Normal esophageal mucosa appears white to tan

Esophageal mucosa is lined by non-keratinized stratified squamous epithelium
Gastric mucosa is lined by columnar glandular epithelium
Selected disorders of the esophagus
Motor disorders: Achalasia
Mechanical injury: Lacerations (Mallory-Weiss syndrome)
Esophagitis: Reflux, infections, drugs, irradiation
Barrett’s esophagus
Malignant neoplasms

Achalasia (failure to relax)
Incomplete relaxation of lower sphincter during swallowing leading to functional obstruction and proximal dilatation
Aperistalsis, incomplete relaxation, increased resting tone
Ganglion cells of the myenteric plexus are diminished or absent
Clinical picture: dysphagia, regurgitation and aspiration
Histology: Inflammation in the area of M. plexus
Hypotheses: autoimmune, viral infections
May occur secondary to Trypanosoma cruzi infection (Chagas disease)
5% develop squamous cell carcinoma, at younger age

Esophageal lacerations (Mallory- Weiss syndrome)
Longitudinal tears at the gastroesophageal junction
Clinical setting: chronic alcoholics after a bout of severe vomiting
Tear may be superficial or deep affecting all layers
Clinical picture: Pain, bleeding, superimposed infection
Hiatal hernia is found in 75% of patients
Most often bleeding stops w/o intervention, but life-threatening hematemesis may occur.
Supportive therapy and balloon tamponade. Healing is prompt with minimal or no residue
Hiatal hernia
Reflux esophagitis
Crohn disease, acute graft versus host disease
Prolonged gastric intubation
Ingestion of irritant substance
Chemotherapy and irradiation
Reflux esophagitis
Reflux of gastric contents into esophagus
Possible etiologies: inadequate function of lower sphincter; sliding hiatal hernia
CP: “heart burn”
Complications: ulceration, bleeding, stricture, Barrett esophagus
Infection-induced esophagitis
More common in patients with impaired immunity
Fungal : Candida
Viruses: Herpes and Cytomegalovirus
Barrett esophagus
A complication of long standing reflux esophagitis
Replacement of squamous epithelium by columnar epithelium with goblet cells
30- to 40-fold greater risk to develop adenocarcinoma
Esophageal varices
Tortuous dilated veins in the submucosa of distal esophagus

Esophageal varices
Etiology: portal hypertension secondary to liver cirrhosis
Asymptomatic until they rupture leading to massive hemorrhage
50% subsides spontaneously
20-30% die during the first episode
Rebleeding occurs in 70% of cases within one year

Esophageal carcinoma
Squamous cell carcinoma
More prevalent worldwide
Risk factors: long-standing esophagitis, achalasia, smoking, alcohol, diet (low vitamins and zinc), genetics
50% in middle 1/3
More common in USA
Occurs on top of Barrett esophagus
More in distal 1/3
1) Cardia
2) Body: Parietal and Chief cells
3) Antrum: Mucin secretion and G-cells that secrete gastrin
Selected disorders of the stomach
Peptic ulcers
Gastric cancer
Chronic Gastritis
Infiltration of the mucosa by chronic inflammatory cells (lymphocytes and plasma cells)
Helicobacter pylori: G-ve bacilli; Noble prize in Medicine 2005, for Barry Marshal & Robin Warren
Autoimmune: rare in USA, autoantibodies to parietal cells (decreased acid and intrinsic factor)
Helicobacter pylori is present in 70-90% of patients with gastric and duodenal ulcers, respectively
Look for intestinal (goblet cell) metaplasia as a precancerous lesion

Helicobacter pylori and associated disorders
Gastritis (chronic and acute), peptic (gastric and duodenal) ulcers
Gastric adenocarcinoma, intestinal type
Gastric lymphoma
Mechanisms of H. pylori-induced pathology
Although the organism is not invasive, it induces intense inflammatory and immune response: cytokines and B-cell activation
Enhances gastric acid secretion
Bacterial products such as urease, lipases and proteases that induce epithelial injury
Acute gastritis “gastropathy”
Injury to the gastric mucosa (erosions) with no significant participation of inflammatory cells
Causes include:
Non-steroidal antiinflammatory drugs
Enterogastric reflux

