mieloma-mc3baltiple.ppt
TRANSCRIPT
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MIELOMA MÚLTIPLE
Dr. Roberto CarrilloBriceño
Internista – Hematóloo
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Re!resentación es"#em$tica
%e la Hemato!o&esis
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Lin'ocitos T & B
Son las células encargadas de la defenza especíca del(I.
Presentan rece!tores en s# membrana ) el TCR enlos lin-focitos T y los AC( en los linfocitos B *, que lespermite recono-cer una enorme variedad de!atóenos.
Esta diversidad de rece!tores viene dada por laexistencia de mltiples segmentos +nicos , ! D " -,que se reagrupan du-rante el desarrollo linfocitario.
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Es"#ema sim!lica%o %elRece!tor %el Lin'ocito B & %el
Lin'ocito T
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Desarrollo Lin'ocitario
#os lin'ocitos T y B se originan en MO a partir de unprogenitor lin-foide comn.
#a diferenciaci$n %acia lin'ocitos B se produce en la MO,pasando por distintos estadios&
cel !ro/B0 cel !re/B0 cel B inma%#ra0 lin'ocito Bma%#ro
Los lin'ocitos T maduran en el Timo0 y al igual que loslin'ocitos B pasan por distintos estadios caracterizados poruna expresi$n diferen-cial de marcadores típicos.
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Clasicación
LI12OCITO( B
Ti!o B/3 Ti!o B /4
Producen 'cs (g) sin T %elta / ama
ayuda de los linf. T y se T al'a – beta5 dividen& B/3a & B/b Hel!er ) CD67* –
Citotó8icos) CD97*
B/4 & re#la%ores ) CD67CD4:7 *.
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Caracter;stica Cel#lar
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DE2I1ICI<1
El mieloma mltiple ! )) " constituye el prototipo degamapatía monoclonal maligna y se caracteriza porproliferaci$n neopl*sica de una clona de c+l#las!lasm$ticas que producen una inmu-noglo+ulina de
car*cter monoclonal.
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=ama!at;as Monoclonales! En'. Inm#no!roli'erati>as
Malinas " curren cuando de una expansi$n neopl*sica de una clona
de C+l#la B, se generan inmunoglo+ulinas idénticas entresí que se indentican en el electro'oretorama porque
tienen una carga eléctrica igual y por lo tanto unamovilidad electroforética %omogénea y simétrica&
? M @ o Monoclonal
Inm#noelectro'oresis %e !rote;nas
ca%enas ca%enas
li>ianas !esa%as
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Orien %e los lin'omas Bsen el %esarrollo %e los
lin'ocitos
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#+ !ro%#cen estas c+l#las
lin'oi%es
!rote;na monoclonal omo+nea
%os ca%enas !esa%as %os ca%enas li>ianas
%e la misma clase %el mismo ti!o
en constraste con las !oliclonales en las c#ales
la s;ntesis %e inm#nolob#linas %e >arias clases %eca%e/ nas !esa%as & %e ambos ti!os %e ca%enasli>ianas.
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Las %i'erentes clases %e
inm#nolob#linas monoclonaes
Son designadas con la letra ma&sc#la quecorresponde a la clase %e ca%ena !esa%a5
I=0 IA0 IM0 IE0 ID =AMED
#as s#bclases son5
I=30 I=40 I=60 IA30 IA4
Sus ca%enas li>ianas que pueden ser&
a!!a ) * Lamb%a
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Las amma!at;as monoclonales secaracterian !or tres con%iciones
im!ortantes
3. Conce!tos monoclonales
4. Ca!aci%a% %e %i'erenciación & nat#ralea %e lasc+l#/las B !roli'erantes.
F. (intomatolo;a Cl;nica
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Intro%#cción Dica !roli'eración %a l#ar a &
/estrucci$n esquelética 0 osteoporosis
osteolísis 0 %ipercalcemia 0 anemia 0 yen ocasiones plasmocitoma extramedular
El e8ceso %e !ro%#cción %e la !rote;na
!#e%e con%#cir a& (nsuciencia renal,infecciones, Síndrome de
%iperviscosidad.
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Etiolo;a
E!i%emiolo;a #as causas MM no est*n esta+lecidas #a incidencia anual es de 12344.444 %.
5epresenta el 36 de todos los tumores. El 346 de todas las %emopatías.
#a edad promedio se sita a los 78 a9os En menores de :: a9os es excepcional.
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Caracter;stica Biolóicas
%e la C+l#la Plasm$tica El MM es #na !roli'eración %e cels L. B. La c+l#la es relati>amente ma%#ra.
Circ#la en la sanre !eri'+rica. Las citocinas inter>ienen en la clona.
