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Practice Questions100 questions

2026 Statistics

Key Facts: Título em Hematologia e Hemoterapia Exam

80 Questions

Official ABHH Theoretical Exam Multiple-Choice Items

Edital Oficial ABHH / AMB

70% (7.0/10.0)

Minimum Passing Grade Benchmark (Nota de Corte)

Regulamento da Prova de Título ABHH

2 Stages

Examination Phases (Prova Teórica + Prova Prática / Teórico-Prática)

Comissão de Título de Especialista ABHH

R$ 1.500 / 3.000

Examination Registration Fee (Sócios ABHH/AMB vs. Não Sócios)

Tabela de Inscrição AMB / ABHH

RQE Definitivo

Permanent Specialist Board Certification Recognized by CFM

Resolução CFM nº 2.330/2023

100 Questions

Comprehensive English-Language OpenExamPrep Practice Bank

OpenExamPrep Practice Bank

The Título de Especialista em Hematologia e Hemoterapia is the official national board certification for Brazilian hematologists and hemotherapists, granted by ABHH and AMB. It assesses comprehensive theoretical knowledge and practical diagnostic competence across red blood cell disorders, hematologic oncology, hemostasis, transfusion medicine, and cell therapy.

Sample Título em Hematologia e Hemoterapia Practice Questions

Try these sample questions to test your Título em Hematologia e Hemoterapia exam readiness. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1A 34-year-old female presents with persistent fatigue, pica (pagophagia), and brittle spoon-shaped nails (koilonychia). Laboratory workup reveals: Hemoglobin 8.4 g/dL, MCV 68 fL, MCH 22 pg, Serum Iron 24 mcg/dL, Total Iron-Binding Capacity (TIBC) 450 mcg/dL, Transferrin Saturation 5.3%, and Serum Ferritin 6 ng/mL. Which laboratory finding most definitively confirms iron deficiency anemia (anemia ferropriva) over anemia of chronic disease / inflammation?

A.Severely decreased serum ferritin (< 15 ng/mL) combined with elevated TIBC.

B.Elevated serum ferritin with normal transferrin saturation.

C.Marked elevation of soluble transferrin receptor (sTfR) with a normal transferrin level.

D.Decreased hemoglobin with an elevated reticulocyte production index (> 3.0).

Explanation: A serum ferritin level below 15 ng/mL (or < 30 ng/mL in clinical practice) is the most specific biochemical marker for absolute total body iron store depletion. In iron deficiency anemia (anemia ferropriva), total iron-binding capacity (TIBC) is elevated and transferrin saturation is markedly reduced (< 16%), whereas in anemia of chronic disease, ferritin is normal or elevated (as an acute-phase reactant) and TIBC is typically decreased or normal.

2A 58-year-old male with a history of chronic autoimmune gastritis presents with progressive paresthesias in a stocking-glove distribution, loss of proprioception and vibratory sense, and memory lapses. Laboratory studies reveal: Hb 7.2 g/dL, MCV 118 fL, Platelets 95 x 10^9/L, Leukocytes 3.2 x 10^9/L, LDH 1,850 U/L, Indirect Bilirubin 2.1 mg/dL, and hypersegmented neutrophils on peripheral blood smear. Which diagnostic metabolite profile is most specific for cobalamin (Vitamin B12) deficiency over folate deficiency?

A.Elevated serum methylmalonic acid (MMA) and elevated serum homocysteine.

B.Elevated serum homocysteine with normal serum methylmalonic acid (MMA).

C.Normal serum methylmalonic acid (MMA) with low erythrocyte folate.

D.Suppressed serum methylmalonic acid (MMA) and elevated serum cobalamin.

Explanation: Vitamin B12 is an essential cofactor for both methylmalonyl-CoA mutase (converting methylmalonyl-CoA to succinyl-CoA) and methionine synthase (converting homocysteine to methionine). Consequently, cobalamin deficiency results in the elevation of both methylmalonic acid (MMA) and homocysteine. In folate deficiency, only homocysteine is elevated, while MMA remains normal.

3A 22-year-old male with known Sickle Cell Disease (Anemia Falciforme - HbSS) is admitted with fever (38.8°C), acute pleuritic chest pain, tachypnea (RR 28/min), and an oxygen saturation of 88% on ambient air. Chest radiography reveals a new alveolar consolidation in the right lower lobe. In accordance with Brazilian Clinical Protocols (PCDT da Doença Falciforme), which emergency therapeutic approach is indicated?

