module 11 restrictive lung disease Flashcards
restrictive PFT
decreased inspiration amount FEV1: gets out less then normal - 2.5L FVC: less out in total - 3.0L FEV1/FVC: 83% - normal
restrictive lung diseases caused by
alterations in
- lung parenchyma
- pleura
- chest wall
- neuromuscular funtion
restrictive lung disease presenting s/s
more effort to expand lungs during inspiration
inc. respiratory rate; rapid, shallow
dec. tidal volume
dyspnea
characteristics of restrictive disorders
dec. vital capacity
dec. total lung capacity
dec. function residual capacity
dec. residual volume
- greater dec. in lung vol. the greater the severity of disease
restrictive disorders ABG
dec. PaO2
normal or dec. PaCO2
inc. pH
overview of restrictive lung disorders
parenchyma - diffuse interstitial lung disease - sarcoidosis - pneumonitis - occupational lung disease atelectatic disorders - ARDS - IRDS infection/inflammatoin plueral space - PTX - effusion neuromuscular disorders chest wall deformities
diffuse interstitial lung disease
restrictive lung disorder also called pulmonary fibrosis 3 pathological patterns - inflammation - fibrosis - destruction Causes thickening of alveolar interstitum
diffuse interstitial lung disease pathogenesis (pulmonary fibrosis)
inj. to alveolar or capillary endothelial cells
- > infiltration of lymphocytes, macrophages, plasma cells
- > obliteration of capillaries, reorganization of lung parenchyma, irreversible fibrosis
- >thickened alveolar wall and interstitium
- > formation of large air filled sacs/cysts and dilated terminal and respiratory bronchioles
diffuse interstitial lung disease s/s
progressive dyspnea irritating non productive cough rapid, shallow breathing clubbing of nail beds bibasilar end-expiratory crackles cyanosis: late anorexia and wt. loss
inflammatory pattern of diffuse interstitial lung disease
triggering event
- occupational, smoking, drugs, CT disease
- > inflammatory response
- > inj. to alveolar capillary basement membrane
- > inc. permeability -> fluids and debris into alveoli
- > fibroblastic proliferation -> deposition of collagen
fibrotic pattern of diffuse interstitial lung disease
inc. mesenchymal and fibroblasts in interstitium
thickened alveolar walls w/ inc. fibrous tissue
-> restriction, dec. compliance, inc. elastic recoil
destruction pattern of diffuse interstitial lung disease
loss of alveolar walls
xray: honeycomb lung
sarcoidosis
acute or chronic systemic disease of unknown cause
immunologic basis
- presence of CD4 T cells
activation of alveolar macrophage to unknown trigger
women in 20-30’s
- 1st degree relative w/ hx inc risk 5x
noncaseating granulomas: fibrotic surrounded by large histiocytes
sarcoidosis pathogenesis
development of multiple, uniform, noncaseating epithelioid granulomas: affect multiple organ systems
Abnormal T cell function
sarcoidosis s/s
malaise fatigue wt loss fever chest discomfort dyspnea dry nonproductive cough erythema nodosum (nodes on lower extremities) macules papules hyperpigmentation subQ nodules hepatosplenomegaly lymphadenopathy iritis uveitis
hypersensitivity pneumonitis
extrinsic allergic alveolitis
restrictive and occupational disease
>300 inhaled organic agents responsible for inflammatory proccess
- genetic predisposition
antigen combines with serum antibody in alveolar walls -> type 3 hypersensitivity reaction -> antigen- antibody complexes -> inflammation and lung tissue injury
leads to diffuse pulmonary fibrosis in upper lobes (hallmark)
hypersensitivity pneumonitis granulomatous inflammation
-> lung tissue injury
- thickening of alveolar walls
- formation of exudate in bronchiolar lumen
- infiltration of lymphocytes, plasma cells, and eosinophils
fibrotic lung changes occur in advanced cases
acute hypersensitivity pneumonitis s/s
4-6 hours after exposure, resolves in 18-24 hours chills sweating myalgia nausea lethargy HA malaise possible fever dyspnea at rest dry cough inc. RR chest discomfort cyanosis (late) crackles in bases
chronic hypersensitivity pneumonitis s/s
progressive diffuse pulmonary fibrosis in upper lobes cough dyspnea fatigue cor pulmonale
pneumoconiosis: occupational lung diseases
parenchymal lung disease caused by inhalation of inorganic dust particles; greater the exposure, the worse the consequence
- anthracosis: coal miners lung/ black lung
- silicosis: silica inhalation
- asbestosis: asbestos inhalation
pneumoconiosis pathogenesis
alveolar macrophages try to engulf and remove particles
macrophages secrete lysozymes to control foreign particle activity
-> damage to alveolar walls causing deposition of fibrous materials
pneumoconiosis s/s
none in early stages physical s/s w/ impaired pulmonary circulation d/t inc. pulm vascular resistance or development of infection - productive cough - dyspnea - progressive fatigue - clubbing of fingers Late - chronic hyposemia - cor pulmonale - respiratory failure