Medical lung diseases

From Libre Pathology
Revision as of 03:55, 4 August 2011 by Michael (talk | contribs)
Jump to navigation Jump to search

The medical lung diseases are a huge topic. Most pathologists have little to do with 'em. They are the domain of respirology. An introduction to lung pathology is in the lung article, along with a general approach.

Acute infectious pneumonia

This is seen by pathologists in autopsy from time-to-time.

Radiologic correlate

  • Air space disease.

Gross pathology

  • Consolidation (the lung parenchyma is firm) - best appreciated by running a finger over the cut surface of the lung with a small-to-moderate amount of pressure.

Microscopy

Features:

  • Alveoli packed with PMNs.
  • +/-Clusters of bacteria - small dots or rods.

Image: Normal alveoli & pneumonia (WC).

Asthma

General

  • The bread and butter of respirology.
  • Associated with atopy.
  • Mast cells thought to play an important role.

Microscopic

Features:[1]

  • Edema.
  • Mucous (plugs).
  • +/-Smooth muscle hypertrophy.
  • +/-Inflammation - especially with eosinophils.
  • +/-Charcot-Leyden crystals (formed from eosinophil granules -- breakdown product).
    • Sharp edge, diamond shaped, intense pink.

Images:

Notes:

  • Leyden in Charcot-Leyden is also seen written as Leiden.
  • Pulmonary cytopathology: Curschmann's spirals - spiral-shaped mucous plugs.[2]

Emphysema

General

  • Usually due to smoking.
  • May be associated with alpha-1 antitrypsin deficiency.
  • Often lumped together with chronic bronchitis and called chronic obstructive pulmonary disease (COPD).[3]

Pathologic classification

Based on morphology:[4]

  1. Centriacinar (centrilobular) - associated with heavy smoking.
  2. Panacinar (panlobular) - associated with alpha-1 antitrypsin deficiency.
  3. Distal (paraseptal) acinar - associated with spontaneous pneumothorax.
  4. Irregular - usu. insignificant.
  • Q. Why does smoking lead to centriacinar emphysema?
  • A. The bad stuff from smoking gets enters the acinus at the centre; ergo, this is the location of the most damage.

Gross

  • Holes (blebs, bullae), usually upper lung field predominant.
  • Lungs may overlap the heart.[5]

Notes:

  • Bleb = (small) vesicle.[6]
  • Bulla = large vesicle.[7]

Microscopic

Features:[5]

  • Large alveoli.
  • Thin septa (no interstitial thickening).

Image:

Chronic bronchitis

General

  • Often seen together with emphysema with which it is lumped together with in the term COPD.
  • It's a clinical diagnosis - criteria:[8]
    • Cough with sputum for thee months in at least two consecutive years.
    • No other cause identified.

Clinical:[8]

  • Blue bloater (carbon dioxide retainers)
  • Develop cor pulmonale.

Microscopic

Features:[8]

  • Mucous gland hypertrophy + mucinous secretions in airway.
  • Goblet cell metaplasia.
  • Bronchiolar inflammation and fibrosis.

Pulmonary edema

General

  • Seen in a number of conditions, e.g. congestive heart failure.

Microscopic

Features:[9]

  • Dilated capillaries.
  • Blood in airspace.
  • Plasma proteins in airspace - light pink acellular junk.
  • +/-Hemosiderin-laden macrophages (heart failure cells).

Organizing pneumonia

General

  • Multiple causes, e.g. transplant rejection, infection.

Clinical diagnoses:

  • Transplant rejection.
  • Cryptogenic organizing pneumonia (COP).
    • AKA bronchiolitis obliterans organizing pneumonia (BOOP).

Microscopic

Features:[10]

  • Distal airway disease -- airways plugged with organizing exudate.
    • "Organized exudate" = fluffy light-staining paucicellular regions with stellate cells (fibroblasts?).

Obliterative broncholitis

General

  • AKA bronchiolitis obliterans.
  • Not the same as Bronchiolitis obliterans organizing pneumonia (BOOP).

Idiopathic interstitial pneumonia

  • Often abbreviated IIP, is a term used for a type of diffuse lung disease.
    • Diffuse lung disease is also known as interstitial lung disease.
      • Diffuse lung disease is probably a better term... as some diseases lumped into this category have involvement of the alveoli, i.e. are not interstitial.

