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202 Cards in this Set
- Front
- Back
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Pattern of colorectal cancer spread
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(1) Direct extension - circumferentially and then through the bowel wall to later invade other abdominaoperineal organs; (2) Hematogenous - portal circulation to liver. THE LIVER IS THE MC SITE OF DISTANT SPREAD; (3) Lymphatic - regionally; (4) Transperitoneal and intraluminal
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Adenomatous poylps
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(1) Premalignant lesions, but most do not develop into cancer. (2) VILLOUS adenomas have higher malignant potential than TUBULAR adenomas; (3) The larger the size, and the greater the number of polyps, the higher the risk of cancer
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IBD and colorectal cancer
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Both UC and Crohn's disease pose an increased risk for colorectal cancer, but UC poses a greater risk than Crohn's disease; Incidence of CRC is 5-10% at 20 years and 12-20% at 30 years with UC
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Familial Adenomatous Polyposis
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(1) AD disease characterized by hundreds of adenomatous polyps in the colon. The colon is always involved, and the duodenum is involved in 90% of cases. Polyps may also form in the stomach, jejunum, and ilieum; (2) Risk of CRC is 100% by 3rd or 4th decade of life (in 100% of familial adenomatous polyposis cases); (3) Prophylactic colectomy is usually recommended
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Gardner's Syndrome [Familial polyposis coli]
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Polyps + osteomas, dental abnormalities, benign soft tissue tumors, desmoid tumors, sebaceous cysts; risk of CRC is 100% by approximately age 40
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Turcot's syndrome
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Ar; Polyps + cerebellar medulloblastoma or GBM
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Peutz-Jeghers Syndrome
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(1) Single or multiple hamartomas that may be scattered through entire GI tract: in small bowel (78%), colon (60%), stomach (30%); (2) Pigmented spots around lips, oral mucosa, face, genitalia, and palmar surfaces; (3) Unlike adenomas, hamartomas have VERY LOW malignant potential; (4) Slightly increased incidence in various carcinomas (stomach, ovary, breast, cervix, testicle, lung); (4) Intussusception or GI bleeding may occur
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Familial juvenile polyposis coli
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(1) Rare; presents in childhood of juvenile; only small risk of CRC; (2) More than 10 and up to hundreds of juvenile colon polyps
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Hereditary nonpolyposis CRC - without adenomatous polyposis
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(1) Lynch Syndrome I (site specific CRC) - early onset CRC; absence of antecedent multiple polyposis; (2) Lynch syndrome II (cancer family syndrome) all features of Lynch I plus increased number and early occurrence of other cancers (e.g., female genital tract, skin, stomach, apncreas, brain, breast, biliary tract)
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Clinical features of CRC
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(1) Abdominal pain is MC presenting symptom. Remember that CRC in the most common cause of large bowel obstruction in adults; (2) Weight loss; (3) Blood in stool; (4) Colonic perforationi sthe most life-threatening presentation; (5) May be asymptomatic
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Signs and symptoms based on specific location of colon tumor
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(1) Right-Sided tumors: Obstruction is unusual because of the larger luminal diameter (the cecum has the largest luminal diameter of any part of the colon), allowing for large tumor growth to go undetected; Common findings: occult blood in stool, iron deficiency anemia, and melena; change in bowel habits is uncommon; triad of anemia, weakness, RLQ mass (occasionally) is present; (2) Left-sided tumors: cmaller luminal diamter - signs of obstruction more common; change in bowel habits more common - alternating constipation/diarrhhea, narrowing of stools ('pencil stools'); hematochezia more common
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Rectal cancer (20-30% of CRC)
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Presents with hematochezia as MC symptom, tenesmus, and rectal mass with feeling of incomplete evacuation of stool (due to mass); rectal cancer has a higher recurrence rate and a lower 5-year survival rate than colon cancer
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What modality is NOT indicated in treatment of colon cancer, although it is used in treating rectal cancer?
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Radiation therapy is not indicated in treatment of colon cancer; however, it is used in treating rectal cancer.
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Treatment of Colon Cancer
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(1) Surgical resection of tumor-containing bowel as well as resection of regional lymphatics; (2) Check CEA before surgery; (3) Adjuvant therapy - postop chemo (5-FU and leucovorin) indicated for Dukes' C colon cancer. For Dukes' B2 or C rectal cancer, 5-FU and XRT are used post-op
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Three types of adenomatous polyps [benign lesions with significant malignant potential]
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(1) Tubular (MC; up to 60-80% of cases) - smallest risk of malignancy; (2) Tubulovillous - intermediate risk of malignancy; (3) Villous - greatest risk of malignancy
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Where are most polyps found?
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In the rectosigmoid region; most patients are asymptomatic, however, in symptomatic patients, rectal bleeding is most common symptom
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Malignant potential of a polyp
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(1) size: larger polyp = greater malignant potential; (2) histologic type; (3) atypia of cells; (4) shape: sessile [flat, more likely to be malignant] vs pedunculated [on a stalk]
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Diverticulosis vs Diverticulitis
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Diverticulosis is pouches in the colon wall. These should be distinguished from diveritculitis, which refers to inflammation or infection of the diverticula and is a complication of diverticulosis
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Diverticulosis : general characteristics
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(1) Caused by increased intraluminal pressure: inner layer of colon bulges through focal area of weakness in colon wall (usually an area of blood vessel penetration); Pt will often feel vague LLQ discomfort, bloating, constipation/diarrhea. RISK FACTORS: [a] low fiber diet - constipation caused intraluminal pressures to increase, [b] family hisory. (2) Prevalence increases with age; (3) MC location is SIGMOID COLON, however, diverticula may occur anywhere in colon
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Diagnosis of diverticulosis
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Barium enema is test of choice; abdominal X-rays are usually normal and are not diagnostic for diverticulosis
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Treatment of diverticulosis
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(1) High-fiber foods (such as bran) to increase stool bulk; (2) Psyllium if patient cannot tolerate bran
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Complications of diverticulosis
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(1) Painless rectal bleeding - seen in up to 40% of patients; is often clinically insignificant and stops spontaneously. No further treatment is necessary in these patients. (2) Bleeding can be severe in about 5% of patients. In many cases, the bleeding stops spontaneously. C-scope may be performed to locate site of bleeding
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Complications of diverticulitis
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(1) Abscess formation; (2) Colovesical fistula - accts for 50% of fistulas 2/2 diverticulitis, 50% close spontaneously; (3) Obstruction - due to chronic inflammation and thickening of bowel wall; (3) Free colonic perforation - uncommon but catastrophic (leads to peritonitis)
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Diverticulitis: general characteristics
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(1) occurs when feces become impacted in the diverticulum, leading to erosion and microperforation; (2) fever, LLQ pain, and leukocytosis. DX: CT w/ contrast. NOTE: barium enema and colonoscopy are contraindicated in acute diverticulitis
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Treatment of diverticulitis
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(1) Initial episode: IV Abx, bowel rest (NPO), IV fluids, mild episodes can be treated on outpt basis if patient is reliable, has few or no comorbid conditions. If symptoms persist for 3-4 days, then surgery may be necessary. (2) Second and subsequent episodes - surgery is rec'd once acute inflammation resolves. Low-residue diet no nuts/seeds rec'd
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Take-home message of diverticulitis vs diverticulosis
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With diverticulosis, barium enema is test of choice, and lower GI bleeding is very COMMON; with diverticulITIS, CT scan with contrast is test of choice [barium enema and c-scope are contraindicated] and lower GI bleeding is very rare
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Angiodysplasia
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aka AV Malformations of the colon; tortuous dilated veins in the submucosa of the colon (usually proximal) wall. COMMON cause of lower GI bleeding in patients over age 60. Bleeding is usually low grade, but 15% may have massive hemorrhave if veins rupture. Diagnosed by colonoscopy, and in about 90% of patients, bleeding stops spontaneously
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What do up to 25% of patients with bleeding AVMs have?