A.Empiric broad-spectrum intravenous antibiotics (including macrolide coverage), aggressive fluid hydration, supplemental oxygen, and prompt red blood cell transfusion (simple or exchange) targeting Hb ~10 g/dL.

B.High-dose corticosteroids alone, strict fluid restriction, and immediate prophylactic anticoagulation with full-dose warfarin.

C.Routine therapeutic phlebotomy to reduce blood viscosity followed by high-dose aspirin.

D.Immediate emergency splenectomy to prevent recurrent splenic sequestration crisis.

Explanation: Acute Chest Syndrome (Síndrome Torácica Aguda - STA) is a leading cause of mortality in sickle cell disease, defined by a new pulmonary infiltrate accompanied by fever, respiratory symptoms, or hypoxemia. Management mandates prompt empiric antibiotics covering *Streptococcus pneumoniae* and atypical pathogens (macrolide/fluoroquinolone), cautious hydration (to prevent pulmonary edema), analgesia, oxygen, and timely transfusion (simple or automated red cell exchange) aiming for Hb around 10 g/dL (or HbS < 30% in severe cases) without exceeding Hb 10-11 g/dL to avoid hyperviscosity.

4A 4-year-old child with homozygous sickle cell disease (HbSS) undergoes routine primary stroke screening with Transcranial Doppler (Doppler Transcraniano - DTC). The examination reveals a time-averaged maximum mean velocity (TAMV) of 215 cm/s in the right middle cerebral artery, confirmed on repeat testing 2 weeks later. According to established guidelines (STOP trial and PCDT MS), what is the appropriate clinical intervention?

A.Initiation of a chronic red blood cell transfusion program (transfusão crônica regular) targeting HbS < 30%.

B.Observation with repeat Transcranial Doppler in 12 months without therapeutic intervention.

C.Immediate initiation of aspirin 100 mg daily as monotherapy without transfusion.

D.Immediate surgical revascularization (encephaloduroarteriosynangiosis) prior to medical therapy.

Explanation: A TAMV >= 200 cm/s on Transcranial Doppler (DTC) in children with HbSS aged 2 to 16 years indicates abnormal arterial velocity and an exceptionally high risk of primary ischemic stroke (> 10% per year). In accordance with the landmark STOP trial and the Brazilian Ministry of Health PCDT, the standard of care is the immediate implementation of a regular chronic red blood cell transfusion regimen to maintain HbS < 30%, which reduces primary stroke incidence by over 90%.

5Hydroxyurea (hidroxiureia) is the cornerstone disease-modifying pharmacotherapy for patients with Sickle Cell Disease (Doença Falciforme). What is the primary molecular and cellular mechanism through which hydroxyurea exerts its main therapeutic benefit in HbSS patients?

A.Induction of fetal hemoglobin (HbF / Hemoglobina Fetal) synthesis, which inhibits intracellular deoxy-HbS polymerization.

B.Direct covalent binding to the beta-globin chain preventing sickle erythrocyte dehydration.

C.Competitive inhibition of splenic macrophages to prolong red blood cell lifespan.

D.Direct enzymatic cleavage of abnormal alpha-globin tetramers.

Explanation: Hydroxyurea acts primarily via ribonucleotide reductase inhibition and soluble guanylyl cyclase activation to stimulate gamma-globin gene transcription, markedly increasing fetal hemoglobin (HbF, alpha2gamma2) production. HbF does not participate in deoxy-HbS polymer formation and physically disrupts HbS polymer fibril elongation, thereby reducing sickling, hemolysis, vaso-occlusive crises, and acute chest syndrome episodes.

6A 29-year-old female presents for pre-conceptional counseling. Hemoglobin electrophoresis identifies Hemoglobin SC disease (HbSC). Compared to patients with homozygous sickle cell anemia (HbSS), which clinical and laboratory feature is characteristically more prominent or preserved in patients with HbSC disease?

A.Higher baseline hemoglobin concentration, persistence of splenomegaly into adulthood, and higher risk of proliferative sickle retinopathy.

B.Lower baseline hemoglobin concentration and rapid autosplenectomy before age 5.

C.Complete absence of vaso-occlusive bone crises and avascular necrosis of the femoral head.

D.Total resistance to acute chest syndrome and thromboembolic events.

