Lipoid pneumonia pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
=== | === Exogenous lipoid pneumonia === | ||
*It is understood that exogenus lipoid pneumonia is the result of chronic body reaction to fatty substance in the alveoli<ref name="GuerguerianLacroix2000">{{cite journal|last1=Guerguerian|first1=Anne-Marie|last2=Lacroix|first2=Jacques|title=Pulmonary injury after intravenous hydrocarbon injection|journal=Paediatrics & Child Health|volume=5|issue=8|year=2000|pages=471–472|issn=1205-7088|doi=10.1093/pch/5.8.471}}</ref>. | |||
*Lipid reaches alveoli by aspiration or inhalation. | |||
*Some mineral oils can cause lung injuries such as gasoline<ref name="DomejMitterhammer2007">{{cite journal|last1=Domej|first1=Wolfgang|last2=Mitterhammer|first2=Heike|last3=Stauber|first3=Rudolf|last4=Kaufmann|first4=Peter|last5=Smolle|first5=Karl Heinz|title=Successful outcome after intravenous gasoline injection|journal=Journal of Medical Toxicology|volume=3|issue=4|year=2007|pages=173–177|issn=1556-9039|doi=10.1007/BF03160935}}</ref>. | |||
*Mineral oils can enter the tracheobranchial tree without causing cough reflex which will bother mucocilliary 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 paranchymal 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 === | |||
<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:
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 tracheobranchial tree without causing cough reflex which will bother mucocilliary 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 paranchymal 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
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.