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Here are 50 hematology pathology flashcards:

Hematology Pathology - 50 Flashcards

Card 1 Q: What is the MCV in microcytic anemia? A: MCV < 80 fL. Causes include iron deficiency, thalassemia, sideroblastic anemia, and anemia of chronic disease.
Card 2 Q: What peripheral smear finding is pathognomonic for iron deficiency anemia? A: Hypochromic, microcytic RBCs with pencil cells (elliptocytes) and target cells.
Card 3 Q: What lab findings distinguish iron deficiency anemia from anemia of chronic disease? A: Iron deficiency: low serum iron, low ferritin, high TIBC. Anemia of chronic disease: low serum iron, high/normal ferritin, low/normal TIBC.
Card 4 Q: What are Heinz bodies and when do they appear? A: Denatured hemoglobin precipitates within RBCs. Seen in G6PD deficiency and alpha-thalassemia. Require supravital staining (crystal violet) to visualize.
Card 5 Q: What is the genetic defect in sickle cell disease? A: Point mutation in codon 6 of the beta-globin gene: glutamic acid → valine (GAG → GTG), producing HbS.
Card 6 Q: What triggers sickling in sickle cell disease? A: Low pO2, acidosis, dehydration, cold temperatures, and high altitude all promote HbS polymerization and sickling.
Card 7 Q: What is the difference between alpha and beta thalassemia? A: Alpha thalassemia: deletion of alpha-globin genes (chromosome 16). Beta thalassemia: point mutations reducing beta-globin synthesis (chromosome 11).
Card 8 Q: What is the most severe form of alpha thalassemia and why is it fatal? A: Hydrops fetalis (deletion of all 4 alpha genes). Results in HbBart (γ4 tetramers) with very high O2 affinity - cannot deliver O2 to tissues. Intrauterine death.
Card 9 Q: What is HbH disease? A: Deletion of 3 alpha-globin genes. HbH = beta4 tetramers. Causes moderate hemolytic anemia; HbH precipitates as inclusions (golf-ball cells on supravital stain).
Card 10 Q: What are the lab findings in beta thalassemia major? A: Severe microcytic hypochromic anemia, elevated HbF and HbA2, massive splenomegaly, target cells, nucleated RBCs, and Cabot rings on smear.
Card 11 Q: What is the Coombs test, and what does a positive direct Coombs indicate? A: The direct Coombs (DAT) tests for antibodies/complement bound to RBCs. Positive = autoimmune hemolytic anemia, hemolytic transfusion reaction, or hemolytic disease of the newborn.
Card 12 Q: What is warm vs. cold autoimmune hemolytic anemia? A: Warm AIHA: IgG antibodies active at 37°C; extravascular hemolysis; associated with SLE, CLL, drugs. Cold AIHA: IgM at <37°C; intravascular hemolysis + Raynaud's; associated with Mycoplasma, EBV.
Card 13 Q: What is hereditary spherocytosis and what protein is defective? A: Autosomal dominant defect in spectrin, ankyrin, or band 3 protein causing RBC membrane instability. Spherocytes lose membrane surface area and are destroyed in spleen.
Card 14 Q: What is the osmotic fragility test? A: Tests RBC resistance to hypotonic solutions. Spherocytes lyse at higher NaCl concentrations (increased fragility) due to reduced surface area:volume ratio.
Card 15 Q: What is G6PD deficiency and what triggers acute hemolysis? A: X-linked recessive defect in G6PD enzyme. RBCs cannot regenerate NADPH → oxidative stress → Heinz bodies → intravascular hemolysis. Triggers: primaquine, dapsone, fava beans, infection, sulfa drugs.
Card 16 Q: What is Paroxysmal Nocturnal Hemoglobinuria (PNH)? A: Acquired clonal stem cell mutation in PIG-A gene. Loss of GPI-anchored proteins (CD55, CD59) that protect RBCs from complement. Results in intravascular hemolysis, thrombosis (especially Budd-Chiari), and cytopenias.
Card 17 Q: How is PNH diagnosed? A: Flow cytometry showing absence of GPI-anchored proteins (CD55, CD59) on RBCs and neutrophils. Ham's test (acidified serum lysis) is the classic but older test.
Card 18 Q: What are the morphological features of microangiopathic hemolytic anemia (MAHA)? A: Schistocytes (helmet cells, fragmented RBCs) on peripheral smear. Elevated LDH, low haptoglobin, negative Coombs. Seen in TTP, HUS, DIC, HELLP.
