11. Acute leukemia: types, etiology, pathogenesis, clinical manifestation, diagnosis, treatment. Flashcards

1
Q

what causes AML ?

A

chemotherapy
radiation
bezene

secondary aml = poorprognosis
to mylodysplastic syndrome
aplastic anemia
myeloproliefrative syndrome

genetic :
down syndrome
and turner

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2
Q

sign and symptoms of AML ?

A

A lack of normal white blood cell production makes people more susceptible to infections

Thrombocytopenia
Epistaxis is defined as acute hemorrhage from the nostril
bleeding and petechiae

gingival involvement = in monocytic AML m4 / m5

bone and joint pain

anemia - weakness , tirendess , pallour

retinal hemorrhages

cns involvemnt = headache ,change in mental status
palsy
highest incidence in relapsed M4 and M5

dic = m3

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3
Q

diagnosis of AML ?

A

cbc

pancytopnea : anemia,
normocytic or macrocyic - due to rapd turnover
thrombocytopenia and granlocytopnea

tumor lysisi syndrome = hyperphosphatemia heprkalemia , hyperurecemia , HYPOKALCEMIA

=====
bone marrow biopsy
20% myeloid blasts

======

blood smear :
Shows many immature blasts with only rare mature segmented granulocytes

romanowsky stain in bone marrow = see alot o the blast cells , and syplasia

esterase

TdT negative

myeloperoxidase stain positive = auer rods
for myeloblast
not monoblasts

sudan black stain

immunophenotyping

=====
real tme pcr = detects known translocation

=========
csf findings of blast cells

====
flow cytometry
cd33 , 34 ,13

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4
Q

what is the treatment for AML ?

A

induction therapy = chemotherapy at high dose
cytarabine 7 days
3 days daunorubicin
10 days

consolidation therapy
After complete remission, 2
-3 cycles of the same drugs

maintencae therapy
monthy chemotherapy

hematopoiec stem cell transplant las resort used inpatents after 1st remission and poor porgnostic factors

======
if m3 = give ATRA
ll trans retinoic acid

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5
Q

what is a complication of AML treatment ?

A

unfortunately not only kills the blasts but also prohibits
the normal haematopoiesis in the bone marrow, the patients basically gain an
aplastic bone marrow

immunoprophylaxis to prevent infections

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6
Q

ALL is more common in whom ?

A

in children - most coomon leukemia in children

new born to 14 years old

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7
Q

etiology of Acute LYMPHOBLASTIC leukemia

A

chemotherapy
radiation
benzene

trisomy 21

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8
Q

what is the diagnosis of ALL

A

pancytopnea
normocytic or macrocytic anemia = due to folic acid deficicny

tumor lysis syndrome

peripheral blood smear - the lymphoblasts have very little cytoplasm to nucleus , so scanty cytoplasm
less prominent nucleoli
NO GRANULES ]coarse chromatin

most than 20 percent of blast cells in bone marrow

positive for TdT marker
and MPO negative
esterase negative

flow cytometry for cd

PAS positive

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9
Q

what is the classification of ALL ?

A

pre - b cells
= trisomy 21 in child
= cd19, cd20
CALA cd10 (acutelymphoblastic leukemia antigen)

t9: 22 bad prognosisi
t12: 21 good prognosis

b cell = ALL

t cells ALL
mass in the mediastinum
cd3 positive
3,4,5,6,7,8

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10
Q

when do people hve acute myeloid leukema and what are the charteristics ?

A

in adults 40-60 years old

and abrupt

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11
Q

what is the classification of AML ?

A

m2 acute myeloblastic leukema
type is the most common
myeloblastic with maturation
t8 :21

m3 = acute promyelocytic leukemia
t15L17 good prognosis
assocaited with DIC
M3 we can treat it with VITAMIN A = ATRA all trans retnoic acid

m5 = monocytic with alot of gum ilfiltration

m4 = myelomonocytic leukrmia

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12
Q

what are the prognosisi of AML according to genetics ?

A

most common good porgnosis t8:21 m2
t15:17 = m3
inversion of 6

intermediate t 19:11

bad
inversion of 3
monomoy 7
5q deletion

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13
Q

what are the bad prognostic factors for aml ?

A

above 50

cytogenetics

treatmnet response mroe than 20 perce blasts in first curse

secondary amp

trilineage myelodysplasia

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14
Q

what are the sympotms of ALL

A

hepatosplenomegaly

neuropathies due to meningeal infiltration

anemia = weakness

pancytopnea :fever , infetions

bleeding

bone pain

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15
Q

what is bad prognosiis in all ?

A

more than 60
wbc over 100,000
philadelphia chromsome 9:22

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16
Q

what is the treatmnet for ALL

A

streoids - prednisone
vincristine
asparginase
daunorubicin

cns prophylassix = by cytarabine and methotrextae intrathecal chemotherapy

induction

consolidation

and maintenace