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The Hematopoietic and Lymphoid Systems PowerPoint Presentation

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Slide 1-

the hematopoietic and lymphoid systems
Slide 2-

hematopathology blood lymphoid organs central: bone marrow thymus peripheral: lymph nodes MALT (Waldeyer´s ring, intestine...) splenic white pulp
Slide 3-

hematopathology leukaemia = neoplastic cells in peripheral blood lymphoma = tumour of the lymph node hemoblastosis primary bone marrow leukaemia + tumoriform lymphomas primary lymph nodes lymphoma + leukemic phase
Slide 4-

bone marrow
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bone marrow weight cca 1,5kg red (hematopoietic) x yellow (adipose) structure: hematopoietic cells: granulopoiesis peritrabecular, erytropoiesis a megakaryocytes intertrabecular and perisinusoidal corroborative elements: makrophages, fibroblasts, mastocytes, plazmocytes, lymfocytes blood sinuses bone trabeculas
Slide 6-

diminished hematopoiesis A) total diminution aplastic anemia (panmyelophtisis) hereditary: Fanconi anemia AR death because of infectious and bleeding complications +/- turn into AML acquired: infectious, irradiation, use of some drugs
Slide 7-

diminished hematopoiesis B) selective one or more of hematopoietic lineages critical is peripheral blood – marrow could be hypercelular = „ineffective hematopoiesis“
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diminished hematopoiesis...anemia 1) anemia ↓ total circulating RBC volume, +/- ↓Hb and ↓O2 hypoxia of tissues = clinical symptoms
Slide 9-

anemia...loss of RBC a) hemorrhage: blood loss anemia hypovolemia → normocytic normochromic anemia → ↑ erytropoiesis (bone marrow) → reticulocytosis, hypochromic anemia
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anemia...hemolytic b) increased rate of RBC destruction: the hemolytic anemias anemia + reactive hyperplastic erytropoiesis bm: ↑erytropoiesis/myelopoiesis, gaucheroid cells +/- extramedullary hematopoiesis Hb -emia, -uria
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anemias..hemolytic..intrinsic I) intrinsic (intracorpuscular) abnormalities of RBC hereditary: 1) disorders of RBC membrane cytoskeleton spherocytosis erythrocytes spheroidal, less deformable and vulnerable to splenic sequestration and destruction AD anemia, splenomegalia a hemolytic icterus
Slide 12-

anemias..hemolytic..intrinsic 2) RBC enzyme deficiencies 3) disorders of Hb synthesis: hem+globin deficient globin synthesis: thalassemia syndromes lack of or decreased synthesis of globin chains: α chains = α thalassemia β chains = β thalassemia ↓ synthesis of Hb → anemia (microcytic hypochromic) + excess of α chains in β thalassemia → insoluble aggregats → damage RBC membrane → reduction of plasticity → phagocytosis, inefective erytropoiesis heterozygous = thalassemia minor homozygous = thalassemia major
Slide 13-

anemias..hemolytic..intrinsic structurally abnormal globin synthesis (hemoglobinopathies): sickle cell anemia structurally abnormal Hb S – on deoxygenation polymerization = gelation or crystallization → microvascular obstruction → ischemic tissue damage + ↑ removing in the spleen = „autosplenectomy“
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anemias..hemolytic..intrinsic acquired membrane defect: paroxysmal nocturnal hemoglobinuria) ↓resistance against C3 granulocytes and plateles affected too → hemolysis, +/- trombotic complications and ↑ susceptibility to infections
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anemias..hemolytic..extrinsic II) extrinsic (extracorpuscular) abnormalities 1) antibody mediated isohemagglutinins erythroblastosis fetalis Rh (mother Rh-, father and child Rh+) antibodies against fetal RBC hydrops fetus universalis, mental retardation, ↑extramedulary hematopoiesis
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anemias..hemolytic..extrinsic autoantibodies idiopathic (primary), drug associated, SLE Coombs tests
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anemias..hemolytic..extrinsic 2) mechanical trauma to RBCs mikroangiopathic hemolytic anemias DIC, TTP mechanic traumatization of erythrocytes dialysis, valves prosthesis 3) infections (malaria)
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anemia...impaired RBC production c) diminished erythropoiesis 1) combination with the others in aplastic anemia 2) pure „erytroblastophtisis“ Blackfan-Diamond syndrom children + thymomas and T-CLL 3) myelophtisic anemia extensive replacement of the marrow by tumours or other lesions → extramedullary hematopoiesis, leukoerythroblastosis
Slide 19-