Histologic classification of IIP

Idiopathic interstitial pneumonia can be subclassified based on histologic appearance into the following patterns:[14][15]

Histology Clinical Correlates Associations
Desquamative interstitial pneumonia (DIP) DIP Smoking
Diffuse alveolar damage (DAD) ARDS, AIP, TRALI ARDS: trauma, infection; TRALI: blood transfusion; AIP: viral (???)
Nonspecific interstitial pneumonia (NSIP) NSIP ???
Respiratory bronchiolitis RB-ILD Smoking
Usual interstitial pneumonia (UIP) CVD, IPF, drug toxicity, pneumoconiosis Allergen (hypersensitivity pneumonitis), idiopathic, autoimmune
Organizing pneumonia Cryptogenic organizing pneumonia autoimmune (???)
Lymphoid interstitial pneumonia (LIP) LIP Viral/autoimmune

ARDS = adult respiratory distress syndrome, AIP = acute interstitial pneumonia, TRALI = transfusion related acute lung injury, CVD = collagen vascular disease, IPF = idiopathic pulmonary fibrosis.


Notes:

  • Usual interstitial pneumonia is the most common type of ILD.[16]

Fibrosis

Histomorphological classification

  1. Hyaline membranes - glassy pink material lining airways & alveoli.
  2. Microscopic honeycombing - "holes" in the lung.
  3. Bronchiolization - ciliated (respiratory) epithelium in distal airway.
  4. Uniform alveolar septal thickening - septae look similar at low power.
  5. Peripheral lobular fibrosis - septae thickening peripheral, HRCT shows: irregular peripheral reticular opacities.[17]
    • Reticular = net-like.[18]
  6. Siderophages in alveoli - macrophages with hemosiderin the alveoli.
  7. Fibrinous pleuritis - peripheral only (based on imaging).
  8. Granulomata, non-necrotizing.
  9. Abundance of vacuolated cells.
  10. Chronic inflammation.
  11. Bronchiolocentric scarring - fibrosis concentrated around airway/assoc. with airway.

Radiologic/gross pathologic DDx by location

Causes of lower lung fibrosis BAD RASH:[19]

  • Brochiolitis obliterans with organizing pneumonia (BOOP).
  • Asbestosis.
  • Drugs (nitrofurantoin, hydralazine, isoniazid (INH), amiodarone).
  • Rheumatologic disease.
  • Aspiration.
  • Scleroderma.
  • Hamman-Rich syndrome (really should be -- interstital pulmonary fibrosis).

Causes of upper lung fibrosis FASSTEN:[20]

  • Farmer's lung.
  • Ankylosing spondylitis.
  • Sarcoidosis.
  • Silicosis.
  • Tuberculosis (miliary).
  • Eosinophilic granuloma.
  • Neurofibromatosis.

Prognosis

  • The pattern and severity of fibrosis seems to be the most important factors prognostically - more important than the underlying cause (ILD, CVD, drug reaction etc.).[21][22]

Patterns of fibrosis:

  • "Linear" - follows alveolar walls, no architectural distortion.
  • UIP-like (honeycombing).

Disease with fibrosis

There are many of 'em.

Diffuse alveolar damage

General

  • Abbreviated DAD.

DAD is the histologic correlate of:

  • Adult respiratory distress syndrome (ARDS).
  • Acute interstitial pneumonia (AIP).
  • Transfusion related acute lung injury (TRALI).

Microscopic

Features:[23]

  • Early:
    • Hyaline membrane: debris (pink crap) lines the alveolar spaces.
  • Intermediate:
    • Macrophage proliferation.
  • Late:
    • Interstitial inflammation.
    • Fibrosis.

Image: Diffuse alveolar damage (WC).