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Aortic stenosis…the cause and effect is unknown
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Acute Mesenteric Ischemia
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Results from a compromised blood supply, usually to the superior mesenteric vessels; 4 types: (1) Arterial embolism [Afib, MI, valvular disease]; (2) Arterial thrombosis [atherosclerotic disease]; (3) Nonocclusive mesenteric ischemia [splanchnic vasoconstriction secondary to low cardiac output, typically seen in critically ill elderly patients; (4) Venous thrombosis
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Clinical Features of Acute Mesenteric Ischemia
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(1) Acute onset of severe abdominal pain disproportionate to physical findings; (2) Pain is due to ischemia and possibly infarction of intestines, analogous to MI in CAD; (2) Signs of intestinal infarction include hypotension, tachypnea, lactic acidosis, fever, and AMS; (3) Check lactate level is acute mesenteric ischemia is suspected
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Chronic Mesenteric Ischemia
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Caused by atherosclerotic occlusive disease of main mesenteric vessels (celiac artery, superior and inferior mesenteric arteries). Results in dull pain - 'abdominal angina' that is typically postprandial (increased demand for splanchnic blood flow)
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Olilvie's Syndrome
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(1) Signs, symptoms, and radiographic evidence of large bowel obstruction, but NO MECHANICAL obstruction; (2) Causes include recent surgery, trauma, serious medical illnesses, and medications; (3) Diagnosis cannot be confirmed until mechnical obstruction of colon is ruled out; (4) Treatment consists of stoppping any offending agent (e.g. narcotics) and supportive measures (IV fluids, electrolyte repletion); (5) Decompression with gentle enemas or NG suction may be helpful. Colonoscopic decompression is usually successful if above measures fail
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Pseudomembranous colitis aka antibiotic associated colitis
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(1) Almost all antibiotics have been associated, but clindamycin, ampicillin, and cephalosporins are most frequently implicated; (2) Profuse watery diarrhea (usually no blood or mucus); (3) Crampy abdominal pain; (3) Toxic megacolon; (4) Demonstration of C. diff toxins in stool is diagnostic, but results take at least 24h to obtain
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Treatment of C. diff
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(1) Metronidazole is drug of choice (cannot be used in infants or pregnant patients); (2) Oral vancomycin is used if patient is resistant ot metronidazole or cannot tolerate it; (3) Cholestyramine ma be used as an adjuvant treatment to improve diarrhea
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Colonic volvulus
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(1) Twisting of a loop of intestine about its mesenteric attachment site; (2) May result in obstruction or vascular compromise [with potential for necrosis and/orperforation if untreated]; (3) MC site is sigmoid colon (75% of cases) and then cecum (25% of cases)
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Diagnosis of volvulus
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(1) Acute onset of colicky abdominal pain; (2) Obstipation, abdominal distention; (3) Anorexia, nausea, vomiting. (4) Plain films may show the 'omega loop sign' of a dilated sigmoid colon or the 'coffee bean sign' indicating a large air-fluid level with distention of cecum and small bowel in a cecal volvulus
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Cirrhosis
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Chronic liver disease characterized by fibrosis, disruption of liver architecture, and widespread nodules in the liver. The fibrous tissue replaces damaged or dead hepatocytes
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What are the two major events 2/2 distortion of liver anatomy that occur during cirrhosis?
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(1) Decreased blood flow through the liver with subsequent hypertension in portal circulation (portal hypertension!) This has widespread manifestations, including ascites, peripheral edema, splenomegaly, and varicosity of veins 'back stream' in the circulation (e.g. gastric/esophageal varices, hemorrhoids); (2) Hepatocellular failure leads to impairment of biochemical functions and decreased albumin synthesis and decreased clotting facor synthesis
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Child's Classification for Cirrhosis
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Estimates hepatic reserve in liver failure. It is used to measure disease severity and is a predictor of morbidity and mortality. Child's class C indicates most severe disease, and Child's class A indicates milder disease
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What are the two most common causes of cirrhosis?
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(1) Chronic viral infection [HepC] and (2) alcoholic liver disease
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Alcoholic liver disease
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Range of conditions from fatty liver (steatohepatitis) to alcoholic hepatitis to cirrhosis (irreversible)
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Other causes of cirrhosis
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(1) Drugs [acetaminophen toxicity, methotrexate]; (2) Autoimmune hepatitis; (3) Primary Biliary Cirrhosis; (4) Inherited metabolic diseases [hemochromatosis, Wilson's disease]; (5) Hepatic congestion 2/2 right-sided heart failure, constrictive pericarditiis; (6) alpha-1 antitrypsin deficiency; (7) Hepatic veno-occlusive disease - can occur after bone marrow transplantation; (8) Nonalcoholic steatohepatitis (NASH)
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Classic signs of chronic liver disease
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(1) Ascites; (2) Varices; (3) Gynecomastia, testicular atrophy; (4) Palmar erythema, spider angiomas; (5) Hemorrhoids; (6) Caput medusae
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Portal Hypertension
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Bleeding (hematemesis, melena, hematochezia) 2/2 esophagogastric varices is the most life-threatening complication of portal HTN; Transjugular intrahepatic portal-systemic shunt (TIPS) to lower portal pressure
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Ascites
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Accumulation of fluid into the peritoneal cavity due to portal HTN (increased hydrostatic pressure) and hypoalbuminemia (reduced oncotic pressure). Clinical features: Abdominal distention, shifting dullness, and fluid wave
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Differential Diagnosis of Ascites
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(1) Cirrhosis, portal HTN; (2) CHF; (3) Chronic renal disease; (4) Massive fluid overload; (5) TB peritonitis; (6) Malignancy; (7) Hypoalbuminemia; (8) Peripheral vasodilation 2/2 endotoxin-induced release of NO, which leads to increased renin and thus secondary hyperaldosteronism; (9) Impaired liver inactivation of aldosterone
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Serum Ascites Albumin Gradient (SAAG)
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If it is >1.1g/dl, portal HTN is very likely. If <1.1g/dl, portal HTN is unlikely and other causes must be considered
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Treatment for ascites
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(1) Bed rest, low sodium diet, and diuretics [furosemide and spironolactone]. [Spironolactone 100-400mg/day + Furosemide 40-160 mg/day]. Note the ratios! 40mg lasix:100mg spironolactone is associated with lower complications
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Hepatic encephalopathy
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Toxic metabolites (there are many, but AMMONIA is believed to be most important) that are normally detoxified or removed by the liver accumulate and reach the brain; See decreased mental function, confusion, poor concentration, even stupor or coma. Asterixis, rigidity/hyperreflexia, Fetor hepaticus - musty odor of breath
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Treatment of Hepatic encephalopathy
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(1) Lactulose prevents absorption of ammonia. Metabolism of lactulose by bacteria in colon favors formation of NH4+, which is poorly absorbed from GI tract, thereby promoting excretion of ammonia; (2) Neomycin - kills bowel flora, so decreases ammonia production by intestinal bacteria; (3) Diet - limit protein to 30-40mg/day
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Hepatorenal Syndrome
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Indicates end-stage liver disease. Progressive renal failure in advanced liver disease 2/2 renal hypoperfusion resulting from vasoconstriction of renal vessels. (1) Often precipitated by infection or diuretics; (2) This is a functional renal failure - kidneys are normal in terms of morphology and no specific causes of renal dysfunction are evident. (3) Clinical features: azotemia, oliguria, hyponatremia, hypotension, low urine sodium (<10mEq/L); (4) Treatment: liver transplantation is the only cure
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Spontaneous bacterial peritonitis
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(1) Infected ascitic fluid; occurs in up to 20% of patients hospitalized by chronic liver disease, associated with high mortality rate of 20-30%; (2) E. coli, Klebsiella, Streptococcus pneumonia; (3) Clinical features include abdominal pain, fever, vomiting, rebound tenderness. SBP may lead to sepsis; (4) Diagnosis is established by paracentesis and examination of ascitic fluid for WBCs (especially PMNs), gram stain with culture, and sensitivities
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Spontaneous bacterial peritonitis one bug or multiple bugs?
