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==Physical examination==
==Physical examination==
==Overview==
On gross pathology, peripheral multifocal lesions is the characteristic finding of adenocarcinoma of the lung.<ref>Adenocarcinoma of the lung. Librepathology 2015. http://librepathology.org/wiki/index.php/File:Adenocarcinoma_%283950819000%29.jpg </ref> On microscopic histopathological analysis, nuclear atypia, eccentrically placed nuclei, abundant cytoplasm, and conspicuous nucleoli are characteristic findings of adenocarcinoma of the lung. Genes involved in the pathogenesis of adenocarcinoma of the lung include [[epidermal growth factor receptor|EGFR]], [[HER2]], [[KRAS]], [[anaplastic lymphoma kinase|ALK]], and [[BRAF]].<ref>{{cite book | last = Stewart | first = Bernard | title = World cancer report 2014 | publisher = International Agency for Research on Cancer,Distributed by WHO Press, World Health Organization | location = Lyon, France Geneva, Switzerland | year = 2014 | isbn = 9283204298 }}</ref>
==Pathogenesis==
* Adenocarcinoma of the lung tends to stain mucin positive as it is derived from the mucus producing glands of the lungs. Similar to other adenocarcinoma, if this tumor is well differentiated (low grade) it will resemble the normal glandular structure. Poorly differentiated adenocarcinoma will not resemble the normal glands (high grade) and will be detected by seeing that they stain positive for mucin (which the glands produce).<ref>{{cite book | last = Stewart | first = Bernard | title = World cancer report 2014 | publisher = International Agency for Research on Cancer,Distributed by WHO Press, World Health Organization | location = Lyon, France Geneva, Switzerland | year = 2014 | isbn = 9283204298 }}</ref>
* To reveal the adenocarcinomatous lineage of the solid variant, demonstration of intracellular mucin production may be performed. Foci of squamous metaplasia and dysplasia may be present in the epithelium proximal to adenocarcinomas, but these are not the precursor lesions for this tumor. Rather, the precursor of peripheral adenocarcinomas has been termed atypical adenomatous hyperplasia (AAH). Microscopically, AAH is a well-demarcated focus of epithelial proliferation, containing cuboidal to low-columnar cells resembling club cells or type II pneumocytes. These demonstrate various degrees of cytologic atypia, including hyperchromasia, pleomorphism, prominent [[nucleoli]]. Lesions of AAH are monoclonal, and they share many of the molecular aberrations that are associated with adenocarcinomas.<ref>{{cite book | last = Kumar | first = Vinay | title = Robbins basic pathology | publisher = Saunders/Elsevier | location = Philadelphia, PA | year = 2007 | isbn = 1416029737 }}</ref>
* This cancer usually is seen peripherally in the lungs, as opposed to [[small cell lung cancer]] and [[squamous cell]] lung cancer, which both tend to be more centrally located.<ref name=Travis95>{{cite journal |author=Travis WD, Travis LB, Devesa SS |title=Lung cancer |journal=Cancer |volume=75 |issue=1 Suppl |pages=191–202 |date=January 1995|pmid=8000996 |doi= 10.1002/1097-0142(19950101)75:1+<191::AID-CNCR2820751307>3.0.CO;2-Y|url=}}</ref><ref name=Kumar-adenocarcinoma>{{cite book |chapter=Chapter 13, box on morphology of adenocarcinoma |author=Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson |title=Robbins Basic Pathology|publisher=Saunders |location=Philadelphia |isbn=1-4160-2973-7 |edition=8th}}</ref>
*Individual susceptibility, active smoking, radon exposure, exposure to high pollution levels, asbestos exposure, occupational or environmental exposure to particular agents or carcinogens. Hydrocarbons cause damage to the DNA and form DNA adducts. Benzo-A-pyrine has effects on inducing p53 mutations and affects molecular signaling pathways such as AKT.