Usual interstitial pneumonia

General

  • It is sometimes used incorrectly as a synoym for idiopathic pulmonary fibrosis.
  • Cannot be diagnosed via bronchoscopic or transbronchial biopsy.[24]

Epidemiology

  • Disease of the old - rare in under 50 years old.[25]
  • Dismal prognosis - mean survival after diagnosis ~ 2.8 years.[21]

Differential diagnosis

UIP is seen in:[26]

  • Idiopathic pulmonary fibrosis.
  • Asbestosis - one ought to see ferruginous bodies.
  • Chronic hypersensitivity pneumonitis (extrinsic allergic alveolitis).
  • Collagen vascular disease.
  • Chronic drug toxicity.[27]

Radiologic

  • Honeycombing - multiple defects that obliterate the normal lung architecture - multiple spherical voids in the lung parenchyma; radiologically these are seen as lucencies.[28]
    • Usually subplural, i.e. peripheral lung.
    • Classically lower lobe predominant.
    • Associated with interstitial thickening. (???)

Note:

  • Cysts - have thin walls (think of emphysema, lymphangioleiomyomatosis et cetera).
    • Cysts may be isolated/not close to a neighbour.
    • Medcyclopaedia defines it as: thin-walled, well-demarcated and >1 cm.[29]

Histology

Features:[30]

  • Fibroblast foci:
    • "Crescent-shaped bulge" of fibroblasts -- a rounded projection of spindle cells into the airspace.
    • Location: in the areas of transisition between active inflammation and old inflammation.[31]
    • Note: Technically, fibroblast foci are composed of myofibroblasts.[32]
  • Interstitial inflammation,
  • Microscopic honeycombing,
    • Typically peripheral - cysts lined by ciliated epithelium.
  • Spatial heterogeneity - patchy lesional distribution (areas of abnormal and normal lung may appear beside one another).
  • Temporal heterogeneity - lesions of differing age side-by-side.[33]

Notes:

  • Disease worse distant from large airways: lower lung field predominance, typically worse at periphery of lobule and lung.[34]
  • Heterogeneity of inflammation: airspace macrophages & inflammation minimal in honeycombed foci.

Asbestosis

General

  • Important to diagnose... asbestosis = compensation.

Microscopic

  • Histologic appearance as for UIP -- plus ferruginous bodies.
    • Segmented twirling batton with long slender fibre within.

Image(s):

Non-specific interstitial pneumonia

  • Abbreviated NSIP.
  • Better prognosis than UIP.
  • Some radiologists and pathologists don't believe in this entity.

Gross/Radiology

  • No honeycombing.
  • Fibrosis usually lower lung zone.
  • Patchy ground glass.

Microscopic

  • Fibrosis:
    • May be uniform.
    • "Linear fibrosis" has a good prognosis - should be mentioned in the report.
      • Linear fibrosis = fibrosis that follows alveolar walls + no architectural distortion.
  • +/-Lymphoid nodules - assoc. with collagen vascular disease.

Notes:

  • Like UIP... also temporally and spatially heterogeneous.
  • Inflammation in NSIP usually more prominent than in UIP.
  • No honeycombing - key difference between UIP and NSIP.

DDx

  • Collagen vascular disease.
  • Drug reaction.
  • Hypersensitivity pneumonitis (extrinic allergic alveolitis).

Hypersensitivity pneumonitis

  • AKA extrinsic allergic alveolitis
  • Exposure to stuffs... e.g. moldy hay - Farmer's lung, atypical mycobacteria - hot tub lung.
  • Upper lung predominant disease (???).

Microscopic

Features:

  • Lesions have centrilobular prominence - important feature. [35]
    • Allergens enter lung through airway which has a centrilobular location.
  • Granulomata (not typically seen in UIP) - important feature.[35]
  • Chronic interstitial inflammation consisting primarily of lymphocytes.
  • Interstitial fibrosis.
  • Air space involvement (alveolitis).

Images:

Lymphocytic lesions of the lung

Diagnosis Key histologic feature Radiology Other diagnostic
Lymphocytic interstitial pneumonia interstitial lymphoid cells, usu. no nodules interstitial pattern
Follicular bronchiolitis/bronchitis lymphoid cell around bronchioles / bronchus, normal parenchyma interstitial pattern
Nodular lymphoid hyperplasia abundant lymphoid cells in nodules nodules /interstitial pattern stains to exclude lymphoma; germinal centres do not exclude lymphoma
Lymphoma (BALToma) abundant lymphoid cells usu. in nodules nodules / interstitial pattern may require stains to prove, germinal centres may be present

Lymphocytic interstitial pneumonia

General

Gross

  • Location: basilar predominance.
  • Increased interstitial markings.