anemia...impaired RBC production 4) iron deficiency anemia most common mikrocytar hypochromic ↓low intake (diets, malabsorptions) x ↑ demands (pregnancy, infancy, chronic blood loss) gross: hypoxic myocardial steatosis marrow normal or hyperplastic erythropoiesis, decline in serrum ferritin and depletion of stainable iron in the bone marrow
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anemia...impaired RBC production 5) megaloblastic anemia disturbance of proliferation and differentiation of erythroblasts → megaloblasts, megakaryocytes nuclear-cytoplasmic asynchrony giant metamyelocytes → hypersegmented neutrophils ineffektive erythropoiesis folate (folic acid) deficiency anemia tetrahydrofolate neurologic abnormalities do not occur
Slide 21-

anemia...impaired RBC production pernicious anemia vitamin B12 (cobalamin) deficiency diet, ↓intrinsic faktor (parietal gastric cells), terminal ileum gross: atrophic glossitis, gastritis, demyelinization
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anemia...impaired RBC production 6) lack of erythropoietin kidney failure, parvovirosis (B19)
Slide 23-

diminished hematopoiesis... leukopenia 2) leukopenia a) lymfopenia hereditary immunity disorders, infections(viral), chronical diseases, steroid therapy
Slide 24-

leukopenia b) neutropenia (granulocytopenia) increased susceptibility to infections marrow failure (aplastic anemia) → agranulocytosis inadequate or ineffective granulopoiesis: certain drugs: benzen, purin and pyrimidin analogs, anthracyklin x idiosyncrastic reaction (chloramfenikol, chlorpromazin, fenylbutazon) accelerated removal or destruction of neutrophils: hypersplenism, certain drugs bm: depend on the underlying basis: ↑ or ↓ granulopoiesis and +/- reaction to infection
Slide 25-

increased hematopoiesis transitory increasing of hematopoiesis 1) ↑erythropoiesis = polycythemia increased erythropoietin levels: appropriate: lung disease, high-altitude living, cyanotic heart disease inappropriate: erythropoietin-secreting tumours, „doping“ bm hypercellular, inappropriate increasing of erythropoiesis no extramedullary hematopoiesis!
Slide 26-

increased hematopoiesis 2) leukocytosis a) lymfocytosis: chronical infections (IM) b) granulocytosis: acute bacterial infections (pyogenic organisms), sterile inflammation (tissue necrosis, burns) → leukemoid reaction (like in CML) c) eosinophilia: allergic disorders, parasitic infestation, drug reaction, certain mlg 3) thrombocytosis: infections, chronical bleeding, tumours, iron deficiency
Slide 27-

myelodysplastic syndromes heterogeneous group of disorders some evidence of bone marrow failure and dysplasia in one or more myeloid cell lineages may evolve to AML chromosomal aberrations primary x secondary (radiotherapy, alkylating agent therapy) bm hypercellular, ↑ erythropoiesis, morphological changes, +/- fibrosis
Slide 28-

myelodysplastic syndromes...histological classification refractory anemia (RA) refractory anemia with ring sideroblasts (RARS) refractory cytopenia with multilineage dysplasia refractory anemia with excess blasts (RAEB) MDS, unclassifiable
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chronic myeloproliferative diseases CMPDs: clonal haematopoietic stem cell disorders characterised by proliferation in the bone marrow of one or more of the myeloid (i.e. granulocytic, erythroid and megakaryocytic) lineages
Slide 30-

CMPD A) chronic myelogenous leukaemia most common adults, 30-60eyars neutrophilic leukocytosis in peripheral blood Ph+ = t(9;22) = Philadelphia chr. bm: hypercellular (↑granulopoiesis, ↑megakaryocytes), +/- fibrosis extramedullary leukaemic infiltration: spleen, liver → accelerated phase → blast phase
Slide 31-

