Download SURGICAL ONCOLOGY

SURGICAL ONCOLOGY
James Taclin C. Banez, MD, FPSGS, FPCS

Study of neoplastic diseases:

ONCOS = tumor
LOGOS = study
Neoplasm:

Altered cell population characterized by
an excessive, non-useful proliferation
of cells that are unresponsive to normal
control mechanisms and to organizing
influences of adjacent tissue.
Neoplasm:
1.
Malignant:

2.
Cancer cells that exhibit uncontrolled
proliferation and impair the function of
normal organs by local tissue invasion
and metastatic spread to distant
anatomic sites.
Benign:

Composed of normal appearing cells
that do not invade locally or
metastasize to other sites
EPIDEMIOLOGY:


Overall cancer death rates shows
slow steady increase
Lower death rates during past
50yrs:
1.
2.

Stomach
Uterus
Increase death ratea:
1.
2.
Lung
pancreas
EPIDEMIOLOGY:
Cancer incidence by sites and sex:
Male
Female
Lung
20% Breast
27%
Prostate
20% Colon & Rectum
16%
Colon & Rectum
14% Lung
11%
Urinary
10% Uterus
10%
Leukemia &
Lymphoma
Skin, pancreas
and oral
8%
Leukemia &
Lymphoma
Skin, pancreas
3-4%
and oral
7%
3-4%
EPIDEMIOLOGY:
Cancer death by sites and sex:
Male
Female
Lung
36% Lung
20%
Colon & Rectum
11% Breast
18%
Prostate
10% Colon & Rectum
14%
Leukemia &
Lymphoma
Pancreas &
Urinary
Leukemia &
Lymphoma
9%
5%
Pancreas & Ovary
each
5%
9%
Urinary & Uterus
4%
each


The most significant 5 yrs survival
rates are achieved in patients w/
cancer of skin, cervix, uterus and
bladder; w/ the lowest survival w/
pancreatic cancer
Females tend to have a greater
number of 5yrs survival w/ cancer
of any given primary site than
males, reason (?)
5 yr survival female
5 yr survival male
= 50%
= 31%
ETIOLOGY:
1.
Chemical carcinogens:
a.
b.
c.
d.
2.
Hydrocarbons from coal tar = skin,
larynx & bronchial CA
Aromatic amines = urinary tract CA
Benzene = leukemia
Asbestos = mesothelioma
Physical carcinogens:
a.
b.
c.
Ionizing radiations = bone cancer
Multiple x-rays = skin/thyroid CA
Atomic bomb (Japan) = leukemia
ETIOLOGY:
3.
Mechanical (chronic irritation):

4.
Marjolin’s ulcer = burn scar cancer
Infection:

Parasitic:


Schistosomas – Liver & bladder CA
Viruses:




Hepatitis B – hepatocellular CA
Epstein-Barr virus – Burkitts lymphoma
Herpes simplex virus 2 – cervical CA
Aids
ETIOLOGY:
4.
Hereditary factors:


5.
Geographic factors:










Familial polyposis – colonic CA
Breast CA – 2-3x in daughters and in younger age
Inc. CA of stomach – Scandinavian,
Iceland and Japan
Inc. CA of liver – South & West Africa
Inc. CA of Nasopharynx – China
Inc. CA of urinary bladder – Egypt
Dec. CA of colon – Black/Africa
Dec. CA prostate / breast – Japan
Dec. CA of uterine/cervix – Israel/Jewish
Dec. CA of skin – Blacks
Customs & environment plays an important role
in the development of CA.
Migration of populations usually causes a shift
towards the patterns of cancer incidence of the
host country
ETIOLOGY:
6.
Precancerous conditions:
a.
b.
c.
d.
e.
f.
Leuplakia
Actinic keratosis
Polyps of colon & rectum
Neurofibromas
Dysplasia of cervix, bronchial
Chronic ulcerative colitis
ETIOLOGY:
6.
Oncogenes & Growth Factors:

RNA tumor viruses cause:
1.
2.
3.
4.

