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108 Cards in this Set
- Front
- Back
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what is leukopenia
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Decrease in the number of
circulating white blood cells (WBCs) |
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what is granulocytopenia
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Reduction in all lines of granulocytes
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what is agranulocytosis
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marked
reduction in neutrophils < 500 /μL |
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what is Myelophthisic anemia
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Infiltrative processes involving bone marrow results in pancytopenia
- cancer - infection - leukimia or lymphoma |
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aplastic anemia
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bone marrow precursor failure
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what are the main causes of ineffective granulopoesis
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B12 and folate deficiencies
myelodysplastic syndromes |
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what is the most common cause of agranulocytosis?
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drug induced
-Chemo -Clorpromazine -Sulfonamides, thiouracil -alcohol |
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Clinical course of neutropenia
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‐ Ulceration/ necrotizing lesions of the gingiva, mouth, pharynx, skin, vagina, anus or GI
invasive bacterial/deep fungal infections, eg Aspergillus, candida |
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Differential diagnosis of pancytopenia
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• Acute leukemia
• Other myelophthisic anemias • Megaloblastic anemia • Aplastic anemia • Autoimmune disease‐SLE, etc. • Myelodysplastic syndromes • Splenic sequestration • Drugs: eg, cancer chemotherapy • Total body radiation, high dose |
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Lymphopenia/Lymphocytopenia
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Absolute lymphs <1200/ μL in adults; < 3000 /μL children
• Causes: ‐ Malnutrition ‐ Congenital immune deficiencies, T cell type ‐ Acquired immune deficiencies: HIV ‐ Corticosteroids ‐ Tuberculosis, ‐ Viral infections‐ type I interferon ‐ Radiation; SLE; |
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Leukocytosis
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‐ Increase in total number of WBCs in
circulation, > 10,000 WBCs/mm3 Neutrophilia ‐ most common in adults Lymphocytosis – common in children |
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what type of cells do you see increased in an acute neutrophilia and what cytokines are responsible
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Band cells
TNF, IL-1 |
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Morphologic changes in neutrophils
with severe inflammation |
• Toxic granulation:
Coarse, darker than normal cytoplasmic granules • Dohle Bodies: Blue staining dilated endoplasmic reticulum • Cytoplasmic vacuoles |
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what is a left shift
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inc in band cells and metamyelocytes
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what is a leukemoid rxn
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high granulocyte count
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leukoerythroblastic rxn
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presence of nucleated red blood
cells and immature neutrophils in peripheral blood smear |
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what causes a leukoerythroblastic rxn
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‐ Primary and metastatic malignancy
‐ Myeloproliferative disorder ‐ Granulomas ‐ Gaucher disease |
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Eosinophilia
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• Absolute eosinophils > 400/mm3
• IL‐5 stimulated differentiation of precursor cells • May be reduced by corticosteroid therapy • Causes: type I hypersensitivity reactions |
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"benign" Lymphocytosis with reactive or atypical lymphs (CD8+ T lymphs)
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‐ Viral infection: infectious mononucleosis
‐‐ likely Dx if reactive lymphs >20% CMV – IM‐like; usually w/o cervical nodes Toxoplasmosis – IM‐like Viral hepatitis and others |
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when do you seen nucleated RBCs
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‐ Rapidly evolving anemias and when < Hb 5g
‐ Post splenectomy ‐ Bone marrow replacement- myelophthisic processes |
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Etiologic and Pathogenic Factors
in White Cell Neoplasia |
• Chromosomal translocations
