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105 Cards in this Set
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nausea, vomiting, diarrhea, abdominal pain, myalgias; low-grade fever
Labs = no fecal WBC; viral culture indicates pathogen (usually unnecessary) |
Viral Gastroenteritis
Self-limited viral infection of GI tract |
Treatment = maintain hydration status; self-limited (48–72 hours)
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Vomiting within several hours of eating, diarrhea later
Source=Fried rice |
Bacterial Gastroenteritis
Bacillus cereus |
Treatment = maintain hydration status; self-limited
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Bloody diarrhea, abdominal pain, fever; rare Guillain-Barré syndrome
Source=Poultry |
Bacterial Gastroenteritis Campylobacter jejuni
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Treatment=Hydration, erythromycin; generally self-limited
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Nausea, vomiting, diarrhea, flaccid paralysis
Source=Honey, home-canned foods |
Bacterial Gastroenteritis
Clostridium botulinum |
Treatment=Botulism antitoxin (not given to infants); self-limited
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Watery diarrhea; gray pseudomembranes seen on colonic mucosa
Source=Antibiotic-induced suppression |
Bacterial Gastroenteritis
Clostridium difficile |
Treatment=Metronidazole, Vancomycin
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Watery diarrhea, vomiting, fever
Source=travelers' Food/water |
Bacterial Gastroenteritis
Escherichia coli (enterotoxigenic) |
Treatment=Hydration; self-limited
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Bloody diarrhea, vomiting, fever, abdominal pain (risk of HUS)
Source=Ground beef, indirect fecal contamination |
Bacterial Gastroenteritis
E. coli type O157:H7 (enterohemorrhagic) |
Treatment=Hydration; self-limited; antibiotics may actually worsen symptoms
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Vomiting, within several hours of eating; diarrhea later
Source=Room-temperature food |
Bacterial Gastroenteritis
Staphylococcus aureus |
Treatment=Self-limited; hydration
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Nausea, abdominal pain, bloody diarrhea, fever, vomiting
Source=Eggs, poultry, milk, fresh produce |
Bacterial Gastroenteritis
Salmonella species (MCC) |
Treatment=Hydration; self-limited; fluoroquinolone for immunocompromised
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Fever, nausea, vomiting, severe bloody diarrhea, abdominal pain (risk of HUS)
Source=food/water, overcrowding |
Bacterial Gastroenteritis
Shigella species |
Treatment=Hydration; self-limited; ciprofloxacin, TMP- SMX in severe cases
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Copious watery diarrhea, signs of dehydration
Source=Water, seafood |
Bacterial Gastroenteritis
Vibrio cholerae |
Treatment=Hydration; tetracycline or doxycycline decreases disease length
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Abdominal pain, watery diarrhea within 24 hr of eating
Source=Seafood (oysters) |
Bacterial Gastroenteritis
Vibrio parahaemolyticus |
Treatment=Hydration; self-limited
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Abdominal pain, bloody diarrhea, right lower quadrant pain, fever
Source=Pork, produce |
Bacterial Gastroenteritis
Yersinia enterocolitica |
Treatment=Hydration; self-limited
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Greasy, foul-smelling diarrhea; abdominal pain, malaise; cysts and trophozoites seen in stool sample
Source=Surface water (usually limited to wilderness or other countries) |
Parasitic and Protozoan Gastrointestinal Infections
Giardia lamblia |
Treatment=Metronidazole; hydration
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Mild to severe bloody diarrhea, abdominal pain; cysts and trophozoites seen in stool sample
Source=Water, areas of poor sanitation |
Parasitic and Protozoan Gastrointestinal Infections
Entamoeba histolytica |
Treatment=Metronidazole, paromomycin
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Watery diarrhea, abdominal pain, malaise in immunocompromised patients; acid-fast stain of stool shows parasites
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Parasitic and Protozoan Gastrointestinal Infections
Cryptosporidium parvum |
Treatment=Control immune suppression; nitazoxanide
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Fever, myalgias, periorbital edema; eosinophilia
Source=Undercooked pork |
Parasitic and Protozoan Gastrointestinal Infections
Trichinella spiralis |
Treatment=Albendazole, mebendazole if CNS or cardiac symptoms
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Mild diarrhea, CNS symptoms
Source=Undercooked pork |
Parasitic and Protozoan Gastrointestinal Infections
Taenia solium |
Treatment=Praziquantel, corticosteroids if >5 cysts
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H/P = possibly asymptomatic; malaise, arthralgias, fatigue, nausea, vomiting, right upper quadrant pain; jaundice, scleral icterus, tender hepatomegaly, splenomegaly, lymphadenopathy
Labs = bilirubinuria, increased aspartate aminotransferase (AST), increased alanine aminotransferase (ALT), increased bilirubin (total), increased alkaline phosphatase |
Hepatitis
RF=IV drug, alcoholism, travel to developing nations, poor sanitation |
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Hepatitis
Picornavirus (single-stranded RNA) by Food (shellfish), fecal-oral |
Hepatitis A
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Treatment=Self-limited; supportive care
Prevention=Vaccine before travel |
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Hepatitis
Hepadnavirus (double-stranded DNA) by Blood, other body fluids (including sexual contact) |
Hepatitis B
Complication=chronic hepatitis (5% adult,90%kid), cirrhosis, hepatocellular carcinoma(3-5%), persistent carrier state, 1% develop fulminant hepatic failure |
Treatment=HBV immediately after exposure in unvaccinated patients; IFN-α or antivirals (lamivudine, adefovir, entecavir)
Vaccine |
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Hepatitis
by Blood, possibly sexual contact Flavivirus (single-stranded RNA) |
Hepatitis C
Complication=chronic hepatitis(80%), cirrhosis(50% of chronic ), slightly increased risk of hepatocellular carcinoma, persistent carrier state |
Treatment=IFN-α; consider ribavirin
NO vaccine |
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Hepatitis D
by Blood; requires coexistent hepatitis B infection Delta agent (incomplete single-stranded RNA) |
Hepatitis D
Complication=Severe hepatitis, cirrhosis, persistent carrier state |
Treatment=IFN-α, Hepatitis B vaccine
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Hepatitis
by Water, fecal-oral Calicivirus (single-stranded RNA) |
Hepatitis E
Complication=High infant mortality in pregnancy |
Treatment=Self-limited; supportive care
No Vaccine |
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Hepatitis B Serology
HBsAg+, HBeAg+, anti-HBs Ab-, anti-HBe Ab-, anti-HBc IgM+ |
Acute infection
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(4–12 wk postexposure)
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Hepatitis B Serology
HBsAg-, HBeAg-, anti-HBs Ab-, anti-HBe Ab-, anti-HBc IgM+ |
Acute infection window period
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(12–20 wk postexposure)
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Hepatitis B Serology
HBsAg+, HBeAg+, anti-HBs Ab-, anti-HBe Ab-, anti-HBc IgG+ |
Chronic infection, active viral replication
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Hepatitis B Serology
HBsAg+, HBeAg-, anti-HBs Ab-, anti-HBe Ab+, anti-HBc IgG+ |
Chronic infection, lesser viral replication
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(good prognosis)
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Hepatitis B Serology
HBsAg-, HBeAg-, anti-HBs Ab+, anti-HBe Ab+, anti-HBc IgG+ |
Past infection (recovered)
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Hepatitis B Serology
HBsAg-, HBeAg-, anti-HBs Ab+, anti-HBe Ab-, anti-HBc IgG- |
Vaccination
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H/P = enlarged and painful glands; pain worsens during eating; parotid glands may have painless swelling
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Salivary gland disorders