Peptic ulcer
Location: stomach or first portion of duodenum
Life time risk is 10% in the USA
More frequent in patients with alcoholic cirrhosis, chronic obstructive pulmonary disease, chronic renal failure and hyperparathyroidism.
Causes include: H. pylori and causes of acute gastritis (especially NSAID)
Clinical features: Epigastric pain (worse at night and relieved by food), bleeding (30%) and perforation (5%; accounts for 2/3 of deaths).
Gastric cancer
Risk factors: diet (nitrites, smoked food, increased salt), chronic gastritis (H. pylori), altered anatomy after resection
On top of intestinal metaplasia
Decreasing in incidence
Glandular morphology
Undefined risk factors
( no known relation to H. pylori)
Signet cell morphology

Small and large bowel
Developmental: Meckel diverticulum
Diarrheal disease:
Infections: viruses, bacteria, protozoa
Idiopathic inflammatory bowel disease
Diverticular disease
Types and causes of diarrheal illness
Secretory diarrhea: loss of intestinal fluid that is isotonic with plasma and persists during fasting
Viruses: rotavirus: destroy the absorptive surface children 6-24 M of age, 130 million cases per year, fecal oral mode of transmission.
Toxin-mediated: Vibrio cholera, E.coli (need time)
Preformed toxin: Stapylococcus aureus (immediate effect)
Excessive laxatives
Types and causes of diarrheal illness, continued
Osmotic diarrhea: secondary to intraluminal fluids with high osmolarity; it abates with fasting.
Specific therapies:
Lactulose therapy: used for constipation and hepatic encephalopathy
Gut lavage before endoscopy
Types and causes of diarrheal illness, continued
Exudative diarrhea: pruluent bloody stool (inflammation of the mucosa and/or hemorrhage)
Infections causing tissue damage: Shigella, Salmonella, Entamoeba histolytica
Infections causing both tissue damage and toxins: Clostridium difficile; with antibiotic therapy, leading to pseudomembranous colitis
Idiopathic inflammatory bowel disease

Entamoeba histolytica: Invasive, amebic colitis and amebic liver abscesses
Giardia lamblia: noninvasive, duodenum and jejunum, diarrhea and malabsorption
Cryptosporidium: self-limited diarrhea in immunocompetent individuals; long course in AIDS patients
Worms: uncommon in USA
Types and causes of diarrheal illness, continued
Exudative diarrhea: pruluent bloody stool (inflammation of the mucosa and/or hemorrhage)
Infections causing tissue damage: Shigella, Salmonella, Entamoeba histolytica
Infections causing both tissue damage and toxins: Clostridium difficile; with antibiotic therapy, leading to pseudomembranous colitis
Idiopathic inflammatory bowel disease
Pseudomembranous colitis
Membranes made of neutrophils and fibrin
Seen in Cl. Difficile infection and in ischemia
Types and causes of diarrheal illness, continued
Exudative diarrhea: pruluent bloody stool (inflammation of the mucosa and/or hemorrhage)
Infections causing tissue damage: Shigella, Salmonella, Entamoeba histolytica
Infections causing both tissue damage and toxins: Clostridium difficile; with antibiotic therapy, leading to pseudomembranous colitis
Idiopathic inflammatory bowel disease

Idiopathic inflammatory bowel disease
Crohn disease
Small bowel and colon (mostly right side)
Patchy involvement
Transmural inflammation, fistulas, strictures, serositis
Non-caseating granulomas
Poor response to surgery
Increased risk for cancer

