Differences in Sxs and histology in Hypersensitivyt Pneumonitis and Silicosis

[LuckiestOne]

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What are some of the differences? Both form non caseating granulomas with chronic inflammatory cells.... Have diffuse nodular densities in the lung x ray..

How do we differentiate those two? Thanks!

 

[ijn]

What are some of the differences? Both form non caseating granulomas with chronic inflammatory cells.... Have diffuse nodular densities in the lung x ray..

How do we differentiate those two? Thanks!

If they write the question without telling you a history of employment or environmental risk factors they're ******ed. Farmer / person with pet birds vs sand blaster / potter / dude who inhales sand for ****s and giggles, etc.

 

[LuckiestOne]

If they write the question without telling you a history of employment or environmental risk factors they're ******ed. Farmer / person with pet birds vs sand blaster / potter / dude who inhales sand for ****s and giggles, etc.

What if it was a farmer? Would they be at risk for more silicosis or hypersensitivity pneumonitis? I think you'd be exposed to lots of silica (sand) and organic dust as a farmer....

While you are here ijn, I'd like to ask you for one more question if that's okay... NBME Spoiler for those who haven't taken it

a 50y/o come with fever, muscle pain,sore throat, non productive cough for 7 days.he had 2similar episode last year.he smoke 2 pack of cigrate daily for 30 years.his temp. is 38.9c. he has rhonchi and crackle. CXR shows consolidation of Rt lower lobe. what mechanism is most likley the cause?

A)inactivation of muramyl depeptide
B)induction of acidification of endosome in alveolar MQ
C)injury of muciciliary escalator
D)stimulation of igM to IgA switching
E)suppretion of cough reflex

I can't seem to understand what this questino is asking. What would you pick as the answer and why? Thanks, ijn.

 

[ijn]

What if it was a farmer? Would they be at risk for more silicosis or hypersensitivity pneumonitis? I think you'd be exposed to lots of silica (sand) and organic dust as a farmer....

The other name for hypersensitivity pneumonitis is farmer's lung or bird fancier's lung. The disease is more of an end point of multiple causes than due to a specific antigen. Dust is a possible cause of hypersensitivity pneumonitis.

You'd have to have a clear history of occupational silica exposure to have a basis for diagnosing silicosis.

While you are here ijn, I'd like to ask you for one more question if that's okay... NBME Spoiler for those who haven't taken it

a 50y/o come with fever, muscle pain,sore throat, non productive cough for 7 days.he had 2similar episode last year.he smoke 2 pack of cigrate daily for 30 years.his temp. is 38.9c. he has rhonchi and crackle. CXR shows consolidation of Rt lower lobe. what mechanism is most likley the cause?

A)inactivation of muramyl depeptide
B)induction of acidification of endosome in alveolar MQ
C)injury of muciciliary escalator
D)stimulation of igM to IgA switching
E)suppretion of cough reflex

I can't seem to understand what this questino is asking. What would you pick as the answer and why? Thanks, ijn.

Smoking injures the mucociliary escalator. Decrease in mucus clearance leads to an increased susceptibility to pneumonia. They could have also written this same question with a person with a history of alcoholism or someone with swallowing problems (secondary to say a stroke).

 

[da Vincis World]

It's very unlikely that they'll get tricky on this type of question.

 

[LuckiestOne]

Thanks everyone

 

[Phloston]

Hypersensitivity pneumonitis is supposedly a mixed-type-III/IV reaction, but in terms of the USMLE, if it's one or the other, type-III is the better bet answer-wise.

I've seen HP show up in practice questions as an arthus reaction, so you're going to have immune complexes. In farmers, Actinomycetes is commonly found in moist hay.

The reason it's partial type-IV is because macrophages still phagocytose antigen, so an infiltrate of T-cells, plasma cells and macrophages is seen histologically.

However the type-III reaction is predominant, so I'd also expect neutrophils alongside those.

In terms of silicosis, we know it induces a restrictive lung disease, so macrophages must phagocytose the SiO2, thereby releasing TGF-beta and other growth factors. This induces collagen production by fibroblasts.

In terms of practice questions, silicosis usually always affects the upper lobes, demonstrates "egg shell" calcifications, and nodularities can be seen. FEV1/FVC should be >80% (restrictive), whereas HP should be obstructive.

 

[Ronin786]

Hypersensitivity pneumonitis is supposedly a mixed-type-III/IV reaction, but in terms of the USMLE, if it's one or the other, type-III is the better bet answer-wise.

I've seen HP show up in practice questions as an arthus reaction, so you're going to have immune complexes. In farmers, Actinomycetes is commonly found in moist hay.

The reason it's partial type-IV is because macrophages still phagocytose antigen, so an infiltrate of T-cells, plasma cells and macrophages is seen histologically.

However the type-III reaction is predominant, so I'd also expect neutrophils alongside those.

In terms of silicosis, we know it induces a restrictive lung disease, so macrophages must phagocytose the SiO2, thereby releasing TGF-beta and other growth factors. This induces collagen production by fibroblasts.

In terms of practice questions, silicosis usually always affects the upper lobes, demonstrates "egg shell" calcifications, and nodularities can be seen. FEV1/FVC should be >80% (restrictive), whereas HP should be obstructive.

Why would HP be an obstructive pattern? Pathoma says that chronic exposure leads to interstitial fibrosis in HP.

Also would Silicosis also have eosinophils present? Cause that could differentiate between the two.

 

[Phloston]

Why would HP be an obstructive pattern? Pathoma says that chronic exposure leads to interstitial fibrosis in HP.

Also would Silicosis also have eosinophils present? Cause that could differentiate between the two.

Repeated damage due to chronic HP could lead to fibrosis, but an acute attack would have to be obstructive secondary to the inflammatory process.

As far as I'm aware, eosinophils are not present in either HP or silicosis. Where did you read that?

Just confirmed on Goljan's Path, p. 300, that HP does not involve IgE or eosinophilia.

Goljan's also doesn't mention eosinophils for silicosis (p. 296-7). It mentions collagen formation and calcification (as we already knew).

 

[Ronin786]

Pathoma mentions that in HP you have granulomas with Eosinophils.

 

[Phloston]

I found an article that says eosinophils can be present in HP:

http://radiographics.rsna.org/content/29/7/1921.full

"Diffuse chronic interstitial inflammatory in-filtrates, primarily consisting of lymphocytes and plasma cells but often including eosinophils, neutrophils, and mast cells. Poorly circumscribed interstitial nonnecrotizing (noncaseating) granulomas consisting of lymphocytes, plasma cells, and epithelioid histiocytes, with or without giant cells."

I think it's just important to know that eosinophils aren't the mainstay of the condition, as they are with type-I hypersensitivities, but that they can be present.

 

[tk0102]

What are some of the differences? Both form non caseating granulomas with chronic inflammatory cells.... Have diffuse nodular densities in the lung x ray..

How do we differentiate those two? Thanks!

Silicotic nodules are present in silicosis and are extremely distinct, consisting of birefringent particles surrounded by "whorled" hyalinized collagen fibres--all of which looks rather glass-y. (Just Google for a picture, and you'll get what I mean.)

he clinical picture is different as well. HP will follow either an acute or chronic course. In acute HP, you'll have fever, cough, dyspnea, etc. within a few hours of exposure. In chronic HP, you'll have malaise and weight loss in addition to dyspnea. In silicosis, however, you'll have the dyspnea, but any inflammatory features.

 

[navigator]

Silicosis doesn't form noncaseating granulomas, right??