Pathology Associates Of Lexington, P.A.
Pathology Associates Of Lexington, P.A.
Pathology Associates Of Lexington, P.A.
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Lung Pathology
Medical:
  • infectious:
  • noninfectious:
    1. BOOP: bronchiolitis obliterans with organizing pneumonia (BOOP) is inflammation of the small airways (bronchioles) and surrounding tissue in the lung. It can affect a small segment of the lung or the entire lung. It can be idiopathic or secondary, related to a historical insult but is not primarily infectious; spaces contain pale, "juicy" fibroplastic polyps or foci [L07-8086]; in 9/07, it was thought that the buttery-flavor, diacetyl, caused "popcorn lung" in microwave popcorn workers & the histology of that is BOOP.
    2. UIP: interstitial fibrosis that is negative for other clues to other entities.
    3. DIP: interstitial fibrosis associated with alveolar filling by pneumocytes.
    4. LIP: interstitial fibrosis Associated with a prominent lymphocytic infiltrate.
    5. tissue eosinophilia on biopsy: asthma, ABPA, eosinophilic pneumonia, other allergic.
    6. collagen vascular disease associtated interstitial fibrosis: broncho-alveolar lavage...BAL...may show eosinophilia.
    7. idiopathic pulmonary fibrosis.
    8. granulomatous: sarcoid (epithelioid), rheumatoid (palisaded).
  • chronic cough causes.
  • infections: CMV nuclear inclusions; AFB or fungal granulomatous (polys...caseation); polys (think bacterial...but there are some non-infectious causes of polys).
  • diffuse alveolar damage (DAD): alveolar spaces lined with fibrin & may see reactive, quite atypical pneumocytes.
    1. inspired agents etiology: toxic...infectious.
    2. shock lung: shock lung without or with transfusion of blood bank products (transfusion associated lung injury...TRALI [newe acute lung injury within 6 hours of a transfusion]). TRALI5 has an incidence of 1:5000 transfusions. DDX is SOB due to fluid overlod (diuretic Rx) vs.TRALI (maybe best to not give diuretic) and has about two proposed mechanisms as of the end of 2007:
      • the antibody payhway: an uncertain anti-leukocyte (anti-WBC; anti-neutrophil) antibody in donor unit binds to an antigen site on the recipient WBCs to start a detrimental, damaging immunological TRALI cascade. Multiparous women tend to carry the highest incidence of these antibodies.
      • the two hit pathway: (1) biological response modifiers...such as cellular or molecular breakdown products or cytokines...in donor blood then (2) get transfused into a recipient whose WBCs are primed or activated (maybe by sepsis) an d the interaction trtiggers TRALI.
  • pulmonary hypertension: [Pulm. Hyperten. Assn.] [Heath-Edwards pulmonary hypertension vasculopathy grades].
  • Post obstructive pulmonary edema syndrome (POPE): induced by inspiration against a closed glottis (negative pressure pulmonary edema), as in drowning or post-extubation (or other events triggering bronchospasm), and can be a cause of minor problems to nearly sudden death.
  • benign nodules:
    • fungal nodules
    • acid fast organism nodules:
    • granulomata without organisms: sarcoid, pneumoconiosis, BCGosis (MERosis)3[T07-183; L07-8188].
  • pulmonary calcification:
    1. metastatic deposits: in general alveolar parenchyma & rarely just bronchial basement membrane zone & subepithelial fibrous stroma (renal failure and/or other chronically hypercalcemic situations).
    2. metaplastic bone: tends to occur in lung having any kind of fibrotic process2.
      • diffuse pulmonary ossification (DPO): innumerable branching linear delicate ossifications felt as gritty, thread-like, stiff-hairbrush-like texture on cut surface [L06-3321; L07-7191] & not broncocentric.
      • tracheobronchopathia osteoplastica: sometimes bronchoscopically visible boney accumulations in bronchial subepithelial stroma.
    3. diffuse bronchial tree cartilagenous calcification: a phenomenon of advancing age.
  • Tumor:
    • lung cancer risk prediction tool @ MSKCC.
    • TTF-1 labels lung adenoca. (but not lung SCC)...primary vs. met. & small-cell NEC.
    • adenoca. vs. mesothelioma [here].
    • benign:
    • uncertain biological potential:
      • Langerhans histiocytosis: S100 pos. monocytoid cells with grooved nuclei [L05-3425].
      • atypical carcinoid: NET too big or too atypical for simple carcinoid
      • atypical adenomatous hyperplasia (AAH...1999): most lesions found incidentally; bronchoalveolar carcinoma like proliferation w/ orderly, amitotic cytohistology...nucleoli often prominent...along alveolar walls (lepidic growth); lesion 5mm or less in size & no papillary or tufting cellularity1,9.
    • malignant: clinicians want to know...
      • primary vs. met.:
        • size pT stage: T2 (>3cm; involves main bronchus =/> 2cm distal to carina; visceral pleural invasion) or higher and/or lymphovascular invasion may need adjuvant treatment.
        • number of nodules pT stage:
          • synchronous double or triple primaries (vs. intrapulmonary mets) ...synchronous primaries may have an incidence as high as 6%10 but a Chinese study11 of 4649 lung cancer cases from 1983-2004 only found 31 cases ...0.6% & cited 3 other studies suggesting between 1 & 3%). Non-BAC & defined(after 11):
            • simutaneous disconnected lesions; and,
            • H&E histology is different...or, if same/similar,
            • if the same by H&E, they are "different" IF:
              • absent special studies, they are in different lobes AND without N2, N3, or M1 status.
              • or if each has some original residual CIS
              • and no cancer in lymphatics common to both (no N1 or N2).
              • no extra-pulmonary mets at time of DX.
              • both should be no worse than stage I.
              • special studies show a clear difference: such as IHC (p53 [our T08-54]), research DNA, EM, ploidy or DNA index differences (if both aneuploid).
          • intrapulmonary satellite nodules in same lobe as primary are pT4 M0 and in another lobe are pT4 M1. Hence, the vital importance of distinguishing mets vs. synchronous [L08-3588].
        • pleura pT stage:
          • pre-op images seem to indicate malignant pleural adhesion, over 50% of the time this is wrong.
          • histology assessment:
            • pT1 vs. pT2: membrane invasion by direct extension (thru the visceral peripulmonary erlastic layers4,8 ) makes pT24,7,8.
            • pT3: adhesed visceral-parietal & direct-extension penetration into parietal of chest, pericardium or mediastinum7.
            • cancer out into or onto pleural surface:
              • intra-pleural skip foci beyond direct extension = pT47.
              • through & out on the free pleural surface implys the set-up for an incipient [T08-54] malignant effusion (pT4) ...but is it the same (6th ed. AJCC has a "clinical" malignant effusion as T4)? AJCC 6th not clear on this for chest7 but is pT4 for colon cancer in abdomen. But, the pleura can be pulled down into the tumor and invasively penetrated (pT2) & sealed off down in this interior space with no call for adjuvant radiation[LMC-07-3392] but may, therefore , call for chemotherapy
      • FS eval. node status: whether any positive nodes (no resection if mediastinal pos.).
      • FS eval. of margins: resect more only if marginal tissue is positive (not if lymphovascular positive only1,9).
      • type of lung malignancy: even when showing malignancy, tiny specimens limit important parameters in classification and therapy choices...
        • bronchioalveolar carcinoma (BAC): neoplastic cells along alveolar walls in lepidic growth pattern & no invasion; mucinous BAC does not respond to tyrosine kinase inhibitors6. Adenocarcinomas with at least 50% lepidic pattern and invasive foci never larger than 5mm do not go to nodes9.
        • small cell neuroendocrine carcinoma: neuroendocrine nuclei with IHC neuroendocrine positivity & malignant features such as elevated Ki67. There are controversies as to carcinoid terminology once proliferation is increased [L08-5641]...even to the point of an occassional lawsuit being filed [].
        • small cell non-neuroendocrine carcinoma: nuclei not neuroendocrine & IHC favoring either adenoca. or SCC [here].
        • non-small cell carcinoma:
          • adenocarcinoma (responds to tyrosine kinase inhibitors6).
            • NOS
            • with BAC features: if at least 50% of tumor has lepidic growth and invasive foci less than 5mm, highly associated with absence of node mets1,9.
            • papillary: has fibrovascular cores.
            • invasive micropapillary6: negative for fibrovascular cores; bad!
          • squamous cell carcinoma: SCC is K903 positive (not responsive to tyrosine kinase inhibitors6); if bronchogenic & (1) pure SCC or (2) NSCLC with dominant % SCC component, avoid anti-endothelial chemo (e.g., Avastin) because of risk of fatal pulmonary bleed6.
          • large cell carcinoma
        • mesothelioma: [IHC]
        • sarcoma
        • lymphoma