Ulcerative colitis
Colon only
Continuous involvement
Superficial inflammation
No granulomas
Good response to surgery
Increased risk for cancer
Types and causes of diarrheal illness, continued
Malabsorption diarrhea (steatorrhea): voluminous bulky stool with increased osmolarity resulting from unabsorbed nutrients and excess fat; usually abates on fasting.
Malabsorption syndromes
Malabsorption syndromes
Defective intraluminal digestion:
pancreatic insufficiency
Defective bile secretion
Mucosal abnormalities:
Disaccharide deficiency (lactose intolerance)
Reduced surface area
Gluten-sensitive enteropathy (Celiac disease)
Surgical resection
Infections: Tropical sprue, whipple disease
Selected malabsorption syndromes
Gluten-sensitive enteropathy (celiac disease): 1:300 persons are affected, hypersensitivity to gliadin, a component of gluten (present in wheat flour) leading to blunted villi and increased intraepithelial lymphocytes. Increased risk for lymphoma.
Tropical sprue: malabsorption and diarrhea after a visit to the tropics. Infectious etiology, responds to antibiotics.
Whipple disease: systemic disease that affects GIT, nervous system and joints. Caused by T. whippelii (gram-positive actinomycete).

Clinical features of malabsorption syndromes
Hematopietic system:
Anemia: iron, folate and B12 deficiency
Bleeding: vitamin K deficiency
Musculoskeletal system:
Osteopenia: calcium and vitamin D deficiency
Endocrine system:
Amenorrhea, impotence, infertility
Purpura: vitamin K deficiency
Dermatitis: vitamin A deficiency
Nervous system:
Peripheral neuropathy: folate and B12 deficiency.

Meckel diverticulum
A blind pouch located in distal small bowel
The most common congenital anomaly of the small intestine; results from failure of the involution of the omphalomesenteric (vitelline) duct
The rule of 2’s:
2% of the population, 2 inches in length, 2 feet proximal to the ileocecal valve, 2 types of heterotopic tissue (pancreas and stomach); 2% are symptomatic.
Symptoms are rare:
Overgrowth of bacteria that depletes vitamin B12 leading to anemia
“Peptic” ulcer and bleeding
Herniation of the mucosa and submucosa through the muscle wall
50% after age 50
Related to low-fiber diet, increased intraluminal pressure and focal defects in muscular layer
Mostly in sigmoid colon
Asymptomatic unless infected
Tumors of the large bowel
Hyperplastic polyps: not precancerous
Adenomatous polyps: precancerous
Familial polyposis syndrome: Autosomal dominant; 500-2500 polyps, 100% risk for developing cancer; mutations in APC gene

Colonic adenocarcinoma:
Almost always arises from adenomatous polyp
Risk factors: low fiber, high fat, decreased vit A, C, E, idiopathic inflammatory bowel disease, familial adenomatous polyposis
Several hits to different genes: APC, k-ras, p53; or DNA mismatch repair genes
Survival depends on stage (depth of invasion and node metastasis)

Colonic adenocarcinoma
Clinical picture: Asymptomatic or fatigue, weakness and iron deficiency anemia in tumors of right side. Left sided tumors may produce bleeding, change in bowel habits and crampy pain
Colonic adenocarcinoma
Course: tumor invades bowel wall and lymphatics/blood vessels with metastasis to lymph nodes, liver, lungs, and bones. 25% of patients have metastatic disease at presentation
Diagnosis is based on endoscopy and biopsy
Prognosis depends on stage (depth of invasion, nodal and distant metastasis), and 5-year survival varies from >90% in stage I, to 4% with distant metastasis.

A 47-year-old man has a history of drinking 1 to 2 liters of whisky per day for the past 20 years. He has had numerous episodes of nausea and vomiting in the past 5 years. He experiences a bout of prolonged vomiting, followed by massive hematemesis. On physical examination in the emergency room, he has vital signs with T 36.8 C, P 110, RR 22, and BP 80/40 mm Hg. His heart has a regular rate and rhythm with no murmurs and his lungs are clear to auscultation. There is no abdominal tenderness or distension and bowel sounds are present. His stool is negative for occult blood. Which of the following is the most likely diagnosis?
Barrett’s esophagus
Esophageal stricture
Esophageal lacerations (Mallory Weiss syndrome)
Esophageal squamous cell carcinoma

