GI&HB Week One

  1. The foregut consists of which 9 structures?
    • Pharynx
    • Esophagus
    • Respiratory System
    • Stomach
    • Liver
    • Gallbladder
    • Pancreas
    • Upper Duodenum
    • Biliary Apparatus
  2. What artery and vein supply the foregut?
    • Celiac Artery
    • Splenic Vein
  3. The midgut consists of what 8 structures?
    • Lower Duodenum
    • Jejunum
    • Ileum
    • Yolk Stalk
    • Cecum
    • Appendix
    • Ascending Colon
    • Proximal 2/3 Transverse Colon
  4. What artery and vein supply the midgut?
    Superior Mesenteric Artery and Vein
  5. The hindgut consists of what 7 structures?
    • Distal 1/3 Transverse Colon
    • Descending Colon
    • Sigmoid Colon
    • Rectum
    • Anus
    • Epithelium of Urinary Bladder
    • Most of Urethra
  6. What artery and vein supply the hindgut?
    Inferior Mesenteric Artery and Vein
  7. These are outpouchings of the mucosa in the posterior pharynx just superior to the cricopharyngeal muscle (upper esophageal sphincter); can cause halitosis as food is trapped in the pouch
    Zenker's Diverticula
  8. An esophageal dismotility disorder in which the wall of the lowest part of the esophagus is scarred or the LES has increased tone. The tube fails to relax completely during a swallow. On barium swallow there is a classic 'bird's beak' appearance as the dilated proximal esophagus tapers down to a narrowing of the distal esophagus close to the diaphragm (near what would be the LES). Main symptoms are dysphagia and regurgitation of non-digested food.
  9. Typically caused by decreased LES tone, which allows backflow of stomach acid and bile salts into the lower esophagus. The acidity and bile acids are irritants to the epithelium of the esophagus and eventually can lead to dysphagia and scarring (Barrett's esophagus/esophogitis) and potentially even esophageal cancer. The dysplastic epithelium in the distal esophagus takes on some of the appearance of gastric mucosa.
    GastroEsophageal Reflux Disease (GERD)
  10. Dilated veins in the submucosal layer of the esophageal wall. Can result from portal hypertension, which is commonly caused by cirrhosis. Patients are at risk of bleeding, which carries a significant morbidity/mortality.
    Esophageal Varices
  11. A craterlike wound that can occur in either the stomach or the duodenum. Can erode through the layers of the organ wall and can perforate through the wall or hemorrhage if left untreated.
  12. Can occur as a result of an enlargement of the esophageal hiatus in the diaphragm, which allows the upper part of the stomach to enter the thorax. When symptomatic it can present in various ways such as chest pain, SOB, or even heart palpitations due to irritation of the vagus nerve. Often asymptomatic.
    Hiatal Hernia
  13. A congenital defect in which the opening of the pylorus is too narrow. Food is thus unable to pass into the duodenum. Children with this typically manifest forceful, "projectile" vomiting within the first 1-2 weeks of life. There is no bile in the vomit.
    Pyloric Stenosis
  14. The duodenum ends at the ligament of _______, which is attached to the right crus of the diaphragm. It contains skeletal muscle from the diaphragm and a fibromuscular band of smooth muscle from the duodenum. When it contracts, the duodenum widens the angle of the duodenojejunal flexure, allowing movement of the intestinal contents.
    Ligament of Treitz
  15. These glands are located in the submucosa of the duodenum. They secrete an alkaline mucus to neutralize the acids from the stomach, provide an alkaline environment for pancreatic enzymes, and lubricate the intestinal wall. The presence of these glands is a key characteristic in identification of the duodenum histologically.
    Brunner's Glands
  16. Remnant of the vitelline duct. It is an outpouching on the antimesenteric side of the ileum approx. 2 ft proximal to the ileocecal junction. It occurs in 2% of the pop., and is 2x more common in males than females. It can contain 2 types of ectopic tissue, and can present as clinically significant abdominal pain at anytime in the first 2 decades of life, but mostly in the first 2 years.
    Meckel's Diverticulum
  17. Characterized by abdominal pain (usually colicky), nausea/vomiting, and abdominal distension. The two most common causes are adhesions from previous abdominal surgeries and incarcerated hernias.
    Small Bowel Obstruction
  18. Inflammation of the mesenteric lymph nodes causing pain (usually in the RLQ) and nausea/vomiting. This can occur as a result of enterocolitis, Yersinia infection or even with (or after) an upper respiratory tract infection, like strep. These kinds of infections can present with symptoms that can be confused with appendicitis.
    Mesenteric Adenitis
  19. A condition of chronic liver disease where hepatocytes have been destroyed and replaced by fibrous scar tissue and regenerated nodules. This impedes normal blood flow through the liver resulting in portal hypertension and the sequelae associated with it.