CMPD B) polycythaemia vera (polycythaemia rubra vera, m. Vaquez-Osler) ↑ erythropoiesis hypertension, thrombosis, haemorrhage bm: initial phase: hypercellular, with increased erythropoiesis + extramedullar infiltration → hepatosplenomegaly +/- blast phase or „spent“ phase
Slide 32-

CMPD C) essential thrombocythaemia proliferation primarly magakaryocytic lineage sustained thrombocytosis in the blood bm: large, mature megakaryocytes D) chronic idiopathic myelofibrosis proliferation of mainly megakaryocytes, associated with reactive deposition of bone marrow connective tissue and extramedullary hematopoiesis
Slide 33-

acute leukaemias causes: complication of certain chromosomal diseases (m. Down, Fanconi anemia, Klinefelter´s syndroma...) radiation chemicals (benzen, alkylating agents, drugs) viruses (HTLV-1) AML, ALL symptoms: combination of aplastic anemia and agranulocytosis bm: leukaemic infiltration, +/- extramedullar infiltration (liver, spleen, kidney, CNS) myelosarcoma („chloroma“)
Slide 34-

acute myeloid leukaemias... histological classification M0...acute myeloblastic l. minimally differentiated M1 ...acute myeloblastic l. without maturation M2...acute myeloblastic l. with maturation M3...acute promyelocytic l. M4...acute myelomonocytic l. M5...acute monocytic l. M6...acute erythroid l. M7...acute megakaryoblastic l.
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acute lymphoblastic leukaemias... histological classification precursor B- and T- cell lymphoblastic leukaemia/lymphoblastic lymphoma
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proliferation of macrophages, histiocytosis A) reactive proliferation of macrophages bone marrow, many causes (hemosiderosis, aiha, viral infections) lysosomal storage diseases (m. Gaucher, Niemann-Pick...)
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proliferation of macrophages, histiocytosis B) hemofagocytic syndroma ↑ proliferation of macrophages or histiocytic precursores → haemofagocytosis → cytopenia + hepatosplenomegaly, fever proliferating macrophages: clonal (mlg histiocytosis) x reaction (infection, Kawasaki, T lymphomas) fatal haemofagocytosis
Slide 38-

proliferation of macrophages, histiocytosis C) histiocytosis X (Langerhans cells histiocytosis) 1) solitary eosinophilic granuloma bng bones (unifocal lytic lesion), skin, lymph nodes, lungs Langerhans cells (Birbeck granules) + eosinophils, +/- plasma cells and lymphocytes 2) m. Hand-Schüler-Christian trias: multifocal lytic lesions of bone + exophtalamus + diabetes insipidus
Slide 39-

proliferation of macrophages, histiocytosis 3) m. Abt-Letterer-Siwe mlg children before 2 years of age cutaneous lesions resembling seborrheic skin eruptions + hepatosplenomegaly, lymphadenopathy, pulmonary lesions, osteolytic bone lesions → anemia and thrombocytopenia, reccurent infections
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metastasis osteolytic x osteoplastic prostate, breast, stomach, lung cancer
Slide 41-

bone marrow necrosis ischemia: vascular collaps in hypercellular marrow metastatic obstruction sickle cell disease, DIC... symptoms: pain, fever, hematopoietic precursors in peripheral blood
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transplantation transplantation: bone marrow, peripheral stem cells autologous x allogenneous (relatives, non-relatives) indications: hematological: tumours, immunodeficiency, anemias, b.m. aplasia non-hematological: tumour metastasis
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transplantation bone marrow suppression → graft hypocellularity → proliferation immunosuppression! GvHD acute x chronic: skin, intestine, liver
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Bleeding disorders cause: defect in the vessel wall platelet deficiency or dysfunction coagulation factors disorder
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bleeding disorders...vascular A) defects in the vessel wall 1) hereditary a) m. Osler-Rendu-Weber (hereditary hemorhagic teleangiektasias) capillary aneurysms in the skin and mucous membranes b) connective tissue disorders m. Ehlers-Danlos Marfan´s syndrome
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bleeding disorders...vascular 2) acquired a) avitaminosis C, ↑ corticosteroids cutaneous, intramuscular, mucosal bleeding b) purpura Henoch-Schönlein circulating IC → skin, kidney
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bleeding disorders...plateles B) plateles deficiency or dysfunction 1) thrombocytopenia a) decresed production aplastic anemia hereditary disorders (sy Bernard-Soulier, grey-plateles sy, m. Wiskott-Aldrich)
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bleeding disorders...plateles b) increased destruction splenomegaly, arteficial valves,... DIC (disseminated intravascular coagulation) activation of the coagulation sequence, leading to formation of thrombi throughout the microcirculation → consumption of plateles and coagulation factors and secondarily activation of fibrinolysis
Slide 49-

