13.01.16 Pathology prof hab. n. med. Andrzej Marszałek LYMPH NODES reactive changes in lymph reactive changes nodes in lymph nodes causes • chronic • acute non-specific – hyperplasia of follicules (è B cells) – enlarged germinal centers • RA • toxo – neutrophils (in sisuses) • HIV (early phase) è bacterial – germinal centers necrosis (abscesses) • without disturbances in node structure • chronic • follicules of different size • different lymphocytes • macrophages (proliferating) reactive chages in lymph nodes reactive chages in lymph nodes • chronic • chronic – hyperplasia of paracortical zone – sisuses enlargement (è macrophages) (è T cells) • neoplasms • EBV • vaccination • drugs • slight changes of the node • „paraimmunoblasts” 1 13.01.16 cat-scratch disease cat-scratch disease • Bartonella (Rochalimaea) henselae morphology: • children/teenagers (90% below 18yrs.) • follicular hyperplasia (early stage) • sefl-limiting è sarkoid-like granulomas (in lymph (nodes enlargement 2 wks è decreased 2-4 nodes) mths) è central necrosis – follicular hyperplasia è neutrophils (abscesses) – hyeplasia of paracortical zone – changes in sinuses – + sometimes changes in: • liver • spleen & bones Actinomycosis actinomycosis def: Pato: • chronic infection caused by Actinomyces • microspy: – most common in head and neck area (after – during 1st phase pyogenic infiltration and trauma, after tooth extraction) abcesses formation (with bacterial colonies) Epidemiology: – then arround abcesses develops intensive fibrosis • Bacteriae could be found on the mucosa or within tonsilar crypts. EBV EBV • Infectious ononukleosis (typical) • clinic (+serology) • teenager/young adult: • Lymph node biopsy NOT needed – ferev, – sorethroat • Atypical cases (lymphadenopaty without – neck lymph node enlargement fever, nor sorethroat, nor spelnomegaly) – slight hepatitis è need to exclud lymphoma – in peripheral blood atypical limphocytes è BIOPSY (cytotoxic T CD8+) 2 13.01.16 EBV Lymphogranuloma venereum • micro: • STD – „blurred” lymph node morphology (immunoblasts in sinuses) • Chlamydia trachomatis (serotypes L1, L2 and L3) – Follicular hyperplasia, multiple macrophages, high mitoses • Endemic in tropical areas – granulocytes • In Western Europe homosexuals (males) – Usually without necrosis – immunoblasty Reed-Sternberg-like immunoblasts – CD20+, CD15-, CD30- Toxoplasmosis Lymphogranuloma venereum (Piringer-Kuchinka lymphadenitis) • 3 phases: • Common obligatory intracellular parasit – early – small foci of necrosis with neutrophils (Toxoplasma gondii) – late – “starry” abscesses surrounded by • Syptomless infection epithelioid cells • Lymph nodes enlargement (usually posterior – abcesses + (fistulas) neck; young females) • in macrophages sometimes visible • Dangerous in pregnant women pathogens (in vacuoles) • From cat feces and raw meet Toxoplasmosis (Piringer-Kuchinka lymphadenitis) • Preserved lymph node structure • Enalrgement of follicles +: – Numerous mitoses – Numerous apoptotic bodies – Small non-caseous granulomas (typically within germinal centers) THYMUS • Sometimes giant cells (Langhans type) 3 13.01.16 myastenia gravis myastenia gravis • AChR on postsynaptic membrane (auto- • Role of T cells (?) Ab) è damage to myocytes • è stimulation of B cells (production of auto-Ab) ● AChR present in normal thymus and on • thymoma (?) myocytes • Proliferation of thymus stromal cells (?) • • Abnormal and numerous dendritic cells ● in thymus may develop ectopic germinal • Role of TLR-4 centers (B cells producing pathogenic Ab) myastenia gravis clinic • 10% with other autoimmune disease (G-B, RA) • autoAb against titin (muscle protein) • 65% with thymus hyperplasia • 25% normal thymus • 10% thymoma SPLEEN • Risk factors: M 50+ with symptoms • Develop in 30-45% patients with thymoma (even after years) splenomegaly • Mass over 1000g • causes: – CML – Gaucher dis. – hairy cell leukemia, – marginal zone B cell lymphoma, – myelofibrosis, – plasmacytoma, – prolymphocytic leukemia 4 .