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Step 2 GI

Step 2 GI
What is the difference between dysphagia and odynophagia?
dysphagia is difficulty swallowing
odynophagia is pain with swallowing
Both indicate abnormalities of the oropharynx or esophagus
How does oropharyngeal dysphagia present?
difficulty passing material from the oropharynx to the esophagus. Involves liquids more than solids. Can be neuro or muscular in origina.
What are some possible causes of oropharyngeal dysphagia?
Parkinson's disease
Myasthenia gravis
prolonged intubation
Zenker's diverticula
How does esophageal dysphagia present?
Obstructive causes: involves solids more than liquids and is generally progressive.
Motility disorders: BOTH liquid and solid dysphagia
What are some possible causes for esophageal dysphagia?
- strictures
- Schatzki rings
- Webs
- carcinoma
- achalasia
- scleroderma
- esophageal spasm
What other types of neck etiologies can cause orophragyneal/esophageal dysphagia?
Anatomic defects
What syndrome does esophageal webs suggest?
Plummer-Vinson Syndrome when present with iron deficiency anemia and glossitis
What diagnostic test can be used to diagnose esophageal dysphagia?
barium swallow followed by endoscopy, mamometry, and/or pH monitoring
If obstructive lesion is suspected, endoscopy with biopsy
What diagnostic test can be used to diagnose odynophagia?
upper endoscopy
What diagnostic test can be used to diagnose oropharyngeal dysphagia?
What infectious esophagitis occurs in AIDS-defining illness?
candidal esophagitis
What is diffuse esophageal spasm?
motility disorder in which normal peristalsis is periodically interrupted by high-amplitude nonperistaltic contractions of unknown etiology. AKA nutcracker esophagus
How does HSV esophagitis present?
oral ulcers.
On endoscopy will see small deep ulcerations
Bx: multinucleated giant cells w/ nuclear inclusions
How is HSV esophagitis treated?
IV Acyclovir
How does CMV esophagitis treated?
retinitis, colitis
Endoscopy: large, superficial ulcerations
Bx: intranuclear inclusions on biopsy
How is CMV esophagitis treated?
IV ganciclovir
How does esophageal spasm present?
chest pain, dysphagia, odynophagia
can be triggered by hot/cold liquids
What causes relief in esophageal spasm?
How is esophageal spasm diagnosed?
Barium swallow: corkscrew-shaped esophagus
Esophageal manometry: high-amplitude, simultaneous contractions
How is esophageal spasm treated?
nitrates and CCB for symptomatic relief
Surgery (esophageal myotomy) for severe, incapacitating symptoms
What type of muscle is the upper 1/3 of the esophagus?
What type of muscle is the lower 2/3 of the esophagus?
smooth muscle
What is achalasia?
motor disorder of the esophagus characterized by impaired relaxation of the lower esophageal sphincter (LES) and loss of peristalsis in the distal 2/3 of the esophagus
What is the hypothesized mechanism of achalasia?
loss or absence of inhibitory ganglion cells in the myenteric (Auerbach's) plexus
How does achalasia present?
progressive dysphagia, chest pain, regurgitation of undigested food, weight loss, nocturnal cough
How is achalasia diagnosed?
Barium Swallow: esophageal dilation with a "bird's beak" tapering of the distal esophagus
Manometry: increased resting LES pressure, incomplete LES relaxation upon swallowing, decreased peristalsis in the body of the esophagus
Endoscopy: r/o mechanical obstruction
How is achalasia treated?
Nitrates, CCB
Endoscopic injection of botulinum toxin into the LES for short term relief
Pneumatic balloon dilation or surgical Heller (myotomy) for definitive treatment options
What is esophageal diverticula?
cervical outpouching through the cricopharyngeal muscle: Zenker's diverticulum. Diverticula cna also occur in the middle/distal third of the esophagus
What is the most common esophageal motility disorder?
2nd most: esophageal diverticula
How does esophageal diverticula present?
chest pain, dysphagia, halitosis, regurgitation of undigested food
How is esophageal diverticula diagnosed?
Barium swallow: demonstrate outpouchings
How is esophageal diverticula treated?
Sx: treat w/ surgical excision of teh diverticulum
Zenker's diverticulum: myotomy of teh cricopharyngeus to relieve high pressure zone
What is the most common type of esophageal cancer worldwide?
What is the most common type of esophageal cancer in teh US/Europe/Australia?
Which esophageal carcinoma is assoc w/ Barrett's esophagus?
What is Barrett's esophagus related to?
chronic GERD
What are major risk factors for SCC?
alcohol use and smoking
How does esophageal cancer present?
progressive dysphagia (solids than liquids), weight loss, odynophagia, GERD, GI bleeding, vomiting
How is esophageal cancer diagnosed?
Barium swallow: narrowing of esophagus w/ an irregular border protruding into the lumen
Endoscopy and bx to confirm dx
CT and endoscopic U/S for staging
How is esophageal cancer treated?
Poor prognosis
Definitive tx: chemoradiation and surgical resection (for high grade Barrett's dysplasia)
Palliative tx: endoscopically placed esophageal stent
What is GERD?
sx reflux of gastric contents into the esophagus, most commonly a result of transient LES relaxation. 2/2 incompetent LES, gastroparesis, hiatal hernia
How does GERD present?
heartburn 30-90min after a meal, worsens w/ reclining, improves with antacids, sitting or standing. Substernal chest pain difficult to distinguish from other causes, sour taste, globus, unexplained cough, morning hoarseness
Exam: benign unless have systemic disease like scleroderma
How is GERD diagnosed?
Hx and clinical impression
Empiric trial of lifestyle modification and medical tx
Barium swallow: to look for hiatal hernia
Esophageal manometry
24hr pH monitoring
Why does esophageal cancer metastasize early?
esophagus lacks a serosa
What are the risk factors for GERD?
hiatal hernia and increased abdominal pressure (obesity, pregnancy)
What other condition is often confused with GERD?
cough-variant asthma
When should endoscopy be performed for GERD pts?
In pts w/ sx unresponsive to initial empiric tx, long-standing, or suggestive of complicated disease (anorexia, weight loss, dysphagia/odynophagia)
Rules out Barrett's esophagus and adenocarcinoma
How is GERD tx?
