Usmle Step 1 -- Dit: Gi

Front 1

Which artery supplies the foregut of the developing embryo? Which structures are contained in this region? Innervation?

Back 1

Celiac artery; stomach, liver, spleen, gall bladder, pancreas, proximal duodenum; Vagus.

Front 2

Which artery supplies the midgut of the developing embryo? Which structures are contained in this region? Innervation?

Back 2

Superior mesenteric artery; distal duodenum to proximal 2/3 of transverse colon; Vagus.

Front 3

Which artery supplies the hindgut of the developing embryo? Which structures are contained in this region? Innervation?

Back 3

Inferior mesenteric artery; distal 2/3 of transverse colon to upper portion of rectum; Vagus.

Front 4

What are the branches of the celiac trunk?

Back 4

Splenic, Left gastric, common hepatic arteries.

Front 5

The left gastroomental artery is a branch of which artery? How about the right gastroomental?

Back 5

Splenic; gastroduodenal.

Front 6

What are the branches of the common hepatic artery?

Back 6

Hepatic artery proper, right gastric artery, gastroduodenal.

Front 7

Who secretes intrinsic factor? What does it do?

Back 7

Parietal cells of the stomach; It binds Vit B12 --> uptake of Vit B12

Front 8

Autoimmune destruction of the parietal cells causes what?

Back 8

Chronic gastritis and pernicious anemia.

Front 9

Who secretes gastic acid?

Back 9

Parietal cells.

Front 10

What stimulates gastric acid secretion from parietal cells? What inhibits it?

Back 10

Stimulated by histamine, ACh, and gastrin. Inhibited by somatostatin, GIP, secretin, prostaglandin.

Front 11

Which artery supplies the foregut of the developing embryo? Which structures are contained in this region? Innervation?

Back 11

Celiac artery; stomach, liver, spleen, gall bladder, pancreas, proximal duodenum; Vagus.

Front 12

Which artery supplies the midgut of the developing embryo? Which structures are contained in this region? Innervation?

Back 12

Superior mesenteric artery; distal duodenum to proximal 2/3 of transverse colon; Vagus.

Front 13

Which artery supplies the hindgut of the developing embryo? Which structures are contained in this region? Innervation?

Back 13

Inferior mesenteric artery; distal 2/3 of transverse colon to upper portion of rectum; Vagus.

Front 14

What are the branches of the celiac trunk?

Back 14

Splenic, Left gastric, common hepatic arteries.

Front 15

The left gastroomental artery is a branch of which artery? How about the right gastroomental?

Back 15

Splenic; gastroduodenal.

Front 16

What are the branches of the common hepatic artery?

Back 16

Hepatic artery proper, right gastric artery, gastroduodenal.

Front 17

Who secretes intrinsic factor? What does it do?

Back 17

Parietal cells of the stomach; It binds Vit B12 --> uptake of Vit B12

Front 18

Autoimmune destruction of the parietal cells causes what?

Back 18

Chronic gastritis and pernicious anemia.

Front 19

Who secretes gastic acid?

Back 19

Parietal cells.

Front 20

What stimulates gastric acid secretion from parietal cells? What inhibits it?

Back 20

Stimulated by histamine, ACh, and gastrin. Inhibited by somatostatin, GIP, secretin, prostaglandin.

Front 21

Who secretes pepsin? Who activates pepsin? What does pepsin do?

Back 21

Chief cells of the stomach; H+ activates pepsin --> protein degradation.

Front 22

What are the sources of HCO3-? What up-regulates its secretion?

Back 22

Pancreas, duodenum, stomach, salivary glands, Brunner's glands; Stimulated release from pancreas and biliary system by Secretin.

Front 23

Name two conditions where salivary secretions are decreased.

Back 23

Damage of CNVII, Sjogren's syndrome.

Front 24

What endocrine syndrome is Z-E association with?

Back 24

MEN I.

Front 25

What is Z-E syndrome?

Back 25

Gastrin-secreting tumor of the pancreas or duodenum. Histo: stomach rugal thickening with acid hypersecretion and recurrent ulcers.

Front 26

What disorder is characterized by an excess of gastrin? What is the treatment?

Back 26

Z-E syndrome; PPIs and OCTREOTIDE (resembles somatostain).

Front 27

What receptors found on gastric parietal cells regulate acid secretion?

Back 27

M3, H2, CCK (gastrin), PG receptors, Somatostatin receptor.

Front 28

What is the most important mechanism of gastric acid secretion by stimulation of the parietal cell by gastrin?

Back 28

Gastrin (from G cells) stimulating ECL cells to secrete histamine --> acts on H2 receptors --> gastric acid secretion.

Front 29

Describe the stimulation of G cells to secrete gastrin.

Back 29

Vagal stimulation --> GRP --> stimulates G cell --> gastrin release.

Front 30

What happens to serum pH at the time of gastric acid secretion?

Back 30

Increased pH d/t "alkaline tide" (Cl-/HCO3- antiporter).

