DASAR-DASAR NEOPLASMA

Dr. Juliana Lina, Sp.PA

Medan - 2017
 Neoplasia = "new growth"

“Suatu massa pertumbuhan jaringan yang abnormal,

tumbuh berlebihan, tidak terkoordinasi dengan
jaringan normal di sekitarnya & tetap bertumbuh
walaupun rangsangan terhadapnya telah dihentikan”
 Neoplasma = Tumor

Oncos

Ilmu yang mempelajari

Oncology tentang tumor

Logos

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 Ganas Jinak

Neoplasma

Kategori ini berdasarkan sifat klinik neoplasma

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 Differentiation between
Benign neoplasm Malignant Manner of
growth neoplasm
Relatively normal Cellulear character Abnormal
Histioid character

•Slight Mitotic activity •Usually great

•Relatively slow & restricted Rate of growth •Rapid & Unrestricted

•Expansive Manner of growth •Invansive & Restructive

•Demarcated, encapsulated Limitation •Not sharply demarcated, not

encapsulated
•Rare Recurrence after simple •Freguent
removal
•Never Metastases •The rule
•Relatively slight Vascularity •Moderate to marked

•Unusual Necrosis & Ulceration •Usual, haemorrhage

•Uncommon Constitutional effects •The rule

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Jinak Ganas
Tidak Kanker
bermetastasis (Latin : crab)

Sembuh dengan Melekat ke jar.

operasi lokal sekitarnya

Note : ukuran Menginvasi &

tumor besar  merusak struktur
serius disekitarnya

Bermetastasis 
kematian
Jinak & Ganas

2 komponen
Mempunyai
dasar

Jar.ikat

Sel
radang P.darah
(host)
 Neoplasma

Jinak Ganas

Parenkim = karsinoma
Akhiran -oma di belakang
jenis sel tumor berasal
Mesenkim = sarkoma

Jar. Ikat = fibroma Kelenjar = adenokarsinoma

Tulang rawan = khondroma

Jar.ikat = fibrosarkoma

Tulang rawan =
Khondrosarkoma
 Nomenklatur Tumor

Asal jaringan Jinak Ganas

Tdd. 1 jenis sel parenkim

Jaringan ikat Fibroma Fibrosarkoma

Lipoma Liposarkoma
Khondroma Khondrosarkoma
Osteoma Osteogenik sarkoma

Endotel & jar. Penunjangnya

P.darah Hemangioma Angiosarkoma

P.limfe Limfangioma Limfangiosarkoma

Sinovium Sinovial sarkoma

Mesotelium Mesothelioma
Pelapis otak Meningioma Invasive meningioma
 Table 6-1. Nomenclature of Tumors

Asal jaringan Jinak Ganas

Sel darah & sel lainnya

Sel hematopoietik Leukemia

Jaringan limfoid Limfoma
Otot

Otot polos Leiomioma Leiomiosarkoma

Otot rangka Rhabdomiosarkoma

Tumor yang berasal dari epitel (parenkim)

Skuamous berlapis Papiloma sel skuamous Karsinoma sel skuamous/

epidermoid
Sel basal / adneksa kulit Karsinoma sel basal

Pelapis epitel kelenjar / duktus Adenoma Adenokarsinoma

Papiloma Karsinoma papilari

Cystadenoma Cystadenokarsinoma
 Ciri-ciri neoplasma jinak & ganas

4 gambaran yang membedakannya yaitu :

Diferensiasi & anaplasia

Laju pertumbuhan

Invasif lokal

Metastasis
Patterns of cell Proliferation
• Hyperplasia
• Dysplasia
• Metaplasia
• Anaplasia
• Neoplasia
Patterns of cell Proliferation

•Metaplasia
• conversion of one type of cell in a tissue to another
type not normal for that tissue

•Anaplasia
• change in the DNA cell structure and orientation to
one another, characterized by loss of differentiation
and a return to a more primitive form.

Neoplasia
• uncontrolled cell growth, either benign or malignant
1. Malignant change in the
target cell, referred to as
transformation
2. Growth of the transformed
cells
3. Local invasion
4. Distant metastases.
 Well differentiated neoplasm
 Resembles mature cells of tissue of origin
 Poorly diffentiated neoplasm
 Composed of primitive cells with little diffrerentiation
 Undifferentiated or “anaplastic” tumor
 Correlation with biologic behavior
 Benign tumors are well differentiated
 Poorly differentiated malignant tumors usually have
worse prognosis
 Pleomorphism
 Size
 shape
 Abnormal nuclear morphology
 Hyperchromasia
 High nuclear cytoplasmic ratio
 Chromatin clumping
 Prominent nucleoli
 Mitoses
 Mitotic rate
 Location of mitoses
 Loss of polarity
 Literallymeans abnormal growth
 Malignant transformation is a multistep process
 In dysplasia some but not all of the features of
malignancy are present

