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  • Many names, same cell
  • ALL blasts look the same on routine stains, whether they are myeloblasts, lymphoblasts, monoblasts, etc.
  • TOXIC GRANULES are EXAGGERATIONS of the marrow’s normal granularity, DOHLE bodies are fragments of remaining dilated rough ER
  • Not only are basophils RARE to find normally, but pure “basophilia” is also VERY rare.
  • Why would monocytosis be linked to granulomatous diseases? Answer: Monocytes are macrophages in circulation, and granulomatous diseaseas are macrophage diseases.
  • EXTRAMEDULLARY HEMATOPOESIS is most common in the spleen, liver, and lymph nodes.
  • If a CML had much more than 10% blasts, you might suspect that the patient was going into a “blast crisis”.
  • This marrow is virtually 100% cellularity!!! This is the HALLMARK of CML, and all the cells are still marrow cells although blasts are INCREASED, i.e., more than 1-2 % This marrow is virtually 100% cellularity!!! This is the HALLMARK of CML, and all the cells are still marrow cells although blasts are INCREASED, i.e., more than 1-2 %
  • This marrow is virtually 100% cellularity!!! This is the HALLMARK of CML, and all the cells are still marrow cells although blasts are INCREASED, i.e., more than 1-2 %. In this CML megakaryocytes are proliferating so what OTHER myeloproliferative disease could this be confused with? Ans: essential thrombocythemia (essential thrombocytosis)
  • Note most of the marrow looks “fibrotic”. What stain could help you confirm that this is fibrous tissue? (trichrome)
  • The most life saving thing you can learn today is how to recognize a blast! HUGE NUCLEUS NUCLEOLI (stain LIGHTER not DARKER than the rest of the nucleus on Wright stain), How many nucleoli does that one blast cell have? Answer: 3 NO cytoplasmic differentiation
  • Many cells from CLL have a “smudge” or “basket” appearance
  • Please those THREE diagnostic features of plasma cells, the malignant plasma cells of MM look like normal plasma cells usually.
  • Normal on left, myeloma on right.
  • Note the “lytic” lesions
  • Blasts, blasts with AUER rods
  • Acute promyelocytic leukemia, remember promyelocytes have BOTH nucleoli AND nonspecific granules, true BLASTS do NOT have granules.
  • In AMML, M4, many of the peripheral leukemic cells look like monocytes, while in M5, Acute Monocytic Leukemia, MOST of them look like monocytes
  • In M6, many of the cells may resemble erythroid cells, in M7, many of the cells may resemble megakaryocytes
  • Know the difference between a myelo-”proliferative” and a myelo-”dysplastic” disease.
  • BENIGN FOLLICULAR HYPERPLASIA. Larger and more numerous than normal follicles. MEDULLA may be compromised.
  • BENIGN SINUS HISTIOCYTOSIS. The cortical area may be compromised. SINUS HISTIOCYTOSIS may be seen in reaction to cancer, even if there are NO tumor cells in the lymph node.
  • “ HAIRY” cell leukemia/lymphoma consists of lymphocytes which look hairy.
  • Most pathologists HATE lymphoma classifications with a passion!
  • I HATE this slide.
  • I HATE this slide even worse.
  • Prognosis of HD disease is related directly of percentage of lymphocytes and inversely to number of RS cells.
  • STERNBERG REED cells are called “lacunar” cells in one of the most common forms of HD called NODULAR SCLEROSING
  • The subcapsular sinus of the lymph node is the FIRST place you will spot a metastatic tumor nest!
  • Notice the “confluence” of WHITE pulp? Could this be lymphoma involvement? Ans: Yes Could this be granulomas? Ans: YES
  • Portal hypertension, prominence of RED pulp
  • Note all these are benign. The commonest MALIGNANT tumor primary to the spleen is a LYMPHOMA
  • Hassal’s corpuscles are fused epithelial reticular cells
  • Transcript

    • 1.