Explanation: Patients with HbSC disease typically maintain higher baseline hemoglobin levels (often 10–12 g/dL) and higher blood viscosity compared to HbSS patients. Because hemolysis is milder, splenomegaly frequently persists into adult life (predisposing to late splenic infarction or sequestration). Additionally, due to higher blood viscosity and localized vaso-occlusion, HbSC patients have a significantly higher incidence of proliferative sickle retinopathy and osteonecrosis compared to HbSS.

7An asymptomatic 24-year-old male of Italian descent has a routine complete blood count (CBC): Hemoglobin 12.8 g/dL, RBC 6.1 x 10^12/L, MCV 64 fL, MCH 21 pg, RDW 12.8% (normal: 11.5–14.5%), and Serum Ferritin 140 ng/mL. The Mentzer index (MCV/RBC) is 10.5. Quantitative hemoglobin electrophoresis demonstrates an HbA2 level of 5.2% (reference: 1.5–3.5%). What is the definitive diagnosis?

A.Beta-Thalassemia Minor (Traço Talassêmico Beta / Heterozygous Beta-Thalassemia).

B.Severe iron deficiency anemia (Anemia Ferropriva).

C.Alpha-thalassemia major (Hydrops Fetalis).

D.Sideroblastic anemia secondary to lead poisoning.

Explanation: The patient exhibits classic features of Beta-Thalassemia Minor (traço talassêmico beta): mild microcytic erythrocytosis (high RBC count relative to Hb), a Mentzer index < 13, normal RDW, normal ferritin, and the diagnostic hallmark of elevated HbA2 (> 3.5%). In contrast, iron deficiency presents with low RBC count, Mentzer index > 13, elevated RDW, low ferritin, and decreased or normal HbA2.

8A 19-year-old female with transfusion-dependent Beta-Thalassemia Major (Talassemia Major) on regular packed red blood cell transfusions undergoes monitoring for transfusion-induced hemosiderosis. Cardiovascular MRI reveals a myocardial T2* of 8 ms (reference: > 20 ms), and hepatic T2* indicates a liver iron concentration (LIC) of 18 mg Fe/g dry weight (reference: < 1.8 mg Fe/g). Which statement regarding iron chelation therapy (quelação de ferro) is correct?

A.Myocardial T2* < 10 ms indicates severe cardiac iron overload with imminent risk of heart failure and arrhythmias, warranting intensive combination chelation therapy (e.g., continuous IV Deferoxamine + Deferiprone).

B.Myocardial T2* of 8 ms is considered normal, so iron chelation should be temporarily paused.

C.Oral Deferasirox monotherapy is contraindicated in any patient with hepatic iron overload.

D.Phlebotomy is the primary therapy for transfusion-dependent thalassemia with severe iron overload.

Explanation: A cardiac MRI T2* value below 10 ms represents severe myocardial iron deposition associated with a high risk of developing acute heart failure and lethal arrhythmias within 12 months. In this high-risk scenario, international and ABHH guidelines recommend aggressive, intensive iron chelation using combination therapy (such as continuous intravenous deferoxamine combined with the intracellular iron-chelator deferiprone) to rapidly remove cardiac iron.

9A 30-year-old male with lifelong chronic microcytic hemolytic anemia and splenomegaly is evaluated. Hemoglobin electrophoresis at neutral pH reveals a fast-migrating hemoglobin band comprising 12% of total hemoglobin, and supravital staining with 1% brilliant cresyl blue demonstrates multiple fine greenish-blue inclusions ('golf-ball' appearance) within mature erythrocytes. What is the molecular basis of this condition?

A.Three-gene alpha-globin deletion (--/-alpha) leading to the formation of unstable beta-4 tetramers (Hemoglobin H disease).

B.Single-gene alpha-globin deletion (-alpha/alpha-alpha) with normal globin chain synthesis.

C.Homozygous beta-globin gene promoter mutation causing complete absence of beta-globin.

D.Four-gene alpha-globin deletion resulting in exclusive gamma-4 tetramer (Hb Bart's) formation.

Explanation: Hemoglobin H (HbH) disease results from the deletion or inactivation of 3 of the 4 alpha-globin genes (--/-alpha). The profound relative excess of beta-globin chains leads to the formation of soluble but unstable beta-4 tetramers (HbH). These precipitate as erythrocytes age, generating characteristic 'golf-ball' inclusion bodies visible upon supravital staining with brilliant cresyl blue.

