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patho exam 2

respiratory disorders part 2

QuestionAnswer
obstructive lung disorders asthma, chronic bronchitis, emphysema, CF, bronchiectasis
bronchiectasis permanent widening and thickening of the airways (bronchi)
obstructive lung disorders impair oxygenation and perfusion
increased work of breathing associated leads to increase in metabolic demand
anatomic airway structure: role of smooth muscles bronchoconstriction and bronchodilation
worsening airway obstruction during exhalation inflammation, loss of support for small airways, bronchoconstriction, mucus in airways (affects movement of air) resistance to airflow
alterations in pulmonary function pulmonary function tests (PTFs)
PTF uses assessment of obstructive lung disorders
PFT types spirometry, body plethysmography, nitrogen washout
tidal volume 500 mL, volume of air inhaled and exhaled during one cycle of normal quiet breathing
inspiratory reserve volume 3000 mL, max volume of air that can be inhaled after TV inhalation
inspiratory capacity 3500 mL, max volume of air that can be inhaled after normal exhalation
expiratory reserve volume 1200 mL, max volume of air that can be exhaled after TV exhalation
vital capacity 4700 mL, max amount of air that can be exhaled in nonforced manner after max inhalation
asthma is a chronic inflammatory disorder of airways
asthma entails recurrent episodes of reversible airway obstruction, hyperreactive airways (very sensitive)
asthma incidence greatest in industrialized countries due to pollution which triggers asthma
risk factors for asthma genetics, obesity, exposure to allergens, irritants, tobacco smoke
how many people in the US with asthma over 28 million which means about 1 in 12 people
asthma etiology unknown
asthma classification considerations clinical presentation, precipitating factors or triggers, allergies
asthma triggers allergies, infections, exercise, medications
asthma types allergic, recurrent
allergic asthma most common allergen causes type 1 hypersensitivity response - an allergen being exposed, basophils put antibodies on their surface
recurrent asthma not very common airways remodeled bronchial smooth muscle hypertrophy, increasing capacity for bronchoconstriction
asthma CMs recurrent chest tightness, SOB, wheezing, cough with our without production of thick sputum, severe asthma episodes
severe asthma episodes entail tachypnea and tachycardia
severity classifications mild intermittent asthma mild, moderate or severe persistant asthma
diagnosis of asthma medical history and physical exam, PFTs before and after bronchodilator use, challenge test, exhaled nitrogen oxide
treatment of asthma environmental control, bronchodilator, anti-inflammatory medications
COPD is not reversible
COPD entails progressive airflow limitations that are not fully reversible, includes chronic bronchitis and emphysema
COPD is linked to cigarette smoking
cigarette smoking accounts for 90% of COPD in industrialized countries - MAIN RISK FACTOR
COPD has a gradual onset with slowly progressive symptoms of dyspnea and SOB
COPD risk factors direct and environmental tobacco use, genetics, occupational exposure, indoor air pollution, severe respiratory tract infections
COPD etiology chronic airflow limitation due to abnormal inflammatory response to inhaled particles and gases in lung
GOLD 1: mild COPD Mild airflow limitation Possible chronic cough and sputum production Possible unawareness of individual that lung function is abnormal
GOLD 2: moderate COPD Worsening airflow limitations, SOB on exertion Possible cough and sputum production Chronic respiratory symptoms lead to person seeking care
GOLD 3: severe COPD Further worsening of airflow limitations, greater SOB Reduced exercise capacity, fatigue, and repeated exacerbations Affect on patient's quality of life
GOLD 4: very severe COPD Severe airflow limitations plus chronic respiratory failure
pathophysiology of COPD airway obstruction results from fixed airways that have increased resistance, slowing the rate of airflow hypercapnia - excess CO2 in the blood hyperinflation of the lungs
types of airway obstructions for COPD chronic inflammation structural remodeling of lung tissue alterations in vascular structure destruction of pulmonary structures
main causes of COPD are cigarette smoking and air pollution
cigarette smoking and air pollution cause continual bronchial irritation and inflammation and breakdown of elastin in CT of lungs
continual bronchial irritation and inflammation leads to chronic bronchitis
chronic bronchitis causes bronchial edema, hypersecretion of mucus, chronic cough, broncospasm
breakdown of elastin in CT of lungs leads to emphysema
emphysema causes destruction of alveolar septa, airway instability (disruption of alveolar walls)
emphysema and chronic bronchitis lead to airway obstruction, air trapping, dyspnea, frequent infections
airway obstruction, air trapping, dyspnea, frequent infections leads to abnormal ventilation-perfusion ratio (high CO2, low O2) hypoxemia, hypoventilation, cor pulmonale
chronic bronchitis originated by inflammation in bronchiole
chronic bronchitis is fixed airway obstruction caused by scarring that thickens basement membrane, increase number and size of mucus glands, loss of support for small airways
chronic bronchitis is the persistent, inflammation induced narrowing of airways
symptoms of chronic bronchitis copious mucus production, chronic productive cough
chronic bronchitis blocks air from going in and out of alveoli, so CO2 is increasing
emphysema damage to lung parenchyma (walls of alveoli), destruction of gas-exchanging pulmonary-surfaces (alveoli), pulmonary hyperinflation (decreased areas where gas can be exchanged)
causes of emphysema cigarette smoking, dont know why but air pollution is also a cause
classifications of emphysema centriacinar and panacinar
centriacinar emphysema loss of elastic tissue on the bronchioles, bronchioles remain in normal structure but lost function to expand so can't inhale and exhale
panacinar emphysema more severe, loss of elastic tissue on the bronchioles and alveoli
pulmonary acini functional units where gas exchange occurs
CMs of COPD depends on whether symptoms of chronic bronchitis or emphysema are dominant
CMs of chronic bronchitis productive cough for three months in 2 consecutive years, progressively worsening dyspnea with SOB and dyspnea on exertion (DOE), hemoptysis (lack of blood O2)
CMs of emphysema increased DOE, barrel chest, respiratory muscles reduction of strength, hypoxemia, foot and ankle swelling
CMs of advanced COPD reduced capacity for gas exchange, deterioration of pulmonary function
physical changes with hyperinflation destruction of alveoli so the capacity of E is decreased significantly
diagnosis of COPD spirometry, body plethysmography, x-ray
treatment of COPD assessment and monitoring, reducing risk factors, managing stable COPD, managing acute exacerbations
real treatment of COPD no real treatment, just monitoring symptoms and manage factors like not smoking, etc.
what does cystic fibrosis affect respiratory system and other organs
CF is the most common lethal genetic disorder
CF is the reabsorption of sodium inhibited in skin, sodium enhanced in epithelial exocrine cells
lifelong morbidity of CF 2-5% of caucasians carry the gene uncommon in blacks and asians
pathophysiology of CF recessive genetic disorder, affects epithelial transport of fluids
gene mutations in CF leads to production of unusually thick and sticky mucus that can clog ducts and airways
reproductive system with CF makes pt sterile
liver/pancreas with CF digestive problems that can be treated with meds
CMs of CF thick pulmonary secretions, frequent respiratory infections (more prone), chronic cough, abdominal distention, large/fatty/foul smelling stool since there are problems with digestive system
diagnosis of CF skin sweat test - sweat is very high in sodium!
treatment of CF abx for secondary infections, vitamin supplements to overcome lack of digestive enzymes due to pancreas problems, pancreatic digestive enzyme replacement
Created by: leh195
 

 



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