All these statements about Barrett’s esophagus are true, except:
It is associated with 30- to 40-fold greater risk to develop adenocarcinoma
It appears as salmon-pink mucosa on endoscopy
It is associated with high risk for esophageal bleeding
It represents replacement of the stratified squamous epithelium by columnar epithelium with goblet cells
It could be a complication of long-standing reflux esophagitis

All these statement about Helicobacter pylori are correct except:
H. pylori organisms are Gram negative bacilli
It is associated with intestinal-type gastric adenocarcinoma
It is associated with gastric lymphoma
It is associated with diffuse-type gastric adenocarcinoma
It is associated with peptic ulcer

A 20-year-old man has noted cramping abdominal pain for the past week associated with fever and low-volume diarrhea. On physical examination, there is right lower quadrant tenderness. Bowel sounds are present. His stool is positive for occult blood. A colonoscopy reveals mucosal edema and ulceration in the ascending colon, but the transverse and descending portions of the colon are not affected. Which of the following microscopic findings is most likely to be present in biopsies from his colon
Entamoeba histolytica organisms
Non-caseating granulomas

A 35-year-old woman has a 10 year history of intermittent, bloody diarrhea. She has no other major medical problems. On physical examination there are no lesions palpable on digital rectal examination, but a stool sample is positive for occult blood. Colonoscopy reveals a friable, erythematous mucosa with focal ulceration that extends from the rectum to the mid-transverse colon. Biopsies are taken and all reveal mucosal acute and chronic inflammation with crypt distortion, occasional crypt abscesses, and superficial mucosal ulceration. This patient is at risk for development of which of the following conditions?
Acute pancreatitis
Colonic adenocarcinoma
Peri-rectal fistula

A 25-year-old man complains of a low volume but chronic, foul smelling diarrhea for the past year. He has no nausea or vomiting. On physical examination there is no abdominal pain or masses and bowel sounds are present. His stool is negative for occult blood. Laboratory studies include a quantitative stool fat of 10 g/day. Upper GI endoscopy is performed with biopsies of the duodenum. The biopsies reveal the absence of villi, and increased surface intraepithelial lymphocytes. Which of the following therapies is most likely to be useful for this man?
Anti-Entamoeba therapy
Gluten-free diet
Surgical resection
Diseases of the liver
Maintaining body metabolic homeostasis:
Lipid and carbohydrate metabolism: production and secretion of glucose
Protein synthesis: albumin, coagulation factors
Detoxification and drug metabolism
Conjugation and excretion of bilirubin
Synthesis and excretion of bile salts

Liver anatomy and histology
Patterns of hepatic injury
Steatosis: accumulation of fat droplets within hepatocytes
Cell death: those cells closer to the central vein are more susceptible to ischemia, toxins and drugs leading to “centrilobular” necrosis
Fibrosis: Irreversible, affect blood flow and hepatocyte function
Cirrhosis: End stage liver disease with diffuse fibrosis and regenerating nodules

Liver cirrhosis
Definition: bridging fibrous septa and parenchymal nodules with disruption of architecture. End stage for many diseases affecting the liver
Clinical consequences of liver disease (life-threatening complications are in yellow)
Hepatic dysfunction:
Decrease synthesis capacity leading to :
Hypoalbuminemia: edema, ascitis, muscle wasting, weight loss
Hypoglycemia: weakness and syncope
Coagulation factor deficiency: bleeding
Decrease detoxification capacity leading to:
Hyperammonemia and increase toxic metabolites: Encephalopathy (altered behavior and disturbances in consciousness that may lead to deep coma and death)
Injury to other organs by active toxins
Hepatorenal syndrome:
Renal failure without intrinsic or functional causes of renal failure. ? Altered blood flow to the kidney.
Clinical consequences of liver disease, continued
Jaundice: yellow discoloration of skin and sclera due to accumulation of bilirubin
Cholestasis: systemic accumulation of bilirubin in addition to bile salts and cholesterol (usually secondary to obstruction)
Portal hypertension in cirrhosis: increased resistance to portal blood flow
Esophageal varices
Malignancy on top of cirrhosis

Accumulation of bilirubin in tissue leading to yellow discoloration of skin and sclera (icterus)
Normal serum level: 0.3-1.2 mg/dl; jaundice appears with levels above 2.0-2.5 mg/dl
Source of bilirubin: the breakdown of senescent red blood cells in the spleen releases heme that changes into bilirubin by specific enzymes.