* activation of proto‐oncogenes in lymphoid neoplasia • Inherited: ‐ Autosomal recessive defects of DNA repair Bloom syndrome, ataxia telangiectasia; Fanconi anemia ‐ Down syndrome (trisomy 21) ‐ Neurofibromatosis, type I • Viruses‐ see lymphoma lecture • Radiation and chemicals (esp. benzene) • Chemotherapy (alkylating agents; some others) • Smoking (myeloid leukemia‐ benzene?) |
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Acute lymphoblastic leukemia/lymphoma
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‐ Involve the bone marrow: leukemia
‐ Involve lymph nodes or extranodal tissues outside of the bone marrow: lymphoma ‐ Present initially as either and progress to the other form of malignancy |
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most common Acute lymphoblastic leukemia
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• Pre‐B immunotype (85%);
‐ TdT; CD10; CD19 positive cells |
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markers for Pre‐T cell neoplasms in ALL
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‐ TdT; CD1, CD2, CD3, CD7 positive cells
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ALL most common in (pre-B type)
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‐ Most common malignancy of childhood
‐ Most cases <15 yrs ‐ Peak age 3 ‐ May occur in adults ‐ More common in males; Caucasians |
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T‐lymphoblastic (pre T) neoplasms
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• Presents as a lymphoma in 50‐70% of cases
‐ Mediastinal mass involving thymus ‐ Respiratory symptoms • Most common in adolescent males ‐ corresponds to thymus reaching maximal size • Rapidly progresses • Worse prognosis than pre‐B type |
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CBC for ALL
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• Anemia: always present
• Thrombocytopenia almost always present • Circulating blasts |
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Bone marrow aspiration and biopsy for ALL
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‐ Hypercellular bone marrow
‐ Blasts‐ predominant cell; >20% • TdT positive blasts in bone marrow, peripheral smear • Primitive cells; large nuclei; delicate chromatin; indistinct nucleoli ‐ PAS positive cytoplasm; myeloperoxidase neg |
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Immunophenotype for ALL
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• Early pre B lymphoblasts may be CD 34 positive
• TdT, both pre‐ B and pre‐T cell types • pre‐B leukemic cells: CD10 (CALLA), CD19, PAX5 • pre‐T leukemic cells CD7 (earliest); CD2, CD3, CD4 and CD8 double positive (latest) |
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ALL: Genotype
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• Hyperploidy >50 chromosomes most common, best prognosis
• t (4; 11) • t (9;22), Philadelphia chromosome ‐ poor prognosis • NOTCH1 gene, T cell neoplasia |
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Pathogenisis of ALL
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blasts accumulate in bone marrow
crowd out normal cells (myelophthisis) Effects on peripheral blood: ‐ anemia, neutropenia and thrombocytopenia ‐ blasts likely to be present |
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Symptoms of ACUTE leukemias
regardless of type |
abrupt and rapidly progressive
fatigue fever ecchymoses, epistaxis, gum bleeding bone pain lymphadenopathy, splenomegaly; hepatosplenomegaly Mediastinal mass‐ pre‐T ALL (resp Sx) CNS and testicular infiltrates |
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CNS sympt of acute leukemia
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‐ Headache
‐ Vomiting ‐ Nerve palsies due to intracranial bleeding |
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Treatment of ALL
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• Combination chemotherapy with prophylactic
CNS treatment ‐ 95% achieve complete remission* ‐ 75% cured • Bone marrow transplantation in adults |
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Prognostic factors in ALL
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• Best prognosis
‐ Age 2‐10 with 50‐60 chromosomes ‐ pre‐B type • Poor prognosis < 2 yrs. old t(9;22) pre‐T type ‐ Adults [25% have t(9;22)] ‐ Peripheral blood blasts >100,000 |
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Acute myelogenous (myelocytic) leukemia pathophysiology
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‐ Blasts accumulate in bone marrow due to acquired genetic alterations
‐‐ translocations involving transcription factors ‐ Suppression of hematopoiesis‐‐> ‐‐ Anemia, neutropenia, thrombocytopenia |
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Classification(s) of AML
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• AML with genetic aberrations
• AML with myelodysplasia‐like features ‐ poor prognosis ‐ aberrations: 5q‐; 7q‐; 20q‐ • AML, therapy‐related: very poor prognosis -alkylating agents -topoisomerase II inhibitor |
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how to classify AML
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• M0 ‐ minimally differentiated, CD34 positive
• M1 ‐ myeloperoxidase positive; rare Auer rods • M2 -Blasts with Auer rods ‐ Myeloperoxidase positive ‐ Most common type of AML • M3‐ (acute promyelocytic leukemia) ‐ Myeloperoxidase positive ‐ Cytoplasmic granules, Auer rods present ‐‐ release of granules causes DIC ‐ t(15;17) PML: RARα (retinoic acid receptor) |
