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14 wbc
This document summarizes diseases of white blood cells and lymphoid tissue. It discusses topics like leukopenia, leukocytosis, lymphoma, leukemia, and myeloproliferative disorders. Specific conditions covered include chronic myelogenous leukemia, polycythemia vera, essential thrombocytosis, multiple myeloma, acute and chronic lymphocytic leukemias. The document reviews normal white blood cell development and function, as well as abnormalities, classifications, symptoms, and characteristics of various malignant proliferations of white blood cells and lymphocytes.
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14 wbc
- 1. DISEASES of WHITECELLS and LYMPHOID TISSUE
- 2. Topics • 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
- 3. WBC/LYMPHOID DISORDERS •Review of Normal WBC Structure/Function • Benign Neutrophil and Lymphoid Disorders • Leukemias • Lymph Nodes • Spleen/Thymus • REVIEW
- 5. NEUTROPHILS • NormalTOTAL 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
- 6. NEUTROPHIL Neutrophil PolymorphonuclearLeukocyte, PMN, PML “Leukocyte” Granulocyte, Neutrophilic granulocyte “Poly-” Polymorph
- 7.
- 8. LYSOSOMAL CONSTITUENTS •PRIMARY • Also called AZUROPHILIC, or NON-specific • Myeloperoxidase • Lysozyme (Bact.) • Acid Hydrolases • SECONDARY • Also called SPECIFIC • Lactoferrin • Lysozyme • Alkaline Phosphatase • Collagenase
- 9. FUNCTIONS • Margination • Rolling • Adhesion • Transmigration (Diapedesis) • Chemotaxis • Phagocytosis: Recognition, Engulfment, Killing (digestion) • Equilibrium with splenic pool
- 10. PELGER-HUET ANOMALY •Genetic • Sometimes ACQUIRED (Pseudo-PELGER-HUET) • All neutrophils look like BANDS • NOT serious, mostly a cute incidental finding
- 11. 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
- 12. LEUKO-penia/NEUTRO-penia Neutropenia/Agranulocytosis •INADEQUATE PRODUCTION • INCREASED DESTRUCTION • 500-1000/mm3 is the DANGER zone!
- 13. 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 productions
- 14. 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
- 15. Leukocytosis/Neutrophilia • Marrowand 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
- 16. NEUTROPHIL INCREASES (e.g.,“NEUTROPHILIA”) • BACTERIA • TISSUE NECROSIS, e.g., MI • DÖHLE BODIES (e.r. remnants) and TOXIC GRANULES are often seen with NEUTROPHILIA • Accompanied by a “LEFT” shift
- 17. EOSINOPHIL INCREASES (i.e.,“EOSINOPHILIA”) • ALLERGIES (esp. DRUG allergies) • PARASITES
- 18. 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
- 19. MONOCYTE INCREASES (i.e.,“MONOCYTOSIS”) • TB • SBE • RICKETTSIAL DISEASES • MALARIA • SLE • IBD, i.e., ULCERATIVE COLITIS
- 20. LYMPHOCYTE INCREASES (i.e.,“LYMPHOCYTOSIS”) • TB • VIRAL –Hep-A –CMV –EBV • Pertussis (whooping cough)
- 21. LYMPHOCYTE INCREASES (i.e.,“LYMPHOCYTOSIS”) • TB • VIRAL –Hep-A –CMV –EBV • Pertussis (whooping cough)
- 22. “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 • Associated with EXTRA-medullary hematopoesis – Chronic Myelogenous “Leukemia” (CML) – P. Vera – Essential Thrombocythemia (aka, Essential Thrombocytosis) – Myelofibrosis
- 23. CML • NOTAT 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”
- 24. CML • Marrow100% 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)
- 27. 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 often progress to myelofibrosis
- 29. 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
- 31. 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
- 33. WBC/LYMPHOID DISORDERS •Review of Normal WBC Structure/Function • Benign Neutrophil and Lymphoid Disorders •Leukemias • Lymph Nodes • Spleen/Thymus • REVIEW
- 34. LEUKEMIAS • MALIGNANTPROLIFERATIONS 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
- 35. 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
- 36. LYMPHOMAS • NODALor 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
- 37. LEUKEMIAS • Acuteor 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!!!!
- 38.
- 39. WHITE CELL NEOPLASMSLeuk/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)
- 40. WHITE CELL NEOPLASMSLeuk/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
- 41. A.L.L./LYMPHOMAS* • SUDDENONSET • 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)
- 42. 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!!!
- 43.
- 44. C.L.L. • Unexplainedsustained (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
- 45.
- 46. C.L.L. • HYPO-gammaglobulinemia • 15% have antibodies against RBC’s or PLATS • CANNOT be classified as separate from lymphomas
- 47. 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)
- 48. PLASMA CELL classicfeatures • OVAL cytoplasm, ROUND nucleus off to side • Cartwheel/Clockface chromatin • Prominent Golgi or “Hoff”
- 49.
- 50. 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
- 51.
