patologi veteriner blok 10
DESCRIPTION
Berbagai ilmu patologi veteriner dasarTRANSCRIPT
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PATOLOGI VETERINER TUMOR
• PATOLOGI VETERINER TUMOR I (ABNORMAL GROWTH-NEOPLASTIC, TATANAMA TUMOR, ANGIOGENESIS, METASTASIS)
• PATOLOGI VETERINER TUMOR II (GENESIS OF CANCER, ETIOLOGI TUMOR DAN MEKANISME DALAM MEMICU TERJADINYA TUMOR)
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PATOLOGI VETERINERTUMOR I
Drh. SITARINA WIDYARINI,MP, PhD
BAGIAN PATOLOGI ANATOMI FKH-UGM
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Kata Kunci Neoplasia:
Newgrowth: neoplasia
Tumour: “swelling” bengkak -- benign growth
Cancer: malignant growth
Carcinogenesis/oncogenesis: proses dari perkembangan cancer (molekuler maupun histopatologi): inisiasi, promosi dan progresi
Transformation: perubahan genetik pada sel yang diturunkan (inherited) pada sel anak (daughter cells)
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Kata Kunci Neoplasia:
Carcinogen: substansi yang dapat menyebabkan terjadinya neoplasia, aksinya melalui ikatan dengan DNA sel target
Oncogen: abnormal gen yang diekspresikan oleh neoplastic cells, derivat proto-oncogen (normal human gen): mutasi, delesi, translokasi-abnormal
Onco suppressor gene: prevent neoplasia: memicu apoptosis dan menghambat proliferasi sel
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Abnomalitas Pertumbuhan:
Non-Neoplastik
Hyperplasia ------------ Hypoplasia Hypertrophy Atrophy Metaplasia ------------- Agenesis/ aplasia
Neoplastik
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Hyperplasia vs Metaplasia:
Hyperplasia
• Peningkatan ukuran jaringan/organ
• Peningkatan jumlah sel penyusunnya
• Peningkatan mitosis• Iritasi, reversible• Melanjut ke neoplasia• Note: proliferasi
Metaplasia
• Perubahan sel dewasa satu menjadi bentuk sel dewasa yang lain
• Epitel cuboid, transitional menjadi epitel squamous
• Adaptasi terhadap lingkungan, reversible
• Melanjut ke neoplasia• Defisiensi vit A: respiratory passage,
radang kronis pada urinary bladder (stone)
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Hyperplasia:
Dapat dikacaukan dengan neoplasia
Terjadi peningkatan proliferasi sel
Secara morfologik sulit dibedakan
Dalam kondisi tertentu ---- neoplasia
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Hyperplasia vs Neoplasia
Hyperplasia
• Stimulus dihilangkan proses akan berhenti
• Tidak merusak struktur jaringan
• Proses diffuse
Neoplasia
• Stimulus dihilangkan proses jalan terus
• Merusak struktur jaringan
• Proses bersifat focal
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Tumour dan Cancer:
Cancer
Neoplasia
Malignancy
Tumour
Benign Growth
Pre-Neoplastic lesion/Pre-Malignant lesion:hyperplasia
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Benign vs Malignant Neoplasm:
Benign• Lambat• Encapsulated
• Non-metastasis
• Sel diferensiasi sempurna
• Sel normal
• Hanya membunuh kalau mengenai organ vital
Malignant• Cepat• Invasif, metastasis
• Sel diferensiasi tidak sempurna/anaplasia
• Sel abnormal
• Selalu mematikan -penanganan cepat
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Normal Epitel Bronkus:
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Hyperplasia Epitel Bronkus:
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Karsinoma Bronkogenik/Lung Cancer:
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Hyperplasia:
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Anaplasia:
Sel yang diferensiasi atau pembelahan atau mitosis yang tidak sempurna (anaplastic cell)
• Variasi dalam bentuk dan ukuran• Rasio nucleolus dan cytoplasma 1/1 (1:4)• Multiple nucleoli• Naiknya jumlah gambaran mitosis dan mitotik index• Naiknya jumlah gambaran abnormal mitosis• Nucleus hyperchromantic • Variasi jumlah chromosome
Note: hystopathology report perubahan pada sel diatas disebut sebagaiatypia
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Anaplasia:
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Anaplasia:
a. hyperchomantic b. Multiple nucleolic. Rasio inti sitoplasma 1:1
a. tripolar, mitosis 3 selb. Hyperchomanticc. Bipolar (normal)
c
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Nomenclature Of Neoplasms:
Berdasar pada histogenesis dan tipe/sifat pertumbuhan dari tumor
Benign ---- akhiran oma
Malignat -- carcinoma (epithelial tissue) dan sarcoma (mesenchymal tissue)
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Nomenclature Of Neoplasms:
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Six Diabolical Superpowers Of Cancer:
• Growth in the absence of normal GO signals
• Growth despite stop signals issued by neighboring cells (lost of contact inhibition)
• Evasion of built-in autodestruct mechanisms
• Ability to stimulate blood vessel construction (angiogenesis)
• Effective immortality• Metastasis
