kuliah dasar molekuler kanker, karsinogenesis, dan interaksi seluler - prof dr ambar mudigdo.ppt
TRANSCRIPT
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BLOK NEOPLASMA
Prof.Dr.Ambar Mudigdo, dr, Sp.PA(K)
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Basic science clinical practice
PromotifPreventifCuratif manageRehabilitatif
Cause of disease : 1.Enviromental factors2.Genetic factor’s
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Diagnostik1.Curatif Manage Perawatan
Theraphy
Etiologi : CausaPredisposisiFaktor berperan
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2. Patogenesis : proses /mekanisme, step by step “Pathway & mechanism”
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3. Morphologi changes :Sub sel:protein,DNA/RNA,gen,Sitokin
Micros SelJaringan
OrganMacrosSistem
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4. Functional changes : Hipo function Hiper function Others
Clinical signal simptoms
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1.Labil cells rapid prolif gut lining
and turn over apitelial cells2.Stable cells slow-prolif
hepatocyt and turn over
3.Permanent cells not able to prolif neurones
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1. Reduced oxygen supply2. Physical agents3. Chemical agents4. Micro organism5. Abnormal immunologic rx6. Nutritional deficiency7. Genetic abnormalities
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To explain : - Why - How
Patologi : general pathsystem path
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General path - Basic reactionSistem path- Spesific resp/organ
4 major aspecs : 1. Etiologi 2. Pathogenese 3. Morphologic changes 4. Functional changes (clinical sign &
symp)
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Physiological proliferation : 1. In somatic growth during fetal
development2.Regeneration : blood cells, mucosa
cells, skin cells (rapid cell turn over)3.Slower cell turn over : liver tissue,
kidney, etc.
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1. Increase in size of individual cellshypertrophy
2. Increase in the number of cellshyperplasia
3. More common : combination 1&2
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A. Physiological enlargement : muscle, uterus, breast
B. Pathological enlargement :result of disease processeg: increased myocardial cell
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Hipertropi : myocardium (enlargement of the heart)
Hiperplasia : - chronic iritation : skin in chronic inflamation- imbalance of hormonal activity : prostat in old age
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Hipertropi : myocardium (enlargement of the heart)
Hiperplasia : - chronic iritation : skin in chronic inflamation- imbalance of hormonal activity : prostat in old age
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Metaplasia : change from one type to another (frequently associated with hiperplasia) in lining epithelia or in conective tissue.
Displasia :disordered growth (frequently precursor of malignancy)e.g : uterine cervic
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1. Progressive : from few cells large tumor
2. Purposeless : irregular, unstructured3. Effects on surrounding tissue : compreses4. Not related to needs of the body : distruction5. Parasitic : blood supply
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1. Intrinsik : - Lesi genetik- Metabolism- Hormonal - dll
2. Ekstrinsik :- Mikrobiologi- Chemical- Physical- Nutritional- dll
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1.Non neoplasma2.Neoplasma
Klinik : BENIGNA MALIGNA
Histol : MESENCHYM EPITEL
-hemopoetic -neuroectoderm
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LEVEL : TUBUH
SYSTEM
ORGAN
JARINGAN
SEL
SUB SEL = CHROMOSOM GEN DNA-RNA /PROTEIN
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BENIGN : + OMA → ADENOMA FIBROMA LIPOMA OSTEOMA
MALIGNA : EPITEL : + CARCINOMA →ADENO CA
MESENCHYM : + SARCOMA → FIBRO SA
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1. Proliferasi tak terkendali2. Progresive3. Purpuseless4. Efek Θ jaringan sekitar/distructive5. Tak bermanfaat6. Parasitik7. Tak tergantung growth factor8. Less adhesive9. metastatic
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BENIGNA MALIGNA
DEFERENSIASI Mature/baik immature / jelek Morfologi sel seperti normal abnormal Pertimbuhan lambat cepat Invasi Θ + Kapsul + Θ Efek yang ditimbulkan kompresi invasi destruksi Gerakan mobil fixedResidif Θ +Klinis desakan destroysOperasi → baik →kombinasi Metastase Θ +Prognose baik buruk
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1. MULTI FAKTOR1. MULTI FAKTOR 2. MULTI HIT2. MULTI HIT 3. MULTI STEP3. MULTI STEP
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1.Faktor external : Lingkungan polusi Budaya Karsinogen Mikro organisme
Radiasi Kimia
2.Faktor internal : Genetik Hormonal Immunologi
Metabolisme
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HIT Beruntun , terus - menerus
Akumulasi lesi gen
Gangguan homeostatis
Onkogen dominant
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1. Inisiasi 2. Promosi 3. Progresi
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N
IN
TC.
PROM
PM EX.
PROG
M
MASS-COMP : - LUMEN-DISTR - VASA. N-INFIL T. OR
META
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MIKRO ORGANISME : VIRUS
BACTERIKARSINOGEN BAHAN KIMIA JAMUR
PHISIK RADIOACTIVE
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VIRUS : HPV : Ca Cervic EBV : Ca
NASOPHARYNX HEPATITIS Ca HEPAR HTLV : LEUKEMIA LIMFOMA
PROTO ONKOGEN - ONKOGEN TUMOR SUP GEN PROG CELL DEATH / APOPTOSIS
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HOMEOSTATIS BALANCE
IMBALANCE : - MUTATION - MULTIPLICATION - DEGRADATION
PROMOTING INHIBITING
ONKOGEN TUM.SUP .GAPOP/PCD.G
DNA REPAIR G.
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INDIVIDUAL SEL DEFERENSIASI :
- Baik , jelek, - tak berdeferensiasi ANAPLASI : atipik PLEOMORPHISM ANISOSITOSIS DISPLASIA
3 S :Size, shape , stainning
KELOMPOK SEL Arsitektur Loss of polarity
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FIBROMA : SUB CUTAN, OVARIUM FIB MOLLE FIB DURUM
KELLOIDMYXOMA : LUNAK , JERNIHLIPOMA : SUB CUTAN PUNGGUNG , PUNDAK, EXTCHONDROMA : JARI
BATAS TEGAS , MELEKAT KERASOSTEOMA : LONG BONE , SKULLMYOMA : LEIO
RHABDO
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Fibro sarcoma Myoma sarcoma : rhabdo
leio Lipo sarcoma Osteo sarcoma Angio sarcoma
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Planocelulare carcinoma Adeno carsinoma Transisional cell carsinoma Undifferentiated cell Ca