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Typically, only one bug is grown (unlike in acute surgical peritonitis). The most common causes are gram negatives [70%] like E. coli and Klebsiella. Gram-positive causes [25%] include streptococcus and enterococcus species
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Diagnosis of SBP
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WBC > 500 or PMN > 250 [most sensitive]
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Treatment of Spontaneous Bacterial Peritonitis
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Drug of Choice: Cefotaxime; repeat tap after 48h and change antibiotics if no decline in PMN
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Wilson's Disease
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(1) Autosomal recessive disorder of copper metabolism; (2) Normally excess copper is excreted by the liver, but the livers of patients with Wilson's disease cannot do so because there is usually a deficiency of ceruloplasmin, a copper-binding protein necessary for copper excretion; (3) Copper accumulates in liver cells, and as hepatocytes die, copper leaks into plasma and accumulates in kidney, cornea, and brain
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Treatment of Wilson's Disease
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(1) Chelating agents - e.g., penicillamine; (2) Zinc - prevents uptake of dietary copper; (3) Liver transplantation; (4) Measure patient's copper levels, urinary copper excretion, ceruloplasmin, and LFTs
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Hemochromatosis
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Autosomal recessive disease of iron absorption; (1) Excessive iron absorption in the intestine leads to increased accumulation of iron (as ferritin and hemosiderin) in various organs; (2) Over many years, fibrosis in involved organs occurs 2/2 hydroxyl free radiacls that are generated by the excess iron; (3) Findings may include signs of liver disease, fatigue, arthritis, impotence/amenorrhea, abdominal pain, and cardiac arrhythmias
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Complications of Hemochromatosis
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(1) Cirrhosis - increased risk of HCC; (2)Cardiomyopathy; (3) Diabetes mellitus; (4) Arthritis; (5) Hypogonadism; (6) Hypothyroidism; (7) Hyperpigmentation of skin ('bronzelike')
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Diagnosis of Hemochromatosis
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(1) Markedly elevated serum iron and ferritin; (2) Elevated transferrin saturation; (3) Decreased TIBC; (4) Liver biopsy required for diagnosis; (5) Genetic testing for chromosomal abnormalities
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Treatment of Hemochromatosis
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(1) Perform repeated phlebotomies - treatment of choice and improves survival dramatically if initiated early in course of disease; (2) Treat any complications e.g. CHF, diabetes, hypothyroidism, arthritis; (3) Liver transplant in advanced cases
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Hepatocellular adenoma
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(1) Benign liver tumor, most often seen in young women (15-40 years of age). OCP use, female sex, and anabolic steroid use are the main risk factors; (2) Patients may be asymptomatic; hepatocellular adenoma may be discovered incidentally on abdominal imaging studies. RUQ pain or fullness may be present; (3) Malignant potential is very low (<1%) however the adenoma may rupture, leading to hemoperitoneum and hemorrhage; (4) Diagnosis is made by CT scan, ultrasound, or hepatic arteriography (most accurate but invasive)
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Treatment of Hepatocellular Adenoma
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(1) Discontinue oral contraceptives; (2) surgically resect tumors >5cm that do not regress after stopping OCPs (otherwise there is a risk of rupture)
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Cavernous Hemangiomas
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(1) Vascular tumors that are usually small and asymptomatic. They are the most common type of benign liver tumor; (2) As the size of the tumor increases (e.g. due to pregnancy or use of OCPs) the symptoms increase and include RUQ pain or mass; (3) Complications (uncommon unless tumor is very large) include rupture with hemorrhage, obstructive jaundice, coagulopathy, CHF secondary to a large AV shunt, and gastric outlet obstruction; (4) BIOPSY IS CONTRAINDICATED due to risk of bleeding; (5) Most cases do not require treatment; consider resection if patient is symptomatic or if there is a high risk of rupture (as with large tumors)
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Focal Nodular Hyperplasia
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(1) Benign liver tumor without malignant potential occurs in women of reproductive age. There is NO ASSOCIATION with oral contraceptives; (2) Usually asymptomatic; hepatomegaly may be present. Treatment is not necessary in most cases
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Hepatocellular Carcinoma (Malignant Hepatoma)
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Accounts for >80% of primary liver cancers and, although rare in the US, accounts for most deaths 2/2 cancers worldwide. TWO TYPES: (1) Nonfibrolamellar [most common] associated with hepB/C and cirrhosis, usually unresectable with very short survival time; (2) Fibrolamellar - usually NOT associated with HepB/C or cirrhosis; Most often resectable, relatively longer survival time; seen most commonly in adolescents and young adults
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Most common malignant liver tumors
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(1) Hepatocellular carcinomas and (2) Cholangiocarcinomas
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Most common benign liver tumor
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Hemangioma
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Nonalcoholic Steatohepatitis (NASH)
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Histology of liver is identical to that in patients with alcoholic liver disease, but these patients do not have a history of alcohol use! Associated with obesity, HLD, DM; usually asymptomatic and a benign course, but cirrhosis develops in 10-15%. Typically discovered on routine lab tests (mild elevation of AST, ALT)
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Gilbert's Syndrome
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Occurs in up to 7% of population - autosomal dominant condition in which there is decreased activity of hepatic uridine diphosphate glucuronyl transferase activity; (2) Common cause of isolated elevation of unconjugated bilirubin; (3) Exacerbated by fasting (crash diets), fever, alcohol, and infection; (4) Asymptomatic in most cases, but occasionally mild jaundice may be present
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Hemobilia
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(1) Blood draining into duodenum via common bile duct; (2) Source fo bleedign can be anywhere along biliary tract, liver, or ampullary region; (2) Causes: truama [most common], papillary thyroid carcinoma, surgery, tumors, infection; (3) Clinical features include GI bleeding (melena, hematemesis), jaundice, and RUQ pain; (4) Arteriogram is diagnostic. Upper GI endoscopy shows blood coming out of ampulla of Vater
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Polycystic Liver Cysts
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(1) Autosomal dominant, usually associated with PCKD; (2) Liver cysts rarely lead to hepatic fibrosis or liver failure; (3) Usually asymptomatic; (4) Treatment unncessary in most cases
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Hydatid Liver Cysts
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(1) Caused by infection from tapeworm Echinococcus granulosus or less commonly, Echinococcus multilocularis; Cysts most commonly occur in right lobe of liver; (2) Small cysts are asymptomatic; large cysts may cause RUQ pain and rupture into the peritoneal cavity, causign fatal anaphylactic shock; (3) Treatment is surgical resection (caution to avoid spilling contents of cyst into peritoneal cavity). Mebendazole is given after surgery
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Pyogenic liver abscess
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(1) MCC is biliary tract obstruction - obstruction of bile flow allows bacterial proliferation; (2) Other causes include GI infection with spread via portal venou system, and penetrating liver trauma (gunshot wound, surgery); (3) Causative organisms include E. coli, Klebsiella, Proteus, Enterococcus,a nd anaerobes; (4) Clinical features include fever, malaise, anorexia, weight loss, nausea, vomiting, RUQ pain, and jaundice. Patients appear quite ill; (5) Diagnosed by ultrasound or CT scan; elevated LFTs; (6) Fatal if untreated - IV antibiotics and percutaneous drainage of abscess reduces mortality to about 5-20%
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What is the MC location of liver abscess?
