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31 Cards in this Set
- Front
- Back
chronic bronchitis
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productive cough for 3 months of the year for 2 consecutive years
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chronic bronchitis pathogenesis
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mucus hypersecretion, hyperplasia of submucosal glands (bronchi), proteases stimulate mucus hypersecretion, increase in goblet cells
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chronic bronchitis clinical findings
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increased bronchial mucus secreting apparatus, reid index more than 0.5, cyanosis and edema. cor pulmonale, heart failure, cancerous transformations
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reid index
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measures the size of the mucous glands
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emphysema
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enlargement of airspaces distal to the terminal bronchioles with destruction of their walls without fibrosis
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emphysema pathogenesis
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smoke causes irritation and mucus secretion, neutrophils contain serine elastase causes destruction of elastic tissue in walls of airspace, inactivation of α-1-antitrypsin (by smoke) which inhibits many proteases including elastase
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centriacinar (centrilobular) emphysema
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most common, usually associated with cigarette smoking, characterized by destruction of the proximal acinus
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panacinar (panlobular) emphysema
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acini are uniformly involved, patients with hereditary α-1antitrypsin deficiency
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localized emphysema
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large area of destruction termed a bulla which may rupture and produce spontaneous pneumothorax
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emphysema clinical findings
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exertional dyspnea, tachypnea, barrel chest, ping puffers, use of accessory muscles of respiration to breathe
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asthma types
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1. atopic - allergen sensitization
2. nonatopic - frequently triggered by respiratory tract infection 3. drug induced asthma - aspirin 4. occupational asthma |
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asthma pathogenesis
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allergen interacts with TH2 cells and IgE antibody bound to the surface of mast cells, type 1 hypersensitivity, inflammatory mediators lead to smooth muscle contraction, mucous secretion, increased vascular permeability
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asthma clinical findings
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tightness in chest and non productive cough, wheezing, ↑respiratory rate, dyspnea, status asthmaticus is severe bronchoconstriction
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pulmonary hypertension
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elevated pulmonary arterial pressure, mean pressure over 24 mm Hg at rest
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primary pulmonary hypertension
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most common in young women, insidious onset of dyspnea, cor pulmonale, heart-lung transplant often required
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secondary pulmonary hypertension
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1. after chronic pulmonary diseases - COPD, pulmonary embolism, tuberculosis
2. after heart disease - left-to-right cardiac shunts 3. thromboembolic pulmonary hypertension - multiple thromboemboli, gradual restriction of pulmonary circulation |
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hypoxemia
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COPD, lung disease, kyphoscoliosis
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obesity-hypoventilation syndrome
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↓ventilatory responsiveness to hypercapnia/hypoxia
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picwikian syndrome
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extreme obesity, cyanosis, irregular breathing, secondary polycythemia, right ventricular hypertrophy, pulmonary hypertension
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pulmonary edema
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increased fluid in the alveolar spaces and lung interstitium
leads to ↓decreased gas exchange, hypoxia, hypertension |
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protective mechanisms of lung against edema (3)
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1. ↓perfusion pressure in lung capillaries 2° ↓right centricular pressure
2. effective drainage of the intersitial space by lymphatics 3. tight cellular junctions between endothelial cells |
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hemodynamic edema
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increased hydrostatic pressure (increased pulmonary venous pressure), decreased oncotic pressure
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cardiogenic pulmonary edema
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↑transmural pressure, ↑hydrostatic pressure, ↑alveolar surface tension,
ultrafiltration rate exceeds capacity, interstitial fluid build up exceeding clearance, alveolar flooding |
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noncardiogenic pulmonary edema
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loss of integrity of alceolar epithelium and capillary endothelium, ↑permeability, disrupted epithelial barrier
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Acute Respiratory Distress Syndrome (ARDS)
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decreased lung compliance, hypoxemia, "white out" on xrays, caused by a large variety of lung insults
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ARDS pathogenesis
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endothelial cells injury causes alveolar fluid build up into interstitial spaces, loss of type 1 pneumocytes causes formation of Hyaline membrane, inflammation, proliferation of pneuomocytes II, fibroblasts deposit collagen in alveolar wall if patient survives acute phase
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ARDS pathology
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acute phase - diffuse alveolar damage, alveolar septa, hyaline membranes
later phase - proliferation of pneuomocytes type II and fribroblasts in interstitial space |
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neonatal respiratory distress syndrome (RDS)
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results from immaturity of the surfactant system at birth, leading cause of morbidity/mortality in infants, very common in premature babies
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RDS pathogenesis
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lack of surfactant causes alveolar collapse during exhalation, inhalation is more difficult and damages alveolar lining
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RDS pathology
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lungs are dark red and airless, alveoli are collapsed, hyaline membranes
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RDS clinical findings
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within an hour of birth: ↑increased respiratory effort with forceful intercostal retraction, ↑respiratory rate, cyanosis, "ground glass" granularity in chest radiographs/"white out" of lungs, long periods of apnea leads to asphyxiation
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