Respiratory Disorders: Flashcards
Epidemiology of Asthma:
About 23 million people (7 million children)
Leading chronic disease for children
Asthma is expected to grow
Third ranking cause of hospitalization among children under 15
High economic cost
Type I hypersensitivity-Asthma
Triggered by innocouous foreign substance (dust, pollen, dander)
Antigens simultaneously bind more than one membrane bound to IgE on a mast cell
(cross-linking process triggers the release of mast cell granules full of histamine )
What are the effects of histamine?
Stimulate bronchoconstriction
Vasodilation and increased capillary permeability causes edema that accum. in the tunica submucosa of the bronchi
Irritation and inflammatory response stimulate the secretion of mucus
What does airway obstruction cause?
Decreased expiratory flow rates
Air trapping
What are some asthma triggers?
Environmental allergens
Air pollutants
Cigarette smoke
Exercise/cold air
Upper airway infection
Genetic predisposition
Clinical Manifestation of asthma:
Cough:
-Hyper-acute= cough non-productive
-Slow-onset/chronic asthma= sufficient mucus to cause productive cough
Wheezing:
-Happens when air is being forced out through constricted bronchi and bronchioles
Insp./Exp. wheezing may be heard at in the last stages of an attack
Tachypnea and dyspnea- use of accessory breathing muscles
Chest tightness and discomfort: inflamm. response induce pain
COPD definition:
Abnormal lung function tests that do not improve over a period of several months
Key is reduced expiratory outflow manifested by prolonged forced expiratory volume in one second
Smoking responsible for 90% of cases
Classification of COPD:
Umbrella term that includes:
-chronic bronchitis
-emphysema
-refractory asthma (irreversible)
-severe bronchiectasis
COPD:Chronic Bronchitis:
Disease caused by chronic inflammation of the bronchi which leads to airways obstruction from hyper-secretion of mucus
Must have cough for at least 3 months out of a year or two consecutive years
Causes of Chronic Bronchitis:
Chronic exposure to irritants- cigarette smoke, (most common cause) coal, mineral dust, etc.
Pathopyshsiology of Chronic Bronchitis:
Recurrent irritation leads to chronic inflammation
Inflammation leads to release of histamines from mast cells as well as leukotrienes and platelet activating factor
Leading to mucus
Bronchial edema: Caused by increased capillary permeability in the tunica submucosa of the bronchi. Narrowed airway lumen and airway obstruction.
Clinical consequences of chronic bronchitis:
Airway Obstruction: edema in bronchial, bronchoconstriction, mucus secretion
Impaired ciliary function: chronic exposure to irritants destroy cilia- mucus secretion also impairs function
Increased risk of resp. infection: chronic mucus production provides warm, wet environment for bacterial colonization (chronic bronchitis easily susceptible to pneumonia due to bacterial infections in bronchi/alveoli)
Clinical Manifestation of Chronic Bronchitis:
Tachypnea, dyspnea (may be at rest) due to decreased ventilation and hypoxemia (low O2)
Hypoxemia manifested by SaO2 (oxygen saturation of hemoglobin) and PaO2 (partial pressure of oxygen in body) caused by airway obstruction and air trapping
Hypercapnia and resp. acidosis manifested by high PaCO2 caused by obstruction to expiratory air flow
Clubbing of fingernails occurs in response to chronic hypoxemia
Polycythemia is when hypoxemia causes the release of erythropoietin. This stimulates proliferation and release of red blood cells from bone marrow.
