bimbingan ukmppd (ukdi) - interna 3 (hematoonkologi)
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BIMBEL UKDI MANTAP
dr. Anindya K. Zahra
dr. Gandhi Anandika Febryantodr. Alexey Fernanda N.
HEMATOONKOLOGI
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RBC1
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Anemia?
Gejala anemia secara umum
lemah, lesu, letih, lelah, penglihatan berkunang-kunang,pusing, telinga berdenging dan penurunan konsentrasi.
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Anemia
Mikrositik
Hipokromik Besi Serum
N
Thalassemia
Sideroblastik
DefisiensiBesi
PenyakitKronik
Normositiknormokromik
Retikulosit
Anemiahemolitik
PerdarahanAkut
N/
AnemiaAplastik
Leukemia, etcMakrositik
Defisiensifolat
Defisiensi
B12
MCV
MCV Normal
MCV
Approach to Anemia: MCV!
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Morfologi Darah Tepi (MDT)
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Anisositosis
Anemia defisiensi besi
Anemia akibat penyakit
kronik
Keracunan tembaga
Anemia sideroblasik
Anemia megaloblastik
Anemia pernisiosa
Mikrositik (8 mikron)
MCV tinggi
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Poikilositosis
Sferosit
Thalassemia
Anemia defisiensi besi
Elliptosis (Ovalosit)
Sel pensil
Sferositosis herediter
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Poikilositosis
Sel Target (Mexican Hat cell,
bulls eye cell)
Thalassemia
Penyakit hati kronik
Stomatosit
Stomatosis herediter
Keracunan timah
Alkoholisme akut
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Poikilositosis
Sel Sabit (sickle cell;
drepanocyte; cresent cell;
menyscocyte)
Hemoglobinopati
Schystosit (fragmented cell;
keratocytes)
Anemia hemolitik
Penyakit keganasan
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Poikilositosis
Sel Spikel
Echynocyte(Burr cell, Crenated
cell, sea-urchin cell)Akantosit (Spurr cell)
Penyakit hati dengan
anemia hemolitik
Paska splenektomi
Penyakit ginjal menahun
(uremia)
Defisiensi piruvat kinase
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Anemia Mi-Hi
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Anemia Mi-Hi
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Angular cheilitis / stomatitis angularis
peradangan sudut mulut
Papil lidah atrofiSmooth tongue
ADB
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ADB: Mikrositik hipokromik
(central pallor >>), Pencil cell (+)
Normal
ADBApusan Darah Tepi
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Terapi ADB
Lini PertamaTerapi Besi Oral
Ferro sulfatmengandung 20 % besi elemental
Sediaan 200 mg, 325 mg (65 mg besi elemental)
Ferro fumaratmengandung 33 % besi elemental
Sediaan 325 mg (107 mg besi elemental)
Ferro glukonatmengandung 12 % besi elemental
Sediaan 325 mg (39 mg besi elemental)
34x sehari dengan besi elemental 5065 mg (3-6 mg besielemental/kg/hari)
Ferro sulfat 3 x 200 mg, 3 x 325 mg
Target : Hb meningkat 1 g/dL dalam 2-3 minggu
Hb terkoreksilanjutkan terapi besi oral hingga 3-4 bulan (untukmengembalikan cadangan besi)
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Oral Iron Therapy
Efek samping Fe Gastric upset (mual, muntah) dan konstipasi
Intoleransi terutama berkaitan dengan besarnya kadar zat besiterlarut yang ada dalam lumen ususdapat dicegah denganmemberikan dosis awal yang rendah(misal : sulfat ferosus 3x100
mg) atau memberikan preparat besi oral bersama dengan makan
Antasida
Fitat (pada sereal) Tanin (pada teh)
Fosfat
Daging
Senyawa sitrat Fruktosa
Asam askorbat
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Anemia Mi-Hi
Th l i k dib h di
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Thalassemia akan dibahas dianemia hemolitik
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Anemia Sideroblastik
Genetic(X-linkedor AD) oracquired(myelodysplasiasyndrome)
Sideroblast:nucleatederythroblast
Ring: iron inperinuclear
mithocondria Iron (+) but
cannot corporateit to Hb
Bone marrow aspirate: ring sideroblast
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Anemia
Mikrositik
Hipokromik Besi Serum
N
Thalassemia
Sideroblastik
DefisiensiBesi
PenyakitKronik
Normositiknormokromik
Retikulosit
Anemiahemolitik
PerdarahanAkut
N/
AnemiaAplastik
Leukemia, etcMakrositik
Defisiensifolat
DefisiensiB12
MCV
MCV Normal
MCV
Approach to Anemia: MCV!