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The right lobe [for both pyogenic and amebic]
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Amebic Liver Abscess
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(1) MC in men [9:1], particularly homosexual men; transmitted through fecal-oral contact; (2) Caused by intestinal amebiasis (Entamoeba histolytica) - the amebae reach the liver via the hepatic portal vein; (3) Clinical features: fever, RUQ pain, nausea/vomiting, hepatomegaly, diarrhea; (4) Serological testing establishes diagnosis; LFTs are often elevated; (5) IV metronidazole is effective treatment in most cases. Therapeutic aspiration of the abscess may be necessary if is large or does not respond to medical therapy
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Budd-Chiari Syndrome
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(1) Liver disease caused by occlusion of hepatic venous outflow, which leads to hepatic congestion and subsequent microvascular ischemia; (2) Course is variable, but most cases are indolent, with gradual development of portal HTN and progressive deterioration of liver function; (3) Rarely, disease is severe and leads to acute liver failure
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Causes of Budd-Chiari Syndrome
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(1) Hypercoagulable states; (2) Myeloproliferative disorders like P. vera - Get A JAK-2! (3) Pregnancy; (4) Chronic inflammatory diseases; (5) Infection, cancer, trauma
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Clinical features of Budd-Chiari
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Resemble those of cirrhosis: hepatomegaly, ascites, abdominal pain in RUQ, jaundice, and variceal bleeding
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Diagnosis of Budd-Chiari
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Hepatic venography; serum ascites albumin gradient >1.1g/dl
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Three major causes of jaundice
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(1) Hemolysis; (2) Liver disease; (3) Biliary obstruction
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General characteristics of jaundice
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(1) Yellow coloration of skin, mucous membranes, and sclerae due to oveproduction or underclearance of bilirubin; (2) Clinical jaundice usually becomes evident when total bili is >2mg/dl;
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Conjugated vs Unconjugated bilirubin
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Conjugated (direct) is loosely bound to albumin and therefore water soluble. When present in excess, it is excreted in urine…therefore DARK URINE IS ONLY SEEN WITH CONJUGATED BILIRUBIN! Unconjugated bilirubin is tightly bound to albumin and therefore not water soluble. It cannot be excreted in urine even fi blood levels are high; it is toxic - the unbound form can cross the BBB and cause neurologic deficits
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Dark urine and pale stools =?
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Conjugated hyperbilirubinemia
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Causes of conjugated hyperbilirubinemia
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Urine positive for bilirubin - due to: (1) Decreased intrahepatic excretion of bilirubin [hepatocellular disease, inherited disorders like Dubin-Johnson or Rotor's syndrome, drug-induced with OCPs, PBC, and PSC]; (2) Extrahepatic biliary obstruction [gallstones, carcinoma of head of pancreas, cholangiocarcinoma, periampullary tumors, extrahepatic biliary atresia]
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Causes of unconjugated hyperbilirubinemia
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Urine negative for bilirubin - due to: (1) Excess production of bilirubin - hemolytic anemias; (2) Reduced hepatic uptake of bilirubin or impaired conjugation [Gilbert's, Drugs [sulfa, PCN, rifampin, radiocontrast], Crigler-Najjar syndrome, Physiologic jaundice of newborn 2/2 immature conjugating system, diffuse liver disease]
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Cholestasis
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Blockage of bile flow (whether intrahepatic or extrahepatic) with a resultant increase in conjugated bilirubin levels; Findings include: jaundice, gray stools, dark urine; pruritus 2/2 bile salt deposition in skin; elevated alk phos, serum cholesterol; skin xanthomas [local accumulation of cholesterol]; malabsorption of fats and fat-soluble vitamins
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Alk Phos levels
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Not specific to liver - also found in bone, gut, and placenta; (1) AlkPhos is elevated when there is obstruction to bile flow (e.g. cholestasis) in any part of the biliary tree. Normal levels make cholestasis unlikely; (2) If levels are VERY HIGH (10-fold increase) think of extrahepatic biliary tract obstruction or intrahepatic cholestasis (e.g. PBC or drug-induced cirrhosis); (3) If levels are mildly elevated, measure GGT to make sure elevation is hepatic in origin. If GGT is also elevated, this trongly suggests hepatic origin; If GGT is normal but AlkPhos is elevated, consider pregnancy or bone disease
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LFT Pearls
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(1) Cholestatic LFTs: markedly elevated alkphos and GGT; ALT and AST slightly elevated; (2) Hepatocellular necrosis or inflammation: normal or slightly elevated alkphos, markedly elevated ALT and AST
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Three types of gallbladder stones
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(1) Cholesterol stones (yellow to green) associated with HLD, obesity, CF; (2) Pigment stones (black) associated with hemolysis 2/2 SCD, thalassemia, HS, artificial cardiac valves or alcoholic cirrhosis; (3) Mixed stones have components of both and acct for the majority of stones
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Biliary colic
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Due to temporary obstruction of cystic duct by a gallstone. Pain occurs as the gallbladder contracts against this obstruction; (2) Pain is typically located in the RUQ or epigastrium; Patients classically report pain after eating and at night; Boca's sign - referred right subscapular pain of biliary colic
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What is the pain in acute cholecystitis caused by?
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Gallbladder wall inflammation; this pain persists for several days
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What is the pain of biliary colic caused by?
