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Exam Review

Key Facts: CMH Hematología Exam

14 Mar 2026

Theoretical exam (UNAM Facultad de Medicina, CU)

CMH certification call

15 Mar 2026

Practical evaluation (CECCOMS, Tlatelolco)

CMH certification call

MXN 6,500

2026 certification fee

CMH certification call

Temario

Official syllabus published by the CMH

CMH

5 years

Certification validity

CONACEM

The CMH certification exam is the CONACEM-recognized hematology board exam in Mexico: a theoretical exam at UNAM followed by a practical evaluation at CECCOMS, held in March (14–15 March 2026; fee MXN 6,500).

Sample CMH Hematología Practice Questions

Try these sample questions to review concepts for the CMH Hematología exam. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1A 42-year-old woman presents with progressive fatigue, cutaneous petechiae, and epistaxis. A complete blood count shows hemoglobin 7.8 g/dL, white blood cell count 3.4 x 10^9/L, and platelets 28 x 10^9/L. Bone marrow aspiration demonstrates 12% myeloblasts with Auer rods, and cytogenetic analysis reveals t(8;21)(q22;q22.1) resulting in the RUNX1::RUNX1T1 fusion. Under the WHO 2022 and International Consensus Classification (ICC) systems, what is the correct diagnosis?
A.Myelodysplastic syndrome with excess blasts type 1 (MDS-EB1), because the blast count is below the 20% threshold
B.Myelodysplastic/myeloproliferative neoplasm unclassifiable, requiring monitoring until blasts exceed 20%
C.Acute myeloid leukemia with RUNX1::RUNX1T1, because this defining genetic abnormality establishes AML below the 20% blast threshold
D.Refractory anemia with excess blasts in transformation (RAEB-t), requiring low-dose cytarabine monotherapy
Explanation: In the WHO 2022 classification, AML with defining genetic abnormalities (including PML::RARA, RUNX1::RUNX1T1, CBFB::MYH11 and KMT2A rearrangements) is diagnosed without a minimum blast count; the exceptions are BCR::ABL1 and CEBPA, which still need ≥20% blasts. The ICC requires ≥10% blasts for AML with recurrent genetic abnormalities (≥20% for BCR::ABL1). A blast count of 12% with t(8;21) therefore meets the AML definition in both systems.
2A 34-year-old male is admitted with severe epistaxis, gingival hemorrhage, and extensive purpura. Laboratory tests show WBC 2.1 x 10^9/L, hemoglobin 8.0 g/dL, platelets 18 x 10^9/L, prothrombin time (PT) 21 seconds (INR 1.8), fibrinogen 78 mg/dL, and elevated D-dimer (>20 mcg/mL). The peripheral smear reveals promyelocytes packed with prominent Auer rods in bundles (faggot cells). Bone marrow aspirate is pending for PML::RARA cytogenetics. What is the immediate, life-saving management step?
A.Immediately administer all-trans retinoic acid (ATRA) along with supportive transfusions of cryoprecipitate and platelets
B.Wait for RT-PCR confirmation of PML::RARA before starting any differentiation agent to prevent toxicity
C.Initiate high-dose broad-spectrum antibiotics and recombinant activated factor VII (rFVIIa) monotherapy
D.Begin full-dose standard '7+3' induction chemotherapy with cytarabine and daunorubicin immediately
Explanation: Acute promyelocytic leukemia (APL) is a medical emergency due to catastrophic disseminated intravascular coagulation (DIC) and primary hyperfibrinolysis. ATRA must be started immediately upon morphological or clinical suspicion, without waiting for genetic or cytogenetic confirmation of the PML::RARA fusion. Aggressive transfusion support targeting fibrinogen >=150 mg/dL (with cryoprecipitate) and platelets >=30-50 x 10^9/L is crucial to prevent fatal intracranial or pulmonary bleeding.
3On day 5 of induction therapy with ATRA and arsenic trioxide (ATO) for newly diagnosed low-risk acute promyelocytic leukemia, a 38-year-old patient develops fever (38.6°C), unexplained dyspnea, a weight gain of 4.5 kg, bilateral pulmonary infiltrates, and a small pleural effusion. The WBC count has risen from 2.5 x 10^9/L to 18.0 x 10^9/L. Blood cultures are drawn. What is the definitive management for this complication?
A.Immediate discontinuation of all oral fluids and administration of high-dose loop diuretics as monotherapy
B.Immediate permanent cessation of both ATRA and ATO, replacing them with broad-spectrum antifungals