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how do you treat a t(15;17) PML: RARα (retinoic acid receptor)
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retinoic acid (ATRA)
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Clinical findings of AML
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‐ neutropenia: fever, infections of oral cavity, skin, lungs, kidneys, bladder by opportunists
‐ anemia: fatigue ‐ thrombocytopenia: ‐‐ Petechiae and ecchymoses ‐‐ Mucosal hemorrhages of GI/GU |
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what is a chloroma
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tissue finding in some cases of AML
‐ Granulocytic sarcoma; myeloblastoma ‐ Localized tumor(s) outside of the bone |
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Laboratory findings of AML
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• Hb, Hct: decreased
• Platelets decreased >85% • Bone marrow > 20% blasts (norm.<5%) • Myeloid markers: myeloperoxidase stain; CD 34; CD 33 and others |
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Prognosis of AML
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• 60% remission; 15‐30% disease free at 5 years
• Poorer prognosis: ‐ over 50 - myelodysplasia; or after chemotherapy; involve chromosomes 5 and 7 - chromosome deletions, - translocation chromosome 11 -- topisomerase II inhibitors |
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Treatment of AML
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• Aggressive combination chemotherapy
• Bone marrow transplantation • PML ‐ Retinoic acid (vitamin A) ‐ or: Arsenic trioxide ‐ followed by combination chemotherapy |
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diff btw Chronic lymphocytic leukemia/
Small lymphocytic lymphoma |
both = Peripheral B‐cell neoplasm
CLL‐ peripheral blood lymphocytosis predominates SLL‐ enlarged lymph nodes predominate ‐‐ diffuse small round cells replace LN |
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Immunophenotype of CLL/SLL
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• B‐cell markers CD19, CD20, CD23 plus CD5
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Prognostic subtypes of CLL/SLL
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CD38; Zap‐70
‐ Zap‐70 negative = good prognosis ‐ Zap‐70 positive = poor prognosis |
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Laboratory findings in CLL
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• Lymphocytosis of > 4000/μL; small round cells
• Smudge cells (basket cells) • Monoclonal Ig spike in some sera • Hypogammaglobulinemia‐common • Autoimmune hemolytic anemia • thrombocytopenia |
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Clinical presentation of CLL/SLL
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• Often asymptomatic
‐ Discovered on lab work • Generalized lymphadenopathy; hepatosplenomegaly • Immune disruption resulting in: ‐ Risk for infection ‐ Autoimmune hematologic disease |
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Treatment of CLL/SLL
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• Therapy is palliative
• Bone marrow transplant may be offered to younger patients • “Gentle chemotherapy” to control symptoms • Immunotherapy with anti‐ CD20; anti‐CD52 |
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Prognosis of CLL/SLL
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• Median survival for CLL 4‐6 yrs
• Long survival if SLL is initial presentation |
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Most common chronic myeloproliferative disease.
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Chronic myelogenous (myelocytic)
leukemia |
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Pathogenesis of CML
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• BCR‐ABL translocation in a pluripotent stem cell
• Philadelphia chromosome Ph1, t(9,22) in 90% |
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Laboratory findings in CML
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• Anemia
• Platelets may be dec. or increased • Neutrophils ALWAYS increased: ‐ Often exceeds 100,000/mm3 ‐ Metamyelocytes; myelocytes; promyelocytes ‐ Blasts in peripheral blood < 10% • Eosinophilia, basophilia usually present • Leukocyte alkaline phosphatase decreased • Hypercellular bone marrow with <20% blasts |
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Clinical presentation of CML
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• Insidious onset
• Fatigue, weakness, weight loss and anorexia • Symptoms of splenomegaly ‐ Dragging sensation in abdomen ‐ Early satiety ‐ LUQ abdominal pain • Hypermetabolism ‐ Fever, night sweats ‐ Increased uric acid |
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Prognosis of CML
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• Median survival is 3 years
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what are the phases of CML
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Chronic- asympt to mild disease
Accelerated- anemia and thrombocytopenia increase or new chromo abnormalities develop Blast crisis- behaves like an acute leukemia, with rapid progression and short survival |