IL/G como 'actor cr#cial !ara !roli'erar. 2actor %e necrosis t#moral a ) T12
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Clasicación
=ama!at;as MonoclonalesA/ Mieloma Mlti!le ! =AMED " y de ca%enas li>ianas
li+res.
Plasmocitoma solitario %e #eso Plasmocitoma e8trame%#lar solitario & mlti!le
Le#cemia %e c+l#las !lasm$ticas. Mieloma nosecretor.
B/ En'erme%a%es lin'o!roli'erati>asMacrolob#linemia %e al%estrom
Macrolob#linemia !rimaria ) IM *
Lin'oma malino
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Clasicación
=ama!at;as monoclonalesC/ En'erme%a%es %e ca%enas !esa%a
En'erme%a%es %e ca%enas !esa%as al'a & beta
En'erme%a%es %e ca%ena & =
D/ Amiloi%osis Primaria
Con mieloma ) sec#n%aria – localia%a *
E/ En'erme%a%es monoclonales %e sinica%o no%eter/
mina%o.
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Princi!ales
mani'estaciones cl;nicas Dolores óseos JK (;n%rome an+mico FK P+r%i%a %e !eso 4:
In'ección 3K 2iebre no in'ecciosa 3 He!atomealia 3F
Es!lenomealia 6 Plasmocitosis e8traóseos 3K
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Datos %e Laboratorio
Hemolobina NKL ::
Pla"#etas 3KK 8 3KN L 3K/3:
Cels !lasm$ticas en m.o. 6K 3: Creatinina Q 4 m%L 4K/4:
Calcio Q 330: m%L 3:/4K
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2enómeno %e Ro#lea#8
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Riñón %el Mieloma
Ins#ciencia Renal El 3K %e los !acientes con mieloma
Ca#sas5 Hi!ercalcemia – Desi%ratación
Cilin%ros %e ca%enas lieras %e!osita%os en lostb#los %istales & colectores.
De!en%e %e la c#ant;a %e la e8creción
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Electro'oresis %e !rote;nas
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Proteinorama
Electro'óretico
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Est#%io c#alitati>o
%e las Inm#nolob#linas
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Lesiones Osteol;ticas
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#esiones steolíticas
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Ra%iora';a %e Tóra8
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Resonancia Man+tica
1#clear
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Dianóstico
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'spirado )edular
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E8amen 2;sico2on%o %e O-o
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E8amen 2;sico
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E8amen 2;sico
Piel / Ten%ones
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Criterios Dianósticos
m;nimos %e Mieloma
Presencia %e 3K %e c+l#las en m.o.
Demostración %e #n !lasmocitoma0 m$s #no %e lossi#ientes criterios5
3/ Com!onente M s+rico Q FKL
4/ Presencia %e ca%enas lieras en orina
F/ Lesiones osteol;ticas
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1ó%#lo c#t$neo mielomatoso
Plasmocitoma
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Plasmocitoma
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2actores Pronósticos
Cl$sicos5
E%a% Esta%o =eneral
Ins#ciencia Renal
Hemolobina
Calcemia Res!#esta al t8.
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2actores Pronósticos
1#e>os 5
B4/ microlob#lina
2ase s;ntesis
Citoen+tica
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Tratamiento La res!#esta es %i';cil con "#imiotera!ia
Mel'alan / ciclo'os'ami%a – !re%nisona –
Poli"#imiotera!ia – ,CMP –
Tratamiento %e mantenimiento – Tratamiento %e reca;%as Tras!lantes %e !roenitores – ICT /
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Tratamiento %e las
Com!licaciones In'ecciones constit#&en #na ca#sa m#&
im!ortante %e morbili%a% & mortali%a%.
Esta%o ran#locito!+nico !or la MT.
(tre!tococc#s !ne#monaie0 Haemo!il#s in#enae & sta!ilococc#s a#re#s.
Ins#ciencia renal0 bacterias ranneati>as – ,ac#nación ne#mocócia. La eritro!o&etina en la anemia
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Tratamiento
%e las Com!licaciones
La !lasma'+resis es ineca en la I.R.=.
La i!ercalcemia – i%ratación – D.asa/l#cocorticoi%es bis'os'onatos –
Com!resión me%#lar – %e8ametasona /
ra%iotera!ia
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Mieloma no (ecretor
1o se !#e%e %etectar com!onente monoclonal s+riconi #rinario !or5
3/ Electro'oresis
4/ Inm#noelectro'oresis o
F/ Inm#no-ación
La inci%encia %e ins#ciencia renal es menor.
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Macrolob#linemia %eal%estrSm
Enfermedades de las cadenas
pesadas.Criolob#linemias monoclonales
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Intro%#cción Consiste en #na !roli'eración monoclonal %e cels B
secretoras %e inm#nolob#linas %e ti!o IM.