Microscopic

Features:[38]

  • Small mature lymphocytes (usually B cells).[39]
  • Plasma cells.
  • +/-Lymphoid follicles.

Negatives:

  • No Vasculitis.
  • No necrosis.

Image: LIP (scielo.br).

DDx:

  • Lymphoma.
  • Follicular bronchitis/bronchiolitis.
  • Nodular lymphoid hyperplasia.
    • This is determined in part by radiology; it has nodules radiographically.

Follicular bronchitis/bronchiolitis

General

Gross/radiology

  • No distinct nodule or mass.
  • Classically: increased reticular marking, i.e. interstitial pattern.

Images: Intersitial pattern - radiographs (ucsf.edu).

Microscopic

Features:[42]

  • Peribronchiolar/peribronchial lymphoid nodules with:
    • Reactive germinal centres.
      • Lack of these should raise suspicion for lymphoma.
    • Plasma cells.
  • +/-Lymphoid nodules in the interlobular septa.

Notes:

  • Lung parenchyma distant from nodule = normal; no lymphocytic infiltrate.

DDx:

Nodular lymphoid hyperplasia

General

  • AKA pseudolymphoma - a term some dislike.[42]
  • Definition - reactive lymphoid cells.

Gross/radiology

  • Has nodules radiographically.

Microscopic

Features:[42]

  • Reactive lymphoid nodules.

Notes:[43]

  • Presence of germinal centres do not exclude lymphoma - may still be a BALToma.
    • BALT = bronchial/bronchus associated lymphoid tissue.

DDx:

Smoking associated disease

Main article: Smoking
  • RB = respiratory bronchiolitis.
  • RBILD = respiratory bronchiolitis interstitial lung disease.
  • DIP = desquamative interstitial pneumonia.
  • Eosinophilic granuloma (of lung) - AKA pulmonary langerhans cell histiocytosis.

All of the above are assoc. with smoking. RBILD & DIP are considered by many to be on a continuum, i.e. RBILD is early DIP.

Respiratory bronchiolitis

  • Diagnosis is based on clinical criteria.

Microscopic

Features:

  • Inflammation.
  • No interstitial lung disease, i.e. no fibrosis.

Respiratory bronchiolitis interstitial lung disease

  • Abbreviated RBILD.

General

  • May be an early version of DIP.

Microscopic

Features:[44]

  • Brown pigmented airspace macrophages - smoker's macrophages.
  • Inflammation of the terminal bronchioles.

Note:

  • The histologic features of RBILD may be present peri-tumoural.

Desquamative interstitial pneumonia

  • Abbreviated DIP.

General

  • Thought to be advanced RBILD.

Microscopic

Features:

  • Brown pigmented airspace macrophages - smoker's macrophages.
  • Architecture preserved; "linear fibrosis".

Notes:

  • Some fields of view may be indistinguishable from RBILD.
  • Amiodarone toxicity, fibrotic NSIP - may appear similar.

Pulmonary Langerhans cell histiocytosis

  • AKA eosinophilic granuloma of lung.

General

Subtypes:[45]

  • Cellular form.
  • Fibrotic form.

One form usually predominates.

Radiology

  • Upper lung zones.

Microscopic

Features:[46]

  • Cellular peribronchiolar nodules with:
    • Langerhans cells - key feature:
      • Pale staining nucleus (H&E) with nuclear infolding - "crumpled tissue paper" appearance.
    • +/-Smoker's macrophages (brown pigmented airspace macrophages).
    • +/-Eosinophilia (may be rare) - significantly narrow DDx.
    • Chronic inflammatory cells (lymphocytes). (???)

IHC

  • Langerhans cells: S100+ and CD1a+.[46]

Granulomatous lung disease

See: Granulomas for an introduction to the general topic.

Most common:

  • Infectious - mycobacterial and fungal.[47]

Noninfectious causes:[47]

  • Aspiration pneumonia.
  • Hypersensitivity pneumonitis.
  • Hot tub lung.
  • Talc granulomatosis.
  • Sarcoidosis.
  • Wegener granulomatosis.

Sarcoidosis

Main article: Sarcoidosis

General

  • Diagnosis of exclusion - infection must be excluded.
  • Radiologic differential diagnosis includes carcinomatosis.[48]

Microscopic

Features:

  • Granulomata, well-formed, non-necrotizing.
    • Negative for microorganisms with special stains (PAS-D, GMS, AFB).
    • Granulomata - interstitial location.