  20. The presence of gallstones in the gallbladder
  21. Inflammation of the gallbladder wall. Tends to occur when a gallstone blocks the cystic duct, which can predispose the organ to bacterial infection. Symptoms include nausea, vomiting, fever, and RUQ pain.
  22. Inflammation of the pancreas. The hallmark symptom is epigastric pain radiating to the back. Nausea and vomiting are also often present. Sequelae include steatorrhea, diabetes mellitus, and pseudocysts. Ranson's criteria are predictive of morbidity and mortality.
  23. Typically the result of abnormal embryonic development, this is a rare condition where the duodenum is surrounded by pancreatic tissue
    Annular Pancreas
  24. The presence of gallstones in the duct system, which can lead to occlusion of the duct
  25. Inflammation of the bile duct wall. The classic symptom triad is fever, jaundice, and RUQ pain. Choledocholithiasis is often a factor which predisposes to bacterial infection. The most common organism is E. Coli
  26. Embryologically, the epithelium of the gut and the parenchyma of glands associated with the digestive tract (e.g., liver and pancreas) are derived from?
  27. Embryologically, the muscular walls of the digestive tract and connective tissues (lamina propria, muscularis mucosae, submucosa, muscularis externa, adventitia, and/or serosa) are derived from?
    Visceral Mesoderm
  28. Describe the formation of the Oral Cavity
    • Anterior 2/3 derived from Stomodeum
    • Posterior 1/3 derived from Foregut
    • Anterior 2/3 and Posterior 1/3 are separated by Oropharyngeal Membrane
  29. The palatoglossal arch is a remnant of which structure?
    Oropharyngeal Membrane
  30. This results if the tracheoesophageal septum is deviated posteriorly. This deviation causes incomplete separation of the esophagus from the laryngotracheal tube and results in a concurrent tracheoesophageal fistula.
    Esophageal Atresia
  31. What are these symptoms indicative of?:
    Maternal polyhydramnios
    Absence of stomach gas on prenatal ultrasound
    Copious, fine white frothy bubbles of mucus, mouth, and nose
    Coughing & choking
    Abdominal distention may occur secondary to collection of air in the stomach
    Esophageal Atresia
  32. This represents narrowing of the esophageal lumen. It is most frequently seen in the distal third of the esophagus. Usually results from incomplete esophageal recanalization during the eighth week of human embryological development.
    Esophageal Stenosis
  33. What are the symptoms of Esophageal Stenosis (2)?
    • Difficulty Swallowing (dysphagia)
    • GERD
  34. The liver and hepatic duct are formed from what structure?
    Hepatic Diverticulum
  35. The gallbladder and cystic duct are formed from what structure?
    Cystic Diverticulum
  36. What structures do the Ventral Pancreatic Bud form?
    • Main Pancreatic Duct
    • Uncinate Process and Inferior Portion of Head of the Pancreas
  37. What structures do the Dorsal Pancreatic Bud form?
    • Superior Head of Pancreas
    • Body and Tail of Pancreas
    • Accessory Bile Duct
  38. This is due to incomplete recanalization of the duodenum. Symptoms include recurrent vomiting, GERD, and peptic ulceration
    Duodenal Stenosis
  39. This is due to no recanalization of the duodenum. Symptoms include maternal polyhydramnios, bile-containing vomitus, and distended stomach
    Dudenal Atresia
  40. This is characterized by the failure of the midgut to return to the abdominal cavity. Herniated intestines are enclosed in umbilical cord and covered in amnion.
  41. This is characterized by the protrusion of viscera directly into the amniotic cavity. It occurs lateral to the umbilicus. It is due to abnormal closure of the body wall. The viscera is not covered by amnion.
  42. The terminal end of the hindgut. Partitioned into urogential sinus and rectum.
  43. When the anal membrane fails to break down it is referred to as?
    Imperforate Anus
  44. The incomplete partitioning of the hindgut is referred to as?
    Urorectal Fistula
  45. This disease is characterized by the absence of parasympathetic ganglia in the gut wall. It is due to a failure of neural crest cells to migrate to the walls of the intestines. Peristalsis is absent in affected regions
    Hirschsprung's Disease
  46. The Dorsal Mesentery consists of (6)?
    • Greater Omentum
    • Mesentery of Small Intestine
    • Mesoappendix
    • Transverse Mesocolon
    • Sigmoid Mesocolon
    • Spleen
  47. The Ventral Mesentery consists of (2)?
    • Lesser Omentum
    • --Hepatogastric Ligament
    • --Hepatoduodenal Ligament
    • Falciform Ligament
  48. A chemical substance produced in the body by an organ, cells of an organ, or scattered cells, having a specific regulatory effect on the activity of an organ or organs
  49. A hormone action in which a hormone binds to receptors on the cell and affects the function of the cell type that produced it