Lifestyle: weight loss, head of bed elevation, reduction of meal size, avoidance of nocturnal meals and substances that decrease LES tone
Pharma: antacids (mild), H2 receptor antagonists (cimetidine, ranitidine; for intermittent sx), PPIs (omeprazole, lansoprazole; chronic and frequent sx). PPIs are preferred for severe or erosive disease
Surgical: for refractor or severe disease. Nissen fundoplication
What are some complications of GERD?
esophagitis, esophageal stricture, aspirationof gastric contents, upper GI bleeding, Barrett's esophagus
What types of foods can exacerbate GERD?
caffeine, alcohol, chocolate, garlic, onions, mints, and nicotine
What is a hiatal hernia?
herniation of a portion of the stomach upward into the chest through a diaphragmatic opening
What are the two common types of hiatal hernias?
Sliding hiatal hernia (95%): GEJ and portion of stomach displaced above diaphragm
Paraesophageal hiatal hernia (5%): GEJ below diaphragm, neighboring portion of the fundus herniates into the mediastinum
How does hiatal hernia present?
How is hiatal hernia dx?
incidental finding on CXR
frequently dx by barium swallow of EGD
How are hiatal hernias tx?
Sliding: medical tx and lifestyle mod to decreased GERD sx
Paraesophageal: surgical gastropexy (attachment of stomach to the rectus sheath and closure of the hiatus) to prevent gastric volvulus
What is gastritis?
inflammation of stomach lining
What is acute gastritis?
rapidly developing, superficial lesions that are often due to NSAIDs, alcohol, H. pylori infxn, and stress from severe illness (burns, CNS injury)
What is Type A chronic gastritis?
occurs at fundus and is due to autoabs to parietal cells. causes pernicious anemia and is assoc w/ other autoimmune disorders, such as thyroiditis. increases the risk of gastric adenocarcinoma
How is Type A gastritis associated w/ pernicious anemia?
the lack of intrinsic factor that is necessary for vitamin B12 absorption due to lack of parietal cells
What is Type B gastritis?
occurs in antrum and may be caused by NSAID use or H. pylori infxn.
How does Type B gastritis present?
ASx, but associated w/ increased risk of PUD and gastric cancer
How do pts w/ gastritis present?
complain of epigastric pain, nausea, vomiting, hematemesis, melena
How is gastritis dx?
Endoscopy: visualize gastric lining
H. pylori infxn: detected by urease breath test, serum IgG abs (which indicate exposure, not current infxn). H. pylori stool antigen, endoscopic biopsy
How is gastritis tx?
Mild: decrease intake of offending agents, antacids, sucralfate, H2 blockers, and/or PPIs
H.pylori confirmed: triple therapy (amoxicillin, clarithromycin, omprazole)
Prophy: H2 blockers/PPIs to pts at risk for stress ulcers (ICU pts)
What is gastric cancer?
malignant tumor in stomach
In what countries is gastric cancer most prevalent?
Korea and Japan
What are the two types of gastric cancer?
1. Intestinal type: thought to arise from intestinal metaplasia of gastric mucosal cells
2. Diffuse type: tends to be poorly differentiated and not associated w/ H. pylori infxn or chronic gastritis
What are the risk factors for intestinal type gastric cancer?
Diet high in nitrites, salt and low in fresh vegetables (antioxidants), H. pylori colonization, chronic gastritis
What are the risk factors for diffuse type gastric cancer?
not assoc w/ H. pylori infxn or chronic gastritis
What unique characteristics are seen on biopsy for diffuse type gastric cancer?
signet ring cells
How do pts with gastric cancer present?
Early signs: indigestion and loss of appetite
Advanced signs: abd pain, weight loss, or upper GI bleeding
How do you dx gastric cancer?
Early: incidentally found on endoscopy
Late: found on endoscopy (high-risk individuals)
How is gastric cancer treated?
Surgery: early detection and removal
five yr survival is <10% for advanced disease
What kind of tumor is gastric adenocarcinoma that metastasizes to the ovary?
Krukenberg tumor
What is assoc with an enlarged left supraclavicular LN? (Virchow's node)
gastric cancer
What is peptic ulcer disease?
damage to gastric or duodenal mucosa caused by impaired mucosal defense and/or increased acidic gastric contents
What causes duodenal and gastric ulcers?
H. pylori
What are other risk factors for PUD?
corticosteroids, NSAID, alcohol, and tobacco use
How does PUD present?
chronic or periodic dull, burning epigastric pain and improves w/ meals (esp duodenal ulcers), worsens 2-3 hrs after eating and can radiate to the back
Other Sx: nausea, hematemesis ("coffee-ground" emesis), blood in the stool (melena or hematochezia)
Exam: epigastric tenderness, active bleeding, + stool guaic
How does acute PUD present?
acute perforation: rigid abdomen, rebound tenderness, guarding, other sx of peritoneal irritation
How is PUD dx?
- AXR to r/o perforation (free air under the diaphragm)
- CBC to assess for GI bleeding (low or decreased hematocrit)
- upper endoscopy: biopsy to confirm PUD and r/o active bleeding or gastric adenocarcinoma (10% of gastric ulcers); barium swallow as alternative
- H. pylori testing
- Recurrent/refractory cases: serum gastrin to screen for Zollinger-Ellison syndrome
After a meal, does pain increase or decrease for gastric ulcers?
decrease for duodenal ulcers
How is acute PUD treated?
- r/o active bleeding w/ serial hct, a rectal exam w/ stool guaiac and NG lavage
- monitor pt's hct and BP and treat w/ IV hydration, transfusion, IV PPIs, endoscopy, and surgery as needed for complications
- if perforation: emergent surgery indicated
What pharma interventions can be used for PUD?
Goal: protect mucosa, decrease acid production, eradicating H. pylori infxn
Mild: antacids, sucralfate, bismuth, misoprostol (a prostaglandin analog) for mucosal protection. PPIs or H2 receptor antagonists may be used to decreased acid secretion
H. pylori infxn confirmed: triple therapy
If recurrent/severe: require chronic sx therapy
What surgical interventions can be used for PUD?
Indications: sx gastric ulcers for >2 months that are refractory to med tx
- r/o gastric adenocarcinoma via endoscopy/upper GI series/barium swallow
- Procedure: parietal cell vagotomy
What are complications of PUD?
hemorrhage (posterior ulcers that erode into gastroduodenal artery)
gastric outlet obstruction
perforation (usually anterior ulcers)
intractable pain
What is Zollinger-Ellison Syndrome?
rare condition characterized by gastrin-producing tumors in the duodenum and/or pancreas that lead to oversecretion of gastrin, which lead to gastric and duodenal ulcers
What syndrome is Zollinger-Ellison syndrome associated w/?
