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BLOK NEOPLASMA
Prof.Dr.Ambar Mudigdo, dr, Sp.PA(K)
Basic science clinical practice
PromotifPreventifCuratif manageRehabilitatif
Cause of disease : 1.Enviromental factors2.Genetic factor’s
Diagnostik1.Curatif Manage Perawatan
Theraphy
Etiologi : CausaPredisposisiFaktor berperan
2. Patogenesis : proses /mekanisme, step by step “Pathway & mechanism”
3. Morphologi changes :Sub sel:protein,DNA/RNA,gen,Sitokin
Micros SelJaringan
OrganMacrosSistem
4. Functional changes : Hipo function Hiper function Others
Clinical signal simptoms
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
1. Reduced oxygen supply2. Physical agents3. Chemical agents4. Micro organism5. Abnormal immunologic rx6. Nutritional deficiency7. Genetic abnormalities
To explain : - Why - How
Patologi : general pathsystem path
General path - Basic reactionSistem path- Spesific resp/organ
4 major aspecs : 1. Etiologi 2. Pathogenese 3. Morphologic changes 4. Functional changes (clinical sign &
symp)
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.
1. Increase in size of individual cellshypertrophy
2. Increase in the number of cellshyperplasia
3. More common : combination 1&2
A. Physiological enlargement : muscle, uterus, breast
B. Pathological enlargement :result of disease processeg: increased myocardial cell
Hipertropi : myocardium (enlargement of the heart)
Hiperplasia : - chronic iritation : skin in chronic inflamation- imbalance of hormonal activity : prostat in old age
Hipertropi : myocardium (enlargement of the heart)
Hiperplasia : - chronic iritation : skin in chronic inflamation- imbalance of hormonal activity : prostat in old age
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
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
1. Intrinsik : - Lesi genetik- Metabolism- Hormonal - dll
2. Ekstrinsik :- Mikrobiologi- Chemical- Physical- Nutritional- dll
1.Non neoplasma2.Neoplasma
Klinik : BENIGNA MALIGNA
Histol : MESENCHYM EPITEL
-hemopoetic -neuroectoderm
LEVEL : TUBUH
SYSTEM
ORGAN
JARINGAN
SEL
SUB SEL = CHROMOSOM GEN DNA-RNA /PROTEIN
BENIGN : + OMA → ADENOMA FIBROMA LIPOMA OSTEOMA
MALIGNA : EPITEL : + CARCINOMA →ADENO CA
MESENCHYM : + SARCOMA → FIBRO SA
1. Proliferasi tak terkendali2. Progresive3. Purpuseless4. Efek Θ jaringan sekitar/distructive5. Tak bermanfaat6. Parasitik7. Tak tergantung growth factor8. Less adhesive9. metastatic
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
1. MULTI FAKTOR1. MULTI FAKTOR 2. MULTI HIT2. MULTI HIT 3. MULTI STEP3. MULTI STEP
1.Faktor external : Lingkungan polusi Budaya Karsinogen Mikro organisme
Radiasi Kimia
2.Faktor internal : Genetik Hormonal Immunologi
Metabolisme
HIT Beruntun , terus - menerus
Akumulasi lesi gen
Gangguan homeostatis
Onkogen dominant
1. Inisiasi 2. Promosi 3. Progresi
N
IN
TC.
PROM
PM EX.
PROG
M
MASS-COMP : - LUMEN-DISTR - VASA. N-INFIL T. OR
META
MIKRO ORGANISME : VIRUS
BACTERIKARSINOGEN BAHAN KIMIA JAMUR
PHISIK RADIOACTIVE
VIRUS : HPV : Ca Cervic EBV : Ca
NASOPHARYNX HEPATITIS Ca HEPAR HTLV : LEUKEMIA LIMFOMA
PROTO ONKOGEN - ONKOGEN TUMOR SUP GEN PROG CELL DEATH / APOPTOSIS
HOMEOSTATIS BALANCE
IMBALANCE : - MUTATION - MULTIPLICATION - DEGRADATION
PROMOTING INHIBITING
ONKOGEN TUM.SUP .GAPOP/PCD.G
DNA REPAIR G.
INDIVIDUAL SEL DEFERENSIASI :
- Baik , jelek, - tak berdeferensiasi ANAPLASI : atipik PLEOMORPHISM ANISOSITOSIS DISPLASIA
3 S :Size, shape , stainning
KELOMPOK SEL Arsitektur Loss of polarity
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
Fibro sarcoma Myoma sarcoma : rhabdo
leio Lipo sarcoma Osteo sarcoma Angio sarcoma
Planocelulare carcinoma Adeno carsinoma Transisional cell carsinoma Undifferentiated cell Ca