White Blood Cell Disorders

histogram
 White Blood Cells
• leukocytes
• protect against disease
• interleukins and colony-stimulating factors
stimulate development
• granulocytes • agranulocytes
• neutrophils • lymphocytes
• eosinophils • monocytes
• basophils
 Neutrophils
• light blue granules in acid-base stain
• lobed nucleus
• other names
• segmenters
• polymorphonuclear leukocyte
• bands (young neutrophils)
• first to arrive at infections
• phagocytic
• 54% - 62% of leukocytes
• elevated in bacterial infections
 Basophils
• deep blue granules is basic stain
• release histamine, heparin
• less than 1% of leukocytes
 Eosinophils

• deep red granules in acid stain

• bilobed nucleus
• moderate allergic reactions
• defend against parasitic worm
infestations
• 1% - 3% of leukocytes
• elevated in worm infestations
and allergic reactions
 Monocytes

• largest blood cell

• kidney-shaped or oval nuclei
• leave bloodstream to become
macrophages
• 3% - 9% of leukocytes
• elevated in typhoid fever,
malaria, tuberculosis
 BLymphocytes
lymphocytes
1) 5-15% of circulating lymphs
2) B-lymph differentiation: B-cells mature in 2
stages-antigen dependent and antigen independent
a.) Antigen dependent: when exposed to an
antigen, the B-cell develops into a plasma cell and
produces antibodies against a specific antigen.
b.) Antigen independent: when a stem cell matures
into a pre B-cell.
 TLymphocytes
lymphocytes
1) 80 % of circulating lymphocytes
2) functions: a) Lyses cells infected with viruses and
tumor targets, lymphokine production. b) T-cells
increase or suppress other lymphs
3) T-Lymph Maturation: a) Pre- T-cells begin in bone
marrow and fetal liver. b) Cells go to Thymus(90%
of pre-T cells die here) c) Cells with the ability to
recognize self survive and go into circulation.
4) Large granular lymphs: slightly larger than T- or
B- cells and have cytoplasmic granules. Thought to
be natural killer (NK) cells.
 T lymphocytes
1. T-cells
 a. Th-Cell Activation ( T-helper)
1) occurs when TH cells recognize an antigen.
2) Requires direct cell contact, IL-1, and IL-2.
 b. Cell mediated immunity (CMI)
1) cytotoxic T-cells (Tc) destroy targets by cell contac
2) mediated by TH lymph
3) cytokines activate other cells involved in the respon
4) NK cells kill targets without being previously
sensitized
 Lymphocytes
c. Tc-cell activity
1) Tc-cells kill targets without antibodies, but
with direct cell contact.
2) The Tc-cells can kill many targets in
succession.
3) TH cells secrete cytokines that activate T cells
4) Main function: remove cells infected with
viruses
5) Tc-cells are CD8 positive
 BB cell
Cellssensitization
sensitization of
andactivation
activation

 Sensitization – the binding of antigens to the B cell

membrane antibodies
 Antigens then displayed on B cell Class II MHC

 TH cells activated by same antigen stimulate B cell

 Active B cell differentiates into Memory B Cell or Plasma
cell
 Plasma cells synthesize and release antibody
 WBC disorders
 reactive increase in number – “philias”   
neutrophilia – bacterial sepsis   
lymphocytosis – viral, Immune   
eosinophilia – allergy & parasites
 decreased number – “penias”
 neutropenia, lymphopenia &
eosinopenia, pancytopenia
 drugs, viral infections, radiation,
chemotherapy etc.
Non-Neoplastic Disorders of
White Blood Cells
 Infectious Mononucleosis
Acute self-limiting disease of adolescents/young
adults
 B-lymphocytotrophic EBV