Albumin bound
Insoluble in water, toxic
Loosely bound to albumin
Water soluble, non-toxic, excreted in urine
Laboratory evaluation of liver disease
Hepatocyte function:
Serum albumin
Prothrombin time: measuring coagulation factors (II, V, VII, X); prolonged in liver cirrhosis
Serum ammonia
Hepatocyte injury (enzymes normally present inside the hepatocytes and released with injury):
Serum aspartate aminotransferase (AST)
Serum alanine aminotransferase (ALT)
Serum lactate dehydrogenase
Biliary excretory function:
Serum bilirubin
Serum alkaline phosphatase
Serum gamma-glutamyl transpeptidase

Laboratory evaluation of liver disease
Searching for etiology:
Hepatitis viral antigens and antibodies
Autoimmune antibodies: for autoimmune hepatitis
Tissue iron and copper: for hemochromatosis and Wilson disease

Selected disorders of the liver
Viral hepatitis
Drug-induced hepatitis
Autoimmune hepatitis
Alcoholic hepatitis
Wilson disease
Neoplasms of the liver

Hepatitis A virus
RNA virus
Mode of transmission: fecal-oral (contaminated water and food)
Incubation period: 2-6 weeks
Virus shedding: 2-3 weeks before and 1 week after appearance of jaundice
50% of population above age 50 are seropositive in USA, no carrier state
No increase risk for chronic hepatitis, or carcinoma
Because viremia is transient, no need to screen donated blood
Hepatitis B virus
dsDNA virus
Mode of transmission: parenteral (blood products, contaminated needles and IV drug abuse), and body fluids (including saliva)
Incubation period: 4-26 weeks
Carrier state: yes, 350 million carriers around the world
Hepatitis B infection: Possible outcomes
Possible outcomes of infection:
Subclinical or acute hepatitis with recovery and clearance (85%); 1% of those may develop fulminant hepatitis and death
Healthy carriers (10%)
Persistent infection (5%): 80% recover and 20% develop chronic hepatitis
20% of chronic hepatitis patients develop cirrhosis and 10% of those develop hepatocellular carcinoma

Hepatitis C
ssRNA virus
Mode of transmission: parenteral, sexual and vertical, 40% unknown source. It is present in the saliva.
Incubation period: 2-26 weeks
Outcomes of infection:

Hepatitis D
Defective RNA virus that needs Hep B capsule to replicate
Mode of transmission: Parenteral
Coinfection of B and D: mild disease with recovery in most cases, <5% chronic hepatitis
Superinfection by D after B: accelerated more severe hepatitis; 80% chronic hepatitis