10A 42-year-old female presents with acute jaundice, dark urine, and dyspnea on exertion. Labs show: Hb 6.5 g/dL, Reticulocytes 8.5% (absolute: 240 x 10^9/L), Total Bilirubin 4.2 mg/dL (Indirect: 3.5 mg/dL), LDH 1,120 U/L, Haptoglobin < 10 mg/dL. Peripheral blood smear reveals prominent microspherocytes and polychromasia. Direct Antiglobulin Test (DAT / Coombs Direto) is strongly positive (3+) for IgG and negative for C3d. What is the first-line therapeutic management?

A.Prednisone 1.0 to 1.5 mg/kg/day orally and oral folic acid supplementation.

B.Emergency splenectomy within 24 hours of diagnosis.

C.Immediate initiation of Eculizumab without immunosuppression.

D.Rituximab monotherapy as initial treatment before considering corticosteroids.

Explanation: Warm Autoimmune Hemolytic Anemia (AHAI por anticorpos quentes) is mediated primarily by polyclonal IgG autoantibodies that bind erythrocyte surface antigens at 37°C, leading to splenic macrophage extravascular phagocytosis (forming spherocytes). The first-line standard treatment is oral prednisone (1.0 to 1.5 mg/kg/day) along with folic acid supplementation to support active erythropoiesis.

About the Título em Hematologia e Hemoterapia Exam

The Título de Especialista em Hematologia e Hemoterapia (TEHH) is the official board certification granted jointly by the Associação Brasileira de Hematologia, Hemoterapia e Terapia Celular (ABHH) and the Associação Médica Brasileira (AMB), under the regulatory oversight of the Conselho Federal de Medicina (CFM). Attaining this title grants physicians the official specialist status and allows registration of the Registro de Qualificação de Especialista (RQE) in Hematology and Hemotherapy in Brazil. The rigorous evaluation spans two stages: an 80-question theoretical examination testing non-malignant hematology, myeloid and lymphoid malignancies, coagulation, transfusion medicine, and stem cell transplantation; and a practical/theoretical-practical station testing morphology slide review (peripheral blood and bone marrow aspirates/biopsies), flow cytometry immunophenotyping plots, immunohematology panels, and clinical emergency management.

Assessment

Two-stage process run by the Associação Brasileira de Hematologia, Hemoterapia e Terapia Celular (ABHH) with the AMB. First stage: an online Prova Teórica of 60 four-option multiple-choice questions delivered on the Educat platform, marked out of 100 points, sat without breaks and preceded by a compulsory pré-teste to check the candidate's hardware, software and proctoring setup. Second stage: an Avaliação Curricular. There is no hands-on practical station examination. The ABHH separately certifies áreas de atuação such as Transplante de Medula Óssea, Hematologia e Hemoterapia Pediátrica and Oncologia Pediátrica, and runs technical proficiency examinations for non-medical professions — all distinct from this título.

Time Limit

2 hours for the online Prova Teórica, with no interval or pause

Passing Score

Set by each annual edital against the 100-point scale of the Prova Teórica, with the Avaliação Curricular considered in the second stage

Exam Fee

R$ 1.200,00 (associados da ABHH) / R$ 1.200,00 (associados da AMB) / R$ 1.500,00 (demais candidatos) (Associação Brasileira de Hematologia, Hemoterapia e Terapia Celular (ABHH) — Associação Médica Brasileira (AMB))

Título em Hematologia e Hemoterapia Exam Content Outline

20%

Anemias e Hemoglobinopatias

Pathophysiology, differential diagnosis, laboratory investigation, and therapeutic protocols for nutritional anemias (iron deficiency / anemia ferropriva, vitamin B12 and folate megaloblastic anemia), hemoglobinopathies (sickle cell disease / anemia falciforme, hemoglobin SC, S-beta thalassemia, alpha and beta thalassemia major/intermedia/minor), autoimmune hemolytic anemias (warm AIHA, cold agglutinin disease), paroxysmal nocturnal hemoglobinuria (PNH / HPN clone flow cytometry), hereditary spherocytosis and elliptocytosis, red cell enzymopathies (G6PD deficiency, pyruvate kinase deficiency), anemia of chronic disease/inflammation, and congenital/acquired sideroblastic anemias.