Image(s):

Pulmonary talcosis

General

  • Associated with herion use.[49]
  • X-ray findings similar to asbestosis.

Microscopic

Features:

  • Granulomas with foreign material.
    • Foreign material often polarizes.

Images:

Miscellaneous diseases

Pneumocytoma

General

  • Previously known as sclerosing hemangioma.
  • AKA sclerosing hemangioma.
  • Derived from type 2 pneumocyte.[50]
  • Progesterone-receptor positive stromal cells.[51]

Epidemiology

  • Female in 40s.[52]
  • Considered benign; excision is curative.
    • Rare case reports of metastases.

Gross

  • Peripheral, solitary.
  • Well-circumscribed.

Microscopy

Features:[52]

  • Mixed cell population.
  • Variable architecture:
    • Papillary.
    • Sclerotic.
    • Solid.
    • Hemorrhagic.
  • +/-Granulomas.

DDx:[53]

  • Papillary adenoma.
  • Neuroendocrine tumour (carcinoid).

IHC

Features:[50]

  • TTF-1 +ve.
  • HNF-3 alpha +ve.
  • HNF-3 beta +ve.

Lymphangioleiomyomatosis

  • Abbreviated LAM.
  • AKA lymphangiomyomatosis.

General

  • Clinical: dyspnea, recurrent pneumothorax.
  • May be an indication for lung transplantation.
  • Non-neoplastic muscle proliferation vs. tumour that can metastasize.[54]

Notes:

Epidemiology

Radiology

  • Bullae/thin walled cysts - distributed in all lung fields.
  • Lymphadenopathy.

Radiologic DDx (of cysts):

  • Eosinophilic granuloma (assoc. with smoking).
  • Interstitial pulmonary fibrosis (UIP).
  • Emphysema.

Microscopic

Features:[57]

  • Spindle cells with small nuclei + larger epithelioid cells with clear cytoplasm and round nuclei.
  • Cyst formation.
  • Thick arterial walls.

Images:

IHC

  • HMB-45 +ve.
  • ER +ve.
  • PR +ve.
  • SMA +ve.

Pulmonary alveolar proteinosis

  • Abbreviated PAP.

General

  • Associated with smoking - particularily in men.[58]

Pathophysiology:

  • GM-CSF (granulocyte-macrophage colony stimulating factor) signaling in macrophages/lack of GM-CSF.
    • GM-CSF is required by alveolar macrophages to clear surfactant.

Classification:[58]

  1. Congenital:
      • Abnormal surfactant.
      • GM-CSF receptor defect.
  2. Secondary:
    • Infections.
    • Haematologic malignancy.
  3. Acquired:
    • Dusts - interfere with macrophage function.

Clinical:

  • Dyspnea & cough - gradual onset.

Radiology

Microscopic

Features:

  • Crap in the alveoli:
  • "Dense bodies" - dead macrophages ("Chatter" in the alveoli).
    • Edema - has pink stuff in the alveoli like PAP but no dense bodies.

DDx - may mimic:[59]

  • Edema.
  • Pneumocystis - exudates foamy & vacuolated.
  • Pulmonary hemorrhage (acute). (???)

Images:

Images of DDx:

Drug reactions

  • Effects are often non-specific.

Website: http://www.pneumotox.com

Pulmonary hypertension

Main article: Pulmonary hypertension

General classification:

  • Primary, i.e. primary pulmonary hypertension, or
  • Secondary, e.g. due to congenital heart disease (like ventricular septal defect), interstitial pulmonary fibrosis.

Non-secondary pulmonary hypertension

Main article: Pulmonary hypertension

Causes:[61]

  • Primary pulmonary hypertension.
  • Pulmonary embolic disease (thromboembolism, and non-thrombotic embolism).
  • Pulmonary capillary haemangiomatosis (PCH).
  • Pulmonary veno-occlusive disease (PVOD).

Severity

Eosinophilic pneumonia

Specific entities:[62]

  • Churg-Strauss syndrome.
  • Acute eosinophilic pneumonia.
  • Chronic eosinophilic pneumonia.
  • Eosinophilic granuloma (pulmonary histiocytosis X, Langerhans cell granulomatosis).

