapping patho: cant fully exhale = high CO2, air trapped in alveoli = increased WOB, lungs hyperinflated, no gas exchange, chronic high co2 and low o2
obstruction: asthma
chronic inflam of bronchial airways (not alveoli) causes bronchial hyperresponsiveness, constriction of airways and variable airflow obstruction that is reversible
chronic disease state with acute exacerbations
asthma: rf
allergies (children), familial link, level of allergen exposure, urban residency, exercise, air pollution (indoor and outdoor), smoke/tobacco, recurrent RTI, gerd, decreased exposure to certain infectious organisms = immunologic imbalance
asthma: phys
antigen exposure (trigger) -> lots of immune cells (dendritic helper T-2, mast, b lymph, neutrophils, basophils, eosinophils
airway inflam
hypersecretion of mucus, airway muscle constriction, swelling bronchial membranes
narrowing breathing passages
wheezing, cough, sob, tightness in chest
asthma: early response
immediate activation, cascade release of inflam mediators occurs within minutes
vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction (bronchoconstriction), mucus secretion
asthma: late response
4-8 hours after, they have already recovered
recruitment of eosinophils, neutrophils, and lymphocytes cause another release inciting same process
asthma: responses
bronchoconstriction = #1 s of asthma attack
inflam -> cause seriousness of disease (long term damage if untreated, irreversible, airway remodeling with chronic asthma)
asthma: diagnose
hx of allergies, recurrent wheeze, dyspnea, course/exercise intolerance
PFT: measure lung function with respect to time, gold standard, decreased EFR, decreased FEV1
asthma: cm
wheeze (classic), SOA (breathless/dyspnea), cough, chest tightness
severe: accessory , distant BS, diaphoresis, dont speak, resp failure = repetitive hacking cough and no BS
asthma: tm
avoid irritants, use PFM
low dose corticosteroids (exacerbations)
short acting beta agonist inhalers for mild (severe = inhaled anti inflam corticosteroids, long acting beta, leukotriene antagonists)
immunotherapy
asthma: status asthmaticus
severe S
unrelenting asthma attach: silent chest, no air movement, pCO2 > 70
life threatening -> IV epinephrine (epi pen)
treat: avoid, drugs (bronchodilators, corticosteroids, o2 therapy)
chronic bronchitis
hypersecretion of mucus and chronic productive cough for 3 mo and 2 yr
chronic bronchitis: cm
persistant productive cough - purulent if also resp infection (freq bc mucus favorable breeding ground)
progresses: increased cough, increased congestion, increased SOA
chronic bronchitis: diagnosis
hx of s, PA, chest imaging, pulmonary function test (decreased FEV1)
by time of treatment seeking, disease is progressive and pathologic changes are irreversible
smokers and vapers
chronic bronchitis: pathophys
inhaled irritants = airway inflam -> infiltration with neutrophils, macrophages, lymphocytes, into bronchial walls
continual bronchial inflam -> bronchial edema, increase in number and size of goblet cell and mucus glands
thick tenacious mucus produced and cant be cleared bc impaired ciliary function: cilia damaged bc inflam/thickened secondary to edema, accumulation of inflam cells, thickened smooth muscle secondary to chronic bronchospasm (fibrosis)
initially only affects larger airways -> eventually all involved