The “multiple hit theory” for adenocarcinoma of the lung states that genetic reproduction is hindered due to the cumulative effect of several toxic insults. Underlying lung disease such as COPD, idiopathic pulmonary fibrosis and tuberculosis may exacerbate the process.
Mutations involving the ras family of oncogenes:
The ras oncogene family has 3 members:
H-ras
K-ras, also determines patient prognosis
N-ras
Mutations of ras affect signal transduction by affecting GTPase activity.They are found in 30 percent of cases.
c-myc
c-raf
tumor suppressor genes retinoblastoma (Rb) and p53
Mutations of APOBEC protein
==Genetics==
* Genes involved in the pathogenesis of adenocarcinoma of the lung include:<ref>{{cite book | last = Stewart | first = Bernard | title = World cancer report 2014 | publisher = International Agency for Research on Cancer,Distributed by WHO Press, World Health Organization | location = Lyon, France Geneva, Switzerland | year = 2014 | isbn = 9283204298 }}</ref><ref name="pmid17625570">{{cite journal| author=Soda M, Choi YL, Enomoto M, Takada S, Yamashita Y, Ishikawa S et al.| title=Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer. | journal=Nature | year= 2007 | volume= 448 | issue= 7153 | pages= 561-6 | pmid=17625570 | doi=10.1038/nature05945 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17625570  }} </ref><ref name="pmid22919003">{{cite journal| author=Davies KD, Le AT, Theodoro MF, Skokan MC, Aisner DL, Berge EM et al.| title=Identifying and targeting ROS1 gene fusions in non-small cell lung cancer. | journal=Clin Cancer Res | year= 2012 | volume= 18 | issue= 17 | pages= 4570-9 | pmid=22919003 | doi=10.1158/1078-0432.CCR-12-0550 | pmc=PMC3703205 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22919003  }} </ref>
:* [[epidermal growth factor receptor|EGFR]] (7p11)
:* [[KRAS]] (12p12)
:* [[BRAF]] (7q34)
:* PIK3CA (3q26)
:* ERBB2 (17q12)
:* Translocation EML4/[[anaplastic lymphoma kinase|ALK]]
:* Tyrosine kinase fusions
::* ALK (2p23), ROS1 (6q22), and RET (10q11)
==Gross Pathology==
* Peripheral lesions
* May be multifocal
===Gallery===
<gallery>
Image:
Lung_adenocarcinoma1.jpg|his subpleural lesion consists mostly of pigmented scar tissue with gray-tan tumor seen predominantly at the periphery.The visceral pleura overlying the tumor is retracted due to traction by underlying scar tissue. This is a good example of what has been called "scar carcinoma". In almost all cases of this type the scar is not a pre-existing lesion but rather represents a desmoplastic reponse to the tumor cells. The basal visceral pleura is involved by tumor<ref>Adenocarcinoma of the lung. Librepathology 2015. http://librepathology.org/wiki/index.php/File:Adenocarcinoma_%283950819000%29.jpg </ref>
</gallery>
==Microscopic Pathology==
* Nuclear atypia
* Eccentrically placed nuclei
* Abundant cytoplasm
* Conspicuous nucleoli
* Nuclear pseudoinclusions
* Lack of intercellular bridges
'''Subtypes'''<ref name=libre>Adenocarcinoma of the lung. Librepathology 2015. http://librepathology.org/wiki/index.php/Adenocarcinoma_of_the_lung#Microscopic Accessed on December 20, 2015</ref>
* Lepidic predominant
:* Tumor grows long the alveolar wall
* Acinar predominant
:* Berry-shaped glands, smaller than lung acini
* Papillary predominant
:* Fibrovascular cores
* Micropapillary predominant
:* Nipple shaped projections without fibrovascular cores
* Solid predominant
:* Sheet of cells
===Gallery===
<gallery>
Image:
Lung_adenocarcinoma2.jpg|Micrograph of mucinous adenocarcinoma of the lung. H&E stain. <ref>Acinar adenocarcinoma. Librepathology 2015. http://librepathology.org/wiki/index.php/File:Mucinous_adenocarcinoma_of_the_lung_--_high_mag.jpg </ref>
Lung_adenocarcinoma3.jpg|Micrograph showing an adenocarcinoma of the lung (acinar pattern). H&E stain. <ref>Mucinous adenocarcinoma. Librepathology 2015. http://librepathology.org/wiki/index.php/File:Acinar_pattern_adenocarcinoma_of_lung_--_intermed_mag.jpg </ref>
</gallery>


