Pancreas

Acute Pancreatitis

  • common disease
  • both sexes; 5th and 6th decades

Classification

  • acute interstitial pancreatitis
  • Acute hemorrhagic pancreatitis

Pathogenesis

  • Caused by pancreatic enzyme release that results in enzymatic autodigestion
  • Theory

Ø  functional or structural duct obstruction coincides with active pancreatic secretion

Ø  small ducts dilate

Ø  disruption of small intralobular ducts

Ø  enzymatic auto digestion

  • Necrosis occurs as a result of the auto-digestion by the enzymes

Ø  Proteases

  • Trypsinogen
  • Chymotrypsin

Ø  Lipase and Phospholipase

  • degrade lipids and membrane phospholipids
  • soap deposits occurs when the fatty acids combine with the cations of the extracellular fluid – fat necrosis

Ø  Elastase

  • digests elastic fibers in vessel wall – hemorrhage
  • prevents dissipation of the enzymes or dilution of the enzymes by the inflammatory edema

Ø  Amylase

  • USEFUL IN LABS

Predisposing Factors

  • chronic alcoholism

Ø  often follows a binge

Ø  most frequent in young men; 3:1 Men:women

Ø  direct chemical irritation of the duodenum results in spasm of the sphincter of oddi which leads to indirect stimulation of pancreatic secretion

  • gallstones

Ø  5x more frequent in patients with pancreatitis

Ø  present in ½ of the cases of acute pancreatitis

Ø  more frequent in women, older persons, and in people with small stones

Ø  structural or functional obstruction of pancreatic duct

  • drugs, trauma, metabolic abnormalities

Pathology

Acute Interstitial pancreatitis

  • Gross

Ø  head of pancreas enlarged, firm, pale, and edematous

Ø  small foci of fat necrosis

  • MICRO

Ø  interstitial edema and leukocytes

Ø  small foci of necrotic pancreas or fat

  • can have peritonitis

Acute hemorrhagic pancreatitis

  • GROSS

Ø  part or all of the pancreas is enlarged

Ø  pulpy grayish yellow mass with foci of blood

Ø  many foci of fat necrosis

  • MICRO

Ø  extensive liquefactive necrosis of the pancreas and fat

Ø  necrotic vessels with hemorrhage

Ø  not very many inflammatory cells

  • Can have peritonitis

Complications

  • Pseudocyst of the pancreas

Clinical Features

Acute Interstitial Pancreatitis

  • sudden onset of epigastric pain – tenderness to deep palpatation
  • Elevated Serum Amylase (Lab marker)
  • Prompt recovery

Acute Hemorrhagic Pancreatitis

  • sudden onset of severe constant agonizing epigastric pain which frequently radiates through to the back and epigastric tenderness
  • nausea, vomiting, shock
  • Elevated serum amylase occurs in hours
  • Serum Lipase rises later and persists 10 days
  • Jaundice may occur
  • 50% mortality

Chronic (Relapsing) Pancreatitis

  • results from multiple mild attacks of acute pancreatitis – scarring occurs each time
  • chronic alcohol abuse indicated in most cases
  • Men > women

Pathology

  • GROSS

Ø  when acute: usual changes of acute pancreatitis

Ø  between acute attacks: pancreas is small, hard, calcareous, ducts become dilated and contain thick fluid of Ca(CO3) stones

  • MICRO

Ø  Extensive fibrosis

Ø  Atrophy and loss of acini and islets of Langerhans

Ø  Chronic inflammatory infiltrate

Ø  Dilated ducts and occasional foci of suppuration

Clinical Features

  • Early Stage

Ø  marked by intermittent or chronic steady, boring, dull or sharp pain

Ø  often has nausea and vomiting

  • Late stage

Ø  characterized by the symptoms of pancreatic insufficiency

Ø  Ex. Steatorrhea, 2o Diabetes mellitus

Ø  Painful seizures

  • TERMINAL EVENT is often attack of acute pancreatic necrosis

Carcinoma of the Pancreas

General

  • 5th most common cause of death from carcinoma in the US (after lung, bowel, breast, and prostate)
  • usually implies a carcinoma of the exocrine pancreas derived from the epithelium of the pancreatic duct
  • Men:Women = 2:1
  • 6th and 7th decade
  • cigarette smokers – 2-2.5 times greater incidence than in non-smokers
  • Classification is as carcinoma of the head or of the body and the tail.