Dysfunction in sublingual, submandibular, or parotid glands resulting from ductal obstruction or inflammation sialolithiasis (ductal stone) in any salivary gland; parotid disease can also be caused by sarcoidosis, infection, or neoplasm |
Treatment = warm compresses, massage, or cough drops may help remove ductal stones; antibiotics and hydration for infection; surgery may be required for relief in refractory cases
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H/P = feeling of “food stuck in throat” when swallowing, cough, solids (mechanical pathology) or solids and liquids (dysmotility) may be difficult to swallow
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Dysphagia
Difficulty swallowing because of oropharyngeal or esophageal transport dysfunction or pain with swallowing (i.e., odynophagia) caused by neuromuscular disorders (e.g., achalasia, motility disorders, scleroderma) or obstruction (e.g., peptic strictures, esophageal webs or rings, cancer, radiation fibrosis) Obstructive pathology tends to limit swallowing of solids; neuromuscular pathology tends to limit swallowing of solids and liquids |
Labs = manometry measures esophageal pressure and may detect neuromuscular abnormality
Radiology = barium swallow before esophagogastroduodenoscopy (EGD) may be helpful for diagnosis |
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H/P = gradually progressive dysphagia of solids and liquids, regurgitation, cough, aspiration, heartburn, weight loss from poor intake
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Achalasia
Neuromuscular disorder of esophagus with impaired peristalsis and decreased lower esophageal sphincter (LES) relaxation because intramural neuron dysfunction |
Labs = manometry shows increased LES pressure, incomplete LES relaxation, and decreased peristalsis
Radiology = barium swallow shows “bird's beak” sign, with tapering at the LES; EGD r/o malignancy Treatment =pneumatic dilation, botulinum injections, or myotomy relieve obstruction; nitrates and calcium channel blockers relax LES, but are rarely used because of simultaneous cardiac effects |
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H/P = chest pain, dysphagia
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Diffuse esophageal spasm
Neuromuscular disorder in which nonperistaltic contractions of the esophagus occur |
Labs = manometry shows nonperistaltic, uncoordinated esophageal contractions
Radiology = barium swallow shows “corkscrew” pattern Treatment = calcium channel blockers, nitrates, or tricyclic antidepressants help reduce chest pain and dysphagia |
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H/P = regurgitation of food several days after eating, bad breath, difficulty initiating swallowing, occasional dysphagia, feeling of aspiration
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Zenker diverticulum
Outpouching in upper posterior esophagus caused by smooth muscle weakness |
Radiology = barium swallow shows outpouching
Treatment = cricopharyngeal myotomy or diverticulectomy Complications = EGD can perforate weakness in esophageal wall; vocal cord paralysis, mediastinitis possible with surgery |
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H/P = burning chest pain (“heartburn”) 30–90 min after eating, sour taste in mouth, regurgitation, dysphagia, odynophagia, nausea, cough; pain may worsen when lying down and lessens with standing
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Gastroesophageal reflux disease (GERD)
Low pressure in LES leads to abnormal reflux of gastric contents into esophagus Risk factors = obesity, hiatal hernia, pregnancy, scleroderma Complications = esophageal ulceration, esophageal stricture, Barrett's esophagus, adenocarcinoma |
Labs = esophageal pH monitoring can detect increased acidity from reflux
Radiology = usually unneeded for diagnosis; EGD, chest radiograph, or barium swallow can help r/o neoplasm, Barrett's esophagus&hiatal hernia Treatment = Elevation of head of bed, weight loss, dietary modification. Initial medications are antacids followed by H2 antagonists (10%–25% effective), proton pump inhibitors (PPI) (60%–75% effective), and promotility agents; Refractory disease may be treated with Nissen fundoplication or hiatal hernia repair |
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H/P = progressive dysphagia (initially solids, later solids and liquids), weight loss, odynophagia, reflux, GI bleeding, vomiting, weakness, cough, hoarseness
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Esophageal cancer
Squamous> adenocarcinoma Barrett's esophagus (columnar metaplasia of distal esophagus secondary to chronic GERD) commonly precedes adenocarcinoma Risk factors = alcohol, tobacco, chronic GERD, obesity (only for adenocarcinoma) Complications = poor prognosis; local extension and metastases frequently present by time of diagnosis |
Labs = biopsy used to make diagnosis
Radiology = barium swallow shows narrowing of esophagus and abnormal mass; MRI, CT w/contrast, or PET scan can determine extension and mets; EGD used to identify mass and perform biopsy Treatment = surgical resection (including total esophagectomy) for early stage disease; radiation and chemotherapy used in nonoperative (advanced) cases or as neoadjuvant therapy to surgery |
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H/P = possibly asymptomatic; symptoms associated with GERD
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Hiatal hernia
Herniation of part of stomach above diaphragm Sliding: gastroesophageal junction and stomach displaced through diaphragm (95% cases) Paraesophageal: stomach protrudes through diaphragm, but gastroesophageal junction remains in normal location Complications = incarceration of stomach in herniation (seen in paraesophageal type) |
Radiology = barium swallow shows portion of stomach above diaphragm; chest radiograph may detect hernia without barium swallow if air in stomach is visible above diaphragm
Treatment = sliding hernias treated w/ reflux control; paraesophageal hernias may need surgical repair (e.g., gastropexy, Nissen fundoplication) |
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H/P = possibly asymptomatic; epigastric pain, indigestion, nausea, vomiting, hematemesis, melena
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Acute Gastritis
Inflammation of gastric mucosa characterized by rapidly developing, superficial lesions; can involve any region of the stomach RF: nonsteroidal anti-inflammatory drug (NSAID) use, alcohol, ingestion of corrosive materials, or stress from severe illness; |
Treatment =
Treat acute form as peptic ulcer disease (PUD) and stop alcohol and offending medications; give H2 antagonists or PPI to patients with severe illnesses |
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Gastritis
Lab=Decreased gastric acid level, decreased gastrin |
Type A Chronic Gastritis
Inflammation of gastric mucosa @ Fundus Ab for parietal cells->low levels of intrinsic factor, vitamin B12 malabsorption, and megaloblastic anemia. Ass. w/ Pernicious anemia, achlorhydria, thyroiditis |
Lab=ratio of pepsinogen isoenzymes useful to detect autoimmune cause
Treatment = requires vitamin B12 replacement |
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Gastritis
Lab=Increased gastric acid level->+ urea breath test; |
Type B Chronic Gastritis
Inflammation of gastric mucosa @ Antrum Helicobacter pylori infection Ass. w/ Peptic ulcer disease, gastric cancer |
Lab=+ IgG Ab to Helicobacter pylori; antral biopsy can detect H. pylori infection
Treatment = eradication of H. pylori through multidrug treatment (typically, PPI, clarithromycin, & either amoxicillin or metronidazole × 7–14 days) |
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H/P = periodic burning epigastric pain that can change (better or worse) with eating, nausea, hematemesis, melena, hematochezia; epigastric tenderness; abdominal rigidity, rebound tenderness, and rigidity seen following acute perforation of ulcer
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Peptic ulcer disease (PUD)
Erosion of gastric and duodenal mucosa 2nd to impaired endothelial defenses and increased gastric acidity RF: ANGST HAM: Aspirin, NSAIDs, Gastrinoma (ZES), Steroids, Tobacco, H. pylori, Alcohol, MEN type I. Complications = hemorrhage (posterior ulcers may erode into gastroduodenal artery), perforation (most commonly anterior ulcers), lymphoproliferative disease |