Entities which may have eosinophilia as prominent feature:

  • AIDS.
  • Lymphoma.
  • Collagen vascular disease.

Churg-Strauss syndrome

Main article: Churg-Strauss syndrome

Microscopic

Features:

Lung transplant pathology

Main article: Lung transplant pathology

This subspecialty is dealt with in its own article.

See also

References

  1. ↑ Klatt, Edward C. (2006). Robbins and Cotran Atlas of Pathology (1st ed.). Saunders. pp. 108. ISBN 978-1416002741.
  2. ↑ Cenci M, Giovagnoli MR, Alderisio M, Vecchione A (November 1998). "Curschmann's spirals in sputum of subjects exposed daily to urban environmental pollution". Diagn. Cytopathol. 19 (5): 349–51. PMID 9812228.
  3. ↑ Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 368. ISBN 978-1416054542.
  4. ↑ Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 368. ISBN 978-1416054542.
  5. ↑ 5.0 5.1 Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 369. ISBN 978-1416054542.
  6. ↑ URL: http://dictionary.reference.com/browse/bleb. Accessed on: 3 August 2011.
  7. ↑ URL: http://dictionary.reference.com/browse/bulla. Accessed on: 3 August 2011.
  8. ↑ 8.0 8.1 8.2 Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 370. ISBN 978-1416054542.
  9. ↑ Klatt, Edward C. (2006). Robbins and Cotran Atlas of Pathology (1st ed.). Saunders. pp. 102. ISBN 978-1416002741.
  10. ↑ Klatt, Edward C. (2006). Robbins and Cotran Atlas of Pathology (1st ed.). Saunders. pp. 110. ISBN 978-1416002741.
  11. ↑ Nicholson AG (November 2002). "Classification of idiopathic interstitial pneumonias: making sense of the alphabet soup". Histopathology 41 (5): 381-91. PMID 12405906. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0309-0167&date=2002&volume=41&issue=5&spage=381.
  12. ↑ Flaherty KR, King TE, Raghu G, et al (October 2004). "Idiopathic interstitial pneumonia: what is the effect of a multidisciplinary approach to diagnosis?". Am. J. Respir. Crit. Care Med. 170 (8): 904-10. doi:10.1164/rccm.200402-147OC. PMID 15256390. http://ajrccm.atsjournals.org/cgi/pmidlookup?view=long&pmid=15256390.
  13. ↑ Kim DS, Collard HR, King TE (June 2006). "Classification and natural history of the idiopathic interstitial pneumonias". Proc Am Thorac Soc 3 (4): 285-92. doi:10.1513/pats.200601-005TK. PMID 16738191. http://pats.atsjournals.org/cgi/pmidlookup?view=long&pmid=16738191.
  14. ↑ Leslie KO, Wick MR. Practical Pulmonary Pathology: A Diagnostic Approach. Elsevier Inc. 2005. ISBN 978-0-443-06631-3.
  15. ↑ "American Thoracic Society/European Respiratory Society International Multidisciplinary Consensus Classification of the Idiopathic Interstitial Pneumonias. This joint statement of the American Thoracic Society (ATS), and the European Respiratory Society (ERS) was adopted by the ATS board of directors, June 2001 and by the ERS Executive Committee, June 2001". Am. J. Respir. Crit. Care Med. 165 (2): 277-304. January 2002. PMID 11790668. http://ajrccm.atsjournals.org/cgi/pmidlookup?view=long&pmid=11790668.
  16. ↑ Visscher DW, Myers JL (June 2006). "Histologic spectrum of idiopathic interstitial pneumonias". Proc Am Thorac Soc 3 (4): 322-9. doi:10.1513/pats.200602-019TK. PMID 16738196. http://pats.atsjournals.org/cgi/pmidlookup?view=long&pmid=16738196.
  17. ↑ http://www.rsna.org/Publications/rsnanews/may06/jrnl_may06.cfm