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Contract of gallbladder against obstructured cystic duct; this pain typically lasts only a few hours
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Acute Cholecystitis
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Obstruction of the cystic duct (NOT infection) induces acute inflammation of the gallbladder wall; (2) Chronic cholecystitis may develop with recurrent bouts of acute cholecystitis; (3) 10% of patients with gallstones develop acute cholecystitis
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Signs of cholecystitis
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RUQ tenderness, rebound tenderness in RUQ; Murphy's sign is pathognomonic - inspiratory arrest during deep palpation of the RUQ; not present in many cases; Hypoactive bowel sounds; Low-grade fever, leukocytosis
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Diagnosis of Acute Cholecystitis
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(1) RUQ U/S is diagnosis of choice - shows thickened gallbladder wall, pericholecystic fluid, distended gallbladder, and presence of stone(s); (2) CT scan is accurate but more sensitive in identifying complications of acute cholecystitis (perforation, abscess, pancreatitis); (3) Radionuclide scan [hepatoiminodiacetic acid] HIDA scan used when ultrasound is inconclusive. If HIDA scan is normal, acute cholecystitis can be ruled out. A positive HIDA scan means the gallbladder is not visualized --> diagnosis of acute cholecystitis is confirmed
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Choledocholithiasis
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Refers to gallstones in common bile duct; primary stones originate in the CBD [usually pigmented stones] whereas secondary stones originate in the gallbladder and then pass into the CBD [usually cholesterol or mixed stones]. These account for 95% of all cases
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Diagnosis of choledocholithiasis
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(1) Elevated total and direct bili, alk-phos; (2) RUQ U/S detects on 50% of cases; (3) ERCP is gold standard and should follow U/S. Diagnostic and therapeutic
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Onset of symptoms in choledocholithiasis
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May signal development of life-threatening complications such as cholangitis and acute pancreatitis. Patients with CBD stones may be asymptomatic for years…
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Cholangitis
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Infection of the biliary tract secondary to obstruction, which leads to biliary stasis and bacterial overgrowth; choledocholithiasis accounts for 60% of cases, other causes include pancreatic and biliary neoplasm, post-op strictures, invasive procedures such as ERCP or PTC, and choledochal cysts
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Charcot's Triad
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RUQ pain, jaundice, and fever - present in only 50-70% of patients with cholangitis
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Reynold's Pentad
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Charcot's triad + septic shock and AMS = highly toxic state that requires emergency treatment
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What is RUQ U/S good at detecting?
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Gallstones and biliary tract dilatation; but not very accurate in detecting CBD stones
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Treatment of cholangitis
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(1) IV Antibiotics and IV Fluids; (2) Close monitoring of hemodynamics, BP, and urine output; (3) Once patient is afebrile for 48hrs, ERCP can be performed for evaluation of underlying condition
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What is the most serious and dreaded complication of acute cholangitis?
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Hepatic abscess - it has a high mortality rate!
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Carcinoma of the gallbladder
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(1) Most are adenocarcinomas and typically occur in the elderly; (2) Associated with gallstones in most cases; other risk factors include cholecystenteric fistula and porcelain gallbladder; (3) Prognosis is dismal - more than 90% die of advanced disease within 1 year of diagnosis
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Porcelain gallbladder
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Intramural calcification of gallbladder wall; prophylactic cholecystectomy is recommended because approximately 50% of patients with porcelain gallbladder will eventually develop cancer of gallbladder
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Primary Sclerosing Cholangitis
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(1) Chronic idiopathic progressive disease of intrahepatic and/or extrahepatic bile ducts characterized by thickening of the bile duct walls and narrowing of their lumens; leads to cirrhosis, portal HTN, and liver failure; (2) Strong association with ULCERATIVE COLITIS (less so with Chron's Disease). UC is present in 50-70% of patients with PSC; often the UC may dominate the clinical picture
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Diagnosis of PSC
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ERCP and PTC are diagnostic studies of choice: see multiple areas of bead-like stricturing and bead-like dilatations of intrahepatic and extrahepatic ducts; lab tests show cholestatic LFTs
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Treatment of PSC
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No curative treatment other than liver transplantation; When a dominant stricture causes cholestasis, ERCP with stent placement for biliary drainage and bile duct dilatation may relieve symptoms; use cholestyramine for symptomatic relief (to decrease pruritus)
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Primary Biliary Cirrhosis
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Chronic and progressive cholestatic liver disease characterized by DESTRUCTION of intrahepatic bile ducts with portal inflammation and scarring. Slowly progressive disease with variable course: may progress to cirrhosis and end-stage liver failure; Auto-immune disease that is often associated with other autoimmune disorders; most common in middle-aged women
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Diagnosis of PBC
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(1) Cholestatic LFTs [elevated LFTs]; (2) Positive anti-mitochondrial antibodies (AMAs) in 90-95% of patients. This is the hallmark of disease; if serum Is positive for AMAs, perform a liver biopsy to confirm; (3) Elevated cholesterol, HDL, IgM; (4) Abdominal U/S to rule ouot biliary obstruction
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Treatment of PBC
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(1) Symptomatic for pruritus (cholestyramine) and osteoporosis (calcium, bisphosphonates, vitamin D); (2) Ursodeoxycholic acid (a hydrophilic bile acid) has been shown to slow progression of disease; (3) Liver transplantation is the only curative treatment available
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Cholangiocarcinoma
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Tumor of intrahepatic or extrahepatic bile ducts: most are adenocarcinomas; (2) Mean age of diagnosis is 7th decade; (3) Located in 3 regions: proximal third of CBD [most common, also called Klatskin's tumor], distal extrahepatic [best chance of resectability], and intrahepatic [least common]. (3) Prognosis is dismal - survival is <1yr after diagnosis
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Risk Factors of cholangiocarcinoma
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(1) PSC is major risk factor in USA; (2) Other risk factors include UC, choledochal cysts, and Clonorchis sinesis infestation in Hong Kong
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Klatskin's Tumors
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Tumors in proximal 1/3 of CBD - involve junction of right and left hepatic ducts; very poor prognosis because unresectable
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Carcinoid Tumors
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(1) Carcinoid tumors originate from neuroendocrine cells and secrete serotonin; (2) The most common site for these tumors is the appendix, but they can be found in a variety of locations (small bowel, rectum, bronchus, kidney, pancreas)
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Carcinoid Syndrome
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Develops in 10% of patients with carcinoid tumors. Excess serotonin secretion leads to cutaneous flushing, diarrhea, sweating, wheezing, abdominal pain, and heart valve dysfunction; Risk factors of mets increase with size of tumor; Mets are rare with appendiceal tumors; ileal tumors have the greatest likelihood of malignancy; surgical resection is treatment of choice
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Acute pancreatitis
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(1) Inflammation of pancreas resulting from prematurely activated pancreatic digestive enzymes that invoke pancreatic tissue autodigestion; (2) Most patients have mild-to-moderate disease, but up to 25% have severe disease
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Causes of acute pancreatitis
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(1) EtOH abuse (40%); (2) Gallstones (40%) that pass into bile duct and block ampulla of Vater; (3) Post-ERCP; (4) Viral infections - mumps, coxsackie B; (5) Drugs - sulfonamides, thiazides, furosemide, estrogens, HIV meds; (6) Post-op complications; (7) Pancreas divisum; (8) Hypertriglyceridemia, hypercalcemia
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Signs and Symptoms of acute pancreatitis
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(1) Abdominal pain, usually in epigastric region, radiating to back in 50% of patients; (2) Often steady, dull, and severe; worse when supine and after meals; (2) Low-grade fever, tachy, hypotensive, leukocytosis; (4) Epigastric tenderness, abdominal distention; (5) Decreased or absent bowel sounds indicate partial ileus; (6) Grey Turner's sign [flank ecchymoses], Cullen's sign [periumbilical ecchymoses] and Fox's Sign [Ecchymoses of inguinal ligament]
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Complications of acute pancreatitis