 Dysplasia may develop into malignancy

 Uterine cervix
 Colon polyps
 Graded as low-grade or high-grade
 Dysplasia may NOT develop into malignancy
 Cellular features
 Local invasion
 Capsule
 Basement membrane
 Metastasis
 Unequivocal sign of malignancy
 Seeding of body cavities
 Lymphatic
 Hematogenous
 Example of breast cancer
 Halsted radical mastectomy
 Sentinel node biopsy
 Prognostic
 Number of involved nodes is an important component of
TNM staging system
 Therapeutic
 Overall risk of recurrence
 Extent of nodal involvement
 Histologic grade and other considerations
 “Adjuvant” chemotherapy
 There are no reliable molecular indicators of malignancy
 The gold standard for diagnosis of cancer remains
routine microscopy.
 Correlation of histologic and cytologic patterns with
clinical outcomes.
 General criteria for malignancy are recognized, they
must be used with caution in specific cases fasciitis
has a more alarming histologic appearance than many
fibrosarcomas, and misdiagnosis can lead to unnecessary
surgery.
Histologic features that favor malignancy include
the following:
 Anaplasia or cellular atypia(correlates with the
aggressiveness of the tumor).
 (1) variation in the size and shape of cells and cell
nuclei (pleomorphism)
 (2) enlarged and hyperchromatic nuclei with coarsely
clumped chromatin and prominent nucleoli
 (3) atypical mitoses
 (4) bizarre cells, including tumor giant cells
 Mitotic activity: Abundant mitoses are characteristic of
many malignant tumors
 Growth pattern: Malignant neoplasms often exhibit a
disorganized and random growth pattern, arrangements
around blood vessels, papillary structures, whorls,
rosettes, and so forth. Malignant tumors often outgrow
their blood supply and display ischemic necrosis.
 Invasion: Malignancy is proved by the demonstration of
invasion, particularly of blood vessels and lymphatics.
 Metastases: The presence of metastases identifies a
tumor as malignant. In metastatic disease, electron
microscopic examination and the demonstration of
specific tumor markers may establish the correct origin.
Metastatic Spread is the
Most Common Cause of
Cancer Death
 Feature Benign Malignant

Differentiation Well differentiated Some degree of anaplasia

Rate of growth Progressive but Variable. Mitoses more
slow. Mitoses few frequent and may be
and normal abnormal
Local invasion Cohesive growth. Poorly cohesive and
Capsule & BM not infiltrative.
breached
Metastasis Absent May occur
 Sun exposure
 Melanomas 6x incidence New Zealand vs Iceland
 Blacks have low incidence of melanoma
 Smokingand alcohol abuse
 Body mass
 Overweight = 50% increase in cancer
 Environmental vs racial factors
 Japanese immigrants to USA
 Viral exposure
 Human papilloma virus (HPV) and cervical cancer
 Hepatitis B virus (HBV) and liver cancer (Africa)
 Epstein-Barr Virus (EBV) and lymphoma
 Age
 Most cancers occur in persons ≥ 55 years
 Childhood cancers
 Leukemias & CNS neoplasms
 Bone tumors
 Genetic predispostion
 Familial cancer syndromes
 Early age at onset
 Two or more primary relatives with the cancer
 Multiple or bilateral tumors
 Polymorphisms that metabolize procarcinogens, e.g.,
nitrites
 Nonhereditary predisposing conditions
 Chronic inflammation
 Precancerous conditions
 Chronic ulcerative colitis
 Atrophic gastritis of pernicious anemia
 Leukoplakia of mucous membranes
The spread of malignant tumors exhibits the
following four characteristics :
 — Infiltration: The tumor cells penetrate the
surrounding tissue .
 — Invasion: The tumor cells penetrate lymph
and blood vessels .
 — Tissue destruction occurs in the vicinity of
the tumor as a result .
 — Metastasis: Tumor cells colonize other
tissuesfar from the original tumor site.
Effects of Cancer

• Disruption of Function- can be due to

obstruction or pressure

• Hematologic Alterations: can impair function of

blood cells

• Hemorrhage: tumor erosion, bleeding, severe

anemia

• Anorexia-Cachexia Syndrome: wasted

appearance of client
Effects of Cancer

• Paraneoplastic Syndromes: ectopic sites with excess hormone

production
– ↑ Parathyroid hormone→ hypercalcemia
– ↑ secretion of insulin→ hypoglycemia
– ↑ Antidiuretic hormone (ADH) → fluid retention, HTN &
peripheral edema

• ↑ Adrenocorticotropic hormone (ACTH): cause excessive

secretion of cortisone (ie: fluid retention, ↑ glucose levels)
 Pain: major concern of clients and families associated with
cancer

• Physical Stress: body tries to respond and destroy neoplasm

Change in bowel or bladder habits

– A person with colon cancer may have

diarrhea or constipation, or he may notice
that the stool has become smaller in
diameter

– A person with bladder or kidney cancer

Unusual bleeding or discharge

– Blood in the stool is often the first sign of

colon cancer

– Similarly, blood in the urine is usually the

first sign of bladder or kidney cancer

– Postmenopausal bleeding (bleeding after

menopause) may be a sign of uterine
cancer
Thickenings or lumps

– Enlargement of the lymph nodes or glands (such

as the thyroid gland) can be an early sign of
cancer

– Breast and testicular cancers may also present as

a lump

• Unexplained anemia

• Sudden unexplained weight loss

Indigestion or difficulty in swallowing

– Cancers of the digestive system, including those

of the esophagus, stomach, and pancreas, may
cause indigestion, heartburn, or difficulty
swallowing

A sore that does not heal

– Small, scaly patches on the skin that bleed or

do not heal may be a sign of skin cancer

– A sore in the mouth that does not heal can

indicate oral cancer
Nagging or persistent cough or hoarseness

– Cancers of the respiratory tract, including lung

cancer and laryngeal cancer, may cause a cough
that does not go away or a hoarse (rough) voice

Obvious change in a wart or mole

– Moles or other skin lesions that change in shape,

size, or color should be reported