Insuficiências Medulares

Diagnostic criteria (bone marrow cellularity < 25%, absolute neutrophil count < 0.5 x 10^9/L, platelet count < 20 x 10^9/L, reticulocytes < 20 x 10^9/L), cytogenetic screening, and therapeutic algorithms (horse ATG + cyclosporine + eltrombopag vs. upfront matched sibling donor HSCT) for acquired severe aplastic anemia (anemia aplástica grave); inherited bone marrow failure syndromes including Fanconi anemia (diepoxybutane/DEB chromosomal breakage test), dyskeratosis congenita (telomere length testing), and Diamond-Blackfan anemia; pure red cell aplasia (aplasia pura de série vermelha, thymoma-associated, parvovirus B19).

22%

Neoplasias Mieloides

Acute Myeloid Leukemia (AML / LMA WHO/ICC classifications, European LeukemiaNet / ELN 2022 risk stratification, molecular genetics NPM1, FLT3-ITD/TKD, CEBPA bZIP, TP53, IDH1/2, KMT2A), Acute Promyelocytic Leukemia (APL / LMA-M3 t(15;17)(q22;q21) PML-RARA, ATRA + arsenic trioxide therapy, differentiation syndrome management), Myelodysplastic Syndromes (MDS / SMD revised IPSS-R and molecular IPSS-M, ring sideroblasts / SF3B1, del(5q) lenalidomide response, hypomethylating agents), Chronic Myeloid Leukemia (CML / LMC BCR-ABL1 transcript monitoring, tyrosine kinase inhibitors imatinib, dasatinib, nilotinib, ponatinib, treatment-free remission criteria), and BCR-ABL1-negative Myeloproliferative Neoplasms (Polycythemia Vera / PV JAK2 V617F, Essential Thrombocythemia / ET CALR/MPL, Primary Myelofibrosis / MFP, ruxolitinib, fedratinib).

22%

Neoplasias Linfoides e Gamopatias Monoclonais

Hodgkin Lymphoma (classical HL, nodular sclerosis, mixed cellularity, lymphocyte-rich, lymphocyte-depleted, nodular lymphocyte predominant HL, ABVD, escalonated BEACOPP, brentuximab vedotin, nivolumab/pembrolizumab), Non-Hodgkin Lymphomas (Diffuse Large B-Cell Lymphoma / DLBCL R-CHOP, cell-of-origin Hans algorithm, double-hit/triple-hit MYC/BCL2/BCL6; Follicular Lymphoma GELF criteria; Mantle Cell Lymphoma cyclin D1 / t(11;14); Burkitt Lymphoma t(8;14) MYC; Marginal Zone Lymphomas MALT; Peripheral T-cell lymphomas), Chronic Lymphocytic Leukemia (CLL / LLC Rai and Binet staging, IGHV mutation status, TP53/del(17p), ibrutinib, acalabrutinib, zanubrutinib, venetoclax), and Plasma Cell Dyscrasias (Multiple Myeloma / Mieloma Múltiplo SLIM-CRAB criteria, R-ISS, VRd / Dara-VRd induction, autologous stem cell transplantation, lenalidomide maintenance, CAR-T and bispecific antibodies; Smoldering Myeloma; MGUS; AL Amyloidosis; Waldenström Macroglobulinemia / MYD88 L265P).

16%

Hemostasia, Trombose e Coagulopatias

Primary hemostasis disorders, Immune Thrombocytopenia (ITP / PTI corticosteroids, IVIg, anti-D, TPO receptor agonists eltrombopag/romiplostim, rituximab, fostamatinib), Thrombotic Microangiopathies (TTP / PTT ADAMTS13 activity < 10%, plasma exchange, caplacizumab; hemolytic uremic syndrome / aHUS eculizumab/ravulizumab), Heparin-Induced Thrombocytopenia (HIT / TIH 4Ts score, anti-PF4/heparin antibodies, direct thrombin inhibitors, fondaparinux), Inherited bleeding disorders (Hemophilia A / Factor VIII deficiency, Hemophilia B / Factor IX deficiency, prophylaxis, emicizumab, inhibitor development and bypass agents; von Willebrand Disease types 1, 2A, 2B, 2M, 2N, 3, desmopressin and VWF concentrates; rare factor deficiencies), Disseminated Intravascular Coagulation (DIC / CIVD ISTH score), Hereditary Thrombophilias (Factor V Leiden, Prothrombin G20210A, Antithrombin, Protein C and S deficiencies), Antiphospholipid Syndrome (APS / SAF Sydney classification criteria, lupus anticoagulant, anticardiolipin, anti-beta-2-glycoprotein I, anticoagulation with VKA), and Venous Thromboembolism (DVT, PE, direct oral anticoagulants / DOACs vs. vitamin K antagonists).