C.Urgent therapeutic leukapheresis to rapidly reduce the circulating white blood cell count
D.Intravenous dexamethasone 10 mg every 12 hours until complete symptom resolution, continuing ATRA and ATO
Explanation: The clinical presentation is classic for differentiation syndrome (formerly retinoic acid syndrome), caused by chemokine release and endothelial activation from differentiating promyelocytes. Standard management is intravenous dexamethasone 10 mg twice daily started at the first clinical suspicion and continued until complete resolution of symptoms and pulmonary infiltrates. ATRA and ATO should be continued unless severe life-threatening respiratory or hemodynamic compromise develops.
4A 54-year-old previously fit man is diagnosed with AML with normal karyotype. Molecular testing reveals an internal tandem duplication of the FLT3 gene (FLT3-ITD) with a high allelic ratio (>0.5) and wild-type NPM1. According to the European LeukemiaNet (ELN) 2022 guidelines and landmark clinical trial evidence (RATIFY), what is the standard frontline induction approach?
A.Low-dose subcutaneous cytarabine monotherapy combined with prophylactic intrathecal methotrexate
B.Standard 7+3 (cytarabine continuous infusion for 7 days plus daunorubicin for 3 days) combined with midostaurin
C.Venetoclax plus decitabine without any systemic anthracycline or multikinase inhibitor
D.Monotherapy with the second-generation FLT3 inhibitor gilteritinib as frontline induction
Explanation: The RATIFY trial demonstrated that adding the multikinase FLT3 inhibitor midostaurin (50 mg orally twice daily on days 8-21) to standard 7+3 induction (cytarabine 200 mg/m2 continuous infusion for 7 days + daunorubicin 60 mg/m2 for 3 days) significantly prolonged overall survival in fit patients with FLT3-mutated (ITD or TKD) AML. Quizartinib added to 7+3 (QuANTUM-First) is an alternative for FLT3-ITD disease. ELN 2022 no longer uses the FLT3-ITD allelic ratio and places FLT3-ITD AML in the intermediate-risk group unless adverse genetic lesions are present. Allogeneic transplantation in first complete remission is generally considered for fit intermediate-risk patients, especially when MRD persists.
5A 77-year-old woman with a history of ischemic cardiomyopathy (left ventricular ejection fraction 32%) is diagnosed with de novo AML (WBC 14 x 10^9/L, bone marrow blasts 35%, normal karyotype, IDH2 R140Q mutation). She is deemed ineligible for intensive anthracycline-based induction. Based on the phase III VIALE-A trial, which frontline regimen provides the greatest overall survival benefit?
A.Azacitidine combined with the BCL-2 inhibitor venetoclax
B.High-dose cytarabine (HiDAC) administered every 12 hours for 6 consecutive doses
C.Supportive care with red blood cell transfusions and hydroxyurea monotherapy
D.Single-agent gemtuzumab ozogamicin administered on days 1, 4, and 7
Explanation: The randomized phase III VIALE-A trial demonstrated that azacitidine combined with venetoclax (a selective oral BCL-2 inhibitor) produced significantly higher complete remission rates (66.4% vs 28.3%) and superior median overall survival (14.7 vs 9.6 months) compared to azacitidine plus placebo in older adults with AML ineligible for intensive chemotherapy. It is the international standard of care.
6A 66-year-old man with a 3-year history of myelodysplastic syndrome treated with erythropoietin presents with progressive pancytopenia. Bone marrow examination shows 26% blasts and a complex karyotype including monosomy 7 and del(5q), establishing therapy-related / secondary AML with myelodysplasia-related changes. Which induction formulation showed statistically superior overall survival over conventional '7+3' in fit older adults with secondary AML?
A.FLAG-Ida (fludarabine, cytarabine, idarubicin, and G-CSF)
B.Standard induction combining cladribine, topotecan, and daunorubicin
C.CPX-351 (dual-drug liposomal encapsulation of cytarabine and daunorubicin at a 5:1 molar ratio)
D.Methotrexate, vincristine, and dexamethasone alternating with cytarabine
Explanation: CPX-351 (Vyxeos) is a fixed 5:1 synergistic molar ratio of cytarabine and daunorubicin encapsulated in 100-nm liposomes. In a pivotal phase III randomized trial in older adults (60-75 years) with secondary AML, therapy-related AML, or AML with myelodysplasia-related changes, CPX-351 demonstrated significantly higher complete remission rates and longer median overall survival (9.56 vs 5.95 months) compared to conventional 7+3.