      • Leukopenia/Neutropenia
      • Leukocytosis
      • Lymphadenitis/Lymphadenopathy
      • (Malignant) Lymphoma
      • NON-Hodgkins Lymphoma
      • Hodgkins Lymphoma (Hodgkins Disease)
      • ALL/CLL (Acute/Chronic Lymphocytic Leukemia)
      • Multiple Myeloma
      • M1/M2/M3/M4/M5/M6/M7
      • Myeloproliferative Disorder
      • CML and Polycythemia Vera
      • Essential Thrombocytosis
      • Splenomegaly
      • Thymoma
      www.freelivedoctor.com
    • 2. WBC/LYMPHOID DISORDERS
      • Review of Normal WBC Structure/Function
      • Benign Neutrophil and Lymphoid Disorders
      • Leukemias
      • Lymph Nodes
      • Spleen/Thymus
      • REVIEW
      www.freelivedoctor.com
    • 3. NEUTROPHILS
      • Normal TOTAL WBC count 6-11 K
      • Neutrophils usually 2/3 of total normal
      • Myeloblast  Promyelocyte  Myelocyte  Metamyelocyte  Band (stab)  Mature Neutrophil (Poly, PMN, Neutrophilic Granulocyte)
      • Produced in red (hematopoetic) marrow, sequester (pool) in spleen, live in peripheral blood, migrate OUT of vascular compartment PRN, live a couple days normally
      www.freelivedoctor.com
    • 4. NEUTROPHIL Neutrophil Polymorphonuclear Leukocyte, PMN, PML “ Leukocyte” Granulocyte, Neutrophilic granulocyte “ Poly-” Polymorph www.freelivedoctor.com
    • 5. NEUTROPHIL MATURATION www.freelivedoctor.com
    • 6. LYSOSOMAL CONSTITUENTS
      • PRIMARY
      • Also called AZUROPHILIC, or NON-specific
      • Myeloperoxidase
      • Lysozyme (Bact.)
      • Acid Hydrolases
      • SECONDARY
      • Also called SPECIFIC
      • Lactoferrin
      • Lysozyme
      • Alkaline Phosphatase
      • Collagenase
      www.freelivedoctor.com
    • 7. FUNCTIONS
      • Margination
      • Rolling
      • Adhesion
      • Transmigration (Diapedesis)
      • Chemotaxis
      • Phagocytosis: Recognition, Engulfment, Killing (digestion)
      • Equilibrium with splenic pool
      www.freelivedoctor.com
    • 8. PELGER-HUET ANOMALY
      • Genetic
      • Sometimes ACQUIRED (Pseudo-PELGER-HUET)
      • All neutrophils look like BANDS
      • NOT serious, mostly a cute incidental finding
      www.freelivedoctor.com
    • 9. CHEDIAK-HIGASHI SYNDROME
      • Also genetic
      • Abnormal LARGE irregular neutrophil granules
      • Impaired lysosomal digestion of bacteria
      • Associated with pigment and bleeding disorders
      • CAN be serious, especially in kids
      www.freelivedoctor.com
    • 10. LEUKO-penia/NEUTRO-penia Neutropenia/Agranulocytosis
      • INADEQUATE PRODUCTION
      • INCREASED DESTRUCTION
      • 500-1000/mm3 is the DANGER zone!