9
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Anemia Hemolitik
Curiga anemia hemolitik: Klinis: Anemia, Jaundice, Splenomegali
Lab: Retikulosit , Bilirubin indirek
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Hemolisis
Letak
Extravascular(90%)
Reticuloendothelial (RE)system
Intravascular(10%)
Penyebab
Intrinsik
Membran
Enzim
Hemoglobin
Extrinsik
Autoimun
Infeksi
Microangiopathy
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Anemia Hemolitik: Defek Intrinsik
Intrinsik
MembranHereditaryspherocyte
Osmotic fragilitytest
Enzim G6PD deficiency G6PD assay
Hemoglobin
ThalassemiaHb
elektroforesis
Sickle cell
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Anemia Hemolitik: Defek Intrinsik
Intrinsik
MembranHereditaryspherocyte
Osmotic fragilitytest
Enzim G6PD deficiency G6PD assay
Hemoglobin
ThalassemiaHb
elektroforesis
Sickle cell
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Membranopathy
Hereditary SpherocytosisMDTSpherocytesOsmotic fragility test
Splenectomy often very effective
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Anemia Hemolitik: Defek Intrinsik
Intrinsik
MembranHereditaryspherocyte
Osmotic fragilitytest
Enzim G6PD deficiency G6PD assay
Hemoglobin
ThalassemiaHb
elektroforesis
Sickle cell
Enzymopathy
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Enzymopathy
G6PD Deficiency
G6PDberfungsi untuk menyediakan jumlah glutathion tereduksi (GSH)
GSHberperan sebagai scavenger terhadap metabolit oksidatifdi dalam
RBC, sebagai sumber NADPH yang melindungi sel dari stress oksidatif
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Anemia Defisiensi G6PD
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G6PD Deficiency
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Anemia Defisiensi G6PD
Harrisons Principles of Internal Medicine 17 Edition, Part 7 Oncology & Hematology, Section 2 Hematopietic Disorders
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Anemia Hemolitik: Defek Intrinsik
Intrinsik
MembranHereditaryspherocyte
Osmotic fragilitytest
Enzim G6PD deficiency G6PD assay
Hemoglobin
ThalassemiaHb
elektroforesis
Sickle cell
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Hemoglobinopathy
Hemoglobin Deffect
Thalassemia
Hb elektroforesis
Sickle cell disease
Thalassemia: microcytic hypochromic anemia,
anisositosis, poikilositosis, target cell
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What is Thalassemia?
Inherited disorders
Defective hemoglobin chains
The two main types:
Alpha
Beta more severe
Hb Elektroforesis HbA2 & HbF
Suspect thalassemia if:
Family history (+)
Microcytic anemia
Jaundice
Bone deformities
Splenomegaly
Appearance early in life
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a Thalassemia minor: often no target cells, but an increase in the number of small erythrocytes
(shown here in comparison with a lymphocyte), so that sometimes there is no anemia.
b More advanced thalassemia minor: strong anisocytosis and poikilocytosis (1), basophilic
stippling (2), and sporadic target cells (3).