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(1) Sterile pancreatic necrosis - infection may develop, but half of all cases resolve spontaneously; (2) Infected pancreatic necrosis - high mortality rate; surgical debridment and antibiotics indicated; (3) Pancreatic pseudocyst - encapsulated fluid collection 2-3 weeks after an attack, lacks epithelial lining of a true cyst; NOTE: pseudocysts may occur at sites distant from pancreas! If cyst is >5cm, drain percutaneously or surgically
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Ranson's Criteria
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Used to determine prognosis and mortality rate in acute pancreatitis; patients with more than 3 or 4 Ranson's criteria should be monitored in an ICU setting
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Chronic Pancreatitis
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Persistent or continuing inflammation of the pancreas, with fibrotic tissue replacing pancreatic parenchyma and alteration of pancreatic ducts (areas of stricture/dilation); eventually results in irreversible destruction of the pancreas with impairment of endocrine and exocrine functions of pancreas
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Causes of chronic pancreatitis
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(1) Chronic alcoholism is MCC (>80% of cases); (2) Other causes include hereditary pancreatitis, tropical pancreatitis, and idiopathic chronic pancreatitis
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Complications of chronic pancreatitis
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(1) Narcotic addiction - probably the MC complication; (2) DM/impaired glucose tolerance caused by progressive loss of islets of Langerhans, eventually appears in up to 70% of patients; (3) Malabsorption/steatorrhea 2/2 pancreatic exocrine insufficiency - occurs when pancreatic enzyme secretion decreases significantly; (4) Pseudocyst formation; (6) Common Bile Duct obstruction
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Treatment of chronic pancreatitis
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(1) Narcotics; (2) NPO/bowel rest; (3) Pancreatic Enzymes + H2 blockers that will inhibit CCK release and gastric acid secretion; (4) insulin if needed; (5) Alcohol abstinence; (6) Frequent, small-volume, low-fat meals - may improve abdominal pain
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Pancreatic Cancer
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(1) Most common in elderly patients, with 75% >60 years old; rare before afe 40, more common in African Americans; (2) 75% are located at the pancreatic head, 20% in the body, and just 5-10% in the pancreatic tail; (3) SMOKING is the most clearly established risk - but also seen with chronic pancreatitis, diabetes, heavy EtOH use, and exposure to benzidine and beta-nephthylamine. Prognosis is dismal - most patients die within a few months of diagnosis
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Clinical features of pancreatic cancer
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(1) Abdominal pain - 90% of patients, may be a vague and dull ache; (2) Jaundice - most common with carcinoma of head of pancreas, less than 10% of patients with cancer involving body and tail of pancreas have jaundice - indicates obstruction of intrapancreatic CBD and is a sign of advanced disease; (3) Weight loss; (4) Recent onset of glucose intolerance; (5) Depression, weakness, fatigue; (6) Migratory thrombophlebitis - develops in 10% of cases; (7) Courvoisier's sign (palpable gallbladder) is present in 30% of patients with cancer involving head of pancreas; presents without pain
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Diagnosis of pancreatic cancer
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(1) ERCP is the most sensitive test for diagnosing pancreatic cancer; it can also distinguish cancer of the head of the pancreas from tumors of CBD, duodenum, ampulla, and lymphomas; (2) CT is preferred test for diagnosis and assessment of disease spread; (3) Tumor markers: CA 19-9 and CEA
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Treatment of pancreatic cancer
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(1) Surgical resection - Whipple's is the only hope for a cure; however, only a minority of tumors are resectable (roughly 10%). The prognosis is grim even after resection, with a 5-yr survival rate of 10%; If a tumor is unresectable and biliary obstruction is present, perform PTC or ERCP with stent placement across the obstruction for palliation
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Aortoenteric fistula
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Rare but lethal cause of GI bleeding. Classic presentation is a patient with a history of aortic graft surgery who has a small GI bleed involving the duodenum before massive, fatal hemorrhage hours to weeks later. Perform endoscopy or surgery during this small window of opportunity to prevent death
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Two most common causes of upper GI bleeding
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(1) PUD - duodenal ulcer, gastric ulcer, gastritis; (2) Esophageal varices
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Two most common causes of lower GI bleeding
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(1) Diverticulosis - most common source of GI bleeding in patients under age 60 - usually painless; (2) Angiodysplasia - most common source in patients over age 60
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Hematemesis
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Vomiting blood; suggests upper GI bleeding. 'Coffee grounds' emesis suggests upper GI bleedign as well as a lower rate of bleeding (enough time for vomitus to transform into 'coffee grounds'
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Melena
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Black, tarry, liquid, foul-smelling stool caused by degradation of hemoglobin by bacteria in the colon; presence of melena indicates that blood has remained in GI tract for several hours; the further the bleeding site is from the rectum, the more likely melena will occur. Suggests upper GI bleeding (esophagus, stomach, or duodenum). Occasionally the jejunum or ileum is the source; it is rare for melena to be caused by a colonic lesion, but if it is, the ascending colon is the most likely site
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Other causes of dark stools
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(1) Bismuth; (2) Iron; (3) Spinach; (4) Charcoal; (5) Licorice
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Hematochezia
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Bright red blood per rectum; usually a lower GI source (typically left colon or rectum); consider diverticulosis, AVM, hemorrhoids, and colon cancers. However, it could also be from an upper GI source that is bleeding very briskly so that blood does not remain in colon to turn into melena. This often indicates heavy bleeding, and patient often has some degree of hemodynamic instability. An upper GI source is present in about 5% to 10% of patients with hematochezia
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Esophageal Cancer
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(1) Squamous cell - occurs in African Americans; risk factors are EtOH and tobacco use; (2) Adenocarcinoma, most common in caucasians and men (5:1 over women); most common in distal third of esophagus/gastroesophageal junction (in 80% of cases). Risk factors: GERD and Barrett's esophagus
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Achalasia
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(1) Acquired motor disorder of esophageal smooth muscle in which the lower esophageal sphincter fails to completely relax with swallowing, and abnormal peristalsis of esophageal body replaces normal peristalsis of esophageal body
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Causes of achalasia
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(1) Majority in US are idiopathic; (2) Adenocarcinoma of proximal stomach is second MCC; (3) Worldwide, Chagas' disease is an important cause
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Achalais and Cancer
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7x increased risk in patients with achalasia of developing esophageal cancer (usually squamous cell) - occurs in 10% of patients 15-25 years after the initial achalasia diagnosis
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Diagnosis of achalasia
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(1) Barium swallow - 'bird's beak' like narrowing of distal esophagus and large, dilated esophagus proximal to the narrowing; (2) Upper GI endoscopy to rule out secondary causes of achalasia (gastric carcinoma) and retention esophagitis or esophageal cancer; (3) Manometry - to confirm diagnosis; reveals failure of LES relaxation and aperistalsis of esophageal body
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Diffuse Esophageal Spasm
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(1) Nonperistaltic spontaneous contraction of the esophageal body - several segments of the esophagus contract simultaneously and prevent appropriate advancement of food bolus; (2) In contrast to achalasia, sphincter function is normal (normal LES pressure)
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Clinical Features of DES
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(1) Noncardiac chest pain that mimics angina and may radiate to the jaw, arms, and back; (2) Dysphagia is common; however, regurgitation of food is uncommon
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Diagnosis of DES
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(1) Esophageal manometry is diagnostic - simultaneous, multiphasic, repetitive contractions that occur after a swallow; sphincter response is normal; (2) Upper GI barium swallow ('corkscrew esophagus') in 50%, which represents multiple simultaneous contractions
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Treatment of DES
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Nitrates and CCBs help to decrease amplitude of contractions; tricyclic antidepressants may provide symptomatic relief
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Sliding vs Paraesophageal Hiatal Hernias
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(1) Sliding hiatal hernias account for >90% of cases. Both the gastroesophageal junction and a portion of the stomach herniate into the thorax throgh the esophageal hiatus in a sliding hiatal hernia. Associated with GERD; (2) Paraesophageal hiatal hernias account for <5% of cases; occurs when stomach herniates into thorax through the esophageal hiatus, but the gastroesophageal junction does not - it remains below the diaphragm. This uncommon hernia can become strangulated and should be repaired surgically