Labs = + urea breath test, IgG Ab, or biopsy detect H. pylori; CBC assess degree of bleeding
Radiology = abdominal x-ray (AXR) to detect perforation (free air under diaphragm seen following perforation); barium swallow AXR can demonstrate collections of barium in ulcerations; EGD for biopsy & detect active bleeding, r/o gastric adenocarcinoma if symptoms lasting >2 months; Treatment = Decrease gastric acid levels with PPI and H2 antagonist; protect mucosa with sucralfate, bismuth subsalicylate, or misoprostol; eliminate H. pylori infection (as described above for treatment of gastritis); Surgery required to repair acute perforations; persistent, non-neoplastic refractory cases may require parietal cell vagotomy or antrectomy |
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PUD: Ab pain Soon after eating, Eating worsen symptoms and cause nausea and vomiting
Age >50 yr old, Helicobacter pylori infection, NSAID users |
Gastric Ulcer
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Lab=Normal/low Gastric acid level; High Gastrin level
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PUD: Ab pain 2–4 hr after eating, Eating make initial improvement in symptoms, with later worsening
Younger patient |
Duodenal Ulcer
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Lab=High Gastric acid level; Normal Gastrin level
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H/P = refractory PUD, abdominal pain, nausea, vomiting, indigestion, diarrhea, steatorrhea, possible history of other endocrine abnormalities
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Zollinger-Ellison syndrome
Syndrome secondary to gastrin-producing tumor most frequently located in duodenum (70% cases) or pancreas Ass w/ malabsorption disorders Complications = occasional w/ other endocrine tumors (e.g., multiple endocrine neoplasia I [MEN I]) 60% of lesions are malignant |
Labs = increased fasting gastrin; + secretin-stimulation test (i.e., administration causes > expected serum gastrin levels); specific gastrin sampling in several pancreatic or abdominal veins can help localize tumor
Radiology = somatostatin receptor imaging using single-photon emission computed tomography (SPECT) can localize tumors; angiography may detect tumor if hypervascular Treatment = surgical resection for nonmetastatic disease w/ localized tumor; PPI and H2 antagonists may ease symptoms; octreotide may help reduce symptoms in metastatic disease |
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H/P = weight loss, anorexia, early satiety, vomiting, dysphagia, epigastric pain; enlarged left supraclavicular lymph node (i.e., Virchow's node) or periumbilical node (i.e., Sister Mary Joseph's node)
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Gastric cancer
Adenocarcinoma (common) or squamous cell carcinoma (rare; caused by invasion from esophagus) affecting stomach Types Ulcerating: resembles ulcers seen in PUD Polypoid: large, intraluminal neoplasms Superficial spreading: mucosal and submucosal involvement only; best prognosis Linitis plastica: all layers of stomach involved; decreased stomach elasticity; poor prognosis RF= H. pylori, family history, Japanese person living in Japan, tobacco, alcohol, vitamin C deficiency, high consumption of preserved foods; males > females Complications = early detection=high cure rate (>70%), poor prognosis in later detection (<15% 5-yr survival) |
Labs = increased carcinoembryonic antigen (CEA), increased 2-glucuronidase in gastric secretions, anemia if active bleeding; biopsy used for diagnosis
Radiology = barium swallow may show mass or thickened “leather bottle” stomach (linitis plastica); EGD used to perform biopsy and visualize ulcers Treatment = subtotal gastrectomy for lesions in distal third of stomach, total gastrectomy for lesions in middle or upper stomach or invasive lesions; adjuvant chemotherapy and radiation therapy |
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H/P = failure to thrive, bloating, and abnormal stools in infants; diarrhea, steatorrhea, weight loss, and bloating in adults; some patients will exhibit depression, anxiety, or arthralgias
Labs = + antiendomysial & antigliadin Ab in serum; biopsy shows loss of duodenal & jejunal villi |
Celiac sprue
Genetic disorder characterized by gluten intolerance (e.g., wheat, barley, rye) Immune-mediated process with antiendomysial & antigliadin antibodies that cause jejunal mucosal damage |
Treatment = removal of gluten from diet (can still eat corn, rice); refractory disease may require corticosteroids
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H/P = failure to thrive, bloating, and abnormal stools in infants; diarrhea, steatorrhea, weight loss, and bloating in adults; some patients will exhibit depression, anxiety, or arthralgias
Acquired disorder in patients living in tropical areas; can present years after leaving tropics |
Tropical sprue
Malabsorption syndrome similar to celiac sprue, with possible infectious or toxic etiology |
Treatment = folic acid replacement, tetracycline; removal of gluten from diet has no effect
Labs = cultures&appropriate serology r/o acute GI infection, celiac sprue, & autoimmune diseases |
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H/P = diarrhea, abdominal pain, flatulence, and bloating after dairy consumption
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Lactose intolerance
Malabsorption syndrome resulting from deficiency of lactase; can also be secondary to Crohn's disease or bacterial overgrowth Lactose not metabolized in jejunum, leading to osmotic diarrhea |
Labs = + lactose tolerance test (i.e., min increase in serum glucose following ingestion of lactose),+ lactose breath hydrogen test after lactose meal
Treatment = lactose-restricted or lactose-free diet; adequate dietary protein, fat, calcium, and vitamins; lactase replacement may benefit some patients |
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H/P = weight loss, joint pain, abdominal pain, diarrhea, dementia, cough, bloating, steatorrhea; fever, vision abnormalities, lymphadenopathy, new heart murmur; severe wasting late in disease course
Labs = jejunal biopsy shows foamy macrophages on periodic acid-Schiff (PAS) stain and villous atrophy |
Whipple disease
Malabsorption disorder 2nd to Tropheryma whippelii infection & likely immune deficiency RF= white males with European ancestry |
Treatment = trimethoprim-sulfamethoxazole (TMP-SMX) or ceftriaxone for 12 months
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H/P=chronic abdominal pain and irregular bowel habits
begins during teens or young adulthood Pain relieved with defecation Stool frequency increases following onset of pain Stools become looser following onset of pain Visible abdominal distention Passage of mucus with stool Feeling of incomplete defecation |
Irritable bowel syndrome (IBS)
Females > males (2 to 1) Manning Criteria (seeH/P) |
Labs = r/o other GI diseases with CBC, electrolytes, stool culture
Radiology = consider AXR, abdominal CT, or barium studies to r/o other GI causes; colonoscopy may be performed in older to r/o neoplasm Treatment = assurance from physician, high-fiber diet, possible psychosocial therapy; antispasmodic, antidepressants, serotonin receptor antagonists have shown use in lessening symptoms |
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H/P = acute abdominal pain out of proportion to examination, bloody diarrhea, vomiting; mild abdominal tenderness
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Ischemic colitis
Ischemia and necrosis of bowel secondary to vascular compromise Caused by embolus, bowel obstruction, inadequate systemic perfusion, medication, or surgery-induced vascular compromise Left side of the colon is most commonly involved in ischemic colitis RF=DM, atherosclerosis, CHF, peripheral vascular disease, lupus Complications = high mortality in cases of irreversible damage |
Labs = increased white blood cell count (WBC), increased serum lactate
Radiology = barium enema shows diffuse submucosal changes from localized bleeding (i.e., “thumb printing”); sigmoidoscopy may show bloody and edematous mucosa; CT may show air within bowel wall and bowel wall thickening Treatment = intravenous (IV) fluids, bowel rest, antibiotics for GI bacteria; surgical resection of necrotic bowel |
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H/P=Abdominal pain, weight loss, watery diarrhea