      www.freelivedoctor.com
    • 11. INADEQUATE PRODUCTION
      • Stem cell suppression, e.g., aplastic anemias
      • DRUGS, esp. CHEMO, MANY antibiotics, aminopyrene, thio-uracil, phenylbutazone
      • DNA suppression due to megaloblastic/myelodysplastic states
      • Kostmann Syndrome (genetic, congenital)
      • Marrow usually shows granulocytic HYPO- plasia, just as in RBC and PLAT decreased production
      www.freelivedoctor.com
    • 12. INCREASED DESTRUCTION
      • Immune mediated
        • By itself (idiopathic), or as in SLE
        • After “sensitization” by many drugs
      • Splenic sequestration, hypersplenism
      • Increased peripheral demand, as in overwhelming infections, esp. fungal
      • Marrow usually shows granulocytic HYPER- plasia, just as in RBC and PLAT increased destructions
        • www.freelivedoctor.com
    • 13. Leukocytosis/Neutrophilia
      • Marrow and splenic pool size
      • Rate of release between pool and circulation
      • Marginating pool
      • Rate of WBCs (neutrophils/monocytes) leaving the vascular compartment
      • NON-vascular pools FIFTY times larger than the vascular pools
      • TNF/IL-1/cytokines stimulate T-cells to produce CSF, the WBC equivalent of EPO
      www.freelivedoctor.com
    • 14. NEUTROPHIL INCREASES (e.g., “NEUTROPHILIA”)
      • BACTERIA
      • TISSUE NECROSIS, e.g., MI
      • DÖHLE BODIES and TOXIC GRANULES are often seen with NEUTROPHILIA
      • Accompanied by a “LEFT” shift
      www.freelivedoctor.com
    • 15. EOSINOPHIL INCREASES (i.e., “EOSINOPHILIA”)
      • ALLERGIES (esp. DRUG allergies)
      • PARASITES
      www.freelivedoctor.com
    • 16. BASOPHIL INCREASES (i.e., “BASOPHILIA”)
      • RARE. Period.
      • But if you want to remember something at least, remember myeloproliferative diseases in which ALL cell lines are increased
      www.freelivedoctor.com
    • 17. MONOCYTE INCREASES (i.e., “MONOCYTOSIS”)
      • TB
      • SBE
      • RICKETTSIAL DISEASES
      • MALARIA
      • SLE
      • IBD, i.e., ULCERATIVE COLITIS
      www.freelivedoctor.com
    • 18. LYMPHOCYTE INCREASES (i.e., “LYMPHOCYTOSIS”)
      • TB
      • VIRAL
        • Hep-A
        • CMV
        • EBV
      • Pertussis (whooping cough)
      www.freelivedoctor.com
    • 19. LYMPHOCYTE INCREASES (i.e., “LYMPHOCYTOSIS”)
      • TB
      • VIRAL
        • Hep-A
        • CMV
        • EBV
      • Pertussis (whooping cough)
      www.freelivedoctor.com
    • 20. “ MYELOPROLIFERATIVE” disorders
      • Also called “chronic” myeloproliferative disorders because they last for years
      • ALL marrow cell lines are affected, splenomegaly
      • Proliferating cells do NOT suppress residual marrow production, and go OUTSIDE marrow  , and EXPAND marrow to fatty appendicular marrow
      • Associated with EXTRA-medullary hematopoesis
        • Chronic Myelogenous “Leukemia” (CML)
        • P. Vera
        • Essential Thrombasthenia (aka, Essential Thrombocytosis)
        • Myelofibrosis
      www.freelivedoctor.com
    • 21. CML
      • NOT AT ALL like an “acute” leukemia, but can develop into one as a condition called a “blast crisis”
      • Age: adult, NOT kids
      • 90% have the “Philadelphia” chromosome, which are aberrations on chromosome #9 (BCR) and #22 (ABL), the BCR-ABL “fusion”
      www.freelivedoctor.com
    • 22. CML
      • Marrow 100% cellular, NOT 50%
      • ALL cell lines increased, M:E ratio massively increased, 50K-100K neutrophils with SIGNIFICANT “left shift”, but not more than 10% blasts
      • SIGNIFICANT SPLENOMEGALY!!!!!
      • Significant breakthrough with BCR-ABL kinase inhibitors!!! (90% remissions)
      www.freelivedoctor.com
    • 23. www.freelivedoctor.com
    • 24. www.freelivedoctor.com
    • 25. Polycythemia Vera
      • All cell lines increased, NOT just RBC
      • HIGH marrow cell turnover stimulates increased purines which often cause gout (10%)
      • BOTH thrombosis AND bleeding risks are present because the increased platelets are AB-normal
      • Do not get “blast” crises, BUT can progress to myelofibrosis
      www.freelivedoctor.com
    • 26. ESSENTIAL THROMOCYTOSIS
      • Platelet count often near 1 million/mm3
      • Often a diagnosis of exclusion.
