reumS ceniksss si a epTy 3 yttsryihseeinvip encoatr,i in wchih het odby esdronps to eainignct deilmac sesacbsntu nda ocusprde i.odnsaebit Tshee itbaseiond in coilnrauitc ehtn inbd to eht gitaninec rsugd nad est off eht mlmnceteop aea.scdc aRtoeuidmh ttihirsar is sloa a Tyep 3 ipiivertsyentshy oanic.ter
)A piosstpAo of acosmaepghr- psoatiops si narylegel ont a eypt of peivsnryiihtytse iort.acen B) tasM lce anlin-eurodagt htsi is artp fo a Tpye 1 ityrsetysipeihnv r/n,esaiayhxaconplati ni wihhc stam clsle nibd gEI on rihte rusacfe, dan EIg igdbinn to eth tetgra enganit unisdce a orioncmaalnfto egcanh in the IgE atth tess ffo atsm lelc ldrote.naianug C) luaarNt lielKr lelC n-kgilli yaspl a eaviytr of oler,s nlgndicui cernca spsrpnesoui adn reutdcnsito of alyrvil efcdtnei le.csl If they plya a lroe ni syyvniriitph,seet it si tpar fo eTyp 2 RHS ni wihhc yeth uwdlo rnpedso to Ig on eth lelc earsuc.f )E elhWe and rlafe n-aiseroct iThs si sola a Tpye 1 H.RS
bumping the OP; extraarticular manifestations are common in RA (i.e. rheumatoid nodules in subcutaneous tissue and lung (+ pneumoconiosis --> Caplan syndrome), interstitial lung disease, pleuritis, pericarditis, anemia of chronic disease, neutropenia+splenomegaly (Felty syndrome), AA amyloidosis, Sjogren syndrome, scleritis, carpal tennel syndrome. (btw I thought RA was local and HSR II)
According to FA 2019, in the section about rheumatoid arthritis, it is given that rheumatoid nodules are due to fibrinoid necrosis. In the pathology chapter in FA, fibrinoid necrosis is said to be an example of type 3 hypersensitivity reaction. In this question stem, the patient is said to have rheumatoid nodules and they ask 'the immunologic mechanism of this patient's inflammation is similar to?' So basically they asked about what type of hypersensitivity reaction is fibrinoid necrosis. The answer: Rheum nodules->fibrinoid necrosis->type 3 HSR->same as serum sickness. Got it wrong btw.
Maybe they went with serum sickness (a type III hypersensitivity rxn) on this question based on the serology used to diagnose RA. Pts with RA have antibodies to immunoglobulin G (IgG), called rheumatoid factors (RFs). It makes some sense that upon these rheumatoid factors reacting with "self" circulating IgG, immune complexes would form that would later deposit in tissues (explaining in part the extraarticular manifestations seen with RA, ex. rheumatoid nodules, pleuritis, pericarditis etc..)
Serum sickness—the prototypic immune complex disease. Antibodies to foreign proteins are produced and 1–2 weeks later, antibody- antigen complexes form and deposit in tissues = complement activation = inflammation and tissue damage. Fever, urticaria, arthralgia, proteinuria, lymphadenopathy occur 1–2 weeks after antigen exposure. Serum sickness-like reactions are associated with some drugs (may act as haptens, eg, penicillin) and infections (eg, hepatitis B).