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defined as airways with less than 2 mm in diameter

and no cartilage 

area between the major airways and lung parenchyma and fundamentally

have a centrilobular location.
Due to its structure (no cartilage and small diameter) they are vulnerable to infectious, inhaled, vascular, pharmacological and immunological injury

decreased diffusion (DLCO); reduced FEV1 (in less degree because it

predominantly identifies airflow obstruction in airways with diameter greater than 2 mm); may be mild restriction due to wide spread of affection

the bronchial wall
centrilobular nodules
air trap can be diffuse or mosaic

perfusion
bronchial wall thickening occurs by cellular infiltration and / or fibrosis, and by the extension of both elements to peribronchial tissue.
Centrilobular nodules are consistent with the anatomical localization of the bronchioles; nodule size is variable.
pattern of “tree-in-bud”

– severe life-threatening respiratory failure
In adults – not so

clear clinical presentation, mostly poorly defined; etiology may include Mycoplasma pneumoniae, RSV, measles, influenza, pertussis, parainfluenza, and adenovirus
RVI symptoms may precede the bronchiolitis
Usually self-limiting

ducts to alveoli.
When inflammation leads to extension of inflammatory

cells into the more distal pulmonary parenchyma, the process is called organizing pneumonia (in past COP was called BOOP – bronchiolitis obliterans organizing pneumonia)
Frequent in COP, also in chronic eosinophilic pneumonia, hypersensitivity pneumonitis, idiopathic pulmonary fibrosis and nonspecific interstitial pneumonia.
may be due to exposure to nitrogen dioxide
HCRT - patchy airspace consolidation, “ground-glass” opacity and small nodular opacities in the periphery and in lower lung areas.
responds to glucocorticoids; the specific regimen depends on the clinical changes and the underlying cause

by antigen stimulation
Well-structured lymphoid follicles are located between the bronchioles

and pulmonary arteries and hyperplasia following compress the light of the bronchioles causing obstruction or complete obliteration
is part of the "lymphoproliferative pulmonary diseases" (LPDs) and is associated with connective tissue diseases (rheumatoid arthritis, Sjögren's syndrome), interstitial lung diseases (ILDs), disorders of mixed collagen-vascular, obstructive diseases of airways and states immunodeficiency including HIV and common variable immunodeficiency (CVID) (secondary FB) , also in lymphoproliferative malignant parenchymal lesions (lymphoma MALT, diffuse large B-cell lymphoma)
CT:
small centrilobular nodules associated, sometimes to peribronchiolar nodules and “ground-glass” areas
"tree-in-bud" pattern, representing impaction with secondary bronchiolar exudate material infection or inflammation
peribronchiolar inflammation and formation of peribronchiolar lymphoid follicles may appear as a “tree-in-bud” on HRCT; which is described as "cotton-in-bud“
Treatment - underlying disease (IVIG, Rituximab, azathioprine), someties macrolides

the respiratory bronchioles; intraluminal macrophages are accompanied by a patchy

submucosal and peribronchiolar infiltrate of lymphocytes and histiocytes; peribronchiolar fibrosis extends in a stellate pattern into contiguous alveolar walls
inflammatory profile in normal smokers is very similar to that of patients with chronic obstructive pulmonary disease (COPD), but less prominent.
May lead to subtle functional alterations in young smokers and may precede the development of emphysema in genetically predisposed patients.
HRCT: diffuse or patchy “ground-glass” opacities, fine nodules, and air trapping, predominantly in the upper lobes.

age
Same name as as idiopathic bronchiolocentric interstitial pneumonia or chronic

bronchiolitis with fibrosis
centrilobular and bronchiolocentric inflammatory infiltrate with peribronchiolar fibrosis and an absence of granulomas; prominent epithelial hyperplasia affecting alveolar septa; squamous metaplasia, goblet cell metaplasia and necrosis have been described
May be related to hypersensitivity pneumonitis
clinical picture: chronic nonproductive cough, progressing faster than HP, no specific interstitial pneumonia (NSIP) or RB-ILD, the other diagnoses have a similar presentation.
PFT - obstructive or restrictive patterns
HRCT - combination of “ground-glass” opacities, traction bronchiectasis, and bronchial wall thickening; latter is a result most advanced peribronchiolar fibrosis
Diff with HP - percentage of lymphocytes in the bronchoalveolar lavage (BAL) is less than 40%.
diagnosis is based on lung biopsy.
treatment is not known. Some patients improve with inhaled or systemic glucocorticoids, but the disease progresses generally in at least half of the patients reported, although ACIF has better prognosis than idiopathic pulmonary fibrosis

or middle-aged patients with identifiable risk factors such as gastroesophageal

reflux disease (GERD), drug abuse and dysphagia
cough, sputum production, dyspnea, and fever in patients with a history of recurrent pneumonia that did not respond to antimicrobial therapy were the most common manifestations
Chest CT findings are micro-nodules and opacities “tree-in-bud”.
management of these patients should focus on the prevention of recurrent aspiration and treatment of GERD.

men and rarely reported outside South-East Asia
affects the lower and

upper respiratory tract, leading to progressive evolution bronchiectasis, recurrent infections and generally sinusitis
Histological injury - respiratory bronchioles, transmural infiltrate of lymphocytes, plasma cells and distinctive lipid-laden “foamy” macrophages, with extension to peribronchiolar tissue. In advanced stages, there´s obstruction and constriction of lumen, proliferation of lymphoid follicles and secondary ectasia of terminal bronchioles. The functional pattern is essentially obstructive.
appears to be a genetic predisposition (HLA-B54 is associated with PBD in Japanese while HLA-A11 in Korean)
 H. influenzae and Pseudomonas auroginosa may be present
CT - small nodular shadows to 2 mm in diameter, diffusely scattered in both lungs that can be invisible by hyperinflation of alveoli and the sign of “tree-in-bud”
treatment – erythromycin, roxithromycin and for extended time and at low doses, mainly for its immunomodulatory effect
survival rate at 10 years of PBD is about 90%

spectrum of exposure to drugs, inhalation, or infection and also

to transplantation of the lung and hematopoietic cells (HSCT)
Injury to the bronchial epithelium seems to initiate the process that may involve the alveoli adjacent to the small pathways, excessive proliferation of granulation tissue that causes obstruction or obliteration of the bronchiolar lumen (constrictive bronchiolitis)
dyspnea, non-reversible airflow limitation with bronchodilators, and normal chest x-ray or pulmonary hyperinflation.

flavoring fumes (diacetyl and 2,3-pentanedione), SRV infection, adenovirus, orMycoplasma pneumoniae,

busulfan, gold or penicillamine treatment, and exposure to combustion air wells in the desert in soldiers, have been described as causes
Rheumatoid arthritis and other rheumatic diseases; inflammatory bowel disease.
graft vs host disease (GVHD) in patients undergoing lung transplantation or HSCT - 6% of allogeneic HSCT and in this group of patient’s survival is only 13% to 5 years; typically develops within the first 2 years of transplantation, although it can occur several years later.
calcineurin inhibitors (cyclosporin, tacrolimus and everolimus), inhibitors of purine synthesis (azathioprine or mycophenolate mofetil) and glucocorticoids

and signs do not follow a typical pattern of asthma

or COPD
or if the patient has a predisposing exposure or condition; for example, symptoms of viral infection, exposure to toxic vapors, history of organ transplantation, or concomitant connective tissue disease.
PFT – initially normal or obstructive pattern with gas trapping and no reversibility with inhaled bronchodilators; then – restrictive and decrease of DLCO

with OB and also survival
FAM (fluticasone, azithromycin and montelukast) have

been used for OB post-transplantation.