Hepatitis E
ssRNA virus
Mode of transmission: waterborne
Incubation period: 2-8 weeks
Endemic in certain populations; 40% in Indian population
Self-limited infection but with higher mortality in pregnant females
The points to remember
Drug-indued hepatitis
Predictable or unpredictable (idiosyncrasy)
Mechanisms: direct toxicity, conversion of drug to an active toxin, immune-mediated
A long list of drugs can cause different forms of injury: hepatitis, fibrosis, granulomas, necrosis, cholestasis, vascular disorders and neoplasia
Example: Acetaminophen overdose induces centrilobular necrosis
Autoimmune hepatitis
More in females (70%)
The absence of serologic markers for viral hepatitis
Elevated serum IgG levels
High titers of autoantibodies (antinuclear, anti-smooth muscle, and anti-microsomal)
Increased frequency of HLA-B8 and DRw3
Associated with other forms of autoimmune disorders such as rheumatoid arthritis and ulcerative colitis
Risk for cirrhosis is 5%
Respond to immunosuppressive drugs
Alcoholic liver disease
100,000 death annually related to alcohol; 20,000 are related directly to end-stage liver cirrhosis; the rest is related to car accidents
Effects on liver:
80% fatty liver (steatosis)
10% alcoholic hepatitis
10% cirrhosis
Short-term ingestion of 80 g (8 beers) of ethanol per day leads to reversible steatosis
Daily ingestion of 160 g for 10-20 years leads to severe injury
Hereditary hemochromatosis
Autosomal recessive disease characterized by increased accumulation of body iron, most of which is deposited in the liver and pancreas.
Mostly due to increased iron absorption and accumulation over the years. Normal total body iron is 2-6 g. In hemochromatosis it may reach 50 gm.
Due to mutations in the hemochromatosis gene (HFE); a gene that regulates iron absorption.
The frequency of being heterozygous is 10% (1 of every ten persons) and that of being homozygous is 0.45% (1 of every 220 persons)
Hereditary hemochromatosis
Excess iron damages DNA, lipids and stimulates collagen formation (fibrosis)
Clinical picture:
Males are more affected; 50-60 years old
Liver cirrhosis, skin pigmentation, diabetes (pancreatic fibrosis), risk for hepatocellular carcinoma.
Diagnosis: elevated serum and tissue iron.
Early detection and therapy by phlebotomy and iron chelators lead to normal life expectancy

Wilson disease
Autosomal recessive disorder characterized by accumulation of copper in liver, brain and eyes, among other organs
The frequency of being heterozygous is 1:200 (less common than hemochromatosis)
The mutated gene (ATP7B) is located on chromosome 13; the mutation leads to failure to excrete copper into bile, and its accumulation in tissue
Clinical picture: neuropsychiatric manifestations, acute and chronic liver disease and Kayser-Fleisher rings in the cornea (green to brown deposits)
Diagnosis: Clinical picture, increased hepatic and urinary copper, and decreased serum ceruloplasmin (a copper binding protein).

Biliary disease
Secondary biliary cirrhosis: secondary to extrahepatic bile obstruction by stones, atresia or tumors
Primary biliary cirrhosis: immune-mediated destruction of intrahepatic bile ducts, more in females, presence of anti-mitochondrial antibodies
Primary sclerosing cholangitis: chronic fibrosis of intra- and extra-hepatic bile ducts; more in men, association with ulcerative colitis
Tumor of the liver
Liver cell adenoma
Occurs in women of childbearing age in relation to oral contraceptives; it regresses on discontinuation of hormones

Liver cell adenoma
Significance of this benign tumor:
It may be mistaken for carcinoma
Subcapsular adenomas are at risk for rupture, especially during pregnancy leading to life-threatening intraabdominal hemorrhage
Hepatocellular carcinoma (HCC)
Risk factors:
Strongly associated with hepatitis B and C infection. The carrier state for hepatitis B carries 200-fold increased risk for HCC
Chronic liver disease (e.g. alcohol)
Hepatotoxins (aflatoxin present on moldy peanuts and grains)
Hepatocellular carcinoma
Clinical picture:
Often patient already has liver cirrhosis, with rapid increase in liver size, worsening ascites, fever and pain; elevated serum alpha fetoprotein levels (>1000 ng/ml)

Metastatic carcinoma
The most common malignant tumors in the liver
Usually multiple lesions
The most common primary sites are colon, lung, breast, pancreas and stomach
Oral manifestation of liver dysfunction
Hematoma, gingival bleeding
Jaundiced mucosa
Glossitis (in alcoholic hepatitis)
Reduced healing after surgery

A 48-year-old man has a long history of chronic alcohol abuse. On physical examination his liver is firm on palpation of the abdomen, but does not appear to be enlarged. An abdominal CT scan reveals that the liver has cirrhosis. He joins a support group for persons with chronic alcohol abuse and he stops drinking. Despite his continued abstinence from alcohol, he most likely remains at risk for development of which of the following diseases?
Liver cell adenoma
Hepatocellular carcinoma
Gallbladder stones

A 28-year-old woman with recent onset of depression ingests an entire bottle (100 capsules, 500 mg each) of a medication containing acetaminophen. She becomes progressively obtunded. Which of the following microscopic findings is most likely to be present in her liver 3 days following this ingestion?
Normal histology
Centrilobular necrosis
Chronic inflammation