Fever, RLQ abdominal mass, abdominal tenderness, perianal fissures&fistulas, oral ulcers blood on rectal examination Lab=ASCA+, hemoccult + |
Crohn's Disease
Entire GI tract may be involved with multiple “skipped” areas; distal ileum most commonly involved; entire bowel wall affected Ass. w/ nephrolithiasis, arthritis, ankylosing spondylitis, uveitis, primary sclerosing cholangitis Complication=Abscess formation, fistulas, fissures, malabsorption, toxic megacolon |
Radiology=Colonoscopy shows colonic ulcers, strictures, “cobblestoning,” fissures, and “skipped” areas of bowel; barium barium enema shows fissures, ulcers, and bowel edema
Treatment=Mesalamine, broad-spectrum antibiotics, corticosteroids, immunosuppressives; surgical resections of severely affected areas, fistulas, or strictures |
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H/P=Abdominal pain, urgency, bloody diarrhea, tenesmus, nausea, vomiting, weight loss
Fever, abdominal tenderness, orthostatic hypotension, tachycardia, gross Lab=pANCA + |
Ulcerative Colitis
Continuous disease beginning at rectum and extending possibly as far as distal ileum; only mucosa and submucosa affected Ass. w/ erythema nodosum, pyoderma gangrenosum, arthritis, uveitis, ankylosing spondylitis, primary sclerosing cholangitis Complication=Significantly increased risk of colon cancer, hemorrhage, bowel obstruction, toxic megacolon |
Radiology=Colonoscopy shows continuous involvement, pseudopolyps, friable mucosa; enema shows “lead pipe” colon without haustra and colon shortening
Treatment=Mesalamine, supplemental iron, corticosteroids, immunosuppressives; total colectomy is curative |
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H/P = dull periumbilical pain followed by nausea, vomiting, and anorexia; pain gradually moves to RLQ and increases; tenderness at McBurney's point (1/3 distance from right anterior superior iliac spine to umbilicus), rebound tenderness, psoas sign (psoas pain on hip extension), fever, Rovsing's sign (RLQ pain w/ LLQ palpation); perforation produces severe pain and distention with rebound tenderness, rigidity, and guarding
Labs = increased WBC w/ left shift |
Appendicitis
Inflammation of appendix with possible infection or perforation Caused by lymphoid hyperplasia (children), fibroid bands (adults), or fecaliths (adults) Complications = abscess formation, perforation |
Lab=CBC
Radiology = AXR or chest x-ray may show fecalith or free air under the diaphragm (due to perforation); CT most sensitive test and may show bowel wall thickening, appendicolith, abscess, phlegmon, free fluid, or right lower quadrant fat-stranding Treatment = appendectomy; antibiotics added (covering Gram-negatives and anaerobes) for ruptured appendix |
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H/P = vague abdominal pain, nausea, vomiting, bloating, no bowel movements, inability to tolerate meals; decreased bowel sounds, no rebound tenderness
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Ileus
Paralytic obstruction of bowel 2nd to decreased peristalsis Caused by infection, ischemia, recent surgery, DM, opioid use |
Radiology = AXR shows distention of affected bowel, air–fluid levels; barium enema can help r/o obstruction
Treatment = stop opioids, make patient NPO (i.e., nothing by mouth); colonoscopic decompression if no resolution |
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H/P = distention, abdominal pain, vomiting, obstipation; possible palpable abdominal mass
Tends to occur in elderly and infants |
Volvulus
Rotation of bowel creates obstruction and possible ischemia; most commonly occurs at cecum and sigmoid colon |
Radiology = AXR may show “double bubble” proximal and distal to volvulus; barium enema shows “bird's beak” for distal volvulus
Treatment = possibly self-limited; colonoscopic decompression of sigmoid volvulus; surgical repair or resection may be required in cecal volvulus or failed colonoscopic detorsion |
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H/P = frequently asymptomatic during uncomplicated diverticulosis; occasional cramping, bloating, flatulence, irregular defecation; possible painless rectal bleeding if erosion into vessel occurs
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Diverticulosis
Outpouchings of colonic mucosa and submucosa that herniate through muscular layer (i.e., diverticulosis); may erode into colonic blood vessel to cause bleeding RF= low-fiber diet, high-fat diet, >60 yr of age Complications = diverticulitis, diverticular colitis (i.e., inflammation of section of colon) |
Radiology = diverticula seen on barium enema and colonoscopy
Treatment = high-fiber diet may help prevent development of additional diverticuli or diverticular bleeding |
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H/P = LLQ pain, nausea, vomiting, melena, hematochezia; abdominal tenderness, possible palpable abdominal mass, fever, abdominal distention
Labs = increased WBC |
Diverticulitis
Obstruction of a diverticulum leading to significant inflammation, focal bowel wall necrosis, and perforation; poor containment of colonic rupture leads to peritonitis Complications = colonic abscess, fistula formation, sepsis |
Labs=CBC
Radiology = CXR or AXR may demonstrate free air under the diaphragm; CT shows increased soft tissue density caused by inflammation, colonic diverticula, bowel wall thickening, and possible abscess formation Treatment = Mild early cases without perforation can be treated by bowel rest (liquids only for at least 3 days) and PO antibiotics (e.g., fluoroquinolone and metronidazole, TMP-SMX and metronidazole, or amoxicillin-clavulanate) Surgery required in most cases to resect involved segment of colon and remove any obstruction or fistula; diverting colostomy performed in cases of peritonitis (reanastomosis in 3 months) Broad-spectrum antibiotics required for any case of bowel rupture |
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H/P=Abdominal pain, vomiting, distention, obstipation
Visible peristaltic waves, ab tenderness,high-pitched bowel sounds, absence of bowel sounds, fever |
Small Bowel Obstruction
Due to Adhesions, incarcerated hernias, neoplasm, intussusception, volvulus, Crohn's disease, congenital stricture |
Radiology=AXR shows ladder-like dilated loops of bowel, air-fluid levels
Treatment=Make patient NPO, maintain hydration; nasogastric decompression may relieve obstruction but, if unsuccessful, surgery is required |
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H/P=Abdominal pain, obstipation, distention, nausea, late feculent vomiting
Palpable mass, ab tenderness, high-pitched bowel sounds, absence of bowel sounds |
Large Bowel Obstruction
Due to Neoplasm, diverticulitis, volvulus, congenital stricture |
Radiology=AXR shows bowel distention proximal to obstruction; barium enema may detect obstruction near rectum
Treatment=Make patient NPO, maintain hydration; colonoscopy may relieve obstruction but, if unsuccessful, surgery is required |
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Internal and external engorged rectal veins causing bleeding (bright-red blood)
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Hemorrhoids
Internal hemorrhoids arise from superior rectal veins above the pectinate line (columnar rectal epithelium); characteristically painless External hemorrhoids arise from inferior rectal veins below the pectinate line (squamous rectal epithelium); frequently painful (especially if thrombosed) |
Radiology = sigmoidoscopy r/o other causes of bleeding
Treatment = warm baths, increase fiber in diet, avoid prolonged straining; sclerotherapy, ligation, or excision can be performed for worsening symptoms |
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Painful, bleeding tears in posterior wall of anus secondary to trauma during defecation or anal intercourse
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Anal fissures
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Treatment = stool softeners, topical nitroglycerin; partial sphincterotomy may be performed for recurrent fissures
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H/P = throbbing rectal pain; fever, tenderness on digital examination
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Anorectal abscesses
Infection of anal crypts, internal hemorrhoids, or hair follicle leading to abscess formation |