==References==
==References==

Revision as of 16:13, 2 March 2018

Physical examination

Overview

On gross pathology, peripheral multifocal lesions is the characteristic finding of adenocarcinoma of the lung.[1] On microscopic histopathological analysis, nuclear atypia, eccentrically placed nuclei, abundant cytoplasm, and conspicuous nucleoli are characteristic findings of adenocarcinoma of the lung. Genes involved in the pathogenesis of adenocarcinoma of the lung include EGFR, HER2, KRAS, ALK, and BRAF.[2]

Pathogenesis

  • Adenocarcinoma of the lung tends to stain mucin positive as it is derived from the mucus producing glands of the lungs. Similar to other adenocarcinoma, if this tumor is well differentiated (low grade) it will resemble the normal glandular structure. Poorly differentiated adenocarcinoma will not resemble the normal glands (high grade) and will be detected by seeing that they stain positive for mucin (which the glands produce).[3]
  • To reveal the adenocarcinomatous lineage of the solid variant, demonstration of intracellular mucin production may be performed. Foci of squamous metaplasia and dysplasia may be present in the epithelium proximal to adenocarcinomas, but these are not the precursor lesions for this tumor. Rather, the precursor of peripheral adenocarcinomas has been termed atypical adenomatous hyperplasia (AAH). Microscopically, AAH is a well-demarcated focus of epithelial proliferation, containing cuboidal to low-columnar cells resembling club cells or type II pneumocytes. These demonstrate various degrees of cytologic atypia, including hyperchromasia, pleomorphism, prominent nucleoli. Lesions of AAH are monoclonal, and they share many of the molecular aberrations that are associated with adenocarcinomas.[4]
  • Individual susceptibility, active smoking, radon exposure, exposure to high pollution levels, asbestos exposure, occupational or environmental exposure to particular agents or carcinogens. Hydrocarbons cause damage to the DNA and form DNA adducts. Benzo-A-pyrine has effects on inducing p53 mutations and affects molecular signaling pathways such as AKT.

The “multiple hit theory” for adenocarcinoma of the lung states that genetic reproduction is hindered due to the cumulative effect of several toxic insults. Underlying lung disease such as COPD, idiopathic pulmonary fibrosis and tuberculosis may exacerbate the process. Mutations involving the ras family of oncogenes: The ras oncogene family has 3 members: H-ras K-ras, also determines patient prognosis N-ras Mutations of ras affect signal transduction by affecting GTPase activity.They are found in 30 percent of cases.

c-myc c-raf tumor suppressor genes retinoblastoma (Rb) and p53 Mutations of APOBEC protein

Genetics

  • Genes involved in the pathogenesis of adenocarcinoma of the lung include:[7][8][9]
  • EGFR (7p11)
  • KRAS (12p12)
  • BRAF (7q34)
  • PIK3CA (3q26)
  • ERBB2 (17q12)
  • Translocation EML4/ALK
  • Tyrosine kinase fusions
  • ALK (2p23), ROS1 (6q22), and RET (10q11)

Gross Pathology

  • Peripheral lesions
  • May be multifocal

Gallery

  • his subpleural lesion consists mostly of pigmented scar tissue with gray-tan tumor seen predominantly at the periphery.The visceral pleura overlying the tumor is retracted due to traction by underlying scar tissue. This is a good example of what has been called "scar carcinoma". In almost all cases of this type the scar is not a pre-existing lesion but rather represents a desmoplastic reponse to the tumor cells. The basal visceral pleura is involved by tumor[10]

    his subpleural lesion consists mostly of pigmented scar tissue with gray-tan tumor seen predominantly at the periphery.The visceral pleura overlying the tumor is retracted due to traction by underlying scar tissue. This is a good example of what has been called "scar carcinoma". In almost all cases of this type the scar is not a pre-existing lesion but rather represents a desmoplastic reponse to the tumor cells. The basal visceral pleura is involved by tumor[10]

Microscopic Pathology

  • Nuclear atypia
  • Eccentrically placed nuclei
  • Abundant cytoplasm
  • Conspicuous nucleoli
  • Nuclear pseudoinclusions
  • Lack of intercellular bridges

Subtypes[11]

  • Lepidic predominant
  • Tumor grows long the alveolar wall
  • Acinar predominant
  • Berry-shaped glands, smaller than lung acini
  • Papillary predominant
  • Fibrovascular cores
  • Micropapillary predominant
  • Nipple shaped projections without fibrovascular cores
  • Solid predominant
  • Sheet of cells

Gallery

  • Micrograph of mucinous adenocarcinoma of the lung. H&E stain. [12]

    Micrograph of mucinous adenocarcinoma of the lung. H&E stain. [12]

  • Micrograph showing an adenocarcinoma of the lung (acinar pattern). H&E stain. [13]

    Micrograph showing an adenocarcinoma of the lung (acinar pattern). H&E stain. [13]

