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
chronic bronchitis: late cm
pulm htn:
increased pulmonary artery P d/t elevated pulmonary venous P, increased pulm BF, pulm vascular obstruction, hypoxemic
S: syncope, DOE, fatigue
can cause R sided HF = cor pulmonale
chronic bronchitis: tm
prevent (dont smoke - if stop before S occur, risk for bronchitis decreases considerably and looks like someone that never smoked)
irreversible -> can be halted if stop smoking
bronchodilators
expectorants/prophylactic abx, CPT, steroids (late or acute exacerbations), home o2
emphysema
abn permanent enlargement of gas exchange airways, accompanied by destruction of alveolar walls
obstruction from inflam and destructive change in lung tissue
major mechanism of airflow limitation if loss of elastic recoil with collapse of airways during exp
emphysema: defined
chronic, irreversible, progressive, destructive
decreased elastic recoil
abn permanent enlargement of air spaces distal to terminal bronchioles secondary destruction of alveolar (pop) walls and capillary beds -> airway remodeling
lung hyperinflation -> destruction from tissue change, not mucus production
obstruction is secondary to change in lung tissue
major mechanism of airflow limitation is less of elastic recoil, causes: smoke, air pollution, freq childhood resp infections, genetics (alpha antitrypsin enzyme deficiency)
emphysema: cm
gradual increase in breathlessness, DOE
eventually SOA at rest: prolonged exp, may become oxygen dependent
wheezing, malN (increased WOB), decreased muscle mass, barrel chest (1:1), pursed lip breathing, decreased breath sounds
emphysema: diagnose
PFT (FEV1 decreased)
CXR: hyperinflate
abg: resp acidosis (increased CO2, decreased pH)
alpha antitrypsin (AAT)
emphysema: tm
dont smoke
bronchodilators and anti inflam agents (mainstay), o2 supplementation, breathing retraining, relaxation techniques, abx for acute infections
chronic bronchitis v emphysema
chronic B: overweight and cyanotic, increased hgb, peripheral edema, ronchi and wheeze, mucus! main issue, hypoxic and cyanotic
emphysema: older and thin (decreased muscle mass, malN), severe dysp, quiet chest (and wheeze), hyperinflation with flat diaphragm, hypercarbic and dyspneic
both!: hypoxic -> decreased o2 and increased co2