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Siklus Sel Normal (Normal Cell Cycle):
Diatur oleh functional phase dan preparation phase
Functional phase: S phase (copy DNA & replikasi DNA) dan M phase (mitosis/ duplikat kromosom antar anak-anak sel)
Preparation phase: Gap 1 (G1) persiapan replikasi dan Gap 2 (G2) persiapan mitosis
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Siklus Sel Normal (Normal Cell Cycle):
Sel yang tidak aktif membelah atau akan dikeluarkan dari siklus dimasukkan dalam GO phase/ non-cycling state
Cell cycle diatur oleh:• Intracelluler & extracelluler factor (growth factor,
mitogen, antimitogen, cell contact dan nutrisi)• Proliferasi sel dalam cycle cell dikontrol oleh produk
gen: tumour suppressor gen dan oncogen
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Siklus Sel Normal (Normal Cell Cycle):
• Tumour suppressor gen: menghambat progresi dari cell cycle (p53 atau TP53)
• Oncogen: memicu kerja cell cycle
• Kematian sel dalam cycle cell: produk gen yang menghambat/ antiapoptosis (bcl2), dan memicu apoptosis (bax)
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Siklus Sel Normal (Normal Cell Cycle):
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Siklus Sel Normal (Normal Cell Cycle):
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Siklus Sel Normal (Normal Cell Cycle):
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Siklus Sel Normal (Normal Cell Cycle):
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Siklus Sel Dan Kanker:
Transformasi normal sel ke tumor sel terjadi karena mutasi gen yang mengontrol siklus sel normal
Gen p53 mengkode protein p53 normal suatu jenis zinc finger gene regulatory protein (GRP) - ditemukan dengan konsentrasi sangat rendah pada sel normal
Produk gen p53 akan menekan siklus sel G1 (hambat Cdk2-cyclin D and E)
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Siklus Sel Dan Kanker:
Anti-oncogen dari p53 -- normal siklus sel- normal sel (gen of the world)
p53 mutan atau p53 null -- fungsi tidak bekerja normal - tumor sel
Tumor sel atau malignant cell: oncogen dan antiapoptosis signal, tumour suppressor gen dan apoptosis signal
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Sel Normal vs Sel Dengan Defek Fungsi P53:
Note: *G1 arrest **no G1 arrest
*
**
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Lost Of Contact Inhibition:
Tumour tissue culture
Tidak menuruti stop signal dari sel tetangga
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Antiapoptosis:
Sel normal --- kerusakan genetik -- aktifkan program bunuh diri/apoptosis
Kanker sel --- kerusakan genetik - tidak aktifkan program bunuh diri - kerusakan diturunkan ke anak sel (disebut juga dengan transnform cell: heritable change has occurred in cell)
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Angiogenesis:
New vascularisation: nutrisi jaringan tumor dan berperan penting untuk metastasis
Tumour angiogenetic factor/TAF diproduksi oleh sel tumor atau sel radang seperti makrofag
Heparin-binding fibroblast growth factor (FGF): kemotaktik dan mitogenik pada endotelial sel dan memicu produksi proteolitik enzim --- penetrasi ke stroma endotel
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Angiogenesis:
TGF-alfa, TGF-beta, EGF, PDGF, VEGF
VEGF -- memicu vaskularisasi di sekitar jaringan tumor
TGF-beta -- memicu pertumbuhan edotelial sel
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Angiogenesis:
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Metastasis:
Penyebaran sel tumor dari satu organ (primer tumor) ke organ lain
• Local invasion: menyebar ke jaringan/ organ sekitar (cervical cancerurinary bladder dan ureter; gastric cancerpancreas)
• Lymphatic: breast cancer axillary lymph node; melanomainguinal lymph node; lung cancermediastinalis lymph node
• Hematogenous: gastric cancer liver; breast cancerbone (hematogenous: liver, brain, bone lung)
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Metastasis:
• Direct seeding across cavity, transcoelomic (across peritoneal cavity): ovarial carcinoma- pseudomyxoma peritonei dan omentum; colorectal cancer abdomen
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Proses Metastasis:
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Proses Metastasis:
Receptor-mediated attachment
Laminin dan fibronectin
Normal sel: high affinity laminin reseptor pada basement membrane/ membrana basalis yang dipolarisasikan pada permukaan membrane sel
Kanker sel: lebih banyak reseptor -- tersebar di seluruh membran sel
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Proses Metastasis:
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Metastasis:
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References:
• “Neoplasia” General Veterinary Pathology, R.G. Thomson, Second Edition (1986)
