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17 Cards in this Set

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Schematic of Pathogenesis of Diffuse ILD
Injury -> Alveolitis -> Cellular and connective tissue response -> repair vs. fibrosis
Some agents of lung injury
Reactive oxygen species
Proteinases, cationic proteins
Immune mechanisms: circulating immune complexes, cellular immunity mediated by cytokines
Direct toxicity: drugs
Arachadonic Acid metabolites
Pathogenesis of interstitial lung disease (alternative)
You have multiple foci of injury that have accumulated over years. You then see a focal fibroblast proliferation. Then, fibroblasts lay collagen. This leads to progression of the disease
Describe lung inflammatory response
Antigen comes in. Macrophages are fixed to the alveolar membrane and they process the antigens. They release chemotactic cytokines that lead to neutrophil recruitment. They all then release agents to impact fibroblasts
What causes a collagen deposition versus resolution?
TH2 responses lead to a humoral response which causes fibroblasts to make collagen

TH1 response involves a cellular response that involves the fibroblasts being turned off so there is resolution

Remember: One good cell

TH1 mediator, IFN gamma is a key
Describe UIP
UIP/IPF- varied histologically from normal to blue and pink stuff. There is some honeycombing. There is spatial and temporal heterogeneity. There are fibroblastic foci (just underneath the epithelial surface).
Describe DIP
accumulations of macrophages within the alveolar space. Less clinically severe
Describe RBILD (respiratory bronchiolitis interstitial lung disease)
Seen only in smokers. Responds well to smoking cessation. Relatively benign
Acute Interstitial Pneumonia (AIP)
This disease has a rapid course over a few weeks from onset to death. See it in acute care facilities. Hyaline membranes can occur (unique). There is a uniform temporal appearance
Nonspecific Interstitial Pneumonia
Uniform appearance.
Prominent interstitial inflammation
Fibrosis is variable and diffuse.
No honeycombing
Common features of ILD
Dyspnea
Cough
Subacute/Insidious onset
Tachypnea
Digital Clubbing
Crackles or Rails
Contrast the clinical features of IIPs
Mean onset for UIPs is older. It has the worst prognosis (5 yr survival)
NSIP has a much better prognosis
DIP has an intermediate prognosis
DIP and NSIP respond to corticosteroids while UIP does not
Physiology of ILDs
Basically a restrictive physiology
-Reduced lung volumes (total lung capacity, residual volume, and functional residual capacity are all reduced in proportion)
-Reduced compliance
-Diffusion impairment
-Hypoxemia (worse with exercis)
What suggests and confirms the restrictive defect in ILD?
Suggestive: reduced vital capacity, normal flows for that volume, and a proportionally normal maximum voluntary ventilation.

Confirmatory: Reduced TLC, compliance, and TLC
Known etilogies of interstitial lung disease
Occupational or environmental- inorganic dusts, organic dusts, gases and fumes

Drugs

Radiation
Unknown etiologies of ILD
This includes most of ILD

Idiopathic pulmonary fibrosis
Sarcoidosis
Collagen-Vascular Diseases (includes lupus and rheumatoid arthritis)
Eosinophilic pneumonias
Wegener's granulomatosis
Therapy of ILDz
Corticosteroids (better for NSIP and DIP)

Azothioprine- cellular immunity

Possibly:
Colchicine, N-acetylcysteine