MEN 1 (pancreas, pituitary, and parathyroid tumors)
How does Zollinger-Ellison present?
unresponsive, recurrent gnawing, burning abd pain and diarrhea, nausea, vomiting, fatigue, weakness, weight loss, and GI bleeding
How is Zollinger-Ellison syndrome dx?
increased fasting serum gastrin levels, increased gastrin following a secretin stimulation test, octreotide scan can localize the tumor
How is Zollinger-Ellison syndrome tx?
Decrease acid production: mod to high dose of PPI
Surgery (avoid possible malignant potential of the tumor): surgical resection
How is diarrhea defined?
>200g feces /day along w/ increased frequency or decreased consistency of stool
What are the four categories of diarrhea?
1) increased motility
2) increased secretion
3) increased luminal osmolarity
4) inflammation
What are the possible causes of acute diarrhea?
Bacteria with preformed toxins
- Staph
- Bacillus
Noninvasive bacteria
- Cholera
- C. Diff
Invasive bacteria
- Salmonella
- Shigella
- Campylobacter
- Yersinia
- Giardia
- Entamoeba histolytica
Opportunistic organisms
- Cryptosporidium
- Isospora
- Microsporidium
What is the most common cause of pediatric diarrhea?
rotavirus (winter)
What are possible causes of chronic diarrhea?
Increased intestinal secretion
- carcinoid
- VIPomas
Malabsorption/osmotic diarrhea
- bacterial overgrowth
- pancreatic insufficiency
- mucosa abnormalities
- lactose intolerance
Inflammatory bowel disease
Altered motility
Osmotic diarrhea
- increased stool osmotic gap and resolution of diarrhea w/ fasting
How is diarrhea diagnosed?
Acute diarrhea does not need lab tests unless have sx of high fever, bloody diarrhea, diarrhea lasting > 4-5 days
Potential labs: stool for fecal leukocytes, bacterial culture, C- diff toxin, and O&P
Procedure: sigmoidoscopy if have bloody diarrhea
How is diarrhea treated?
- If not suspicious for bacteria: antidiarrheals (loperamide, bismuth salicylate) and oral rehydration
- suspicious of bacterial infxn: avoid antimotility agents and consider abx after stool studies have been sent
- identify underlying cause and treat sx w/ loperamide, opioids, octreotide, or cholestyramine
- oral rehydration: if cannot take PO fluids, hospitalize and give IV fluids, replete electrolytes and treat underlying cause
What is the causative agent for diarrhea associated w/ ingestion of raw eggs or dairy?
If after stool electrolytes, osmolality, weight/24 hrs, quantitative fat and an increased osmotic gap is detected, what causes of diarrhea should be considered?
Increased fecal fat
- malabsorption syndromes
- pancreatic insufficiency
- bacterial overgrowth
Normal fecal fat
- lactose intolerance
- sorbitol
- lactulose
- laxative abuse
If normal osmotic gap is detected after diarrhea tests what causes should be considered?
Normal stool weight
- factitious diarrhea
Increased stool weight
- >1000 g: secretory or laxative abuse
What clues indicate C. diff infxn?
- recent abx (penicillins, cephalosporins, clinda)
- recent hospitalization
What complications can result from C. diff infxn?
toxic megacolon
What is a possible complication of EHEC?
Abx and antidiarrheal tx must be avoided because can increase HUS risk
What is the causative organism of osteomyelitis in sickle cell pts?
What is malabsorption?
inability to absorb nutrients as a result of an underlying condition
What are some underlying conditions that can cause malabsorption?
bile salt deficiency (bacterial overgrowth, ileal disease)
short bowel syndrome
mucosal abnormalities (celiac disease, Whipple's disease, tropical sprue)
pancreatic insufficiency
How do pts with malabsorption present?
frequent, loose, watery stools and/or pale foul-smelling, bulky stools assoc w/ abd pain, flatus, bloating, weight loss, nutritional deficiencies, and fatigue
How is malabsorption treated?
Etiology dependent
Celiac sprue: gluten-free diet

If severely affected, need TPN, immunosuppresants, and anti-inflammatory meds
What is lactose intolerance?
Deficiency of lactase (brush-border enzyme that hydrolyzes the disaccharide lactose into glu and galactose)
How does lactose intolerance present?
Abd bloating, flatulence, cramping, watery diarrhea following milk ingestion
How is lactose intolerance dx?
Empiric lactose-free diet
H2 breath test: reveals increased breath hydrogen following ingestion of lactose load (indicates metabolism of lactose by colonic bacteria)
How is lactose intolerance tx?
avoidance of dairy products
lactase enzyme replacement
What is carcinoid syndrome?
liver metastasis of carcinoid tumors (hormone-producing enterochromaffin cells) that most commonly arise from the ileum and appendix and produce vasoactive substances such as serotonin and substance P
How does carcinoid syndrome present?
cutaneous flushing, diarrhea, abd cramps, wheezing, right-sided cardiac valvular lesions
Sx usually occur after eating, exertion, or excitement
How is carcinoid syndrome dx?
High urine levels of serotonin metabolite 5-HIAA are diagnostic
Octreotide scan to localize
How is carcinoid syndrome tx?
Symptoms: octreotide
Surgery: debulking of tumor mass
What is IBS?
idiopathic functional disorder that is characterized by changes in bowel habits that increase w/ stress as well as by abdominal pain that is relieved by bowel mvts
What kind of condition is associated w/ IBS?
psychiatric disorders
half of IBS pts have comorbid psychiatric disorders
How does IBS present?
abd pain, change in bowel habits (diarrhea and/or constipation), abd distension, mucous stools, relief of pain w/ bowel movt
Systemic sx rare: doesn't awaken from sleep, no vomiting, no weight loss
Exam: mild abd tenderness
How is IBS dx?
Dx of exclusion
R/O other GI causes: CBC, TSH, electrolytes, stool cultures, abd films, barium contrast studies, manometry to assess sphincter fxn
How is IBS tx?