Increased hematocrit (polycythemia) is an attempt by bone marrow to increase oxygen delivery to tissues
COPD Emphysema:
Disease characterized by loss of alveolar recoil and destruction of septa between adjacent alveoli- leading to decreased alveolar surface area impairing gas exchange
Etiology of Emphysema:
Alpha 1 antitrypsin deficiency -Small percentage are caused by this a genetic lack of enzyme so it’s called Primary Emphysema
Alpha 1 antitrypsin problems are also root of acquired emphysema
Pathophysiology of Emphysema:
Alpha 1 antitrypsin deficiency is when its not active in the lung tissue
If alpha 1 antitrypsin in not active in the lungs, elastases produced by alveolar macrophage will dominate leading the enzymatic digestion of elastin and other proteins
Normally elastin fibers on the outside of the alveoli help expel air during exhalation
Breakdown of this elastin reduces expiratory air flow and increased residual volumes
Etiology of Emphysema:
-Inhibition of Alpha 1 antitrypsin
-Majority of cases caused by acquired inhibition of alpha 1 (causes same effect as deficiency)
-Secondary emphysema caused by smoking cigarettes
(smokers have 20% chance of developing emphysema)
Pathophysiology of Emphysema:
Septal destruction- septa between individual alveoli are destroyed from the protease leading to permanent enlargement of alveoli
Capillaries that lie between the alveolar septa also get destroyed as the alveolar wall disappear
Clinical consequences of emphysema:
Loss of elastin causes the alveoli to over-inflate during inhalation
Loss of elastin also reduces alveolar recoil resulting in air trapping
Air trapping causes functional obstruction to airflow in the lungs
Reduced surface area for gas exchange (V-Q mismatching and hypoxemia result)
Hypoxemia and hypercapnia- air trapping leads to decreased in inspired O2. Loss of elastin make it difficult to expel CO2 from alveoli
Loss of alveoli and pulmonary capillaries decrease the available surface area for gas exchange
Hypercapnia:
Increased CO2 in arterial blood caused by hypoventilation of the alveoli
Often overlooked
Clinical Manifestations Emphysema:
Dypsnea on exertion which progresses to dyspnea at rest (due to decreased ventilation/resulting hypoxemia)
Tachypnea and use of accessory muscles
Prolonged expiration manifested by decreased forced expiratory volume in one second
Increased A-P diameter of chest (barrel chest) due t increased RV from air trapping
Complications of COPD:
-Frequent lung infections
-Increased risk of osteoporosis due to oral corticosteroids
-Problems with weight
-emphysema may need to gain weight
-chronic bronchitis may need to lose weight
-pneumothorax (damage lung structures and allow air to leak into chest cavity)
-sleep problems
Respiratory Infection: Pneumonia
Infection of lung parenchyma
Bacteria causes of pneumonia:
Gram Positive: strep and staph
Gram negative: klebsiella, E coli, enterobacter, etc.
Viral causes of pneumonia:
Influenza virus, RSV, parainfluenza, adenovirus, SARS
Causes 2-35% in adults (more in children)
Higher hospital rates from viral PNA. in persons >60 yo
COPD and asthma frequently complicated by resp. viral infections
Immunocompromised increased risk
Viral Causes of Pneumonia-Influenza
Annual winter epidemics 6-8x weeks
Transmitted by small particles aerosols
2-3 incubation period
5-7 days max virus shedding
Viral Causes of Pneumonia-RSV
2nd most common cause of viral PNA in older adults
Major cause of serious lower resp tract infections in young children
Important pathogen for adults, esp elderly and chronic lung disease pt’s or immunocomp.
Classifications of Pneumonias:
Community acquired-
-mortality rate much lower in patient’s not admitted to ICU (nearly 40%)
Nursing home acquired
Nosocomial/Hospital acquired-
- > 48 hrs post discharge Incidence much higher with mechanical ventilation (mortality near 70% in patients with HAP)
-Increases length of stay by 7-9 days
-failure of therapy/pathogen resist./host factors/antibiotic resistance
Ventilator-associated
Pathophysiology of pneumonia:
Inflammatory response to pathogen:
-increased capillary perm. allows fluid into interstitial tissue/alveoli
Decreased function area of gas exchange leads to hypoxemia and hypercapnia:
-resp. rate and depth of respirations increase
Mucous production increases:
-helps decrease gas exchange
Clinical Manifestations of Pneumonia:
Consolidation:
