Acute Leukemia and Lymphoma R

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Acute Leukemia + Malignant Lymphoma ( 2011 )

1 4th

year – female

Leukemia

Acute Chronic

Myeloid Acute myeloid leukemia Chronic myeloid leukemia

Lymphoid Acute lymphoblastic

leukemia

Chronic lymphoid leukemia

Acute Leukemia

It occurs abruptly ( suddenly )

In normal individuals there are 2 % of primitive cells (blasts) inside their B.M

Differentiation of BM ( Figure.1)

Patients with acute leukemia have 20 % or more of these immature cells inside their B.M

(accumulative inside the B.M )

Acute leukemia Chronic leukemiaSudden onset Gradual onset ( slowly progressive )

Accumulation of more than 20% of immature

cells inside the BM (blasts )

Accumulation of mature cells (mature leukocyte )

History : sudden high fever associated with chest

infection , GIT problems or bleeding problems

Figure 1: Bone Marrow differentiation




2 4th

year – female

• Predisposing Factors:

AL is a multi system hypothesis. Could occur in uterine life or acquired during the life .possible causes

that may contribute in the developing of the disease :

1-

Ionizing radiation ( even the therapeutic doses )

2- Chemicals , e.g. : benzene

3- Viruses .e.g. : EBV , CMV , HIV

4- Exposure to environmental hazards & air pollution

5- Genetic predisposition , e.g.: translocation , mutations

• Incidence :

ALL has two peaks : in childhood age then in adult age . in a childhood group the curable rate is

about 90% with chemotherapy while in adult the curable rate is 20% with chemotherapy . many

of those who developed ALL in adult age need BM transplantation (Figure.2 )

AML : is common in adult (Figure.2 )

Figure 2: incidence rate of ALL & AML with

age group



Acute Leukemia + Malig

3 4th

Classification 1- T-lymphoc

2- B-lymphoc

3- precursors

Cli

General • Bone

a- An

b- Ne

c- Th

Organ infiltration

(MCQs)

Santury sites o

because of its

lymphoblasts c

tend to have C

also infiltrate t

the testis and

Patients usuall

lymphadenop

splenomegaly

testicular mas

Hypervicosity

syndrome

It is more com

cause of hyper

sludge togethe

1- Luckostasis

2- CNS proble

, confusion

3- Kidney (wh

4- Ear : tinnit

A

ant Lymphoma ( 2011 )

year – female

ALL & AML

ALL AM

tes

te

According to the FAB cla

M0 = no differentiation

M1 = >3% MPO; 20% AMM2= inc gran; Auer rods

M3= inc promyelocytes

M4= myelomono

M5= monoblastic

M6= erythroleukemia

M7= megakaryocytic

ical presentations( classical Finding )

arrow failure

emia(normochromic normocytic) : fatigue , pallor ,h

utropenia : recurrent infection ( form his/her own f

omopcytopenia : bruise , purpra , bleeding tenden

f lymphoblsats:

mall sizes ,

an cross the BBB and

S infiltration . it can

e coporacavernosa in

roliferate there.

y present with

thy ,hepato-

CNC complains or

es

M3 (promylocytic)

and patient in most o

with DIC( lymphoblas

tissue factors that ov

coagulation cascade

M4 & M5 (monocytic

tissues . patient may

hyperplasia or subcu

Patients may present wi

manifestations except in

M5 leuckemiaOther Finding

on in AML than ALL because of the large size of ce

iscosity refers to the increase in number of blasts c

r .as a result the following complications may occur

: heart pushes now against high resistance HF

ms : due to inadequate O2 saturation ( blood flow v

, syncopic attack , loss of consciousness

ich has very fine blood supply): hematoriua , acute

s , HL ( may be the 1st

complication )

Figure

of pati

A- gum

B- Chlo

B

L

sification :

L

eadache

lora)

cy

tends to over bleed

f the time presents

ts in M3 release

er activate the

)

) tend to infiltrate

present with gum

taneous nodules

h no specific

case of M3 , M4 or

lls in AML. The actual

ell which are tend to

:

ery slow) delusion

renal shut down

: Clinical presentations

nt with AML

hyperplasia

romas




4 4th

year – female

• Diagnosis work up of AL :