Medicina Transfusional e Hemoterapia

Blood component preparation, quality control, storage conditions, and clinical transfusion triggers (Packed Red Blood Cells / Concentrado de Hemácias, Platelet Concentrates / Plaquetas randômicas e aférese, Fresh Frozen Plasma / Plasma Fresco Congelado, Cryoprecipitate / Crioprecipitado); Special blood component processing (leukocyte reduction / desleucocitação, gamma irradiation for prevention of TA-GVHD, saline washing); Immunohematology testing (ABO forward and reverse grouping, RhD typing, Rh phenotyping, unexpected red cell antibody screening / PAI, antibody identification panels, direct antiglobulin test / TAD, immediate spin and indirect antiglobulin crossmatching); Hemolytic Disease of the Fetus and Newborn (DHPN, maternal anti-D prophylaxis guidelines); Therapeutic Apheresis (plasma exchange, red cell exchange, therapeutic leukocytapheresis/plateletpheresis); and Acute and Delayed Transfusion Reactions (TRALI, TACO, Acute Hemolytic Transfusion Reaction / RHAT, Febrile Non-Hemolytic Reaction / RNFH, allergic/anaphylactic reactions, Post-Transfusion Purpura, Transfusion-Associated Graft-versus-Host Disease / DECH-AT).

Transplante de Células-Tronco Hematopoéticas e Terapia Celular

Indications for Autologous HSCT (Multiple Myeloma, relapsed/refractory Hodgkin and aggressive Non-Hodgkin Lymphomas) and Allogeneic HSCT (AML, ALL, MDS, Severe Aplastic Anemia, high-risk MPN); Conditioning regimens (Myeloablative Conditioning / MAC vs. Reduced-Intensity Conditioning / RIC); Donor selection (HLA-matched sibling, matched unrelated donor / MUD, haploidentical donor with post-transplant cyclophosphamide / PTCy, umbilical cord blood); Graft-versus-Host Disease (acute GVHD organs: skin, GI tract, liver; chronic GVHD NIH consensus criteria; prophylaxis with calcineurin inhibitors, methotrexate, PTCy; first-line corticosteroids and second-line ruxolitinib); Post-transplant complications (Sinusoidal Obstruction Syndrome / VOD defibrotide, CMV reactivation preemptive therapy, Post-Transplant Lymphoproliferative Disorder / PTLD rituximab); Chimeric Antigen Receptor (CAR) T-cell therapy (anti-CD19 and anti-BCMA indications in B-cell ALL, DLBCL, and Multiple Myeloma; Cytokine Release Syndrome / CRS grading and IL-6 receptor antagonist tocilizumab; Immune Effector Cell-Associated Neurotoxicity Syndrome / ICANS grading and dexamethasone).

How to Pass the Título em Hematologia e Hemoterapia Exam

What You Need to Know

Passing score: Set by each annual edital against the 100-point scale of the Prova Teórica, with the Avaliação Curricular considered in the second stage
Assessment: Two-stage process run by the Associação Brasileira de Hematologia, Hemoterapia e Terapia Celular (ABHH) with the AMB. First stage: an online Prova Teórica of 60 four-option multiple-choice questions delivered on the Educat platform, marked out of 100 points, sat without breaks and preceded by a compulsory pré-teste to check the candidate's hardware, software and proctoring setup. Second stage: an Avaliação Curricular. There is no hands-on practical station examination. The ABHH separately certifies áreas de atuação such as Transplante de Medula Óssea, Hematologia e Hemoterapia Pediátrica and Oncologia Pediátrica, and runs technical proficiency examinations for non-medical professions — all distinct from this título.
Time limit: 2 hours for the online Prova Teórica, with no interval or pause
Exam fee: R$ 1.200,00 (associados da ABHH) / R$ 1.200,00 (associados da AMB) / R$ 1.500,00 (demais candidatos)

Keys to Passing

Work through all 100 available questions
Review every answer and explanation
Track weak areas and revisit them
Use our AI tutor for tough concepts

Título em Hematologia e Hemoterapia Study Tips from Top Performers

1Master Peripheral Blood and Bone Marrow Morphology: Train extensively on characteristic microscopic findings including Auer rods, dysplastic megakaryocytes/erythroblasts, smudge cells (manchas de Gumprecht), Reed-Sternberg cells, schistocytes, spherocytes, and plasma cells (flame cells, Russell bodies).

