Categories: Pathology

PANCREAS, Its Acute and Chronic Disorders

PANCREAS

INTRODUCTION

The pancreas is a gland organ. It is located in the abdomen. It is part of the digestive system and produces insulin and other important enzymes and hormones that help break down foods.

  • Its name has been driven from the Greek word

“Pankreas” meaning (all flesh) • It has an endocrine and exocrine function.

  • Pancreas is a transversely oriented retroperitoneal organ extending from the “C” loop of the duodenum to the hilum of the spleen.
  • It is 20cm in length weighting 85 to 90gm.
  • Pancreas has a body and a tail.
  • The main pancreatic duct is known as the duct of wirsung.
  • Which drain into the duodenum at the papilla of vater.
  • Its accessory pancreatic duct is known as the duct of Santorini.
  • Embryologically it arises from the fusion of dorsal and ventral outpouchings of the foregut.
  • The endocrine portion is composed of about one million clusters of cells, the islets of Langerhans which secrete…
  1. Insulin.
  2. Glucagon.
  3. Somatostatin
  • The exocrine part is composed of acinar cells that produce enzymes for digestion.
  1. ▫ Amylase
  2. Lipase & some proenzymes (Trypsinogen, Chymotrypsinogen, Proelastase etc…)

NORMAL PANCREAS

PATHOLOGICAL LESIONS OF PANCREAS

EXCOCRINE PART OF PANCREAS

A) Inflammatory

  1. Acute pancreatitis
  2. Chronic pancreatitis

B) Neoplasm

  1. Benign

  • Serous cystadenoma
  • Mucinous cystadenoma
  • Intraductal papillary mucinous neoplasms (IPMNs)
  1. Malignant

  • Serous cystadenocarcinoma
  • Mucinous cystadenocarcinoma
  • Infiltrating ductal adenocarcinoma

C) Cysts

  1. A non-neoplastic cyst (pseudocyst)
  2. Congenital cyst

D)ENDOCRINE PART OF PANCREAS

Non-tumors lesions

  • Diabetes Mellitus  (DM)

Endocrine neoplasm (Tumours lesions)

  • Insulinoma (hyperinsulinism)
  • Gastrinoma (Zollinger Ellison syndrome)
  • Other rares
  1. α –cell tumors (glucagonoma)
  2. δ –cell tumors somatostatinomas)
  3. VIPomas

ACUTE PANCREATITIS

DEFINITION:-

  • An acute pancreatitis is a group of reversible lesions characterized by inflammation of the pancreas ranging in severity from edema and fat necrosis to parenchymal necrosis with severe hemorrhage.

ETIOLOGIC FACTORS:-

Metabolic

  1. Alcoholism
  2. Hyperlipoproteinemia
  3. Hypercalcemia
  4. Drugs (e.g. thiazide diuretics)
  5. Genetic

Mechanical

  1. Trauma
  2. Gallstones
  3. Iatrogenic injury
  • Preoperative injury
  • Endoscopic procedures with dye injection

Vascular

  1. Shock
  2. Atheroembolism
  3. Polyarteritis nodosa

Infectious

  1. Coxsackievirus
  2. Mycoplasma pneumonia

LESS COMMON CAUSES OF ACUTE PANCREATITIS

  • Obstruction of the pancreatitis duct.
  • Inherited alterations genes including germline mutations.
  • 10% to 20% unknown (Idiopathic)

PATHOGENESIS

  • Autodigestion of the pancreatic by inappropriate activated pancreatic enzymes leading to inflammation small vessel thrombosis resulting in activation of trypsinogen which is an important triggering event in acute pancreatitis.
  • Pancreatic duct obstruction leading to leakage of lipase causing focal fat necrosis resulting in periacinar inflammatory reaction.
  • Primary acinar cell injury.
  • Defective intracellular transport of proenzyme.

PROPOSED PATHWAY IN PATHOGENESIS

MORPHOLOGY

  • Microvascular leakage causing edema.
  • Necrosis of fat by lipolytic enzymes.
  • Acute inflammatory reaction.
  • Proteolytic destruction of pancreatic parenchyma.
  • Destruction of blood vessels with subsequent interstitial hemorrhage.

In severe cases…

  • Acute necrotizing pancreatitis a fact acinar and ductal tissue as well as islets of Langerhans leading to…

▫ Red black hemorrhage with chalky fat necrosis found in the omentum and the mesentery resulting in

Hemorrhagic pancreatitis

CLINICAL FEATURES

  • Medical emergency presenting severe abdominal pain (Acute Abdomen)
  • Systemic effects.
  1. Leukocytosis
  2. Hemolysis
  3. Disseminated intravascular coagulation (DIC)
  4. Dehydration
  5. Acute respiratory syndrome
  6. Diffuse fat necrosis
  7. Vascular collapse leading to shock with acute renal tubular necrosis.

LAB. DIAGNOSIS

  • Elevation of serum amylase within 1st 24 hours.
  • Increased serum lipase level within 72 hours.
  • Hypocalcemia resulting from precipitation of calcium sops in fat necrosis.

Radiological diagnosis:-

  • Direct visualization of the enlarged inflamed pancreas by ultrasound and CT.

ACUTE PANCREATITIS GROSS

ACUTE PANCREATITIS MICROSCOPIC

PANCREATIC PSEUDOCYST, GROSS

CHRONIC PANCREATITIS

DEFINITION:-

  • Inflammation of pancreas with the destruction of exocrine parenchyma, fibrosis & destruction of endocrine parenchyma.