  50. A mode of hormone function in which hormone synthesized in and released from endocrine cells binds to its receptor in nearby cells of a different type and affects their function
  51. A mode of hormone function in which hormone synthesized in and released from endocrine cells binds to its receptor in nearby cells of a neural type and affects their function
  52. What gastrointestinal site does Secretin (S) act on?
    Small Intestine
  53. What gastrointestinal site does Gastrin (G) act on?
    • Gastric Antrum
    • Duodenum
  54. What gastrointestinal site does Cholecystokinin (I) act on?
    Small Intestine
  55. What gastrointestinal site does Glucagon (A) act on?
  56. What gastrointestinal site does Insulin (B) act on?
  57. What gastrointestinal site does Pancreatic Polypeptide (PP) act on?
  58. What gastrointestinal site does Somatostatin (D) act on?
    • Pancreas
    • Stomach
    • Small & Large Intestine
  59. What gastrointestinal site does GIP (GIP) act on?
    Small Intestine
  60. What gastrointestinal site does Motilin (Mo) act on?
    Small Intestine
  61. What gastrointestinal site does Histamine (ECL) act on?
  62. Which 3 gastrointestinal peptides are the only ones that meet the criteria to be designated a "hormone" and act as true hormones?
    • Gastrin
    • Secretin
    • Cholecystokinin
  63. What syndrome is associated with the peptide Gastrin and manifests with ulcers and diarrhea?
  64. What syndrome is associated with the peptide Serotonin and manifests with the symptoms of flushing, diarrhea, and bronchospasm?
  65. What syndrome is associated with the peptide Vasoactive Intestinal Peptide and manifests with voluminous watery diarrhea?
    Verner-Morrison (VIPoma)
  66. What syndrome is associated with the peptide Insulin and manifests with hypoglycemia?
  67. What syndrome is associated with the peptide Glucagon and manifests with Diabetes, and migratory necrolytic erythema?
  68. What syndrome is associated with the peptide Somatostatin and manifests with Cholelithiasis, Diabetes, and Steatorrhea?
  69. What syndrome is associated with Pancreatic Polypeptide and manifests with mass effect?
  70. What is the single most important stimulant of acid secretion? This hormone interacts in a paracrine manner on local parietal cell H2 receptors to increase acid secretion, and acts via H3 receptors on D cells to suppress somatostatin release.
  71. This hormone interacts with muscarinic (M3) receptors producing a direct cholinergic action on parietal cells and D cells. It also has a neurocrine action to release histamine & suppress somatostatin. It acts to increase acid secretion.
  72. This hormone is released into the bloodstream from G cells (gastric antrum). It likely binds CCK-2 receptor on ECL cells to stimulate acid secretion via stimulation H2 release (indirect).
  73. This hormone has an important role in modulating gastrin release. It is an inhibitor of parietal cell function.
  74. This hormone has a meal stimulated release into the bloodstream. Its net effect is inhibitory. It is mediated through stimulation of D cell release somatostatin.
    Cholecystokinin (CCK)
  75. This hormone is secreted by virtually every epithelial, non-epithelial gastric cell. It inhibits acid secretion.
    Prostaglandins (PG)
  76. Commonly an adenocarcinoma that arises in the head of the organ. Patients may present with painless jaundice and/or pruritis due to hyperbilirubinemia. Once symptoms occur, the disease is usually at advanced stage. Smoking and chronic ETOH contribute to the risk factors for this
    Pancreatic Cancer
  77. Outpouching of the mucosa and submucosa through weak areas in the muscle wall. Most commonly located in the sigmoid colon as this area is subject to increased pressure. Complications include inflammation, bleeding and infection. This is commonly seen as a history of constipation, LLQ pain and a positive test for fecal blood occult (Guiac test) or frank red blood per rectum. Agressive antibiotics for multi-organismal infections would be the treatment as well as pain control.
  78. Dilated veins in the anal canal. Internal ones are not painful and are above the pectinate line whereas externals are painful and below the pectinate line. Straining secondary to constipation and pregnancy are common causes. These can be managed with high-fiber diets or surgically removed
  79. An acute inflammation of the appendix that is usually the result of an infection. It may be predisposed by an occluding fecolith. Pain usually begins in the periumbilical region and then moves down and right to McBurney's Point as the somatic nerves in the peritoneum are involved. Perforation is a very serious complication that can be lethal so this always warrants surgical consultation
  80. Which organs are retroperitoneal?
    • Thoracic Esophagus
    • Rectum
  81. Which organs are secondarily retroperitoneal?
    • Pancreas
    • Duodenum
    • Ascending and Descending Colon
  82. Which one of the following produces inappropriate hypergastrinemia?

