Neonatal respiratory distress syndrome pathophysiology: Difference between revisions

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{{Neonatal respiratory distress syndrome}}
{{Neonatal respiratory distress syndrome}}
{{CMG}}
{{CMG}}{{AE}}{{Vanya}}
 
==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==
==Pathophysiology==
The lungs are developmentally deficient in a material called [[pulmonary surfactant|surfactant]], which allows the [[alveoli]] to remain open throughout the normal cycle of inhalation and exhalation. Surfactant is a complex system of [[lipid]]s, [[protein]]s and [[glycoprotein]]s which are produced in specialized lung cells called Type II cells or Type II pneumocytes. The surfactant is packaged by the cell in structures called [[lamellar bodies]], and extruded into the alveoli. The lamellar bodies then unfold into a complex lining of the alveoli. This layer reduces the surface tension of the fluid that lines the alveolar walls. During exhalation the walls of the alveoli come in contact and surface tension tends to cause them to stick together, preventing re-inflation. By reducing surface tension, surfactant allows the alveoli to re-expand with inspiration. Without adequate amounts of surfactant, the alveoli collapse and are very difficult to expand. Microscopically, a surfactant deficient lung is characterized by collapsed alveoli alternating with hyperaerated alveoli, vascular congestion and, in time, [[hyaline]] membranes. Hyaline membranes are composed of [[fibrin]], cellular debris, [[red blood cell]]s, rare [[neutrophil]]s and [[macrophage]]s. They appear as an eosinophilic, amorphous material, lining or filling the alveolar spaces and blocking gas exchange. As a result, blood passing through the lungs is unable to pick up oxgen and unload carbon dioxide from the alveolar spaces. Blood oxygen levels fall and carbon dioxide rises, resulting in rising blood acid levels and [[hypoxia]]. Structural immaturity, as manifest by low numbers of alveoli, also contributes to the disease process. Therapeutic oxygen and positive-pressure ventilation, while potentially life-saving, can also damage the lung. The diagnosis is made by the clinical picture and the chest xray, which demonstrates decreased lung volumes (bell-shaped chest), absence of the thymus (after about 6 hours), a small (0.5-1 mm), discrete, uniform infiltrate (sometimes described as a "ground glass" appearance) that involves all lobes of the lung, and air-bronchograms (ie the infiltrate will outline the larger airways passages which remain air-filled).  In severe cases, this becomes exaggerated until the cardiac borders become inapparent (a 'white-out' appearance).
===Physiology===
===Gross Pathology===
The normal physiology of [name of process] can be understood as follows:
The characteristic [[pathology]] seen in babies who die from RDS was the source of the name "hyaline membrane disease". These waxy-appearing layers line the collapsed tiny air sacs ("[[alveoli]]") of the lung. In addition, the lungs show bleeding, over-distention of airways and damage to the lining cells.
 
===Pathogenesis===
*The exact pathogenesis of [disease name] is not completely understood.
OR
*It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
*The progression to [disease name] usually involves the [molecular pathway].
*The pathophysiology of [disease/malignancy] depends on the histological subtype.
 
==Genetics==
[Disease name] is transmitted in [mode of genetic transmission] pattern.
 
OR


The organs generally showed no abnormalities other than those of immaturity expected at this gestational age. There was moderate diffuse subarachnoid hemorrhage and a small amount of blood in the pleural and pericardial cavities.
Genes involved in the pathogenesis of [disease name] include:
*[Gene1]
*[Gene2]
*[Gene3]


[http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
OR


<div align="left">
The development of [disease name] is the result of multiple genetic mutations such as:
<gallery heights="175" widths="175">
Image:Infant respiratory distress syndrome 1.jpg|This is a gross photograph of lung demonstrating hyaline membrane disease (Infant respiratory distress syndrome) and atelectasis.
</gallery>
</div>


===Microscopic Pathology===
*[Mutation 1]
*[Mutation 2]
*[Mutation 3]


<div align="left">
==Associated Conditions==
<gallery heights="175" widths="175">
Conditions associated with [disease name] include:
Image:Infant respiratory distress syndrome 4.jpg|This high-power photomicrograph of liver shows more clearly the immature blood cell precursors (arrows) which represent extramedullary hematopoiesis of the liver. The liver is a normal site of fetal hematopoiesis and, for this stage of gestation, extramedullary hematopoiesis of the liver is normal.
Image:Infant respiratory distress syndrome 5.jpg|This low-power photomicrograph of lung demonstrates hypercellular pulmonary interstitium and small air spaces (as compared to adult lungs).
Image:Infant respiratory distress syndrome 6.jpg|This is a medium-power photomicrograph showing a large bronchus with cartilage. Interstitial congestion with numerous red cells is apparent. Even at this magnification hyaline membranes (arrows) can be seen lining the alveoli.
</gallery>
</div>


<div align="left">
*[Condition 1]
<gallery heights="175" widths="175">
*[Condition 2]
Image:Infant respiratory distress syndrome 7.jpg|This high-power photomicrograph shows an airway with adjacent lung tissue. Some alveoli have hyaline membranes (arrows). There is severe congestion of the interstitium throughout this section.  
*[Condition 3]
Image:Infant respiratory distress syndrome 8.jpg|This medium-power photomicrograph shows the pink acellular homogeneous material lining the alveoli which comprises the hyaline membranes (arrows). The interstitium shows congestion, as in previous sections.
 
Image:Infant respiratory distress syndrome 9.jpg|This higher-power photomicrograph shows more clearly the hyaline membranes (arrows) and the congestion in the interstitium.  
==Gross Pathology==
</gallery>
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
</div>
 
<div align="left">
==Microscopic Pathology==
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].


<gallery heights="175" widths="175">
Image:Infant respiratory distress syndrome 2.jpg|This is a low-power photomicrograph of a triangular-shaped section of lung (1) and an oblong section of liver (2). The lack of open air spaces in this neonatal lung indicates its immaturity.
Image:Infant respiratory distress syndrome 3.jpg|This is a low-power photomicrograph of liver which contains dark blue-stained cells in the hepatic sinusoids. These are immature blood cell precursors and this represents extramedullary hematopoiesis of the liver.
</gallery>
</div>
==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
[[Category:Needs overview]]
 
 
[[Category:Pediatrics]]
[[Category:Pediatrics]]
[[Category:Pulmonology]]
[[Category:Pulmonology]]

Latest revision as of 15:00, 31 August 2021

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Vanya Vohra, M.B.B.S[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

Physiology

The normal physiology of [name of process] can be understood as follows:

Pathogenesis

  • The exact pathogenesis of [disease name] is not completely understood.

OR

  • It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
  • [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
  • Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
  • [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
  • The progression to [disease name] usually involves the [molecular pathway].
  • The pathophysiology of [disease/malignancy] depends on the histological subtype.

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

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