Pathology

  • GROSS

Ø  poorly defined nodular mass

Ø  can extend into adjacent tissues or organs

Ø  gray-white, hard or scirrhous tissue replaces the normal lobules

  • MICRO

Ø  adenocarcinoma embedded in the dense fibrous stroma

Ø  lymphatic and blood vessel penetration is frequent

Carcinoma of the Head of the Pancreas

  • bile duct involvement occurs quickly
  • obstruction of the bile duct and jaundice occur early
  • changes occur in the distal pancreas due to the bile duct obstruction
  • Hepatobiliary dysfunction kills before the tumor becomes widely disseminated
  • Usually spreads to regional lymph nodes (70%) and liver (50%); may invade duodenum
  • CLINICAL FEATURES TO MAKE IT STAND OUT: abdominal pain and obstructive jaundice
  • Usually does not metastasize to the peritoneum

Carcinoma of the Body and Tail of the Pancreas

  • metastases more frequent, massive, and more widespread
  • Peritoneal metastases common (75%); Lymph node (90%) and Liver (85%)
  • Clinical Features

Ø  Abdominal pain in the epigastrium and left upper abdominal quadrant

Ø  Worse at noght and in supine position

Ø  Depression, rapid weight loss, anorexia, and ascites are common

Ø  Trousseau’s sign – migratory thrombophlebitis

Ø  Diagnosis – fine needle biopsy

Ø  Death in an average of 6 months from onset of symptoms

Islet Cell Tumors

  • rare compared to tumors of the exocrine pancreas
  • adults
  • may be single, multiple, benign, or malignant.

Ø  Insulinoma (Beta-cell tumor) – THE MOST COMMON ISLET CELL TUMOR

Ø  Gastrin-Zollinger-Ellison Syndrome – endocrine tumor producing gastrin with resultant gastric hypersecretion and recalcitrant peptic ulcer disease

Ø  MENs (Multiple Endocrine Neoplasia Syndromes)

I.                 MEN I (Werner syndrome) – Parathyroids, pituitary, adrenals, pancreatic isles, and thyroid; peptic ulceration occurs.

II.               MEN II (Sipple’s syndrome) – pheochromacytomas, thyroid (medullary CA), parathyroid, NOT PANCREAS OR PEPTIC ULCERATION

Gallbladder

Cholelithiasis: stones in the gallbladder or extra-hepatic biliary tree

  • very common; can be symptomatic or asymptomatic
  • adults; women > men; whites > blacks

Classification of Stones

  • based upon composition
  • in industrialized countries, ¾ of all gallstones consist 1o of cholesterol

Cholesterol Stones

  • women have a 3x greater risk of developing cholesterol stones
  • pure cholesterol stones are uncommon
  • Mixed cholesterol stones

Ø  MOST COMMON TYPE OF ALL GALLSTONES

Ø  Consist of: cholesterol, bile pigment, calcium, and protein

Ø  Multiple stones

Calcium pigment stones

  • black or crown
  • pure ones uncommon
  • Compocition: Ca and bile pigments, brown stones have some sholesterol
  • Gallbladder usu normal
  • Multiple, small, irregularly shapes, hard, brittle
  • Black stone are harder

Normal gallbladder function

  • place where bile is concentrated and acidified
  • inorganic salts and H2O are reabsorbed which concentrates the large organic solute, esp. cholesterol
  • Cholesterol maintained in solution stored in mixed micelles

Etiology and Pathogenesis of Gallstones

Cholesterol Stones

  • Supersaturation of bile with cholesterol

Ø  can result from increased production of cholesterol of a decrease of bile salts or phospholipids

Ø  required but not sufficient alone

Ø  7 alpha-hydroxylas deficiency

Ø  obese people have enhances cholesterol secretion

  • Nidus or Nucleation

Ø  mucinous glycoproteins secreted by the gallbladder epithelium provide the nidus

Ø  may have a deficiency of anti-nucleating factor.

