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Limfadenitis Limfoma Hodgkins

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Textbook Reading LYMPHADENITIS DAN HODGKIN LYMPHOMAOleh Chyntia Giska Aryunisari, S. Ked (0818011012) M. Dzikrifishofa, S. Ked (0818011073) Ricky Pebriansyah, S. Ked (0818011091)

Pembimbing : dr. Wien Wiratmoko, Sp. PA dr. Resti Arania, Sp. PA dr. Muhartono, Sp. PAKEPANITERAAN KLINIK PATOLOGI ANATOMI RUMAH SAKIT UMUM DAERAH Dr. Hi. ABDUL MOELOEK BANDAR LAMPUNG 15 Maret 2013

I. LYMPHADENITIS

Definition Radang yang terjadi pada kelenjar limfa karena infeksi, merupakan suatu reaksi mikroorganisme yg terbawa oleh limfa dari daerah yg infeksi ke kelenjar limfa regional. Peradangan pada satu atau beberapa kelenjar getah bening hiperplasia kelenjar getah bening hingga terasa membesar secara klinik.

Classification1. Spesific Lymphadenitis Kronis (TBC). 2. Non-Spesific Lymphadenitis Akut, Kronis.

SPECIFIC LYMPHADENITIS TB Lymphadenitis

ACUTE NONSPECIFIC LYMPHADENITIS Lymph nodes undergo reactive changes whenever they are challenged by microbiologic agents, cell debris, or foreign matter introduced into wounds or into the circulation. Cervical region -teeth or tonsils Axillary region Inguinal region - secondary to infections in the extremities. Mesenteric lymph nodes draining acute appendicitis.

Morphology Swollen Gray red and engorged HistologicallyLymphoid follicles with large germinal centres and numerous mitotic figures. Macrophages with particulate debris Neutrophilic infiltration Suppurative

CHRONIC NONSPECIFIC LYMPHADENITIS Follicular Hyperplasia Paracortical Hyperplasia Sinus Histiocytosis

Follicular Hyperplasia Humoral immune responses (sel B) Two distinct regions : A dark zone : proliferating blast-like B cells (centroblasts). A light zone : B cells with irregular or cleaved nuclear contours (centrocytes). Tingible body macrophages. Causes : RA, Toxo, Early HIV.

Features reactive follicular hyperplasia: (1) Preservation of the lymph node architecture, include interfollicular T-cell zones and sinusoid, ; (2) Variation in shape and size of lymphoid nodules; (3) Frequent mitotic figures, phagocytic macrophages, and recognizable light and dark zones. Sometimes accompanied by marginal zone B-cell hiperplasia.

Paracortical Lymphoid Hyperplasia Cellular immune response. Reactive changes within the T cell regions. Activated T cells (immunoblasts) three to four times the size of resting lymphocytes, have round nuclei, chromatin, prominent nucleoli, moderate of pale cytoplasm. Immunologic reactions induced by drugs (Dilantin), acute viral, mononucleosis, and vaccination against certain viral diseases.

Sinus Histiocytosis (Reticular Hyperplasia) The lining lymphatic endothelial cells are hypertrophied, and macrophages are greatly increased in number Distension and prominence of the lymphatic sinusoids. May be particularly prominent in lymph nodes draining cancer, such as Ca of breast.

II. HODGKIN LYMPHOMA

HODGKINS DISEASEMerupakan neoplasma lymphoid Keganasan tersering pada dewasa muda terutama usia 32 tahun Dapat disembuhkan pada kebanyakan kasus

KlinisTerdapat benjolan di kelenjar lymp Demam Keringat malam hari

Penurunan berat badan 10% selama 6 bulan

Clinical Stage of Hodgkins and Non Hodgkins Lymphomas (Ann Arbor Classification) STAGE DISTRIBUTOR OF DISEASE

I Involvement of a single lymph node region (I) or involvement of a single extralymphatic organ or site (IE). II Involvement of two or more lymph node regions on the same side of the diaphragm alone (II) or with involvement of limited contiguous extralymphatic organ or tissue (IIE).

STAGE

DISTRIBUTOR OF DISEASE

III Involvement of lymph node regions on both sides of the diaphragma (III), which may include the spleen (IIIS) and/or limited contiguous extralyphatic organ or site (IIIE, IIIES). IV Multiple or disseminated foci of involvement of one or more extralymphatic organs or tissues with or without lymphatic involvement.

Perbedaan KlinisHodgkins Non Hodgkins Seringkali terjadi pada KGB perifer dan multipel tidak seringkali

mengenai 1 kelompokan KGB (cervical, mediastinum/ paraaortic Penyebaran menjalar Kgb mesenterial dan Waldeyers ring jarang dikenai Jarang extranodal

sering

Klasifikasi WHO: 1. Nodular sclerosis 2. Mixed cellularity 3. Lympocyte Rich 4. Lymphocyte depletion 5. Lymphocyte predominance

Reed Sternberg Sel (RS sel) sel besar (15-45 m) binucleated/ bilobed kadang nuclei multiple Nucleolus besar (owl eyed) dikelilingi halo yang cerah variasi lain Lacunar Cell sering pada nodular sclerosis

Selain dengan adanya RS cell, untuk mendiagnosis dibutuhkan background berupa sel inflamasi non neoplasma

Nodular SclerosisTerdapat variant RS sel - Lacunar sel

Jaringan ikat kolagen yang membagi jaringan lymphoid menjadi nodule-nodule

Lacunar Cell:

sel besar inti satu dengan anak inti banyak sitoplasma pucat

Dengan formalin fixasi, sitoplasma tampak retraksi Lacunae

Pada jenis ini: fibrosis (+) RS sel jarang

Mixed Cellularity Hodgkins DiseaseSuatu tipe antara limphocyt predominan dan lymphocyt depletion RS sel banyak Lymphocyt tidak sebanyak pada bentuk lymphocyt predominan Tampak banyak eosinofil, plasma sel, histiosit area-area nekrosis/ fibrosis kadang ada

sering pada laki-laki

Lymphocyte-Rich Type Karakteristik Banyak terdapat limfosit reaktif

limfanodus tidak terlihat menyebar, tetapi kadang dapat ditemui Berhubungan dengan infeksi EBV pada 40% kasus Prognosis baik

Lymphocyte Depletion TypePrevalensi 5% dari kasus Dewasa > muda, HIV positif, Infeksi HBV menigkatkan resiko

Karakteristik Sedikit limfosit dan banyak sel Reed-Stenberg (RS)

Prognosis : Kurang baik dibanding tipe limfoma hodgkin yang lain

Lymphocyte Depletion Type

Lymphocyte Predominan TypePrevalensi 5% kasus

Karakteristik Sebagian besar limfosit kecil yang matur dan Histiosit (L&H) Popcorn cell

Prognosis : Sangat baik

Lymphocyte Predominan Type

Etiologi Limfoma HodgkinSel asal tumor = Belum pasti Penelitian Sel limfosit b centrum germinativum

Etiologi EBV Peningkatan NF-kB

Patogenesis Limfoma Hodgkin

Prognosis = Baik Angka kesembuhan stadium 1 dan 2 = 90% 5 years dissease free stadium 3 dan 4 = 60-70%

New Problem Terapi meningkatkan resiko terjadinya secondary cancer

DAFTAR PUSTAKA Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 7th ed. Philadelphia, W.B. Saunders, 2007. Journal modern pathology @2013 United States and Canadian Academy of Pathology. Webphatology.com@2003-2011 Dharam M. Ramnani, M.D.