    Pernicious Anemia
    Antral-predominant H. pylori infection
    H. pylori pangastritis
    High dose PPI therapy
    Idiopathic gastric acid secretion
    Antral-predominant H. pylori infection
  83. What are three important constituents of saliva, and what is their function?
    • Bicarbonate: neutralizes refluxed gastric acid
    • Amylase: starch digestion
    • Lysozyme, lactoferrin, IgA: innate and aquired immune protection
  84. Saliva is secreted from what type of cells? What is the main component of saliva?
    • Acinar Cells
    • Water
  85. What duct is associated with the Parotid Gland?
    Stensen's Duct
  86. What duct is associated with the Submandibular Gland? What two nerves are associated?
    • Wharton's Duct
    • Lingual Nerve and CN XII
  87. What two ducts are associated with the Sublingual Gland?
    • Duct of Rivinus
    • Bartholin's Duct
  88. What supplies the innervation to the Submandibular and Sublingual Glands?
    • Superior Cervical Ganglion (sympathetic)
    • Submandibular Ganglion (parasympathetic)
  89. Striated and Intercalated ducts are primarily found in the serous, not mucous glands. Striated ducts inject ______ into the lumen and take _____ from the lumen. Intercalated ducts inject ______ into the lumen and take _____ from the lumen. They therefore produce hypotonic fluid.
    • HCO3 & Cl
    • K & Na
  90. What happens without adequate saliva (Xerostomia) (4)?
    • Dental Caries
    • Candidiasis
    • Burning Mouth
    • Aphthous Ulcers
  91. Suck/swallow pattern is developed by ____ weeks gestation in full term infants.
  92. What are the functions of the larynx (3)?
    • Airway protection
    • Pressure valving
    • Phonation
  93. What are the three methods for management of Dysphagia?
    • Compensation
    • Rehabilitation
    • Surgery
  94. Secondary peristalsis of the smooth muscle portion of the esophagus can be produced even in the absence of vagal input by a network of what neuron type?
    Enteric Neurons
  95. What is the primary inhibitory neurotransmitter involved in esophageal peristalsis?
  96. Bolus transport through the esophagus becomes progressively impaired with peristaltic amplitudes of ____ mm Hg or less
  97. What are the three primary motor functions of the stomach?
    • Storage: to act as a reservoir
    • Mixing: preparation of ingested materials and formation of chyme
    • Emptying: delivery of nutrients to the small intestine
  98. This is defined as microscopic inflammation of stomach mucosa (biopsy needed to diagnose). There is a poor correlation between the histology (dense inflammatory infiltrate in lamina propria of the mucosal layer) and clinical symptoms, which consists of:

    Epigastric Pain

    This is commonly secondary to infectious or autoimmune etiologies.

    The chronic form of this disease is usually clinically silent but a risk factor for peptic ulcer disease and gastric neoplasms.
  99. This is defined as mucosal damage/regeneration with minimal or no associated inflammation (usually detected by endoscopy). The spectrum of damage for this disease includes:

    Erosions: superficial mucosal necrosis
    Small Ulcers: necrosis extending to muscularis mucosa
  100. What are the two forms of chronic gastritis?
    • Environmental Metaplastic Atrophic Gastritis (EMAG)
    • Autoimmune Metaplastic Atrophic Gastritis (AMAG)
  101. In this form of chronic gastritis, there is involvement of the antrum and body with mucosal atrophy and intestinal metaplasia. Chronic H. pylori infection is seen in at least 85% of these patients.
    Environmental Metaplastic Atrophic Gastritis (EMAG)
  102. In this form of chronic gastritis, there is autoimmune destruction of body/fundic glands. This form accounts for <5% of all cases of chronic gastritis. In this form, antibodies to parietal cell, and intrinsic factor lead to achlorhydria/pernicious anemia.
    Autoimmune Metaplastic Atrophic Gastritis (AMAG)
  103. This is a form of Gastropathy that can be caused by aspirin or other NSAIDs , which block COX-1, which is responsible for prostaglandin synthesis/mucosal defense. Alcohol, especially when combined with NSAIDs, is another common cause.
    Reactive Gastropathy
  104. This is defined as a break in the gastroduodenal mucosa. It has an appreciable depth at endoscopy, and there is histologic evidence of involvement of the submucosa. This generally occurs as a result of an imbalance of aggressive (Gastrin, Pepsin) and defensive factors in the stomach and duodenum.
    The lifetime risk of developing these is ~10%, with duodenal > Gastric ~4:1.
    About 4% are malignant
    Natural history is greatly altered by H. pylori, with 70% of duodenal etiologies thought to be a result of H. pylori infection
    Peptic Ulcers
  105. What is the diagnosis?:

    Classic Symptoms: burning/gnawing epigastric pain relieved by antacids

    Complicated Disease: N&V, weight loss, hematemesis, melena, or acute peritonitis
    Peptic Ulcer Disease
  106. What are the treatment options for Peptic Ulcers?
    • Antacids
    • H-2 Receptor Antagonists (block H-2 receptor on parietal cells)
    • PPIs (block proton pump on parietal cells)
    • Mucosal Protective Agents
    • H. Pylori Antibiotics
  107. What is the diagnosis?:

    Most common causes are diabetes (50% of pts with longstanding diabetes mellitis will develop) and postsurgical (vagotomy, esophagofundectomy, fundoplication, and antrectomy can variably affect gastric emptying).

    Symptoms: early satiety, prolonged epigastric fullness, epigastric pain, N&V (chewed food from a prior meal -- yesterday's breakfast).