  • Growth by accretion
  • Risk factors for increased cholesterol secretion

Ø  increasing age

Ø  obesity

Ø  certain ethnic groups

Ø  familial

Ø  high calorie and high cholesterol diets

Ø  metabolic abnormalities

Pigment stones (black or brown)

  • increased conc. Of bilirubin in the bile precipitates as Calcium bilirubinate
  • BLACK STONES

Ø  old and undernourished people

Ø  chronic hemolysis

Ø  cirrhosis

Ø  no known predisposing cause in most patients

  • BROWN STONES

Ø  found more frequently in intrahepatic and extrahepatic bile ducts than in gallbladder

Ø  bacterial cholangitis associated with these almost always

Ø  increased unconjugated bilirubin in the bile

Effects of Gallstones

  • Irritation
  • Obstruction of the biliary duct
  • Cystic duct

Ø  dilatation of BG—intense RUQ pain occurs

  • Common bile duct

Ø  may pass into the intestine or obstruct

Ø  Effects of common bile duct obstruction

  • biliary colic
  • obstructive jaundice
  • ascending cholangitis
  • biliary cirrhosis
  • acute pancreatitis or fibrosis of ampulla with persistent obstruction
  • Biliary fistula

Symptoms of Gallstones

  • most are asymptomatic
  • symptoms occur from irritation or obstruction
  • Distension of Gallbladder

Ø  pain

Ø  reflex disturbances

  • Obstruction of common bile duct – obstructive jaundice

Acute cholecystitis

  • less common than chronic; usually superimposed on chronic

Etiology

1)     cystic duct obstruction

2)     distension of GB with compression of BVs

3)     impaired blood flow and bile action causes mucosal injury

4)     2o bacterial infection due to the obstruction

Pathology

  • GROSS

Ø  distended GB with congested serosa and a fibrinous exudate

Ø  Gallstones almost always present

Ø  Edema and congestion of the wall of the gallbladder with foci of hemorrhage and ulceration of mucosa

Ø  Gangrene may occur

Ø  Hydrops or Empyema of the GB may occur if obstruction persists

  • MICRO

Ø  congestion, edema, and hemorrhage, modest neutrophils

Ø  chronic changes present

Ø  extensive necrosis and inflammation

  • Clinical Features of Acute cholecystitis

Ø  Severe biliary colic (pain in RUQ)

Ø  Tenderness and rigidity of the RUQ

Ø  Fever and leukocytosis

Ø  Palpable GB

Chronic cholecystitis

Etiology

  • chronic mechanical and chemical irritation by stones
  • repeated attacks of acute can also cause

Pathology

  • GROSS

Ø  thickened wall and firm with fibrous peritoneal adhesions

Ø  stones almost always present

Ø  atrophic mucosa or it is rigid and pitted

Ø  dilated cystic duct

  • MICRO

Ø  atrophic mucosa

Ø  fibrotic wall with chronic inflammation in all layers

Ø  “Rokitansky-Aschoff sinuses”

Ø  calcified wall in long standing cases

Symptoms

  • chronic indigestion with episodes of biliary colic
  • pain sometimes referred to the right subscapular region
  • large fatty meals aggrevate symptoms

Treatment of Cholelithiasis

  • cholecystectomy if symptomatic
  • exploration of common bile duct also
  • shock wave lithotripsy &/or litholytic drugs

Carcinoma of the Gallbladder

ADENOCARCINOMA is the most common tumor of the GB (90%)

  • usually associated with cholelithiasis and chronic cholecystitis
  • more common in women than in men
  • almost always incurable by time of discovery

Clinical features

  • symptomatic cholelithiasis for a number of years
  • dull RUQ pain, palpable mass, hepatomegaly, weight loss, jaundice
  • extensive local spread and early metastases

Pathology

  • GROSS

Ø  large mass of hard gray-white, thickens the wall or forms a bulky mass

Ø  liver infiltration occurs

  • Spread

Ø  liver and along ducts almost always

Ø  regional lymph nodes and liver and peritoneum

Carcinoma of the Extrahepatic Bile

  • men more than women
  • uncommon
  • unknown cause

Pathology

  • Sites of predilection

Ø  distal bile duct with ampulla of Vater

Ø  common bile duct

Ø  hepatic duct

Ø  confluence of hepatic ducts with common bile duct (Klatskin tumor)

  • GROSS

Ø  periampullary tumors are soft and papillary

Ø  others are hard and infiltrative

Ø  Local spread and metastases like the GB

  • MICRO

Ø  most are adenocarcinomas

Clinical Features

  • Obstructive Jaundice
  • Upper abdominal pian, hepatomegaly, and palpable GB may be present
  • Most are incurable by time of presentation

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