7A 49-year-old male presents with early satiety, left upper quadrant fullness, and night sweats. Physical examination reveals splenomegaly palpable 7 cm below the left costal margin. Laboratory studies show WBC 96 x 10^9/L with a left-shifted myeloid series (myelocytes, metamyelocytes, basophilia 4%, blasts 1%), hemoglobin 11.2 g/dL, and platelets 420 x 10^9/L. Bone marrow cytogenetics demonstrates t(9;22)(q34.1;q11.2). Which oncoprotein with deregulated constitutive tyrosine kinase activity causes this disorder?
A.FLT3 internal tandem duplication tyrosine kinase receptor
B.BCR::ABL1 fusion oncoprotein (p210)
C.JAK2 V617F pseudokinase domain mutant protein
D.PML::RARA hybrid nuclear retinoic acid receptor
Explanation: Chronic myeloid leukemia (CML) is hallmarked by the reciprocal translocation t(9;22)(q34.1;q11.2), creating the Philadelphia chromosome. This juxtaposes the ABL1 proto-oncogene on chromosome 9 with the BCR gene on chromosome 22, producing the chimeric BCR::ABL1 fusion transcript encoding the constitutively active p210 tyrosine kinase that drives unregulated granulocytic proliferation.
8A 51-year-old patient with chronic-phase CML has been receiving first-line imatinib 400 mg daily for 12 months. Routine molecular monitoring by quantitative RT-PCR on the International Scale (IS) demonstrates a BCR::ABL1 transcript level of 0.06% (IS). According to the European LeukemiaNet (ELN) milestones, how is this response classified?
A.Treatment failure, requiring immediate switch to third-line therapy with ponatinib
B.Warning response, necessitating dose escalation of imatinib to 800 mg daily
C.Complete cytogenetic response only, without achieving major molecular response
D.Optimal response, having achieved a major molecular response (MMR / MR3.0)
Explanation: Under ELN criteria, an optimal response at 12 months of TKI therapy is defined as achieving a major molecular response (MMR or MR3.0), which corresponds to BCR::ABL1 <= 0.1% on the International Scale (a 3-log reduction from the standardized baseline). A transcript level of 0.06% represents MMR (MR3.0) and is classified as an optimal response.
9A 53-year-old male with chronic-phase CML who initially achieved MMR on nilotinib develops secondary resistance with loss of MMR and rising BCR::ABL1 transcripts to 12% over 6 months. BCR::ABL1 kinase domain mutational analysis detects a T315I gatekeeper mutation. Which tyrosine kinase inhibitor is indicated and approved to overcome this mutation?
A.Ponatinib
B.Dasatinib
C.Bosutinib
D.Imatinib at 800 mg daily
Explanation: The T315I gatekeeper mutation substitutes isoleucine for threonine at position 315 in the ATP-binding pocket of ABL1, creating steric hindrance that confers cross-resistance to first-generation (imatinib) and second-generation TKIs (dasatinib, nilotinib, and bosutinib). Ponatinib is a rationally designed third-generation TKI whose carbon-carbon triple bond accommodates the bulky isoleucine side chain, making it highly active against T315I. Asciminib at high dose (200 mg BID) is also approved for T315I.
10A 61-year-old man presents with severe pruritus after warm showers (aquagenic pruritus), burning pain and erythema in his fingertips (erythromelalgia), and dizziness. Physical examination shows facial plethora and splenomegaly. Laboratory evaluation demonstrates hemoglobin 19.8 g/dL, hematocrit 59%, WBC 12.8 x 10^9/L, platelets 490 x 10^9/L, and a subnormal serum erythropoietin level (<2 mIU/mL). Which molecular genetic alteration is present in over 95% of patients with this disorder?
A.CALR exon 9 insertion/deletion mutation
B.MPL W515L/K transmembrane domain point mutation
C.JAK2 V617F point mutation in exon 14
D.BCR::ABL1 fusion gene resulting from t(9;22)
Explanation: The patient exhibits classic features of Polycythemia Vera (PV). The somatic point mutation JAK2 V617F (valine to phenylalanine substitution at codon 617 in exon 14, disrupting the auto-inhibitory pseudokinase domain JH2) is present in >95% of patients with PV. The remaining ~3-5% of PV cases harbor mutations in JAK2 exon 12.