  18. ↑ http://dictionary.reference.com/browse/reticular
  19. ↑ TN05 R13.
  20. ↑ TN05 R13.
  21. ↑ 21.0 21.1 Bjoraker JA, Ryu JH, Edwin MK, et al. (January 1998). "Prognostic significance of histopathologic subsets in idiopathic pulmonary fibrosis". Am. J. Respir. Crit. Care Med. 157 (1): 199-203. PMID 9445300. http://ajrccm.atsjournals.org/cgi/content/full/157/1/199.
  22. ↑ AC UBC S.425.
  23. ↑ Klatt, Edward C. (2006). Robbins and Cotran Atlas of Pathology (1st ed.). Saunders. pp. 103. ISBN 978-1416002741.
  24. ↑ Leslie, Kevin O.; Wick, Mark R. (2004). Practical Pulmonary Pathology: A Diagnostic Approach (1st ed.). Churchill Livingstone. pp. 186. ISBN 978-0443066313.
  25. ↑ AC UBC S.102.
  26. ↑ Wick, Mark R.; Leslie, Kevin (2005). Practical pulmonary pathology: a diagnostic approach. Edinburgh: Churchill Livingstone. ISBN 0-443-06631-0. OCLC 156861539.
  27. ↑ Rossi SE, Erasmus JJ, McAdams HP, Sporn TA, Goodman PC (2000). "Pulmonary drug toxicity: radiologic and pathologic manifestations". Radiographics : a review publication of the Radiological Society of North America, Inc 20 (5): 1245-59. PMID 10992015.
  28. ↑ http://www.medcyclopaedia.com/library/topics/volume_v_1/h/honeycombing.aspx
  29. ↑ http://www.medcyclopaedia.com/library/topics/volume_v_1/l/lung_cyst.aspx
  30. ↑ Leslie, Kevin O.; Wick, Mark R. (2004). Practical Pulmonary Pathology: A Diagnostic Approach (1st ed.). Churchill Livingstone. pp. 186-9. ISBN 978-0443066313.
  31. ↑ http://www.epler.com/IPFWhat%27sIPFDiseaseInformation2.htm
  32. ↑ Leslie, Kevin O.; Wick, Mark R. (2004). Practical Pulmonary Pathology: A Diagnostic Approach (1st ed.). Churchill Livingstone. pp. 189. ISBN 978-0443066313.
  33. ↑ H. 8 July, 2009.
  34. ↑ AC UBC S.103.
  35. ↑ 35.0 35.1 PMID 16061708.
  36. ↑ URL: http://emedicine.medscape.com/article/299643-overview. Accessed on: 2 June 2010.
  37. ↑ 37.0 37.1 Nicholson AG (August 2001). "Lymphocytic interstitial pneumonia and other lymphoproliferative disorders in the lung". Semin Respir Crit Care Med 22 (4): 409–22. doi:10.1055/s-2001-17384. PMID 16088689.
  38. ↑ URL: http://emedicine.medscape.com/article/299643-diagnosis. Accessed on: 2 June 2010.
  39. ↑ AFIP atlas of nontumour pathology. 2002. Vo. 2. P.265. ISBN 1-881041-79-4.
  40. ↑ Aerni MR, Vassallo R, Myers JL, Lindell RM, Ryu JH (February 2008). "Follicular bronchiolitis in surgical lung biopsies: clinical implications in 12 patients". Respir Med 102 (2): 307–12. doi:10.1016/j.rmed.2007.07.032. PMID 17997299.
  41. ↑ Kinane BT, Mansell AL, Zwerdling RG, Lapey A, Shannon DC (October 1993). "Follicular bronchitis in the pediatric population". Chest 104 (4): 1183–6. PMID 8404188.
  42. ↑ 42.0 42.1 42.2 AFIP atlas of nontumour pathology. 2002. Vo. 2. P.277. ISBN 1-881041-79-4.
  43. ↑ AFIP atlas of nontumour pathology. 2002. Vo. 2. P.281. ISBN 1-881041-79-4.
  44. ↑ Leslie, Kevin O.; Wick, Mark R. (2004). Practical Pulmonary Pathology: A Diagnostic Approach (1st ed.). Churchill Livingstone. pp. 197-8. ISBN 978-0443066313.
  45. ↑ 45.0 45.1 Leslie, Kevin O.; Wick, Mark R. (2004). Practical Pulmonary Pathology: A Diagnostic Approach (1st ed.). Churchill Livingstone. pp. 234. ISBN 978-0443066313.