Treatment = antibiotics, surgical incision and drainage
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H/P = mild pain during defecation; possible visible site draining pus
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Rectal fistula
Formation of tract between rectum and adjacent structures from unknown cause or secondary to IBD or abscess formation |
Treatment = fistulotomy; treat patients with Crohn's disease w/ antibiotics & immunosuppressants unless refractory disease
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H/P = usually asymptomatic; obstruction of sinus leads to mildly painful cyst with drainage (possibly purulent); small cysts can progress to larger abscesses
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Pilonidal disease
Presence of one or more cutaneous sinus tracts in the superior midline gluteal cleft Obstruction of sinus tract by hair or debris can lead to cyst and abscess formation |
Treatment = incision and drainage of abscesses; surgical closure of sinus tracts may prevent recurrence
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H/P = possibly asymptomatic; abdominal pain; possible carcinoid syndrome (i.e., flushing, diarrhea, bronchoconstriction, tricuspid/pulmonary valvular disease) caused by serotonin secretion by tumor (only seen with liver metastases or extragastrointestinal involvement)
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Carcinoid tumor
Tumors arising from neuroectodermal cells that function as amine-precursor-uptake and decarboxylation (APUD) cells Most commonly in appendix, ileum, rectum, stomach |
Labs = increased 5-HIAA in urine, serum serotonin level
Radiology = CT or indium-labeled octreotide scintigraphy can localize tumor Treatment = tumors <2 cm have very low incidence of metastases and should be resected; tumors >2 cm have high risk of metastases and require extensive resection; metastatic disease treated with IFN-α, octreotide, and embolization |
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H/P = change in bowel habits (more common in left-sided disease), weakness, right-sided abdominal pain (in right-sided disease), constipation, hematochezia, melena, malaise, weight loss; abdominal or rectal mass may be palpated
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Colorectal cancer
Neoplasm of large bowel or rectum; most commonly adenocarcinoma Risk factors = family history, ulcerative colitis, colonic polyps, hereditary polyposis syndromes, low-fiber/high-fat diet, previous colon cancer, alcohol, smoking, DM Spreads to regional lymph nodes; metastasizes most commonly to lung and liver Prevention =Regular screening for colon cancer recommended in patients >50 yr of age Annual fecal occult blood test (FOBT) Flexible sigmoidoscopy every 5 yr (in addition to FOBT) Colonoscopy is more sensitive than sigmoidoscopy |
Labs = + stool guaiac test, decreased hemoglobin & hematocrit; biopsy is diagnostic; CEA useful for monitoring treatment success and cancer recurrence
Radiology = barium enema may detect lesion; colonoscopy may detect lesion and obtain biopsy specimens; CT or PET used to determine local extent of disease and spread of metastases Treatment = Surgical resection, regional lymph node dissection; adjuvant chemotherapy in cases of positive lymph nodes; palliative resections are helpful in metastatic disease to reduce symptoms and remove obstruction Preventative colectomy may be indicated for hereditary syndromes Duke's classification can be used for prognosis; CEA may be followed after treatment to monitor for recurrence |
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Bright-red blood (e.g., hematochezia) suggests a rapid or heavy bleed; dark blood (e.g., melena, coffee-grounds emesis) suggests either blood that has passed through much of the GI tract or has been sitting in the stomach for some time
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GI Bleeding
Upper:PUD, Mallory-Weiss tears (longitudinal esophageal tears secondary to violent retching), esophagitis, esophageal varices, gastritis Lower:diverticulosis, neoplasm, ulcerative colitis, mesenteric ischemia, AVMs, hemorrhoids, Meckel's diverticulum |
Radiology = NG tube lavage to r/o upper/rapid->EGD or colonoscopy shows most sources of bleeding; barium studies may detect defects; angiography can help locate AVMs; technetium scan can locate Meckel's diverticulum
Treatment = fluid replacement is vital; transfusion for increased blood loss; some small bleeds stop automatically; treat underlying cause; PPI for upper GI bleeds until gastric cause ruled out; prophylactic antibiotics in patients with a known history of cirrhosis; sclerotherapy may help stop bleeding from varices; vasopressin may stop bleeding from AVMs and diverticula; surgical resection of tumors and diverticula may be needed |
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H/P=Acute epigastric pain radiating to back, nausea, vomiting, Grey Turner's sign (bluish discoloration of flank), Cullen's sign (periumbilical discoloration), fever, tachycardia; hypotension, shock if severe
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Acute Pancreatitis
Initially, results from leak of pancreatic enzymes into pancreatic and surrounding tissues; later caused by pancreatic tissue necrosis; RF=Gallstones, alcoholism, trauma, hypercalcemia, hyperlipidemia, drugs Complication=Complications Pancreatic abscess, pseudocyst, necrosis, fistula formation, renal failure, chronic pancreatitis, hemorrhage, shock, DIC, sepsis, respiratory failure Ranson's Criteria for mortality: GA LAW on admission: Glucose >200 mg/dL, AST >250 IU/L, LDH >350 IU/L, Age >55 yr, WBC >16,000/mL; Calvin & HOBBeS in48hr: Calcium <8 mg/dL, Hct decrease >10%, O2 (Pao2) <60 mm Hg, BUN increase >5 mg/dL, Base deficit >4 mEq/L, Sequestration of fluid >6 L. |
Labs=Increased amylase and lipase
Radiology=AXR may show dilated loop of bowel near pancreas (sentinel loop) or right colon distended until near pancreas (colon cutoff sign); CXR may show pleural effusion, hemidiaphragm elevation; CT may show pseudocyst or enlarged pancreas; US may detect gallstones Treatment=Hydration, pain control with opioids, nasogastric suction, make patient NPO, stop offending agent, prophylactic antibiotics for GI bacteria; debridement of necrotic tissue |
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H/P=Recurrent epigastric pain, steatorrhea, weight loss, nausea, constipation
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Chronic Pancreatitis
RF=Alcoholism, congenital defect Complication=Ductal obstruction, pseudocyst, malnutrition, glucose intolerance, pancreatic cancer |
Labs=Mildly increased amylase and lipase, glycosuria
Radiology=Abdominal radiograph may show pancreatic calcifications; CT may show calcifications, pancreatic enlargement, or pseudocyst; ERCP may be helpful for diagnosis Treatment=Stop alcohol use, opioid analgesia, enzyme supplementation; surgery may be required to repair ductal damage |
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H/P = possibly asymptomatic; recent acute pancreatitis, epigastric pain; fever
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Pancreatic pseudocyst
Fluid collection arising from pancreas consisting of enzyme-rich fluids contained in sac of inflamed membranous tissue Complications = rupture, hemorrhage, abscess formation |
Labs = increased WBC, increased amylase; aspiration of pseudocyst demonstrates very high amylase content
Radiology = pseudocyst visible on ultrasound (US) or CT Treatment = possibly self-resolving; drainage (surgical, endoscopic, or percutaneous) indicated if lasting >6 wks, painful, or rapidly growing; débride necrotic pancreatic tissue |
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H/P = abdominal pain radiating to back, anorexia, nausea, vomiting, weight loss, fatigue, steatorrhea; jaundice (if bile duct obstructed); palpable, nontender gallbladder (i.e., Courvoisier's sign); splenomegaly (if in tail), palpable deep abdominal mass, ascites
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Exocrine pancreatic cancer
Adenocarcinoma of pancreas most commonly in head of pancreas RF= chronic pancreatitis, DM, family history, tobacco, high-fat diet; male > female Complications = usually not detected until progressed; 5-yr survival <2%; 20–30% 5-yr survival following successful Whipple procedure; migratory thrombophlebitis (i.e., Trousseau's syndrome) |