      • The RAREST of all myeloproliferative disorders
      • Giant platelets usually. Why? Ans: Quicker release from marrow (RPW/RDW)
      • Massively increased megakaryocytes in the marrow
      www.freelivedoctor.com
    • 27. PRIMARY MYELOFIBROSIS
      • Rapid progressive marrow fibrosis
      • Oldest age group of all the MPD’s, >60
      • Can follow other MPD’s. Why?
      • Usually the most extensive extramedullary hematopoesis because the marrow is NOT the primary site of hematopoesis
      • LEUKOERYTHROBLASTOSIS
      • Like CML, 10-20% can progress to AML
      www.freelivedoctor.com
    • 28. www.freelivedoctor.com
    • 29. WBC/LYMPHOID DISORDERS
      • Review of Normal WBC Structure/Function
      • Benign Neutrophil and Lymphoid Disorders
      • Leukemias
      • Lymph Nodes
      • Spleen/Thymus
      • REVIEW
      www.freelivedoctor.com
    • 30. LEUKEMIAS
      • MALIGNANT PROLIFERATIONS of WHITE BLOOD CALLS
      • In the case of neutrophilic precursors, the primary process is marrow and peripheral blood, but can involve any organ or tissue which receives blood
      • In the case of lymphocytes, there is an intimate concurrence with malignant lymphomas
      www.freelivedoctor.com
    • 31. Leukemias vs. Lymphomas
      • All leukemias of lymphocytes have lymphoma counterparts
      • Primary lymphomas can have “leukemic” phases, including multiple myelomas
      • Any myeloid leukemia can infiltrate a lymph node, or any other site, but if/when it does it is NOT called a lymphoma, but simply a myeloid infiltrate INTO a lymph node
      • ALL lymphomas are malignant proliferations of lymphocytes
      • ALL leukemias involve bone marrow changes
      www.freelivedoctor.com
    • 32. LYMPHOMAS
      • NODAL or EXTRANODAL
      • T or B
      • SMALL or LARGE CELLS
      • FOLLICULAR or DIFFUSE
      • Hodgkins or NON-Hodgkins
      • “ F.A.B. classification” is currently popular this week (FrenchAmericaBritish), for the NON-Hodgkins lymphomas
      www.freelivedoctor.com
    • 33. LEUKEMIAS
      • Acute or Chronic
      • Myeloid or Lymphocytic
      • Childhood or Adult
      • All involve marrow
      • All ACUTE leukemias suppress normal hematopoesis, i.e., have anemia, thrombocytopenia
      • Most have chromosomal aberrations
      • Some can respond DRASTICALLY to chemo, most notably ALL in children, even be cured!!!!
      www.freelivedoctor.com
    • 34. BLAST www.freelivedoctor.com
    • 35. WHITE CELL NEOPLASMS Leuk/Lymph
      • Many have chromosomal translocations
      • Can arise in inherited and/or genetic diseases:
        • Downs Syndrome (Trisomy 21)
        • Fanconi’s anemia (hereditary aplastic anemia)
        • Ataxia telangiectasia
      • May have a STRONG viral relationship:
        • HTLV-1 (lymphoid tumors)
        • EBV (Burkitt Lymphoma)
        • Human Herpesvirus-8 (B-Cell Lymphomas )
      www.freelivedoctor.com
    • 36. WHITE CELL NEOPLASMS Leuk/Lymph
      • Can be caused by H. Pylori (gastric B-Cell lymphomas)
      • Can follow celiac disease (gluten sensitive enteropathy  T-Cell lymphomas)
      • Are common in HIV, T-Cell lymphomas, CNS lymphomas
      www.freelivedoctor.com
    • 37. A.L.L./LYMPHOMAS*
      • SUDDEN ONSET
      • ANEMIA, BLEEDING, FEVER
      • Bone pain, adenopathy, hepatosplenomegaly
      • CNS: headaches, vomiting, nerve palsies
      • (* NB: These are pretty much the symptoms of A.M.L. too and vice versa)
      www.freelivedoctor.com
    • 38. A.L.L./LYMPHOMAS
      • “ Lymphoblasts” which can give rise either to T or B cells are the cells of malignant proliferation
      • All lymphocytic leukemias CANNOT be classified independently of lymphomas because they all have lymphoma counterparts
      • A.L.L. mostly in children
      • Most have chromosomal changes, hyperploidy, Philadelphia chromosome, translocations
      • SIGNIFICANT response to chemo: 90% remission, 75% CURE!!!