CBC

Peripheral blood film

BM aspiration &trefine biopsy

Flow cytometry (immunophenotyping )

Cryptogenic test ( karyotype analysis )

ALL AML

CBC WBCs( rarely in subleukemic –

leukemia )

Lymphocytes

Neutrophils ,platlates , Hb

WBCs

In case of M4 , M5 : monocyte

Neutrophils, lymphocyte ,platlates , Hb

Blood film Increase NO. oflymphoblasts in the

peripheral tissue . it lacks the

specifity because in viral infection

you may see these cells in theperiphery

Bone marrow

aspiration

Presence of 20% and more of blasts in BM is a diagnostic

Bone marrow biopsy All the normal cells are suppressed and increase NO. of blasts ( immature )

Flow cytometry To differentiate between the BM origin or non BM then to differentiate the myloid from

lymphoid then to distinguish the subtypes of both .for example :

1- the presence of TDT ( a surface marker on blast cells) is characteristic for ALL

2- the presence of Auer rod ( an eosinophilic needle like structure in the cytoplasm

) is characteristic of AML

Cryptogenic test

(karyotypeanalysis )

The presence of Philadelphia

chromosome “trans (19-22)”indicates poor prognosis of ALL

- M3 shows trans (15-17) abnormality

Other genetic

diagnostic method

FISH

PCR

Microarrays




5 4th

year – female

Lymphoma

A-Hodgkin’s lymphoma :

Bimodal age distribution : young & old age

It is a curable disease by chemotherapy

• Predisposing factors :

EBV

HCV

House hold probe : more than one member in a family + environmental causes

HIV : through immunosuppression

• Clinical presentation :

It has to start in L.N L.N enlargement ( superficial – intra-thoracic – intra-abdominal )

intra-abdominal L.N may lead to pressure manifestation : bowel obstruction

The enlargement L.Ns are rubbery in consistency , firm , big in size & non-tender (painless)

B-symptoms : fever , wt loss ( > 10% / 6 months) , night sweats (drenching > 38 ) Itching is one of the symptoms and it is due to presence of basophilia and eosinophilia

• Pathognemonic cells :

Owl eyes “ Reed- sternberng “ cells – muted B-cell

Big nucleus , 2 big inclusions

• Investigation :

1- Hx& Ex

2- L.N BIOPSY ( excesional biopsy ) : the best form cervical

In patients with shortness of breath , take it from the thoracic with CT-guided

DON’T take FNA

3- Cytology

a- Reed- sternberng cells with inflammatory background

b- Types : according to WHO classification :

Nodular sclerosis ( young age & female )

Mixed cellurity( older age)

Lymphocytic depleted

Lymhphocytic –predominant

c- Staging : an arble staging system :

Stage I : 1 L.N gp.

Stage II : 2 L.N gp. above the diaphragm

Stage III : 2 L.N above & below the diaphragm

Stage IV : distant metastasis

Each stage further subdivided into :

A lack of B cells

B present of B cells

X L.N larger than 10 cm




6 4th

year – female

4- CT scan of the neck – chest – abdomen – pelvic : to stage correctly to give appropriate

treatment

5- BM aspiration &trephinebiopsy : to see BM involvement

• Always remember : Hodgkin’s lymphoma is a disease of primary L.N involvement and it isspread in ordinary fashion ( contiguity )

B- Non-Hodgkin’s lymphoma :

- Hetergenousdisease : can involve extra-lymphatic system from the beginning

- L.N enlargement is haphazard

• Predisposing factors :

- Same as Hodgkin’s lymphoma

- Patients with autoimmune disease ( Celiac disease or UC ) or those who are immune

compromised have more tendency to develop Non-Hodgkin’s lymphoma

• Investigation :

- Take skin biopsy in Mycosis fungoides(sézarýssyndrome )or from the lung (pleural effusion ) or

from L.N

- NHL is difficult to staging

• Specific types :

1- H.pylori : it causes peptic ulcer disease or gastritis but some cases developMALT lymphoma

( mucosa –associtiated –lymphoid tissue lymphoma )

2- EBV related : can lead to Burkitt’s Lymphomapatient presents with jaw lesion

Done by

Scientific Committee – female – 2011

Documents

Acute Leukemia and Lymphoma R