Labs = possible hyperglycemia; increased CEA and CA 19-9 tumor markers; increased bilirubin (total and direct) and increased alkaline phosphatase with bile duct obstruction; biopsy used to make diagnosis
Radiology = CT shows mass, dilated pancreas, local spread, and dilated bile ducts; US also useful for imaging mass, but not as sensitive as CT; endoscopic retrograde cholangiopancreatography (ERCP) locates tumors not seen with CT Treatment = Nonmetastatic disease limited to head of pancreas may be resected with Whipple procedure (i.e., removal of pancreatic head, duodenum, proximal jejunum, common bile duct, gallbladder, and distal stomach) Lesions in body or tail rarely amenable to surgery, but can be resected via subtotal pancreatectomy if found early Adjuvant chemotherapy may be beneficial in respectable disease Enzyme deficiency treated with replacement therapy Stenting of pancreatic ducts, biliary ducts, or duodenum can be performed as palliative therapy in advanced disease |
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H/P = headache, visual changes, confusion, weakness, mood instability, palpitations, diaphoresis
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Insulinoma
Insulin-secreting β-islet cell tumor causing hypoglycemia Insulinomas are almost always solitary; multiple insulinomas may be seen in MEN 1. |
Whipple's triad=symptoms of hypoglycemia while fasting, hypoglycemia, and improvement in symptoms w/ carbohydrate load
Labs = increased fasting insulin, spontaneous hypoglycemia, positive C-peptide Radiology = CT, US, or indium-labeled octreotide scintigraphy may be useful for localizing tumor Treatment = surgical resection; diazoxide or octreotide may relieve symptoms in nonresectable disease |
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H/P = exfoliating rash (migratory necrolytic erythema); symptoms of DM refractory; abdominal pain, diarrhea, weight loss, mental status changes;
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Glucagonoma
Glucagon-secreting α-cell tumor causing hyperglycemia Complications = frequently malignant; poor prognosis |
Labs = hyperglycemia, increased glucagon; biopsy confirms diagnosis
Radiology = CT or endoscopic US may localize tumor Treatment = surgical resection if localized lesion; octreotide, IFN-α, chemotherapy, and embolization may be used in metastatic disease |
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H/P = watery diarrhea, weakness, nausea, vomiting, abdominal pain
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VIPoma
Vasoactive intestinal peptide (VIP)-producing tumor of non–β-islet cells |
Labs = increased serum VIP, stool osmolality suggests secretory cause
Radiology = CT may detect tumor Treatment = surgical resection for localized tumors; corticosteroids, chemotherapy, octreotide, and embolization used in metastatic disease |
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H/P = postprandial abdominal pain (worst in right upper quadrant [RUQ]), nausea, vomiting, indigestion, flatulence; RUQ tenderness, palpable gallbladder
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Cholelithiasis
Gallstone formation in the gallbladder that can cause cystic duct obstruction Most stones are composed of cholesterol; others are calcium bilirubinate (i.e., pigmented stones) secondary to chronic hemolysis RF = age >40 yrs, obesity, female, multiparity, oral contraceptive use, total parenteral nutrition (TPN), recent rapid weight loss, family history, DM, Complications = recurrent stones, acute cholecystitis, pancreatitis |
Radiology = US may show gallstones; AXR will only show some pigmented stones (because of high iron content from bilirubin)
Treatment = dietary modification (decrease fatty food intake), bile salts (dissolve stones), shock wave lithotripsy (uses sound waves to break up stones); cholecystectomy is typically performed in symptomatic patients |
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H/P = RUQ pain radiating to back, nausea, vomiting, anorexia; fever, palpable gallbladder, RUQ tenderness; symptoms more severe and longer in duration than typical cholelithiasis
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Acute cholecystitis
Inflammation of gallbladder commonly caused by gallstone obstruction of cystic duct; acalculous cholecystitis can occur in patients on TPN or in those who are critically ill Complications = perforation, gallstone ileus, abscess formation |
Labs = increased WBC; increased bilirubin (total and direct) and increased alkaline phosphatase seen when condition related to impacted stone or cholangitis
Radiology = US may show gallstones, sludge, or thickened gallbladder wall; hepatic iminodiacetic acid (HIDA) scan will detect cystic duct obstruction (gallbladder fails to fill normally during scan) Treatment = hydration, antibiotics, cholecystectomy (frequently delayed after 24–48 hrs of supportive care); patients with more mild symptoms can be treated with lithotripsy and bile salts; patients who are not stable for surgery can be treated with ERCP delivery of stone solvents |
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H/P = Jaundice, fever, RUQ tenderness;RUQ pain, chills; change in mental status or signs of shock seen in severe cases
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Cholangitis
Infection of bile ducts secondary to ductal obstruction RF=cholelithiasis, anatomic duct defect, biliary cancer |
Labs = + blood cultures, increased WBC, increased bilirubin (total and direct), increased alkaline phosphatase, increased AST and ALT, increased amylase with associated pancreatic inflammation
Radiology = US may detect obstruction; HIDA scan is more sensitive Treatment = hydration, IV antibiotics, endoscopic biliary drainage followed by delayed cholecystectomy; severe symptoms demand emergency bile duct decompression and relief of obstruction |
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H/P = similar symptoms to acute cholecystitis; anorexia, weight loss, abdominal pain radiating to back; palpable gallbladder, jaundice
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Gallbladder cancer
Adenocarcinoma of gallbladder associated with cholelithiasis, chronic infection, and biliary tract disease; generally poor prognosis |
Labs = increased bilirubin (total and direct), increased alkaline phosphatase, increased cholesterol; biopsy provides diagnosis
Radiology = abdominal radiograph may show calcified gallbladder (i.e., porcelain gallbladder); US or endoscopic US may detect invasive mass; ERCP can localize lesion and perform biopsy Treatment = cholecystectomy, lymph node dissection, partial removal of adjacent hepatic tissue; adjuvant radiation therapy and chemotherapy may reduce recurrence rates and are used as primary therapies in unresectable disease |
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H/P = asymptomatic for many years of alcoholism; anorexia, nausea, vomiting late in disease course; abdominal tenderness, ascites, splenomegaly, hepatomegaly, fever, jaundice, testicular atrophy, gynecomastia, digital clubbing
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Alcohol-related liver disease
Progressive liver damage secondary to alcoholism Initially characterized by fatty deposits in liver; reversible with alcohol cessation Continued alcoholism causes hepatic inflammation and early necrosis Progressive damage results in cirrhosis Complications = cirrhosis, hepatic encephalopathy, coagulation disorders |
Labs = increased ALT, increased AST, increased γ-glutamyl transferase (GGT), increased alkaline phosphatase, increased bilirubin (total and direct), prolonged prothrombin time (PT), increased WBC; biopsy provides diagnosis (fatty liver, many polymorphonuclear leukocytes (PMNs), areas of necrosis)
Treatment = cessation of alcohol use, thiamine, folate, high caloric intake (2,500–3,000 kcal/day); liver transplant is a consideration in patients who are able to maintain abstinence from alcohol |
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H/P = symptoms follow continuum from early liver diseases; weakness, weight loss, GI bleeding; hepatomegaly, splenomegaly, jaundice, ascites, abdominal wall varicosities (i.e., caput medusae), spider telangiectasias, palmar erythema, digital clubbing, Dupuytren's contractures in hands, testicular atrophy, gynecomastia, possible mental status changes (from encephalopathy), asterixis (i.e., asynchronous flapping of hands)