      www.freelivedoctor.com
    • 39. A.L.L. www.freelivedoctor.com
    • 40. C.L.L.
      • Unexplained sustained (months) lymph count of > 4000/mm3 is CLL, usually picked up on CBC
      • M>F
      • Lymphs look normal and are NOT blasts
      • No need for marrow exam for dx, but progressive involvement of marrow, nodes, and other organs is the usual biologic behavior
      • Liver can be involved portally or sinusoidally
      • Translocations RARE, but trisomies and deletions common
      www.freelivedoctor.com
    • 41. C.L.L. www.freelivedoctor.com
    • 42. C.L.L.
      • HYPO-gammaglobulinemia
      • 15% have antibodies against RBC’s or PLATS
      • CANNOT be classified as separate from lymphomas
      www.freelivedoctor.com
    • 43. MULTIPLE MYELOMA
      • DEFINED AS A MALIGNANT PROLIFERATION OF PLASMA CELLS
      • Can have a “leukemic” phase, but the BONE MARROW is the usual primary site of origin
      • Usually have MONOCLONAL GAMMOPATHIES
      • Secrete Heavy and Light chains, and Light chains in the urine is known as Bence-Jones protein
      • Usually have elevated IL-6 (bad prognosis)
      www.freelivedoctor.com
    • 44. PLASMA CELL classic features
      • OVAL cytoplasm, ROUND nucleus off to side
      • Cartwheel/Clockface chromatin
      • Prominent Golgi or “Hoff”
      www.freelivedoctor.com
    • 45. MONOCLONAL “SPIKE” on SPE www.freelivedoctor.com
    • 46. MULTIPLE MYELOMA
      • BONE DESTRUCTION
      • Various deletions and translocations
      • Plasma cells usually 1-3% of marrow, but >20% or plasma cells in SHEETS is diagnostic
      • Plasma cells usually look normal
      • IgG >> IgA, other immunoglobulins are rare
      • Staph, Strep, E. coli infections
      • Bleeding
      • Amyloidosis
      • RENAL FAILURE
      www.freelivedoctor.com
    • 47. Multiple Myeloma: Skull X-ray www.freelivedoctor.com
    • 48. “ Solitary” Plasmacytoma
      • Progression to MM is “inevitable”, with time, perhaps 10-20 years even
      www.freelivedoctor.com
    • 49. M.G.U.S.
      • M onoclonal G ammopathy of U nknown S ignificance, i.e., no plasma cell proliferation is found
      • Age related
      • 1% of 50-year olds, 3% of 70-year olds, etc.
      • Same chromosomal aberrations as MM, but generally follow a BENIGN course
      www.freelivedoctor.com
    • 50. Other “GAMMOPATHIES”
      • Waldenstrom’s MACROglobulinemia (associated with lymphomas)
      • Heavy Chain Disease (associated with lymphomas)
      • AMYLOID , follows MM and/or chronic granulomatous diseases
      www.freelivedoctor.com
    • 51. A.M.L.
      • GENETIC ABERRATIONS INHIBIT DIFFERENTIATION
      • Many have various TRANSLOCATIONS
      • F.A.B. classifies them as M0  M7
      • MORE than 20% of BLASTS are needed in the marrow for a diagnosis of acute leukemia!!! (i.e., ANY kind of BLAST
      • NORMALLY, a marrow should have only about 1-2 % blasts
      www.freelivedoctor.com
    • 52. A.M.L.
