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Haemopoiesis
According to age
Fatty tissue replacment
in long bones
Haemopoiesis
50% of the
marrow is fat.
reversion to
haemopoiesis
FatHaemopoietic tissue
So the normal
cellularity is
50%
Stem cell
 Undifferentiate
 Self renewal
 Rare
 CD34+ CD38-
1stem cell = million
Growth Factors
Proliferation
differentiatio
maturation
apoptosis
Diagnostic methods
Why ?
Treatment
prognosis
Peripheral blood
EDTA
CBC
DBC
Evaluate cell shape
Diagnostic methods
Bone Marrow Aspiration
Bone Marrow Biopsy
0.5 - 3 ml
Heparin, EDTA
1-2 cm
Diagnostic methods
Painfull !!!!!
Bone Marrow Aspiration
Bone Marrow Biopsy
Evaluate cellularity
Percentage of each
lineage
Dysplastic cell
Diagnostic methods
Lymph node biopsy
Cytochemistry
Myeloperoxidase ,Esterase, Sudan black, Terminal
deoxynucleotidyl transferase , leukocyte ALP
Immunofenotyping (CD)
Cytogenetics , Molecular tests
Diagnostic methods
Originate from
BM
Lymphatic system
Mechanisim: mutation in stem
cell
Proliferation
Apoptosis
Haematological cancers
Haematological cancers
mature immature
chronic acute
survival
survival
Classification
• HL
• NHL
• CML
• PV
• ET
• IM
• ALL
• AML
• CLL
Leukemia
Myeloprolif
-erative
disorder
lymphoma
MM
MDS
HCL
General Symptoms
Fever
Recurrent infections
Bruising
petechial
bleeding
Fatigue
Pale
Night
sweats
Lymphoad-
enopathy
Weight
loss
Spleno-
megaly
Bone
pain
Statistics
The20MostCommonCancersin2010
8%ofcancers
Statistics
Neoplasm in the
haemopoeitic tissue
Leukeamia
Monoclonal
proliferation
of leukocyte
lineage
Infiltration
BM,
blood,…
BM failure
leukocytosis
No specific reason
Risk factor
Etiology
environmental
Risk factor
Etiology
host
• Genetic disorders
(down, fanconi,
bloom)
• Immunodeficiency
Leukeamia
Leukemia
acute
acute lymphoblastic leukemia
(ALL)
acute myelogenous leukemia
(AML)
chronic
chronic lymphocytic leukemia
(CLL)
chronic myelogenous leukemia
(CML)
Leukeamia
Monoclonal Blast proliferation (myelo
/ lympho)
Useless cells !!!!
Affect haemopoiesis
(BM failure)
Acute Leukemia
WHO criteria
According to blasts in BM
Acute Leukemia
Above 20%
Acute leukemia
Below 20%
MDS
Acute Lymphoblastic Leukemia
(ALL)
ALL- Clinically
Bone marrow failure
• Anemia
• Bleeding
• Infections
Infiltration
• Hypatosplenomegaly
• Adenolymphopathy
• Bone pain
FAB:
Morphologically 3 types
of ALL
(L1, L2, L3)
ALL- Diagnosis
Peripheral blood
• RBC
• Platelet
• WBC
• Lymphoblast
ALL- Diagnosis
Peripheral blood
• RBC
• Platelet
• WBC
• Lymphoblast
ALL- Diagnosis
Peripheral blood
• RBC
• Platelet
• WBC
• Lymphoblast
ALL- Diagnosis
Bone marrow aspirate
• hypercellularity
• high lymphoblast
>20%
Immunofenotyping
Blood /BM
Differential diagnosis
Cytochemistry
ALL (-) peroxidase
AML (+) peroxidase
ALL- Diagnosis
Any age , mostly Adult (65 old)
incidence rate x 20 times + down syndrome
Acute Myelogenous Leukemia (AML)
