BLOK NEOPLASMA

Prof.Dr.Ambar Mudigdo, dr,

Sp.PA(K)

Basic science

clinical practice
Promotif
Preventif
Curatif
Rehabilitatif

Cause of disease :
1. Enviromental factors
2. Genetic factors

manage

1.Curatif
Perawatan

Diagnostik
Manage
Theraphy

Etiologi :

Causa
Predisposisi
Faktor berperan

2. Patogenesis : proses /mekanisme,

step by step
Pathway & mechanism

3. Morphologi changes :
Sub sel:
protein,DNA/RNA,gen,Sitokin
Micros Sel
Jaringan
Organ
Macros
Sistem

4. Functional changes :

Hipo function

Hiper function

Others
Clinical signal simptoms

1. Labil

cells
gut lining

rapid prolif
and turn over

apitelial cells
2. Stable cells
hepatocyt
3. Permanent

neurones

cells

slow-prolif
and turn over
not able to prolif

1.
2.
3.
4.
5.
6.
7.

Reduced oxygen supply

Physical agents
Chemical agents
Micro organism
Abnormal immunologic rx
Nutritional deficiency
Genetic abnormalities

To explain
Patologi :

: - Why
- How
general path
system path

General path Sistem path -

Basic reaction
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
development
2. Regeneration : blood cells, mucosa
cells, skin cells (rapid cell turn over)
3. Slower cell turn over : liver tissue,
kidney, etc.

1.
2.
3.

Increase in size of individual cells

hypertrophy
Increase in the number of cells
hyperplasia
More common : combination 1&2

A.

Physiological enlargement :
muscle, uterus, breast

B.

Pathological enlargement :
result of disease process
eg: 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.
2.
3.
4.
5.

Progressive

: from few cells

large tumor
Purposeless
: irregular,
unstructured
Effects on surrounding tissue
: compreses
Not related to needs of the body : distruction
Parasitic
: blood supply

1.

Intrinsik

2.

Ekstrinsik :

:
- Lesi genetik
- Metabolism
- Hormonal
- dll
-

Mikrobiologi
Chemical
Physical
Nutritional
dll

1.Non neoplasma
2.Neoplasma
Klinik

: BENIGNA
MALIGNA

Histol

: MESENCHYM
EPITEL
-hemopoetic
-neuroectoderm

LEVEL :

TUBUH
SYSTEM
ORGAN
JARINGAN
SEL
SUB SEL =

CHROMOSOM
GEN
DNARNA /PROTEIN

BENIGN : + OMA ADENOMA

FIBROMA
LIPOMA
OSTEOMA
MALIGNA :
EPITEL

: + CARCINOMA
ADENO CA

MESENCHYM : + SARCOMA
FIBRO SA

1.
2.
3.
4.
5.
6.
7.
8.
9.

Proliferasi tak terkendali

Progresive
Purpuseless
Efek jaringan sekitar/distructive
Tak bermanfaat
Parasitik
Tak tergantung growth factor
Less adhesive
metastatic

BENIGNA

MALIGNA
DEFERENSIASI
jelek
Morfologi sel
Pertimbuhan
Invasi
+
Kapsul

Efek yang ditimbulkan

destruksi
Gerakan
Residif
Klinis

Mature/baik
seperti normal
lambat

immature /
abnormal
cepat

+
kompresi
mobil

desakan

invasi
fixed
+
destroys

 1.
2.
3.

MULTI FAKTOR
MULTI HIT
MULTI STEP

1.Faktor external : Lingkungan polusi

Budaya
Karsinogen
Mikro organisme
Radiasi
Kimia
2.Faktor internal : Genetik
Hormonal
Immunologi
Metabolisme

HIT
menerus

Beruntun , terus -

Akumulasi lesi gen

Gangguan homeostatis
Onkogen dominant

1.
2.
3.

Inisiasi
Promosi
Progresi

MASS
-COMP : -DISTR -INFIL

IN

TC.
M
PROM
PROG

PM

EX.

META

LUMEN
VASA. N
T. OR

KARSINOGEN

MIKRO ORGANISME : VIRUS

BACTERI
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

PROMOTING
ONKOGEN

INHIBITING
TUM.SUP .G
APOP/PCD.G
DNA REPAIR G.

HOMEOSTATIS BALANCE

IMBALANCE

: - MUTATION
- MULTIPLICATION
- DEGRADATION

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
KELLOID
MYXOMA
: LUNAK , JERNIH
LIPOMA
: SUB CUTAN
PUNGGUNG , PUNDAK, EXT
CHONDROMA : JARI
BATAS TEGAS , MELEKAT
KERAS
OSTEOMA
: LONG BONE , SKULL
MYOMA
: LEIO
RHABDO

Fibro sarcoma
Myoma sarcoma : rhabdo
leio
Lipo sarcoma
Osteo sarcoma
Angio sarcoma

Planocelulare carcinoma
Adeno carsinoma
Transisional cell carsinoma
Undifferentiated cell Ca