      • M0 Minimally differentiated
      • M1 AUER rods rare (COMMON)
      • M2 AUER rods common (COMMON)
      • M3 Acute PRO-myelocytic leukemia
      • M4 AMML (myelo-Mono cytic) (COMMON)
      • M5 Monocytic
      • M6 ErythroLeukemia
      • M7 Acute Megakaryocytic leukemia
      • NOTE: Diagnosis is CONFIRMED by special markers, not just visual identification
      www.freelivedoctor.com
    • 53. M0  M2 www.freelivedoctor.com
    • 54. M3 www.freelivedoctor.com
    • 55. M4-M5 AMML Normal “classic” monocyte www.freelivedoctor.com
    • 56. M6-M7 www.freelivedoctor.com
    • 57. A.M.L.
      • Anemia
      • Thrombocytopenia (bleeding)
        • Petechiae
        • Ecchymoses
      • Fever
      • Fatigue
      • Lymphadenopathy
      • 60% respond, BUT only 20 % are free of remission after 5 years, WORSE than A.L.L.
      www.freelivedoctor.com
    • 58. MYELO-DYSPLASTIC SYNDROMES
      • Increased risk of acute leukemias
      • But, UNLIKE the myeloPROLIFERATIVE syndromes, NOT a hypercellular marrow
      • Spontaneous or drug related (even > 5 yrs!)
      • Has marrow ABERRATIONS
        • REFRACTORY ANEMIAS
        • RINGED SIDEROBLASTS (Fe in mitochondria)
        • Nuclear “BUDDING”
        • EXCESS BLASTS , but LESS than 20%
        • About, say 25% develop into acute leukemias
      www.freelivedoctor.com
    • 59. Ring Sideroblasts and “BUDS” www.freelivedoctor.com
    • 60. LYMPH NODES
      • Normal Structure, Function
      • Benign enlargement/Benign disease
        • Acute
        • Chronic (follicular vs. “sinus histiocytosis”)
      • Lymphomas/Malignant Lymphomas
        • Adjectives of various classifications
        • Features
        • STAGING
      • Metastatic disease TO lymph nodes
      www.freelivedoctor.com
    • 61. www.freelivedoctor.com
    • 62. CORTEX ---SUB-capsular Sinus ---Follicles (Pri? Or second.?) ---PARA-follicular zone MEDULLA Blood flow? Lymph flow? www.freelivedoctor.com
    • 63. Definition of TERMS
      • Lymphadenopathy
      • Lymphadenitis
      • Dermatopathic
      • Normal size?
      • Palpation
      • What to do if a lymph node is enlarged?
      • Diffuse/Follicular
      • T/B/NK, Small/Large, Cleaved/Non-cleaved
      • Precursor/Peripheral
      • HD/Non-HD
      www.freelivedoctor.com
    • 64. BENIGN ENLARGEMENT
      • Also called LYMPHADENITIS, and HYPERPLASIA
      • Can be ACUTE (tender), or CHRONIC (non-tender)
      • Usually SUBSIDE in, say, less than 6 weeks
      • FOLLICULAR HYPERPLASIA is enlargement of the cortical secondary follicles and increase in number of the cortical secondary follicles
      • SINUS HISTIOCYTOSIS is prominence in medullary sinuses (also called “reticular” hyperplasia)
      www.freelivedoctor.com
    • 65. www.freelivedoctor.com
    • 66. www.freelivedoctor.com
    • 67. (MALIGNANT) LYMPHOMAS
      • Terms in historic classifications:
        • Diffuse/Follicular, Small/Large, Cleaved/Non-cleaved
        • Hodgkins (REED-STERNBERG CELL) /NON-Hodgkins
        • Lukes, Rappaport, etc.
        • Working Formulation, WHO, NIH, FAB, Intl., etc.