7.
Carcinomas
Sarcoma
Leukemia
Lymphomas
Retrovirus have an enzyme that alters
the viral genomic RNA resulting to
abnormal growth and differentiation of
the cell.
Multi-factorial:

Lung / breast CA
CANCER BIOLOGY
1.
Morphologic changes:





Rise from a single cell
Revert to more primitive cell types
Normal orderly tissue patterns are lost
or replaced by the random pilling up
of malignant cells w/o definite pattern
High index of mitoses
Invasion of adjacent sturctures
CANCER BIOLOGY
2.
Biochemical changes:



Changes in DNA, RNA and chemical
architecture results to LOSS of CONTACT
INHIBITION to proliferation and intercellular
adhesiveness
Reversion of normal cellular biochemistry to
that of the embryonal cells that produces
EMBRYONAL subs. (CEA, alpha fetoprotein)
Also produced biologically active subs.
Normally produced by the cells.
(hyperparathyroidism); also that are not
normally produced by the cells of origin
(bronchogenic CA=ACTH)
CANCER BIOLOGY
3.
Growth rates of neoplasm:


Doubling time is doubled
Takes 30 doubling time to produce
1cm nodule
CANCER BIOLOGY
4.
Effector mechanism in tumor
immunity:

Host provides a number of effector
mechs. That destroys the tumor:
a.
b.
c.
d.
e.
f.
Tumor-antigen-specific antibodies
Mononuclear phagocytes
Natural killer cells
Cytotoxic T lymphocytes
Neutrophils
K cells
CANCER BIOLOGY
4.
Effector mechanism in tumor
immunity:

Tumor Necrosis Factor (TNF):


Cytokines produced by monocytes,
machrophage, endothelial cells, large
granular lymphocytes and neutrophils
Properties:
a. Direct cytotoxicity for certain cells
b. Stimulation of procoagulant activity by
vascular endothelial cells
c. Induction of fever by direct effect on the
hypothalamic thermoregulatory center
CANCER PATHOLOGY
A.
Classification of Neoplasm:
Carcinoma – arising from epithelial cells
Sarcoma – arise from connective tissue
and cells of mesenchymal origin
(fibrous, muscular, fatty, vascular &
skeletal).
CANCER PATHOLOGY
B.
Grading of malignancy:
Broders classified carcinoma into 4 grades
according to:
1.
Degree of differentiation
2.
Appearance of cells, their nuclei and the
number of mitotic figures
Grade I – least malignant
Grade IV – most malignant

Carcinoma in Situ:

Has cytologic characteristic of malignant
tumors but w/ no detectable invasion into
the surrounding tissue or infiltration into
deeper cell layers
ROUTES OF SPREAD:

Metastasis may entirely dominate the
clinical picture, while the primary tumor
remains latent and asymptomatic
1.
2.
3.
4.
Direct extension
Lymphatic spread

Common in epithelial neoplasms of all types
(except for basal cell CA)
Vascular spread

Either thru the thoracic duct or by the
invasion of blood vessels

Capillaries are almost invaded, veins invaded
frequently but arteries rarely.

More common in sarcomas
Spread through serous cavities

Peritoneal seedings (gastrointestinal CA)
CLINICAL MANIFESTATION:

The onset of neoplastic state is
difficult to date (asymptomatic).
Seven Danger Signals of Cancer
(Direct manifestation):
1. Change in bowel or bladder habits
2. A sore that does not heal
3. Unusual bleeding or discharge
4. Thickening or lump in breast or
elsewhere
5. Indigestion or difficult in swallowing
6. Obvious change in wart or mole
7. Nagging cough or hoarseness
CLINICAL MANIFESTATION:
Indirect or Systemic Manifestation:
1.
Secondary to metastasis

2.
Cachexia
Secondary to none metastatic:
a.
b.
c.
d.
Ectopic production of known hormones
Secretion of unidentified, hormone like
substances
Toxic substances secreted from the
tumor
Autoimmune – host is sensitized to an
antigen from the tumor
CLINICAL MANIFESTATION:
Signs of Expansile growth:
1. Obstruction
2. Destruction
Signs of Infiltrative Growth:

1.
2.
3.
Tumor infiltrates the nerves
Pain
Numbness
paralysis
CLINICAL MANIFESTATION:
Signs of Tumor necrosis (Bleeding &
Infection):



Tumor may become necrotic, ulcerate
and bleed
Fatigue and weakness in right colon
cancer due to anemia
Inflammation caused by cecal CA can
mimic the clinical symptoms of acute
AP or cholecystitis.
Unknown primary tumors prsenting
as metastases
DIAGNOSIS OF CANCER:
A.
Clinical History:

1.
2.
3.
4.
5.
6.
7.
8.
9.
Warning signs for Cancer:
Weight loss
Loss of Appetite
Bleeding or a discharge from any body orifice
or nipple
Sore that is slow to heal
Persistent cough or wheeze
Change in voice
Difficulty of swallowing
Change in bowel habit
Growing lump in the skin, breast, abdomen
or muscle
DIAGNOSIS OF CANCER:
B.
Physical Examination:


C.
Palpable masses (movable, nonmovable)
LN enlargement
Laboratory Examination:


Blood examination
Radiological procedure:

X-ray, esophagoram, Barium enema,
mammography, thyroid scan, CT scan,
MRI
DIAGNOSIS OF CANCER:
C.
Laboratory Examination:


Endoscopy:

Bronchoscopy, esophagoscopy, gastroscopy,
proctosigmoidoscopy, colonoscopy,
cystoscopy
Biopsy:

To document presence of malignancy

Types:
1.
2.
3.
o
Needle biopsy (cytological)
Incisional biopsy
Excisional biopsy
Rapid frozen biopsy / exfoliative cytology
(Pap smear)
STAGING OF CANCER:
A.
Clinical Staging of Cancer:
TNM:
Stage
Stage
Stage
Stage

I = cancer confined to it’s primary site
II = more locally advanced disease
III = metastasis to regional LN
IV = metastasis to distant sites
Use all information available prior to 1st
definitive treatment:
STAGING OF CANCER:
B.
Post-surgical Resection Staging:

C.
Re-treatment Staging:

D.
Pathological Staging:
 The extent of disease using all data available at the
time of surgery and on examination of a completely
resected specimen.
Restaging is necessary for additional or secondary
definitive treatment after a (disease-free) interval
following 1st treatment.
Autopsy Staging;

Used only when the cancer is 1st diagnosed at
autopsy.
CANCER TREATMENT:
Interdisciplinary Approach:
Surgical resection 55% (40% alone)
2. Radiation therapy 34% (16% alone)
3. Chemotherapy 22% (alone or combination)
Surgery & radiation tx represents
treatment of cancers that remains
localized to it’s primary site or regional
LN.
Chemotherapy and Immunotherapy
– tx effective against tumor cells already
metastatic to distant organ sites.
1.


CANCER TREATMENT:
GOALS of Therapy:

Vary w/ extent of the cancer:
1.
Localized w/o evidence of spread:

Eradicate the cancer and cure THE PATIENT
2.
Spread beyond the local site:
 Control patient’s symptoms and to
maintain maximum activity for the
longest possible period of time.
CANCER TREATMENT:
CRITERIA of Incurability:
1. Distant metastasis (most common)
2. Evidence of extensive local infiltration of
adjacent organs or structures


Pt’s general condition and the presence of
any coecisteing disease must be considered
in planning therapy.
The PSYCHOLOGICAL makeup of the patient
and the patient’s life situation must be
considered.
CANCER TREATMENT:
SURGICAL RESECTION:
A. Surgical Curative Resection:

Wide local resection:
 Low grade malignancy
 Basal cell CA of the skin
 Radical Local Resection:
 High grade malignancy
 En Bloc LN dissection for breast,
esophagus, gastric, colorectal CA
B.
Surgical Palliative Resection:
1.
2.
3.
To relieve symptoms
To prolong a useful comfortable life
Gastrojejunostomy, colostomy
CANCER TREATMENT:
RADIOTHERAPY:


Destroy tumor with preservation of
anatomic structures
Direct toxic effect to cells due to
ionization of water
CANCER TREATMENT:
CHEMOTHERAPY:
Antimetabolites:


Inhibit enzymes of nucleic acid synthesis
Methotrexate & 5-FU
Alkylating agents:


Substitute alkyl grp for the hydrogen
atom
Alkylation of DNA molecule interferes
with replication in transcription
CANCER TREATMENT:
CHEMOTHERAPY:
Antibiotics:



From soil fungi
Forms stable complexes with DNA and
inhibit synthesis of DNA and RNA
Actinomycin D, Doxorubicin, Bleomycin
Vinca Alkaloids:


Bind to microtubular proteins necessary
for cell division causing cell death during
mitosis
Vincristine & Vinblastine
CANCER TREATMENT:
IMMUNOTHERAPY:



Inhibit proliferation of cancer cells w/o
affecting function of normal cells
Stimulates the host to generate specific
immune response to its tumor-vaccine from
tumor cells
TUMOR SPECIFIC ANTISERUM:



Murine monoclonal antibodies
Immunotoxins
None-specific immunotherapy=BCG vaccine
PROGNOSIS:
DETERMINANTS:





Site of origin of primary tumor
Stage of the disease
Histologic features of the cancer
Host immune factors
Age of the patients