 Fever, sore throat, generalized adenitis

 ↑ atypical lymphocytes (60%), humoral

antibody response, hepatitis, febrile rash
 Infectious Mononucleosis
 Lab: + heterophil reaction (monospot test),
+ specific antibodies for EBV (EBNA, VCA, EA)
 EBV potent transforming virus: B-cell
lymphomas, especially immunosuppressed organ
and BMT recipients
X-linked lymphoproliferative disorder-inability to mount an
immune response to EBV, boys with SH2D1A gene
mutation.
 Cat Scratch Disease
Acute self-limited lymphadenitis of childhood
(<18 y/o)
 caused by Bartonella henselae (related to
rickettsiae)
 axillary and neck adenopathy occurs 2
weeks after a feline scratch / splinter or
thorn injury that regresses in 2-4 months
 raised inflammatory nodule/vesicle/eschar
 Cat scratch disease
 Biopsy: sarcoid-like “stellate”
granulomas/microabscess with central
necrosis filled with PMNs
 Skin test: + CSD skin antigen test
 Treatment: Antibiotics ???
 Useful in immunocompromised patients
(i.e. doxycycline, erythromycin)
Neutrophilia
Toxic Granulation
Leukemoid Reaction
Lymphocytosis
Lymphocytosis - Virocytes
Neoplastic Disorders
Hema-Oncology
 Introduction
 No benign neoplasms – All are considered
malignant or premalignant.
 Neoplastic cells flood blood stream – Leukemia
 Commonly arise in marrow (myelo/ly) or Lymph
node (lymphoid),
 Spread to blood & other RES tissues rarely to
other organs
 Symptoms are due to deficient normal
hematopoiesis. RBC, WBC & Plt.
Neoplastic Proliferations of WBCs
 Myeloid Neoplasms
 AML

 Chronic myeloproliferative disorders (MPD)

 Myelodysplastic syndromes (MDS)

 Lymphoid Neoplasms
 NHL, Hodgkin’s Lymphoma, lymphocytic
leukemias, plasma cell dyscrasias
 Histiocytic Neoplasms
 Leukemia - Clinical Features
 Anemia (low RBC)
 Fever - Infections (low WBC)
 Bleeding tendency (low PLT)
 Tender bones, lymphadenopathy,
spleenomegaly etc. (leukemic infiltration)
 Leukemia Classification
 Acute Leukemias
 Acute Myeloid Leukemia - AML

 AML M0, M1, M2, M3, M4, M5, M6 & M7

 Acute Lymphoid Leukemia - ALL

 ALL - L1, L2 & L3 - maturity

 Chronic Leukemias
 Chronic Myeloid Leukemia- CML

 Chronic Lymphoid Leukemia - CLL

 Acute Leukemias (AML/ALL)
 Block in differentiation – “blasts” w/ prolonged
generation time
 Accumulation of “blasts’
 Result from a clonal expansion
 Failure of maturation
 Suppress normal hematopoiesis

1. ↓ in normal RBCs, WBCs and PLTs
2. Aim of TX is to reduce the leukemic clone to allow
reconstitution with the progeny of remaining
normal stem cells
 Acute Leukemias (AML/ALL)
Clinical features
 Abrupt onset
 Symptoms related to BM depression
 Fatigue from anemia, fever from infection,
bleeding from thrombocytopenia
 Bone pain and tenderness
 BM expansion with subperiosteal infiltration
 Generalized adenopathy, hepatosplenomegaly
(ALL>AML)
 CNS manifestations (ALL>AML)
 Headache, vomiting, nerve palsies
 Acute Leukemias (AML/ALL)
 Laboratory
 Leukocytosis (>100,000 or <10,000) with “blasts” in
circulation and BM
 Lymphoblasts: with + PAS aggregates
 Myeloblasts: + myeloperoxidase
 Immunophenotyping
 Tdt (DNA polymerase): + in 95% of ALL
 Lineage specific markers: CD19 (B cell), CD2 (T cell)
 Karyotyping (predictive of prognosis)
 Usually nonrandom abnormalities
 Pre - B: Hyperdiploidy assoc with t(12,21) - good
Ph chromosome - poor
 platelet coagulation

petechiae, purpura hematoma, joint bleeding

 ALL-Acute Lymphocytic Leukemia

 ALLs comprise 80% of childhood leukemia

(peaks at age 4) and are usually pre-B phenotype
 FAB classification L1, L2 & L3
 CD10 +ve, Pre B cell type common
 Growth failure, Fever, Anemia
Lymphadenopathy, bleeding.
 Moderate Hepatosplenomegaly
Organomegaly
ALL:Cervical Lymphadenopathy
Mediastinal Lymphadenopathy - ALL
ALL-L1
ALL-L2
ALL-L3
Chronic Lymphocytic Leukemia
 Elderly age
 Anemia, fever & bleeding – slow over years.
 Lymphocytosis & Lymphadenopathy
 Spleen, & liver enlargement
 Common B cell (CD5 +ve)
CLL
CLL – Blood Film
CLL: Smudge Cells
CLL: Balloon Cells
 Myeloid Neoplasms