Front 31

Who secretes Somatostatin?

Back 31

D cells of the pancreas and GI mucosa.

Front 32

Who secretes GIP? What are its exocrine and endocrine functions? What stimulates its release?

Back 32

K cells of the duodenum and jejunum; Exocrine: decreased gastric acid secretion; Endocrine: increased insulin secretion; Stimulated by fatty acids, amino acids, and oral glucose.

Front 33

What drug can stimulate Motilin (thereby stimulating migrating motor complexes) in patients with ileus?

Back 33

Erythromycin.

Front 34

A patient with a pancreatic VIPoma will have what symptom?

Back 34

Copious diarrhea.

Front 35

The vagus nerve stimulates G cells to release gastrin; however, the administration of a muscarinic antagonist such as atropine will NOT INHIBIT the release of gastrin. Why?

Back 35

The nt is GRP, not ACh. Boo yeah.

Front 36

Which G protein is coupled to the H2 receptor in the parietal cell?

Back 36

Gs

Front 37

What is a major pharm consideration for Cimetidine?

Back 37

It is a potent INHIBITOR of CYP-450.

Front 38

What is a major toxicity of Misoprostol?

Back 38

It increases uterine tone --> ABORTIFACIENT.

Front 39

What is the clinical use of Mosprostol?

Back 39

It's a PGE1 analog, so it increases production/secretion of the gastric mucous barrier and decreases acid production --> prevention of NSAID-induced peptic ulcers; maintenance of PATENT DUCTUS ARTERIOSUS. Also used to induce labor.

Front 40

Overuse of this drug can cause constipation.

Back 40

Aluminum hydroxide.

Front 41

Overuse of this drug can cause diarrhea, hyporeflexia, hypotension, and cardiac arrest.

Back 41

Magnesium hydroxide.

Front 42

Overuse of this drug can cause hypercalcemia and rebound acid increases.

Back 42

Calcium carbonate.

Front 43

What drug is used to control vomiting and what is its mechanism of action? Toxicities?

Back 43

Odansetron; 5-HT3 antagonist -- central-acting antiemetic; can cause headache and constipation. Safe in pregnancy.

Front 44

At which receptor does Metoclopramide act? What effects does it have and what is it used to treat?

Back 44

D2 receptor antagonist; Increases resting tone, contractility, LES tone, and motility -- treatment for GERD, diabetic gastroparesis, and post-op gastroparesis.

Front 45

What is are the toxicities to be aware of when using Metoclopramide?

Back 45

Increased Parkinson's sx, contraindicated in patients w/small bowel obstruction.

Front 46

What causes acute gastritis?

Back 46

Stress and NSAID use, alcohol, uremia, burns (CURLING'S ulcer), brain injury (CUSHING'S ulcer) -- increased vagal input to parietal cells).

Front 47

What are the two types of chronic gastritis?

Back 47

Type A -- Auto-antibody to parietal cells = decreased HCl, gastrin, IF --> pernicious anemia.
Type B -- Most common. Caused by H.PYLORI and increases risk of MALT LYMPHOMA.

Front 48

Hypertrophic rugae of stomach + protein loss + parietal cell atrophy are characteristic of what disease?

Back 48

Ménétrier's disease.

Front 49

What are the two most common causes of gastric ulcers?

Back 49

H.pylori and NSAID use.

Front 50

Is pain greater or lessened by eating when you have a gastric ulcer? Duodenal ulcer?

Back 50

Pain is greater when you are eating if you have a gastric ulcer, but decreased if you have a duodenal ulcer (HCO3- is secreted when you eat -- soothes ulcer).

Front 51

Which type of peptic ulcer increases your risk of carcinoma?

Back 51

Gastric ulcer.

Front 52

What is the treatment for peptic ulcers?

Back 52

Triple therapy: PPI, clarithromycin, and amoxicillin.

Front 53

Which drugs are used for traveler's diarrhea?

Back 53

Bismuth, sucralfate.

Front 54

What enzyme is inhibited by PPIs?

Back 54

H+/K+ ATPase.

Front 55

An infant presents to the ER with vomiting. What presenting features would lead you to suspect congenital pyloric stenosis?

Back 55

~2-6 weeks old, nonbilious projectile vomiting, palpable "olive" mass in epigastric area, metabolic alkalosis (hypokalemic, hypochloremic).

Front 56

What is the most common type of stomach cancer? What is pathognomonic for stomach cancer?

Back 56

Adenocarcinoma; Signet ring cells.

Front 57

What risk factors are associated with stomach cancer?

Back 57

Nitrosamines, chronic gastritis.

Front 58

Where is Vichow's node located? Sister Mary Joseph's node?

Back 58

Left supraclavicular node, d/t mets from STOMACH; subcu periumbilical met from stomach.

Front 59

Describe Krukenberg's tumor.

Back 59

Bilateral mets to ovaries from stomach -- you'll see SIGNET RING cells in the OVARY!