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Treatment of CML
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• Temporary control with leukapheresis
• *Long‐term control with Imatinib (BCR-ABL antagonist) - *Current treatment of choice; remission in 90% • Bone marrow transplant: 75% chance for cure |
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Hairy Cell Leukemia
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• RARE B‐cell neoplasm of Middle aged men (typically)
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Morphology/immunophenotype of hairy cell leukemia
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‐ Hair‐like projections by phase‐contrast
‐ Packed bone marrow: dry tap common ‐ Positive for CD 19, CD20, CD11c, CD22 ‐Postgerminal center B memory cell |
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Clinical: hairy cell leukemia
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• Splenomegaly‐MASSIVE and common
• Lymph nodes NOT enlarged • Pancytopenia from marrow replacement and splenic sequestration • High incidence atypical Mycobacteria infection |
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Prognosis of Hairy cell leukemia
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‐ Long‐lasting remissions with alpha interferon and nucleoside analogs
‐ With therapy, 95% survive 5 years; 80% 10 yrs. ‐w/o therapy: median survival 50 mon. |
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Myelodysplastic Syndromes MDS
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Group of clonal stem cell disorders characterized by
‐ ineffective hematopoiesis resulting in cytopenias ‐ increased risk‐transformation to AML |
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what is t‐MDS
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therapy related
‐‐ Myelosuppressive drugs (cancer chemotherapy; topoisomerase inhibitors and others) ‐‐ Radiation therapy ‐ Onset 2‐8 yrs after exposure ‐ Early transform into AML is likely • Pathogenesis: stem cell genetic damage |
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Peripheral Blood Morphology of MDS
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• Pancytopenia*
• MCV frequently increased • Poikilocytosis • hypogranular cells or toxic granulation • pseudo‐Pelger‐Huet cells (binucleated granulocytes) • Giant platelets |
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Bone Marrow Morphology of MDS
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• Hypercellular marrow
• Megaloblastoid maturation • Ringed sideroblasts |
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Clinical features of MDS
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• refractory anemia (does not respond to treatment) or pancytopenia
‐ Weakness, infections and bleeding • 5 q‐ syndrome occurs in older women ‐ megaloblastoid anemia w ringed sideroblasts ‐ platelet count normal ‐ better prognosis |
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Prognosis for MDS
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• Refractory anemia may survive to 5 years
• Median survival all types 9‐29 months • Poorer prognosis for t‐MDS; high blasts |
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Treatment of MDS
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supportive with frequent transfusions
or bone marrow transplantation |
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Polycythemia vera, PCV
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• Uncommon
• Neoplasm arising in a multipotent myeloid stem cell characterized by erythrocytosis (polycythemia) • Granulocytosis and thrombocytosis also universally • Splenomegaly ‐congestion ‐ Extramedullary hematopoiesis |
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Pathophysiology of PCV
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Erythroid reproduction and growth is independent of erythropoietin
‐ Due to activating point mutation in JAK2 pathway |
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Morphology of PCV
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‐ Hypercellular bone marrow; normal M:E (myeloid: erythroid) 4:1
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Clinical course of polycythemia vera
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• Insidious onset; mean age 60
• Plethoric (“excess of body fluids”) and cyanotic complexion • Splenomegaly • Hypertension in 70% • Headache, dizziness • Histamine from basophils: ‐ Peptic ulceration ‐ Intense pruritis • Hyperuricemia and gout in 10% • Risk of bleeding ‐ Due to stagnant flow; platelet dysfunction ‐ Major hemorrhage in 5‐10% ‐ Epistaxis, bleeding from gums • Thromboses: presenting symptom in 25% ‐ DVT, MI, stroke, bowel infarction ‐ Hepatic vein: Budd‐Chiari syndrome |
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Treatment and prognosis of
Polycythemia vera |
• Treatment: phlebotomy, JAK inhibitors
• Median survival 10 yrs with regular phlebotomy |
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Laboratory findings in Polycythemia vera
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• Hematocrit: 60+%