 Acute myeloblastic leukemias (AML)

 block in differentiation → ”myeloblasts”
 Chronic myeloproliferative disorders
(CMPD)
 no block in terminal differentiation, but
with dysregulated growth
 Myeloid neoplasms
 Myelodysplastic syndromes (MDS)
 Disordered terminal differentiation
 Dysplastic BM precursors
 “cytopenias”
 “Blurred divisions”-MDS and CMPD
transform to AML
 Acute Myeloblastic Leukemia
 Usually adults, incidence ↑ with age
 Diverse:
 Predominant line of differentiation
 Cell maturity
 S/Sx like lymphoblastic leukemia, due to
BM failure: fatigue, pallor, bleeding,
infections, & “granulocytic sarcoma”, no
significant lymphadenopathy, moderate
splenomegaly
Acute Myeloblastic Leukemia
 Diagnosis:
 Morphology
 Myeloblasts
 Auer rods
 Histochemistry
 Immunophenotype
 Karyotype
 Acute Myeloblastic Leukemia
 Morphology: blasts with delicate nuclear
chromatin, azurophilic granules and “Auer rods”
 Classification: good, intermediate, bad risk based
on karyotyping (ie, good risk aberrations t[8,21],
inv [16] )
 M3 t(15,17) results in abnormal PML/RARA
fusion protein that blocks differentiation at
promyelocytic stage which is overcome by
retinoic acid (ATRA)
 Acute myeloblastic leukemia
 Histochemistry: MPO positive
 Immunophenotype
 Myeloid associated antigens:

CD13, CD14, CD15, CD64, CD33

 Platelet associated antigens:

GPIIb/IIIa, CD42b, CD61, CD41

 Course:
 Conventional therapy -15 -30% disease free survival
 Stem cell transplant
 Acute Myeloblastic Leukemia

 Prognosis depends on cytogenetic risk

categories: 5 year survival
 70 - 90% - AML with t(15;17) with
ATRA + CT
 10 - 30% - AML with multiple
cytogenetic aberrations
 Acute myeloblastic leukemia
 Indication for stem cell transplant or bone
marrow transplant: very high risk in first
remission or after relapse
 Results of BMT in AML : 30 - 50 % cure
rate at 5 years, but at a price of 15 - 35%
transplant related mortality within 100 days
 FAB Classification of AML
Class Morphology Comments
M0 blasts lack cytologic markers 2-3%

M1 very immature myeloblasts 20% (Ph chromosome

-worsens prognosis)
M2 myeloblasts & promyelocytes 30%, t,(8;21) good prognosis

M3 hypergranular promyelocytes 5-10% DIC, t(15,17)

“many Auer rods”

M4 myelocytic & monocytic diff. 20-30%, inv16/del16q better

prognosis
M5 monoblasts & promonocytes 10%, pediatric age-young
adults, 11q23 abnormalities
M6 erythroblasts > myeloblasts 5%, older adults

M7 megakaryocytic blasts myelofibrosis

AML-M0 - Undifferentiated
 Acute Myeloid Leukemia: M1
Myeloblasts without Differentiation
 Acute Myeloid Leukemia: M2
Myeloblasts with Some Differentiation
AML-M2 - with maturation
AML-M3 - Auer Rods
AML-M4 - Myelomonocytic
Acute Myeloid Leukemia: M5
Monocytic Leukemia
AML-M6 : Erythroleukemia
Acute Myeloid Leukemia: M6
Erythroleukemia
AML-M7 : Megakaryocytic
Acute Myeloid Leukemia: M7
Megakaryocytic Leukemia
AML-M5 - Gum Hypertrophy
 Lymphoid Neoplasms
 Vary in clinical presentation/behavior
 Leukemias: arise from the BM and circulate
peripherally
 Lymphomas: tumor masses in LN and organs
 Plasma cell dyscrasias: bone mass with
systemic Sx related to inappropriate
production of complete/partial monoclonal Ig
polypeptide
 Lymphoid neoplasms
 Can spread to LN, spleen, liver and BM
 Involve the peripheral blood – “leukemia”
 Controversial classification: clinical,
morphologic, phenotypic and genotypic
 Lymphoid Neoplasms
 Derived from a SINGLE transformed cell
“monoclonal”
 Disrupt normal immune regulation:
 Immunodeficiency
 Autoimmunity
 80-85% B-cell origin: CD10, CD19, CD20 &
surface Ig
 15% T-cell origin: CD2, CD3, CD4, CD7 &CD8
 NK tumors rare: CD15 & CD56
 Lymphoid neoplasms
 Points:
 Tdt - immature T/B cells (lymphoblasts)
 CD13, CD14, CD15, CD64 – myeloid cells
 CD34 - stem cells, early myeloid and
lymphoid progenitor cells
 Lymphoma
 Tumors of lymphoid tissue
 Lymphadenopathy
 Fever
 Hodgkins lymphoma
 Non-Hodgkins lymphoma
 Hodgkin vs. Non-Hodgkin
Lymphoma
HL NHL
 Localized to single  Multiple peripheral LN
axial group of LN  Noncontiguous spread
 Orderly spread by  Common mesenteric &
contiguity Waldeyer ring
 Rare mesenteric &  Extranodal common
Waldeyer ring
 Extranodal uncommon
Right neck mass
Lymphoma