Front 60

An infant shows up in the ER with early bilious vomiting, proximal stomach distention causing a "double bubble" sign on x-ray. You also notice that the infant has Down's Syndrome. What is your diagnosis?

Back 60

Duodenal atresia.

Front 61

What causes pancreas divisum?

Back 61

Failure of the dorsal and ventral pancreatic buds to fuse at 8 weeks.

Front 62

What are the retroperitoneal structures?

Back 62

"SAD PUCKER": Suprarenal gland, aorta, duodenum (2nd, 3rd, and 4th parts), pancreas (except tail), ureters, colon, kidneys, esophagus, rectum (upper 2/3).

Front 63

Which GI ligament contains the portal triad and may be compressed during surgery?

Back 63

Hepatogastric ligament.

Front 64

Which GI ligament attaches the spleen to the posterior abdominal wall?

Back 64

Falciform ligament.

Front 65

Which GI ligament attaches the spleen to the stomach?

Back 65

Gastrosplenic ligament.

Front 66

Which GI ligament contains the splenic artery and vein?

Back 66

Splenorenal ligament.

Front 67

What are the secreting cells of the duodenum and what do they secrete?

Back 67

S cells --> somatostain
I cells --> CCK
K cells --> GIP

Front 68

In the 10th week of development the midgut returns from its herniation through the umbilical ring and rotates around which vessel?

Back 68

SMA.

Front 69

What is the term for persistence of herniation of abdominal contents into the umbilical cord, covered by peritoneum?

Back 69

Omphalocele.

Front 70

What is the term for extrusion of the abdominal contents through the abdominal folds, not covered by peritoneum and located lateral to umbilicus?

Back 70

Gastrochisis.

Front 71

A newborn is having trouble feeding. He vomits milk when fed and has a gastric bubble on x-ray. What type of defect is likely?

Back 71

Tracheoesophageal fistula.

Front 72

What is the most common subtype of tracheoesophageal fistula?

Back 72

Blind upper esophagus. Lower esophagus connected to trachea.

Front 73

Where is the Zenker's diverticulum located? What symptoms does it cause?

Back 73

Herniation of the mucosa at the junction of the pharynx and the esophagus. Causes halitosis (bad breath), obstruction, dysphagia.

Front 74

Where is a traction diverticulum located? Epiphrenic diverticulum?

Back 74

Near the midpoint of the esophagus; Immediately above the LES.

Front 75

Why is an omphalocele worse than gastrochisis?

Back 75

Omphalocele usually contains a PROTRUDING LIVER, which is never seen with gastrochisis. Also, the risk of other anomalies is higher when an omphalocele is present.

Front 76

What happens at the GE junction?

Back 76

Transition from non-keratinzing stratified squamous cell epithelium to intestinal columnar epithelium.

Front 77

What purpose does NO serve in the GI tract? What happens if there is a loss of NO secretion?

Back 77

Increases smooth muscle relaxation, especially at the LES. Loss of NO secretion --> increased LES tone --> ACHALASIA.

Front 78

What is the underlying defect in achalasia? Presentation? Dx?

Back 78

Loss of myenteric (Auerbach's) plexus --> no relaxation of LES. Progressive dysphagia to solids and liquids. "Bird's beak" appearance on barium swallow. Also, increased risk of esophageal carcinoma.

Front 79

What bug and AI disease can cause achalasia?

Back 79

T. cruzi --> Chagas disease. Scleroderma (CREST syndrome). Remember, the "E" in "CREST" stands for Erica, not esophageal dysmotility.

Front 80

From which part of the developing foregut is the pancreas derived?

Back 80

Foregut.

Front 81

From which part of the developing embryo is the spleen derived? Who gives the spleen its blood supply?

Back 81

Dorsal mesentery. Celiac artery (artery of the foregut, ya'll!).

Front 82

Keeping this in mind: Latin annularis, from anulus, "a ring", what is an annular pancreas and what's the big deal?

Back 82

The ventral pancreatic bud encircles the 2nd part of the duodenum and can cause narrowing.

Front 83

What other anomalies is the annular pancreas associated with?

Back 83

Meckel's diverticulum, esophageal and duodenal atresia, imperforate anus, Down's, polyhydraminos.

Front 84

What are the two nervous system bundles that run through the GI tract and where are they located?

Back 84

Myenteric (Auerbach's) plexus -- muscularis externa. Meissner's plexus -- Submucosa.

Front 85

What is Mallory-Weiss syndrome? Who usually shows up with this?

Back 85

Mucosal lacerations at the gastroesophageal junction due to SEVERE VOMITING. Alcoholics and bulimics.

Front 86

What is Boerhaave syndrome.

Back 86

TRANSMURAL esophageal rupture due to VIOLENT retching.

Front 87

What can cause an esophageal stricture?

Back 87

Lye ingestion, acid reflux, scleroderma, neoplasm.

Front 88

What is the triad for Plummer-Vinson syndrome?