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Mallory-Weiss S yndrome
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(1) Mucosal tear at (or just below) the GE junction as a result of forceful vomiting or retching usually occurs after repeated episodes of vomiting, but it may occur after one episode; (2) Most commonly associated with binge drinking in alcoholics, but any disorder that causes vomiting can induce the mucosal tear; (3) Hematemesis is always present - varies from streaks of blood in vomitus to massive bright red blood; (4) Upper endoscopy is diagnostic; (5) Rx: surgery - oversewing tear or angiographic embolization if bleeding continues, but this rarely is necessary. Acid suppression is used to promote healing
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Mallory-Weiss vs Boerhaave's
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If tear is mucosal and at the GE junction, it is referred to as Mallory-Weiss; if tear is transmural and causes esophageal perforation, it is referred to as Boerhaave's Syndrome
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Plummer-Vinson Syndrome
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Upper Esophageal Webs that cause dysphagia 2/2 iron deficiency anemia; Also see koilonychia (spoon-shaped fingernails) and atrophic oral mucosa; 10% of patients develop SCC of oral cavity, hypopharynx, or esophagus, therefore it is considered a premalignant lesion
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Schatzki's Ring (Distal Esophageal Webs)
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(1) Circumferential ring in lower esophageus always accompanied by sliding hiatal hernia; (2) Usually asymptomatic, but mild to moderate dysphagia may be present; (3) Usually due to ingestion of alkali, acids, bleach, or detergents in suicide attempts
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Zenker's diverticulum
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Found in upper 1/3 of esophagus; failure of cricopharyngeal muscle to relax during swallowing leads to increased intraluminal pressure that causes outpouching of mucosa through an area of weakness in pharyngeal constrictions; (2) Clinical features include dysphagia, regurgitation, halitosis, weight loss, and chronic cough
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Traction diverticula
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Located in midpoint of esophagus near the tracheal bifurcation. It is due to traction from contiguous mediastinal inflammation and adenoathy (pulmonary TB). TB causes hilar node scarring, which causes retraction of esophagus. It is usually asymptomatic and does not require treatment
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Epiphrenic diverticula
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Found in lower 1/3 of esophagus; usually associated with spastic esophageal dysmotility or achalasia. Symptoms of dysphagia are more often relatd to the underlying motility disorder, unless diverticulum is very large
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What is the cause of both proximal (Zenker's) and distal (epiphrenic) diverticula?
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An underlying motility disorder; surgical treatment is aimed at correcting the motility disorder (i.e., myotomy). Diverticultomy is of secondary importance
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Esophageal Perforation
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(1) Etiology: blunt trauma, medical tubes and instruments, forceful vomiting (Boerhaave's syndrome) that is associated with alcoholic binges and bulimia; (2) Clinica features: pain, tachycardia, hypotension, tachypnea, dyspnea, fever, Hamman's sign ('mediastinal crunch') produced by heart beating against air-filled tissues, pneumothorax, or pleural effusion; (3) Contrast esophagram is definitive diagnostic study; (4) CXR shows air in mediastinum
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Time interval between esophageal perf and surgery
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MOST IMPORTANT FACTOR in determining survival; if delayed beyond 2h, mortality rate and likelihood of fistulization increase
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Peptic Ulcer Disease
|
(1) H. pylori; (2) NSAID use; (3) Acid hypersecretion - Zollinger-Ellison
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Acute gastritis
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Inflammation of gastric mucosa - multiple causes: (1) NSAIDs; (2) H. pylori; (3) EtOH; (4) smoking; (5) caffeine
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Chronic gastritis
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H. pylori is the MCC - over 80% of cases! Autoimmune gastritis leads to chronic atrophic gastritis with serum antiparietal and anti-intrinsic factor antibodies and development of pernicious anemia!
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Gastric Cancer
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(1) Majority are adenocarcinomas; (2) Rare in US, most common in Japan. Lesions: (1) ulcerative carcinoma - ulcer through all layers; (2) polypoid carcinoma - solid mass projects into stomach lumen; (3) superficial spreading - most favorable prognosis; (4) Linitis plastica - 'leather bottle' infiltrates early through all layers, stomach wall is thick and rigid, poor prognosis
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Krukenberg's Tumor
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Metastasis to the ovary of gastric carcinoma
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Blumer's shelf
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Metastasis to the rectum (pelvic cul-de-sac) [can palpate on rectal examination]
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Sister Mary Joseph's node
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Metastasis of gastric carcinoma to periumbilical lymph ode
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Virchow's node
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Metastasis to the supraclavicular fossa nodes
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Irish's node
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Metastasis to the left axillary adenopathy
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Gastric Lymphoma
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A type of non-Hodgkin's lymphoma that arises in the stomach; clinical features are similar to those of adenocarcinoma of the stomach (e.g. abd pain, wt loss, anorexia); EGD with biopsy is standard for dx (same as adenocarcinoma of stomach)
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Small Bowel Obstruction
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Dehydration is a key event in SBO. Intestinal distention causes reflex vomiting, increased intestinal secretion proximal to the point of obstruction, and decreased absorption. This leads to hypochloremia, hypokalemia, and metabolic alkalosis; The resulting hypovolemia leads to systemic findings such as tachycardia, hypotension, tachypnea, altered mental status, and oliguria
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Causes of SBO
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(1) Adhesions from previous abdominal surgery - MCC in adults; (2) Incarcerated hernias - second MCC; (3) Malignancy, intussusception, Crohn's disease, carcinomatosis, and SMA syndrome
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Proximal vs Distal SBO
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Proximal: frequent vomiting, severe pain, minimal abdominal distention. Distal: less frequent vomiting, and significant abdominal distention
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Large Bowel Obstruction
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Causes: volvulus, adhesions, hernias, colon cancer (MCC); Results in less fluid and electrolyte disorder than SBO
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Clinical Features of SBO
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(1) Cramping abdominal pain - if pain is continuous and severe, strangulation may be present; (2) Nausea, vomiting - may be feculent; (3) Obstipation (absence of stool and flatus); (4) Abdominal distention
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Diagnosis of SBO
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(1) Abdominal plain films - dilated loops of small bowel, air-fluid levels proximal to point of obstruction, and minimal gas in colon; (2) Barium enema - to rule out colonic obstruction if plain films do not distinguish small fromlarge bowel obstruction; barium enema identifies site of obstruction; (3) Upper GI series - with small bowel follow-through if above are not diagnostic
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Treatment of SBO
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(1) IV fluids to establish adequate urine output; add K+ to fluids to correct hypokalemia; (2) NG tube to empty stomach (gastric decompression; (3) Antibiotics; (4) Surgery indicated for complete obstruction, partial obstruction that is persistent and/or associated with constant pain, or if strangulation is suspected. Perform exploratory laparatomy with lysis of adhesions and resection of any necrotic bowel
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Paralytic ileus
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Peristalsis is decreased or absent (no mechanical obstruction present); Causes include medications (narcotics and anti-cholinergics), post-op state s/p abdominal surgery, spinal cord injury, metabolic disorders, (esp. hypokalemia), and peritonitis; Abdominal plain films show a uniform distribution of gas in the small bowel, colon, and rectum (in contrast to small bowel or colonic obstruction); Failure to pass contrast medium beyond a fixed point is diagnostic; TREATMENT: IV fluids, NPO, correction of electrolyte imbalances (esp. hykokalemia), NG suction, and placement of a long tube if ileus persists postop
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Celiac Sprue
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(1) Hypersensitivity to gluten resulting in weight loss, abdominal distention, bloating, and diarrhea; (2) Biopsy of small bowel reveals flattening of villi, which causes malabsorption; (3) Strict adherence to a gluten-free diet is essential.