bleeding disorders...plateles thrombotic thrombocytopenic purpura (TTP) thrombocytopenia, fever, microvessel obstruction symptoms → microangiopathic hemolytic anemia hyaline thrombi in the microcirculation hemolytic-uremic syndrome (HUS) E.coli kidney cortex necrosis, intestinal bleeding
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bleeding disorders...plateles idiopathic thrombocytopenic purpura (ITP) autoimmune origin destruction in the spleen → splenectomy bm +/- increased megakaryopoiesis
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bleeding disorders...plateles 2) platelet dysfunction adhesion disorder (Bernard-Soulier, m. von Willebrand) aggregation disorder (thrombasthenia Glanzmann) secretion disorder: tromboxan A2 inhibition (aspirin)
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bleeding disorders...coagulation factors C) coagulation disorders 1) hereditary deficiencies a) hemophilia A (classic hemophilia) f VIII (severe = activity < 1%!) X chromosoma (new mutation x familiar) easy bruising and massive hemorrhage after trauma or operative procedures, „spontaneous“ hemorrhages – joints (hemarthroses) → progressive deformities b) hemophilia B (Christmas disease) f IX
Slide 53-

bleeding disorders...coagulation factors 2) acquired a) DIC b) liver diseases synthesis of coagulation factors (fibrinogen, prothrombin, fV, VII, IX-XI) + anticoagulation and fibrinolytic factors c) vitamin K food, synthesis in the large intestine (bacterias) d) anticoagulation therapy
Slide 54-

lymph vessels and nodes
Slide 55-

lymphatic vessels A) lymphoedema lymph is protein-rich → lymphostasis leads to fibroproduction, +/- infectious and ulcerative complications 1) hereditary = Milroy´s disease valvular disorder 2) acquired lymphoedema lymphoedema praecox secondary lymphoedema: obstruction and lymphostasis (mlg, inflammatory changes)
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lymphatic vessels B) lymphangiectasia focal extension of lymphatic vessels skin, small intestine (chylangiectasia) → lymforhea (chylothorax...)
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lymphatic vessels C) lymphangiitis lymph vessels draining the primary (infectious) focus β hemolytic streptococci + regional lymphadenitis clinical: red subcutaneous line histology: lymphangiitis simplex lymphangiitis purulenta: pus + fibrin → spreading → abscesses, trombophlebitis
Slide 58-

lymfatic nodes...structure cells: lymphocytes, dendritic cells (FDRC, IDRC), macrophages with apoptotic bodies, NK cells follicles = B zone lymphocytes from the bm → primary follicle → immunity stimulation → germinal centres = secondary follicle, immunity answer → polarization of germinal centres germinal centres: B cells augmentation, selection Ag high affinity clones → plasma cells differentiation → migration into medulla, waiting to secondary immunity answer
Slide 59-