        • B
        • T
        • PRECURSOR (less mature looking)
        • PERIPHERAL (more mature looking )
      www.freelivedoctor.com
    • 68. DIFFUSE LYMPHOMA www.freelivedoctor.com
    • 69. FOLLICULAR LYMPHOMA www.freelivedoctor.com
    • 70. LARGE CELL LYMPHOMA www.freelivedoctor.com
    • 71. SMALL CELL LYMPHOMA www.freelivedoctor.com
    • 72. “ CLEAVED” CELL LYMPHOMA www.freelivedoctor.com
    • 73. “ Hairy” Lymphocyte www.freelivedoctor.com
    • 74. FEATURES of LYMPHOMAS
      • The Antigen receptor genes re-arrangement PRECEDES malignant transformation, so the cells are MONOCLONAL, NOT the usual POLYCLONAL
      • 85% B-cell, 15% T-Cell
      • The tumor cells congregate wherever T and B cell congregate normally however
      • DISRUPTED or “EFFACED” normal architecture, obliterated subcapsular sinus
      • HD/Non-HD staging CRUCIALLY IMPORTANT, esp. HD. Why? HD grows more “linearly”
      www.freelivedoctor.com
    • 75. LATEST CLASSIFICATION
      • NON-HODGKIN
        • PRECURSOR B
        • PERIPHERAL B
        • PRECURSOR T
        • PERIPHERAL T
      • HODGKIN’S DISEASE (i.e., HODGKINS LYMPHOMA)
      www.freelivedoctor.com
    • 76. PRECURSOR B
      • Precursor B LYMPHOBLASTIC LEUKEMIA/LYMPHOMA
      www.freelivedoctor.com
    • 77. PERIPHERAL B
      • CHRONIC LYMPHOCYTIC LEUKEMIA/LYMPHOMA
      • B-Cell PRO-lymphocytic LEUKEMIA
      • Lymphoplasmacytic
      • Splenic and Nodal Marginal Zone
      • EXTRA-nodal Marginal Zone
      • Mantle Cell
      • Follicular
      • Marginal Zone
      • Hairy Cell Leukemia
      • Plasmacytoma/Multiple Myeloma
      • Diffuse B Cell
      • BURKITT LYMPHOMA (Starry Sky)
      www.freelivedoctor.com
    • 78. PRECURSOR T
      • Precursor T LYMPHOBLASTIC LEUKEMIA/LYMPHOMA
      www.freelivedoctor.com
    • 79. PERIPHERAL T and NK
      • T-Cell PRO-Lymphocytic Leukemia
      • Large Granular
      • Mycossis fungoides/Sezary Cell syndrome (skin)
      • Peripheral T-Cell
      • Anaplastic large cell
      • Angioimmunoblastic T-Cell
      • Enteropathy-associated T-Cell
      • Panniculitis-like
      • Hepatosplenic gamma-delta
      • Adult T-Cell
      • NK/T Cell nasal
      • NK-Cell leukemia
      www.freelivedoctor.com
    • 80. LYMPHOCYTE MARKERS (CD-) i.e., LYMPHOCYTE ANTIGENS
      • T-Cell: 1,3,4,5,8
      • B-Cell: 10 (CALLA), 19,20,21,23,79a
      • Mono/Mac: 11c, 13, 14, 15, 33, 34
      • STEM: 34
      • RS: 15, 30
      • All: 45 (Leukocyte Common Antigen)
      • NK: (16, 56)
      www.freelivedoctor.com
    • 81. HODGKINS DISEASE
      • NEED R-S (Reed-Sternberg, or Sternberg-Reed) cells for correct diagnosis
        • NODULAR SCLEROSIS (Young Women), the R-S cells may be called “LACUNAR” cells
        • MIXED CELLULARITY
        • Lymphocyte RICH
        • Lymphocyte POOR
        • Lymphocyte PREDOMONANCE
      www.freelivedoctor.com
    • 82. STERNBERG-REED CELL www.freelivedoctor.com
    • 83. STAGING, HD & NHD
      • I ONE NODE or NODE GROUP
      • II MORE than ONE, but on ONE side of diaph.