• Plasma volume increased • WBC 12,000‐50,000/μL (5,000‐10,000) • Platelets 500,000+ ( normal <450,000) ‐ Giant forms present; functional deficits • Erythropoietin very low • JAK2 mutation present in 97% |
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Essential Thrombocytosis
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‐ Thrombocytosis >600,000
‐ JAK2 mutation - absence of other MPD features • Uncommon MPD |
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clinical Essential thrombocytosis
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‐ Thrombosis and hemorrhage
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Labs for ET
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‐ Peripheral smear: large platelets
‐ Bone marrow: increased megakaryocytes ‐ Functional platelet defects |
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Primary Myelofibrosis
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• Definition: Clonal neoplastic transformation
of a multipotent myeloid stem cell ‐ Fibrosis of bone marrow “myelofibrosis” ‐ Hematopoiesis in other organs |
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Pathophysiology of Myelofibrosis
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• JAK2 mutations in 50%
• Neoplastic megakaryocytes release PDGF and TGF‐ß = fibrosis of bone marrow ‐‐>extramedullary hematopoiesis |
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Clinical presentation of Myelofibrosis
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• Fatigue, weight loss, night sweats
• Massive splenomegaly~3000 gm • Hyperuricemia |
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mech of death for Myelofibrosis
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‐ Infection
‐ Bleeding or thrombosis ‐ Transformation to AML |
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Laboratory findings in Myelofibrosis
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• Anemia: normocytic normochromic
• Leukoerythroblastosis ‐‐ Left shifted WBCs ‐‐ Nucleated RBCs (normoblasts) ‐ Tear drop erythrocytes • Platelets increased; giant forms |
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Pathogenesis of lead toxicity
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• Inhibits heme enzymes
‐ Ferrochelatase ‐ δ – aminolevulinic acid dehydratase • Interferes with remodeling of epiphyseal cartilage in children • Inhibits healing of fractures • Competition for calcium ions ‐ Bone storage, nerve transmission deficits, - brain developmental defects • Inhibition of membrane‐associated enzymes ‐ Hemolysis of RBCs ‐ Renal damage and hypertension • Impaired metabolism of 1, 25 DH vitamin D |
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Consequences of lead exposure:
Nervous system |
• Adults
‐ Headache and dizziness ‐ Memory loss ‐ Peripheral nerve demyelination ‐‐ Wrist and foot drop • Children ‐ Encephalopathy ‐ Mental deterioration: IQ impaired; hearing loss • Anemia – hypochromic,microcytic ‐‐basophilic stippling of RBC • colic, diarrhea, anorexia • Oral lead line; radiodense deposits in bone • Infertility in men ‐ Failure of implantation of fertilized ovum ‐ Delayed puberty in girls ‐ Gout (renal injury) ‐ Hypertension ‐ Fanconi syndrome in children - reduced IQ in children |
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Langerhans Cell Histiocytosis
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Proliferative disorders of immature dendritic (Langerhans) cells
Morphology of langerhans ‐‐ Birbeck granules by EM ‐ CD1a; HLA‐DR; S‐100 expression |
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Letterer Siwe disease; Clinical (LCH)
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- any age; most under age 2 yrs
- Seborrheic eruption (skin rash) - Hepatosplenomegaly; lymphadenopathy - Pulmonary lesions ‐ anemia; thrombocytopenia ‐ progression to osteolytic bone lesions - Rapidly fatal w/o therapy; responds well to chemotherapy |
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Eosinophilic Granuloma (LCH)
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• Langerhans cells are mixed with eosinophils, lymphs, plasma cells, PMNs
• Most common in children, young adults • Common locations: bone, calvarium, ribs, femur • also occur in skin, stomach, lungs of smokers • May regress spontaneously; may require local excision; prognosis good |
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Hand‐ Schuller – Christian triad
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- children
• Eosinophilic granulomas of calvarial bone • Exophthalmos • Diabetes insipidus |
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Plasma Cell Neoplasms (Dyscrasias)
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• Neoplasms of terminally differentiated B cells
• Monoclonal gammapathy |
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Multiple Myeloma
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Plasma cell neoplasm forms tumors
at multiple sites within the bone marrow |
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Pathophysiology of Multiple Myeloma
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• Plasma cell infiltrates of bone cause
osteoclastic/ lytic bone destruction (via IL-6 production) • Production of excess immunoglobulin predisposes for: ‐ Serum hyperviscosity ‐ Proteinuria with renal damage ‐ Suppression of normal humeral immunity |