Psych: reassurance from MD. Sx not all in their head
Dietary: fiber supplements (psyllium) may help
Pharma: TCAs, antidiarrheals (loperamide), antispasmodics (anticholinergics, such as dicyclomine)
What is small bowel obstruction?
blocked passage of bowel contents through small bowel. Fluid and gas can build up proximal to obstruction, leading to fluid and electrolyte imbalances and significant abd discomfort
What are the causes of SBO?
adhesions from a prior abd surgery (60%), hernia (10-20%), neoplasms (10-20%), intussusception, gallstone ileus, stricture due to IBD, volvulus
How does SBO present?
cramping abd pain w/ a recurrent crescendo-decrescendo pattern at 5-10 min intervals
Vomiting follows pain, early emesis is bilious and nonfeculent if the obstruction is prox but feculent if it is distal
Exam: distention, tenderness, prior surgical scars/hernias, bowel sounds are high-pitched tinkles, peristaltic rushes
What is an emergent presentation of SBO?
Fever, hypotension, rebound tenderness, tachycardia, peritonitis, disappearance of peristalsis-->surgical EMERGENCY
How does partial obstruction present?
continued passage of flatus, but no stool
Complete obstruction: no flatus or stool (obstipation)
How is SBO dx?
Labs: CBC show leukocytosis, COMP show dehydration and metabolic alkalosis (vomiting). If see lactic acidosis, suggest bowel necrosis and need for emergent surgical intervention.
AXR: stepladder pattern of dilated small bowel loops, air-fluid levels, paucity of gas in the colon
If there is radiopaque material at the cecum on AXR along with sx of SBO, what does that suggest?
gallstone ileus
How is SBO treated?
Partial Obstruction: supportive care (NPO status, NG suction, IV hydration, correction of electrolyte abnormalities, Foley catheterization to monitor fluid status
Surgery indications: complete obstruction, vascular compromise, and/or sx lasting >3 days w/o resolution
- Ex Lap w/ lysis of adhesions, resection of necrotic bowel, evaluation for stricture, IBD, and hernias
- second look laparotomy or laparoscopy may be performed 18-36 hrs after initial surgical tx to reevaluate bowel viability if ischemia is a concern
What is an ileus?
loss of peristalsis w/o structural obstruction
What are risk factors for an ileus?
recent surgery/GI procedure
severe medical illness
electrolyte imbalances
medications that slow GI mobility (anticholinergics, opiods)
How does ileus present?
diffuse, constant, moderate abd discomfort; nausea vomiting (w/ eating); absence of flatulence or bowel mvts
DRE: to rule out fecal impaction in elderly pts
How is ileus dx?
AXR (supine): diffusely distended loops of small and large bowel
AXR (upright): air-fluid levels
Gastrografin study: r/o partial obstruction
CT: r/o neoplasm
How is ileus tx?
Discontinue/decrease narcotics and other drugs that reduce bowel motility
Temporarily decrease/discontinue oral feeds
Initiate NG suction/parenteral feeds, as necessary
Replete electrolytes as needed
What is mesenteric ischemia?
decrease mesenteric blood supply leading to insufficient perfusion to intestinal tissue and ischemic injury
What are some causes of mesenteric ischemia?
acute arterial occlusion (SMA)
thrombosis (due to atherosclerosis)
embolism (Afib or decreased ejection fraction)
nonocclusive arterial disease (low cardiac output, arteriolar vasospasm)
venous thrombosis (due to hypercoabulable states)
How does mesenteric ischemia present?
- sudden onset of severe abd pain out of proportion to exam
- h/o prior episodes of similar abd pain after eating "intestinal angina"
- nausea/vomiting, diarrhea, bloody stools
Early exam: unremarkable
Late exam: may show peritoneal signs (bowel infarction)
How is mesenteric ischemia dx?
Labs: leukocytosis, metabolic acidosis, increased lactate, increased amylase, increased LDH, increased CK
AXR/CT: bowel wall edema ("thumbprinting") and air w/in the bowel wall (pneumatosis intestinalis)
Mesenteric angiography: gold standard for arterial occlusive disease
How is mesenteric ischemia tx?
- volume resuscitation, broad-spectrum abx, optimization of hemodynamics and avoidance of vasoconstrictors
- anticoagulation for arterial or venous thrombosis or embolism
Surgery: early lap for acute arterial occlusive disease or if evidence of peritonitis or clinical deterioration
- angioplasty and thrombectomy +/- endovascular stenting for acute arterial thrombosis
- embolectomy for acute arterial embolism
- resection of infarcted bowel
What are the complications of mesenteric ischemia?
sepsis/septic shock, multisystem organ failure, death
What is diverticular disease?
outpouchings of mucosa and submucosa (false diverticula) that herniate through the colonic muscle layers in areas of high intraluminal pressure; most commonly found in sigmoid colon
What is the most common cause of acute lower GI bleeding (>40yo)?
What are the risk factors for diverticular disease?
low-fiber and high-fat diet
advanced age (65% occur in those > 80yo)
connective tissue disorders
What is diverticulitis?
inflammation and potentially perforation of diverticulum secondary to fecalith impaction
How does diverticulosis present?
bleeding that is painless and sudden, hematochezia with sx of anemia (fatigue, lightheadedness, dyspnea on exertion)
How does diverticulitis present?
LLQ abd pain, fever, nausea, vomiting, constipation.
Perforation is a serious complication that leads to peritonitis and shock
How is diveritcular disease dx?
Labs: leukocytosis
AXR: r/o free air, ileus, obstruction
Colonoscopy/barium enema: see outpouchings
AVOID sigmoidoscopy/colonoscopy in diverticulitis b/c of possible perforation
CT: to look for abscess/free air if no improvement b/c of severe disease
How is diverticular disease treated?
Uncomplicated diverticulosis: high-fiber diet/fiber supplements
Diverticular bleeding: bleeding usually stops spontaneously, transfuse and hydrate as needed, if bleeding does not stop, angiography w/ embolization or surgery
Diverticulitis: bowel rest (NPO), NG tube placement, broad-spectrum abx (flagyl, fluoroquinolone or 2nd/3rd gen cephalosporin) if pt is stable. AVOID barium enema, flexible sigmoidoscopy if diverticulitis suspected
If perforated: perform immediate surgical resection of diseased bowel via a Hartmann's procedure w/ a temporary colostomy
How does LBO present?
constipation/obstipation, deep and cramping abd pain (less intense than SBO), N/V (less than SBO but more commonly feculent)
How does the exam of LBO differ from SBO?
significant distention, tympany, and tenderness; examine for peritoneal irritation or mass; fever or signs of shock suggest perforation/peritonitis or ischemia/necrosis
What are the common causes of LBO?