Row of
enlarged
lymph nodes
 Hodgkins Lymphoma

 Children & adults – double peak.

 Lymphadenopathy, painless, firm
 Fever, Eosinophilia
 Reed-Sternberg cells - B lymphocytes.
 ? Viral etiology
Splenomegaly

Spleen
Hodgkins lymphoma
 Non-Hodgkins Lymphoma
 Fever, anemia, infections
 Marked Lymphadenopathy
 No RS cells or eosinophilia
 Large group of different lymphomas
 Clinical – low, intermediate & high grade.
 Cell type – B cell, T cell, Histiocyte & other

 Histology – Follicular & diffuse.

 Lymphoid Neoplasms
 Precursor B-cell Neoplasms
 Peripheral B-cell Neoplasms
 B-cell CLL/SLL
 Mantle cell lymphoma
 Follicular Lymphoma
 MALT lymphoma
 Plasma cell myeloma
 Burkitt Lymphoma
 Lymphoid neoplasms
 Precursor T-cell Neoplasms
 Peripheral T/NK Cell Neoplasms
 Mycosis fungoides/Sezary syndrome
 Hodgkin's Lymphoma
 Nodular Sclerosis
 Mixed cellularity
 Summary of More Common Lymphoid Neoplasms
Entity Frequency Morphology Comments

SLL/CLL 3-4% of lymphomas Diffuse pattern, CD5 + Old age

30% of leukemias Small Mature B cell Indolent
lymphocytes Express sIg* Gen.adenopathy

Follicular 40% of adult Follicular pattern, CD10+, BCL2+ Same as above

lymphoma lymphomas Germinal center Mature B cells t (14,18)
cells Express sIg Difficult to cure

Burkitt <1% of lymphomas Intermediate size CD 10+, sIg Endemic in Africa

lymphoma in the US NUCLEOLI Mature B cells Rapid spread
“starry sky” ↑ ImmunoSx Px

Plasma cell Most common Plasma cells w/ Mature B cells Bone lesions, ↑ Ca
myeloma lymphoid neoplasm nucleoli and Ig with cIg** Plasmacytoma
in adults inclusions Renal insufficiency

M. fungoides/ Most common type Usually small cells CD4+, CD3+ Local/generalized
Sezary of cutaneous with convoluted Mature T cells skin involvement
syndrome lymphoma nuclei Very indolent

* sIg – surface immunoglobulin **cIg – cytoplasmic immunoglobulin

 NHL- Histologic types

Diffuse - & - Follicular

 NHL- Histologic types

Small – Intermed. – Large

 Plasma Cell Dyscrasias
 B-cell neoplasm
 Expansion of a single clone of Ig-secreting cell ---
↑ in serum level of a single homogeneous Ig or
its fragments (M component)
 called “monoclonal gammopathies”

 MGUS: M component + in normal elderly people

 Types: Multiple Myeloma, localized
plasmacytoma, lymphoplasmacytic lymphoma,
heavy chain disease, primary amyloidosis, MGUS.
 Multiple Myeloma
 Most common malignant plasma cell dyscrasia
1. Clonal plasma cell (myeloma cells) proliferation (BM)
 by IL-6 produced by fibroblasts and macrophages