Back 88

Dysphagia (d/t esophageal webs), glossitis, Iron-deficiency.

Front 89

What is pathognomonic for Barrett's esophagus? What type of neoplasia is this?

Back 89

Presence of goblet cells in the distal esophagus. METAPLASIA.

Front 90

What causes Barrett's esophagus? What does it predispose the patient to?

Back 90

GERD; Adenocarcinoma.

Front 91

What are the risk factors for SCC of the esophagus?

Back 91

Alcohol use, cigarettes, achalasia.

Front 92

Which is more common worldwide, SCC or adenocarcinoma of the esophagus?

Back 92

SCC > Adenocarcinoma worldwide. SCC = Adenoca in the U.S.

Front 93

What are the risk factors for adenocarcinoma of the esophagus?

Back 93

Barrett's esophagus, nitrosamines.

Front 94

Where are Brunner's glands located and what do they do?

Back 94

They are located in the submucosa of the proximal duodenum; secrete HCO3- in response to acidic contents entering the duodenum from the stomach.

Front 95

When might you see hypertrophied Brunner's glands?

Back 95

Peptic ulcer disease.

Front 96

Which pancreatic proenzyme is converted to its active form by enterokinase/enteropeptidase in the duodenum?

Back 96

Trypsinogen.

Front 97

What enzymes does the pancreas secrete?

Back 97

α-amylase, lipase, phospholipase A, colipase, Proteases (secreted as "zymogens" then converted to active form -- trypsin, chymotrypsin, elastase, carboxypeptidase).

Front 98

Which enzyme converts the pancreatic proteases to their active form?

Back 98

Trypsin.

Front 99

What enzymes are involved in carbohydrate digestion? What is the rate-limiting step?

Back 99

Salivary amylase, pancreatic amylase, oligosaccharide hydrolases (RLS -- at brush border of intestine).

Front 100

How does cystic fibrosis affect the GI system?

Back 100

Abnormally thick mucus plugs cause pancreatic insufficiency, malabsorption (especially of fat soluble vitamins), steatorrhea, and meconium ileus in newborns.

Front 101

What are the possible etiologies of acute pancreatitis?

Back 101

"GET SMASHED": GALLSTONES, ETHANOL, trauma, scorpion sting, mumps, AI disease, steroids, hypertriglyceridemia/hypercalcemia, ERCP, drugs (sulfas).

Front 102

What are the sx of acute pancreatitis? Labs?

Back 102

Epigastric pain radiating to back, anorexia, nausea; Elevated amylase and lipase..also "sentinel sign" on x-ray -- inflamed pancreas halts peristalsis and causes an air bubble in adjacent duodenum.

Front 103

What are the major risk factors for chronic pancreatitis?

Back 103

Alcoholism, smoking. Increased risk of pancreatic adenocarcinoma.

Front 104

You see calcification of the pancreas... what do you think?

Back 104

Chronic pancreatitis.

Front 105

What is the tumor marker associated with pancreatic adenocarcinoma?

Back 105

CA 19-9 (also CEA, less specifically).

Front 106

What is the clinical presentation of pancreatic adenocarcinoma?

Back 106

1. Abd pain radiating to back.
2. Weight loss (d/t malabsorption + anorexia)
3. Migratory thrombophlebitis (Trousseau's syndrome)
4. Obstructive jaundice w/palpable gall bladder (Courvoisier's sign).

Front 107

What is the typical presentation of a patient with pancreatic insufficiency? How is it treated?

Back 107

Fat-soluble vitamin deficiency, anorexia, nausea, and epigastric pain radiating to back; Tx includes replacement of pancreatic enzymes + limiting fat intake.

Front 108

What bug can cause wicked gallstones?

Back 108

Clonorchis sinensis (Oriental liver fluke).

Front 109

An infant born at 35 wks arrives in your ER one week after birth. She has acute abdominal distress, GI bleeding, large intestinal perforation, and sepsis. What is your diagnosis?

Back 109

Necrotizing enterocolitis.

Front 110

Which carbohydrates are absorbed by enterocytes? What transporters get them across the cell membrane?

Back 110

Galactose, fructose and glucose. SGLT1 transports galactose and glucose; GLUT-5 transports fructose.

Front 111

What lipoprotein is required for a chylomicron to get out of the cell and into the circulation? In which disease is this mechanism disfunctional?

Back 111

ApoB48. Abetalipoproteinemia.

Front 112

An elderly man shows up in your ER with cardiac arrhythmia, arthralgias, and neuro sx. An intestinal biopsy shows PAS+ foamy macrophages in the lamina propria. What's your diagnosis? What bug causes this?

Back 112

Whipple's disease; T. whippelii (gram-positive).

Front 113

What are the syndromes that can cause malabsorption?

Back 113

"These Will Cause Devastating Absorption Problems": Tropical sprue, Whipple's disease, Celiac sprue, Disaccharide deficiency, Abetalipoproteinemia, Pancreatic insufficiency.