References

  1. ↑ Adenocarcinoma of the lung. Librepathology 2015. http://librepathology.org/wiki/index.php/File:Adenocarcinoma_%283950819000%29.jpg
  2. ↑ Stewart, Bernard (2014). World cancer report 2014. Lyon, France Geneva, Switzerland: International Agency for Research on Cancer,Distributed by WHO Press, World Health Organization. ISBN 9283204298.
  3. ↑ Stewart, Bernard (2014). World cancer report 2014. Lyon, France Geneva, Switzerland: International Agency for Research on Cancer,Distributed by WHO Press, World Health Organization. ISBN 9283204298.
  4. ↑ Kumar, Vinay (2007). Robbins basic pathology. Philadelphia, PA: Saunders/Elsevier. ISBN 1416029737.
  5. ↑ Travis WD, Travis LB, Devesa SS (January 1995). "Lung cancer". Cancer. 75 (1 Suppl): 191–202. doi:10.1002/1097-0142(19950101)75:1+<191::AID-CNCR2820751307>3.0.CO;2-Y. PMID 8000996.
  6. ↑ Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson. "Chapter 13, box on morphology of adenocarcinoma". Robbins Basic Pathology (8th ed.). Philadelphia: Saunders. ISBN 1-4160-2973-7.
  7. ↑ Stewart, Bernard (2014). World cancer report 2014. Lyon, France Geneva, Switzerland: International Agency for Research on Cancer,Distributed by WHO Press, World Health Organization. ISBN 9283204298.
  8. ↑ Soda M, Choi YL, Enomoto M, Takada S, Yamashita Y, Ishikawa S; et al. (2007). "Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer". Nature. 448 (7153): 561–6. doi:10.1038/nature05945. PMID 17625570.
  9. ↑ Davies KD, Le AT, Theodoro MF, Skokan MC, Aisner DL, Berge EM; et al. (2012). "Identifying and targeting ROS1 gene fusions in non-small cell lung cancer". Clin Cancer Res. 18 (17): 4570–9. doi:10.1158/1078-0432.CCR-12-0550. PMC 3703205. PMID 22919003.
  10. ↑ Adenocarcinoma of the lung. Librepathology 2015. http://librepathology.org/wiki/index.php/File:Adenocarcinoma_%283950819000%29.jpg
  11. ↑ Adenocarcinoma of the lung. Librepathology 2015. http://librepathology.org/wiki/index.php/Adenocarcinoma_of_the_lung#Microscopic Accessed on December 20, 2015
  12. ↑ Acinar adenocarcinoma. Librepathology 2015. http://librepathology.org/wiki/index.php/File:Mucinous_adenocarcinoma_of_the_lung_--_high_mag.jpg
  13. ↑ Mucinous adenocarcinoma. Librepathology 2015. http://librepathology.org/wiki/index.php/File:Acinar_pattern_adenocarcinoma_of_lung_--_intermed_mag.jpg

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Cirrhosis Microchapters

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Causes

Differentiating Cirrhosis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

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Echocardiography or Ultrasound

Other Imaging Findings

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Medical Therapy

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History and Symptoms

  • History should include:
    • Appearance of bowel movements
    • Travel history
    • Associated symptoms
    • Immune status
    • Woodland exposure

References

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Other Imaging Findings

Other diagnostic studies

Other Diagnostic Studies

  • Breath hydrogen test

==

Overview

References

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Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Cirrhosis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Tertiary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

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Case #1

Sandbox:Cherry On the Web

Most recent articles

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Risk calculators and risk factors for Sandbox:Cherry

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3] Associate Editor(s)-in-Chief:

Video codes

Normal video

{{#ev:youtube|x6e9Pk6inYI}} {{#ev:youtube|4uSSvD1BAHg}} {{#ev:youtube|PQXb5D-5UZw}} {{#ev:youtube|UVJYQlUm2A8}}

Video in table

{{#ev:youtube|5ucSlgqGAno}}

Floating video

Title
https://https://www.youtube.com/watch?v=ypYI_lmLD7g%7C350}}

Redirect

  1. REDIRECTEsophageal web

synonym website

https://mq.b2i.sg/snow-owl/#!terminology/snomed/10743008

Image

Normal versus Abnormal Barium study of esophagus with varices


Image to the right

C. burnetii, the Q fever causing agent
C. burnetii, the Q fever causing agent

Image and text to the right

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Gallery

References

  1. ↑ 1.0 1.1 1.2 Neuroendocrine tumor of the pancreas. Libre Pathology. http://librepathology.org/wiki/index.php/Neuroendocrine_tumour_of_the_pancreas

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REFERENCES

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