• “Neoplasia” Pathologic Basis of Disease, S.L. Robbins, Third Edition (1986)
• “Neoplasia” Robbins Pathologic Basis of Disease, R.S. Contran, (1996)
• “Neoplasia” Basic Pathology, M.D.Kumar, (2003)
• Cancer Principles and Practice of Oncology,V.T. DeVita, (1997)
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PATOLOGI VETERINERTUMOR II
Drh. SITARINA WIDYARINI,MP, PhD
BAGIAN PATOLOGI ANATOMI FKH-UGM
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Genesis Of Cancer:
Somatic mutation theory
• Cancer terjadi karena mutasi gen (carcinogen-- mutagen)
• Pada pasien xeroderma pigmentosa/XP -- DNA excision repair enzim tidak mampu atasi mutasi untuk mencegah munculnya tumor kulit (SCC) pada pasien XP-- autosomal recessive
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Genesis Of Cancer:
Epigenetic theory
• Cancer terjadi karena kegagalan diferensiasi dari sel/ penyebab diluar gen
• Beberapa tumor bisa mengalami regresi (UV/chemical-induced cancer)
• Beberapa tumor ganas diferensiasi sel masih terlihat nyata (well-defferentiated)/ pada kasus SCC
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Genesis Of Cancer:
Somatic mutation theory
• Standard Dogma (mutasi gen -- eliminasi protein dari tumor suppressor gen dan mengaktifkan oncoprotein)
• Modified Dogma (Peningkatan random mutasi pada genom dari pre-cancer cell)
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Genesis Of Cancer:
• Early Instability Dogma
• All Aneuploidy Dogma
- Abrasi dari kromosom-- genomic
instability-- mutasi - Perubahan genetic yang bervariasi
--tumor
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Penyebab Kanker:
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Viral Carcinogens:
DNA oncogenic viruses
• Adenoviruses
• Poxviruses• Papovaviruses/papillom
a viruses
• Herpesviruses
RNA oncogenic viruses/ oncorna virus
• Avian leucosis
• Bovine leukemia virus• Murine osteosarcoma
virus
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DNA Oncogenic Viruses:
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RNA Oncogenic Viruses (Oncorna Virus):
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Viral Carcinogens:
Kasus ditemukan pada hewan maupun manusia Pada manusia:
• Infeksi Eppstein Barr Virus/ EBV (family herpes virus) --- Burkitts lymphoma, B-cell lymphoma (pada pasien infeksi HVI, dan pasien transplantasi organ), nasopharyngeal carcinoma (NPC)
• Herpes simplex ---HPV-> cervical cancer
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Chemical Carcinogens:
Direct Acting Carcinogen
Procarcinogens --- metabolic activation
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Chemical Carcinogens:
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Chemical Carcinogens:
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Initiator & Promotor
INITIATOR:• Zat yang secara sendiri dapat menstimulir
timbulnya cancer (DMBA, BP, AAF)
PROMOTER:• Zat yang secara sendiri tidak dapat menimbulkan
cancer, tapi apabila diberikan bersama initiator dalam dosis sub-carcinogenic dapat menimbulkan cancer (hormon/DES, phorbol ester, croton oil, TPA)
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Initiator & Promotor:
Zat yang dapat beraksi sebagai initiator sekaligus promoter dalam menstimulasi cancer
Complete Carcinogens
UV, 4-nitroquinoline-1-oxide
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Chemical Carcinogens:
Metabolisme PAH
• K regio
• Melibatkan Mixed-function oxidase (MFOs)- suatu sistem enzim yang mengandung berbagai bentuk sitokrom P450
• Proximate carcinogen dan ultimate carcinogen
(diol epoksida)
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Chemical Carcinogens:
Ikatan Kovalen DNA Sel dan Diol Epoksida PAH
• Epoksida bersifat elektrofilik
• Binding to DNA- adduct formation
• Basa guanin --kesalahan pemilihan basa -- guanin-adenin
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Chemical Carcinogens:
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Physical Carcinogens:
UV radiation
Ionizing radiation • Atomic bombs
• X-ray
• Gamma rays• Particulate (alpha, beta, protons, neutron)
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Physical Carcinogens:
UVB-induced DNA damage• Cyclobutane pyrimidine dimers/CPD (most)• 6-4 photoproduct
UVA-induced DNA damage• Reactive oxygen species (singlet oxygen,
superoxide dan hydroxyl radical)• Oxidised base 8-hydroxyguanosin (8-OHdG)
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References:
• “Neoplasia” General Veterinary Pathology, R.G. Thomson, Second Edition (1986)
• Cancer Principles and Practice of Oncology,V.T. DeVita, (1997)
• “Neoplastic Disease and Anticancer Drug” Texbook of Pharmacology, Bowman WC. Rand MJ, (1989)
• “Neoplasia” Robbins Pathologic Basis of Disease, R.S. Contran, (1996)
• “Neoplasia” Basic Pathology, M.D.Kumar, (2003)