About the CMH Hematología Exam

Independent CMH hematology certification study practice by OpenExamPrep. The Consejo Mexicano de Hematología, A.C., recognized by CONACEM, certifies hematologists through a theoretical exam at the UNAM Facultad de Medicina and a practical evaluation at CECCOMS, Tlatelolco. The 2026 stages were held on 14 and 15 March 2026 and the fee was MXN 6,500. The official exam is in Spanish; this bank is an independent English-language MCQ study adaptation of the theoretical component, built from the CMH temario, current international guidelines and NOM-253-SSA1-2012. It is not an official translation or simulation, and the practical stage is not simulated.

Exam sponsor: Consejo Mexicano de Hematología, A.C. (CMH). The requirements and fees below concern the certification or admission exam, separate from our free practice resources.

Assessment

Two in-person stages in Mexico City: a written theoretical exam at the UNAM Facultad de Medicina (Ciudad Universitaria) followed the next day by a practical evaluation at CECCOMS, Tlatelolco (14 and 15 March 2026). The CMH publishes an official temario but no item count, duration or percentage pass mark. This bank groups practice into myeloid neoplasms, lymphoid and plasma-cell neoplasms, benign hematology, hemostasis and transfusion (including NOM-253-SSA1-2012), and transplantation and cellular therapy (an OpenExamPrep study grouping).

Time Limit

Not published

Passing Score

not-published

Exam / Certification Fees

MXN 6,500

Exam sponsor website

Fees, eligibility, and exam policies can change. Confirm them with the exam sponsor before applying or paying.

Official sources

Our practice resources: topics covered

We aim to reflect publicly available exam outlines and topic information in our study resources. Coverage, format, and difficulty may differ from the actual exam, and we cannot guarantee that every detail is accurate or current. Confirm exam requirements, fees, and policies with the official exam sponsor.

Core section (weight not published)

Neoplasias Hematológicas Mieloides

Acute myeloid leukemia (WHO/ICC 2022 classifications, cytogenetics, targeted therapies: venetoclax, midostaurin, IDH inhibitors), myelodysplastic syndromes (IPSS-R, IPSS-M, hypomethylating agents, luspatercept, 5q- syndrome), and myeloproliferative neoplasms (CML BCR-ABL1 monitoring and TKI resistance, PV JAK2 V617F, essential thrombocythemia, primary myelofibrosis)

Core section (weight not published)

Neoplasias Linfoides y Gammapatías Monoclonales

Acute lymphoblastic leukemia (Ph-positive/negative, blinatumomab, inotuzumab, CAR-T), non-Hodgkin lymphomas (DLBCL, follicular, mantle cell, Burkitt), Hodgkin lymphoma (ABVD, brentuximab vedotin, Deauville PET response criteria), chronic lymphocytic leukemia (del(17p)/TP53, BTK inhibitors, venetoclax), and multiple myeloma (SLiM-CRAB criteria, VRd induction, Dara-VRd, autologous SCT eligibility)

Core section (weight not published)

Hematología Benigna, Fisiología Eritrocitaria y Anemias

Severe aplastic anemia (Camitta criteria, immunosuppression with horse ATG + cyclosporine + eltrombopag vs matched sibling donor HSCT), paroxysmal nocturnal hemoglobinuria (flow cytometry CD55/CD59, complement inhibitors), autoimmune hemolytic anemia (warm IgG vs cold agglutinin disease), megaloblastic anemia (B12 vs folate deficiency), iron metabolism, and thalassemias

Core section (weight not published)

Hemostasia, Trombosis y Medicina Transfusional

Immune thrombocytopenia (corticosteroids, IVIG, TPO receptor agonists), thrombotic microangiopathies (TTP ADAMTS13 deficiency, plasma exchange, caplacizumab), heparin-induced thrombocytopenia (4Ts score, non-heparin anticoagulants), hemophilias (factor replacement, emicizumab, Bethesda assay inhibitors), von Willebrand disease, antiphospholipid syndrome, DOACs, and blood component safety under NOM-253-SSA1-2012