COLON CANCER, diverticulitis, volvulus, fecal impaction, benign tumors
What other conditions need to be r/o in LBO?
SBO, paralytic ileus, appendicitis, IBD, Ogilvie's syndrome (pseudo-obstruction)
How is LBO tx?
obstruction can be relieved w/ a gastrografin enema, colonoscopy, rectal tube, surgery often needed
If ischemic colon, usually requires partial colectomy w/ a diverting colostomy
Treat underlying cause (neoplasm)
What bacteria is assoc w/ colon cancer?
Strep bovis
How does colon cancer often present?
ASx--screening should catch based on risk factors
Sx based on location
R-sided lesions: bulky, ulcerating masses that lead to anemia from chronic occult blood loss. Pts may complain of weight loss, anorexia, diarrhea, weakness, vague abdominal pain. Obstruction is rare
L-sided lesions: "apple-core" obstructing masses. Pts complain of change in bowel habits (decreased stool caliber, constipation, obstipation), colicky abd pain, and/or blood-streaked stools. Obstruction common.
Rectal lesions: BRBPR, often w/ tenesmus and/or rectal pain. Hemorrhoid coexisting common.
How is colon cancer dx?
Labs: CBC (microcytic anemia), occult blood in stool
Sigmoidoscopy: evaluate rectal bleeding, suspicious left-sided lesions
Colonoscopy: right-sided lesions w/ colonoscopy
Air-contrast barium enema: to look for additional lesions
Endorectal ultrasound: determine degree of invasion of rectal cancer
Metastatic work-up: CXR, LFTS, abd/pelvic CT
How is colon cancer treated?
Surgical resection of 1mary cancer and LN dissection for staging
Rectal Lesions depends on location
- Abdominoperineal resection: for distal lesions <10cm from the anal verge, when the sphincter cannot be preserved, the rectum and anus are resected and a permanent colostomy is placed
- Low anterior resection: For proximal lesions >10cm from the anal verge, a primary anastomosis is created btw the colon and rectum
- Wide local excision: for small, low-grade, well-differentiated tumors in the lower third of the rectum
Adjuvant chemo: if + LN. considered for rectal cancers
Follow/ serial CEA levels (diagnostically nonspecific, but useful for monitoring recurrence)
Metastasis work-up: colonoscopy, LFTs, CXR, abd CT
What is ischemic colitis?
due to lack of artieral blood supply to colon. severity depends on superficial mucosa vs. full-thickness necrosis
Where is ischemic colitis most likely?
left colon in watershed area at the splenic flexure
How does ischemic colitis present?
crampy lower abd pain assoc w/ bloody diarrhea.
fever and peritoneal signs suggest infarction
How is ischemic colitis dx?
Labs: leukocytosis
Flexible sigmoidoscopy/colonoscopy: assess colonic mucosa
How is ischemic colitis tx?
Supportive Tx: bowel rest, IV fluids, broad-spectrum abx
Surgery: w/ resection if infarcted, fulminant colitis, obstruction 2ndary to ischemic stricture
What is a known complication to AAA repair because of sacrificing inferior mesenteric artery?
ischemic colitis
What are usual causes of UGI bleeding?
PUD, esophagitis/gastritis, Mallory-Weiss tear, esophageal varices
What are the usual causes of LGI bleeding?
diverticulosis (60%), IBD, hemorrhoids/fissures, neoplasm, AVM
What locations is UC usually?
rectum ALWAY involved
extends proximally in continuous fashion
Inflammation and ulceration are limited to mucosa and submucosa
What locations is Crohn's usually?
any portion of GI tract
ileocecal region in a discontinuous pattern ("skipped lesions")
rectum often spared
transmural inflammation
How does UC usually present?
bloody diarrhea, lower abd cramps, tenesmus, urgency
Exam: reveal orthostatic hypotension, tachycardia, abd tenderness, frank blood on rectal exam, extraintestinal manifestations
How does Crohn's usually present?
Abd pain, abd mass, low-grade fever, weight loss, watery diarrhea
Exam: reveal fever, abd tenderness or mass, perianal fissures, fistuals, and extraintestinal manifestations
What are extraintestinal manifestations of UC?
aphthous stomatitis, episcleritis/uveitis, arthritis, primary sclerosing cholangitis, erythema nodosum, pyoderma gangrenosum
What are the extraintestinal manifestations of Crohn's disease
aphthous stomatitis, episcleritis/uveitis, arthritis, primary sclerosing cholangitis, erythema nodosum, gallstones, nephrolithiasis, and fistulas to the skin, bladder, or btw bowel loops
How is UC dx?
CBC, AXR, stool cultures, O&P, stool assay for C. diff
Colonoscopy: diffuse and continuous rectal involvement, friability, edema, and pseudopolyps
Bx: definitive
How is Crohn's dx?
CBC, AXR, stool cultures, O&P, stool assay for C. Diff
Upper GI series w/ small bowel follow-through
Colonoscopy: aphthoid, linear, stellate ulcers, strictures, "cobblestoning" and "skip lesions", "creeping fat" may also be present during laparotomy
Bx: definitive
How is UC tx?
Meds: 5-ASA agents (sulfasalazine, mesalamine) topical or oral; corticosteroids and immunomodulating agents (azathioprine) for refractory disease
Total proctocolectomy: curative
- for long-standing or fulminant colitis or toxic megacolon
- decrease cancer risk
How is Crohn's tx?
5-ASA agents; corticosteroids and immunomodulating agents (azathioprine, infliximab) if no improvement is seen
Surgical resection: necessary for suspected perforation, stricture, fistula, or abscess; may recur anywhere in the GI tract
Does UC have a high risk of cancer?
markedly increased risk of colon cancer in long-standing cases (monitor w/ frequent fecal occult blood screening and yearly colonoscopy w/ multiple biopsies after eight yrs of disease)
What is an inguinal hernia?
abnormal protrusion of abdominal contents (usually the small intestine) into inguinal region through a weakness or defect in the abd wall
What is the difference btw an indirect and direct hernia?