Card 19 Q: What is the pathophysiology of TTP? A: Deficiency of ADAMTS13 (vWF-cleaving protease) → ultra-large vWF multimers → platelet microthrombi → MAHA + thrombocytopenia. Classic pentad: MAHA, thrombocytopenia, fever, renal failure, neurological symptoms.
Card 20 Q: What distinguishes TTP from HUS? A: TTP: predominantly neurological symptoms, severe ADAMTS13 deficiency. HUS: predominantly renal failure, often triggered by Shiga toxin (E. coli O157:H7), normal ADAMTS13.
Card 21 Q: What is DIC? A: Disseminated intravascular coagulation - systemic activation of coagulation consuming clotting factors and platelets. Causes both thrombosis and bleeding. Triggers: sepsis, trauma, obstetric complications, malignancy.
Card 22 Q: What are the lab findings in DIC? A: Prolonged PT, PTT, and thrombin time; low fibrinogen; elevated D-dimer and FDPs; thrombocytopenia; schistocytes on smear.
Card 23 Q: What is the most common cause of polycythemia vera, and what mutation is involved? A: JAK2 V617F mutation (present in ~95% of cases). Results in EPO-independent erythroid proliferation.
Card 24 Q: What are the diagnostic features of polycythemia vera? A: Elevated hematocrit (>49% men, >48% women), JAK2 mutation, subnormal serum EPO, bone marrow hypercellularity. Symptoms: plethora, pruritus after bathing, erythromelalgia, splenomegaly.
Card 25 Q: What is the Philadelphia chromosome and which leukemia is it associated with? A: t(9;22) translocation creating BCR-ABL fusion gene (constitutively active tyrosine kinase). Hallmark of Chronic Myeloid Leukemia (CML). Targeted by imatinib (Gleevec).
Card 26 Q: What is the blast crisis in CML? A: Transformation to acute leukemia (>20% blasts) - either AML or ALL. Accelerated phase precedes it (10-19% blasts). Poor prognosis.
Card 27 Q: What is the FAB classification of AML? A: M0-M7 based on morphology/cytochemistry. Most important: M3 (acute promyelocytic leukemia, APL) - t(15;17), PML-RARA fusion, Auer rods, high DIC risk, treated with ATRA.
Card 28 Q: What are Auer rods and in which disease are they found? A: Pink needle-like cytoplasmic inclusions in myeloblasts - crystallized azurophilic granules. Pathognomonic for AML (especially M3/APL). Never in ALL.
Card 29 Q: What is the most common leukemia in adults? A: Chronic Lymphocytic Leukemia (CLL). B-cell neoplasm (CD5+, CD19+, CD20dim, CD23+). Smudge cells on smear. Indolent course.
Card 30 Q: What is Richter's transformation? A: Transformation of CLL into an aggressive large B-cell lymphoma (usually DLBCL). Presents with rapid lymph node enlargement, B symptoms, elevated LDH. Poor prognosis.
Card 31 Q: What is the most common leukemia in children? A: Acute Lymphoblastic Leukemia (ALL). B-cell ALL is most common. t(12;21) ETV6-RUNX1 = best prognosis. t(9;22) BCR-ABL = worst prognosis.
Card 32 Q: What is the immunophenotype of T-cell ALL? A: CD2+, CD3+, CD5+, CD7+, TdT+. Often presents as mediastinal mass in adolescent males (thymocyte origin). Associated with NOTCH1 mutations.
Card 33 Q: What is the hallmark translocation of Burkitt lymphoma? A: t(8;14) - MYC gene (chromosome 8) juxtaposed to IGH enhancer (chromosome 14). Results in MYC overexpression and rapid cell proliferation. "Starry sky" pattern on histology.
Card 34 Q: What is the "starry sky" pattern in Burkitt lymphoma? A: Sheets of dark-blue lymphoma cells (sky) interspersed with macrophages containing apoptotic debris (stars). Reflects extremely high proliferation rate (Ki-67 ~100%) with rapid cell death.
Card 35 Q: What is Hodgkin lymphoma and what are the key diagnostic cells? A: Malignancy of B-lymphocyte origin. Reed-Sternberg cells (RS cells): large binucleated cells with prominent "owl-eye" nucleoli, CD15+, CD30+, CD45-.
Card 36 Q: What are the four subtypes of classical Hodgkin lymphoma by prognosis? A: Best to worst: Lymphocyte-predominant > Nodular sclerosis (most common) > Mixed cellularity > Lymphocyte-depleted (worst prognosis, associated with HIV).