2Integrate WHO/ICC 2022 and ELN 2022 Classifications: Memorize defined cytogenetic and molecular categories for AML (NPM1, FLT3-ITD, CEBPA, TP53, t(8;21), inv(16), t(15;17)) and MDS (IPSS-R, IPSS-M, SF3B1, del(5q)).

3Know Brazilian Clinical Protocols (PCDT) and International Guidelines: Review Ministry of Health PCDT recommendations for sickle cell disease (hydroxyurea, transcranial Doppler), aplastic anemia, hemophilia prophylaxis, and immune thrombocytopenia.

4Internalize Transfusion Medicine Triggers and Reaction Algorithms: Clearly distinguish between TRALI (neutrophil activation, non-cardiogenic pulmonary edema, normal BNP/wedge pressure) and TACO (volume overload, elevated BNP, hypertension, response to diuretics), and master immediate management steps for acute hemolytic transfusion reactions.

5Understand Modern Targeted Therapeutics & Cellular Therapy: Review mechanisms of action, clinical indications, and adverse effects of BTK inhibitors (ibrutinib, acalabrutinib), BCL-2 inhibitors (venetoclax), FLT3 inhibitors (midostaurin, gilteritinib), bispecific T-cell engagers, and CAR-T cell therapy (cytokine release syndrome and ICANS management).

6Practice Timed Case Vignettes Across All Sub-Disciplines: Work through the full 100-question practice set with comprehensive rationales to identify diagnostic and pharmacological nuances across red cell disorders, oncology, hemostasis, and hemotherapy.

Frequently Asked Questions

What is the Título de Especialista em Hematologia e Hemoterapia (TEHH)?

The Título de Especialista em Hematologia e Hemoterapia is the official medical board certification recognized by the Associação Médica Brasileira (AMB) and the Conselho Federal de Medicina (CFM), administered by the Associação Brasileira de Hematologia, Hemoterapia e Terapia Celular (ABHH). It formally certifies a physician as a specialist in Hematology and Hemotherapy and qualifies them for the Registro de Qualificação de Especialista (RQE).

What are the eligibility requirements to register for the ABHH specialist examination?

Candidates must hold an active registration with their Regional Medical Council (CRM), be in good standing, and have completed either: (a) a medical residency program (Residência Médica) in Hematologia e Hemoterapia accredited by the Comissão Nacional de Residência Médica (CNRM/MEC), or (b) documented clinical practice and professional training in the specialty for a minimum number of years specified in the official annual announcement (Edital ABHH/AMB).

How is the ABHH specialist title exam structured?

The examination is divided into two main stages: (1) Prova Teórica, an objective multiple-choice examination with 80 questions covering the broad spectrum of hematology, hematologic oncology, hemostasis, transfusion medicine, and bone marrow transplantation; and (2) Prova Prática / Teórico-Prática, evaluating real-world clinical and laboratory competencies, including microscopic blood and marrow morphology, flow cytometry interpretation, coagulopathy workups, and transfusion medicine scenarios.

What is the minimum passing score for the ABHH exam?

Candidates must obtain a minimum passing grade of 7.0 out of 10.0 (70%) on both the theoretical and practical evaluation components according to the official certame notice (Edital).

Which professional society administers the exam?

The examination is administered by the Associação Brasileira de Hematologia, Hemoterapia e Terapia Celular (ABHH) in institutional partnership with the Associação Médica Brasileira (AMB). The ABHH is the sole AMB-convened society representing hematology and hemotherapy in Brazil (official portal: abhh.org.br).

Why is this OpenExamPrep practice bank authored in English?

This practice bank is an English-language study adaptation designed to deliver high-yield conceptual mastery for physicians, hematology fellows, and international medical trainees. It maintains all authentic Brazilian clinical terminology (e.g., ABHH, AMB, CFM, SUS, PCDT, anemia ferropriva, púrpura trombocitopênica imune, mieloma múltiplo, concentrado de hemácias) within standardized bilingual vignettes.