Increase non-lympho blasts:
erythroblast, megakaryoblast, monoblast,
myeloblast
Immunofenotyping to differ them
Accombined by genetic disorders e.g:
t(8;21), t(15;17)
AML
FAB
8 types according to cell differentiation
,maturation
AML
M0: minimally myeloid differentiated
M1: without maturation beyond the
myeloblast stage
M2: with maturation
M3: hypergranular promyelocytic
M4:myelomonocytic
M5: monoblastic (M5a) / monocytic (M5b)
M6: erythroleukaemia
M7: megakaryoblastic
Rare types (e.g. eosinophilic, natural killer)
AML - classification
Bone marrow failure
• Anemia
• Bleeding
• Infections
Infiltration
• Hypatosplenomegaly
• Adenolymphopathy
• Bone pain
• gum hypertrophy
AML- Clinically
M1
Blood smear
myeloblasts
Auer Rods
AML- Diagnosis
M1
BM aspirate
Blast 90%
AML- Diagnosis
M2
Blood smear
promyelocytes
AML- Diagnosis
M2
BM aspirate
Blast 30-80%
AML- Diagnosis
M3
Blood smear
Promyelocytes
Auer rods
AML- Diagnosis
M3
Blood smear
Promyelocytes
Auer rods
AML- Diagnosis
M3
BM aspirate
Blast <30%
AML- Diagnosis
M4
Blood smear
Myeloblast
monoblast
AML- Diagnosis
M5
Blood smear
Monoblast
(M5a)
Promonocytes ,
monocytes
 (M5b)
AML- Diagnosis
M5
Monocytes and its
procurser
 + esterase (red)
AML- Diagnosis
M6 need BM sample
AML- Diagnosis
M0 , M7 similar
smear with ALL
M7
megakaryoblasts
>30%
AML- Diagnosis
AML- Diagnosis
Peripheral blood
• RBC
• Platelet
• Neutropenia (M2)
neutrophilia
Hematological Malignancies 1/2

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Hematological Malignancies 1/2

Editor's Notes

  1. الحياة الجنينية يقوم الكيس المحي مع الكبد و الطحال و من ثم نقي العظم بعد الولادة فالمكان الوحيد للتصنيع هو النقي. الرضع تشارك جميع العظام تقدم العمر يحصل نمو لنسيج دسم
  2. للعودة للحالة المنتجة للدم عند الحاجة كما في فقر الدم الانحلالي حتى أن الكبد و الطحال قادران
  3. واحدة من كل 20 مليون خلية منواة بالنقي تشبه الخلايا اللمفية الصغيرة
  4. تأتي من مكونات النسيج الضام في النقي و من نسج أخرى ( مثل erythropoietin
  5. B ذاكرة أو الى خلايا بلازمية مفرزة لل immunoglobulin.
  6. قد لا يلاحظ التكاثر الورمي في الدم بل يبقى لفترة في النقي. القمة الامامية للعظم الحرقفي و في بعض الحالات يمكن البزل من عظم القص الخزعة عند عدم القدرة على بزل النقي كما في حالات تليف النقي
  7. يزداد معدل حدوثها مع تقدم العمر و تتطور عند الكبار
  8. الاضطرابات التكاثرية النقوية
  9. يرتبط مع burkitt’s lymphoma Human T-cell leukemia-lymphoma virus
  10. عوز المناعة الوراثي
  11. اول تنين
  12. متوسط عمر 5
  13. اضطراب وظيفة الكريات البيض وقلة العدلات
  14. البيض غالباً مرتفعة على حساب الارومات وقد تكون طبيعية او ناقصة يوجد تصنيف آخر لل WHO يأخذ الاختبارات الجينية و الجزيئية بعين الاعتبار الى جانب الصفات الشكلية و المناعية و الكيميائية. L1 الارومات متفاوتة الحجم و تصل حتى ضعفي الحجم الطبيعي ,نسبة النواة إلى السيتوبلاسما عالية.
  15. في L2 الارومات اكبر من النمط الاول , ذات شكل غير منتظم و السيتوبلاسما فيها أكثر.