      • III BOTH sides of diaph., but still in nodes only
      • IV OUTSIDE of NODES, e.g., liver, marrow, etc.
      • A No systemic symptoms
      • B fever and/or night sweats and/or 10% weight loss
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    • 84. METASTATIC CARCINOMA
      • Perhaps the single most important staging and prognostic feature of tumors
      • The metastatic cells FIRST enter into the SUBCAPSULAR SINUS
      • The tumor may replace the entire node and enlarge it
      • The tumor may be focal
      • The tumor usually looks the same as it’s primary or other metastases
      • The tumor usually ENLARGES the node
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    • 85. METASTATIC SQUAMOUS CELL CARCINOMA www.freelivedoctor.com
    • 86. METASTATIC ADENOCARCINOMA www.freelivedoctor.com
    • 87. SUBCAPSULAR SINUS www.freelivedoctor.com
    • 88. SPLEEN
      • 150 grams POST-LUQ (just like kidney, 1/10 of liver)
      • Bordered by diaphragm, kidney, pancreas, splenic flexure, stomach
      • SMOOTH & GLISTENING capsule
      • 50% RED pulp, 50% WHITE pulp
      www.freelivedoctor.com
    • 89. www.freelivedoctor.com
    • 90. ABNORMAL SPLEEN www.freelivedoctor.com
    • 91. ABNORMAL SPLEEN www.freelivedoctor.com
    • 92. SPLENIC FUNCTION
      • REMOVE OLD BLOOD CELLS
      • MAJOR SECONDARY ORGAN of the IMMUNE SYSTEM
      • HEMATOPOIESIS
      • SEQUESTER (POOL) BLOOD CELLS
      • 15% of body’s PHAGOCYTIC activity is in the spleen (liver has >80)
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    • 93. SPLENOMEGALY
      • CONGESTIVE vs INFILTRATIVE
      • HYPERSPLENISM
        • Anemia
        • Leukopenia
        • Thrombocytopenia
      • DECISION for SPLENECTOMY
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    • 94. SPLENOMEGALY
      • INFECTIONS: TB, Mono, Malaria, Fungus
      • PORTAL HTN: CHF, CIRRHOSIS, PV Thromb.
      • LYMPHOHEMATOGENOUS: Leuk, Lymph
      • IMMUNE: RA, SLE
      • STORAGE: Gaucher, Niemann-Pick
      • MISC: Amyloid, mets (melanoma, lymphoma, Germ cell tumors of testis)
      LONG STANDING CONGESTION breeds FIBROSIS www.freelivedoctor.com
    • 95. INFARCT www.freelivedoctor.com
    • 96. PRIMARY TUMORS (RARE)
      • HEMANGIOMA
      • LYMPHANGIOMA
      • fibroma
      • osteoma
      • Chondroma
      • LYPHOMA
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    • 97. MISC
      • Congenital Absence (very rare)
      • “ Accessory” spleens (very common)
      • RUPTURE
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    • 98. THYMUS
      • Mother of all T-Cells
      • Massive in newborns, virtually absent in the elderly, bilobed
      • Under manubrium
      • 1) Thymocytes
      • 2) Epithelial Ret. Cells
      • 3) Hassal’s Corpuscles
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    • 99. HASSAL’s CORPUSCLES www.freelivedoctor.com
    • 100. DISEASES
      • HYPOPLASIA/APLASIA
              • DiGeorge Syndrome
      • CYSTS (incidental)
      • THYMOMAS
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    • 101. THYMOMAS
      • ALL (most) thymomas show counterparts of BOTH lymphoid as well as epithelial reticular cells, hence, the classic name “LYMPHOEPITHELIOMA”
        • Benign thymoma: (encapsulated)
        • Malignant Thymoma I: (locally invasive)
        • Malignant Thymoma II: (easily metastasizable )
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