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31 Cards in this Set

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chronic bronchitis
productive cough for 3 months of the year for 2 consecutive years
chronic bronchitis pathogenesis
mucus hypersecretion, hyperplasia of submucosal glands (bronchi), proteases stimulate mucus hypersecretion, increase in goblet cells
chronic bronchitis clinical findings
increased bronchial mucus secreting apparatus, reid index more than 0.5, cyanosis and edema. cor pulmonale, heart failure, cancerous transformations
reid index
measures the size of the mucous glands
enlargement of airspaces distal to the terminal bronchioles with destruction of their walls without fibrosis
emphysema pathogenesis
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
centriacinar (centrilobular) emphysema
most common, usually associated with cigarette smoking, characterized by destruction of the proximal acinus
panacinar (panlobular) emphysema
acini are uniformly involved, patients with hereditary α-1antitrypsin deficiency
localized emphysema
large area of destruction termed a bulla which may rupture and produce spontaneous pneumothorax
emphysema clinical findings
exertional dyspnea, tachypnea, barrel chest, ping puffers, use of accessory muscles of respiration to breathe
asthma types
1. atopic - allergen sensitization
2. nonatopic - frequently triggered by respiratory tract infection
3. drug induced asthma - aspirin
4. occupational asthma
asthma pathogenesis
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
asthma clinical findings
tightness in chest and non productive cough, wheezing, ↑respiratory rate, dyspnea, status asthmaticus is severe bronchoconstriction
pulmonary hypertension
elevated pulmonary arterial pressure, mean pressure over 24 mm Hg at rest
primary pulmonary hypertension
most common in young women, insidious onset of dyspnea, cor pulmonale, heart-lung transplant often required
secondary pulmonary hypertension
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
COPD, lung disease, kyphoscoliosis
obesity-hypoventilation syndrome
↓ventilatory responsiveness to hypercapnia/hypoxia
picwikian syndrome
extreme obesity, cyanosis, irregular breathing, secondary polycythemia, right ventricular hypertrophy, pulmonary hypertension
pulmonary edema
increased fluid in the alveolar spaces and lung interstitium

leads to ↓decreased gas exchange, hypoxia, hypertension
protective mechanisms of lung against edema (3)
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
hemodynamic edema
increased hydrostatic pressure (increased pulmonary venous pressure), decreased oncotic pressure
cardiogenic pulmonary edema
↑transmural pressure, ↑hydrostatic pressure, ↑alveolar surface tension,

ultrafiltration rate exceeds capacity, interstitial fluid build up exceeding clearance, alveolar flooding
noncardiogenic pulmonary edema
loss of integrity of alceolar epithelium and capillary endothelium, ↑permeability, disrupted epithelial barrier
Acute Respiratory Distress Syndrome (ARDS)
decreased lung compliance, hypoxemia, "white out" on xrays, caused by a large variety of lung insults
ARDS pathogenesis
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
ARDS pathology
acute phase - diffuse alveolar damage, alveolar septa, hyaline membranes
later phase - proliferation of pneuomocytes type II and fribroblasts in interstitial space
neonatal respiratory distress syndrome (RDS)
results from immaturity of the surfactant system at birth, leading cause of morbidity/mortality in infants, very common in premature babies
RDS pathogenesis
lack of surfactant causes alveolar collapse during exhalation, inhalation is more difficult and damages alveolar lining
RDS pathology
lungs are dark red and airless, alveoli are collapsed, hyaline membranes
RDS clinical findings
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