Front 114

What serum antibodies are associated with celiac sprue?

Back 114

Anti-Gliadin and anti-tissue transglutaminase.

Front 115

Which specific organs are involved in the absorption of vitamin B12? Which test is done to figure out the cause of B12 deficiency?

Back 115

Salivary glands, stomach (IF!), pancreas, terminal ileum; Schilling Test.

Front 116

What part of the GI tract is affected by Crohn's disease? Describe the gross and microscopic morphology.

Back 116

Any part can be affected -- 80% of the time it occurs in the terminal ileum. ALWAYS SPARES THE RECTUM. Skip lesions are common; Morph: TRANSMURAL inflammation, cobblestoning mucosa, creeping FAT, ulcers, fissures, fistulas, bowel wall thickening ("STRING SIGN" on barium swallow), noncaseating GRANULOMAS and lymphoid aggregates.

Front 117

What are some of the extraintestinal manifestations of Crohn's disease?

Back 117

Migratory polyarthritis, erythema nodosum, immunologic disorders, kidney stones.

Front 118

What drugs are used in the treatment of Crohn's?

Back 118

Corticosteroids (obviously, it's an AI disorder), Infliximab (Anti-TNF agents), 5-ASA agents.

Front 119

Describe the MOA for the 5-ASA agents used to treat Crohn's.

Back 119

Mesalamine, sulfasalazine: combo of an antibacterial (sulfapyridine) and an anti-inflammatory (5-ASA) -- the cool thing is IT STAYS IN THE GUT because it's actived in the terminal ileum/colon.

Front 120

Which carbohydrates are absorbed by enterocytes? What transporters get them across the cell membrane?

Back 120

Galactose, fructose and glucose. SGLT1 transports galactose and glucose; GLUT-5 transports fructose.

Front 121

What lipoprotein is required for a chylomicron to get out of the cell and into the circulation? In which disease is this mechanism disfunctional?

Back 121

ApoB48. Abetalipoproteinemia.

Front 122

An elderly man shows up in your ER with cardiac arrhythmia, arthralgias, and neuro sx. An intestinal biopsy shows PAS+ foamy macrophages in the lamina propria. What's your diagnosis? What bug causes this?

Back 122

Whipple's disease; T. whippelii (gram-positive).

Front 123

What are the syndromes that can cause malabsorption?

Back 123

"These Will Cause Devastating Absorption Problems": Tropical sprue, Whipple's disease, Celiac sprue, Disaccharide deficiency, Abetalipoproteinemia, Pancreatic insufficiency.

Front 124

What serum antibodies are associated with celiac sprue?

Back 124

Anti-Gliadin and anti-tissue transglutaminase.

Front 125

Which specific organs are involved in the absorption of vitamin B12? Which test is done to figure out the cause of B12 deficiency?

Back 125

Salivary glands, stomach (IF!), pancreas, terminal ileum; Schilling Test.

Front 126

What part of the GI tract is affected by Crohn's disease? Describe the gross and microscopic morphology.

Back 126

Any part can be affected -- 80% of the time it occurs in the terminal ileum. ALWAYS SPARES THE RECTUM. Skip lesions are common; Morph: TRANSMURAL inflammation, cobblestoning mucosa, creeping FAT, ulcers, fissures, fistulas, bowel wall thickening ("STRING SIGN" on barium swallow), noncaseating GRANULOMAS and lymphoid aggregates.

Front 127

What are some of the extraintestinal manifestations of Crohn's disease?

Back 127

Migratory polyarthritis, erythema nodosum, immunologic disorders, kidney stones.

Front 128

What drugs are used in the treatment of Crohn's?

Back 128

Corticosteroids (obviously, it's an AI disorder), Infliximab (Anti-TNF agents), 5-ASA agents.

Front 129

Describe the MOA for the 5-ASA agents used to treat Crohn's.

Back 129

Mesalamine, sulfasalazine: combo of an antibacterial (sulfapyridine) and an anti-inflammatory (5-ASA) -- the cool thing is IT STAYS IN THE GUT because it's actived in the terminal ileum/colon.

Front 130

What are the characteristics of IBS?

Back 130

Abdominal pain or discomfort associated with 1+ of the following: relieved by defecation, change in stool frequency, change in stool form.

Front 131

Compare and contrast Meckel's diverticulum with an omphalomesenteric cyst.

Back 131

Both involve the vitelline duct. Meckel's is due to persistence of the duct, whereas an omphalocele is due to cystic dilatation of the duct.

Front 132

What is the most common congenital anomaly of the GI tract?

Back 132

Meckel's diverticulum.

Front 133

What are the "five 2's" of Meckel's diverticulum:

Back 133

1. 2" long
2. Within 2' of the ileocecal valve
3. Affects 2% of the population
4. Commonly presents in the first TWO years of life
5. May have 2 types of epithelia (gasric/pancreatic).

Front 134

What are the common causes of small bowel obstruction?