Card 37 Q: What is diffuse large B-cell lymphoma (DLBCL)? A: Most common non-Hodgkin lymphoma in adults. Aggressive B-cell lymphoma. CD19+, CD20+. BCL-2 and BCL-6 rearrangements common. Treated with R-CHOP.
Card 38 Q: What translocation is associated with follicular lymphoma and what does it do? A: t(14;18) - BCL-2 gene moved next to IGH enhancer → BCL-2 overexpression → blocked apoptosis. Cells accumulate without dying. Indolent but incurable.
Card 39 Q: What is MALT lymphoma? A: Mucosa-Associated Lymphoid Tissue lymphoma - extranodal marginal zone B-cell lymphoma. Gastric MALT associated with H. pylori; can regress with H. pylori eradication. t(11;18) in H. pylori-negative cases.
Card 40 Q: What is multiple myeloma? A: Malignant proliferation of plasma cells in bone marrow producing monoclonal immunoglobulin (M-protein). CRAB criteria: hyperCalcemia, Renal failure, Anemia, Bone lesions (lytic).
Card 41 Q: What is the difference between MGUS, smoldering myeloma, and multiple myeloma? A: MGUS: M-protein <3g/dL, BM plasma cells <10%, no CRAB. Smoldering: M-protein ≥3g/dL or BM plasma cells 10-60%, no CRAB. Multiple myeloma: CRAB criteria present or BM plasma cells >60%.
Card 42 Q: What are Bence-Jones proteins? A: Free light chains (kappa or lambda) in urine. In myeloma, excess monoclonal light chains are filtered by kidneys. Can cause "myeloma kidney" (cast nephropathy) and tubular damage.
Card 43 Q: What is Waldenström's macroglobulinemia? A: Lymphoplasmacytic lymphoma producing IgM M-protein. Hyperviscosity syndrome: visual changes, headache, bleeding, Raynaud's. MYD88 L265P mutation in >90%. Treated with plasmapheresis for hyperviscosity.
Card 44 Q: What are the morphological features of plasma cells? A: Eccentric nucleus with "clock-face" chromatin, prominent perinuclear hof (clear zone = Golgi), abundant basophilic cytoplasm. Russell bodies = immunoglobulin-filled inclusions.
Card 45 Q: What is hemophilia A vs. hemophilia B? A: Hemophilia A: Factor VIII deficiency (X-linked recessive). Hemophilia B (Christmas disease): Factor IX deficiency (X-linked recessive). Both: prolonged PTT, normal PT and bleeding time.
Card 46 Q: What is von Willebrand disease (vWD) and which type is most common? A: Deficiency or dysfunction of vWF. Type 1 (most common, 75%): quantitative partial deficiency. Type 2: qualitative defect. Type 3: complete absence. Prolonged bleeding time + PTT; normal PT.
Card 47 Q: What is the coagulation defect in liver disease? A: Liver produces all clotting factors except vWF and factor VIII (made by endothelium). Deficiency of factors II, V, VII, IX, X, XI; prolonged PT (Factor VII has shortest half-life). Also thrombocytopenia from hypersplenism.
Card 48 Q: What is heparin-induced thrombocytopenia (HIT)? A: IgG antibodies against heparin-PF4 complex activate platelets → thrombocytopenia + paradoxical thrombosis. Diagnosis: 4Ts score + anti-PF4 antibody. Treat: stop heparin, use direct thrombin inhibitor (argatroban).
Card 49 Q: What is the 5T mnemonic for diagnosing TTP? A: Thrombocytopenia, Thrombotic microangiopathy (MAHA with schistocytes), Temperature (fever), Trouble with kidneys (renal failure), Trouble with brain (neurological symptoms).
Card 50 Q: What is the significance of the leukemoid reaction vs. CML? A: Leukemoid reaction: reactive leukocytosis (WBC >50,000) from infection/stress - high LAP (leukocyte alkaline phosphatase) score, no Philadelphia chromosome, toxic granulation. CML: low LAP score, Philadelphia chromosome/BCR-ABL present, basophilia.
That's 50 hematology pathology flashcards covering:
  • RBC disorders (cards 1-18): anemias, hemolytic disorders, morphology
  • Coagulation disorders (cards 19-22, 45-49): DIC, TTP, HUS, hemophilias, vWD, HIT
  • Myeloproliferative disorders (cards 23-25): polycythemia vera, CML
  • Leukemias (cards 26-32, 50): AML, ALL, CML, CLL
  • Lymphomas (cards 33-40): Hodgkin, NHL subtypes, Burkitt, DLBCL, follicular, MALT
  • Plasma cell dyscrasias (cards 41-44): myeloma, MGUS, Waldenström's
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