Indirect hernia: hernia of abd contents through the internal and then external inguinal rings and eventually into the scrotum (in males). Lateral to epigastric vessels
Direct hernia: herniation of the abd contents through the floor of Hesselbach's triangle. Hernial sac contents do not traverse the internal inguinal ring; they herniate directly through the abd wall and are contained w/in the aponeurosis of the external oblique muscle. Medial to epigastric vessels
Which is more common, an indirect hernia or direct hernia?
inguinal is most common in both genders
What causes an indirect inguinal hernia?
congenital patent processus vaginalis
What causes a direct inguinal hernia?
acquired defect in the transversalis fascia from mechanical breakdown that increases w/ age
How are hernias treated?
Surgery: b/c of risk of incarceration and strangulation
- open or laparoscopic
Direct: correct defect in transversalis fascia
Indirect: isolate and ligate the hernial sac and reduce the size of the internal inguinal ring to allow only the spermatic cord structures in males to pass through
What is Hesselbach's triangle?
bounded by inguinal ligament, inferior epigastric artery and rectus abdominis
What is biliary colic?
Results from transient cystic duct blockage from impacted stones
What are the risk factors for biliary colic?
Other risk factors
- OCP use
- rapid weight loss
- + fam hx
- chronic hemolysis (pigment stones in sickle cell disease)
- small bowel resection
How does biliary colic present?
postprandial abd pain (RUQ) that radiates to subscapular area or the epigastrium. pain is abrupt and followed by gradual relief. Assoc w/ n/v, fatty food intolerance, dyspepsia, and flatulence
Exam: ASx or palpable gallbladder
What are black gallstones likely a result of?
What are brown gallstones likely a result of?
How is biliary colic/cholelithiasis dx?
AXR: not helpful
What is the treatment for biliary colic/cholelithiasis?
- laparoscopically for symptomatic
If gallstones in common bile duct:
Nonsurgical candidates:
- dietary modification
What are complications of cholelithiasis?
recurrent biliary colic
acute cholecystitis
ascending cholangigis
gallstone ileus
gallstone pancreatitis
What is acute cholecystitis?
prolonged blockage of cystic duct caused by an impacted stone that leads to obstructive distension, inflammation, superinfection, and possibly gangrene of the gallbladder (acute gangrenous cholecystitis)
What is acalculous cholecystitis?
absence of cholelithiasis in pts who are chronically debilitated, those who are critically ill in the ICU or on TPN and trauma or burn victims
How does acute cholecystitis present:
RUQ pain, nausea, vomiting, fever
More severe and longer duration sx than for biliary colic
Exam: RUQ tenderness, inspiratory arrest during deep palpation of the RUQ (Murphy's sign), low-grade fever, mild icterus, possible guarding/rebound tenderness
How is acute cholecystitis dx?
Labs: Leukocytosis
U/S: stones, bile sludge, pericholecystic fluid, thickened gallbladder wall, gas in gallbladder, ultrasonic Murphy's sign
HIDA scan: (only if U/S is equivocal). Nonvisualization of the gallbladder on HIDA suggests acute cholecystitis
How is acute cholecystitis tx?
Broad spectrum IV abx
IV fluids
replete electrolytes
- If early or unstable, cholecystecomy
- If stable and/or with multiple comorbidities (DM) delay cholecystectomy until acute inflammation resolves (4-6wks)
Where does the cystic artery pass through?
triangle of Calot, comprising the common hepatic duct, the cystic duct, and inferior border of the liver
What are complications of acute cholecystitis?
gangrene, empyema, perforation, emphysematous gallbladder (due to infxn by gas-forming organisms), fistulization, gallstone ileus, sepsis, abscess formation
What is choledocolithiasis?
Gallstones in common bile duct
How does choledocolithiasis present?
varying sx based on degree of obstruction, duration of obstruction, and extent of bacterial infxn
- biliary colic, jaundice, fever, and pancreatitis
How is choledocolithiasis dx?
Labs: increased Alk phos and total bilirubin
How is choledocolithiasis tx?
ERCP w/ sphincterotomy followed by semi-elective cholecystectomy
- may need common bile duct exploration
What is the mechanism of gallstone pancreatitis?
when gallstones in the ampulla also obstruct the pancreatic duct
What is ascending cholangitis?
acute bacterial infxn of biliary tree that occurs due to obstruction (choledocholithiasis) or primary sclerosing cholangitis (progressive inflammation of biliary tree assoc w/ UC)
What are other causes of ascending cholangitis?
bile duct stricture
malignancy (biliary or pancreatic)
What organisms are implicated in ascending cholangitis?
Gram negs
- E. coli
- Enterobacter
- Pseudomonas
How does ascending cholangitis present?
Charcot's triad:
- RUQ pain
- Jaundice
- fever/chills
Reynold's pentad (acute suppurative cholangitis)
- Charcot's traid
- septic shock
- altered mental status
What is Reynold's pentad?
- Charcot's traid
- septic shock
- altered mental status
How is ascending cholangitis dx?
Labs: leukocytosis, increased bilirubin, increased Alkphos, blood cultures
U/S or CT: not necessary b/c clinical dx
MRCP: most useful imaging and noninvasve
ERCP: dx and tx (biliary drainage)
How is ascending cholangitis tx?
Admit to ICU
Hydration and BP support
broad spectrum ABx
- if acute suppurative cholangitis--> emergent bild duct decompression via ERCP/sphincterotomy, percutaneous transhepatic drainage, or open decompression
What is a gallstone ileus?
mechanical obstruction resulting from passage of large (>2.5cm) stone into the bowel through a cholecystoduodenal fistula
Obstruction is at the terminal ileum (TI/ileocecal valve)
How does a gallstone ileus present?
no hx of biliary sx
present as an SBO (subacute)
How is gallstone ileus dx?
Pneumobilia (gas in the biliary tree)
- upper GI series w/ small bowel follow-through showing TI obstruction
How is gallstone ileus tx?
Laparotomy w/ stone extraction (enterolithotomy) or manipulation into colon
What is PSC?
idiopathic disorder characterized by inflammation, fibrosis and strictures of extra-and intrahepatic bile ducts
Does PSC affect men or women?
young men w/ IBD (UC)
How does PSC present?
progressive jaundice, pruritis, fatigue
How is PSC dx?
Labs: increased alkphos, increased bilirubin
MRCP/ERCP: multiple bile duct strictures w/ dilatations btw strictures
Liver biopsy: periductal sclerosis ("onion skinning")
How is PSC tx?
high dose ursodeoxycholic acid, endoscopic dilation and short-term stenting of bile duct strictures; liver transplantation
What type of cancer are PSC pts at risk for?