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Thalassemia
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Splenomegaly
Splenomegaly & Extramedullary hematopoiesis
FACIES RODENT FACIES COOLEY
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FACIES RODENTFACIES COOLEY
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ThalasemiaTransfusi PRC
Indikasi Hb < 8 g/dL
Hb > 8 g/dL, bila keadaan umum kurang baik, anoreksia, gangguan aktivitas,gangguan pertumbuhan, adanya pembesaran limpa yang cepat, dan perubahanpada tulang
Pemberian dan kecepatan pemberian
Diberikan sampai target Hb 12 g/dL, tidak boleh melebihi 15 g/dL
Bila Hb > 5 g/dL berikan 10-15 mL/kg/kali dalam 2 jam atau 20 mL/kg/kali dalam3-4 jam
Bila Hb < 5 g/dL berikan 5 mL/kg/kali dengan kecepatan 2 mL/kg/jam. Beri oksigen
Pemantauan dan kontrol
Kontrol 2-4 minggu sekali bagi penderita thalasemia lama
Kadar ferritin dan besi serum diperiksa tiap 6 bulan
Fungsi organ dipantau tiap 6 bulan
Pemeriksaan marker hepatitis B dan C
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Chronichemolysis
Iron overload Tissue damage
Thalassemia
Excess ironfree hydroxyl radicalsROS
Insoluble iron complexesdeposited inbody tissues
Mechanism
Pituitary impaired growth Heart cardiomyopathy, heart failure
Liver hepatic cirrhosis
Pancreas diabetes mellitus
Gonads hypogonadism, infertility
Clinical sequelae of iron overload
Iron Chelating Agent
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Iron Chelating Agent
(Deferoxamine/Deferiprone/Deferiprox/ICL670 )
TRANSFUSI PRC BERKALA
IRON CHELATING
Indikasi iron chelating agent
- Ferritin >1000 mg/dL & saturasi transferrin serum >50 %
- Transfusi >5 L, transfusi >10 kali, transfusi > 1 tahun
Deferiprox = 75
mg/kg/hari, dibagi 3
dosis, per oral
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ThalassemiaIndikasi Splenektomi
Limpa terlalu besar (Schuffner IV-VIII atau >6
cm)risiko ruptur
Hipersplenisme dini : jika jumlah transfusi
>250 mL/kg dalam 1 tahun terakhir
Hipersplenisme lanjut : pansitopenia
Splenektomi dilakukan pada usia >5 tahun (
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Anemia Hemolitik: Defek Ekstrinsik
Extrinsik
Autoimun
Warm
Cold
MicroangiopathyProstheticvalves etc
Infeksi Malaria, etc
Autoimmune Hemolytic Anemia
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Autoimmune Hemolytic AnemiaWarm & Cold AIHA
Warm (70 %) Cold (30 %)
Maximally bindRBCs at
37C 0 to 4C
Clinical Acute and severe
Collagen disease, idiopathic
Post infectious, idiopathic
Younger age group Older age group
Mediated byautoandibodies
IgG IgM(cold agglutinin)which fixescomplement (C3), antibodi Donath-
Landsteiner
Mechanism IgG-coated RBCspartially
ingested by the macrophages of
the spleenmicrospherocytes
extravascular hemolysis
IgM + RBCactivate complement
C3 coated RBCagglutination
intravascular hemolysis
Treatment Corticosteroid
Splenectomy (if steroid isnt
adequate)
Avoidance of cold
Corticosteroid and splenectomy
wasnt effective
Transfusion therapy in AIHA is challenging, and the most compatible
red blood cells should be given
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Coombs Test
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Autoimmune Hemolytic Anemia
Warm AIHA:
spherocytes
Mi i hi A i
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Microangiopathic Anemia
Cause: Microvascular disease (DIC, TTP etc) Heart valve prostheses
Trauma / implanted devices
Schistocytes and microspherocytes noted on the blood smear
f
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Anemia Defisiensi EPO
Anemia padachronic kidney
disease (CKD)
(mulai pada
stage III) Anemia
normositik
normokromik
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Anemia Aplastik
Pansitopeniayang disertaihiposelularitas sumsumtulang
Etiologi =
idiopatik (sebagian besar),
Radiasi Obat & bahan kimia
kemoterapi, benzena, gold,kloramfenikol,hidantoin,carbamazepine
Infeksi virushepatitis,
virus Ebstein-Barr, CMV,parvovirus, HIV-1
Penyakit imun
Hemoglobinuriaparoksismal nokturnal
Kehamilan
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5 L (lemah, letih, lesu, lalai, lupa)
Pucat, pusing, jantung berdebar,dispnea, penglihatan kabur, telingaberdenging
Anemia
Perdarahan mukosa
Perdarahan bawah kulit (memar)Trombositopenia
Rentan terhadap infeksi
DemamLeukopenia
Anemia AplastikManifestasi Klinis
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Anemia Aplastik
Gambaran histologis anemia aplastik pada biopsi sumsum tulang
Gambaran hiposeluler, banyak terisi lemak
ThalassemiaApproach to Anemia: MCV!
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Anemia
Mikrositik
HipokromikBesi Serum
N
Thalassemia
Sideroblastik
DefisiensiBesi
PenyakitKronik
Normositiknormokromik
Retikulosit
Anemiahemolitik
PerdarahanAkut
N/
AnemiaAplastik
Leukemia, etcMakrositik
Defisiensifolat
DefisiensiB12
MCV
MCV Normal
MCV
Approach to Anemia: MCV!
