Malignant lymphomas Flashcards
(43 cards)
all Bm cells arise form
immature stem cells
Bm chnage depens on severity of injury
slight injury–>^BM cellularity
sever–>decerased BM celllarity
–>occurance of bm DYSPLASIA
APLASTIC ANEMIA
etiologt
can develop into
etio
priamry: unkown
secondary: drugs, tocins, infeciton-virla, radiaiton
pathophysoo
-destruction of BM stem cell–>PANCYTOPENIA
develop into->MDS OR AML
megaloblastic anemia
causes and pathophys
causes
1. deficemy of vit B12
-autoimmune gastritis: IF
-malabsorptiona nd maldigestion syndrome
-food deficit
2. folic acid deficecny: alcholics, poor socisal
pathophys:
-unsufficent DNA syntheiss–>destruciton of erythroid stem cells–>anemia
PERNICIOUS ANEMIA
MYELOPID NEOPLASIA GENERAL
-clonal disorders of undiff/stem resp. progenitor cells of hemopoieses
lesions:
-^prolif
-disorder/blocakge of maturaito
cancers of myeloid cells (the bone marrow cells that make red cells, white cells, platelets).
Main types:
Acute Myeloid Leukemia (AML) → lots of immature blasts, aggressive.
Myeloproliferative Neoplasms (MPNs) → overproduction of mature cells, slower course.
Myelodysplastic Syndromes (MDS) → bad, dysfunctional cells, bone marrow failure.
Overlap syndromes (mixed features).
MDS etiology+pathogeneis+MORPH
-injurt of stemcells of hemopoiesis
-radiation, tocicn, chemo, inherited
patho
- unefective hemopoesis
-decresed sensitivty of hemopoietic cell to GF+^cellualr apoptosis
-not incresed prolif of clonal population
-acc of genetic abonarlitis of stem cells–>distubance of maturaito–>acc of blast–>ACUTE LEUCEMIA
mopho: hypercellualr BM
classification of mds
- accordinng to linage
- Single–>SLD
-MLD, RS(ring siderobalst–>MDS-RS-SLD/MLD), MDS-U - acording to blast in Bm resp peripheral bllod
-1=5-9%
-2= 10-19% - specific genetic abnormalit
-5q
clinical manifestaiton of MDSS
OBVI PANCYTOPENIA-bm DONT WORK
- BM FAILURE
-aneima
-dyserytropeoieses
-hypocia of tissue
- failure
-impared thrombocyte
myeloprolipherative neoplasm (MPN)
dosroder affecting the myeloid stem cell of hemopoiesis–>affected ALL 3 LINES OF HEMOPOIESOS
-^PROLIF OF LINES+COMPLETED MATURATION–>
-lead to BM fibrosis–>reduction of hemopoieisi
clincal MPN
-^/red prolif of eryhto–>POLYGLOBULIA/ANEMIA
-^prolif of granulo–>NEUTROPHILIA
-^prolif of mega–>THROMOCYTOSIS
-^pooling and destruction of blood clels in spleen—>PSLENOMEGALY
-BM fibrosis–>ANEMIA, NEUTROPENIA, THMBOCYTOPENIA
-extrmedullary hemopoiesi in spleen&liver–>HEPATOSPLENOMEGALY
Genetic MPN
phildelphia chroosme=formation of bcr/abl fusion gene
Ph positive MPD–>chronic myelogenous leukemia (CML
ph neg mpd
Ph neg mpd
pylocytemia vera -PV
esssentila thrombocytaemia -ET
primary myelofibrosis-PMF
common muation JAK 2
mutation of calreticuline gene in jak2 is neg in
ET, PMF
The presence of JAk2 mutation enables:
To distinguish ph1 negative MPN from CML
CML general+morpho
most often MPD
-mostly older
-Ph1 chromo POS
morpho
-hypercellular BM
-prolif granulopoiesis w maturation
-^megakryocye
-BLOOD reduces
-BM fibrosis
clnical CML
first
-leukocytois, thrmobocytsos, anemia, splenomegaly and heptomegaly
-fatigue, weight loos, nigtsweaat
later
-thrombocytopenia,anemia
-spkenomegaly
-balst transformaiton
polycytehmia vera
general
msmot common of ph neg
trilinear prolif!!!!!!
ERYTHROPOIESIS IIS MOS TPROMINENT
obliteration of Bm hemopoiesis by diffue reticulin/collagen fibrosis!
PV general
early
-polyglobulia, thrmobocytosis, leukocytosis
-hypertension, thromosis->heart infarciton, rbain
-embosm, fatique
-visial
-hyperuricemia
-HEAPTOSPLENOMEGALY
terminal
-BM failure
PRONGOSIS
-10Y
essential thrmocotthemai
-morpho
-clinical
-slightly hypercellualr
-MONOLINEAR prolif fo MEGARYOTIC LINEAGE
-reticulin fibrosis
clincial
-mostly asym
-thrombocytosis-throboembolic and haemorrhaig complicatoin, infarctoin, splenomegaly
-slow fibrosis=BEST PROGNOSI OF MPD-15 Y
Primary myelofibros-PMF
MORPHO
end
clinical
-hypercell bm
-BILINEAR-MGK &GRANULO
-RED OF HEMO
-fbirotic BM obliteration is end result
clincial:
- asymptomatic moslty
early: leukocytoss+thrombocytosis like ET
advanced: leukocytosis, anemia, thrombocytopenia, fatique, dyspnoe, weight loss, ngiht sweat
-heaptosplenomegalu:very common!!!
acute leukemia(aml) pathogeneis
-absolute blocakeg of maturation in some point hemopoiesis
-acc of immature precursos befroe blocage
types
1.acute lymphoid leukemia: childhood
2. acute myeloid: 70%%, middle/older
acc of imature precurso in BM->hypercell BM, red of all cell lines,reful fo blast into blood
AML
Bm failure->anemia, dyspnoe, weigloss,
-neutropenia
-thrombocytopenia
immature balst in blood->leucaemia, infiltartion of other orgns of hemopoes, skin, soft, kindey, cns
localised infilatrtion of blasts
myeloid sarcoma
myelosarcoma=localized infilatrtion of myeloblasts
-skull, sternum, vertebral colom
etio:
-PB and BM involvnetn of aml
-realps of AML
plasma cell myeloma
diffue tumurous burden of plasma cell in BM, extramee manifestaion in adavnced idsease
clincial mani+labratory: hypercalcemia, renal damage, anemia, bone lesions, proteinuria, hyperurisemia,hypoalbumenia