  16. النمط L3 نادرجداً تكون فيه الخلايا منتظمة الشكل ذات سيتوبلاسما محبة للقلوي بشدة ,مع وجود حويصلات في بعض الخلايا حديثاً يصنف حسب WHO على انه مرحلة ابيضاضية في سياق NHL و ليس ابيضاض حاد
  17. خلايا نقوية اولمفية ناضجة او طلائع B , T
  18. في M0 , M1 الخلايا المسيطرة هي myeloblasts و هي خلايا كبيرة بنسبة (نواة : سيتوبلاسما) مرتفعة , مع وجود نوية او اثنتان. في M1 تحوي السيتوبلاسما حبيبات صغيرة تدعى عصيات اور Auer Rods
  19. في M1 تشكل الارومات 90% من خلايا النقي المنواة , و تظهر كخلايا متوسطة الى كبيرة الحجم فيها نواة دائرية او بيضوية تحوي نوية او اثنتان . قد تظهر بعض الحبيبات والحويصلات و Auer rods في السيتوبلاسما
  20. في M2 توجد سليفة الخلية النقوية promyelocytes التي تحوي حبيبات اكثر من الارومات النقوية .
  21. في M2 توجد نفس الارومات لكنها تشكل 30-80% من خلايا النقي المنواة . مع تمايز اكثر من10% من الخلايا الاخرى الى سلاسل المحببات (promyelocytes to neutrophils) . و 20% من الخلايا يتمايز لسلسلة الوحيدات.
  22. النمط M3 مميز بأن سيتوبلاسما promyelocyte مليئة بحبيبات كبيرة و قد توجد حزم من Auer rods . يوجد نمط يدعى M3 variant يصعب تشخيصه بفحص اللطاخة الدموية .تكون promyelocyte بدون حبيبات أو حبيبات ناعمة كالغبار مع وجود حزم Auer rods ,وتوجد العديد من الخلايا سليفة النقوية ذات نواة مفصصة ثنائية.
  23. يوجد نمط يدعى M3 variant يصعب تشخيصه بفحص اللطاخة الدموية .تكون promyelocyte بدون حبيبات أو حبيبات ناعمة كالغبار مع وجود حزم Auer rods ,وتوجد العديد من الخلايا سليفة النقوية ذات نواة مفصصة ثنائية.
  24. الخلايا سليفة النقوية الشاذة promyelocyte تكون اكبر من الارومات الطبيعية, و ذات نواة باشكال مختلفة. الستوبلاسما فيها حبيبات كبيرة حمراء او بنفسجية مع وجود Auer rods . و في النمط المتغاير تكون السيتويلاسما عديمة الحبيبات أو فيها حبيبات ناعمة جداً.
  25. في M4 نشاهد الارومات النقوية و ارومات الوحيدات . ارومة الوحيدات اكبر و حجم السيتوبلاسما اكبر و محبة للقلوي , و قد تكون دائرية بنواة دائرية أو ذات شكل غير منتظم بنواة مفصصة . كما نلاحظ فيM4 ان الارومات تشكل 30-89% من خلايا النقي.
  26. M5 يقسم الى تحت نمطين اذا كانت الخلايا المسيطرة هي ارومة الوحيدات monoblast (M5a) ,و اذا وجدت خلايا سليفة الوحيدات promonocytes او وحيدات ناضجة monocytes (M5b) سليفة الوحيدات اكبر و ذات سيتوبلاسما اكثر قلوية و حبيبية اكثر من الوحيدات.
  27. M6 تشكل طلائع الكريات الحمر الشاذة اكثر من 50% من خلايا النقي, تبدي هذه الخلايا ضخامة و تعدد النوى
  28. ذات اشكال مختلفة pleomorphic و تفرق عن الارومات الاخرى بصبغة Romanowsky او بالتنميط المناعي
  29. الصفيحات و في حالات نادرة زيادة الصفيحات.