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Megaloblastic Anemia
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Anemia Megaloblastic Vitamin B12
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Anemia MegaloblasticVitamin B12
Deficiency
Anemia Megaloblastikukuran eritrosit
membesar dan hampir sama dengan leukosit
Tampak neutrofil dengan hipersegmentasi
Perbandingan eritrosit dan leukosit
pada keadaan normal
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Tatalaksana Defisiensi Folat & B12
Defisiensi asam folat
Asam folat 1-5 mg/hariselama 1-4 bulan
Dosis 1 mg/hari biasanyasudah efektif
Defisiensi vitamin B12
Vitamin B12 parenteral (IMatau SC) 1 mg/hari selama 1minggu
Dilanjutkan dengan 1
mg/minggu selama 4 minggu,lalu 1 mg/bulan
Sediaan oral sama efektif,tetapi membutuhkankompliansi pasien (1-2
mg/hari) Sediaan oral kurang efektif
apabila terdapat gangguanabsorpsi vitamin B12 digastrointestinal
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Komponen Darah
WholeBlood
Komponen lengkap
Perdarahan masifatau hipovolemik
Packed RedCell (PRC)
Eritrosit yangdipisahkan dari
plasma
Anemia tanpapenurunan
komponen darah lain
WashedRed Cell
PRC dicuci NaCl
fisiologis,menghilangkanantibodi yang
menempel di plasma
Penderita transfusi
berulang ataumengalami demam
pada transfusisebelumnya
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Komponen Darah
PlateletConcentrate
Trombosit
Trombositopenia,profilaksis (operasi),
Fresh FrozenPlasma
All coagulationfactor
Multiple coagulationfactor deficiency,
DIC
Cryoprecipitate
Fibrinogen, vonWillebrand factor,factor VIII, factor XIII
and fibronectin.
Haemophilia A, VonWillebrandsdisease,
Hipofibrinogenemia
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HemogramDifferential Leukocytes Count
Mulai dengan sel basofil / eosinofil / neutrofil
batang / neutrofil segmen / limfosit / monosit Nilai normal hitung jenis pada dewasa
- Basofil : 0 - 1 %
- Eosinofil : 1 3 %
- Neutrofil Batang : 2 6 %- Neutrofil Segmen : 50 70 %
- Limfosit : 20 40 %
- Monosit : 2 8 %
Stab
Neutrophil
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Bleeding timemenilai
fungsi hemostasis primer
(aktivitas platelet)
Clotting timemenilai fungsi
hemostasis sekunder (aktivitas
faktor koagulasi)
coagulation
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coagulation
cascade
waterfall
PT
APTT
TT
*
Fibrinolysis system
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Fibrinolysis system
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20
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ITP
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ITPManifestasi Klinis
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Terapi ITP
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Terapi ITP
ITP: antiplatelet antibody
platelet destruction
Indikasi : AT < 20.000 atau perdarahan
Prednisone 1 mg/kg/hari (2 minggu)
Kortikosteroid
Indikasi : severe, life-threatening bleeding, atau anak dengan AT
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Intravascu lar Coagulat ion)
Clinical manifestation of DIC
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b di i f
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Lab diagnosis of DIC
DIC Screening : bleeding time (>>) , PT (>>), APTT
(>>) , platelet count (), AT III (
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Evans Syndrome
Definisi
AIHA (direct Coombstest +) dan immune-mediatedthrombocytopenia tanpa adanya penyebab yang mendasari
Manifestasi Klinis Trombositopenia (76%), anemia (67%), neutropenia (24%),
pansitopenia (14%), hemolitik
Manajemen
Stabilisasi fungsi kardiovaskular dan respirasi
Transfusi PRC
Prednison (first line), IvIg
H h S h l i P
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Henoch-Schonlein Purpura
Definisi
Gangguan imun akut yang diperantarai oleh IgAvaskulitis general yang melibatkanpembuluh darah kulit, GI tract, ginjal, sendi, dan paru / CNS (jarang)
Manifestasi Klinis
Gejala prodromal : sakit kepala, anorexia, demam Ruam (95-100% kasus), terutama melibatkan tungkai. Lesi urtikaria atau macula
eritematosa, berkembang menjadi papul pucat lalu purpura
Nyeri perut dan muntah
Nyeri sendi, terutama di tungkai bawah dan ankle
Edema subkutan, edema skrotum
Feses berdarah
Manajemen
Suportif, analgetik, corticosteroid
H h S h l i P
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Henoch-Schonlein Purpura
Characteristic rash of Henoch-Schnlein purpura.