    Exam may reveal epigastric tenderness and/or distention, succussion splash
  108. What do the common bile duct and ventral pancreatic duct drain through?
    Major Duodenal Papilla
  109. What complex regulates drainage of bile ducts?
    Sphincter of Oddi
  110. This is a clinical syndrome of acute abdominal pain associated with significant elevation of serum amylase and lipase. It can be caused by gallstones (most common cause), alcohol, as well as hypertriglyceridemia, medications, post-ERCP, genetic, pancreatic divisum, etc.
    Acute Pancreatitis
  111. Clinical syndrome (pain, steatorrhea, diabetes) due to permanent and progressive damage to pancreatic parenchyma. This is characterized initially by pain and later by endocrine and exocrine insufficiency. The pain is caused by pancreatic duct obstruction with increased PD pressure. This is a scarring disease -- can cause stricture in the duct leading to pseudocysts. 90% of the gland must be lost before a loss in function is seen. The most common cause is alcohol abuse, followed by genetic causes.
    Chronic Pancreatitis
  112. This pancreatitis type is related to pancreatic duct obstruction caused by gallstones.

    It is Diagnostic if:
    GB or CBD stones on US
    ALT > 3x normal at presentation
    Gallstone Pancreatitis
  113. Acute pancreatitis of this type is more commonly seen in men, and has a younger median age of 39. What is it?
  114. Acute pancreatitis of this type is more commonly seen in women, with an older median age of 69. What is it?
  115. What are some of the common drug related causes of acute pancreatitis?
    • Asparaginase
    • Azathioprine
    • 6-MP
    • Didanosine (DDI)
    • (HIV meds, immunosuppressants, anti-epileptics
  116. This is a rare cause of acute pancreatitis. Serum triglycerides are usually > 1000 mg/dL (normal = 150). It may cause chronic disease, and can be drug-induced: alcohol, estrogens, isotretinoin, HIV-protease inhibitors.
  117. In this form of pancreatitis, high-risk patients are YOUNG FEMALES with normal ducts, SO dysfunction, and they are anicteric. Procedural risk factors include difficult cannulations, pancreatic injections, acinarization, and sphincterotomy.
    Endoscopic Retrograde Cholangio Pancreatography (ERCP)-Induced Pancreatitis
  118. This is an anatomic abnormality seen in about 7% of the population, and is a risk factor for acute pancreatitis. In this abnormality, the ducts don't fuse as they normally would (Santorini [minor] Duct and Wirsung [major] Duct)--therefore, the dorsal duct ends up draining the majority of the pancreas through a much smaller opening
  119. What is the diagnosis?:

    Abdominal Pain -- very severe, often radiating back to the thoracic spine
    Abdominal Tenderness
    Fever -- low grade

    Lab Tests: increased WBC, increased Serum Amylase, increased Serum Lipase
    Acute Pancreatitis
  120. In acute pancreatitis, _____% have a mild form, with only 3-4 day hospitalization required. ____% have a more severe form, and of those, ____% develop organ failure and infection, and result in death.
    • 85%
    • 15%
    • 1%
  121. What are the three most common danger signs for Severe Acute Pancreatitis?
    • Shock with Tachy
    • Low BP
    • Poor Systemic
  122. The Apache II Calculator is a test used to predict severity for acute pancreatitis. It gives a risk of in-hospital death, and a score of >____ is predictive of a more severe course.
  123. The normal value for Hemoconcentration is 40-45. If a low score is seen, then what is unlikely to develop?
    Severe/Necrotizing Disease
  124. There are early changes seen in what lab test in relation to mortality in acute pancreatitis?
  125. What management is required for the mild form of acute pancreatitis?
    • Monitoring for signs of organ failure
    • NPO
    • IV Hydration
    • NG Suction if ileus or vomiting
    • Pain Management
  126. What are the management techniques used for severe acute pancreatitis?
    • Vigorous fluid resuscitation
    • Support organ failure
    • Antibiotics?
    • Vigilance for pancreatic infection
    • Nasojejunal feeding
    • Manage local complications
  127. This is a local complication of acute pancreatitis characterized by an area of pancreatic juice enclosed by nonepithelialized wall (acute or chronic). It takes 2-3 weeks to develop.
  128. What are four local complications of acute pancreatitis?
    • Necrosis: region of nonviable pancreatic parenchyma due to disrupted vascular atrophy
    • Fluid Collection: peripancreatic fluid without well defined borders or wall
    • Pseudocyst: area of pancreatic juice enclosed by nonepithelialized wall
    • Abscess: circumscribed region of pus usually due to infection of pseudocyst
  129. How can chronic pancreatitis be diagnosed?
    • Calcifications of plain film or CT
    • Overt steatorrhea
    • 24 hr fecal fat < 7 grams
    • EUS (most sensitive)
  130. What methods of pain relief are used for chronic pancreatitis?
    • Discontinue alcohol
    • Give analgesics, including narcotics
    • Supress secretin
    • Modify neural transmission
    • Relieve obstruction
  131. This is the most common method used to relieve obstructions causing chronic pancreatitis. In this surgical technique, a v-shaped wedge is taken out of the anterior part of the pancreas and a loop of the jejunum is brought up and sown on to the side of the pancreas. This allows the pancreatic juice to get into the bowel without transversing the whole length of the duct.
    Lateral Pancreaticojejunostomy
  132. What surgical technique, used for pain management in chronic pancreatitis, involves removing the head of the pancreas, which seems to be the pain pacemaker in the disease?
    Pylorus Preserving Whipple
  133. Why does the pain improve over time in chronic pancreatitis?
    Because the gland burns out over time, resulting in the pain improving as function worsens
  134. In this form of pancreatitis, the pancreas becomes inflamed with lymphoplasmacytic cell infiltrate. This frequently presents as a mass that mimics pancreatic cancer, or as a diffusely swollen sausage-like pancreas. There is an irregular, narrowed duct, and periductal lymphoplasmacytic inflammation and fibrosis occur. There are IgG4, autoimmune markers, and it is steroid responsive.
    Autoimmune Pancreatitis
  135. Are the following pancreatic cysts malignant or benign?