Back 134

Adhesions (75%), bulge or hernia, cancer or tumors (most often from met CRC).

Front 135

Where does intussusception occur most commonly? How does it present? Treatment?

Back 135

Ileocecal junction; young child with colicky abdominal pain, currant jelly stools, possible recent adenovirus infection, spontaneously resolves; Tx is barium enema.

Front 136

Someone you know has sudden onset of SEVERE, DIFFUSE ABDOMINAL PAIN, bloody diarrhea, pain after eating, weight loss, may or may not be elderly. What's your diagnosis and where is the hot spot within the GI tract for this to occur?

Back 136

Ischemic colitis; splenic flexure and distal colon.

Front 137

Where and in whom does angiodysplasia typically occur? What's the pathogenesis?

Back 137

Terminal ileum, cecum, ascending colon; occurs in elderly patients; Due to TORTUOUS DILATION OF VESSELS --> bleeding. Along with CRC is one of the MOST COMMON CAUSES OF GI BLEEDING IN THE ELDERLY.

Front 138

What characteristic of a carcinoid tumor determines whether or not a patient will develop carcinoid syndrome?

Back 138

LOCATION! If the tumor or its mets are contained within GI tract, 5-HT undergoes 1st pass metab in liver and no sx arise.

Front 139

What type of tumor comprises 50% of small bowel tumors? What type of cells is it composed of? What is its most common location?

Back 139

Carcinoid tumor; Neuroendocrine cells producing 5-HT; Appendix, ileum, and rectum.

Front 140

What are the classic symptoms of carcinoid syndrome? Labs? Tx?

Back 140

Bronchospasm, flushing, diarrhea, R-sided heart murmur; elevated 5-HIAA in urine; Tx with Octreotide.

Front 141

What are the symptoms of pellagra? What causes pellagra?

Back 141

Diarrhea, Dermatitis, Dementia; Deficient Vitamin B3 (Niacin) or its precursor, tryptophan.

Front 142

What enzyme is responsible for the conjugation of bilirubin? What drug increases the activity of this enzyme? When is this clinically useful?

Back 142

UDP-glucuronyl transferase. Phenobarbital. Tx w/ phenobarb is used in patients with Crigler-Najjar syndrome, type II.

Front 143

In which hereditary hyperbilirubinemia is UDPGT activity decreased and patients are asymptomatic unless under stress?

Back 143

Gilbert's syndrome.

Front 144

In which hereditary hyperbilirubinemia is UDPGT activity completely absent and treatment includes plasmaphoresis and phototherapy?

Back 144

Crigler-Najjar syndrome, type I.

Front 145

In which hereditary hyperbilirubinemia do you see a grossly black liver and elevated conjugated hyperilirubinemia?

Back 145

Dubin-Johnson syndrome.

Front 146

What would LFTs look like in an individual with alcoholic hepatitis? What would the histology reveal.

Back 146

AST:ALT >1.5; MALLORY bodies + necrotic, swollen hepatocytes.

Front 147

What drugs should you give to patients with cirrhosis of the liver and portal hypertension?

Back 147

Propranolol: Portal HTN
Diuretics +/- abx: Ascites
Vit K: Replace coag factors
Lactulose: Detox

Front 148

What enzyme is elevated in obstructive liver disease (HCC), obstructive biliary disease, and bone disease?

Back 148

Alkaline phosphatase.

Front 149

If ALP is elevated, how would you distinguish between a liver pathology or bone pathology?

Back 149

Get a GGT --> it's associated with BILIARY epithelium.

Front 150

What is the mechanism by which aspirin can cause Reye syndrome?

Back 150

ASA metabolites --> inhibit mitochondrial enzymes --> inhibition of β-oxidation --> decreased filtration of toxic blood substances = HEPATIC ENCEPHALOPATHY.

Front 151

What causes nutmeg liver? What will you see grossly? Clinically?

Back 151

Right-sided heart failure (you'll see JVD) and Bud-Chiari syndrome; blood backs up in the liver --> mottling of liver --> centrilobular congestion and necrosis --> "cardia cirrhosis".

Front 152

What is seen in Budd-Chiari syndrome? What conditions are associated with Budd-Chiari syndrome?

Back 152

Occlusion of hepatic veins and/or IVC cause POST-HEPATIC portal HTN --> centrolobular congestion and necrosis (nutmeg liver) --> congestive liver disease. Distinguished from cardiac cirrhosis by ABSENCE OF JVD!! Assoc w/hypercoaguable state, polycythemia vera, pregnancy, HCC.

Front 153

What medications are used to treat chronic hepatitis B and C infections?

Back 153

Hep B: IFN-α
Hep C: IFN-α + Ribavarin

Front 154

Which antibodies can be used to help make the diagnosis of autoimmune hepatitis?