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P li it i
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Polisitemia
P li it i V
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Polisitemia Vera
Kelainan neoplastik yang ditandai dengan peningkatan eritorosit (disertaidengan leukositosis dan trombositosis)
Sering tidak bergejala (asimptomatik)
Peningkatan volume dan viskositas eritrositsakit kepala, malaise,dyspnea, fatigue, gangguan penglihatan
Peningkatan turnoversel darahhiperurisemiarisiko gout dan batu
saluran kemih
Hiperviskositastrombosisstroke, TIA, DVT, infark miokard, oklusiarteri vena retina
Polisitemia
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Polisitemia
K it i PV l h PVSG
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Kriteria PV oleh PVSG
KATEGORI A KATEGORI B
1. Total volume RBC 36 ml/kg pada
pria, 32 ml/kg pada pria
2. SaO2 > 92%
3. Splenomegali
1. Trombositosis >400.000/mm3
2. Leukositosis >12.000/mm3 (tanpa
demam/infeksi)
3. Leukocyte alkaline phosphatase score>100
4. Serum vitamin B12 >900 pg/ml atau
serum UB12BC >2.200 pg/ml
KRITERIA DIAGNOSIS PV
A1 + A2+ A3 atau A1 + A2 + 2 kategori B
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KEGANASAN HEMATOLOGI
Le kemia
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LeukemiaCBC Acute Chronic
Hb (anemia (anemia)
AL (leukositosis) (leukositosis)
AT (trombositopenia) - N/- in CML blast crisis
Diff count blast cells (nucleoli (+)) immature granulocytes (allstage of maturation)
Myeloid (AML) Lymphoid (ALL) Myeloid
(CML)
Lymphoid CLL
80-90% caseAdult & children
Myeloblast >20%
Auer rod (+)
Children>>
Limfoblast >20%
AdultsPhiladelphia
chromosom
>55 yoLimfositosis
>50rb
*Pansitopenia may present in the early sign of leukemia
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Auer rod
nucleoli
AML M1:
AML without
maturation
Myeloblast > 80-90%
AML-M3
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AML-M3
Hypergranular: consist of procoagulant
(promote coagulation activity)induce DIC
Multiple Auer rod
promyelocytes
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ALL-L1: small uniform cells
ALL-L3: large varied cells with
strongly basophilic cytoplasm &
vacuoles (bubble-like features)
ALL-L2: varied cell, large blast cells
with prominent nucleoli & cytoplasm
and with more heterogeneity
ALL-L1: uniform cell, small blast cell
with scanty cytoplasm
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Blast
transformationAccelerated
phase
Chronic
phase
biphasic
triphasic
several years
several years
Fase:
Kronik: blast 15%
Acute/Blast crisis: blast >30% (mirip AML)
Chronic Myeloid Leukemia
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Chronic Myeloid Leukemia
90% of patients with CML have a chromosomeabnormalityknown as Philadelphia( Ph)
chromosomein the leukaemic blasts. It results
from translocation between 9 and 22chromosomes t( 9,22). This translocation can
be detected by cytogenetics or polymerase
chain reaction (PCR)
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Chronic Lymphoid Leukemia
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Chronic Lymphoid Leukemia
Leucocytic count is 50-200x109/L or higher,the absolute lymphocyte is > 5x109/L and
may be up to 300x109/L. Between 70-99% of
white cells in the blood film appear as smalllymphocytes
Lymphoma Maligna : Hodgkin & Non-
Hodgkin(85%)
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Hodgkin(85%)
B symptoms (+) in Hodgkin.
NHLB symptoms (+) in
advance & late stage
Lymphoma Hodgkin VS Non Hodgkin
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Lymphoma Hodgkin VS Non-Hodgkin
Lymphoma Hodgkin Lymphoma Non-Hodgkin
Dijumpai gambaran sel B neoplastik
raksasa (Reed Sternberg)
Gambaran klinis tampak lebih jelas dan
bermanifestasi sistemik
Pola penyebaran teraturke jaringan
sekitar
Penyebarannya difus (tidak teratur)
Jarang mengenai limfonodi mesenterium
dan cincin Walldeyer
Sering mengenai limfonodi mesenterium
dan cincin Walldeyer
Jarang mengenai sistem di luar kelenjargetah bening
Sering ekstranodal
Terlokalisasi dan sering mengenai 1
kelenjar getah bening
Mengenai banyak kelenjar getah bening
Hodgkin Lymphoma
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Hodgkin Lymphoma
Owls EyesReed Stenberg cell (+)
Hodgkin Lymphoma
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Hodgkin Lymphoma
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TERIMA KASIH
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