    Serous Cystadenoma
    Mucinous Cystadenoma
    Intraductal Papillary Mucinous Neoplasm (IPMN)
    • Benign
    • Pre-malignant
    • Pre-malignant or Malignant
  136. What are the two gallstone types?
    • Cholesterol Stones
    • Pigmented Stones
  137. What are the two causes of Cholesterol Stones?
    • Cholesterol Hypersection: rapid weight loss, estrogens, progesterone, obesity, high calorie diet
    • Bile Acid Deficit: estrogens, racial differences, ileal disease, cholestatic liver disease
  138. What is the cause of Pigmented Stones?
    Increased unconjugated bilirubin: hemolysis, cirrhosis, biliary infections
  139. What is the cause of Cholesterol and Pigmented Stones both?
    Gallbladder stasis: progesterone, prolonged fasting
  140. The highest frequency of Gallstones is seen in which countries/racial groups?
    • American Indians
    • Sweden
    • Chile
    • Czech
    • Hispanics
  141. Over 90% of Gallstone complications are preceded by what? What are some other common causes?
    • Biliary Colic
    • Acute Cholecystitis, Choledocholithiasis, Acute Cholangitis, Acute Pancreatitis
  142. Which type of Gallstones are of a Crystalline consistency, located in the Gallbladder +/- common duct, are Lucent, and Metabolic?
  143. Which type of Gallstones are composed of calcium salts (PO4, CO3), of a Hard consistency, located in Gallbladder and Bile Ducts, Opaque, and associated with Hemolysis and Cirrhosis?
    Black Pigmented Gallstones
  144. Which type of Gallstones are composed of Calcium Soaps (palmitate, stearate), are of a Soft, Greasy consistency, located in the Common Duct, Lucent, and associated with Infection, Inflammation, and Infestation?
    Brown Pigmented Gallstones
  145. This complication of Gallstones may occur post-prandially (after a fatty meal). It is characterized by a steady increase in intensity over 15 min, and is localized to the epigastrium, RUQ, and occasionally the substernal region. It has right shoulder/scapular radiation. The pain is steady and lasts 30 min - 3 hrs.
    Biliary Colic
  146. This is characterized by obstruction of the cystic duct (10% acalculous), pain lasting > 3 hrs localized to RUQ, vomiting, tenderness in RUQ (Murphy's Sign), fever, leukocytosis common, and jaundice in 10-15%.
    On US, thickened GB wall, pericholecystic fluid, ultrasonographic Murpy's sign, and air in GB wall (gangrenous cholecystitis) can all be seen.
    Radionucleotide Scanning reveals Technicium-iminodiacetic acid (IDA) given IV, Isotope excreted in bile, and absence of GB filling (indicative of cystic duct obstruction)
    Acute Cholecystitis
  147. Most gallstones are asymptomatic and do not require treatment. However, recurrent biliary colic, complications, or porcelain gallbladder can be indications for what type of therapy?