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Cirrhosis
Persistent liver damage leading to necrosis and fibrosis of hepatic parenchyma Caused by alcoholism, chronic HBV or HCV infection, chronic bile duct obstruction, biliary and hepatic parenchymal diseases, drugs, toxins Complications = portal hypertension, varices (caused by venous hypertension), ascites, hepatic encephalopathy (because of poor filtering of blood), renal failure, spontaneous bacterial peritonitis |
Labs = increased ALT, increased AST, increased GGT, increased alkaline phosphatase, decreased albumin, anemia, decreased platelets, prolonged PT; paracentesis of ascites shows fluid with <2.5 g/dL protein, WBC <300/µL, normal glucose level, and decreased amylase; biopsy shows fibrosis and hepatic necrosis
Radiology = US detects small, nodular liver Treatment = nonreversible, but progression may be halted; stop offending agent (e.g., alcohol); treat varices with β-blockers or sclerotherapy to reduce bleeding risk; lactulose, neomycin, and low-protein diet may improve encephalopathy; liver transplant may be needed in progressive cases |
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H/P = ascites, abdominal pain, change in mental status (from hepatic encephalopathy), hematemesis (caused by esophageal varices), symptoms of cirrhosis; hepatomegaly, splenomegaly, fever, abdominal wall varices, testicular atrophy, gynecomastia
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Portal hypertension
Increase in portal vein pressure giving it a higher pressure than the inferior vena cava; may result from prehepatic, intrahepatic, or posthepatic causes Prehepatic causes include portal vein thrombosis Intrahepatic causes include cirrhosis, schistosomiasis, parenchymal disease, and granulomatous disease Posthepatic causes include right-sided heart failure, hepatic vein thrombosis, and Budd-Chiari syndrome (i.e., hepatic vein thrombosis secondary to hypercoagulability) Shunting of blood into systemic veins causes varices in several locations |
Labs = increased ammonium (NH4+); paracentesis shows ascites with albumin > serum albumin by at least 1.1 g/dL, increased WBC, and normal glucose
Radiology = CT may show ascites and obstructing mass; EGD may show esophageal varices Treatment = Salt restriction and diuretics for ascites IV antibiotics for bacterial peritonitis Dialysis for renal failure Lactulose, neomycin, and low-protein diet for hepatic encephalopathy Vasopressin or sclerotherapy for bleeding varices Hepatic shunting via laparotomy or transjugular intrahepatic portal-caval shunting (TIPS) is short-term solution for severe disease; liver transplant often required as eventual treatment in progressive cases |
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systemic infection and comorbid portal hypertension
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Spontaneous bacterial peritonitis
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paracentesis will show >250 PMN/µL, total protein >1 g/dL, glucose <50 mg/dL, and lactate dehydrogenase (LDH) > normal serum LDH.
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H/P = abdominal pain, polydipsia, polyuria, arthralgias, impotence, lethargy; pigmented rash (bronze hue), hepatomegaly, testicular atrophy; may see symptoms and signs that resemble DM and CHF
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Hemochromatosis
Autosomal-recessive disease of iron absorption Excess iron absorption causes iron deposition in liver, pancreas, heart, and pituitary, leading to eventual fibrosis Rarely is result of chronic blood transfusions or alcoholism Complications = cirrhosis, hepatoma, CHF, DM, hypopituitarism |
Labs = increased iron, increased percentage saturation of iron, increased ferritin, increased transferring saturation, slightly increased AST and ALT; biopsy shows increased iron content in liver
Treatment = weekly or biweekly phlebotomy until normal iron, then monthly phlebotomy; avoid excess alcohol consumption; deferoxamine for iron chelation |
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H/P = psychiatric disturbances (e.g., depression, neuroses, personality changes), loss of coordination, dysphagia; jaundice, tremor, possible green-brown rings in cornea (i.e., Kayser-Fleischer rings), hepatomegaly; signs may precede symptoms
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Wilson's disease
Autosomal-recessive disorder of impaired copper secretion, primarily in young adults Excess copper deposits in liver, brain, cornea Complications = fulminant hepatic failure, cirrhosis |
Labs = decreased serum ceruloplasmin, increased urinary copper, slightly increased AST and ALT; biopsy shows increased copper deposits in liver
Treatment = trientine or penicillamine for copper chelation; life-long zinc for maintenance therapy; dietary copper restriction (no organ meats, shellfish, chocolate, nuts, or mushrooms), supplementary vitamin B6; liver transplantation may be needed in cases of liver failure |
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H/P=cirrhosis & panlobular emphysema
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α1-Antitrypsin deficiency
Autosomal-recessive disorder with decreased α1-antitrypsin production Most symptoms arise from emphysemic component of disease |
Labs = increased AST, increased ALT; pulmonary function tests (PFTs) demonstrate obstructive disease
Treatment = liver transplant or lung transplant may be needed in severe cases; enzyme replacement may be helpful in stopping disease progression |
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H/P = possibly asymptomatic; fatigue, pruritus, arthralgias; jaundice, xanthomas, skin hyperpigmentation, hepatosplenomegaly
Labs = increased alkaline phosphatase, increased GGT, normal AST and ALT, increased cholesterol, increased bilirubin (total and direct) later in disease course; + antinuclear antibody (ANA), + antimitochondrial antibodies; |
Primary biliary cirrhosis (PBC)
Autoimmune disease with intrahepatic bile duct destruction leading to accumulation of cholesterol, bile acids, and bilirubin RF= rheumatoid arthritis, Sjögren syndrome, scleroderma; female > male |
Labs = increased alkaline phosphatase, increased GGT, normal AST and ALT, increased cholesterol, increased bilirubin (total and direct) later in disease course; + antinuclear antibody (ANA), + antimitochondrial antibodies; workup may indicate comorbid autoimmune diseases; biopsy shows inflammation and necrosis in bile ducts
Treatment = ursodeoxycholic acid improves liver function and reduces symptoms; colchicines or methotrexate can be added in more severe cases; liver transplant needed in progressive disease |
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H/P = possibly asymptomatic; fatigue, pruritus, RUQ pain; fever, night sweats, jaundice, xanthomas
Labs = increased alkaline phosphatase, increased GGT, normal AST and ALT, increased cholesterol, increased bilirubin (total and direct), possible + perinuclear antineutrophil cytoplasmic antibodies (pANCA); Radiology = ERCP shows stricturing and irregularity of extrahepatic and intrahepatic bile ducts (i.e., “pearls on string”) |
Primary sclerosing cholangitis (PSC)
Progressive destruction of intrahepatic and extrahepatic bile ducts leading to fibrosis and cirrhosis RF= ulcerative colitis; male > female |
Labs = increased alkaline phosphatase, increased GGT, normal AST and ALT, increased cholesterol, increased bilirubin (total and direct), possible + perinuclear antineutrophil cytoplasmic antibodies (pANCA); biopsy appears similar to that for PBC
Treatment = ursodeoxycholic acid, methotrexate, corticosteroids; endoscopic stenting of strictures; surgical resection of affected ducts and liver transplant may be required in progressive cases |
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H/P = mild jaundice following fasting, exercise, or stress
Labs = increased indirect bilirubin <5 mg/dL |
Gilbert's disease
Autosomal-recessive or dominant disease with mild deficiency of glucuronosyltransferase |
Treatment = none necessary
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H/P = persistent jaundice and central nervous system (CNS) symptoms (due to kernicterus) in infants