Back 154

+ ANA
+ ANTI-SMOOTH MUSCLE ANTIBODY
+ Anti-liver-kidney microsomal antibody

Front 155

Leishmania donovani causes spiking fever, hepatosplenomegaly and pancytopenia. How is this bug transmitted? How is it treated? What does it look like under the microscope?

Back 155

SANDFLY; Sodium stibogluconate; Macrophages containing "amastigotes".

Front 156

Entamoeba hystolytica causes liver abcesses, RUQ pain, and bloody diarrhea. What do you see under the microscope? How is this treated?

Back 156

Flask-shaped ulcer if submucosal rupture occurs; it eats RBCs so you'll see RBCs in the cytoplasm of this bugger; Tx with metronidazole and iodoquinol.

Front 157

A young man presents with ataxia and tremors. He has a sick liver and brown pigmentation in a ring around the periphery of his cornea. What treatment should he receive.

Back 157

Penicillamine -- he has Wilson's disease.

Front 158

What is the classic triad of symptoms in hemochromatosis? What lab tests are used to dx? What is the tx?

Back 158

Cirrhosis, DM, skin pigmentation ("Bronze Diabetes"); Increased ferritin, increased iron, increased transferrin saturation, decreased TIBC; tx phlebotomy. These patients are at risk of CHF AND HCC!

Front 159

α1-antitrypsin deficiency causes liver and lung pathology. How does it do this?

Back 159

Misfolded gene product protein aggregates in hepatocellular ER --> cirrhosis with PAS-positive globules in the liver. In the lung, decreased inhibition of neutrophil elastase --> decreased elasticity of lungs --> panacinar emphysema.

Front 160

What are the risk factors for hepatic angiosarcoma?

Back 160

Vinyl chloride and arsenic exposure.

Front 161

What are the risk factors for the development of HCC? What tumor marker is associated w/HCC? To where does HCC metastasize?

Back 161

α1-antitrypsin deficiency, chronic HBV or HCV infection, Wilson's disease, alcoholic cirrhosis, carcinogens (aflatoxin from Aspergillus), hemochromatosis; α-FETOPROTEIN -- check serial levels of this!!! Mets to LUNGS.

Front 162

What is the fate of bilirubin after it is conjugated and secreted into the GI tract?

Back 162

Converted to urobilinogen by gut bacteria --> 80% excreted in feces, 20% gets recycled or excreted by kidney as urobilin.

Front 163

What enzyme is functioning sub-optimally in newborns with physiologic jaundice?

Back 163

UDP-glucuronyl transferase.

Front 164

What serum antibody is associated with primary biliary cirrhosis? How does this disease present?

Back 164

Anti-mitochondrial antibody (AMA); Presents with actinic pruritis and NO JAUNDICE early on (aka anicteric pruritis). This is an autoimmune process.

Front 165

What are the histological features and ERCP findings of primary sclerosing cholangitis? What other GI disease is this associated with? Any serum markers?

Back 165

Concentric onion-skinning fibrosis of the bile duct and alternating strictures and dilation with "beading" of intra and extrahepatic bile ducts; Associated with ulcerative colitis; +p-ANCA.

Front 166

What is the most common type of gallstone? What are the risk factors for developing these?

Back 166

Cholesterol stones; RFs: Female, fat, fertile, forty.

Front 167

When might you pigmented gallstones?

Back 167

In patients with chronic hemolysis or Clonorchis sinensis infection.

Front 168

What is Charcot's triad?

Back 168

Indicators of cholangitis: jaundice, fever, RUQ pain.

Front 169

What is Murphy's sign?

Back 169

Inspiratory arrest on deep palpation due to pain resulting from CHOLECYSTITIS.

Front 170

According to Golijan, what are the only two things you need to know about gallstones?

Back 170

Biliary colic and air in the biliary tree.

Front 171

What bug causes inflammation of the biliary tract? How do you treat this infection?

Back 171

Clonorchis sinensis from undercooked fish; tx is Praziquantel.

Front 172

What GI problems are associated with Down Syndrome?

Back 172

Duodenal atresia, Hirschsprung, Anular pancreas, Celiac sprue.

Front 173

What is the primary defect in Hirschsprung disease?

Back 173

FAILURE OF NEURAL CREST CELLS TO MIGRATE = Lack of ganglion cells/eneteric nervous plexuses (Auerbach's and Meissner's plexuses).

Front 174

What is the most common cause of appendicitis in adults? Children? What is the presentation?

Back 174

Obstruction d/t fecalith; lymphoid hyperplasia following infection; Initial diffuse periumbilical pain followed by localization to McBurney's point.

Front 175

What is the most common tumor of the appendix?

Back 175

Carcinoid tumor.

Front 176

Where is the most common location for a carcinoid tumor? What are the classic sx of carcinoid syndrome?

Back 176

Appendix; Tumor of the neuroendocrine cells = increased levels of 5HT3 --> R-sided heart murmur, diarrhea, flushing, bronchospasm.

Front 177

What condition can carcinoid syndrome lead to?