ETIOLOGY:-

  • Long term alcohol abuse is usually seen in middle age males.
  • Less common causes

▫ Long-standing obstruction of the pancreatic duct by pseudocysts, calculi, trauma, neoplasms.

▫ Tropical pancreatitis is seen in Africa & Asia due to malnutrition.

▫ Hereditary pancreatic & idiopathic

PATHOGENESIS

  • Ductal obstruction by concretions due to high level of protein needs to ductal which may calcify & form calculi which obstructs the pancreatic duct.
  • Toxic metabolic toxins including alcohol exert a direct toxic effect on acinar cells leading to the accumulation of lipids resulting in fibrosis of acinar cells.
  • Oxidative stress promotes the fusion of lysosomes & zymogen granules, acinar cell necrosis, inflammation & fibrosis.
  • Necrosis-fibrosis repeated episodes of acute pancreatitis need for chronic pancreatitis.

COMPARISON OF SEQUELAE OF ACUTE AND CHRONIC PANCREATITIS

MORPHOLOGY

  • Paranchymical fibrosis sparing islets of Langerhans.
  • Dilation of pancreatic duct grossly gland is hard & some time calcified.
  • Microscopically interlobular and interlobular ducts are dilated and contain protein plugs.
  • Ductal epithelial may be atrophied or hyperplastic or may show squamous metaplasia.

CLINICAL FEATURES

  • Moderate to severe abdominal pains.
  • Back pain.
  • Diabetes militias due to pancreatic insufficiency.
  • Attack of jaundice.
  • Vague attack of indigestion.

LAB. DIAGNOSIS:-

  • Increase the level of serum amylase
  • Low level of albumin.
  • Increase level serum bilirubin.

CHRONIC PANCREATITIS

SEROUS CYST ADENOMA

MUCINOUS CYST ADENOMA

PANCREATIC CARCINOMA

(Infiltrating Ductal Adenocarcinomas)

  • 4th leading cause of cancer death in the USA. • The highest mortality rate of any cancer
  • 5-year survival rate is < 5%.

Precursors pancreatic cancer:-

  • Progression in pancreas from non-neoplastic epithelium to histologically well-defined noninvasive lesions in small ducts and ductules to invasive carcinoma (pancreatic intraepithelial neoplasias “PanINs”)
  • PanINs are found in pancreatic parenchyma adjacent to infiltrating carcinoma

MOLECULAR CARCINOGENESIS

  • It is a genetic disease (disease of inherited & acquired mutations in cancer-associated genes)
  • K-RAS gene (chromosome 12p) is the most frequently altered oncogene in pancreatic cancer

(80% to 90%)

  • P16 gene (chromosome 9p) is the most frequently inactivated tumor suppressor gene

(> 90%)

  • Inactivation of P53 tumor suppressor gene (chromosome 17p) is seen in 50% – 70% of patients.
  • SMAD4 is inactivated in 55% of pancreatic CA.
  • Other genes.

▫ AKT2 (10% – 20%). MYB gene (6q) in 10%

▫ BRCA2, AIB1, MKK4, TGFβ-R1, TGFβ-R2.

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ETIOPATHOGENESIS

  • The disease of elderly people usually seen between the ages of 60 to 80.
  • More common in blacks as compared to white.
  • Environmental influence (smoking) is believed to be double the risk of pancreatic carcinoma.
  • Fat rich diet is another contributed factor.
  • Chronic pancreatitis with a history of smoking and alcohol has a strong association with carcinoma.
  • Minor factor includes diabetes mellitus, familial clustering & number of inherited genetic syndromes.

MORPHOLOGY

  • 60% of cancer arises from the head of the gland.
  • 15% form body & 5% form tail.
  • 20% involving the entire gland.
  • The majority of the pancreatic carcinoma is ductal adenocarcinoma having a feature of …
  1. Gland formation
  2. mucin secretion
  3. Peripancreatic tissue invasion.
  4. Intense non-neoplastic host reaction comprising of fibroblast, lymphocytes & extracellular matrix (desmoplastic response)

▫ Mostly there is obstruction of common bile duct leading to distention of biliary tree.

▫ Locally invade to spleen, adrenals vertebral column, transverse colon  & stomach.

▫ Peripancreatic, gastric, mesenteric, omental, & porta hepatic lymph nodes are involved.

▫ Distant metastatic involve lungs & bones.

Microscopy:-

  • moderately to poorly differentiated adenocarcinoma reveal.
  1. Abortive tubular structures
  2. Cell cluster and aggressive infiltrating growth
  3. Lymphatic invasion is also seen
  4. Malignant glands are atypical, irregular, small & bizarre-looking lined by anaplastic epithelial cells.
  5. Rare variants are…
  6. Acinar cell carcinoma, adenosquamous carcinoma & undifferentiated carcinoma with osteoclast-like giant cells.

ADENOCARCINOMA GROSS

ADENOCARCINOMA MICROSCOPIC

CLINICAL FEATURES

  • Obstructive jaundice in most of the cases.
  • Weight loss, anorexia & generalized malaise
  • Migratory thrombophlebitis (Trousseau sign) in 10% cases due to the elaboration of platelet aggregating factors & procoagulant form the tumor are its necrotic products.
  • < 20% pancreatic cancer is resectable at the time of diagnosis.
  • Endoscopic ultrasonography & CT have great importance in diagnosis & performance of percutaneous needle biopsy.

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