  46. ↑ 46.0 46.1 Leslie, Kevin O.; Wick, Mark R. (2004). Practical Pulmonary Pathology: A Diagnostic Approach (1st ed.). Churchill Livingstone. pp. 237. ISBN 978-0443066313.
  47. ↑ 47.0 47.1 Mukhopadhyay S, Gal AA (May 2010). "Granulomatous lung disease: an approach to the differential diagnosis". Arch. Pathol. Lab. Med. 134 (5): 667–90. PMID 20441499.
  48. ↑ URL: http://www.radiologyassistant.nl/en/46b480a6e4bdc. Accessed on: 23 May 2010.
  49. ↑ Davis, LL. (Dec 1983). "Pulmonary "mainline" granulomatosis: talcosis secondary to intravenous heroin abuse with characteristic x-ray findings of asbestosis.". J Natl Med Assoc 75 (12): 1225–8. PMC 2561715. PMID 6655726. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2561715/.
  50. ↑ 50.0 50.1 Yamazaki, K. (Jul 2004). "Type-II pneumocyte differentiation in pulmonary sclerosing hemangioma: ultrastructural differentiation and immunohistochemical distribution of lineage-specific transcription factors (TTF-1, HNF-3 alpha, and HNF-3 beta) and surfactant proteins.". Virchows Arch 445 (1): 45-53. doi:10.1007/s00428-004-1023-3. PMID 15138814.
  51. ↑ Einsfelder, BM.; Müller, KM. (Sep 2005). "["Pneumocytoma" or "sclerosing hemangioma": histogenetic aspects of a rare tumor of the lung]". Pathologe 26 (5): 367-77. doi:10.1007/s00292-005-0751-8. PMID 15731902.
  52. ↑ 52.0 52.1 Keylock, JB.; Galvin, JR.; Franks, TJ. (May 2009). "Sclerosing hemangioma of the lung.". Arch Pathol Lab Med 133 (5): 820-5. PMID 19415961.
  53. ↑ URL: http://www.med.muni.cz/biomedjournal/pdf/2004/01/37_42.pdf. Accessed on: 17 June 2010.
  54. ↑ Taveira-DaSilva, AM.; Pacheco-Rodriguez, G.; Moss, J. (Mar 2010). "The natural history of lymphangioleiomyomatosis: markers of severity, rate of progression and prognosis.". Lymphat Res Biol 8 (1): 9-19. doi:10.1089/lrb.2009.0024. PMID 20235883.
  55. ↑ 55.0 55.1 http://emedicine.medscape.com/article/299545-overview
  56. ↑ Schiavina, M.; Di Scioscio, V.; Contini, P.; Cavazza, A.; Fabiani, A.; Barberis, M.; Bini, A.; Altimari, A. et al. (Jul 2007). "Pulmonary lymphangioleiomyomatosis in a karyotypically normal man without tuberous sclerosis complex.". Am J Respir Crit Care Med 176 (1): 96-8. doi:10.1164/rccm.200610-1408CR. PMID 17431222.
  57. ↑ http://emedicine.medscape.com/article/299545-diagnosis
  58. ↑ 58.0 58.1 Trapnell BC, Whitsett JA, Nakata K (December 2003). "Pulmonary alveolar proteinosis". N. Engl. J. Med. 349 (26): 2527-39. doi:10.1056/NEJMra023226. PMID 14695413. http://content.nejm.org/cgi/content/extract/349/26/2527.
  59. ↑ Leslie, Kevin O.; Wick, Mark R. (2004). Practical Pulmonary Pathology: A Diagnostic Approach (1st ed.). Churchill Livingstone. pp. 248. ISBN 978-0443066313.
  60. ↑ Leslie KO (May 2009). "My approach to interstitial lung disease using clinical, radiological and histopathological patterns". J. Clin. Pathol. 62 (5): 387–401. doi:10.1136/jcp.2008.059782. PMC 2668105. PMID 19398592. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2668105/.
  61. ↑ Bush A (December 2000). "Pulmonary hypertensive diseases". Paediatr Respir Rev 1 (4): 361-7. doi:10.1053/prrv.2000.0077. PMID 16263465.
  62. ↑ http://emedicine.medscape.com/article/301070-overview

External links

Retrieved from "https://librepathology.org/w/index.php?title=Medical_lung_diseases&oldid=6308"