Back 177

PELLAGRA: Excessive 5HT3 synthesize --> decreased TRYPTOPHAN (precursor to 5HT3) --> decreased Niacin (Vit B3) --> Pellagra --> Dermatitis, Dementia, Diarrhea.

Front 178

What is the most abundant bacteria in the colon of most individuals?

Back 178

B. fragilis.

Front 179

Which pathological lesions of the colon are considered precursors to malignancy? Which colon pathology has the most malignant potential?

Back 179

Adenomatous polyps. Villous polyps (think "VILLainOUS).

Front 180

Where are most colonic polyps found?

Back 180

Rectosigmoid colon.

Front 181

What is the most common non-neoplastic polyp of the colon? Where is it likely to be found?

Back 181

Hyperplastic polyp, completely benign. >50% are found in the rectosigmoid colon.

Front 182

A patient presents with multiple nonmalignant hamartomas throughout the GI tract. You notice this patient also has hyperpigmented lips, hands, and genitalia (on closer examination, of course). What is the diagnosis? What is the inheritance pattern? What type of cancer is this patient at an increased risk for?

Back 182

Peutz-Jegers syndrome.
Autosomal dominant.
CRC.

Front 183

Iron-deficiency anemia in males over 50 yrs and post-menopausal women should raise your suspicion of what disease? What is the tumor marker for this disease? What will you see on a barium enema x-ray?

Back 183

CRC.
CEA tumor marker.
"Apple core" lesion.

Front 184

What is the presentation of CRC with regard to location? What are the sx associated with CRC in each location?

Back 184

Rectosigmoid > Ascending > Descending.
Ascending: exophytic, iron deficiency, weight loss.
Descending: infiltrating mass, obstruction, colicky pain, hematochezia.

Front 185

What are the risk factors for CRC?

Back 185

IBD, tobacco use, Peutz-Jegers syndrome, Juvenile polyposis syndrome, large villous adenomas, S. bovis bacteremia.

Front 186

Familial Adenomatous Polyposis is associated with what gene? What is the defect? What is the presentation?

Back 186

Autosomal dominant mutation of the APC gene on CHROMOSOME 5q21.
100% progress to CRC.
THOUSANDS of polyps.
PANCOLONIC, always involve rectum.
Prophylactic resection of bowel.

Front 187

What is Gardner's syndrome?

Back 187

FAP + osseous and soft tissue tumors, retinal hyperplasia.

Front 188

What is Turcot's syndrome?

Back 188

FAP + malignant CNS tumor.

Front 189

Which segment of the bowel is affected in Hereditary Non-Polyposis Colorectal Cancer (HNPCC)/Lynch Syndrome? What is the genetic defect?

Back 189

Proximal colon.
Autosomal dominant mutation in the DNA mismatch repair genes.
80% progress to CRC.

Front 190

What are the two molecular pathways associated with development of CRC?

Back 190

1. APC/β-catenin (chromosomal instability) pathway = 85%
2. Microsatellite instability pathway = 15%

Front 191

Which gene mutations is the Microsatellite instability pathway of CRC associated with?

Back 191

MMR gene mutations --> sporadic and HNPCC/Lynch syndrome.

Front 192

What is the series of mutations that occurs in the APC/β-catenin pathway of CRC?

Back 192

Loss of APC gene --> colon at risk.
K-RAS mutation --> adenoma.
Loss of p53 --> carcinoma.

Front 193

What is the most common cause of massive lower GI bleeding? Where does this most commonly occur?

Back 193

Diverticulosis. Sigmoid colon.

Front 194

I say "Left-sided appendicitis", you say...

Back 194

Diverticulitis.

Front 195

How is diverticulitis treated?

Back 195

Abx: Metronidazole + ONE of these:
TMP:SMX
Levofloxacin
Ciprofloxacin

Front 196

What weird kind of fistula can present with diverticulitis?

Back 196

Colovesical. Fistula between colon and bladder. Pee air!

Front 197

I am a volvulus. Where might I like to live and within whom? What problem can I cause?

Back 197

Cecum and sigmoid colon. Elderly folks. Obstruction and infarction.

Front 198

What is the arterial and venous supply to the anus above and below the pectinate line?

Back 198

Above pectinate line: superior rectal artery (branch of inferior mesenteric) and superior rectal vein.
Below pectinate line: inferior rectal artery (branch of internal pudendal artery) and inferior rectal vein.

Front 199

Colonoscopy reveals friable mucosa extending from RECTUM to distal transverse colon. Imaging reveals a "lead pipe" appearance due to loss of haustra. Diagnosis? Tx?

Back 199

Ulcerative colitis.
Tx with ASA preparations (sulfasalazine). 6-MP. Infliximab. Colectomy.

Front 200

What is a major complication of ulcerative colitis? What are the extraintestinal manifestations of ulcerative colitis?

Back 200

Markedly increased risk of CRC.
Pyoderma gangrenosum. Primary sclerosing cholangitis. Ankylosing spondylitis. Uveitis.