Mention the common findings in AML
1_Anemia: pallor fatigue weakness
2_thrombocytopenia: bleedind bruisisng.
3_fever that fails to respond to therapy.
4_splenomegaly, hepatomegaly, lympadenopathy
5_bone tenderness.
what are the hematological and bone marrow findings in AML
1_hema: normocytic normochromic anemia, occasionally macrocytic but don’t response to B12 or B9.
nucleated RBC, anisocytosis, poikilocytosis.
platlete count is moderatly depressed(hypogranular and giant).
WBC is variable.
BM: hypercellular, with blasts> 20% to deffrintiate it from MDS
Mention the FAB classification of AML
M0 A myeloblastic L minimaly defferntiated.
M1 AML without maturation
M2 AML with maturation
M2 baso(with basophil blasts)
M3 hypergranular promylelocytic L
M3 variant (hypogranular bilobed, micro).
M4 myelomonocytic L
M5 monocytic L (M5a poorly dif, M5b well deff).
M6 erythroleukemia
M7 megakaryocytic leukemia.
Explain some charecters of M0
explain some charecters of M1
explain some charecters of M2
explain some charecters of M3
-seen in younger patients
-most common finding: bleeding
-serious complications: DIC
-80-100% have t(15:17)
- unique treatment (all trans retinoic acid).
- two forms: typical hypergranular
variant hypogranular
what are the special characters of M4
what are the special characters of M5
Schilling
what are the special characters of M6
DiGuglieumo
what are the special characters of M 7
mention the complications of AML
1_infection
2_bleeding, DIC
3_tumer lysis syndrome
4_leukostasis
Mention the causes of AML
1_radiation 2_chemical drugs «leukemogens» 3_onchogens 4_protoonchogens 5_genetic factors 6_viruses«C RNA»
Do you memorize the table of Cytochemical differntiation of acute leukemia?
subtype.MPO.SBB. PAS. ANAE. AP
M0; + + - - -
M1,2,. +++ ++ + - - +m2
M4. -/++ +/++ - + +
M5. -/+ -/+ - +++ +
M6. - - + + - +
M7. - - - - -
BALL. - - ++ - -
TALL. - - - - +
Regarding polycythemia vera:
A_clinical features and complications.
B_lab findings.
C_critria to diagnose
A_
1_plethooric appearance, iching after hot shower
2_symptoms of slow circulation (cardia, neuro, GIT)
3_symptoms of increased metabolism(sweating, weigt loss)
4_bleeding tendency
5_HSM
6_Complications: CML, myelosclerosis, RF, thrombosis, gout, peptic ulcer.
B:
1_increased Hb, HC, blood viscosity
2_low ESR
3_High WBC C with slight shift«metamyelocyte», H basophils
4_plat c high, decrease level of PF3
5_BM, hypercellular, hyperplasia of erythroid series, Low iron stores, high reticulin.
6_LAP high
7biochemstry: high B12 and B12 binding ptn, low erythropoitein, ferretin, folate.
hyperurecemia and H LDH.
C
1_Jak 2+: Hct> 52% m,> 48% female.
2_Jak2-: major: Hct> 60% m,> 56%f
no secondary erythrocytosis.
palbable splenomegaly, aquired genetic abnormalities«except Jak, BCR-ABL».
minor:
plat> 450×106
Neutrophils> 10 ×106
radiographic splenomegaly
low serum erythropoitein
*4major criteria or 3 major+2minor for diagnosis.
Regarding IM:
1_cause
2_clinical features
3_lab findings
1_primary: idiopathic and un common
secondary: infiltration by malignancy or infection or chemicals or irradiation.
2_progressive anemia, splenomegaly,hepatomegaly, fibrosis.
bleeding due to dysmegakaryocytopoisis is the most constant feature.
osteosclerosis, bone pain, malaise.
3_leukocytosis with leukoerythroblastic picture, tear drop cells, NRBCs, immature myloid cells.
BM is hypercellular and fibrotic «dry tap».
Regarding ET: 1_how to diagnose it 2_most common diorders in patients 3_lab findings 4_male: female ratio 5_plat function
1_by exclusion of other MPD and non hematological illness associated with increased plat count.
2_bleeding or thrombotic problems
3_high platlete c; exceed 1million, with a minimum of 6 m.
Hb low, hypochromic microcytic anemia, with splenic atrophy«target cells, HJ bodies, NRBCS, acanthocytes.
WBC C increased in 50%.
ALP N or H
B12 and uric acid increased.
BM: hypercellular, megakaryocytic hyperplasia, polypoid of the nuclei, giant forms and clusters.
4_equal
5_mean extent of aggregation is lower than normal.
memorize the table of differential diagnosis of MPD
Gallery
Mention the clinical features of CML
1_minimal intensity symptoms, fatigue, anorexia, weigt loss, abdominal discomfort. 2_pain due to splenic infarction 3_hemorrhage 4_gout, visual disturbance 5_neuro abnormalities (piriapism).
when dose ANP value change?
1_increase in: PV, ET, A leukemia,leukemoid reaction,carcinoma, MM,HL,osteomyelosclerosis,prenicous anemia,sepsis,sarcoidosis, fever secondary to infections.
2_decrease or ansent: congenital hypophosphatase, CML, PNH, sideranemia, rheumatic disease
What are the lab findings in CML
1_moderate anemia «normocyticnormochromic»… severe later.
2_leukocytosis up to 500k,mainly «segmented neutrophils, myelocytes comprise 10-50%»
3_increased lymphocytes, monocytes.
4_plat normal or increase
5_hyperurecemia, hyperuricosuria, H LDH, H serum K, NAP < 6%.
6_BM: hypercellular, mainly myeloid series, erythropoiesis is normal, somtimes dyserythrotic.
7_M: E ration increased
8_megakaryocyte are prominent and usually smaller than normal.
What are the stages of CML
1_ Chronic phase: blood;
GP: shift to left, psudopleger, esinophilia, basophilia.
EP: Normoblasts, anisocytosis.
THP: increase plat, immature, anisocytosis.
BM: GP: hyperplasia, shift, esino baso
EP: decreased
THP: increased with normal form.
2_Accelerated phase: Blood: GP: shift, blast<20%, basophils<30% EP: normo, anisocytosis. THP:normal or decrease anisocytosis. BM: GP:shift,blast 15_20%, basophilia EP: D. THP: normal or D.
3_Blast crisis: Blood GP: blast increase EP: anisocytosis, polychromesia, normoblasts THP:decrease or absent, anisocytosis. BM: GP: blast> 30% EP: D. THP: D