    References:
    1. BWD's shared notes April 2007, highlights from USCAP 2006 meeting, Current Controversies in Diagnosis and Staging of Lung Cancer.
    2. Leslie KO & Wick MR, Practical Pulmonary Pathology, 813 pages, 2005.
    3. Hill CA, "Thoracic Tuberculosis, Mycobacteriosis, MERosis, and BCGosis in a Cancer Treatment Center", Radiology 153(2):311-316, November 1984.
    4. Butnor KJ, et. al., "Interobserver Agreement on What Constitutes Visceral Pleural Invasion by Non-small Cell Carcinoma...an Internet-based Assessment of International Current Practices", AJCP 128:638-647, October 2007.
    5. lead article CAP Today October 2007.
    6. article CAP Today November 2007, pages 93-94.
    7. AJCC Manual, 6th Edition (2002).
    8. Butnor KJ, et. al., "Interobserver Agreement on What Constitutes Visceral Pleural Invasion by Non-small Cell Lung Carcinoma", AJCP 128(4):638-647, October 2007.
    9. Farver CF, "Current Controversies in Diagnosis and Staging of Lung Cancer"...Medscape CME, Highlights of 2006 USCAP meeting.
    10. Rosai J, Rosai and Ackerman's Surgical Pathology, 2 vol. text 2977 pages, 2004.
    11. Feng FY, Zhang DC, Liu XY, Wang YG, Mao YS, "Surgical treatment and prognosis of synchronous double primary lung cancer: a report of 31 cases", Ai Zheng [Chinese Journal of Cancer] ;24(2):215-8, Feb. 2005 [author e-mailed an English translation to EBS 5/08].
    12. Kamiya K, et. al, "Histopathological features and prognostic significance of the micropapillary pattern in lung adwnocarcinoma", Mdern Pat. 21(8):992-1001, August 2008.
    13. about neuroendocrine tumors: Oberg K, " Expert Rev Anticancer Ther.", 2003; 3(6): 863-877.

    (posted 25 November 2002; latest addition 13 August 2008)
 
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