Labs = increased indirect bilirubin >5 mg/dL |
Crigler-Najjar syndrome
Autosomal-recessive disease with severe deficiency in glucuronosyltransferase Complications = early kernicterus can cause permanent CNS damage |
Treatment = phototherapy, plasmapheresis, calcium phosphate combined with orlistat; liver transplantation is an option
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H/P = frequently asymptomatic; possible RUQ fullness
Women with history of oral contraceptive use |
Benign tumors (e.g., hepatic adenoma, focal nodular hyperplasia, hemangiomas, hepatic cysts)
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Radiology = CT, MRI, or angiography detects hypervascular liver mass
Treatment = frequently untreated; larger tumors may be resected or embolized to prevent rupture |
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H/P = RUQ pain, weight loss, malaise, anorexia, diarrhea, dyspnea; jaundice, hepatomegaly, bruit over liver, ascites
Labs = increased α-fetoprotein; slightly increased AST and ALT, increased alkaline phosphatase, increased bilirubin (total and direct); |
Hepatocellular carcinoma (hepatoma)
RF = HBV or HCV infection, cirrhosis, hemochromatosis, Aspergillus infection, schistosomiasis Complications = poor prognosis; portal vein obstruction, Budd-Chiari syndrome, liver failure Paraneoplastic syndromes associated with hepatoma include hypoglycemia, excessive RBC production, refractory watery diarrhea, hypercalcemia, and variable skin lesions. |
Labs = biopsy provides diagnosis, but risks causing substantial hemorrhage
Radiology = CT, MRI, or US shows liver mass; angiography may show increased vascularity; PET can be used to determine extent of spread Treatment = surgical resection of small tumors (lobectomy or partial hepatectomy) and chemotherapy; transplant may be an option for limited disease; radiofrequency ablation and chemoembolization are options for unresectable tumors |
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H/P = coughing and cyanosis during feeding, food may fill blind pouch, abdominal distention, possible history of aspiration pneumonia
Pediatric |
Tracheoesophageal fistula
Malformation of trachea and esophagus resulting in tract formation between structures (see Figure 3-17) Frequently associated with esophageal atresia |
Radiology = chest radiograph following nasogastric tube insertion demonstrates malformation (tube in lung or blind pouch)
Treatment = surgical repair |
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H/P = symptoms begin a few weeks after birth; nonbilious emesis, projectile emesis; palpable epigastric olive-sized mass
Pediatric |
Pyloric stenosis
Hypertrophy of pyloric sphincter causing obstruction of gastric outlet |
Radiology = barium swallow shows thin pyloric channel (i.e., string sign); US shows increased pyloric muscle thickness (see Figure 3-18)
Treatment = pyloromyotomy |
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H/P =hematochezia, bilious vomiting, lethargy, poor feeding, diarrhea; abdominal distention, abdominal tenderness; signs of shock in severe cases
Pediatric |
Necrotizing enterocolitis
Idiopathic mucosal necrosis and epithelial cell sloughing RF = preterm birth, low birth weight |
Labs = metabolic acidosis, decreased Na+
Radiology = abdominal radiograph shows bowel distention, air in bowel wall, portal vein gas, or free air under the diaphragm Treatment = TPN, IV antibiotics, broad-spectrum antibiotics, nasogastric suction, surgical resection of affected bowel |
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H/P = obstipation, vomiting, failure to pass stool; abdominal distention
Pediatric |
Hirschsprung's disease
Absence of bowel autonomic innervation causing bowel spasm and obstruction |
Labs = bowel biopsy shows absence of ganglia
Radiology = AXR demonstrates dilated bowel; barium enema shows proximal dilation (megacolon) with distal narrowing Treatment = colostomy and resection of affected area |
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H/P = sudden abdominal pain that lasts <1 min and is episodic; palpable sausage-like abdominal mass, ab tenderness; pallor, sweating, vomiting, bloody mucus in stool (i.e., currant jelly stool);
Pediatric |
Intussusception
Telescoping of bowel into adjacent segment of bowel, leading to obstruction; most frequently proximal to ileocecal valve RF= Meckel's diverticulum, Henoch-Schönlein purpura, adenovirus infection, cystic fibrosis Complications = bowel ischemia (appendix particularly susceptible) Intussusception is the most common cause of bowel obstruction in the first 2 yrs of life. Intussusception in an adult is considered cancer until proven otherwise and usually will require surgical reduction. |
Labs = increased WBC
Radiology = barium enema will show obstruction; US or CT may detect abnormal bowel Treatment = barium enema may reduce defect; surgery required for refractory cases |
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H/P = asymptomatic; occasionally presents with painless rectal bleeding, intussusception, diverticulitis, or abscess formation
Pediatric |
Meckel's diverticulum
Common remnant of vitelline duct that exists as outpouching of ileum and may contain ectopic tissue Meckel's diverticulum rule of 2s—males 2 times more common than females, occurs within 2 ft of ileocecal valve, 2 types of ectopic tissue (gastric, pancreatic), found in 2% of the population, most complications occur before 2 yrs of age |
Radiology = gastric mucosa may be detected by technetium radionucleotide scan (i.e., Meckel's scan)
Treatment = surgical resection if symptomatic |
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H/P = jaundice, scleral icterus; lethargy, high-pitched cry, seizures, and apnea seen with kernicterus
Pediatric |
Neonatal jaundice
Physiologic (common): physiologic undersecretion, breast-feeding failure; resolve within 2 wks Increased hemolysis: maternal-fetal ABO incompatibility, hereditary RBC abnormalities, glucose 6-phosphate dehydrogenase (G6PD) deficiency Bilirubin overproduction without hemolysis: hemorrhage, maternal-fetal transfusion Hepatic abnormalities: Gilbert's syndrome, Crigler-Najjar syndrome, biliary atresia Kernicterus is deposition of bilirubin in basal ganglia and hippocampus and may cause permanent damage; results from extremely high serum bilirubin and is typically only seen with hepatic abnormalities |
Labs = frequently indirect hyperbilirubinemia (due to hemolysis); jaundice developing with initial 24 hrs after birth, total bilirubin >15 mg/dL, or direct bilirubin >2 mg/dL suggests nonphysiologic cause
Treatment = phototherapy used for physiologic jaundice lasting several days; suspected nonphysiologic causes should be worked up and may require exchange transfusion; intravenous immunoglobulin may reduce need for exchange transfusion in cases of maternal-fetal blood type incompatibility |
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H/P = look for leads to organic causes; screen for abuse
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Failure to thrive
Children below 3rd-percentile weight for age or failure to gain weight appropriate for age May be due to underlying illness or neglect |
Labs = urinalysis, CBC, blood culture, urine culture, serum electrolytes, cystic fibrosis testing, and caloric intake records may be helpful in making diagnosis
Treatment = high-calorie diet, treat underlying disorder; educate parents in proper nutrition and feeding; contact social support services in cases of neglect or abuse |
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Colorectal Cancer Staging/TMN
Tumor confined to bowel wall |
Duke Class A, TMN I
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Cure Rate 90%
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Colorectal Cancer Staging/TMN
Penetration of tumor into colonic serosa or perirectal fat |
Duke Class B, TMN II
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Cure Rate 80%
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Colorectal Cancer Staging/TMN
Lymph node involvement |
Duke Class C, TMN III
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Cure Rate <60%
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Colorectal Cancer Staging/TMN
Distant metastases |
Duke Class D, TMN IV
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Cure Rate 5%
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