Lipoid pneumonia pathophysiology: Difference between revisions
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** Leakage from vessels | ** Leakage from vessels | ||
** Prolonged hypoxia | ** Prolonged hypoxia | ||
** Local oxygen and carbon dioxide tension.<br /> | ** Local oxygen and carbon dioxide tension. | ||
*Endogenous lipoid pneumonia can be caused by transbronchial dissemination of cancer cell breakdown products<ref name="TamuraHebisawa1998">{{cite journal|last1=Tamura|first1=A.|last2=Hebisawa|first2=A.|last3=Fukushima|first3=K.|last4=Yotsumoto|first4=H.|last5=Mori|first5=M.|title=Lipoid Pneumonia in Lung Cancer: Radiographic and Pathological Features|journal=Japanese Journal of Clinical Oncology|volume=28|issue=8|year=1998|pages=492–496|issn=0368-2811|doi=10.1093/jjco/28.8.492}}</ref>. | |||
*Poorly differentiated adenocarcinoma cells secreting mucin is the most common neoplastic reason. | |||
*Another mechanism suggested is anoxic tissue injury stimulating various enzymes such as phospholipase and mono-oxygenases<ref name="TakiNakazima1986">{{cite journal|last1=Taki|first1=Takao|last2=Nakazima|first2=Tomoko|last3=Emi|first3=Yohko|last4=Konishi|first4=Yohichi|last5=Hayashi|first5=Akira|last6=Matsumoto|first6=Makoto|title=Accumulation of surfactant phospholipids in lipid pneumonia induced with methylnaphthalene|journal=Lipids|volume=21|issue=9|year=1986|pages=548–552|issn=0024-4201|doi=10.1007/BF02534050}}</ref>. | |||
*These enzymes activation in turn cause modification of LDL cholesterol, enhancing lipid uptake by alveolar macrophages similar to atherogenesis.<br /> | |||
==Genetics== | ==Genetics== | ||
[Disease name] is transmitted in [mode of genetic transmission] pattern. | [Disease name] is transmitted in [mode of genetic transmission] pattern. | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ramyar Ghandriz MD[2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Exogenous lipoid pneumonia
- It is understood that exogenus lipoid pneumonia is the result of chronic body reaction to fatty substance in the alveoli[1].
- Lipid reaches alveoli by aspiration or inhalation.
- Some mineral oils can cause lung injuries such as gasoline[2].
- Mineral oils can enter the tracheobronchial tree without causing cough reflex which will bother mucociliary transport system chronically.
- Injected lipids mechanism of further producing lipid pneumonia is more complicated:
- It is suggested that the lung is the first capillary bed encountered during circulation, bearing the majority of damage.
- as the lipid goes inside the alveoli, it is trapped and hard to expectorate, this condition may be worsen by associated neurological and gastrointestinal disorders affecting swallowing or cough.
- Lipids in alveoli form emulsion and then consumed by macrophages via phagocytosis.
- Since the alveolar macrophages cannot metabolize consumed fatty substance, oil is repeatedly released into alveoli after death of these macrophages.
- The oil released, illicits a giant-cell granulomatosis reaction.
- In fresh lesions, lipid-laden macrophages are seen.
- In advanced lesions larger vacuoles and inflamatory infiltrates are seen in alveolar and bronchial walls and septa.
- In oldest lesions fibrosis and parenchymal destruction around large lipid-containing vacuoles is seen.
- Staining can help demonestrating whether vacuoles are filled with lipid or not:
- Oil red O
- Sudan black
Endogenous lipoid pneumonia
- The pathogenesis of endogenous pneumonia is still not well understood[3][4][5].
- The mechanism may be related to several mechanisms such as:
- Retained epithelial secretion
- Cell breakdown
- Leakage from vessels
- Prolonged hypoxia
- Local oxygen and carbon dioxide tension.
- Endogenous lipoid pneumonia can be caused by transbronchial dissemination of cancer cell breakdown products[6].
- Poorly differentiated adenocarcinoma cells secreting mucin is the most common neoplastic reason.
- Another mechanism suggested is anoxic tissue injury stimulating various enzymes such as phospholipase and mono-oxygenases[7].
- These enzymes activation in turn cause modification of LDL cholesterol, enhancing lipid uptake by alveolar macrophages similar to atherogenesis.
Genetics
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
- [Gene1]
- [Gene2]
- [Gene3]
OR
The development of [disease name] is the result of multiple genetic mutations such as:
- [Mutation 1]
- [Mutation 2]
- [Mutation 3]
Associated Conditions
Conditions associated with [disease name] include:
- [Condition 1]
- [Condition 2]
- [Condition 3]
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Guerguerian, Anne-Marie; Lacroix, Jacques (2000). "Pulmonary injury after intravenous hydrocarbon injection". Paediatrics & Child Health. 5 (8): 471–472. doi:10.1093/pch/5.8.471. ISSN 1205-7088.
- ↑ Domej, Wolfgang; Mitterhammer, Heike; Stauber, Rudolf; Kaufmann, Peter; Smolle, Karl Heinz (2007). "Successful outcome after intravenous gasoline injection". Journal of Medical Toxicology. 3 (4): 173–177. doi:10.1007/BF03160935. ISSN 1556-9039.
- ↑ Burke, M; Fraser, R (1988). "Obstructive pneumonitis: a pathologic and pathogenetic reappraisal". Radiology. 166 (3): 699–704. doi:10.1148/radiology.166.3.3340764. ISSN 0033-8419.
- ↑ "www.thoracic.org" (PDF).
- ↑ Cohen, Allen B.; Cline, Martin J. (1972). "In VitroStudies of the Foamy Macrophage of Postobstructive Endogenous Lipoid Pneumonia in Man1–3". American Review of Respiratory Disease. 106 (1): 69–78. doi:10.1164/arrd.1972.106.1.69. ISSN 0003-0805.
- ↑ Tamura, A.; Hebisawa, A.; Fukushima, K.; Yotsumoto, H.; Mori, M. (1998). "Lipoid Pneumonia in Lung Cancer: Radiographic and Pathological Features". Japanese Journal of Clinical Oncology. 28 (8): 492–496. doi:10.1093/jjco/28.8.492. ISSN 0368-2811.
- ↑ Taki, Takao; Nakazima, Tomoko; Emi, Yohko; Konishi, Yohichi; Hayashi, Akira; Matsumoto, Makoto (1986). "Accumulation of surfactant phospholipids in lipid pneumonia induced with methylnaphthalene". Lipids. 21 (9): 548–552. doi:10.1007/BF02534050. ISSN 0024-4201.