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restrictive pulmonary disorders
result from decreased lung expansion
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Restrictive pulmonary disorders
[characteristics]
- decrease in vital capacity (VC), lung capacity (FRC), residual volume (RV)
- greater the decrease in lung volume, greater the severity of disease
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Fibrotic interstitial lung disease
[etiology]
characterized by thickening of alveolar interstitium
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Diffuse Interstitial lung disease
[pathogenesis]
- immune reaction
- Inflammation
- Fibrosis
- Destruction
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Diffuse Interstitial lung disease [pathogenesis]
immune reaction
- begins with injury to alveolar epithelial or capillary endothelial cells
- interstitial and alveolar wall thickening
- increased collagen bundles in interstitium
- lung tissue becomes infiltrated
- persistent alveolitis leads to obliteration of alveolar capillaries, reorganization of lung parenchyma, irreversible fibrosis
- lead to large air-filled sacs (cysts) with dilated terminal and respiratory bronchioles
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Diffuse Interstitial lung disease [pathogenesis]
inflammation
- occurs early, reversible
- triggering event leads to inflammatory response and increased inflammatory cells
- ---injury leads to increased membrane permeability and movement of fluid/debris into alveoli
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Diffuse Interstitial lung disease [pathogenesis]
Fibrosis
- fibroblastic proliferation and deposition of large amt of collagen
- caused by increased mesenchymal cells and fibroblasts in interstitium
- Alveolar walls become thickened w/ increased amts of fibrous tissue
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Diffuse Interstitial lung disease [pathogenesis]
destruction
- end-stage disease
- loss of alveolar walls
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Diffuse Interstitial lung disease
[clinical manifestations]
- progressive dyspnea w/ exercise w/ desaturation
- rapid-shallow breathing
- irritating, nonproductive cough
- clubbing of nail beds
- bibasilar end-expiratory crackles (Valcro rales)
- Cyanosis
- anorexia, wt loss
- inability to increase cardiac output with exercise
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Diffuse Interstitial lung disease
[diagnosis]
- CXR
- PFT
- open lung biopsy
- transbronchial biopsy
- Gallium 67 scan
- bronchoalveolar lavage
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Diffuse Interstitial lung disease
[treatment]
- smoking cessation
- avoid environmental exposure to cause
- anti-inflammatory agents
- immunosuppressive agents
- lung transplant
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Sarcoidosis
[etiology]
- chronic common in 3rd-4th decade of life
- Activation of alveolar macrophage to unknown trigger
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Sarcoidosis
[pathogenesis]
development of multiple, uniform, noncaseating epithelioid granulomas
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Sarcoidosis
[clinical manifestations]
- malaise, fatigue
- wt loss
- fever
- dyspnea of insidious onset
- dry, nonproductive cough
- erythema nodosum
- macules, papules, hyperpigmentation, and subcutaneous nodules
- hepatosplenomegaly, lymphadenopathy
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Sarcoidosis
[diagnosis]
- leukopenia, anemia
- increased eosinophil count, elevated sedimentation rate
- increased Ca levels
- elevated liver enzymes
- anergy
- elevated angiotensin-converting enzyme in active disease
- Gallium 67 scan
- PFTs
- Bronchoalveolar lavage
- transbronchial lung biopsy
- CXR
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Sarcoidosis
[stages 1]
normal
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Sarcoidosis
[stage 1]
- good prognosis
- hilar adenopathy alone
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Sarcoidosis
Stage 2
hilar adenopathy and bilateral pulmonary infiltrates
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Sarcoidosis
stage 3
pulmonary infiltrates w/o adenopathy
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Sarcoidosis
stage 4
- advanced fibrosis w/ evidence of honeycombing,
- dilar retraction, bullae, cysts, and emphysema
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Sarcoidosis
[treatment]
- corticosteroids
- immunosuppressive agents
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Hypersensitivity pneumonitis
[etiology]
- aka extrinsic allergic alveolitis
- restrictive and occupational disease
- predominant in nonsmokers
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Hypersensitivity pneumonitis
[pathogenesis]
- genetic predispose
- agent suggest by pt history
- agent confirmed by precipitating antibodies in serum
- antigen combines with serum antibody in alveolar walls; leads to type III hypersensitivity rxn
- antigen-antibody complexes then elicit granulomatous inflammation leading to lung tissue injury
- must have delayed hypersensitivity (type IV) rxn to antigen to develop pneumonitis
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hypersensitivity pneumonitis
[clinical manifestations]
Acute
- symptoms after 4-6 hrs and resolve in 18-24hrs
- general:chills, sweating, shivering
- myalgias
- nausea
- malaise, lethargy
- headaches
- Respiratory symptoms:
- dyspnea at rest
- dry cough
- tachypnea
- chest discomfort
- physical findings
- cyanosis
- crackles in lung bases
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hypersensitivity pneumonitis
[clinical manifestations]
intermediate
- acute febrile episodes
- progressive pulmonary fibrosis with cough
- dyspnea, fatigue
- cor pulmonale (R sided heart failure due to lung disorders)
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hypersensitivity pneumonitis
[clinical manifestations]
Chronic (hallmark)
progressive, diffuse pulmonary fibrosis in upper lobes
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hypersensitivity pneumonitis
[treatment]
- ID ofeending agent and prevent further exposure
- oral corticosteroids
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Occupational lung diseases
[etiology]
- result from inhalation of toxic gases or foreign particles
- atmospheric pollutants have large effect on occupational respiratory diseases
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Occupational lung diseases
What particles
- pneumoncniosis
- anthracosis
- silicosis
- asbestosis
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occupational lung disease
[predisposing factors]
- preexisting lung disease
- exposure to atmospheric pollutants
- duration of dust exposure
- amt of dust conc.