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Morphology of Multiple Myeloma
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• Skeletal defects
‐ Punched out osteolytic defects of bone ‐‐ Vertebral column; Ribs and skull ‐ Produces bone pain; hypercalcemia • Myeloma kidney ‐ Bence‐Jones light chain protein precipitates in tubules forming eosinophilic casts • Bone marrow plasmacytosis ‐ Russell bodies ‐‐ Ig cytoplasmic inclusions ‐ Mott cells‐ multiple Russell bodies, grapelike ‐ Dutcher bodies‐‐Ig nuclear inclusions • Systemic amyloidosis in 10%: |
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Clinical features of Multiple Myeloma
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• Most common malignant bone tumor
• More common in African‐Americans • Peak age: 50‐60 years; may arise from MGUS • Bone pain: severe low back pain, fracture • Hypercalcemia in 25%: confusion, weakness • Recurrent bacterial infections • Renal insufficiency • Symptoms of amyloidosis • Hyperviscosity syndrome in 7% |
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Lab findings in Multiple Myeloma
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• M protein
• Bence‐Jones protein in urin • Bone marrow plasmacytosis • rouleaux (stack of coin arrangements of RBCs) |
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Multiple Myeloma Diagnostic Criteria
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• Plasmacytosis of >10% in bone marrow
• Monoclonal protein in serum or urine • Evidence of end organ damage, one or more of the following: ‐ C: hypercalcemia ‐ R: renal insufficiency ‐ A: anemia ‐ B: bone lesions |
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Treatment of multiple myeloma
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• Palliative; incurable disease
- corticosteroids; bisphosphonates ‐ Thalidomide; Bortezomib + stem cell transplant have been shown to extend survival • Survival w/o therapy: 6‐12 months ‐ with therapy: 3 years average |
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Solitary plasmacytoma
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Localized tumor of plasma cells
no M component precedes development of multiple myeloma by 10‐20 years • May be extraosseous‐ curable by surgery |
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Monoclonal gammapathy of uncertain
significance (MGUS) |
• M protein in asymptomatic individual:
no other evidence of myeloma ‐ Most common monoclonal gammapathy - precancer |
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Lymphoplasmacytic Lymphoma
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• Indolent B‐cell neoplasm of older adults
• 30% of cases secrete monoclonal IgM‐‐> hyperviscosity syndrome (Waldenstrom’s macroglobulinemia) |
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Morpholorgy of Lymphoplasmacytic Lymphoma
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‐ PAS positive Russell and Dutcher bodies
• No punched out bone lesions • Involves lymph nodes, liver, spleen ‐ Lymphs: B cell markers‐ CD 19; CD 20 + ‐ Plasmas cells: monoclonal immunoglobulin |
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Clinical features of
Lymphoplasmacytic Lymphoma |
• Fatigue, weight loss
• Lymphadenopathy • Hepatosplenomegaly • Anemia, due to: ‐ Bone marrow replacement ‐ Autoimmune hemolytic anemia due to cold agglutinins ‐10% • Hyperviscosity syndrome |
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Waldenstrom’s macroglobulinemia
Hyperviscosity syndrome |
• Visual impairment
• Neurologic symptoms ‐ Headaches, dizziness, stupor, deafness • Bleeding • Cryoglobulinemia ‐ Raynaud’s phenomenon ‐ Cold urticaria and livedo reticularis |
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Treatment and of lymphoplasmacytic lymphoma with Waldenstrom’s macroglobulinemia
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• Plasmapheresis used to control hyperviscosity
• Indolent; progressive • May transform to large B cell lymphoma |
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Functions of the spleen
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• Filtration of unwanted elements from blood
‐ RBCs ‐ Cleans inclusions from RBCs Howell Jolly, Heinz bodies ‐ Removes bacteria ‐ Removes macromolecules ‐ Removes cell debris • Major secondary organ in the immune system extramedullary hematopoiesis • Reserve pool and storage site ‐ 30‐40 ml RBCs ‐ 30‐40% of platelets |
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Splenic sequestration/ hypersplenism
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• Hypersplenism triad
‐ Splenomegaly ‐ Reduction in one or more elements in the blood: anemia, thrombocytopenia or leukopenia ‐ Compensatory bone marrow hyperplasia |
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Neoplasms of the spleen
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• Metastases to spleen:
‐ Malignant melanoma ‐ Lung cancer |
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Causes of “spontaneous” splenic rupture
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‐‐ Infectious mononucleosis
‐‐ Malaria, typhoid ‐‐ Acute splenitis ‐‐ Leukemia |