2. Lytic bone lesions

 Translocation involving IgG on Chromosome 14
 M component:
 IgG (60%), IgA (25%), Κ or λ (20%), rare IgM, IgD, IgE
 Light chains excreted in urine as Bence Jones protein
 Light chain disease - light chains only (no M component)
 80% of patients will synthesize complete Ig
molecules and excess light chains
 Multiple Myeloma
 Lytic bone lesions throughout skeletal system
 “punched out lesions” on X-ray
 Vertebral column > ribs > skull >pelvis >femur
 Medullary cavity → erode cancellous bone → cortical bone
 Resorption by cytokines produced by myeloma cells (Il-6,
TNF, IL-1ß)
 D/D lymphoplasmacytic lymphoma – no lytic lesions
 Diagnosis:
Bone Marrow: plasma cells (with abnormal features)
 Characteristic “punched out lesions”,
 Serum and urine electrophoresis

 Plasma cell infiltration in other tissue (spleen, liver, etc.)

 Myeloma Nephrosis + calcification
 Multiple Myeloma
 Clinical Features:
 Bone pain – pathologic fractures, hypercalcemia
 CNS Sx from hypercalcemia
 Anemia – BM effacement by plasma cells
 Infections – suppression of normal Ig secretion
 Hyperviscosity syndrome – excessive secretion and
aggregation of myeloma proteins
 Renal failure
 Amyloidosis (5-10%)
 Nonsecretory myelomas (1%) - Ig present in the
plasma cell masses only not in serum or urine
 Course: progressive, 2-4 years median survival
Myeloma – Bone Marrow
Chronic Myeloproliferative Syndromes
 Neoplasms, Slow, Chronic, Proliferation - ?Bgn
 Increased, Functionally abnormal cells.
 Extramedullary hemopoiesis - Organomegaly
 Progress to Leukemia – end stage
 Classification:
 Polycythemia rubra vera (PV)
 Chronic Myeloid Leukemia (CML)

 Essential Thrombocythemia (ET)

 Myelofibrosis (MF)
MPS: Classification
 Causes of High Hct/polycythemia
 Relative or spurious erythrocytosis
 Hemoconcentration secondary to dehydration
 (diarrhea, diaphoresis, diuretics, deprivation of
water, emesis, ethanol, etc.)
 Absolute erythrocytosis (True ):
 Tissue hypoxia - High altitude, Pumonary disease,
respiratory def. Right to left cardiac shunts,
Carbon monoxide intoxication, High oxygen-
affinity Hb.
 High EPO - Renal disease, Tumors eg. HCC.
 Androgen therapy
 Primary - Polycythemia vera
 Polycythemia vera (PV)
 Adults (40-60)
 Trilineage clonal proliferation (from a single neoplastic
stem cell)
 absolute ↑ rbc mass but with ↓ Epo

 D/D: relative polycythemia ↑ Epo

 Clinical: thrombotic/hemorrhagic symptoms

 plethora/cyanosis, pruritus, headache, GI/gum/nose
bleeding, gout, stroke, Budd-Chiari syndrome
 Lab: ↑ RBC (6-10M/uL), ~60% Hct, ↑ WBC/PLTs
 BM: hypercellular (trilineage) + fibrosis
 Polycythemia vera (PV)

Course:
 Natural history - progressive transition to a “spent
phase” towards MMMF
 BM fibrosis → EM hematopoiesis (splenomegaly)
 Leukemia transformation
 Less frequent than CML
 AML (2%) in those treated with phlebotomy
 AML (15%) in those treated with RT,
chlorambucil
MPS - P. Rubra Vera (PV)
Chronic myelogenous leukemia
 Adults, usually 40-50
 Philadelphia chromosome
 Clinical: slow onset, nonspecific s/sx, marked
splenomegaly
 Lab: leukocytosis (>100,000)
 PMNs, myelocytes, eosinophils, basophils, <5% “blasts”
 BM: hypercellular (granulocytic/megakaryocytic)
 D/D: leukemoid reaction (↑LAP)
 Course: 50% accelerated phase
 ↑ anemia, ↓ PLTs, ++ cytogenetic abn, blastic crisis
 Chronic myelogenous leukemia
(CML)
Course:
 50% abrupt blast crisis:
 30%: Tdt + blasts that express B lineage (+CD19/20)
 70%: “myeloblasts”
 Clonal gene rearrangements
 50% accelerated phase
 ↑ anemia, ↓ PLTs, ++ cytogenetic abn, with final
acute leukemia transformation (blastic crisis)
Treatment: Gleevec (Imatinib®)
Tyrosine kinase that targets BCR-ABL fusion protein
Chronic Myeloid Leukemia:
 Blood Film
Plenty of
Platelets