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Serology with Celiac Sprue
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(1) Anti-endomysial antibodies and (2) Tissue-transglutaminase antibodies
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Crohn's Disease: Definition
|
Disease of unknown etiology characterized by chronic transmural inflammation with granulomas and with a predilection for involvement of the terminal ileum.
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Crohn's or UC: Discontinuous with skip areas of intervening normal bowel
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Crohn's Disease
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Crohn's or UC: Transmural inflammation with involvemnt of mesentery and regional lymph nodes
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Crohn's Disease
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|
Crohn's or UC: May involve the intestinal tract from the mouth to the anus
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Crohn's Disease
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Crohn's Disease: Clinical features
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(1) Diarrhea of a moderate degree (4-5 BM daily), (2) pain, often a steady mild right lower quadrant discomfort, occasionally with superimposed colic, and (3) fever, usually below 102F orally. The course is variable but in general is that of gradual deterioration, with shorter and shorter asymptomatic intervals. The patient may complain of fatigue and difficulty in maintaining body weight. Anemia is common.
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Crohn's Disease: Complications
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Small bowel obstruction and fistula formation are the most common complications. Fistula may form between bowel and adjacent structures, such as skin, vagina, bladder, etc. Spontaneous free perforation and gross bleeding are less frequent.
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Crohn's Disease: Radiographic findings
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Cobblestone appearance to complete loss of the mucosal pattern with a rigid pipe-like appearance.
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Crohn's Disease: Pharmacotherapy
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The drugs used include 5-amino salicylates (e.g., Azulfidine), corticosteroids, 6-mercaptopurine, cyclosporine, antibiotics such as metronidazole, and newer immune modulators.
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Crohn's Disease: Surgical options
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Surgery is best reserved for complications because it can not cure the disease.
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Crohn's Disease: Systemic complications
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Systemic complications are common and include arthritis, iritis, erythema nodosum, clubbing, liver disease, gallstones, kidney stones, amyloid, malabsorption.
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Ulcerative Colitis: Definition
|
Chronic mucosal inflammatory disease of unknown etiology. The disease primarily affects children and young adults and the course is one of exacerbation and remissions. For practical purposes, the rectum is always involved and the process may extend proximal to involve the left colon or entire colon (universal disease). The mucosa of the terminal ileum may also be involved (back wash ileitis).
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Crohn's or UC: Inflammatory process confined to mucosa and submucosa
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Ulcerative colitis
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Crohn's or UC: Microscopic ulcerations
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Ulcerative colitis
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|
Crohn's or UC: Visual inspection may reveal a granular, friable mucosa, or large areas denuded of mucosa (ulcerated) with remaining areas of inflamed mucosa with undermined edges (pseudopolyps)
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Ulcerative colitis
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Crohn's or UC: Crypt abscesses with predominantly PMNs
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Ulcerative colitis
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|
Crohn's or UC: The sigmoidoscopic finding of mucosal friability is one of the most important diagnostic features
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Ulcerative colitis
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|
Crohn's or UC: Bowel involved in a continuous ring beginning in rectum, extending upward for a variable distance
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Ulcerative colitis
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Mild Ulcerative Colitis: Clinical Features
|
60% of cases. Disease limited to distal colon, severe diarrhea and bleeding are absent, no systemic symptoms. Hospitalization is rare, prognosis is good
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Moderate Ulcerative Colitis: Clinical Features
|
25% of cases. Diarrhea, 4-5 stools/day with cramps and low grade fever. Mild-moderate bleeding. Hospitalization for many, with a dramatic response to steroids. Prognosis is poor, and most require surgery
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Severe Ulcerative Colitis: Clinical Features
|
15% fo cases. 'Fulminant' with sudden onset of symptoms, constant diarrhea and bleeding with high fever. Patient is dangerously ill, dehydrated, weak, febrile. Abdominal tenderness, labs reveal anemia and hypoalbuminemia. Prognosis is very poor, and most require emergency or early surgery
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Treatment of UC
|
Azulfidine (5-ASA), Steroids [short-term benefit, use dependent on clinical status of patient].
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Surgical indications for total colectomy in UC
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(1) Complications that are immediately life threatening, such as colon perforation or cancer; (2) because of the grave clinical condition of the patient such as uncontrolled bleeding, toxic megacolon lasting 96 hours, or severe disease not remitting within 2 weeks on therapy; (3) conditions of no immediate threat to life such as severe morbidity, effects of steroids, growth retardation, severe systemic complications.
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Complications of UC
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Local - hemorrhoids 20%, pseudopolyps 15%, anal fissures 12%, recto-vaginal fistula 0.2%. Major - megacolon, perforation, massive hemorrhage, stricture, carcinoma. Systemic complications are many and may affect the liver, joints, eyes, skin, blood etc.
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Extraintestinal manifestations of IBD
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(1) Eye lesions- episcleritis, anterior uveitis; (2) Skin lesions - erythema nodosum - esp in Crohn's, pyoderma gangrenosum - esp in UC; (3) Arthritis - most common extraintestinal manifestation of IBD: migratory monoarticular arthritis, ankylosing spondylitis, sacroiliitis; (4) Thromboembolic-hypercoagulable sate - can lead to DVT, CVA, PE; (5) Primary Sclerosing Cholangitis in UC
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