PANCREATIC CANCER

Submitted to:
Murphy G. French, PTRP

Date:
May 13, 2010

Submitted by:
Christopher Bebanco
Frances Anne Cabanacan
BSPT-3A
ANATOMY AND PHYSIOLOGY

 The pancreas is a racemose gland located in the retro-peritoneum. It is

approximately 15cm in length and 2 to 3cm thickness, and it weighs about 90g.
The pancreas is divided into a head, body and tail. The head is position over the
vena cava and is lodged within the first three portion of the duodenum. The body
and tail occupy a position slightly above and behind the head, extending
transversely behind the stomach to almost touch the spleen.

 Both endocrine and exocrine functions are vested in the pancreas. Secretory
cells, called acini, line the multiple small alveoli that together form the lobules of
the exocrine pancreas. The lobules contain small ducts to receive secretions
from the alveoli. These small ducts empty pancreatic secretions into the
Wirsung’s canal, which runs from the tail to the head and empties into the
duodenum. A branch of the main duct, the duct of Santorini, is in the upper half of
the head and empties into the duodenum.

 Each day, 300 to 800 mL of pancreatic juice is secreted directly into the
duodenum. The major exocrine components are electrolytes and the digestive
enzymes trypsin, amylase, and lipase. These enzymes are responsible for the
hydrolysis of protein, starch, glycogen, and fats. Endocrine products of insulin,
gastrin, and glucagon are released directly into the blood stream. Most endocrine
tissue is contained in the tail and distal body of the pancreas.

DEFINITION

 Malignancy of the pancreas

 Called “SILENT DISEASE”

 Fifth of the most fatal cancer

How Pancreatic cancer develop?

 Cells in the pancreas acquires damage to its DNA

 Single cancer cell mutate and divides rapidly. Become a tumor

 Cells from the tumor travel elsewhere in the body through blood or lymphatic
system

Stages of Pancreatic cancer

 Stage 0: no spread

- pancreatic cancer is limited to a single layer of cells in the pancreas.

 Stage 1: Local growth

- PC is limited to pancreas

Stage 1A- PC has grown to be less than 2 cm.

Stage 1B- Greater than 2 cm.

 Stage 2: Local spread

- PC ha grown outside the pancreas

  Stage 3: Wider spread

- tumor has expanded into nearby major blood vessels or nerve, but PC
can’t be seen in other organs.

 Stage 4: Confirmed spread

- PC is found in distant organs.

ETIOLOGY

 Exact cause remain unclear

 Low socioeconomic groups

 Cigarette smoking

 Presence of Chronic disease state

-- Diabetes mellitus

-- Chronic pancreatitis

-- Prior cholecystectomy

 Occupational Exposure

-- DDT

-- benzidine

-- dry cleaning agents

-- polychlorinated biphenyls (PCBs)

-- beta- napthtylamine

 Advanced Age

 Male gender

 Genetics

 Family history of pancreatic cancer

 Familial syndromes

 BRCA1 and BRCA2 mutations

 Familial atypical multiple mole melanoma syndrome (FAMMM)

 Hereditary pancreatitis syndrome

 Epidemiology

 It occurs in all ages

 Race and ethnicity

 Male to female ratio is 1:1.5

Clinical Manifestation
  Cancer of the pancreas has an insidious onset. In nine of ten individuals, cure is
impossible by the time cancer is discovered. The early signs and symptoms are
vague and often referred to other or organs and systems. Careful assessment
and extensive inquiry into the character, onset, duration, and modulators of
presenting signs and symptoms will greatly aid definitive diagnosis.
Manifestations of disease differ according to the location of the tumor in the
pancreas.

Signs and symptoms/clinical manifestation

 Head of the pancreas

 Pain in epigastric region

 Profound weight loss

 Progressive jaundice

 Body of pancreas

 Excruciating pain

 Vomiting

 Tumor

 Tail of pancreas

 Generalize weakness

 Gripping upper abdominal

 Vague digestion

 Anorexia

 Unexplained weight loss

 Carcinoma production

PATHOPHYSIOLOGY

 Pancreatic cancer arise fronmexocrine and endocrine portions of the pancreas

Ductal Adenocarcinoma

- pancreatic tumor arise from exocrine cell in the ducts

 75% of PC occur in the head or neck of the pancreas

-- produce obstruction of both pancreatic and common bile duct. Causes JAUNDICE

-- obstruction of the superior mesentery and portal vein. Produce

GASTROESOPHAGEAL VARICES AND CLINICAL HEMORRHAGE.

-- Invade the duodenum. Produce Ulceration and duodenal obstruction.

 15-20% occur in the body of the pancreas

 5-10% occur in the tail

-- tumors in body and tail in pancreas can lead to splenic venous occlusion.
  Tumors in the peritoneal surface can obstruct veins and may result to Ascites.

 PC first metastasize to regional lymph nodes, then to liver, less commonly to the
lungs.

 Directly invade the duodenum, stomach and colon.

 Metastasize in the surface in the abdominal cavity via peritoneal spread,

adrenals, bone, brain and skin.

Apudomas

- Tumors in endocrine pancreas, rare neoplasm of the islet of langerhans.

- “Apud” acronym fpr amine precursor and uptake and decarboxylation.

- Contains neurosecretory granules.

- Endocrine neoplasms are fatal because they secrete abnormal amounts of

hormones, such as insulin.

PROGNOSIS

 Extremely poor prognosis

 90% of patient with untreated carcinomas of pancreas die within a year of the
time the diagnosis is made

 Resectable cases also have poor prognosis

 Presence of jaundice (survival time from 2 to 4 ½ months)

 Combination of radiotherapy and chemotherapy (survival time from 6 to 10

months)

Cause of illness is often short (in a series)

- Half lived 10 ½ months from the first symptom

- 6 months from the time of diagnosis

- Half being dead within 3 ½ months

American Joint Committee (AJC), using Tumor-Node-Metastasis (TNM) in 1 year

survival rate

 33% for stage 1

 15% for stage 2

 11% for stage 3

 Overall % year survival rate is less than 5%

Treatment

 Surgery

 Total pancreactectomy

 Pancreatoduodenectomy
  Regional pancreatectomy

 Distal pancreatectomy

 Palliative surgical procedures

 Postoperative care

 Chemotherapy

 Radio therapy

 Suppportive therapy

REFERENCES

 Adams J., Paulter C., Paudya K., (1983), Clinical oncology: a multidisciplinary
approach. American Cancer Society.

 Sir Ronald Bodley Scott, Cancer the Facts(1979). Great Brittain. R. Clay and Co.
Ltd. Bungay

 DeVita V. Jr., Hellman S., Roseberry S., Cancer: Principles and Practice of
Oncology, Vol.1, 2nd Edition. (1985) J>B Lippincott Company

 Groenwald S., Frogge M., Goodmann M., Yarbro C. Cancer Nursing: princilples
and practice. Second edition(1990).Jones and Barlett Publishers