Megakaryocyte
MPS : E.T. Bleeding
MPS : E.T. Thrombocytosis

BM & PS
 Myeloid metaplasia w/
myelofibrosis (MMMF)
 Early occurrence of “spent phase”
-may begin with PV or CML features
 Clinical: Marked hepatosplenomegaly, anemia
and thrombocytopenia
 Etiology: fibroblastic proliferation (polyclonal)
by PDGF and TGF-ß
 BM: hypocellular with diffuse fibrosis
 Lab: PS-leukoerythrocytosis, no Ph chromosome
 Course: 5-15% “blast crisis”
MPS : M.F. Organomegaly
MPS : MF - Radio Iron Study
 Myelodysplastic Syndromes
 Clonal stem disorder: maturation defect, ineffective
hemotopoiesis, ↑↑ AML transformation
 Etiology: idiopathic, post CT or RT
 BM: hypercellular PS: pancytopenia
 Unstable stem cell clone prone to mutations → AML
 Cytogenetics: 5 and 7 (loss or long arm deletions)
 Clinical: adults with hemorrhages, anemia, infection
 Treatment:
 Poor response to CT (underlying stem cell failure)
 May respond to T cell immunosuppressants
 Myelodysplastic Syndromes:
 Excess proliferation in marrow.
 But functional & Structural abnormality

 Ineffective Myelopoiesis.

 Peripheral pancytopenia.

 Also known as Refractory Anemia’s

 Not responding to hematenics.

 Myelodysplastic Syndromes:
FAB classification
 RA : Refractory Anemia (Blasts <1%)
 RARS : RA with Ring Sideroblasts (<1%)

 RAEB : RA with excess blasts (<5%)

 RAEB in T : RAEB in transformation (>5%)

MDS - Dysplastic Erythroblasts
MDS: - Ring Sideroblast
 Histiocytic Neoplasms
Langerhans cell histiocytosis
 Langerhans cell proliferation (+HLA-DR/CD1)
 “HX bodies” (Birbeck granules)
 3 conditions that are different expressions of the same
disorder:
 Hand Schuller Christian disease
 “HSC triad”- exophthalmos, diabetes insipidus,
calvarial bone lesions
 Letterer-Siwe disease: < 2 y/o, skin lesions,
hepatosplenomegaly, osteolytic bone lesions
 Eosinophilic granuloma: unifocal vs. multifocal
Disorders of the Thymus and Spleen
 Hyperplasia of the thymus
 + lymphoid follicles within the medulla
 M. gravis, SLE, rheumatoid
 Thymoma
 Splenomegaly
 Disorders of the thymus and spleen
 Thymoma (neoplastic epithelial cells)
 Benign thymoma: cytologically/biologically benign
 Malignant thymoma:
 Type I : cytologically benign/biologically aggressive
 Type II: thymic carcinoma (5%)
 usually squamous cell carcinomas
 Lymphoepithelioma-resemble NSP carcinomas
with EBV genome, anaplastic epithelial cells in a
background of benign lymphocytes
 Splenomegaly
 Massive splenomegaly (>1000 g)
 Chronic myeloproliferative disorders
(CML,MMMF)
 CLL (less massive)

 Hairy cell leukemia, lymphomas, malaria, Gaucher

 Moderate splenomegaly (500-1000 g)

 Chronic congestive splenomegaly (portal HTN0

 Hereditary spherocytosis

 AIHA, Amyloidosis, NP disease, TB

 splenomegaly
 Mild splenomegaly (<500 g)
 Acute splenitis

 Infectious mononucleosis

 Acute splenic congestion

 Summary
 Leukemias – Starts in marrow spread to blood
 Anemia, infections & Bleeding
 Enlargement of Liver, Spleen lymphnodes
 Acute/Chronic & Myeloid & Lymphoid.

 Lymphomas – Tumors of lymphnodes.

 Fever & lymphadenopathy
 Types - Hodgkins & non- hodgkins, special types.

 Premalignant conditions
 MDS: Myelodysplastic syn – Less & Dysplastic
 MPS: Myeloproliferative dis -Excess & abnormal