If labs show an elevated AST and ALT, what kind of liver disease does this suggest?
hepatocellular injury
If labs show an elevated alk phos and bilirubin, what kind of liver disease does this suggest?
What drugs can cause a hepatitis?
What are some potential causes for increased alkphos and bilirubin?
Intrahepatic Cholestasis
- medications
- postop
- sepsis
Biliary Obstruction
- stone
- stricture
- cancer
What are some causes of isolated hyperbilirubinemia?
- hemolytic anemia
Defective conjugation
- Gilbert's syndrome
- Crigler-Najjar syndrome
Defective excretion
- Dubin-Johnson syndrome
- Rotor's syndrome
How does acute hepatitis present?
Viral prodrome: malaise, fever, joint pain, fatigue, URI sx, nausea, vomiting, changes in bowel habits
Followed by Jaundice and RUQ tenderness
Exam: jaundice, scleral icterus, tender hepatomegaly, possible splenomegaly, lymphadenopathy
How does chronic hepatitis present?
chronic liver disease: jaundice, fatigue, hepatosplenomegaly
How is acute viral hepatitis dx?
Labs: dramatically increased ALT and AST, bilirubin/alkphos
Hepatitis serology
How is autoimmune hepatitis dx?
Labs: increased AST/ALT and bilirubin and alkphos
ANA, anti-smooth muscle antibody, and antimitochondrial antibody
How is hemachromatosis dx?
Labs: increased AST/ALT and bilirubin and alkphos
iron saturation
How is Wilson's disease dx?
Labs: increased AST/ALT and bilirubin and alkphos
How is chronic hepatitis dx?
ALT and AST are increased for > 6 months w/ concurrent increase in alkphos/bilirubin and hypoalbuminemia
Severe cases: PT prolonged (all clotting factors except factor VIII are produced by the liver)
How is hepatitis treated?
Severe alcoholic hepatitis: steroids
Autoimmune hepatitis: immunosuppression
Chronic HBV: IFN-alpha, lamivudine, adefovir
Chronic HCV: peginterferon, ribavirin
End-stage Liver failure: liver transplantation
Fulminant hepatic failure: ICU mgmt and emergent transplant
What are complications of chronic hepatitis?
cirrhosis, liver failure, hepatocellular carcinoma
What is cirrhosis?
fibrosis and nodular regeneration resulting from hepatocellular injury
What are causes of cirrhosis?
chronic hepatitis, biliary tract disease (primary biliary cirrhosis, primary sclerosing cholangitis), R-sided heart failure, constrictive pericarditis, Budd-Chiari syndrome (hepatic vein thrombosis secondary to hypercoagulability)
How does cirrhosis present?
Jaundice, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy (asterixis, altered mental status), gastroesophageal varices, coagulopathy, renal dysfxn. Weakness, anorexia, and weight loss (if advanced)
Exam: enlarged, palpable, firm liver. Stigmata of portal HTN, signs of liver failure
How is cirrhosis dx?
Labs: decreased albumin, increased PT/PTT, and increased bilirubin, anemia or thrombocytopenia (secondary to hypersplenism), hepatitis serologies, autoimmune studies, serum ferritin, ceruloplasmin, alpha-antitrypsin
U/S: liver size, presence of ascites, patency of splenic and hepatic veins
Bx: bridging fibrosis, nodular regeneration
What is the SAAG?
Serum-ascites albumin gradient (SAAG)
SAAG = serum albumin-ascites albumin\
- SAAG>1.1 = portal HTN
--presinusoidal = splenic or portal vein thrombosis, schistosomiasis
--sinusoidal = cirrhosis, massive hepatic metastases
--postsinusoidal = RHF, constrictive pericarditis, Budd-Chiari syndrome

-SAAG <1.1 = protein leakage
--nephrotic syndrome
--malignancy (ovarian cancer)
What are some physiologic signs of portal htn?
esophageal varices (hematemesis)
Peptic ulcer (melena)
Caput medusae
What are some physiologic signs of liver cell failure?
scleral icterus
fetor hepaticus
spider nevi
loss of sexual hair
bleeding tendency
testicular atrophy
ankle edema
How is ascites treated?
- sodium restriction and diuretics (furosemide and spironolactone)
- r/o infxn and neoplastic cause by performing paracentesis to obtain SAAG, cell count w/ diff and cultures
How is SBP tx?
SBP (fever, abd pain, AMS)
- check peritoneal fluid if there is a possibility of infxn; fluid is + if there are >250 PMNs or >500WBCs
- Tx w/ abx (3rd gen cephalosporin) to cover both gram + Enterococcus and gram - E. coli and Klebsiella organisms until a causative organism is identified
How is hepatorenal syndrome tx?
How is hepatic encephalopathy tx?
due to decreased clearance of ammonia
precipitated by dehydration, infxn, electrolyte abnormalities, and GI bleeding
treat w/ dietary protein restriction, lactulose, and rifaximin
How is esophageal varices tx?
monitor for GI bleeding; treat medically (B-blockers, octreotide), endoscopically (band ligation) or surgically (portocaval shunt)
consider liver transplant for pts w/ advanced disease
What is PBC?
autoimmune disorder characterized by destruction of intrahepatic bile ducts
Does PBC commonly affect men or women?
Middle-aged women w/ other autoimmune conditions
How does PBC present?
progressive jaundice, pruritis, malabsorption of the fat soluble vitamins (A, D, E, K)
How is PBC dx?
Labs: increased alk phos, increased bilirubin, +antimitochondrial ab, increased cholesterol
How is PBC tx?
Ursodeoxycholic acid (slows progression of disease); cholestyramine for pruritis, liver transplant
What are the most common risk factors for developing hepatocellular carcinoma in the US?
cirrhosis and chronic HCV
What are the most common risk factors for developing hepatocellular carcinoma worldwide?
aflatoxins and HBV infxn
How does hepatocellular carcinoma present?
RUQ tenderness, abd distention, signs of chronic liver disease such as jaundice, easy brusability, and coagulopathy. Cachexia and weakness may also be present
Exam: tender enlargement of the liver
How is hepatocellular carcinoma dx?
U/S or CT: mass
Labs: abnormal LFTs, significantly elevated AFP
Bx: definitive dx
How is hepatocellular carcinoma tx?