Hepatitis C infection is characterized by which one of the following:
Absence of carrier status
Highest incidence of chronic hepatitis among other viral hepatitis
No increase risk for hepatocellular carcinoma
It can be transmitted by eating contaminated food

50 year-old male presented with jaundice and pruritus. Lab studies show elevated serum conjugated bilirubin and alkaline phosphatase. ALT and AST levels were only slightly elevated. The most likely diagnosis is:
Hepatitis B
Hepatitis C
Extrahepatic bile duct obstruction
Autoimmune hepatitis

The Pancreas
The Pancreas
85% exocrine: enzymes for digestion
Acute and chronic pancreatitis
Cystic fibrosis
15% endocrine: insulin, glucagon and others

Pancreatic exocrine enzymes
Acute pancreatitis
Acute pancreatitis
Clinical presentation: abdominal pain radiating to the back, elevated serum amylase and lipase, hypocalcemia
Rise in serum lipase is more specific for pancreatitis.
Complications: infections, abscess, pseudocyst
Mortality is high: 20-40%, from shock, sepsis or acute respiratory failure, acute renal failure, disseminated intravascular coagulation

Chronic pancreatitis
Progressive destruction of pancreatic parenchyma and its replacement by fibrosis
Predisposing factors: alcohol, hypercalcemia or idiopathic
30% of idiopathic cases have been found to have mutation in CFTR gene
Complications: Pseudocyst, malabsorption, 2ry diabetes
Diagnosis: abdominal pain, malabsorption, calcifications on X-ray

Pancreatic adenocarcinoma
The 5th most frequent cause of death from cancer
Risk factors: smoking
CP: symptoms are late; pain and jaundice
Prognosis is poor: 5% survive for 5 years

Islet cell tumors
Rare compared to adenocarcinoma
Insulinomas: secrete insulin ? hypoglycemia ? behavioral changes, confusion and coma. Over 90% are benign
Gastrinomas: secrete gastrin ? increase acid production ? duodenal and gastric ulcers
Gallstones (cholelithiasis)
Afflict 10% of adult population in Western countries
Costs of management: $6 billion a year
20 million patients are estimated to have gallstones totalling several tons
Made of cholesterol, bilirubin and calcium salts with different concentrations
Two types: cholesterol and pigmented stones
Western > others
Advancing age
Female sex
Hyperlipidemia and bile stasis
Asian > Western
Hemolytic anemia
Biliary infection
Acute cholecystitis
Calculous: acute inflammation of a gallbladder that has stones. It may represent a medical emergency; no associated infection initially
Acalculous: no stones, in severely ill patients, severe trauma, burns and sepsis

The risks factors for developing acute pancreatitis include all of the following except:

All of the following statement about pigmented gallstones are correct except:
Hyperlipidemia is a risk factor
Hemolytic anemias could be a cause
Biliary infections may be present
They are more common in Asians

A 38-year-old woman has experienced episodes of light-headedness, irritability, and difficulty concentrating at her work for the past year. On physical examination there are no abnormal findings. Laboratory studies show her hemoglobin is 14.2 g/dL. An abdominal CT scan shows a 1 cm mass in the tail of the pancreas. Which of the following is the most likely diagnosis?
Pancreatic adenocarcinoma
Pancreatic pseudo-cyst
Chronic pancreatitis

A 50-year-old man gives a history of chronic alcohol abuse. He has had bouts of abdominal pain in the past year. For the past month, he has had more frequent and worsening abdominal pain. Physical examination reveals right upper and left upper quadrant pain with guarding. An abdominal plain film radiograph reveals no free air, but there is extensive peritoneal fluid collection along with dilated loops of small bowel. An abdominal CT scan reveals a 7 to 8 cm cystic mass in the tail of the pancreas. Which of the following is the most likely diagnosis?
Pancreatic adenocarcinoma
Metastatic carcinoma
Pancreatic pseudocyst
Acute pancreatitis