lymph nodes...structure medulla lymphatic tissue between medullar sinuses small lymphocytes, plasma cells paracortex = T zone mainly CD4 T cells, small venules T lymphocytes 70% of lymphocytes in lymph node and 80-90% in blood sinuses incoming lymph vessels → subcapsular (marginal) sinus → interfollicular → medulla → outgoing vessels
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lymph nodes...regressive changes A) regressive changes and circulatory disorders 1) infarction vasculitis tumorous infiltration vascular transformation of sinuses 2) atrophy lipomatous hyalin 3) pigmentation 4) amyloidosis 5) storage diseases
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lymph nodes...inflammation B) lymphadenitis 1) acute nonspecific inflammation of regional lymph node clinicaly: enlarged, erythematous lymph nodes histology: ↑ follicles, mitoses, sinuses filled with granulocytes, histiocytes +/- healing with fibrous scarse
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lymph nodes...inflammation 2) chronic nonspecific lymphadenitis etiology: a) follicular hyperplasia etio: tonsillitis, respiratory infections, RA, syphilis, AIDS histology: ↑ germinal centers, fanciful shapes, many mitoses, blastic forms of cells – could be misinterpreted like mlg lymphoma!
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lymph nodes...inflammation progressive transformation of germinal centres connection with HD (paragranuloma) m. Castleman (angiofollicular hyperplasia) „lolly pops“ follicles unifocal bng x multifocal fatal
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lymph nodes...inflammation b) paracortical hyperplasia etio: viruses (IM, HSV), inoculation, some drugs histology: enlarged paracortex, with many IDRC, small follicles in the periphery of the lymph node, T imunoblasts c) reactive sinusoidal histiocytosis etio: reactive (different Ag) histology: dilated sinuses filled with histiocytes
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lymph nodes...inflammation m. Rosai-Dorfman (masive sinusoidal histiocytoses) intrasinusoidal macrophages with emperipolesis d) mixed reactive hyperplasia etio: toxoplasmosis (epitheloid granulomas)
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lymph nodes...inflammation 3) granulomatus purulent epitheloid granulomas with central necrosis with accumulation of neutrophils cat scratch disease veneric lymphogranuloma (Chl.trachomatis) mesenterial lymphadenitis (Y.enterocolitica) ulcus molle (H. ducreyi)
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lymph nodes...inflammation 4) granulomatous necrotic tularemia (Fr. tularensis) plague (Y. pestis) anthrax (B. antracis) 5) granulomatous tuberculoid granulomas without central necrosis sarcoidosis, m. Crohn... 6) TBC lymphadenitis miliary x caseous productive
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lymph nodes...inflammation 7) granulomatous reaction to lipid materials m. Whipple lipid vacuoles, around epitheloid histiocytes, intracytoplasmic PAS+ material 8) granulomatous reaction to foreign bodies silicic material in prosthesis
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lymph nodes...neoplasms
Slide 70-

lymph nodes...neoplasms C) neoplasms, malignant lymphomas 1) m. Hodgkin (HD) group of disesases presence of distinctive neoplastic giant cells: Reed-Sternberg cells, Hodgkin cells, admixed with a variable infiltrate of reactive, nonmalignant inflammatory cells young people
Slide 71-

lymph nodes...neoplasms...HD classification: nodular lymphocytic predominance Hodgkin lymphoma „classic“: lymphocyte rich HL (LR-CHL) nodular sclerosis (NS-CHL) mixed cellularity (MC-CHL) lymfocyte depleted (LD-CHL)
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lymp nodes...neoplasms...NHL 2) non Hodgkin lymphomas predominance of neoplastic cells elder patients B and T cells
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lymph nodes...neoplasms...B-NHL a) B-NHL chronic lymphocytic leukaemia/small lymphocytic lymphoma (CLL/SLL) follicular lymphoma (FCL) mantle cell lymphoma (MCL) marginal zone lymphoma (MZL): SMZL, ENMZL=MALT, NMZL hairy cell leukaemia (HCL) diffuse large B-cell lymphoma (DLBCL) Burkitt lymphoma
Slide 74-

chronic lymphocytic leukaemia/small lymphocytic lymphoma (CLL/SLL) elderly patients naive lymphocytes indolent type of lymphoma
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follicular lymphoma (FCL) middle aged patients centrocytes and centroblasts indolent course but rellapsing!
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mantle cell lymphoma (MCL) „diffuse centrocytoma“ agressive type of lymphoma t(11;14) – cyklin D1
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marginal zone lymphoma (MZL) mucosa associated lymphoid tissue (MALT) – GIT, bronchi… association with chronic inflammation
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diffuse large B-cell lymphoma (DLBCL) „waste basket“ transformation of small cell lymphomas aggresive course x good reaction to therapy
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Burkitt lymphoma endemic x sporadic younger patients association with EBV infection
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lymph nodes...neoplasms...B-NHL plasma cell neoplasms: monoclonal gammopathy of undetermined significance (MGUS) lymphoplasmacytic lymphoma (LPL), m. Waldenström plasmacytoma multiple myeloma
Slide 81-