Descrita en 3N66 como #n s;n%rome5 anemia –%i$tesis emorr$ica – lin'a%eno!at;as eneralia%as– inltración %e m.o. !or cels lin'o!lasmocitarias – &ele>ación %e las lob#linas s+ricas /.
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Lin'ocitosis
C+l#las Plasm$ticas
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Bió!sia %e 1ó%#lo Lin'$tico
Lin'ocitos Plasmocitoi%es
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Cl;nica
(;ntomas iniciales Astenia 63 Di$tesis Hemorr$ica F3
P+r%i%a %e !eso 39 (;ntomas 1e#rolóicos 34 Trastornos >is#ales 3K In'ecciones 9 Dolores óseo & artralias 6 2enómeno %e Ra&na#% F 1in#no N
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Princi!ales %atos
e8!loratorios He!atomealia 63 Es!lenomealia 6K
A%eno!at;as FG Cambios en el 'on%o %e o-o 4N
Trastornos ne#rolóicos 39 Pr!#ra 34
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(;n%rome %e Hi!er>iscosi%a%
2on%o %e O-o
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Laboratorio Anemia normoc;tica normocrómica FK E8iste lin'ocitosis en #n FK Trombocito!enia en #n 4K ,E( m#& acelera%a
Pilas %e mone%a ) ro#lea#8 *.
En to%os e8iste el com!onente M. Criolob#linas0 en #n 3:. Anemia emol;tica crónica – e8tra>asc#lar /
Eritrocitos ar#!a%os
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Eritrocitos ar#!a%os'orman%o
; pilas en monedas”
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Trastornos %e la Coa#lación Prote;nas "#e !reci!itan con el 'r;o0 se enc#entran
en el 3: %e los !ctes con M0 el : !ro%#censintomatolo;a.
La criolob#lina em!iea a !reci!itar a T 44C & s#concentración s+rica 4KL.
El 3K %e los casos0 la IM reacciona con ant;enoses!ec;cos %e los eritrocitos a T a FJC0 %an%ol#ar a #na AHCrónica.
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PARAPROTEU1A(
Trastornos %e la Hemostasia Alteración %e la '#nción !la"#etaria D+cit %e 'actores ,III0 , & ,II Amiloi%osis asocia%a0 las emorraias !#e%en ser
%ebi%as a #na inacti>ación in >i>o %el 'actor V
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Mastocito C+l#la Ceba%a
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Criolob#linemias
Monoclonales
(on inm#nolob#linas "#e !reci!itan a ba-as tem!erat#ras.
Pro>ocan5 is"#emia & lceras en el c#er!o0%e%os0ore-as0nari & !iel.
Los com!le-os inm#nolob#l;nicos !#e%en %e!ositarse en elriñón & %ar ins#ciencia renal.
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(intomatolo;a %e las
criolob#linas monoclonales
Di$tesis emorr$ica
2enómeno %e Ra&na#%
Is"#emia0 lceras & necrosis
Artritis
Ins#ciencia renal
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Ti!os %e Criolob#linemias
Ti!o I 5 com!onente monoclonal ) IM0 I= o IA * "#eacta !or si mismo como #na criolob#lina. C#an%o s#
concentración es ele>a%a0 s# !reci!itación en!e"#eños >asos !#e%e %ar5
>asc#litis
is"#emia e
incl#so necrosis.
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Criolob#linemiaTi!o I
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Criolob#linemiaTi!o II
Ti!o II 5 inm#nolob#lina monoclonal "#e !osee
acti>i%a% antic#er!o 'rente a otro com!onentes+rico.
La >ariante m$s 'rec#ente %e este trastorno es laIM monoclonal 'rente a I= !oliclonal.
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Amiloi%osis
Este !a%ecimiento '#e %escrito !or ,ircoW eincl#&e #n r#!o %e !a%ecimientos "#e tienen encomn el %e!ósi/to en %i>ersos óranos & te-i%os%e #n material omo+/neo & amor'o llama%oamiloi%e !or s# ani%a% con el &o/%o
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Clasicación %e los %osr#!os
#as 'ormas eneralia%as y las 'ormas localia%as
Amiloi%osis !rimaria en #n soloórano
Asocia%os a mieloma & o sistema
macrolob#linemia Amiloi%osis sec#n%arias Amiloi%osis ere%o'amiliares
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C#a%ro Cl;nico
La !artici!ación %el riñón es comn & a >eces !#e%elle>ar a la m#erte.
El coraón se a'ecta & los !acientes !#e%en s#'rir %e IC.
(e !#e%e a'ectar el sistema res!iratorio & ner>ioso.
Es abit#al la ne#ro!at;a !eri'+rica0 los %e!ósitoscerebrales %e amiloi%e !ro%#cen %eterioro mental) (in%. %e Aleimer *