    What form of this therapy is associated with shorter hospital stays, earlier return to normal function, as well as the complications of a higher incidence of bile duct injuries; contraindication for pregnancy, peritonitis/extensive inflammation, and extensive scarring/adhesions; and cannot treat bile duct stones?
    • Cholecystectomy
    • Laproscopic Cholecystectomy
  148. This is a distinct clinical entity within gallstone disease with a high rate of perforation (70%). The usual setting is severe/critical illness: trauma, extensive burn, major surgery. Pathogenesis is likely related to stasis or ischemia.
    Acalculous Cholecystitis
  149. What is the diagnosis/pathogenesis?:

    Ambulatory patients with chronic/recurrent biliary-type pain.
    No gallstones or sludge on US.
    HIDA scan with CCK-stimulated GB ejection fraction -- normal less than or equal to 35%
    Lap cholescystectomy results in symptom relief in 80-95% of patients with abnormal EF -- the more abnormal the EF, the more likely symptoms will be eradicated by cholecystectomy.
    Gallbladder Dyskinesia
  150. Choledocholithiasis affects 5-15% of patients with symptomatic gallstones. This always requires treatment. What are the two treatment options?
    • ERCP with sphincterotomy and stone extraction
    • Cholecystectomy with common bile duct exploration
  151. What is the diagnosis?:

    This is an infection in the biliary tree above an obstruction (e.g. stone or stricture)

    It is usually due to a gram negative rod, enterococcus

    Presents with the Charcot Triad (50-75%):
    RUQ Pain

    Reynold's Pentad: add Hypotension and Confusion

    Treated with antibiotics and biliary drainage
    Acute Cholangitis
  152. This therapy for Gallstones is composed of Ursodeoxycholic Acid.

    Must have patent cystic duct and adequate emptying based on oral cholecystogram

    Noncalcified, small (<1 cm), cholesterol stones are ideal

    80% effective in ideal circumstances

    Requires 9-12 months; high (50%) recurrence rate

    What is the therapy?
    Oral Dissolution Therapy
  153. What is the diagnosis?:

    Disease of older women
    Strong association with gallstones
    80% present with incurable disease
    Often detected at time of cholecystectomy for "stones"
    Median survival is 5-6 months; 5 yr survival is rare
    Gallbladder Cancer
  154. What is the diagnosis?:

    Chronic cholestatic disease of the liver and bile ducts
    Inflammation, stricturing intra- and extra hepatic ducts
    Hepatic fibrosis
    2:1 male predominance

    Clinical Manifestations:
    Cholestasis, pruritis
    Metabolic Bone Disease
    Dominant Strictures
    Cholangiocarcinoma -- 10-15x risk
    Colon Cancer -- at even higher risk than those with UC without this
    About 70-80% of these patients also have UC, and about 5-10% of UC patients have this
    Immunopathogenic etiology, not well understood
    Frequent Autoantibodies: p-ANCA, ASMA, ANA
    Primary Sclerosing Cholangitis (PSC)
  155. What is the treatment for Primary Sclerosing Cholangitis (PSC)?
    • No pharmacotherapy shown to be effective
    • ERCP for evaluation/sampling/dilation of dominant strictures
    • Liver Transplantation
  156. This is a cancer of the intrahepatic or extrahepatic biliary epithelium.
    Risk factors include PSC (30%), and choledochal cysts
    2/3 involve the bifurcation ("Klatskin tumors")

    This has a poor prognosis (5-10% survival)

    Treatment includes: Resection, Liver Transplantation, Palliation of Jaundice, Chemoradiation, and Photodynamic Therapy
Card Set
GI&HB Week One