lymph nodes...neoplasms...T-NHL b) T-NHL peripheral T cell lymphoma (PTL) anaplastic large T cell lymphoma (ALCL) angioimmunoblastic T cell lymphoma (AILT) adult T cell leukaemia mycosis fungoides/Sezary syndrom
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anaplastic large T cell lymphoma (ALCL) young patients typical translocation t(2;5)
Slide 83-

mycosis fungoides/Sezary syndrom primary skin lymphoma → generalisation = Sezary syndrom
Slide 84-

spleen
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spleen structure: white pulp: lymphoid tissue red pulp: venous sinuses → hilus splenomegaly: venosthasis, inflammation, neoplasms hypersplenism = increased function → cytopenia hyposplenism → susceptibility to certain bacterial infections
Slide 86-

spleen...regressive changes, circulatory disorders A) inborn anomalies accessory spleens = spleniculi B) regressive changes and circulatory disorders 1) amyloidosis secondary (AA) +/- hyposplenism
Slide 87-

spleen...regressive changes, circulatory disorders 2) storage diseases 3) hemolytic anemias ↑ splenic function → splenomegaly hereditary spherocytosis 4) chronic perisplenitis 5) splenic infarction white (embolization, vasculitis) red (thrombosis of lienal vein)
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spleen...regressive changes, circulatory disorders 6) chronic venosthasis 7) splenic rupture, bleeding traumatic
Slide 89-

spleen...inflammation A) inflammation 1) acute septic tumour reaction to general infection x tumour lysis clinically: tense capsula, soft tissue histology: red pulp cellular, small abscesses (central pyemia)
Slide 90-

spleen...inflammation 2) chronic inflammatory tumour chronic infections (IE) histology: red pulp hyperemia, reactive hyperplasia of the white pulp malaria TBC, histoplasmosis, leishmaniosis, trypanosomiasis AIDS
Slide 91-

spleen...tumours D) tumours and pseudotumours 1) cystic formations posttraumatic pseudocysts parasitary cysts 2) hamartoma (splenoma) nodule histology: chaotic sinuses a fibrous tissue = incorrect arrangement of the red pulp +/- hypersplenism
Slide 92-

spleen...tumours 3) hemangioma histology: cavernous blood spaces, thrombosis 4) littoral cell angioma phagocytosis → pancytopenia 5) inflammatory pseudotumour histology: inflammatory cells + fibroproduction
Slide 93-

spleen...tumours 6) malignant lymphomas primary: SMZL secondary: more often secondary infiltration by NHL, HD, CML, HCL 7) epithelial metastasis microscopically
Slide 94-

thymus
Slide 95-

thymus...structure structure: lobulus cortex and medulla mixture of T lymphocytes and a epithelial cells = lymphoepithelial organ cortex: mainly T lymphocytes lymphatic follicles without germinal centres medulla: thymocytes, Hassal bodies
Slide 96-

thymus...function function: production of small lymphocytes with cellular immunity TdT a CD1 → maturation → CD4 a CD8 → postthymic lymfocytes in medulla: CD4 (helpers/inducers), CD8 (suppressor/cytotoxic), loss of TdT a CD1 → blood, peripheral lymphatic organs main role intrauterine and in childhood
Slide 97-

thymus...dysgenesis A) thymic dysgenesis primary immunodeficiency syndromes (diGeorge, Nezelof...)
Slide 98-

thymus...regressive changes B) regressive changes 1) lipomatous atrophy (involution) puberty – involution with increase of adipous tissue = ↓ thymocytes, calcification of Hassal bodies... 2) acute (accidental) involution etio: corticosteroids – stress histology: fragmentation of cortical thymocytes, cystic transformation of Hassal bodies, lymfocytes disappeared, in cortex only spindle epithelial cells
Slide 99-

thymus...hyperplasia C) thymic hyperplasia primary hyperplasia myasthenia gravis histology: lymphoid hyperplasia, lymphatic follicles with germinal centres Ab anti acetylcholin-receptors
Slide 100-

thymus...neoplasms D) neoplasms 1) thymomas epithelial thymic cells + lymphocytes local manifestation association with myasthenia gravis 2) neuroendocrinne tumors 3) germinal cells tumours (teratoma, seminoma) bng, cystic 4) malignant lymphoma