- particle size of pollutant
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Occupational lung disease
[pathogenesis]
- pollutants interfere and paralyze cilia
- inference with ciliary action
- alveolar macrophages try to engulf and remove
- macrophages secrete lysozymes to control foreign particles activity
- enzymes damage alveolar walls causing deposition of fibrous materials
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occupational lung disease
[clinical manifestations]
- symptoms depend on predisposing factor
- pneumonconiosis produces no signs/symptoms in early stage
- usually symptom free up to 10-20 yrs with chronic exposure
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occupational lung disease
[late clinical features]
- chronic hypoxemia
- cor pulmonale
- respiratory failure
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Occupational lung disease
[treatment
- preventive measures
- corticosteroids
- bronchodilators
- O2 therapy
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ARDS - Acute respiratory distress syndrome
[etiology]
occurs in assoc with other pathophysio processes
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ARDS
[causes]
- severe trauma
- sepsis
- aspiration of gastric acid
- fat emboli syndrome
- shock
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ARDS
[pathogenesis]
- widespread pulmonary inflammation leads to:
- noncardiogenic pulmonary edema assoc with leaky pulmonary capillaries
- atelectasis assoc. with lack of surfactant (decrease surface tension in small alveoli and prevents from collapsing)
- fibrosis(hyaline membranes)
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ARDS
[characteristic abnormalities]
- injury to alveoli fr wide variety of disorders
- changes in alveolar diameter
- injury to pulmonary circulation
- disruptions in O2 transport and utilization
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ARDS
common findings
severe hypoxemia caused by intrapulmonary shunting of blood
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ARDS
[clinical manifestations]
Early and Late
- EArly:
- sudden marked respiratory distress
- slight increase in pulse rate
- dyspnea
- low PaO2
- shallow, rapid breathing
- Late:
- tachycardia
- tachypnea
- hypotension
- marked restlessness
- crackles, rhonchi on auscultation
- use of accessory muscles
- intercostal and sternal retractions cyanosis
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ARDS
hallmark
hypoxemia refractory to increased levels of supplemental O2
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ARDS
[treatments]
- mostly supportive
- ID underlying cause
- maintain fluid and electrolyte balance
- block system inflammatory cells
- adequate oxygenation
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IRDS
infant respiratory distress syndrome
[etiology]
- Hyaline membrane disease
- syndrome of premature neonates
- primary cause: lack of surfactant
- risk factors:
- birth prior to 25 wks gestation
- birth at advanced gestational age
- poorly controleld diabetes in mother
- deliveries after antepartum hemorrhage
- C section w/o antecedent labor
- perinatal asphyxia
- 2nd twin
- previous infant with RDS
- Rh factor incomp.
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IRDS
[clinical manifestations]
- shallow respirations, diminished breath sounds
- intercostal, subcostal, sternal retractions
- flaring of nares
- hypotension, bradycardia
- peripheral edema
- low body temp
- oliguria
- tachypnea
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IRDS
[treatment]
- prevent
- maintain adequate oxygen level
- mechanical ventilation with PEEP or continuous positive airway pressure
- exogenous surfactant adm
- high freq. ventilation
- antibiotics
- supportive therapy
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Pneumothorax
[etiology]
- accumulation of air in the pleural space
- primary cause: also, trauma
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pneumothorax
[pathogenesis]
open 'sucking' chest wall wound
- air enters during inspiration but cannot escape during expiration
- --leads to shift of mediastinum
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Pneumothorax
[clinical manifestations]
- small pneumothoraces usually not detect on physical
- tachycardia
- decreased/abset breath sounds on affected side
- hyperresonance
- sudden chest pain on affected side
- dyspnea
tension and large spontaneous pneumothorax = emergency situations
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Pneumothorax
[treatment]
- management depends on severity of problem and cause of air leak
- lung collapse: may or may not hospitalized/ treat symptomatically
- --chest tube placement with H2O seal and suction
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Pleural effusion
[etiology]
- collection of fluid/pus in pleural cavity as result of another disease process
- 5-15 ml of serous fluid contained in pleural space
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Flail chest
[etiology]
- results from multiple rib fractures r/t trauma to chest wall
- ribs fractured at 2 distant sites
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pneumonia
why and causes
inflammatory rnx in alveoli and interstitium caused by infectious agent
- causes:
- aspiration of oropharyngeal secretions composed of normal bacterial flora/ gastric contents
- inhalation of contaminants
- contamination fr. systemic circulation
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Pneumonia
classifications
- community acquired
- hospital acquired
- bacterial (G(+)) - Staphyl & Strept
- fungal (aspergillus)
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Pneumonia
[clinical manifestations]
- severity of disease and patient age causes variation in symptoms
- crackles and bronchial breath sounds over affected lung tissue
- chills
- fever
- cough, purulent sputum
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Pneumonia
[treatment]
antibiotic therapy
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Pulmonary tuberculosis
[etiology]
- prior infection
- malnourishment, immunosuppression
- living overcrowded condition
- incarcerated persons
- immigrants
- elderly
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Pulmonary tuberculosis
[clinical manifestations]
- history of contact with infected person
- low grade fever
- cough
- night sweats
- fatigue
- wt loss
- malaise
- anorexia
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Pulmonary tuberculosis
[treatment]
- administer multiple drugs (antibiotics) which org is susceptible
- add at least 2 agents to drug regimen when tx failure is suspected
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