Core section (weight not published)

Trasplante de Progenitores Hematopoyéticos y Terapia Celular

Autologous vs allogeneic HSCT indications, conditioning regimens, acute and chronic graft-versus-host disease (MAGIC biomarkers, corticosteroid therapy, ruxolitinib), post-transplant opportunistic infections (CMV, EBV-PTLD, invasive aspergillosis), sinusoidal obstruction syndrome (defibrotide), and CAR-T cell toxicity management (CRS and ICANS)

Preparing for the CMH Hematología Exam

What You Need to Know

  • Passing score: not-published
  • Assessment: Two in-person stages in Mexico City: a written theoretical exam at the UNAM Facultad de Medicina (Ciudad Universitaria) followed the next day by a practical evaluation at CECCOMS, Tlatelolco (14 and 15 March 2026). The CMH publishes an official temario but no item count, duration or percentage pass mark. This bank groups practice into myeloid neoplasms, lymphoid and plasma-cell neoplasms, benign hematology, hemostasis and transfusion (including NOM-253-SSA1-2012), and transplantation and cellular therapy (an OpenExamPrep study grouping).
  • Time limit: Not published
  • Exam / certification fees: MXN 6,500 Official sources

Using Our Practice Resources

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

CMH Hematología: Suggested Study Strategy

1Master the 2022 WHO and ICC classifications of acute myeloid leukemia, paying particular attention to genetic defining lesions (such as PML::RARA, RUNX1::RUNX1T1, CBFB::MYH11, NPM1, and biallelic/in-frame CEBPA) and ELN 2022 risk stratification.
2Review first-line targeted therapies across hematologic malignancies, including venetoclax combinations in unfit AML and CLL, FLT3 inhibitors (midostaurin, gilteritinib), BTK inhibitors (ibrutinib, acalabrutinib), and anti-CD38 monoclonal antibodies (daratumumab) in multiple myeloma.
3Thoroughly understand the diagnostic workup and acute management of hematologic emergencies: thrombotic thrombocytopenic purpura (TTP: ADAMTS13 activity, urgent plasma exchange and caplacizumab), acute promyelocytic leukemia (prompt ATRA initiation prior to genetic confirmation), and hyperleukocytosis.
4Memorize the mandatory Mexican requirements under NOM-253-SSA1-2012 for blood component preparation, viral screening, irradiation indications to prevent transfusion-associated GVHD, and the clinical distinction and management of TRALI versus TACO.
5Rehearse the management of post-transplant complications, including acute and chronic graft-versus-host disease (GVHD) diagnostic staging, first-line methylprednisolone dosing, second-line ruxolitinib indications, and cytomegalovirus (CMV) preemptive monitoring and treatment.

Frequently Asked Questions

What is the CMH hematology certification exam?

The Examen de Certificación en Hematología is administered by the Consejo Mexicano de Hematología, A.C. (CMH), the council recognized by CONACEM for the specialty. Certification is valid for 5 years and is renewed through recertification.

How is the CMH certification exam administered?

The exam has two in-person stages in Mexico City: a written theoretical exam at the UNAM Facultad de Medicina (Ciudad Universitaria) and, the next day, a practical evaluation at CECCOMS, Tlatelolco. In 2026 these were held on 14 and 15 March. Documents are submitted through SIGME.

What is the fee and passing score for the CMH examination?

The 2026 fee was MXN 6,500. The CMH does not publish a percentage pass mark or the number of items.

What topics and standards are evaluated on the exam?

The CMH publishes an official certification temario. Core areas include myeloid and lymphoid neoplasms, plasma cell disorders, red cell disorders and marrow failure, hemostasis and thrombosis, transfusion medicine under NOM-253-SSA1-2012, and hematopoietic cell transplantation.

Does this OpenExamPrep question bank simulate the practical CECCOMS examination?

No. This practice bank is an independent English-language study adaptation focused strictly on the written theoretical knowledge component of the specialty examination. Practical stations, microscope slide interpretations, and oral clinical simulations conducted at CECCOMS are not simulated.

Why is this OpenExamPrep question bank written in English?

The official CMH exam is administered in Spanish. This bank is an independent English-language MCQ study adaptation built on the CMH temario, international guidelines and landmark trials, with Mexican references such as NOM-253-SSA1-2012 kept where relevant. It is not an official translation or simulation.