Small tumors/early detection
- aggressive tumor resection
- orthotopic liver transplantation
Chemotherapy and radiation
- not effective, but can be used to shrink large tumors prior to surgery (neoadjuvant tx)
- serial AFP for monitoring
- prevent exposure to hepatic carcinogens
- vaccinate against hepatitis in high-risk individuals
What is hemachromatosis?
hyperabsorption of iron w/ parenchymal hemosiderin accumulation in the liver, pancreas, heart, adrenals, testes, pituitary, kidneys
How is hemachromatosis inherited?
autosomal recessive
occurs in males of northern european descent and is rarely dx before 50s
What is secondary hemachromatosis?
occurs w/ iron overload and common in pts receiving chronic transfusion tx (ex- alpha thal) and alcoholics (increased iron absorption)
How does hemachromatosis present?
abd pain, sx of DM, hypogonadism, arthropathy of the MCP joints, heart failure, cirrhosis
Exam: bronze skin pigmentation, pancreatic dysfxn, cardiac dysfxn (CHF), hepatomegaly, testicular atrophy
How is hemachromatosis dx?
Labs: increased serum iron, percent saturation of iron, ferritin w/ decreased transferrin, fasting transferrin saturation (serum iron divided by transferrin level), glucose intolerance and mildly elevated AST and alk phos
Bx: determines hepatic iron index
Hepatic MRI
HFE gene mutation screen
How is hemachromatosis tx?
weekly phlebotomy: when serum iron levels decrease, perform maintenance phlebotomy every 2-4 mo
Deferoxamine: used for maintenance tx
What are complications of hemochromatosis?
cirrhosis, hepatocellular carcinoma, cardiomegaly leading to CHF and/or conduction defects, DM, impotence, arthropathy, hypopituitarism
What is Wilson's disease?
Decreased ceruloplasmin and excessive deposition of copper in the liver and brain due to deficient copper-transporting protein
Is Wilson's disease heritable?
Yes, autosomal recessive defect on Chromosome 13
How does Wilson's disease present?
hemolytic anemia, liver abnormalities (jaundice secondary to hepatitis/cirrhosis), neurologic (loss of coordination, tremor, dysphagia), psychiatric (psychosis, anxiety, mania, depression)
What physical exam findings are unique to Wilson's disease?
Kayser-Fleischer rings in the cornea, jaundice, hepatomegaly, asterixis, choreiform movts, and rigidity
How is Wilson's disease dx?
Labs: decreased serum ceruloplasmin, increased urinary copper excretion, increased hepatic copper
How is Wilson's disease tx?
dietary copper restriction (avoid shellfish, liver, legumes), penicillamine (copper chelator that increases urinary copper excretion, administer w/ pyridoxine), possibly oral zinc (increases fecal excretion)
What are risk factors for acute pancreatitis?
gallstones, alcoholism, hypercalcemia, hypertriglyceridemia, trauma, drug side effect (thiazide diuretics), viral infxns, post-ERCP, scorpion bites
What are risk factors for chronic pancreatitis?
alcoholism, gallstones, hyperparathyroidism, hyper cholesterolemia, cystic fibrosis, idiopathic
How does acute pancreatitis present?
severe epigastric pain (radiating to the back); nausea, vomiting, weakness, fever, shock
Exam: discoloartion (Grey Turner's sign) and periumbilical discoloration (Cullen's sign)
How does chronic pancreatitis present?
recurrent episodes of persistent epigastric pain, anorexia, nausea, constipation, flatulence, steatorrhea, weight loss, DM
How is acute pancreatitis dx?
increased amylase, lipase, decreased calcium
AXR: if severe: "sentinel loop" or "colon cutoff sign"
U/S or CT: enlarged pancreas w/ stranding, abscess, hemorrhage, necrosis, pseudocyst
How is chronic pancreatitis dx?
increased or normal amylase and lipase, decreased stool elastase, glycosuria, pancreatic calcifications, mild ileus on AXR and CT "chain of lakes"
How is acute pancreatitis tx?
removal of the offending agent
Supportive care: IV fluids/electrolyte replacement, analgesia, bowel rest, NG suction, nutritional support, O2, "tincture of time"
IV abx, respiratory support, surgical debridement if necrotizing pancreatitis is present
How is chronic pancreatitis tx?
analgesia, exogenous lipase/trypsin and medium-chain fatty-acid diet, avoidance of causative agents (EtOH), celiac nerve block, surgery for intractable pain or structural causes
What are complications of acute pancreatitis?
pancreatic pseudocyst, fistual formation, hypocalcemia, renal failure, pleural effusion, chronic pancreatitis, sepsis
What are complications of chronic pancreatitis?
chronic pain, malnutrition/weight loss, pancreatic cancer
What is Ranson's criteria on admission?
GA LAW (mortality increases w/ more signs)
Glucose >200
LDH> 350
What is Ranson's criteria after 48hrs?
Ca <8.0
Hematocrit decreased by >10%
PaO2 <60
Base excess>4 mEq/L
BUN increase by >5mg/dL
Sequestered fluid >6L
Where is pancreatic cancer usually found?
75% are adenocarcinomas in the head of the pancreas
What are the risk factors for pancreatic cancer?
smoking, chronic pancreatitis, 1st degree relative w/ pancreatic cancer, high-fat diet
How does pancreatic cancer present?
abd pain radiating toward the back, obstructive jaundice, loss of appetite, nausea, vomiting, weight loss, weakness, fatigue, indigestion
Usually Asx until late
Exam: palpable, nontender gallbladder (Courvoisier's sign) or migratory thrombophlebitis (Trousseau's sign)
How is pancreatic cancer dx?
CT: pancreatic mass, dilated pancreatic and bile ducts, extent of vascular involvement (SMA, SMV, and portal vein) and metastasis (hepatic)
ERCP or endoscopic ultrasound for visualization
CA-19-9 often elevated, but measure lacks sensitivity and specificity
How is pancreatic cancer tx?
Most palliative b/c present w/ metastatic disease
If no evidence of metastasis: Whipple procedure (pancreaticodudenectomy) and mass is at pancreatic head
- 5-FU and gemcitabine to improve short-term survival, but long-term prognosis is poor (5-10% five year survival)
What is the classic presentation of pancreatic cancer?
painless progressive obstructive jaundice