- 52. “Solitary” Plasmacytoma •Progression to MM is “inevitable”, with time, perhaps 10-20 years even
- 53. M.G.U.S. •Monoclonal Gammopathyof Unknown Significance, 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
- 54. Other “GAMMOPATHIES” •Waldenstrom’s MACROglobulinemia (associated with lymphomas) • Heavy Chain Disease (associated with lymphomas) •AMYLOID, follows MM and/or chronic granulomatous diseases
- 55. A.M.L. • GENETICABERRATIONS 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
- 56. A.M.L. • M0Minimally 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
- 57.
- 58.
- 59. M4-M5 AMML Normal“classic” monocyte
- 60.
- 61. 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.
- 62. 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
- 63. Ring Sideroblasts and“BUDS”
- 64. 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
- 66. CORTEX ---SUB-capsular Sinus ---Follicles (Pri? Or second.?) ---PARA-follicular zone MEDULLA Blood flow? Lymph flow?
- 67. 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
- 68. 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)
- 71. (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)
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- 78. 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”
- 79. LATEST CLASSIFICATION •NON-HODGKIN –PRECURSOR B –PERIPHERAL B –PRECURSOR T –PERIPHERAL T • HODGKIN’S DISEASE (i.e., HODGKINS LYMPHOMA)
- 80. PRECURSOR B •Precursor B LYMPHOBLASTIC LEUKEMIA/LYMPHOMA
- 81. 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)
- 82. PRECURSOR T •Precursor T LYMPHOBLASTIC LEUKEMIA/LYMPHOMA
- 83. PERIPHERAL T andNK • 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
- 84. 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)
- 85. 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
- 86.
- 87. 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
- 88. 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
- 89. METASTATIC SQUAMOUS CELLCARCINOMA
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- 92. SPLEEN • 150grams 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
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- 96. 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)
- 97. SPLENOMEGALY • CONGESTIVEvs INFILTRATIVE • HYPERSPLENISM –Anemia –Leukopenia –Thrombocytopenia • DECISION for SPLENECTOMY
- 98. 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
- 99.
- 100. PRIMARY TUMORS (RARE) • HEMANGIOMA •LYMPHANGIOMA • fibroma • osteoma • chondroma
- 101. MISC • CongenitalAbsence (very rare) • “Accessory” spleens (very common) •RUPTURE
- 102. THYMUS • Motherof all T-Cells • Massive in newborns, virtually absent in the elderly, bilobed • Under manubrium • 1) Thymocytes • 2) Epithelial Ret. Cells • 3) Hassal’s Corpuscles
- 103.
- 104. DISEASES •HYPOPLASIA/APLASIA »DiGeorge Syndrome •CYSTS (incidental) •THYMOMAS
- 105. 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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Editor's Notes
- #2 Classical features of peripheral white cells
- #5 Classical features of peripheral white cells
- #7 Many names, same cell
- #8 ALL blasts look the same on routine stains, whether they are myeloblasts, lymphoblasts, monoblasts, etc.
- #17 TOXIC GRANULES are EXAGGERATIONS of the marrow’s normal granularity, DOHLE bodies are fragments of remaining dilated rough ER. Wiki lists the differential diagnosis of Dohle bodires as: Burns Infections Physical trauma Neoplastic diseases Wissler’s disease May-Hegglin anomaly Chédiak-Steinbrinck-Higashi’s syndrome
- #20 Contrary to urban legends, monocytosis is NOT seen in infectious “mono”nucleosis, but lymphocytosis IS!
- #23 EXTRAMEDULLARY HEMATOPOESIS is most common in the spleen, liver, and lymph nodes.
- #25 If a CML had much more than 10% blasts, you might suspect that the patient was going into a “blast crisis”.
- #26 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 %
- #27 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)
- #29 This marrow is 90% cellular and looks a lot like CML. This is P. vera
- #31 Note that this is NOT a marrow biopsy but a smear, so TRUE marrow cellularity cannot be assessed, however MOST of the cells are megakaryocytes!
- #33 Note most of the marrow looks “fibrotic”. What stain could help you confirm that this is fibrous tissue? (trichrome)
- #46 Many cells from CLL have a “smudge” or “basket” appearance
- #50 Normal on left, myeloma on right.
- #52 Note the “lytic” lesions
- #60 In AMML, M4, many of the peripheral leukemic cells look like monocytes, while in M5, Acute Monocytic Leukemia, MOST of them look like monocytes
- #61 In M6, many of the cells may resemble erythroid cells, in M7, many of the cells may resemble megakaryocytes
- #70 BENIGN FOLLICULAR HYPERPLASIA. Larger and more numerous than normal follicles. MEDULLA may be compromised.
- #71 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.
- #78 “HAIRY” cell leukemia/lymphoma consists of lymphocytes which look hairy.
- #87 STERNBERG REED cells are called “lacunar” cells in one of the most common forms of HD called NODULAR SCLEROSING
- #92 The subcapsular sinus of the lymph node is the FIRST place you will spot a metastatic tumor nest!
- #95 Notice the “confluence” of WHITE pulp? Could this be lymphoma involvement? Ans: Yes Could this be granulomas? Ans: YES
- #96 Portal hypertension, prominence of RED pulp
- #101 Note all these are benign. The commonest MALIGNANT tumor primary to the spleen is a LYMPHOMA
- #104 Hassal’s corpuscles are fused epithelial reticular cells
- #107 Benign, Malignant I, and Malignant II